Datasets:

zhengyun21

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PMC-Patients

like 107

3952284-1

noncomm/PMC003xxxxxx/PMC3952284.xml

Live Birth Following a Term Pregnancy in a Non-communicating Rudimentary Horn of a Unicornuate Uterus

Mrs. J.O. was a 32-year old secondigravida who had one previous vaginal delivery of a set of twins. She booked for antenatal care in the index pregnancy at a Catholic Mission Hospital in Cross River State Nigeria at a gestational age of 28+2 weeks. Prior to booking however, the pregnancy had been complicated by intermittent vaginal bleeding, abdominal pain and anemia for which she received care in several private hospitals from the 10th week of gestation to about the 24th week of gestation when the bleeding ceased spontaneously. Ultrasound scans performed in the course of her evaluation for the bleeding revealed different findings from the absence of intra-uterine gestational sac to single intrauterine gestation of compatible gestational age. One scan suggested hemoperitoneum and the possibility of a heterotopic pregnancy. All scans were performed outside the mission hospital.\nAt booking, she had no complaints. General physical examination was normal and the uterine fundal height was compatible with her gestational age with an indeterminate fetal lie. Fetal heart tones were normal. Her packed cell volume was 30.9 L/L and other routine investigations were normal. During her antenatal care subsequently, she only complained of occasional non-specific generalized abdominal discomfort.\nShe had an elective cesarean section at 37 weeks gestation for a persistent oblique breech presentation and a “low lying placenta.” The abdominal cavity was entered through a Pfannenstiel incision. The baby was delivered through a low transverse uterine incision. Difficulty with delivery of the placenta resulted in heavy bleeding and prompted exteriorization of the uterus with the placenta. This revealed a morbidly adherent placenta in a non-communicating compartment in the left uterine cornu. The compartment was continuous with the left fallopian [Figures and ]. Further hemorrhage was controlled by the application of a size 18 G Foley's catheter as a tourniquet at the level of the uterine isthmus such that both uterine arteries and the right infundibulopelvic ligament were compressed. Following this, the rudimentary horn, placenta and membranes were resected en-bloc with the left fallopian tube while preserving the left ovary. The uterine wall was repaired in two layers with No. 1 chromicised catgut. Two units of cross-matched and screened whole blood were transfused intra-operatively. The baby was female and weighed 2.2 kg. She had no obvious anomaly. Post-operative packed cell volume was 30.3 L/L. Mother and baby were discharged on the 6th post-operative day. Post-natal clinic visit at 6 weeks was unremarkable. Histology of the excised tissue showed “oedematous thin smooth muscle layer enclosing dense eosinophilic areas containing a mixture of blood clots, decidual cells and few chorionic villi. Tubal epithelium also appeared oedematous.”

[[32.0, 'year']]

F

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{'6710493-1': 1}

3952285-1

noncomm/PMC003xxxxxx/PMC3952285.xml

Primary Labial Tuberculosis: A Rare Presentation

A 24-year-old male presented with a 15 days history of persistent swelling of upper lip that ulcerated 2 days ago. He denied any history of trauma, fever, cough, weight loss, and drug or tobacco usage and his past medical and dental history was non-contributory. The patient was thin built with normal vital signs. There was no lymphadenopathy. A diffuse, non-tender swelling of lower lip with mild eversion of the lip was present []. A reddish pink granular lesion involving the vermillion border, labial mucosa, floor of the mouth, and the mandibular anterior gingiva was seen. The lesion had patchy areas of brown crustation, bleeding and purulent discharge []. A provisional diagnosis of Chelitis granulomatosis was made with a differential diagnosis of Baelz disease, tuberculous granulomatosis, sarcoidosis, a deep mycosis, primary syphilis, leishmaniasis, Squamous cell carcinoma, and non-Hodgkin's lymphoma. Plain chest radiograph and complete hemogram were within normal range. Serologies for syphilis and Leishmania, Mantoux test, and Enzyme-linked immunosorbent assay (ELISA) for HIV gave a negative result. An incisional biopsy from the lesion was undertaken that revealed numerous necrotizing epitheloid granulomas with Langhans type giant cells. Ziehl-Neelsen staining showed multiple rods like acid fast bacilli, confirming the diagnosis of primary labial tuberculosis [Figures and ]. The patient was started on anti-Koch's therapy in consultation with the physician with culture report awaited. Culture report obtained after 6 weeks confirmed mycobacterium tuberculous infection. Anti-Koch's therapy administered in this case consisted of four drug regimen, that is, rifampicin, isoniazide, ethambutol, and pyrazinamide for 6 months. The patient was regularly followed-up for next 6 months. The lesions regressed significantly within 15 days of beginning of the therapy and healed completely within 2 months [].

[[24.0, 'year']]

M

{'15641968': 1, '11601825': 1, '20486998': 1, '8705586': 1, '10673784': 1, '16037775': 1, '27795773': 1, '15996739': 1, '7595805': 1, '11352389': 1, '21493882': 1, '24669346': 2}

{}

3952286-1

noncomm/PMC003xxxxxx/PMC3952286.xml

A Type-II First Branchial Cleft Anomaly Presenting as a Post-Auricular Salivary Fistula: A Rare Presentation

A 12-year-old female presented to Otolaryngology Department of our hospital with a history of intermittent watery discharge at the time of meals from an opening behind her right ear for last 3 years. It began with a swelling behind the ear with intermittent pus discharge from the right ear. After some days, the post-auricular swelling spontaneously ruptured with pus discharge. The same site was then marked by a persistent small opening in the skin which discharged clear fluid intermittently, more at the time of meals. The ear discharge stopped, once the discharge began from the post-auricular region. There was no history of purulent discharge from the opening. She denied any history of trauma, hearing loss or any other swelling. On examination, there was a small cutaneous opening near mastoid tip behind the ear lobule, which discharged clear fluid (saliva) on pressing the parotid gland []. External auditory canal and tympanic membrane were normal. Audiological tests were normal.\nComputed tomography (CT) sialography carried out after cannulation of right Stensen's duct and injection of radio-opaque contrast revealed a fistulous tract connecting the sub segmental duct of the parotid gland extending along the pre-tragus region in subcutaneous plane up to mastoid tip after passing inferior to external auditory canal [Figure and ].\nThe patient underwent superficial parotidectomy through an S-shaped incision with excision of the tract. The tract was superficial to the branches of the facial nerve and ended into the parotid gland []. The facial nerve branches were completely visualized and preserved. Histopathology revealed sinus tract comprising of ectodermal components and acini of the parotid gland [].

[[12.0, 'year']]

F

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{}

3952287-1

noncomm/PMC003xxxxxx/PMC3952287.xml

Systemic Lupus Erythematosus Presenting as Acute Adrenal Insufficiency: A Rare Clinical Presentation

A 20-year-old female unmarried regularly menstruating presented to us with a history of anorexia, progressive darkening of the face and hands for the last 3 months and 4 days history of fever and vomiting. Patient also gave a history of periorbital puffiness and multiple joint pains for the last 2 months.\nOn examination, patient had pallor, puffiness of face, hyperpigmentation over face, nose and lips []. Vital examination revealed pulse rate of 90 beats/min and blood pressure of 90/60 mm Hg supine and 80/50 mm Hg standing. Rest of the general and systemic examination was unremarkable. Investigations revealed hemoglobin of 9.3 g/dl, Leukocyte count of 2200/mm3, Platelet count of 60,000/mm3. Kidney function tests, Liver function tests, serum calcium, and electrolytes were normal. Spot urine examination revealed pus cells of 2-3/high power field, no red blood cells and casts and albumin was ++. Chest X-ray showed right mid and lower zone infiltrates., 24 h urine examination showed 1.2 g of protein per day. Blood and urine cultures were sterile.\nPatient was put on intravenous fluids and antibiotics were started empirically. Bone marrow examination performed in view of pancytopenia revealed hypercellular marrow with megaloblastoid and erythoid maturation with adequate iron stores. Antinuclear antibodies and antidouble stranded deoxyribonucleic acid (DNA) antibodies were positive. Patient was labeled as a case of SLE and renal biopsy was carried out in view of proteinuria. Histopathological examination of the biopsy tissue showed features consistent with focal lupus nephritis, International Society of Nephrology/Renal Pathology Society (ISN/RPS) class III, National Institute of Health (NIH) activity score of 9/24 and chronicity 3/12 []. Immunofluorescence showed immune deposit pattern suggestive of SLE. Echocardiography was normal. Patient continued to be in hypotension even on inotropic support and her clinical condition remained same. Based on clinical parameters, adrenal insufficiency was suspected. After taking 8 am sample for cortisol, patient was started on steroids. Serum antiadrenal antibody test showed results as 3 U/ml (normal range < 1 U/ml). Patient showed dramatic improvement in clinical parameters and hemodynamics. Morning cortisol levels were 7.5 μg/dl (normal range > 15 μg/dl). A short synecthen test (SST) using 250 mcg synecthen carried out after stopping steroids showed 30 min value of 10 μg/dl and 60 min value of 12 μg/dl. Computed tomographic scan of the abdomen was normal. Thyroid function test was normal. Antithyroid peroxidase antibody levels were normal.\nPatient was managed as a case of SLE with lupus nephritis with adrenal insufficiency and was discharged on steroids and hydroxychloroquine in a satisfactory clinical condition.

[[20.0, 'year']]

F

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{'4223953-1': 1, '8323633-1': 1}

3952288-1

noncomm/PMC003xxxxxx/PMC3952288.xml

Hydroxycut-induced Liver Toxicity

A 27-year-old man with no significant past medical history presented as a referral from a community hospital for evaluation of hepatitis, initially diagnosed as choledocholithiasis. The patient complained of fever, chills, and abdominal pain (achy in the Right Upper Quadrant and epigastrium) for the past 2 weeks, nausea, and vomiting of clear liquids without blood for a 1 week, and jaundice for 2 days. Records from referring facility indicated that patient had MRCP-Magnetic Resonant Cholangio Pancreatography that demonstrated cholelithiasis, but it did not show any signs of cholecystitis. An abdominal ultrasound revealed sludge and gallstones in the gallbladder.\nFurther questioning revealed that patient had been studying to be a physical trainer at a local college. He exercised vigorously at least 3 times/week. Patient stated that he was “prescribed” a set of supplements (Hydroxycut, Black powder, mitotropin, xenadrine, arson, and L-glutamine powder 23) by his local nutrition center.\nAfter admission in the hospital, hepatology consult was called. When patient was admitted, liver enzymes panel showed: AST-Aspartate Aminotransferase: 3800 U/L, ALT-Alanine aminotransferase: 5100 U/L, total bilirubin: 14.7 mg/dl, direct bilirubin: 10.0 mg/dl and alkaline phosphatase: 99 mg/dl, all correlated with the degree of jaundice seen. Additional tests included a urine toxicology screen, immunological studies for liver (anti-nuclear antibodies, anti-smooth muscle antibodies, and anti A liver/kidney microsomal antibodies), serum acetaminophen level, serum ceruloplasmin level, and genetic tests for hemochromatosis; all of them were negative. Liver biopsy showed signs of acute liver failure.\nHematoxylin and eosin stain of the liver biopsy specimen is shown in Figures and . shows extensive patchy areas of necrosis as in acute fulminant hepatitis with sparing of biliary tract. shows lymphocytic infiltration of the portal tracts and lobular parenchyma.\nPatient was asymptomatic during the hospital stay and was planned to discharge with trending down of liver enzymes by discontinuation of Hydroxycut and conservative management. The patient was advised to follow-up with Hepatology. On follow-up visit after 2 weeks of discharge, Labs: AST: 669 U/L, ALT: 1965 U/L, Total Bilirubin: 4.5 mg/dl, Alkaline phosphatase: 128 mg/dl, PT: 1.1.

[[27.0, 'year']]

M

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{'5867608-1': 1, '5143754-1': 1, '7057255-1': 1}

3952309-1

noncomm/PMC003xxxxxx/PMC3952309.xml

Refractory Status Epilepticus Spontaneously Resolved by Parturition

The patient was a 27-year-old primigravida who was diagnosed as epilepsy with cortical dysplasia 21 years before. Her previous seizures were reasonably controlled by topiramate, carbamazepine, and pregabalin. At 23 weeks of pregnancy, her seizure frequency progressively increased. She came to the ER in a confused mental state with intermittent convulsive movements in her arm that lasted for a few hours. On neurological examination, her mental status was stuporous, but there were no focal neurological deficits. Initial electroencephalography (EEG) revealed very frequent and sharp medium- to high-voltage waves in the left fronto-centro-parietal area that built up repetitive high-voltage, generalized sharp, and wave complexes for 10 to 20 sec, which suggested SE. These ictal rhythms were correlated with initial head and eyeball deviation that was secondary to generalized tonic-clonic seizures. Between the seizures, consciousness was not regained. Except for the pregnancy, there were neither precipitating factors nor laboratory abnormalities.\nShe was admitted to the ICU, and she was managed with a continuous infusion of intravenous midazolam under continuous EEG (c-EEG) monitoring. On the EEG, very frequent sharp waves with repetitive ictal rhythms appeared in the left centro-parieto-occipital area. Midazolam was titrated up to 5.5 mg/kg/h, but the ictal rhythms with clinical seizures were not successfully controlled. On the fifth hospital day (HD 5), midazolam was dosed up to 17 mg/kg/h, her blood pressure was reduced to 80/50, but the repeated seizures were not controlled. We added 3,000 mg of levetiracetam per day. Midazolam was tapered slowly from HD 10 to HD 16, and then her mental state and EEG findings were improved except for an occasional brief seizure. On HD 32, she was transferred to the ward with c-EEG monitoring. However, three days later, very frequent generalized seizures occurred again. Phenytoin, phenobarbital, and pentobarbital were sequentially loaded for a few days with intervals, but SE continued.\nOn HD 43, at 29 weeks of pregnancy, a cesarean section was performed. After the parturition, the EEG gradually improved. The EEG performed the day after parturition showed only intermittent median voltage sharp waves in the left centro-parietal area. Her mentality gradually improved, and accordingly, previous anti-SE drugs were gradually tapered out. She was discharged with an alert mental status, and the discharge medications were topiramate (300 mg), pregabalin (450 mg), levetiracetam (3,000 mg), and phenobarbital (180 mg). Her baby was raised in the newborn section because of premature and low birth weight. However, he did not show any other neonatal problems.

[[27.0, 'year']]

F

{'18479400': 1, '14692912': 1, '18158256': 1, '18840393': 1, '4054760': 1, '17996636': 1, '19398682': 1, '24649442': 2}

{}

3952310-1

noncomm/PMC003xxxxxx/PMC3952310.xml

Encephalitis Associated with Acute Hepatitis A

A 27-year-old man visited our hospital because of a sudden-onset generalized convulsion. He had been overworking and had slept less than 5 hours a day for the previous month. A week prior to the hospital visit, the patient had developed a fever and generalized myalgia but had not taken any medicine. High fever, anorexia, and generalized malaise appeared. On the day of the hospital visit, he could not be awakened, and he showed no responses to any stimulus. Finally, he developed a generalized tonic-clonic seizure that lasted for about three min and that was accompanied by cyanosis, upward eyeball deviation, and tongue biting.\nOn physical examination at the emergency department, the patient’s body temperature rose up to 38.7°C. He did not show jaundice, hepatosplenomegaly, nor ascites. He was confused and could not follow the examiner’s verbal commands appropriately, and he often attempted to run out of the bed while yelling incomprehensible words and abuses. Neck stiffness was found on neurologic examination. Positive or negative myoclonic jerk was not observed.\nBrain computed tomography and magnetic resonance imaging showed no abnormalities. Diffuse slowing without epileptiform discharges was observed on electroencephalography (EEG) recordings. The cerebrospinal fluid (CSF) was clear, and its pressure was measured at 16.0 cmH2O, with 20 leukocytes/μL (95% lymphocytes), protein levels of 70.5 mg/dL, and normal glucose levels (63.0 mg/dL). Blood tests showed that white blood cell counts were increased to 17,230 cells/μL. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ-glutamyl transpeptidase levels were increased to 441, 1294, and 460 IU/L, respectively. Total bilirubin and direct bilirubin levels were normal (0.6 mg/dL and 0.2 mg/dL, respectively). Creatine phosphokinase levels were elevated up to 14,500 IU/L. Serum ammonia levels were normal (24 μg/dL).\nSeizure did not relapse after 30 min of continuous infusion of 15 mg/kg of phenytoin mixed with normal saline. He regained consciousness on the second admission day and became fully conscious the following day. Intravenous acyclovir was given for two days because of the clinical suspicion of herpes encephalitis, which was discontinued after observing the clinical improvement and the detection of the IgM antibody of HAV. The patient’s score on the Korean version of the mini-Mental Status examination (K-MMSE) score was 30 on the fifth admission day. Serum and CSF IgM antibodies of herpes simplex type 1, 2, and varicella zoster were negative. Polymerase chain reaction (PCR) of the CSF for HAV and enterovirus were also negative. AST and ALT levels decreased to 125 and 432 IU/L on the seventh admission day. He was discharged without any sequela. During the year after discharge, he had been seizure-free with normal EEG recordings.

[[27.0, 'year']]

M

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3952312-1

noncomm/PMC003xxxxxx/PMC3952312.xml

Two Patients Diagnosed with Juvenile Myoclonic Epilepsy by First-Ever Status Epilepticus in Adult Life

A 52-year-old woman presented with generalized tonic-clonic seizure (GTCS) at the first seizure attack. In general, she was healthy, and only suffered from mild headache in the past few months.\nDuring the night before visiting the ER, she showed inappropriate behavior, confusion, and disorientation. A few hours later, she showed GTCS lasting for 1–2 minutes, and then, remained in a mild confusion state in the ER. There were no abnormal findings on the brain MRI and in the CSF analysis.\nDuring the confusion state, on the EEG, there were repetitive, high voltage generalized polyspikes and waves with flat periods () which subsided after intravenous injection of lorazepam. Detailed history taking revealed previous occasional absence-like episodes and myoclonic jerks. The patient’s younger sister also suffered from epilepsy since childhood.\nThe epileptic discharges were all abolished on the follow-up EEG.\nThe patient was diagnosed as JME and there has been no recurrence of seizures with sodium valproate medication.

[[52.0, 'year']]

F

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{'3952312-2': 2}

3952312-2

noncomm/PMC003xxxxxx/PMC3952312.xml

Two Patients Diagnosed with Juvenile Myoclonic Epilepsy by First-Ever Status Epilepticus in Adult Life

A woman, aged 39 visited the ER with transient loss of consciousness (LOC). W Anamnesis showed that, when she was 27 years old, during excessive working at night, she experienced one episode of LOC without convulsions.\nBoth the brain MRI scan and the EEG performed at that time were normal. Recently, she felt exhausted because of her night job. In the ER, she was alert and could follow all commands, but showed mild confusion. Focal neurological signs were not observed, and brain imaging was normal. Generalized polyspikes and slow waves repetitively occurred on the EEG ().\nThe pathologic waves disappeared after IV injection of lorazepam.\nThe EEG recorded on the following day showed normal background activity and decreased slow wave activity.\nWith careful history taking, we found out that she also experienced a myoclonic jerk soon after awakening. She was diagnosed as JME, and no further seizures occurred after sodium valproate administration.\nDue to the occurrence of hand tremor, the sodium valproate treatment was changed to lamotrigine during the follow-up period.

[[39.0, 'year']]

F

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{'3952312-1': 2}

3952315-1

noncomm/PMC003xxxxxx/PMC3952315.xml

Seizure Localization in Patients with Multiple Tubers: Presurgical Evaluation in Tuberous Sclerosis

The patient was a 30-year-old woman who had history of epilepsy since 3-year-old. She was transferred to our epilepsy clinic for the video-electroencephalography (VEEG) monitoring for presurgical evaluation. She was right handed, high school graduate, and unemployed. Physical examination revealed shagreen patch on her right lumbar region and few hypomelanotic macules on her back. Neurological examination revealed no remarkable neurological deficit. She reported to have monthly psychic and, or abdominal aura which often evolves to complex partial seizure, while on valproate, topiramate, carbamazepine, and pregabalin. Caregivers reported that she fumbles her right fingers and shows lip smacking during her seizures, and does not respond to questions. She reported only one episode of generalized tonic clonic seizure which occurred before taking anti-epileptic drugs. Caregivers also reported the change in the personality. She became aggressive and violent, mostly addressed to caregivers.\nIntellectual assessment revealed IQ score of 83 which indicates low average level. Her neuropsychological test indicated bilateral frontal lobes and right temporal lobe dysfunction. Beck’s depression inventory score was 33 and Beck’s anxiety inventory score was 34, indicating severe depressive and anxious state.\nAn 8-day Video-EEG monitoring study demonstrated frequent interictal epileptiform activity localized to right frontotemporal region. Five seizures and one aura were recorded. Semiology was psychic, and, or abdominal aura which evolves to automotor seizure with right hand fumbling. Ictal EEG exhibited two seizures with maximum amplitude over the right frontotemporal electrodes, and three were obscured by artifacts. Remarkably, all five seizures had theta range rhythm build up at right frontotemporal electrodes (). The brain magnetic resonance imaging (MRI) study revealed multiple cortical tubers including a prominent on right anterior temporal cortex with loss of normal gray-white differentiation, and other scattered cortical tubers are located at right middle, and superior frontal gyri, right insula, left medial frontal and Lt parietal regions.\nRadiotracer for ictal SPECT was injected at 24 seconds from the onset of 56 second duration habitual seizure. Ictal single photon emission computed tomography (SPECT) findings were concordant to the localization of ictal EEG onset. The hyperperfusion was regionalized to right anterior temporal area. This also anatomically correlated with cortical tuber seen at the right anterior temporal pole. Furthermore subtracted ictal-interictal SPECT co-registered with MRI (SISCOM) revealed hyperperfusion at the right temporal pole and anterior temporal region (). Other cortical tubers seen in the brain MRI shows no definite regional perfusion changes. The ictal EEG at the timing of injection was rhythmic 5 Hz theta rhythm in right frontotemporal region. Brain 18F-fludeoxyglucose positron emission tomography (FDG-PET) reveals right anterior to posterior temporal regions hypometabolism, especially involving mesial temporal area (). The genetic test confirms the gene mutation in TSC1 (c.2389C>T). Further evaluation for other symptoms of tuberous sclerosis including abdominal and thoracic CT scan were unremarkable.

[[30.0, 'year']]

F

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{'3952315-2': 2}

3952315-2

noncomm/PMC003xxxxxx/PMC3952315.xml

Seizure Localization in Patients with Multiple Tubers: Presurgical Evaluation in Tuberous Sclerosis

The patient was a 23-year-old male who had a history of epilepsy since 8-year-old. He was transferred to our clinic for the presurgical evaluation. He was bi-handed, college graduate, and unemployed. Physical examination revealed shagreen patch on his lumbar region, no other definite dermatologic abnormalities were seen. Neurological examination revealed no remarkable neurological deficit. He reported seizures consisting of automotor seizure and generalized tonic clonic seizure once in a year, and psychic auras several times per month while on valproate, topiramate, lamotrigine, and clonazepam. He reported infrequent complex partial seizures and secondary generalization. He also complained about the severe disability in concentration following polytherapy. He reported that seizures are provoked by loud music, thus he avoids earphone use or places with loud speakers, which withdraws him from normal social activities. Caregivers also reported the change in the personality and aggressive behavior since high school years. Intellectual assessment revealed IQ score of 108 which is average level.\nDuring the six-day VEEG monitoring the patient experienced approximately five seizures and one aura. Semiology was psychic aura to unresponsive dialeptic seizure which then evolves to left versive seizure and generalized tonic clonic seizure. The video-EEG study revealed frequent interictal epileptiform activity, maximal over the right frontotemporal region with frequency of 3–6 per minute. These seizures all were lateralized to right hemisphere: three started from right frontotemporal area, and one from posterior temporal area (). Ictal discharges of all four seizures had theta range rhythm build up at right frontotemporal area. The brain MRI revealed multiple cortical tubers located at right hippocampus, inferior, and superior frontal gyri, left middle frontal gyrus, left mesial frontal cortex, left parietal cortex, and left occipital cortex. Radiotracer for ictal SPECT was injected at 34 seconds from the onset of 104 second duration habitual seizure. SISCOM revealed hyperperfusion at right temporal cortex (more on mesial) (). Brain PET reveals right temporal lobe hypometabolism, especially involving mesial and basal cortex (). He carried a disease-associated mutation in TSC1 (c.2578delG). His abdominal and thoracic CT scan showed no abnormal findings.

[[23.0, 'year']]

M

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{'3952315-1': 2}

3952316-1

noncomm/PMC003xxxxxx/PMC3952316.xml

An Unusual Case of Herpes Simplex Viral Encephalitis Following Acute Retinal Necrosis after Administration of a Systemic Steroid

A 57-year-old man was referred to Samsung Medical Center with abrupt confusion, fever, and loss of vision in both eyes. The patient was in his usual state of health until two weeks prior, when he began to develop sudden loss of vision in his right eye. In another hospital, he was diagnosed with retinal vasculitis in his right eye and was prescribed oral prednisolone, 60 mg/day for three days, followed by 120 mg/day for three days. The retinal vasculitis did not respond to oral prednisolone, so he was treated with intravenous methylprednisolone, 1 g/day for five days. Two days after initiation of intravenous methylprednisolone, he complained of decreased vision in his left eye. One week after initiation of intravenous methylprednisolone, he became drowsy and high fever occurred, and he was then referred to Samsung Medical Center. On neurological examination, he was drowsy and confused to time and place orientation. Mini-mental status examination was 18. He consistently complained of severe headache and bilateral ocular pain. However, his extraocular movement did not show any limitation in all directions. Neck stiffness and meningeal irritation sign were not definite. Other focal neurologic deficits were not found.\nHis brain magnetic resonance imaging (MRI) showed a hyper-intense lesion in the left medial temporal and bilateral medial occipital areas on T2-weight images, suggestive of HSE (). Cerebrospinal fluid (CSF) study revealed 11 cells/mL (lymphocytes 90%), low protein (19.3 mg/dL), and normal range glucose concentration (63 mg/dL compared to 110 mg/dL in serum). An empirical antiviral agent (acyclovir 30 mg/kg/d) was administered intravenously. One week later PCR of the CSF was revealed to be positive for HSV-1 DNA. On the night of admission, the patient experienced a generalized tonic-clonic seizure during sleep. His electroencephalography showed sharp waves in left or right anterior temporal areas (F7T7, F8T8 maximum) with a frequency of 1/min and diffuse slow waves. An antiepileptic drug (phenytoin 300 mg/d) was administered and no more epileptic seizure recurred.\nOn the day of admission, his visual acuity was perception of light in both eyes. Fundus examination showed retinal hemorrhage, confluent retinal necrosis affecting almost the whole retina, vascular sheathing involving both arterioles and venules, optic disc swelling, and exudative retinal detachment in both eyes (). Fluorescein angiography revealed multiple vascular occlusions and vascular leakage. Ultrasonography shows retinal detachment in both eyes (). Infectious retinitis including acute retinal necrosis was suspected, but in terms of the location of necrosis, his clinical features were not typical of ARN Diagnostic vitrectomy confirmed the presence of HSV-1. Finally, he was diagnosed with ARN with optic neuropathy by HSV-1.\nAfter administration of intravenous acyclovir for 14 days, his systemic symptoms consistent with encephalitis slowly resolved, but his vision was not restored. On follow-up examination, retinal necrosis did not progress, but he still suffered from severe bilateral ocular pain with partial improvement of the exudative retinal detachment (). Thus, intravitreal ganciclovir injection (5,000/0.05 μg/mL) causes pain relief and decreased intraocular inflammation. But his visual acuity could not perceptany light. Bilateral rhegmatogenous retinal detachment with optic atrophy was found six weeks later, thus vitrectomy with silicone oil tamponade was done in the right eye.

[[57.0, 'year']]

M

{'34716288': 1, '11320015': 1, '31464954': 1, '8172275': 1, '9227211': 1, '31138593': 1, '20079537': 1, '13129871': 1, '21770880': 1, '11248101': 1, '9744385': 1, '33530932': 2, '21113344': 1, '17972228': 1, '10682968': 1, '18852442': 1, '24649457': 2}

{'7851902-1': 1}

3952319-1

noncomm/PMC003xxxxxx/PMC3952319.xml

Klüver-Bucy Syndrome with Isolated Bilateral Hippocampal Atrophy Following Status Epilepticus

A 31-year-old man who had no significant medical history presented with status epilepticus. He had headache, fever of 39° and generalized tonic clonic seizure without recovery of consciousness. His vital sign was stable except fever. On neurological examination, there was no abnormality except stuporous mental status between frequent generalized tonic clonic seizures. Initial blood tests showed no leukocytosis and normal level of inflammatory markers (C-reactive protein and erythrocyte sedimentation rate). Cerebrospinal fluid (CSF) was clean and contained 108 leukocytes/mm3 (83% polymor-phonuclear leukocytes and 17% lymphocytes) with normal glucose (78 mg/dL) and protein (42 mg/dL). Serologic testing of blood and CSF was normal. Initial brain MRI showed T2 hyperintensity and swelling of isolated bilateral hippocampus, especially CA1 region without any abnormal lesion in other areas ().\nOn the day of admission, we assumed that the patient had herpes encephalitis, and started maximum dosage of acyclovir (15 mg/kg three times a day) which is the hospital protocol for treatment of herpes encephalitis. Electroencephalography (EEG) showed frequent spike and waves on bilateral fronto-temporal areas dominantly on temporal areas, so we started antiepileptic drugs (initial phenytoin loading with subsequent add-on of levetiracetam, oxcarbazepine and topiramate) and midazolam-coma therapy. Further serologic tests including polymerase chain reaction (PCR) for herpes species were negative and no bacteria and viruses were grown. He recovered from status epilepticus three weeks later, but afterwards he developed KBS which is characterized by hyperphagia (he ate a large amount of food six to seven times a day), hypersexuality (he wanted to have a sex with the nurses, his ex-girlfriend and his mother), hypermetamorphosis, global amnesia (memory registration was normal, but recall was impaired) and dysosmia. On the 46th day of hospitalization, the score of his Korean-version of mini-mental status examination was 20/30 (orientation to time- 3/5, orientation to place- 2/5, immediate recall- 3/3, delayed recall- 0/3, attention and calculation- 3/5). Since we considered that his symptoms occurred due to secondary temporal lobe epilepsy, we performed an EEG, but his EEG showed no definite epileptiform discharges. Forty-five days later, follow-up brain MRI showed isolated bilateral hippocampal atrophy (). Finally, we concluded that he had a KBS, and the patient was discharged on the 58th day of hospitalization and his cognitive dysfunction is persistent with minimal improvement for six months follow-up.

[[31.0, 'year']]

M

{'7936288': 1, '15365793': 1, '441166': 1, '2360478': 1, '2803598': 1, '9879850': 1, '7731534': 1, '9447506': 1, '27530874': 1, '24649454': 2}

{}

3952320-1

noncomm/PMC003xxxxxx/PMC3952320.xml

Vigabatrin-Induced Generalized Epileptiform Discharges in a Patient with Focal Epilepsy

A 21-year-old man has been treated for a seizure disorder in the Department of Neurology since he was 15 years old. At the age of nine years old, he suffered the first seizure attack. The beginning of his seizures was a visual aura, right side hemianopsia, usually accompanied by a headache, and then he stares vacantly and does not respond to verbal commands. The frequency of the seizures was two to three times per year.\nWhen he was 13 years old, he had started to take an unknown species of antiepileptic drug. But because of the bankruptcy of the hospital he was treated in, he stopped the medication when he was 14 years old. He suffered a generalized tonic-clonic seizure under the drug withdrawal state. Just after the seizure he visited another hospital. Valproic acid (VPA) monotherapy did not change the seizure frequency under poor drug compliance. He heard that there were no abnormal findings on the two EEGs checked in that hospital.\nThe patient visited the pediatric department of our hospital when he was 15 years old. There were no abnormal findings in the brain MRI taken at that age; VGB was added on and VPA was tapered; his prescription was adjusted to high dosage of VGB (3,500 mg/day) by a pediatrician. Five months after his visit to the pediatric department, he suffered another complex partial seizure, and the pediatrician in charge referred the patient to the department of Neurology. Since then, he had been seizure free for four years and eight months while taking 3,000 mg/day of VGB. He also did not report any absence attack during that period. However, he had another complex partial seizure starting with visual aura when he was 20 years old; that was his last seizure.\nEEGs were recorded periodically in our hospital after the use of VGB since the first visit in the pediatric department. In eight of the consecutive nine EEGs recorded over approximately four years, the diffuse bursts of 2–2.5 Hz spike-and-wave complexes were observed repetitively (). The occurrences of the abnormal discharges in each EEG were several to frequent during the 30 min recording. In another EEG recorded five months after the last seizure at when he was 20 years old, the generalized epileptiform discharges were also observed intermittently. Just after that EEG recording, 600 mg/day of VPA was added to his medication, and the tapering of VGB was started.\nFour months after starting of the drug changes, another EEG was done. The patient’s prescription at that time was 600 mg/day of VPA plus 1,000 mg/day of VGB. In the EEG recorded under that medication, several clusters of spikes on the occipital area of the left hemisphere were observed (). There was no burst of the 2–2.5 Hz spike-and-wave complexes on that EEG. One month after the EEG recording, the VGB medication was stopped after tapering. When the patient was 21 years old, four months after the EEG recording, another EEG was recorded; no epileptiform discharges were observed in that EEG. The medication at that time was 600 mg/day of VPA.

[[21.0, 'year']]

M

{'9818915': 1, '9746003': 1, '1690139': 1, '1650272': 1, '12536034': 1, '7732767': 1, '9371946': 1, '2796603': 1, '24649455': 2}

{}

3952324-1

noncomm/PMC003xxxxxx/PMC3952324.xml

Two Cases of Chromosome 22q11.2 Deletion Syndrome Diagnosed in 12-Year-Old Boys with Hypocalcemic Seizures

A 12-year-old boy presented with a new onset generalized tonic-clonic seizure. He is the first child of a phenotypically normal mother. The patient was born at term after an uneventful pregnancy by an uncomplicated caesarean section with low birth weight of 2,900g (10–25th percentile). At 8 months the child underwent surgical repair of a cleft palate and at age 2 years had two episodes of febrile convulsion. He had a learning disability in his school-aged years. On family history, his father had a prominent forehead, small down-turned mouth, micrognathia, and nasal voice (). He had not undergone any prior specific evaluation, but seemed to have normal intelligence without any neuropsychiatric symptoms including a seizure history.\nPhysical examination revealed prominent forehead, small down-turned mouth, micrognathia (), and repaired cleft palate with not well formed uvula (). His height was 146 cm (25–50th percentile) and weight was 38.5 kg (25–50th percentile). Chvostek’s and Trousseau’s signs were negative. He had mild mental retardation with an intelligence quotient (IQ) of 68 on the Korean version of Wechsler Intelligence Scale for Children (K-WISC).\nThe electrocardiogram (ECG) was abnormal due to a prolonged corrected QT interval and the chest radiograph failed to show a thymus shadowing. Computed tomography (CT) of the heart revealed right aortic arch (), and CT of the brain showed multiple calcifications in the bilateral basal ganglia and both frontal white matters (). The electroencephalogram (EEG) revealed generalized intermittent slow waves without any epileptiform discharges.\nLaboratory tests showed hypocalcemia (calcium 6.5 mg/dL, ionized calcium 2.8 mg/dL), hyperphosphatemia (9.1 mg/dL) and normal level of magnesium (1.8 mg/dL). Parathyroid hormone (PTH) was decreased to 4.76 pg/mL (reference range 15–65 pg/mL) and 25-vitamin D3 was decreased to 13.6 ng/mL (reference range 30–60 ng/mL). Peripheral blood count, hepatic, renal and thyroid function tests were all normal except thrombocytopenia (144,000/μL). Immunological studies showed normal levels of Immunoglobulins but T cell subpopulation analysis was abnormal. T lymphocyte was decreased to 42.8 %/μL (reference range 52–78%/μL), CD4/CD8 T cell ratio was decreased to 0.79 (reference range 0.8–3.0).\nFluorescent in situ hybridization (FISH) analysis was performed using peripheral blood and chromosomal study was carried out using DiGeorge/VCFS TUPLE1 region probe (22q11.2) with an ARSA control probe (22q13) which confirmed a 22q11.2 deletion. His father revealed the same chromosomal abnormality, which suggests paternal inheritance in this case.\nThe patient was treated with calcium citrate and calcitriol. He remained asymptomatic with normalization of his serum calcium level with medications.

[[12.0, 'year']]

M

{'9350810': 1, '15967641': 1, '9781025': 1, '8230162': 1, '28690994': 2, '11005797': 1, '886353': 1, '16793949': 1, '24649462': 2}

{'3952324-2': 2, '5495981-1': 1}

3952324-2

noncomm/PMC003xxxxxx/PMC3952324.xml

Two Cases of Chromosome 22q11.2 Deletion Syndrome Diagnosed in 12-Year-Old Boys with Hypocalcemic Seizures

A 12-year-old boy presented with a new onset generalized tonic-clonic seizure. He is the second child of phenotypically normal parents, born at term after an uneventful pregnancy by an uncomplicated caesarean section with low birth weight of 2,800 g (10–25th percentile). At age 1 year, the child underwent surgical repair of patent ductus arteriosus. At age 6 and 7 years, he had two episodes of febrile convulsion. He had a learning difficulty in his school-aged years. He did not have any family history of similar clinical conditions.\nPhysical examination was abnormal due to a prominent forehead, small down-turned mouth, micrognathia and bifida uvula. His height was 155.8 cm (90–97th percentile) and weight was 59.7 kg (75–90th percentile). Chvostek’s and Trousseau’s signs were negative. On neurological evaluation, his verbal fluency was decreased.\nThe ECG showed a prolonged corrected QT interval and chest X-ray failed to show a thymus shadowing. The brain CT revealed calcification located in the left basal ganglia (). The EEG was abnormal due to generalized intermittent slow waves without any epileptiform discharges.\nLaboratory tests showed hypocalcemia (calcium 6.9 mg/dL, ionized calcium 3.8 mg/dL), hyperphosphatemia (8.3 mg/dL) and normal level of magnesium (1.7 mg/dL). PTH was normal with 21.91 pg/mL (reference range 15–65 pg/mL) and 25-vitamin D3 was decreased to 22.9 ng/mL (reference range 30–60 ng/mL). Peripheral blood count, hepatic and renal function tests were all within normal range except mild thrombocytopenia (130,000/μL). A 22q11.2 deletion was confirmed by a FISH analysis.\nThe patient was treated with calcium citrate and calcitriol. He remained asymptomatic with normal serum calcium level with medications.

[[12.0, 'year']]

M

{'9350810': 1, '15967641': 1, '9781025': 1, '8230162': 1, '28690994': 2, '11005797': 1, '886353': 1, '16793949': 1, '24649462': 2}

{'3952324-1': 2, '5495981-1': 1}

3952326-1

noncomm/PMC003xxxxxx/PMC3952326.xml

A Case of Psychogenic Dizziness Mimicking Vestibular Epilepsy

A 28-year-old man presented to our clinic three days after his first episode of vertigo. The patient was suffering from frequent episodes of severe spinning vertigo with mild nausea; each episode lasted for a few minutes. The patient complained of a severe whirling sensation with a clockwise direction during the ictus, and experienced a dull headache after the ictus. The patient reported that he did not suffer from agoraphobia, panic symptoms, or any recent stressful conditions. Nor was the ictus accompanied by ear symptoms, such as tinnitus, hearing loss, or aural fullness, and there were no other symptoms, such as paresthesia, motor deficit, or visual disturbances, including field defect, metamorphopsia, or color change. His symptom was not predictable and occurred without any position change. The patient did not lose consciousness during the onset of the symptom, and his family members had not witnessed any eyeball deviation or head turning during the episodes. The patient had no history of motion sickness or migraine. However, he had undergone an operation in the left cerebral hemisphere for the treatment of Moyamoya disease (encephaloduroarteriosynangiosis, EDAS) 3 years ago. Brain MRI revealed the presence of an osteoplastic craniotomy scar in the left lateral convexity (). No nystagmus was observed and his symptoms were not evoked by the hyperventilation maneuver. The patient showed bilaterally symmetrical saccade and smooth pursuit. A cerebellar function test was normal and a caloric test and audiometry showed normal responses. We assumed that the ictus was a manifestation of vestibular epilepsy. Therefore, the patient was admitted to the Epilepsy Monitoring Unit (EMU). He was monitored continuously for 24 hours a day with video and computerized EEG equipment. However, the episodes of vertigo were not accompanied by any significant EEG changes, such as sharp waves and spikes. Therefore, we suspected that the episodes might be psychogenic dizziness. The patient was responsive to benzodiazepine medication and psychological encouragement.

[[28.0, 'year']]

M

{'9153437': 1, '3047705': 1, '13831894': 1, '24649463': 2}

{}

3952329-1

noncomm/PMC003xxxxxx/PMC3952329.xml

Simple Partial Status of Forced Thinking Originated in the Mesial Temporal Region: Intracranial Foramen Ovale Electrode Recording and Ictal PET

A 50-year-old, ambidextrous woman was referred for the management of intractable partial seizures which began at the age of 13. During the first several years, she reported experiencing recurrent episodes of flash-backs which she described as “very familiar scenes passing by me”. She also reported olfactory hallucinations which consisted of odd smells. At the age of 17, she started to have complex partial seizures (CPS) which were associated with different types of psychic auras such as déjà-vu, jamais-vu, and FT. These auras were experienced alone or in various combinations. She also had experienced two prolonged episodes of continuous FT which lasted for several days after clusters of CPS. She recalled these episodes of FT as “I forgot something that I should do”. Despite systematic trials of antiepileptic drugs (AED), she was still having two to three episodes of CPS monthly, and she decided to receive epilepsy surgery.\nShe had no prior medical history, including febrile seizure. A bedside neurological examination was unremarkable. Neuropsychological test revealed an average level of intelligence, and her memory was average in visual and borderline in verbal modalities. Magnetic resonance imaging showed left hippocampal sclerosis ().\nVideo-EEG monitoring disclosed interictal epileptiform discharges in the left temporal region with a maximum amplitude at the sphenoidal electrode (SP1). Two episodes of CPS without aura were recorded after AED withdrawal. These started with brief eye blinking, subtle limb automatisms, and body rocking. She then developed moaning, right facial tonic spasms, right arm dystonia, and left head and body rotations. The ictal EEGs showed diffuse attenuation of background activity before the clinical onset, followed by delayed rhythmic 5–6 Hz theta activity in the left temporal region, 15s and 28s after the clinical onset, respectively.\nIctal 99mTc-ethylcysteinate dimer single photon emission computed tomography showed increased blood flow in the left temporal and parietal lobes (). We elected to place intracranial foramen ovale electrodes (FOE) under local anesthesia because the ictal EEG onset was diffuse and there was a significant delay of lateralizing discharges after the clinical ictal onset.\nInterictal EEG showed frequent epileptiform discharges at the left FOE without any obvious changes in the scalp electrodes. After the placement of the FOE, she experienced 18 episodes of brief CPS overnight. Ictal EEG revealed that the onset in the left FOE consisting of rhythmic β fast activity with superimposed polyspikes for 6–10s. This evolved to higher amplitude rhythmic theta activity in the left temporal scalp electrodes, 10–20s later.\nThe CPS clustering was successfully terminated by the intravenous administration of lorazepam, and she resumed taking AEDs including lamotrigine 100 mg, valproate 300 mg, topiramate 150 mg, and pregabalin 75 mg bid. However, she started complaining of continuous FT. The content of FT, quoted as her saying, was “I have something that I must do”, and the similar content of FT had occurred as either habitual auras or prolonged aura episodes after CPS cluster. She well recognized that there was nothing that she actually should do, but she was not able to stop this line of thinking. These thoughts caused unnecessary anxiety. The EEG showed a continuous 1–1.5 Hz periodic pattern of polyspikes and slow wave complexes on the left FOE during the persistent FT (). Her bedside neurological examination including memory function did not show any definite abnormality. She did not have any problem in daily life. The simple partial status persisted for five days.\nBrain 18F-fluorodeoxyglucose PET during the episode of FT showed a focal hypermetabolism in the left mesial temporal region (). The PET data was analyzed using MRIcro () and statistical parametric mapping 8 (SPM8) (). The patient’s PET images were initially transferred to the Analyze format with MRIcro and spatially normalized to our institutional PET template using the affine transformation of SPM8. Afterwards, the images were smoothed with a 12-mm FWHM Gaussian kernel and a statistical analysis was set up to compare the patient and the control subjects (n=32) with a two-sample t-test. We used a voxel height threshold at p=0.001 (uncorrected) and the minimal cluster size as 100 voxels. The SPM map was superimposed on the normalized T1 template using ANALYZE 5.0 (Biomedical Imaging Resource, Mayo Foundation, Rochester, MN, USA).This demonstrated increased metabolism in the left hippocampus, the left parahippocampal gyrus, and the right cerebellum (). A Wada test with intracarotid injection of thiopental revealed bilateral language and right memory dominance (6 versus 0 out of 10 items). The patient underwent a left anterior temporal lobectomy. The pathology was consistent with hippocampus sclerosis. No further seizure including aura had developed during the 56 months follow-up after the surgery.

[[50.0, 'year']]

F

{'13117140': 1, '6698944': 1, '9339883': 1, '31951969': 1, '8320551': 1, '27486431': 1, '1543059': 1, '7771296': 1, '8710129': 1, '3346692': 1, '3779297': 1, '34908691': 2, '7125603': 1, '24649451': 2}

{'8611604-1': 1, '8611604-2': 1, '8611604-3': 1}

3952330-1

noncomm/PMC003xxxxxx/PMC3952330.xml

Staged Total Callosotomy for Lennox-Gastaut Syndrome: A Case Report

A 6 year-old boy was born at 34 weeks’ gestation to healthy parents with birth weight of 3,540 g after an uneventful pregnancy. He had no family history of epilepsy or focal neurologic sign, but he had delayed development in fine motor and language areas since before 12 months of age. His first seizures, myoclonic seizures, occurred at the age of 8 months, and he was started on antiepileptic drugs (AEDs). At the time of his admission to our hospital at the age of 27 months, he was suffering from multiple types of seizures including drop attacks, generalized tonic seizures, and atypical absence seizures. His EEG showed generalized slow spike and wave discharges with multifocal spikes (), and he was diagnosed as having LGS. Brain magnetic resonance imaging (MRI) showed no abnormalities. Despite various antiepileptic drugs (valproate, topiramate, zonisamide, and clobazam) and a ketogenic diet, his seizures remained uncontrolled. Long term video EEG monitoring for 48 hours showed a dozen seizures a day. The seizure semiology consisted of suddenly dropping his head with losing his tone, thus suggesting myoclonic-atonic seizures. Ictal EEG showed diffuse generalized bursts of polyspike discharges with very brief electromyographic activities. His social quotient was reported to be 27. At the age of 36 months, he underwent anterior 2/3 corpus callosotomy. He achieved a post-operative seizure-free state for 3 months, after which he developed a relapse of his seizures. EEG performed at post-operative 10 months revealed frequent generalized spike and wave discharges and generalized paroxysmal fast activities. His seizures did not respond to either additional vagus nerve stimulation or to medical treatment at that time. As diffusion tensor imaging showed remaining callosal fibers in the splenium, we decided to perform a second total callosotomy (). After the second total callosotomy, the patient maintained a seizure-free state for 27 months and with EEG normalization (). He is still on the medication of valproic acid, topiramate, zonisamide, and clobazam. Developmental test performed after the second surgery showed no remarkable progress by that time. However, according to his parents, his cognitive function is improving compared to that of his pre-operative state.

[[6.0, 'year']]

M

{'18799327': 1, '15118994': 1, '6790275': 1, '8504787': 1, '17005346': 1, '8686549': 1, '16830167': 1, '19245287': 1, '17825516': 1, '14580615': 1, '18539083': 1, '8410248': 1, '24649449': 2}

{}

3952331-1

noncomm/PMC003xxxxxx/PMC3952331.xml

Effectiveness of Topiramate in Medically Complicated Patients with Status Epilepticus or Acute Refractory Seizures

A 48-year-old woman with no history of seizures was admitted to the hospital in poor health. The patient was diagnosed with paroxysmal nocturnal hemoglobinuria (PNH) 20 years prior to admission and had been treated as an outpatient with oral steroids. RBC transfusions were performed once a month. The routine blood tests on admission revealed pancytopenia (hemoglobin 4.4 g/dL, hematocrit 13.3%, WBC 730/mm3, and a platelet count of 52,000/mm3) and acute renal failure (BUN 126.5 mg/dL and creatinine 9.23 mg/dL). Continuous renal replacement therapy (CRRT) was performed in the intensive care unit. On the third hospital day, GCSE developed. Treatment was started with a LZP injection followed by DPH infusion. However, the GCSE continued. A loading dose of TPM (800 mg) was administrated via a nasogastric tube. By the next day, the continuous seizures were under control and the patient was responsive to verbal stimulation. However, intermittent brief seizures occurred several times under a maintenance dose of TPM (300 mg bid) during the subsequent two days. After three days of TPM administration the seizures stopped. The follow-up EEG showed no epileptiform discharges. The diffusion-weighted MRI revealed multifocal high signal intensity involving the occipital lobes, the right basal ganglia and the subcortical white matter of the prefrontal gyri on the diffusion and T2-weighted images. The identified lesions showed increased values on the ADC map, suggesting vasogenic edema or a posterior reversible encephalopathy (PRES). The EEG showed multifocal sharp waves and intermittent generalized slow waves. The TPM was maintained at a dose of 200 mg bid, and there was no further seizure activity. However, aspiration pneumonia and sepsis developed, and the patient died on the 15th hospital day.

[[48.0, 'year']]

F

{'30855319': 1, '14510830': 1, '12760428': 1, '34586297': 1, '11218054': 1, '19087119': 1, '12683704': 1, '14698713': 1, '17044824': 1, '11784388': 1, '28004305': 1, '16822255': 1, '21711264': 1, '20050893': 1, '12552056': 1, '16142991': 1, '10530681': 1, '11983039': 1, '32705422': 1, '16426869': 1, '28759588': 1, '24649446': 2}

{'3952331-2': 2}

3952331-2

noncomm/PMC003xxxxxx/PMC3952331.xml

Effectiveness of Topiramate in Medically Complicated Patients with Status Epilepticus or Acute Refractory Seizures

A 56-year-old woman was admitted to the hospital with impaired mental status. The patient had a history of multiple myeloma (stage IIIa) diagnosed three years prior to the admission; she received chemotherapy several times, but the disease was refractory to chemotherapy. VAD chemotherapy using vincristine, doxorubicin and dexamethasone was started. However, generalized seizures developed during the third cycle of chemotherapy, and the patient became unresponsive with her eyes deviated to the right side. The routine blood tests revealed pancytopenia (hemoglobin 5.2 g/L, hematocrit 14.4%, WBC 4,570/mm3, and a platelet count of 15,000/mm3), and septic shock developed. Continuous EEG monitoring showed bilateral rhythmic slow waves dominating the frontal area. NCSE was diagnosed and TPM (300 mg bid) was administrated. The epileptiform discharges disappeared after five days, the patient recovered and was responsive. However, the blood culture revealed Staphylococcus epidermidis, and she died on the 49th hospital day from septic shock.

[[56.0, 'year']]

F

{'30855319': 1, '14510830': 1, '12760428': 1, '34586297': 1, '11218054': 1, '19087119': 1, '12683704': 1, '14698713': 1, '17044824': 1, '11784388': 1, '28004305': 1, '16822255': 1, '21711264': 1, '20050893': 1, '12552056': 1, '16142991': 1, '10530681': 1, '11983039': 1, '32705422': 1, '16426869': 1, '28759588': 1, '24649446': 2}

{'3952331-1': 2}

3952334-1

noncomm/PMC003xxxxxx/PMC3952334.xml

Nocturnal Frontal Lobe Epilepsy Presenting as Obstructive Type Sleep Apnea

A 20-year-old man visited our sleep center because of snoring and sleep apnoea; the symptoms had started two years prior. He worked for the military, and his apnea and snoring were bothering colleagues in the barracks. His daily life was normal, and he had neither a family history nor a medical history of seizures and had previously been healthy. His Epworth Sleepiness Scale (ESS) score was 14 out of 24, which suggested moderate excessive daytime sleepiness. He especially complained of severe sleepiness in the morning. No parasomnia events or periodic limb movements during sleep had been reported. No tongue biting was reported, but he reported recent occasional enuresis. Physical examination revealed no apparent abnormalities. His body mass index (BMI) was 23.1 kg/m2.\nOvernight polysomnography was performed. Sleep efficiency was 81.9%, wakefulness after sleep onset (WASO) time was 59.2 minutes (17.8%), and his arousal index was 28.7/h. Stage 1 and 2 sleep were increased; however, stage 3 and REM sleep were decreased. He experienced nine apneas and two hypopneas during PSG, each episode lasted 20–40 seconds. His apnea/hypopnea index (AHI) was 2.7/h. These apneic episodes consisted of respiratory cessation accompanied by chest and abdominal movements of the obstructive type. All hypopnea was typical hypopneas. Seven out of nine apneic episodes were accompanied by rhythmic paroxysmal discharges in the bifrontal areas on EEG; clinically, five of the episodes progressed to tonic movement of all four limbs, and two episodes showed apneas only. All that seven episodes occurred during NREM sleep (two in stage 1, four in stage 2, and the others in stage 3). The other apnea and hypopnea did not accompany tonic movement.\nThe next night, a 16-channel video-EEG monitoring was performed to classify these events and to determine the temporal relationship of apnea onset and Ictal discharge. Ten apneic events with ictal discharges preceding the apnoea were recorded throughout the night. Ictal EEG showed paroxysmal rhythmic discharges in the range of 9 to 10Hz in the bifrontal area starting just before onset of the apneic episodes. The interictal EEG was normal, and brain MRI showed no specific abnormality. Ictal SPECT revealed increased cerebral blood perfusion in the right frontal region (). Given these findings, we concluded that these events were epileptic seizures presenting as obstructive sleep apnoea. Carbamazepine therapy was initiated, and the nocturnal episodes were decreased.

[[20.0, 'year']]

M

{'28374233': 1, '10356056': 1, '19255415': 1, '10612352': 1, '19110889': 1, '19933056': 1, '10996549': 1, '8404744': 1, '9696531': 1, '24649450': 2}

{}

3952375-1

noncomm/PMC003xxxxxx/PMC3952375.xml

Nonfunctional Islet Cell Tumor of the Pancreas in a Patient with Tuberous Sclerosis: A Case Report with Literature Review

A 63-year-old-woman was referred to our department with a complaint of abdominal pain. Upon physical examination, skin lesions were detected and a firm mass was palpable in the upper quadrant of the abdomen. Laboratory findings were unremarkable. She was referred to the radiology department for a computed tomography (CT) examination of the abdomen. A biphasic contrast enhanced CT was also performed on a 16-slice CT system (Somatom Sensation, Siemens, Erlangen, Germany). An intravenous injection of 130 mL contrast media (iopamidol with an iodine concentration of 300 mg/mL) was given at a rate of 4 mL/s. Scanning was initiated after a delay of 25 s and 70 s after infusion of contrast material for the arterial phase and venous phase images, respectively. Scanning parameters were as follows: Slice collimation, 16 × 1.5 mm; table feed/rotation, 18.0 mm; rotation time, 0.5 s; KV 120; effective mAs 160, slice thickness, 2 mm.\nCT examination revealed a 9 × 6 cm mass with discrete nodular calcifications in the head of the pancreas. The mass showed heterogeneous enhancement in the arterial phase and homogenous enhancement in the venous phase [Figure and ]. The gastroduodenal artery was seen encased by the pancreatic mass. There were also multiple lesions in the liver ranging in diameter from 3 to 25 mm. Some of the lesions showed homogenous fat-density; however, others had heterogeneous areas of soft-tissue density and fat-density that were suggestive of AML. Lesions with homogenous fat-density did not show any enhancement in both the arterial and the venous phase images []. In lesions containing both a soft tissue component and a fat component, the nonfat component was enhanced markedly in the arterial phase and showed isohypodensity in the venous phase. Four lesions ranging from 3 to 12 mm in diameter had no fat components. These lesions had homogenous enhancement in the arterial phase image and became isohypodense in the venous phase image []. There were also multiple fat-containing lesions in both kidneys compatible with AML [] as well as multiple small discrete sclerotic lesions in the vertebrae. A cranial CT revealed multiple calcified subependymal nodules []. Unfortunately, as the patient was claustrophobic she did not undergo a magnetic resonance imaging (MRI) investigation.\nThe diagnosis of tuberous sclerosis was established on the basis of radiologic findings of renal and hepatic AML, calcified subependymal nodules, and vertebral sclerotic lesions with a clinical finding of adenoma sebaceum. Ultrasound-guided fine-needle aspiration of the pancreatic mass was performed using a 20-gauge needle. Histological examination of the cell-block preparations of the mass showed solid sheets of neuroendocrine-appearing cells characterized by large eosinophilic cytoplasm with moderate nuclear pleomorphism []. Immunochemical staining showed the cells were positive for synaptophysin and a few tumor cells were positive for chromogranin. On the basis of the morphologic and immunohistochemical findings, the lesion was diagnosed as ICT. Since the patient's serum levels of the pancreatic hormones were within the normal limits, ICT was considered as a nonfunctioning lesion.

[[63.0, 'year']]

F

{'3024343': 1, '22826391': 1, '18508996': 1, '18672238': 1, '22173120': 1, '28357779': 1, '7820027': 1, '12409579': 1, '19610144': 1, '18722871': 1, '22169969': 1, '24678435': 2}

{}

3952376-1

noncomm/PMC003xxxxxx/PMC3952376.xml

Non-resolving Findings in a Long-term Radiographic Follow-up of an Infant with Acute Paraffin Oil Aspiration

This was a case report of a 5-month-old male infant who was admitted as an emergency case to a secondary care hospital with acute onset of high-grade fever and respiratory distress. The chest X-ray showed bilateral extensive consolidation involving mainly the lower lobes of the lungs. He was placed on broad spectrum antibiotics and bronchodilatory inhalers, in response to which he showed no clinical improvement over a period of 2 days. Therefore, and in view of his deteriorating clinical status, he was urgently transferred to our hospital for further management.\nUpon arrival, the infant was in respiratory distress requiring 4 L/min of oxygen to keep his oxygen saturation above 90%. Further examination of the infant revealed dysmorphic features such as low set ears, generalized muscular hypotony, and delayed psychomotor development. Additional questions on patient history identified that at the age of 5-months the child had accidentally ingested paraffin oil administered by his 3-year-old brother. This prompted consideration of a probable diagnosis of acute exogenous LP. Computed tomography (CT) scan [] revealed extensive bilateral consolidations in the lower lobes. Bronchoscopy was performed which did not reveal any significant anatomical abnormalities or foreign bodies. The BAL aspirate was opalescent with a supernatant halo of fat and showed an increased number of macrophages. BAL was sent for microbiological studies including Gram staining, Ziehl-Neelsen staining, and bacterial and fungal cultures. The microbiological results were all negative. The cytologic study showed numerous foamy macrophages with intracytoplasmic and extracellular droplets of fat with a positive histochemical confirmation of acute LP with Oil Red O stain. (Oil Red O is a fat-soluble dye used for staining of lipids and triglycerides.) Total lavage was not performed as it was considered too risky in view of the critical status of the patient and the signs of hypoxia he demonstrated during the procedure.\nA corticosteroid therapy regimen was introduced which led to an improvement of his general condition. The infant remained in our hospital for a total of 5 months showing gradual clinical improvement. Before discharge an additional bronchoscopy and BAL was performed that showed a clear aspirate with no supernatant fat and fewer lipid-laden macrophages. Further, an additional CT scan was performed which showed persistent findings with minimal improvement []. 7-years after the incident, the patient was admitted for a complete workup. He underwent spirometry, which revealed a forced vital capacity (FVC) equal to 85% of predicted value, a forced expiratory volume in 1 s (FEV1) of 79% of predicted value. FVC and FEVI values over 80% of predicted value are considered normal. FEV1/FVC ratio was 81%, which was within the normal range (approximate range: 75-80%) for healthy adults. The reversibility test was negative. The patient could not undergo further pulmonary function testing (lung volume, diffusing capacity of lung for carbon monoxide). BAL revealed far fewer lipid-laden macrophages, while the CT scan showed resolution of the consolidations, but evidence of residual interstitial findings [].

[[5.0, 'month']]

M

{'19283836': 1, '34877333': 2, '17876572': 1, '3991256': 1, '19820809': 1, '14561906': 1, '20028911': 1, '20118714': 1, '26821544': 1, '10767479': 1, '24678434': 2}

{'8610930-1': 1}

3952380-1

noncomm/PMC003xxxxxx/PMC3952380.xml

Symmetrical Chorioretinal Colobomata with Craniovertebral Junction Anomalies in CHARGE Syndrome - A Case Report with Review of Literature

A 27-year-old woman presented with complaints of poor vision in both eyes and inability to hear since birth. She had undergone surgical ligation of patent ductus arteriosus (PDA) in childhood. There was no feeding difficulty in childhood. She had retarded growth and development and a characteristic facial appearance. There was bilateral Grade I/II microtia [].\nHer vision was 20/2000 in both eyes. Ocular adnexa, ocular motility, and anterior segment were normal in both eyes. There was no iris coloboma but symmetrical, large colobomata involving the optic nerve, choroid, and retina were present [Figure and ]. The colobomata included the macula. There were no neurological dysfunction or limb abnormalities.\nThere was severe to profound sensorineural deafness on pure tone audiometry examination and brain stem evoked response audiometry with identifiable peak V on 125 dB stimulus in both ears. Echocardiography revealed normal cardiac chamber dimensions and valve morphology with no residual shunt across PDA closure.\nUltrasound examination of the abdomen revealed an infantile uterus. X-ray KUB (kidney, urether, and bladder) region and serum calcium were within normal limits.\nMagnetic resonance imaging (MRI) revealed bilateral hypoplasia of vestibule, lateral semicircular canals, and cochlea with visualization of about 1½-turns [Figure and ]. Vestibulo-cochlear nerves on both sides were of smaller size than the adjacent facial nerves with narrow internal acoustic meatus. There was basilar invagination with short clivus, fused C2 and C3 vertebrae, and partially occipitalized atlas []. There was a large posterior global defect with adjacent deformed and thinned out sclera around the optic disc in both eyes []. The brain was normal.\nChromosomal analysis revealed normal female karyotype (46 XX chromosomes) in all the metaphases analyzed. CHD7 gene analysis could not be done.\nA diagnosis of CHARGE syndrome was arrived at by satisfying three major criteria prelisted by Blake et al., namely, i) Coloboma (retina and choroid), ii) Characteristic ear abnormalities, and iii) Cranial nerve dysfunction (sensorineural deafness), plus three minor criteria, namely, i) Cardiovascular malformations, ii) Growth deficiency, and iii) Distinctive face. The criteria for typical CHARGE syndrome according to Verloes are also met, namely, two major criteria of i) Coloboma (choroid) and ii) Hypoplastic semi-circular canals, plus three minor criteria of i) Rhombencephalic dysfunction (sensorineural deafness), ii) Abnormal external ear, and iii) Malformation of mediastinal organs (heart).\nProphylactic laser retinopexy was done in both the eyes along the border of the coloboma to reduce the risk of future retinal detachments. Her corrected visual acuity was 20/2000 in both eyes.\nHer two sisters and mother were found to be normal.

[[27.0, 'year']]

F

{'2466227': 1, '458518': 1, '469662': 1, '31649160': 1, '17299439': 1, '28059674': 1, '15666308': 1, '9559509': 1, '19112063': 1, '29854496': 2, '6166737': 1, '20186815': 1, '9545604': 1, '30237300': 1, '29622552': 1, '24678437': 2}

{'5952563-1': 1}

3952390-1

noncomm/PMC003xxxxxx/PMC3952390.xml

The first linezolid-resistant Enterococcus faecium in India: High level resistance in a patient with no previous antibiotic exposure

We report a case of a 72-year-old female, known diabetic for last 16 years, was admitted to the intensive care unit (ICU) of a tertiary care hospital with sudden onset unconsciousness for approximately 12 h first noticed when patient was not responding when her family tried to wake her up from sleep, patient was on oral hypoglycemic drugs with poor glycemic control. The patient was also hypertensive, which was controlled on medication. Patient did not have any history of convulsions, fever, vomiting, headache, trauma or any neurodeficit in the past.\nAt the time of admission, the patient neurological score was 5/15 as per Glasgow Coma scale. The pulse was 88/min, blood pressure-140/80 mm Hg, respiratory rate of 16/min and was irregular with bilateral vesicular breath sounds. The capillary blood glucose was 28 mg/dL. The other blood investigations were as follows: Total leukocyte count-16,200/mm3 with neutrophil predominance, serum alanine aminotransferase (ALT) -31 IU/mL, serum aspartate aminotransferase (AST) -71 IU/mL, alkaline phosphatase-22 IU/L, total protein-4.8 g/dL, albumin-2.4 g/dL, urea-54 mg/dL, creatinine-1.2 mg/dL, total bilirubin-0.6 mg/dL, conjugated bilirubin 0.3 mg/dL. Computerized tomographic scan on admission showed signs of focal ischemia. She was diagnosed as a case of hypoglycemic encephalopathy with hypoxic brain damage. She was intubated and put on ventilator support. The patient's glycemic status was restored and the patient was started on piperacillin + tazobactam empirically, to cover against any aspiration pneumonia, given the long period of unconsciousness of the patient.\nOn day 3 of treatment, she was showing some response to a painful stimulus, but the blood sugar was remaining uncontrolled fluctuating in between 221 mg/dL and 350 mg/dL. On day 4 of treatment, she developed low grade fever for which the endotracheal secretions were sent for culture. Acinetobacter baumanii with significant colony count (>106 colony forming units) was isolated, which was sensitive to netilmicin and polymixin B. The blood cultures sent on day 3 showed no growth and the chest X-ray showed mild right sided basal opacity. Patient was started on netilmicin and cefepime.\nOn day 7 of treatment, the patient developed high grade fever. The blood investigations were showed total leukocyte count of 8400/mm3 with neutrophilic predominance and serum creatinine of 2 mg/dL. The catheterized urine sample and blood were sent for culture. The urine culture showed a significant growth of Escherichia coli which was sensitive to meropenem, poymyxin B, cotrimoxazole and nitrofurantoin. On the basis of the culture reports, meropenem was added to the treatment regimen, but the general condition of the patient deteriorated, with total leukocyte counts dropping to 4000/mm3.\nThe blood cultures sent on day 7 and day 8 showed growth of E. faecium, which was identified by standard laboratory procedures.[] The antibiotic susceptibility of the isolate was performed by Kirby Bauer disc diffusion technique as per Clinical and Laboratory Standards Institute (CLSI guidelines), which showed the organism to be sensitive to vancomycin, but more remarkably the isolate was resistant to linezolid showing no zone around the disc by the disc diffusion technique [].[] Disk diffusion testing was performed with 30-μg linezolid disks (BBL, Becton Dickinson). E-test linezolid strips with a concentration gradient corresponding to 0.016-256 μg/mL were utilized with Mueller-Hinton agar as described by the manufacturer (Hi Media laboratories Mumbai) to determine the MIC of theisolate, but the isolate did not show any zone of inhibition, indicating that the MIC of the isolate was more than 256 μg/mL []. The MIC of the isolate was further determined by agar dilution method (using 0.5, 1, 2, 4, 8, 16, 32, 64, 128, 256, 512 and 1024 μg/mL) was conducted in accordance with CLSI standards[] using a linezolid preparation obtained from the manufacturer (Pfizer, India) which showed the MIC of the isolate was 1024 μg/mL. Automated susceptibility testing by the Vitek 2 system using the antimicrobial susceptibility testing (AST) GP-61 card (bioMérieux) was performed according to the manufacturers’ instructions. The categorical interpretation of results was based on CLSI guidelines.\nPatient was started on vancomycin but her condition further deteriorated and she was declared dead on day 15 of admission.\nThe cultures from the other patients in the ICU, did not reveal any similar organisms, unlike other case reports where isolation of linezolid resistant enterococci from one patient was usually associated with clonally related isolates, being isolated from other patients in the same wards.[]

[[72.0, 'year']]

F

{'31143752': 2, '18391028': 1, '16982791': 1, '15071066': 1, '34572664': 1, '31160854': 1, '16517903': 1, '12766857': 1, '28969155': 1, '28250623': 1, '31504566': 1, '12407134': 1, '16517918': 1, '24678466': 2}

{'6510087-1': 1, '6510087-2': 1}

3952391-1

noncomm/PMC003xxxxxx/PMC3952391.xml

Isolation of Mycobacterium branderi, an unusual species from an acute myelogenous leukemia patient

The present case report is about a 31-year old male patient who presented to our medical center with a productive cough, hemoptysis and chest pain for a month. He had a history of pulmonary tuberculosis (TB) twice over the last 10 years. In the first episode, he was treated with the World Health Organization category (CAT) I standard regimen including: Isoniazid (H), Rifampin (R), Pyrazinamide (Z) and Ethambutol (E) for 6 months (2HRZE/4HR). In the second episode, a CAT II regimen including streptomycin in the 1st 2 months (2HRZES/1HREZ/5HRE) was prescribed for 8 months.[] His treatment was successful, however one year after completion of the second therapy, he presented with respiratory symptoms to our hospital. His vital signs were within the normal limits. On physical examination, he was pale and afebrile with generalized wheezing and bilateral bronchial rhonchi. Laboratory studies revealed the following values: Total white blood cell (WBC) count: 103,600 cells/ul with 5% neutrophils, 14% mature monocytes, 11% lymphocyte and more than 20% immature nucleated cells of myeloid lineage some with monocytoid morphology; hemoglobin 5.8 g/dl; platelets 233,000 cells/ul and erythrocyte sedimentation rate 125 mm/h. All other biochemical tests were unremarkable. Chest X-ray and spiral computed tomography scan of the thorax showed a cavitary lesion in the right upper lobe surrounding diffuse infiltrates with pleural thickening. There were also some areas of nodular infiltrate demonstrating a “ tree-in-bud” appearance in left lung [].\nA sputum smear was positive for acid-fast bacilli, so anti-TB regimen (CAT I) was initiated, culture and drug susceptibility testing were initiated. In addition, bone marrow biopsy was performed and AML – M4 was diagnosed by histopathological examination, based on published criteria.[] Chemotherapy agents consisting Danurubicin 70 mg/q12h plus Cytarabine 1600 mg/q12h were started. The patient was transferred to the intensive care unit due to fever and severe neutropenia (WBC 880 cells/ul) on the 6th day of chemotherapy and Meropenem 1 g/q8 h, Vancomycin 1 g/q12h and Itraconazole 100 mg/daily were initiated.\nThe polymerase chain reaction (PCR) of deoxyribonucleic acid collected from sputum sample of patient (based on IS6110 primer) was negative for Mycobacterium tuberculosis complex. The Mycobacterium identification was performed by PCR-restriction fragment length polymorphism (RFLP) polymorphism analysis and subsequently M. branderi was isolated from the sputum of the patient. A 440 bp fragment of hsp65 gene was first amplified (based on TB11, TB12 primer) and then the PCR product digested using BstEII and HaeIII restriction endonucleases.[] The obtained digested pattern (BstEII; 235,211 bp: HaeIII; 130,106,80,41,37 bp) was compared with the standard strains published on database[] []. To further confirm the identification of M. branderi pure colonies were isolated at 25°C and 45°C within 3 weeks of incubation. Differentiation of M. branderi from Mycobacterium celatum was done based on phenotypic characteristic of colonies and pigment production. The colonies of M. branderi had not produced pigment.\nThe susceptibility testing observed for the clinical isolate included resistance to Isoniazid and Rifampin.\nThe anti-TB drugs were stopped and treatment was modified to Clarithromycin 500 mg/q12 h, Ciprofloxacin 500 mg/q12h and Doxycycline 100 mg/q12 h. This combination regimen was well tolerated and the patient's symptoms resolved. After 1 month of treatment, sputum smear and culture conversion was reported.\nFollowing discharge from hospital, mycobacterial treatment was continued for 12 months and our patient remained smear negative and free of pulmonary symptoms in follow-up appointments.

[[31.0, 'year']]

M

{'10806169': 1, '11473995': 1, '22184566': 1, '8711643': 1, '17507546': 1, '22879540': 1, '1500501': 1, '9279284': 1, '15973015': 1, '22706597': 1, '26180788': 1, '12370992': 1, '8590682': 1, '11015432': 1, '8381805': 1, '24678467': 2}

{}

3952392-1

noncomm/PMC003xxxxxx/PMC3952392.xml

Reactivation of latent melioidosis presenting with acute pyelonephritis and bacteremia

The present case report is about an 81-year-old Indian male patient who presented to the emergency room with the complaining of worsening fevers, chills, dysuria and decreased appetite over a 3-week period. His medical history included diabetes mellitus, chronic obstructive pulmonary disease, hypertension, benign prostatic hyperplasia and dyslipidemia. His surgical history was unremarkable and he was taking atenolol and lovastatin as an out-patient. He reported that he had been to the emergency room 1 month ago for the treatment and management of lower gastrointestinal bleed secondary to colitis. During that admission, he developed a urinary tract infection for which he was treated with oral levofloxacin as an out-patient. He denied any history of smoking. He also denied any illicit drug or alcohol use. The patient emigrated from India to the United States of America (USA) over 40 years ago. The last time he travelled out of the USA was to India 2 years ago. His symptoms began approximately 3 weeks prior. On admission, he was febrile, with a temperature of 102°F. He was hemodynamically stable, but in obvious discomfort complaining of weakness and dizziness. On physical examination, he had suprapubic tenderness and right cost overtebral/flank tenderness, but no other physical abnormalities. His prostate exam was unremarkable. Initial laboratory work-up revealed an elevated leukocyte count of 13 × 103 with a left shift. His urine analysis revealed 10-15 red blood cells per high power field, 50 leukocytes per high-power field, positive bacteria with positive nitrates and leukocyte esterase and few hyaline casts. A chest X-ray was unremarkable, but a computed tomography scan of the abdomen and pelvis [] revealed wedge-shaped enhancement defects in the right kidney suggestive of pyelonephritis. We drew blood and urine cultures which both grew non-lactose fermenting, aerobic and motile Gram-negative rods which were identified to be B. pseudomallei. The patient was treated with a 2-week course of imipenem/cilastatin, followed by oral trimethoprim-sulfamethoxazole for eradication therapy for 4 months. As the result of the treatment regimen, the patient clinically improved and he was asymptomatic at the 4 months follow-up.

[[81.0, 'year']]

M

{'10975006': 1, '21152057': 1, '2665001': 1, '32161067': 1, '10476750': 1, '11718367': 1, '11964912': 1, '26787155': 1, '32494583': 1, '30148016': 2, '24678468': 2}

{'6107038-1': 1}

3952412-1

noncomm/PMC003xxxxxx/PMC3952412.xml

Lacunar infarction with oral contraceptives: An unusual case report

A 35-year-old previously healthy female patient on ‘Sukhi’ for contraception for the last 3 years presented to the Emergency Department of S.C.B. Medical College and Hospital, Cuttack in November 2011, with complaints of sudden onset (45 min earlier) of slight paralysis of the right side of her body and the inability to express herself by speech, writing, or signs. She was afebrile, alert, oriented with blood pressure of 122/98 mm Hg, pulse rate 100/min. She was a non-smoker, not a known diabetic or hypertensive, but there was history of repeated abortions in the past. General physical examination was normal with normal intact memory. Fundoscopic findings were normal although neurological examination revealed right sided hemiparesis with upward right babinski reflex. On investigations the parameters such as hemogram, ESR, random blood sugar, kidney function tests, liver function tests, electroencephalogram, electrocardiogram, serum cholesterol, serum electrolytes, urine analysis and X-ray chest were within normal limits. Plasma amino acid, vascular profile, and metabolic profile (including levels of homocysteine, ammonia, and lactate) were also within normal limits. Hemoglobin electrophoresis also revealed normal bands. Additional tests such as prothrombin time, activated partial thromboplastin time, antinuclear antibody test, anticardiolipin antibody immunoglobulin levels, protein C level and antithrombin III level were within normal limits.\nHowever a non-contrast enhanced computed tomography of brain showed a LACI [] which was confirmed on a magnetic resonance imaging scan. The patient was then hospitalized and treated with intravenous unfractionated heparin, which was then switched on to subcutaneous enoxaparin. After 7 days, her condition completely improved and she was discharged with oral warfarin.

[[35.0, 'year']]

F

{'1983896': 1, '15946211': 1, '16682663': 1, '2493841': 1, '5814299': 1, '8555935': 1, '12616980': 1, '24672184': 1, '8838483': 1, '9740116': 1, '20300047': 1, '24672193': 2}

{}

3952413-1

noncomm/PMC003xxxxxx/PMC3952413.xml

Conservative treatment of a femoral neck fracture following nail removal

A 67-year-old woman was treated for a pertrochanteric fracture (AO classification 31-A1.2) following a low-energy fall at home with closed reduction and internal fixation with a locked IMN (Bi-Nail, Gruppo Bioimpianti, Peschiera Borromeo, Italy). At three weeks, she was walking with full weight bearing without support, and bony union had occurred by 12 weeks. Eighteen months after surgery, the fracture had clinical and radiographical signs of complete healing. Twenty months after the operation, the patient complained of continuous discomfort over the great trochanter; anteroposterior view documented the apex of the implant protruding proximally and the lag screw that was set in the center of the neck [].\nDue to this discomfort, the need for IMN removal was felt. The day after the removal of the hardware, the patient complained of a left inguinal pain that increased during weight bearing. No traumatic events occurred postoperatively. Standard X-rays were taken and no fracture signs were present. Due to persistence of pain, two days later, further plain radiographs were taken showing a dubious fracture of the femoral neck. In addition, a computed tomography (CT) scan was performed, documenting a subcapital femoral neck fracture, which was classified as Garden's grade II [].\nIn this condition, a stable osteosynthesis could hardly be achieved as screw-holding power would have been reduced by the recent removal of a lag screw, making it more prone to the risk of cutting out and consequent screw loosening, especially in an elderly patient. In view of the minimally displaced impacted fracture and the rapid reduction of the symptoms at rest, conservative management with medication and close X-ray monitoring was conducted. The patient was allowed to walk with bilateral crutches with no weight bearing on the left limb, and was discharged after 10 days. Antiosteoporotic therapy was started with calcium and vitamin D supplementation in addition to antiresorptive drugs. At the radiographic follow-up at 30 days, no displacement was detected and the fracture line was not visible any more. Six months postoperatively, radiographs showed complete healing of the fracture []. At the clinical follow-up at six months, the patient had returned to previous daily activities, and clinical assessment showed a satisfactory range of motion with no pain on walking.

[[67.0, 'year']]

F

{'19809775': 1, '16078057': 1, '11716853': 1, '3343269': 1, '27274491': 1, '9308538': 1, '10149962': 1, '15645267': 1, '12670137': 1, '19484169': 1, '4064399': 1, '8746322': 1, '24672194': 2}

{}

3952414-1

noncomm/PMC003xxxxxx/PMC3952414.xml

Endometrial cartilaginous metaplasia: A case report with literature review

A 38-year-old multiparous female, with obstetric score of gravida 4, Para 4, live birth 4, abortion 0, presented with third degree uterovaginal prolapse (recto, cysto, and enterocele) for which she underwent transvaginal hysterectomy. Duration between the last pregnancy and hysterectomy was 7 years. There was no previous history of any intrauterine contraceptive device insertion. Also, there was no history of previous surgical intervention like dilatation and curettage after the last pregnancy or between pregnancies. There was no history of discharge per vagina, fever, or pelvic pain.\nHer menstrual cycles were regular, 5-7 days/30 days. However, a history of passage of clots and dysmennorhoea was present.\nHysterectomy specimen received for histopathological examination revealed the uterus with cervix measuring 8 × 3 × 2 cm. The cut section showed a tiny gray-white smooth, glistening rice grain like lesion measuring approximately 0.6 × 0.2 cm was embedded in the substance of uterus. An intramural fibroid measuring 2 cm in diameter, firm in consistency, showing whorled appearance was noted [Figures and ].\nMicroscopic examination revealed unremarkable squamocolumnar junction of cervix with squamous metaplasia of few cervical glands. Chronic inflammatory infiltrate was noted in cervical stroma.\nA section from the endometrium incidentally showed a solitary focus of well-formed hyaline cartilage in the endometrial stroma. Transition between stromal and cartilaginous cells was evident, which helped us to identify it as metaplastic. The surrounding endometrial tissue showed secretory changes. Inflammatory reaction and necrosis were absent. No evidence of granuloma was observed. Myometrium revealed adenomyotic foci with an intramural fibroid [].\nA histological diagnosis of endometrial cartilaginous metaplasia with adenomyosis and leiomyoma-uterus was made.

[[38.0, 'year']]

F

{'11832650': 1, '19008603': 1, '27790592': 1, '21209755': 2, '24672184': 1, '468134': 1, '26261678': 1, '19185859': 1, '8981150': 1, '21126963': 1, '24672195': 2}

{'2970784-1': 1}

3952898-1

noncomm/PMC003xxxxxx/PMC3952898.xml

Soil-acquired cutaneous nocardiosis on the forearm of a healthy male contracted in a swamp in rural eastern Virginia

A 45-year-old man presented to a local urgent care medical center in Roanoke, Virginia, with complaints of pain and a swelling on his right wrist. The patient reported having scratched his right wrist while playing paintball in eastern Virginia 3 weeks prior. He reported slipping while running through a swamp and received a small cut on the volar aspect of his right wrist. Two weeks later, he noticed a pimple-like lesion developing at the same site on his right wrist. The lesion quickly grew in size and then ulcerated. The patient’s temperature was 36.3°C (97.3°F). On physical examination, a large abscess, 1 inch × 4 inches in diameter was noted on the volar aspect of his right wrist, with erythema spreading along the anterior surface of his distal forearm ( and ). A chain of enlarged and tender lymph nodes was palpable going up the arm and surrounding the right axillary area.\nBecause of the severity of his condition, the patient was taken to the emergency room at Carillion Medical Center, where surgical drainage of the abscess was carried out and the pus was sent for culture and sensitivity testing. The emergency room physician suspected the patient had a methicillin- resistant Staphylococcus aureus infection and the patient was prescribed tetracycline, trimethoprim-sulfamethoxazole, and vancomycin. Blood tests revealed a peripheral white blood cell count of 5,500/mm3 (normal 4,000–10,500/mm3) with a differential of neutrophils, lymphocytes, and monocytes of 55.9%, 33.3%, and 6.2%, respectively (normal 42%–75%, 21%–51%, and 2%–13%, respectively). Laboratory studies revealed a hemoglobin of 14.0 g/dL (normal 13–16 g/dL), a hematocrit of 41.2% (normal 37%–49%), and a platelet count of 223,000/mm3 (normal 130,000–400,000/mm3). Urine analysis was negative for blood, leukocytes, protein, and glucose. A comprehensive metabolic panel revealed total protein of 6.6 g/dL (normal 6.0–8.3 g/dL), albumin of 4.6 g/dL (normal 3.2–5.5 g/dL), glucose of 77 mg/dL (normal 70–99 mg/dL), creatinine of 1.03 mg/dL (normal 0.5–1.4 mg/dL), calcium of 9.7 mg/dL (normal 8.5–10.7 mg/dL), total bilirubin of 0.3 mg/dL (normal <1.3 mg/dL), aspartate transaminase of 21 IU/L (normal 10–42 IU/L), and alanine transaminase of 20 IU/L (normal 10–60 IU/L). Three days later, culture of pus yielded colonies of Nocardia brasiliensis. After consultation with the infectious disease service, the tetracycline and vancomycin were stopped and the patient was continued on double-strength oral trimethoprim-sulfamethoxazole tablets (800–160 mg) once every 12 hours for 30 days. The patient reported remarkable improvement in his symptoms by day 5 after initiation of treatment with trimethoprim-sulfamethoxazole. Most of the lymphatic spread had resolved and only some erythema and swelling were seen at the area of the original lesion. A chest X-ray was reported as normal.\nFour weeks later, the patient returned for follow-up of his cutaneous nocardiosis infection. The site on his wrist was completely closed and there was no longer any erythema present. The patient retained a residual scar at the infection site (). His axillary lymph nodes were still enlarged and tender. The patient continued on double-strength oral trimethoprim-sulfamethoxazole tablets (800–160 mg) every 12 hours for a further 60 days. On follow-up after 2 months, the patient reported that he was doing well.

[[45.0, 'year']]

M

{'17374898': 1, '18578712': 1, '15544704': 2, '30237721': 2, '22469352': 1, '7923055': 1, '20349680': 1, '15871308': 1, '23712786': 1, '22219309': 1, '32602372': 2, '17194827': 1, '11688533': 1, '10987735': 1, '17539844': 1, '17350499': 1, '1568812': 1, '6340623': 1, '14532173': 1, '23392396': 1, '12398218': 1, '14431196': 1, '13900489': 1, '23680413': 1, '23966490': 1, '21304201': 1, '16614249': 1, '24244780': 1, '16882297': 1, '32435172': 1, '33193422': 1, '20463251': 1, '376887': 1, '12967747': 1, '19171991': 1, '15533065': 1, '22341733': 1, '23112367': 2, '7747092': 1, '24093436': 1, '3284465': 1, '23188464': 1, '14656414': 1, '6374833': 1, '21727716': 1, '8055469': 1, '24247124': 1, '20306281': 1, '10864621': 1, '12574299': 1, '21155087': 1, '11923355': 1, '17428927': 1, '24634589': 2}

{'3482810-1': 1, '534796-1': 1, '7328479-1': 1, '6136398-1': 1, '6136398-2': 1, '6136398-3': 1, '6136398-4': 1}

3953170-1

noncomm/PMC003xxxxxx/PMC3953170.xml

Transanal Evisceration Caused by Rectal Laceration

We present the case of an 81-year-old woman without interesting medical precedents excepting a moderated cognitive deterioration (with partial dependence for activities of daily living). She was taken to the hospital by her relatives after they found her in the bathroom presenting with intestinal loops exiting through her anus. The presence of a rectal prolapse was not among her precedents ().\nOn the first exploration, we recognized an abdominal excavation, which was painless on palpation, and we observed many small intestine loops with a congestive aspect exiting through the anus. When the patient arrived, she was hypotensive and tachycardic. After the first resuscitation attempt, an urgent blood test was requested, and the results showed albumin, 3; C-reactive protein, 47.3 mg/dL; and 19,700 leukocytes with neutrophilia, indicating an urgent need for surgery. The patient was taken to the operating room less than two hours after the beginning of the symptoms, and during the surgery, her hemodynamic condition remained the same.\nFor the surgery, the patient was placed in a modified lithotomy position, and two areas (abdominal and perineal) were prepared. After checking the difficulty of reducing the intestine exclusively through the anus, we performed an exploratory laparotomy, which revealed the absence of small intestine loops in the cavity; these had been moved to the pelvis and this was causing an important traction of the mesentery root. As a result, a manual reduction of the loops to the cavity through intraperitoneal traction was done; this was controlled from the perineal field. After the reduction had been completed, a 3 to 4 cm lineal craniocaudal perforation in the antimesenteric portion of the upper rectum was objectified (RIS II/AAC III). An important flaccidity of the entire pelvic musculature which contained a large rectovaginal pouch was observed, which resulted in both the superior rectum and the peritoneal reflection leaning on the pelvic floor (). The peritoneal cavity was abundantly washed with hot saline, and after some minutes, the loops initiated a visible peristalsis and took on a normal coloration. Later, the superior rectum and the sigmoid colon were dissected until the promontory, and an anterior resection of the rectum and a terminal colostomy in the left iliac region (Hartmann's procedure) were performed ().\nLater, the patient's relatives told us that she had difficulties defecating and had frequently manipulate herself to extract her feces. The patient was admitted to the intensive care unit for 3 days where she remained hemodynamically stable and her ventilatory support was ceased without incidence. She had a slow recovery, and on the 6th day tolerated oral intake well. She was discharged after 13 days, and two months later remained asymptomatic.

[[81.0, 'year']]

F

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{'3338229-1': 1}

3953172-1

noncomm/PMC003xxxxxx/PMC3953172.xml

Iatrogenic Rectal Diverticulum With Pelvic-Floor Dysfunction in Patients After a Procedure for a Prolapsed Hemorrhoid

A 42-year-old man with a 4-month history of constipation came to the hospital. The patient complained of excessive effort for evacuation, unsuccessful attempts, and long periods spent in the bathroom. Medical history included a hemorrhoidectomy four years earlier. He is a current smoker with a smoking history of 10 packs/yr.\nA review of the symptoms showed no abnormality, except constipation. Physical examination revealed normal rectal tone and intact anorectal inhibitory reflex. Laboratory findings showed no specific abnormality. On sigmoidoscopy, a feces-filled pocket with a 2-cm-sized opening was located just above the anorectal junction (). After the fecal material had been removed by using forceps, which took about one hour, a huge rectal diverticulum was seen (). The rectal mucosa surrounding the saccular lesion was normal, except for mild hyperemia and edema. There was no evidence of a fistula. The colon transit time was in the normal range (), and anorectal manometry showed a reversed defecation index with increased anal and rectal pressure at straining, consistent with pelvic floor dysfunction, type I (). Defecography showed a filled defect with a broad base at the anterior wall of the rectum, leading to lumen narrowing. These findings seemed to be associated with the excessive effort for evacuation (). Pelvic magnetic resonance imaging confirmed the diagnosis of rectal diverticulum outpouching through the muscular layer of the intestine in the left posterolateral direction ().\nAs a huge rectal diverticulum with fecalith can cause severe inflammation or sepsis, we decided to perform surgery. The patient underwent a transanal diverticulectomy and a direct rectal-wall repair. After the operation, the chief complaint, constipation, was lessened. He was discharged without any complications from the surgery and with no remaining symptoms. At the two-month follow-up, no abnormalities, except for a minimal saccular lesion, were found on sigmoidoscopy.

[[42.0, 'year']]

M

{'28273604': 1, '12432288': 1, '15973098': 1, '33791335': 1, '31890199': 2, '12195201': 1, '11888463': 1, '15622575': 1, '18618073': 1, '10711924': 1, '11557901': 1, '15864208': 1, '24639972': 2}

{'6926126-1': 1}

3953352-1

noncomm/PMC003xxxxxx/PMC3953352.xml

Sonographic Evaluation of the Peripheral Nerves in Hereditary Neuropathy With Liability to Pressure Palsies: A Case Report

A 73-year-old, right-handed woman visited our hospital in September 2010, complaining of right foot drop and numbness on right lower leg in the previous month. There was no history of diabetes, trauma or any other polyneuropathy. She had undergone a lumbar disc operation five years previously. In particular her first son and grandson had a history of transient monoparesis of upper limbs that spontaneously resolved.\nNeurological examination revealed weakness of right foot dorsiflexion and eversion (Medical Research Council scale grade 3) and reduced pinprick and touch sensations on the dorsal side of the right foot and the lateral aspect of the lower leg. Deep tendon reflexes at both knees and ankles were decreased.\nElectrodiagnostic studies showed a right peroneal neuropathy around the knee level and chronic bilateral L5 radiculopathy. The sonographic examinations demonstrated swelling of right common peroneal nerve around the fibular head level (cross-sectional area [CSA], 18 mm2), compared with contralateral side (CSA, 9.6 mm2).\nSix months later, while she was recovering from foot drop, she had another presentation with wrist drop on the right side. Electrodiagnostic studies were performed to rule out radial neuropathy. Motor nerve conduction studies showed prolonged distal latency and reduced compound muscle action potential amplitude in the right median nerve and no response in the right peroneal nerve. The ulnar nerve's segmental conduction velocities across the elbow were decreased (). In sensory nerve conduction studies, sensory nerve action potentials (SNAP) of both median nerves and right superficial peroneal nerve were not generated. The distal sensory latency was prolonged, and SNAP amplitude was reduced in both ulnar nerves (). In needle electromyography, ulnar innervated muscles including the abductor digiti minimi, first dorsal interosseous, and flexor carpi ulnaris showed large amplitude, long duration and polyphasic motor unit action potentials (MUAP) with reduced recruitment. In the forearm muscles innervated by radial nerve, extensor digitorum communis and extensor indicis proprius showed no MUAP. However brachioradialis and extensor carpi radialis longus muscles did not show any abnormalities. Median innervated muscles, such as abductor pollicis brevis and flexor carpi radialis, showed long duration and polyphasic MUAP. In lower limb muscles, abnormal spontaneous activities and large amplitude, long duration and polyphasic MUAP with reduced recruitment were demonstrated in right peroneal innervated muscles, such as tibialis anterior and peroneus longus (). These electrodiagnostic studies suggested not only right radial neuropathy, but also bilateral median, ulnar neuropath and right common peroneal neuropathy. The clinical findings and electrodiagnostic findings suggested HNPP, and the diagnosis was confirmed by genetic test demonstrating a PMP22 gene deletion.\nPeripheral nerves of the upper and lower extremities were examined by ultrasonography with an HD15 ultrasound system (Philips Ultrasound Inc., Bothell, WA, USA) using a 7-12 MHz linear array transducer. We traced most of the peripheral nerves, which were typically measured in previous studies about normal reference values of CSA in sonography, including median nerve at the level of carpal tunnel inlet and outlet in the forearm at the antecubital fossa and mid-humerus, ulnar nerve at the wrist and elbow, mid-humerus and radial nerve in the forearm and spiral groove level, common peroneal nerve at the fibular head level, tibial nerve at the popliteal fossa, sciatic nerve in the distal thigh and cervical roots at the C5-8 level. All measurements were done on the right side. CSA was measured using a direct tracing method just inside the hyperechoic rim of each nerve, and the CSA findings were compared with normal reference values [-].\nThe CSA of the median nerve at the carpal tunnel inlet and outlet (CSA, 10.8 mm2 and 9.8 mm2; normal value <6.7 mm2) and in the forearm (CSA, 12.7 mm2; normal value <10.7 mm2) was enlarged (). However the CSA of median nerve at the antecubital fossa (CSA, 13.1 mm2; normal value <13.2 mm2) and mid-humerus level (CSA, 10.9 mm2; normal value <13.1 mm2) was not swollen. The CSA of ulnar nerve was enlarged at the elbow (CSA, 9.3 mm2; normal value <8.3 mm2), but not in the wrist (CSA, 4.6 mm2; normal value <8.1 mm2), and not in the mid-humerus level (CSA, 5.0 mm2; normal value <7.9 mm2). The radial nerve was not swollen in the forearm (CSA, 5.5 mm2; normal value <14.3 mm2) or at the spiral groove level (CSA, 5.1 mm2; normal value <13.3 mm2). In the lower limb, the CSA of common peroneal nerve at the fibular head level was enlarged (CSA, 16.2 mm2; normal value <12.1 mm2) (). However, other nerves of lower extremity were not swollen: the tibial nerve at the popliteal fossa (CSA, 23.5 mm2; normal value <55.9 mm2) and the sciatic nerve in the distal thigh (CSA, 49.9 mm2; normal value <80.6 mm2). The cervical nerve roots (C5-8) were not enlarged at any root level: C5 root (CSA, 6.8 mm2; normal value <7.8 mm2), C6 root (CSA, 10.3 mm2; normal value <12 mm2), C7 root (CSA, 11.6 mm2; normal value <14.2 mm2) and C8 root (CSA, 9.8 mm2; normal value <14.4 mm2) ().

[[73.0, 'year']]

F

{'18351581': 1, '17321837': 1, '23055312': 1, '33572591': 1, '33359733': 1, '12210462': 1, '10734269': 1, '18440055': 1, '22102454': 1, '19697380': 1, '24639934': 2}

{}

3953353-1

noncomm/PMC003xxxxxx/PMC3953353.xml

Stepwise Rehabilitation of the Triple Amputee Combined With Dysfunction of the Sound Limb

A 36-year-old man, who had splenectomy history due to trauma when he was 10 years old, visited the emergency room due to abdominal pain and vomiting on November 15th, 2010. He developed septic shock, so norepinephrine was applied for 5 days and peripheral ischemia of four extremities occurred. The patient underwent right knee disarticulation, left trans-femoral amputation and right elbow disarticulation on December 21th, 2010 (). He underwent skin flap operation of the right knee and left hand skin defect area on January 10th and 24th, 2011, and joint range of motion exercise and isometric exercise were performed. After the operation wound healing, he was admitted to the Severance Rehabilitation Hospital for prostheses measurement and rehabilitation on March 5th, 2011.\nConsidering the patient's young age, we set the final goals as gait, independency of ADL and going back to work. During the initial stage of the rehabilitation program, we focused on upper extremity function improvement and independency improvement on wheelchair level activity. After this short-term goal had been reached, gait training and car training were planned. Finally, before discharge, we planned to do computer training since he used computer a lot for his marketing business.\nBefore admittance to our hospital, the patient had a psychiatric consultation due to depression. There was no objective data for the depression score, but he showed clinically meaningful level of depression, so he took antidepressant medication. After symptoms improved, medication was stopped, and he no longer took the pills after being admitted to our hospital. Since his limb was amputated when he was on shock status, he finally recognized amputation after recovering from the shock. This made him feel negative body image of himself, and thus he went through anorexia and sociophobia. But, after admission to our hospital, he accepted his situation and got over with negative body image and wanted active rehabilitation. We helped him get actively involved in the rehabilitation program by inspiring a sense of accomplishment from stepwise functional recovery. Sometimes he felt the depression, but he did not want to take the medication. Continuous support from his family and inducing motivation made him feel better, so he could actively participate in the rehabilitation program. The patient's motivation was increased particularly by setting short-term goals that considered the patient's condition and by sharing the rehabilitation program with the patient. When he was admitted, the stump sites were relatively fine: right elbow disarticulation site was club shape and stump length from acromion was 32 cm; right knee disarticulation site was cylindrical shape and stump length from great trochanter was 44.6 cm; and left trans-femoral amputation site was conical shape and stump length from great trochanter was 33.3 cm. Skin condition and soft tissue shrinkage of all three amputation sites were relatively fine with no bony spurs or neuroma. There had been phantom pain and phantom sensation on stumps, but they decreased during gait training with the prostheses. Also, his left hand was 2nd, 3rd, 4th, and 5th distal interphalangeal joint disarticulation status, skin flap site was fragile, and there were blisters due to friction during the rehabilitation program. This condition of the sound limb made the rehabilitation program more difficult for the patient. At first, passive range of motion of the left wrist joint flexion was 40° and extension was 30°. In addition, 1st web space length was 2 cm, but we could achieve 4 cm of 1st web space after left hand stretching exercise (). Due to the contracture and weakness of the left hand, he could not do opposition before intensive training, however, he was finally able to do tip pinch using thumb and 2nd finger when he picked up something like a tissue. Manual muscle power test (MMT) of upper extremities on admission showed grade 4 on both shoulder joints in terms of flexion, extension, abduction and adduction, grade 3 on the left elbow and wrist joint in terms of flexion and extension, and grade 2 on the left hand in terms of flexion and extension. MMT of lower extremities on admission showed grade 3 on both hip joints in terms of flexion, extension, external rotation and internal rotation. After strengthening exercise, the left hand muscle power improved to grade 3, and the hip joint muscle power improved to grade 4 together with strengthening exercise and Cybex (Cybex 770+TMC) isokinetic training. Since he had stayed in the intensive care unit (ICU) for a long time, deconditioning and impaired pulmonary function also made his rehabilitation program more difficult. Vital capacity (VC) on admission was 3,480 mL (75.9% of predictive value) and peak cough flow (PCF) on admission was 450 mL. We guided him to buy an Ambu bag and trained him to do air stacking exercise, and finally, VC/PCF reached to 5,300 (115%)/650.\nDuring the 2nd week of the program, he was fitted with the right elbow disarticulation prosthesis. Elbow disarticulation socket, elbow flexion device control unit, elbow lock control cable, outside locking hinge, constant friction wrist unit, and figure of 8 harness were used. Artificial hand was used for cosmetic reasons during work, and bimanual activity training was performed. Even though he was originally right handed, we planned to make sound left hand as the dominant hand at first. His left hand function test was impossible due to the contracture and weakness on admission, but after training, pinch power showed 1.8 kg and Box and Block Test showed 33 points. However, there still remained some limitations to using the left hand as the dominant hand. First, the motion of the left wrist was limited as flexion 50° extension 50°, and skin condition was still thin and fragile. Second, due to remaining contracture, it seemed hard to bear his weight with the left hand, even though the left hand function was recovered. So, we changed our plan and decided his right hand as the dominant hand and trained each hand the same proportionally. Before intensive gait training, we measured wheelchair (MIKI U2; MIKI Korea, Daegu, Korea), did ADL training with prosthesis on wheelchair level, and made him improve independency and use walking aid more efficiently after. Sitting balance was good on admission but ADL training had not been done; so Functional Independence Measure (FIM) score of self care subunit was 6 points. So intensive ADL training was done and he finally could don upper prosthesis by himself using pull over sweater method. But, since dressing, eating and grooming still needed minimal assistance due to the impaired hand fine motor function, ADL training was done consistently until discharge. On occupational therapy, ADL training, such as spoon use, drinking with a cup, and buttoning and unbuttoning, was done and as a result, follow-up FIM score improved to 12 after 1 month and 25 on discharge. He was able to do upper dressing by himself, although it took 2 minutes and 30 seconds. We decided on the dominant leg as the right leg because of the longer stump length on the right side. We also decided on the height of 162 cm, which is shorter than his original height of 167 cm, to improve stability by lowering the center of gravity. The patient was fitted with right knee disarticulation prosthesis with end bearing socket, polycentric knee, endoskeletal shank and dynamic solid ankle cushion heel (SACH) foot on the 6th week of the program. In addition, he was fitted with left trans-femoral amputation prosthesis with quadrilateral socket, polycentric knee, endoskeletal shank and dynamic SACH foot on the 8th week of the program. Parallel bar weight shift training was started on the 9th week of the program. On the 10th week of the program, he started gait training with anterior walker without wheels, and he finally could walk 100 m using anterior walker without pause (). After starting intensive gait training, we analyzed the gait pattern and found that the left leg was dragged on swing phase. We shortened the left leg by a quarter inch and it improved the gait pattern. During rehabilitation program, doctor, physical therapist, occupational therapist, and prosthetist regularly met twice a week and discussed the prostheses fitting, hand function recovery, and gait pattern. This multidisciplinary team approach made the patient more motivated and rehabilitation program more efficient.\nCane gait seemed to be difficult for him due to the left hand contracture and weakness. We decided to gait with a walker indoors and use an electronic wheelchair outdoors. Family education, such as stump site management, was done and occupational rehabilitation program, such as ADL training and computer training, was done for going back to work. We rented a car for disabled people and trained him to move to the driver's seat and drive short distance with electronic wheelchair. And we also gave him information about repair costs of a car for the disabled. He could use a computer mouse by himself, but since the typing speed was too slow, a universal cuff was used for faster speed. On discharge, ADL independency was increased up to 90 point of FIM score and 56 point of Modified Barthel Index score, which were 48 point and 20 point on admission, respectively ().\nFunctional level status also improved. He was at absolute bed rest status on admission, but at the time of discharge, he could come to sit by himself and gait with anterior walker. After discharge, we follow up on him constantly. He is successfully goes back to work using an electronic wheelchair and performs almost all of ADL by himself without help on wheelchair level.

[[36.0, 'year']]

M

{'12296984': 1, '907454': 1, '9881614': 1, '5676572': 1, '420566': 1, '9111458': 1, '24639935': 2}

{}

3953354-1

noncomm/PMC003xxxxxx/PMC3953354.xml

Videofluoroscopy-Guided Balloon Dilatation for the Opening Dysfunction of Upper Esophageal Sphincter by Postoperative Vagus Nerve Injury: A Report on Two Cases

A 62-year-old man had cervical spinal cord injury (neurological level, C8; American Spinal Injury Association D [ASIA-D]) after accidental fall. He underwent anterior fixation on C3-C7 and laminoplasty by posterior approach after four weeks, on the same level. After the second operation, sudden dyaphagia occurred. The patient could not swallow food and showed aspiration sign during mealtime. On physical examination, he presented hoarseness and deviated tongue to the left. Left vocal cord palsy was found on laryngoscopy. He was diagnosed as palsies of left vagus and hypoglossal nerves.\nFor the treatment plan, videofluoroscopic swallow study (VFSS) with 2 mL and 5 mL of radiopaque yogurt pudding and mineral water was done. The patient could not swallow the food, and aspiration was evoked by an overflowing of pyriform sinus remnant (). For 5 weeks, he was nourished by nasogastric tube and had conventional dysphagia therapy for UES opening, which included manual laryngeal elevation and Shaker exercise for five days a week. The patient showed no improvement.\nWe performed videofluoroscopy-guided balloon dilatation of UES. Checking images on fluoroscopy, 16-Fr Foley catheter with deflated balloon was inserted through the nasal cavity until the balloon part of catheter was estimated to be under the lower margin of UES. Then balloon was gently inflated using 3 mL of contrast media, and we pulled the inflated catheter slightly upward, locating the balloon at middle of UES (). We kept balloon at UES for 30 seconds so that UES could be dilated mechanically. If the balloon was thrown upward from UES, we promptly deflated and repositioned the balloon at UES and continued the procedure. The procedure was done ten times with one minute interval per session. At the end of each session, VFSS with yogurt pudding was done. When UES opening improved as much as possible to start pudding intake, VFSS was performed three days after the session. When VFSS demonstrated no aspiration and pyriform sinus residue was less than 10% of width, the ballooning treatment was terminated. Before and after ballooning, we measured clinical symptom score, disability rating scale for swallowing impairment and the amount of pyriform sinus residue [] ().\nAfter six ballooning sessions with a periodic interval of five days per month, pyriform sinus residue decreased from grade 3 to 1 () without aspiration (). The patient started oral intake. The clinical symptom score and disability rating score also improved from 9 to 0 and 4 to 0, respectively. Other neurologic symptoms like tongue deviation, vocal cord palsy and hoarseness continued for four months after the termination of ballooning. Dysphagia has not recurred for over a year.

[[62.0, 'year']]

M

{'11726859': 1, '26361588': 1, '9246397': 1, '20308522': 1, '22427310': 1, '32871899': 1, '21997884': 1, '18097197': 1, '17023244': 1, '12389853': 1, '24639936': 2}

{'3953354-2': 2}

3953354-2

noncomm/PMC003xxxxxx/PMC3953354.xml

Videofluoroscopy-Guided Balloon Dilatation for the Opening Dysfunction of Upper Esophageal Sphincter by Postoperative Vagus Nerve Injury: A Report on Two Cases

A 72-year-old man who had a retropharyngeal abscess underwent abscess removal surgery. After the operation, he complained of dysphagia. He was diagnosed as right vagus nerve palsy, showing hoarseness and abnormal position of right vocal cord on laryngoscopy.\nVFSS demonstrated a firmly closed UES. The patient could not swallow food and liquid through UES at all, and aspiration occurred by pyriform sinus residue with grade 3 (). He was nourished by nasogastric tube for six weeks and had conventional dysphagia therapy without any improvements. He received eleven trials of videofluoroscopy-guided balloon dilatation for two months with the same method as described in case 1. The UES opening improved, and no aspiration was observed in the final VFSS (). He could swallow 5 mL of yogurt pudding in four swallowing efforts to reach grade 0 of pyriform sinus residue () and started oral intake. The clinical symptom score and the disability rating score improved from 10 to 4 and 4 to 1, respectively. Other neurologic symptoms continued for two months after the termination of ballooning. Dysphagia has not recurred for over a year.

[[72.0, 'year']]

M

{'11726859': 1, '26361588': 1, '9246397': 1, '20308522': 1, '22427310': 1, '32871899': 1, '21997884': 1, '18097197': 1, '17023244': 1, '12389853': 1, '24639936': 2}

{'3953354-1': 2}

3953357-1

noncomm/PMC003xxxxxx/PMC3953357.xml

Right Calf Claudication Revealing Leriche Syndrome Presenting as Right Sciatic Neuropathy

A 52-year-old male with a past history of hypertension and bony fusion of the thoracolumbar spine (from 11th thoracic to 2nd lumbar vertebrae) due to tuberculous spondylitis, was presented to the department of orthopedic surgery. He was a heavy smoker and complained of right foot pain, claudication in his right calf, impaired gait functions, and muscle wasting on the right lower limb, which had begun 7 months prior to the visit.\nMagnetic resonance imaging (MRI) of the thoracolumbar spine showed severe kyphotic curvature in the thoracolumbar spine, and central canal stenosis on the 10th and 11th thoracic vertebra level with a relatively well preserved lumbar spinal canal ().\nThe first impression of his attending surgeon was that he had spinal stenosis, related to severe thoracolumbar kyphosis. However, his symptoms were not well correlated to the MRI findings; and his condition did not improve, despite undergoing two weeks of medication. Subsequently, he took an electrophysiologic study at the department of neurology. The nerve conduction study revealed reduced amplitude of the right tibial and peroneal compound motor action potential, and the sural sensory nerve conduction study result was within the normal range (). Needle electromyography showed abnormal spontaneous activities in the right tibialis anterior, peroneus longus, short head of the biceps femoris, gastrocnemius, extensor digitorum brevis, and the abductor hallucis. On volition, the giant motor unit action potential was noted in the tibialis anterior (). These electrophysiologic findings were suggestive of partial right sciatic neuropathy. They concluded that the patient's foot pain and claudication were caused by sciatic neuropathy, combined with lumbar spinal stenosis, and maintained medication for neuropathic pain.\nTwo months later, he visited the department of rehabilitation medicine for an impairment rating and disability determination, and was still complaining of right foot pain and right leg claudication. We focused on the previously diagnosed non-traumatic right sciatic neuropathy noting his medical history; and performed an extended examination to reveal an undiscovered cause of neuropathy, or other possible causes of his symptoms. He described right leg intermittent claudication affecting the buttocks, and a burning ache radiating to the calves and foot. His claudication was exacerbated during walking and slightly relieved when resting. Upon physical examination, we were able to palpate diminished femoral and popliteal pulses on the right lower limb compared with the other side. On neurologic examination, the sensory test showed hypesthesia in the right lateral knee and foot, and sole of the foot. The motor power of the right lower limb was above grade four in all tested muscle groups, but was slightly weaker than the left side. Atrophy was also found in the right calf, anterior leg and foot muscle, and deep tendon reflexes were hypoactive in the right lower limb.\nComputed tomography (CT) angiography was performed to rule out the possibility that the symptoms were caused by ischemic disease. CT angiography of the lower extremities showed an occlusion of the infrarenal abdominal aorta, and bilateral common iliac and right external iliac arteries; and collateral circulations to both the internal iliac arteries and left external iliac artery were also observed. However, there were no significant findings that could cause sciatic neuropathy, such as mass lesions (). These findings were compatible with Leriche syndrome. Therefore, we concluded that our patient had Leriche syndrome causing ischemic injury of the right sciatic nerve.\nHe was referred to the department of surgery and underwent a bilateral axillo-femoral and femoro-femoral bypass graft. After the bypass surgery, his symptoms including claudication and right foot pain were relieved; but hypesthesia and motor weakness of the lower limb arising from sciatic neuropathy persisted at the time of the last follow-up visit, 8 months after the surgery.

[[52.0, 'year']]

M

{'31952498': 2, '34066172': 2, '17859070': 1, '20488654': 1, '14557504': 1, '22504264': 1, '8175074': 1, '8931570': 1, '23177034': 1, '7451792': 1, '11239320': 1, '20411392': 1, '24639938': 2}

{'8150991-1': 1, '6966837-1': 1}

3953525-1

noncomm/PMC003xxxxxx/PMC3953525.xml

Secondary Aneurysmal Bone Cystic Change of the Chondroblastoma, Mistaken for a Primary Aneurysmal Bone Cyst in the Patella

A 29-year-old woman presented to our clinic with a 3-month history of left knee pain. The patient had no significant previous medical history or trauma. Pain was aggravated after going up and down the stairs. On physical examination, she had localized tenderness in the lateral aspect of the patella. However, there was no evidence of a soft-tissue mass and overlying skin lesion. Further, no joint effusion was noted. She had full range of motion and the neurocirculatory status was normal. Laboratory studies indicated that all inflammatory markers were within the normal limits. Radiographic examination revealed a well-defined osteolytic lesion with a sclerotic margin in the lateral aspect of the patella, and there was no pathologic fracture or periosteal reaction (). A technechium-99m bone scan showed an increased uptake isolated to the lateral aspect of the left patella. Magnetic resonance imaging (MRI) was also conducted, which showed a partially multilobulated and septated mass in the lateral aspect of the patella. A fluid-fluid level was noted in this mass with T1-low and T2-high signal intensity. The margins of the lesion were well defined and a cortical break was not seen in the anterior and posterior cortex of the patella (). Based on the imaging studies, the preoperative diagnosis was foremost aneurysmal bone cyst or simple bone cyst.\nAt surgery, there was no abnormality in the soft tissue around the patella. The lesion was aspirated using a needle and about 2 mL bloody fluids were discharged from the cavity. The lesion was a cystic cavity and was surrounded by a gray or brownish tissue. Multiple fragments of hemorrhagic soft tissue admixed with recognizable bone fragments were revealed. Curettage was completely performed and cauterization of the inner wall of the cavity was thoroughly done. After massive saline irrigation, the cavity was filled with autogenous iliac bone chips.\nMicroscopically, sheets of chondroblasts were intermingled with fine eosinophilic chondroid matrix. The chondroblasts showed oval shaped nuclei with moderate eosinophilic cytoplasm. Several multinucleated giant cells were scattered. Occasional mitotic figures were also identified. The indented nuclear grooves were characteristic nuclear features. Blood-filled cystic cavities were present in the chondroblastoma, consistent with secondary aneurysmal bone cyst ().\nThe final diagnosis was chondroblastoma with a secondary aneurysmal bone cyst. Post-operatively, the patient was ambulating without a limp and had a normal, pain-free range of motion. At the 3-month follow-up, she had returned to her usual daily and recreational activities. Radiologically, the grafted bones were well incorporated and there were no other abnormal symptoms and no recurrent evidence in the patella at the post-operative 1.5-year follow-up ().

[[29.0, 'year']]

F

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{}

3953526-1

noncomm/PMC003xxxxxx/PMC3953526.xml

Localized Nodular Tenosynovitis Originated near the Medial Plicae

A 41-year-old male was admitted to the hospital with a major complaint of left knee pain that began 3-4 years ago. There was no specific history of trauma or infection on the left knee. The patient reported intermittent knee pain and feeling of irritation (catching) during flexion and extension of the knee that had been present for 3-4 years. Due to persistent pain and irritating feeling upon squatting and over 100° of flexion, activities involving knee flexion was impossible. Since 18 months ago, a mass was palpable on the skin in the medial side of the left knee, and it moved underneath the skin when pressed by the hand. When the mass was checked or palpated on the medial skin of the knee, the pain with locking worsened, whereas when it was not palpated after being pressed underneath the skin, the feature of the symptom was similar but the severity was relieved. On physical examination, a mass with the size of a bean was observed on the medial surface of the patella, and tenderness was present. Simple radiography did not demonstrate any shadow of mass or local bony erosion, and the joint space appeared normal.\nOn magnetic resonance imaging (MRI), the area where the medial plicae is present inferomedial to the patellofemoral joint showed equal intermediate-low signal intensity on T1 images and a 8×11×7 mm sized oval-shaped mass with a low signal intensity was found on T2 images (). On the contrast enhanced images, findings of specific enhancement and effusion of synovial fluid or synovitis were not present.\nOn arthroscopic examination, a yellowish oval shaped mass of pedunculated type protruding through the patellofemoral joint was found. No abnormal findings of hypertrophy of the medial plicae were found and the articular cartilage of the patella and femur was not injured. We made a high anterolateral portal as a viewing portal. En bloc resection of the mass was done through the anteromedial working portal (). The size of the resected mass was 14×10×11 mm and it was a yellowish solid tissue with clear margin, and the color inside was dark-brown ().\nIn hematoxylin and eosin stain, pathologic studies showed histiocyte, fibrous tissue, and giant cells. Multinucleated giant cells mixed in a collagen stroma and macrophage that has eaten hemosiderin were found. It was diagnosed as localized nodular tenosynovitis originating from synovium just above the medial plicae (). Pain and mechanical symptoms were relieved immediately after surgery. During the 1-year follow-up, no recurrence of preoperative symptoms or abnormalities was found in physical examination.

[[41.0, 'year']]

M

{'22733940': 1, '7794435': 1, '26261570': 1, '32160509': 2, '11078555': 1, '12861198': 1, '8141018': 1, '24639948': 2}

{'7489121-1': 1}

3953527-1

noncomm/PMC003xxxxxx/PMC3953527.xml

Acute Simultaneous Ruptures of the Anterior Cruciate Ligament and Patellar Tendon

A 32-year-old male visited our clinic with a major complaint of severe pain in the right knee that started to occur when he managed to stop running over the second base that he had run toward while playing baseball. The right leg that was planted on the second base at the time of injury produced a crackling sound when the knee was flexed with a valgus force applied and severe swelling of the right knee, range of motion (ROM) restriction due to pain, and approximately 40° of extension lag were present. Simple plain radiography showed patella alta on the lateral view (), but other abnormal findings, such as a fracture, were not observed. Magnetic resonance imaging (MRI) was performed to identify if there is an accompanying injury, which revealed a complete tear of the patellar tendon and complete tears of the ACL and the medial collateral ligament (MCL) at the femoral attachment sites, and increased signal intensity in the lateral meniscus led us to suspect an injury to the meniscus ().\nAt 6 days after injury, primary suture repair of the patellar tendon with ACL reconstruction was carried out. The patellar tendon repair preceded the ACL reconstruction. Initially, a 10cm longitudinal skin incision extending from the middle of the patella through the center of the patellar tendon to the tibial tuberosity was made to expose the ruptured patellar tendon. The patellar tendon was completely torn in the midsubstance, the torn end had a frayed mop-end appearance, and the tear extended to the medial retinaculum (). Taking consideration into the shape of the torn end and the distally narrowing anatomical shape of the patellar tendon, the torn end was longitudinally divided into three equal sections, and three core sutures of the patellar tendon were determined. The center of the distal end was repaired with a Fiberwire (Arthrex, Naples, FL, USA) suture using the Krackow method. Two longitudinal bone tunnels were created in the patella using a 2.0-mm Kirschner wire. A suture was passed through the tunnel and pullout repair with the proximal end was performed on the anterosuperior patella with the knee in 45° flexion. The proximal end was sutured with two Fiberwire sutures at medial 1/3 and lateral 1/3 points using the Krackow method. A bone tunnel parallel to the tibial tuberosity was created, through which the sutures were passed and pullout suture with the distal torn end was done. At the torn ends, end-to-end anastomosis was performed additionally (. Subsequently, an anterolateral portal, an anteromedial portal, and an accessory far medial portal for anatomical ACL reconstruction were created through the skin incision. An arthroscope was introduced into the joint. The presence of a transverse tear in the posterior horn of the lateral meniscus that was not clearly identifiable on MRI was confirmed. It was repaired using an all inside technique with two PDS (polydioxanone monofilament; Ethicon Inc., Somerville, NJ, USA) sutures. A complete tear of the ACL at the femoral attachment site was confirmed, and reconstruction was done using an Achilles tendon allograft to avoid a donor site injury (). For anatomical ACL reconstruction, a femoral tunnel was created at the center of the femoral attachment of the ACL using the transportal technique and a tibial tunnel was made at the center of the tibial attachment site using Pinn-ACL tibial guide (Linvatec, Largo, FL, USA). With the calcaneal fragment of the Achilles tendon allograft placed toward the femur, the graft was fixated to the femur using a metal interference screw and to the tibia using a bioabsorbable interference screw with the knee in 20° flexion, and a metal staple was used for additional fixation. Following ACL reconstruction, a primary suture for the medial retinaculum and the patellar tendon sheath was carried out. The complete tear of the MCL at the femoral attachment site was conservatively treated: after 2 weeks of splint immobilization, rehabilitation therapy was administered so that the range of flexion could be gradually increased.\nFor the 14 postoperative days, the patient was treated with compression dressing, application of ice, and elevation of the leg with a long leg splint applied, to reduce swelling. From day 1 after surgery, quadriceps strengthening exercises were recommended. From the second postoperative week, the long leg splint was replaced with a limited motion knee brace and the patient was encouraged to perform flexion exercises within pain-free ranges. The range of flexion was gradually increased to 30° at the 2nd postoperative week, to 60° at the 4th postoperative week, and to 90° at the 6th postoperative week. Weight bearing ambulation was not allowed until 6 weeks after surgery due to the meniscal repair.\nMRI scan at 6 month after surgery showed well-maintained continuity of the ACL and patellar tendon and no abnormal findings in other soft tissue, such as the meniscus (). At 1-year postoperative follow-up, 0°-140° of flexion was possible, and no changes were detected in the Lachman and pivot shift tests. The Lysholm score was satisfactorily high (94 points). Other than discomfort in the knee after long or knee-straining activities, no complication was reported.

[[32.0, 'year']]

M

{'22439127': 2, '29051869': 2, '26566349': 1, '16022228': 1, '8827310': 1, '6938816': 1, '16171641': 1, '17210443': 1, '22110304': 1, '6985557': 1, '34327033': 2, '28456816': 1, '24639949': 2}

{'3307214-1': 1, '8302369-1': 1, '5635187-1': 1}

3953546-1

noncomm/PMC003xxxxxx/PMC3953546.xml

Posterior interosseous nerve syndrome due to intramuscular lipoma

A 48-year-old woman presented with spontaneous inability to extend the fingers of the left hand. She noticed a gradually increasing inability to extend the fingers over 6 months. She was unable to perform her domestic activities because of weakness and paresis of the hand; she denied any trauma or other diseases. Examination revealed a swelling of 5 × 3 cm in the anterolateral aspect of the left forearm in the region of the brachioradialis muscle just below the elbow. The swelling was firm in consistency, immobile, not fixed to the skin; there were no dilated veins over the swelling or signs of inflammation. The elbow function was normal, as was the flexor strength of the wrist and fingers; however, there was a decrease in the extension strength of the wrist and metacarpophalangeal joints of the fingers and thumb (power 3/5). There was no sensory deficit. Magnetic resonance imaging of the elbow objectified an intramuscular mass, of 8-cm-long axis depending on the supinator muscle, pathognomonic of a lipoma (Figs. and ). Surgical excision was recommended. General anesthesia was administered, and an incision was made over the mass. The incision of the supinator muscle exposed a fatty encapsulated mass (Fig. ). The dissection of the mass revealed that it is constricting the PIN (Figs. and ). The nerves were carefully released, and a lipoma was removed. The PIN was preserved, without damage (Fig. ). Histological examination of the tumor confirmed it to be a benign lipoma (Figs. and ). In the early postoperative period, the radial nerve recovered its function. A physiotherapy program was started 2 weeks after surgery. The patient recovered well, and 6 weeks after surgery, she resumed her activities. No local recurrence was detected at 18 months after surgery.

[[48.0, 'year']]

F

{'4015361': 1, '10393751': 1, '8088179': 1, '2398202': 1, '4288961': 1, '3038920': 1, '30050744': 2, '4652058': 1, '2022830': 1, '2323127': 1, '8836068': 1, '4745615': 1, '8116382': 1, '4288960': 1, '12475510': 1, '1430948': 1, '2584252': 1, '3561611': 1, '12195259': 1, '3755996': 1, '16076062': 1, '34094741': 2, '10190625': 1, '16630914': 1, '24634698': 2}

{'8164879-1': 1, '6059519-1': 1}

3953739-1

noncomm/PMC003xxxxxx/PMC3953739.xml

A case of hepatic portal venous gas due to viral gastroenteritis

A 71-year-old man with a medical history of diabetes mellitus type II, hypertension, dyslipidemia, and hypothyroidism presented with complaints of acute-onset nausea, vomiting, and abdominal pain. The patient also reported diarrhea, but denied any fevers or chills. The patient had no history of any manipulation of the gastrointestinal system. A physical examination revealed mild abdominal tenderness, pronounced in the upper-and lower-right quadrants, with no peritoneal signs. A computed tomography (CT) scan demonstrated no evidence of an acute intra-abdominal disturbance (). An extensive amount of gas, however, was found in the portal venous system (). Due to the patient’s clinical presentation and stable condition, a conservative management plan, including intravenous fluids and taking nothing by mouth, was implemented.\nCT scanning was repeated 3 hours later. Although the results reflected a diminished amount of portal venous gas, there was no evidence of any acute abdominal pathology that may have caused the hepatic portal venous gas (). After the patient’s nausea, vomiting, and abdominal pain resolved, no further medical interventions were ordered. On day 2 of hospitalization, the patient’s dietary restrictions were lifted and he was discharged. At the 1-month follow-up examination, the patient reported no health problems; a colonoscopy was performed, and results were within normal limits.

[[71.0, 'year']]

M

{'11735870': 1, '637584': 1, '30775674': 2, '13249015': 1, '33042664': 2, '27180229': 1, '19653334': 1, '24696625': 2}

{'7535866-1': 1, '6366390-1': 1}

3953743-1

noncomm/PMC003xxxxxx/PMC3953743.xml

New-onset ascites as a manifestation of virologic relapse in patients with hepatitis C cirrhosis

A 53-year-old woman with CHC genotype 1, biopsy-proven cirrhosis, and previous partial response to polyethylene glycosylated (PEGylated) interferon and ribavirin was started on telaprevir-based therapy. Cirrhosis was well compensated, without ascites or edema before and during therapy. Pretreatment laboratory evaluation revealed albumin 4.4 g/dL, aspartate aminotransferase (AST) 115 U/L, alanine aminotransferase (ALT) 120 U/L, alkaline phosphatase 191 U/L, total bilirubin 1.1 mg/dL, hemoglobin 16.3 g/dL, platelet count 183,000/μL, and hepatitis C virus (HCV) viral load 3,210,000 IU/mL. Upper endoscopy was negative for varices. Therapy was complicated by anemia requiring ribavirin dose reduction and erythropoietin therapy and rash that resolved after discontinuation of telaprevir. Viral load was 110 IU/mL at treatment week three and undetectable at week eight. PEGylated interferon and ribavirin were discontinued after 48 weeks of therapy. HCV viral load remained undetectable from week eight until the end of therapy. Laboratory evaluation at week 45 revealed albumin 2.7 g/dL, AST 125 U/L, ALT 67 U/L, total bilirubin 1.3 mg/dL, hemoglobin 10.1 g/dL, and platelet count 49,000/μL. Weight at the end of therapy was 132 lb (60 kg). One month after discontinuation of therapy, the patient presented with 5 lb weight gain (weight 137 lb) and new-onset ascites. Evaluation revealed albumin 3.1 g/dL, AST 77 U/L, ALT 44 U/L, total bilirubin 0.8 mg/dL, blood urea nitrogen (BUN) 8 mg/dL, creatinine 0.7 mg/dL, hemoglobin 13.5 g/dL, platelet count 105,000/μL, and virologic relapse with HCV viral load of 228 IU/mL. Abdominal magnetic resonance imaging (MRI) revealed a cirrhotic morphology, abdominal ascites, and recanalization of the umbilical vein and left retroperitoneal varices consistent with portal hypertension. The patient refused diagnostic paracentesis. An echocardiogram was obtained, which revealed normal left ventricular systolic and diastolic functions and right ventricular systolic pressure, with no sign of pulmonary hypertension. Ascites rapidly responded to sodium-restricted diet and diuretic therapy (spironolactone 50 mg, furosemide 20 mg daily). Repeat laboratory evaluation after control of ascites revealed an albumin level of 3.9 g/dL. Repeat viral load 3 months after the end of therapy was 528,810 IU/mL. Repeat abdominal MRI 7 months after therapy cessation showed no ascites.

[[53.0, 'year']]

F

{'22384189': 1, '3829877': 1, '7639225': 1, '11870385': 1, '24127561': 1, '18609142': 1, '20196120': 1, '20346533': 1, '13684979': 1, '18397389': 1, '18208570': 1, '23177279': 1, '19231019': 1, '21946021': 1, '23268517': 1, '17544878': 1, '18593587': 1, '20795462': 1, '18059233': 1, '24696626': 2}

{'3953743-2': 2}

3953743-2

noncomm/PMC003xxxxxx/PMC3953743.xml

New-onset ascites as a manifestation of virologic relapse in patients with hepatitis C cirrhosis

A 61-year-old woman with CHC genotype 1, biopsy-proven cirrhosis, and previous nonresponse to three courses of interferon-based therapy was started on telaprevir-based therapy. Cirrhosis was well compensated, without evidence of ascites or hepatic encephalopathy. Upper endoscopy was negative for esophageal varices. Laboratory evaluation revealed albumin 2.7 g/dL, AST 132 U/L, ALT 81 U/L, alkaline phosphatase 394 U/L, total bilirubin 0.8 mg/dL, hemoglobin 13.3 g/dL, platelet count 156,000/μL, and HCV viral load 71,600 IU/mL.\nAfter initiation of telaprevir-based therapy, the patient achieved rapid virologic response. Side effects of therapy included anemia, requiring ribavirin dose reduction and erythropoietin therapy. Treatment was noteworthy for stable hypoalbuminemia, with albumin level 2.1 g/dL without edema or ascites. She completed 12 weeks of telaprevir-based therapy, but therapy was discontinued at treatment week 31 due to a severe facial rash requiring systemic steroids for 2 days. HCV viral load remained undetectable from treatment week four until the end of therapy. Laboratory evaluation at the end of therapy revealed albumin 2.1 g/dL, AST 64 U/L, ALT 32 U/L, alkaline phosphatase 347 U/L, total bilirubin 1.3 mg/dL, hemoglobin 10.8 g/dL, and platelet count 80,000/μL. Weight at the end of therapy was 122 lb.\nThe patient presented 1 month later with 8 lb weight gain (weight 130 lb) over 2 weeks, new ankle edema, and abdominal distention. Abdominal ultrasound showed moderate ascites. HCV viral load was undetectable, albumin 2.9 g/dL, AST 71 U/L, ALT 37 U/L, alkaline phosphatase 309 U/L, total bilirubin 1.5 mg/dL, BUN 13 mg/dL, and creatinine 0.7 mg/dL. The patient refused diagnostic paracentesis. An echocardiogram was obtained, which revealed normal left and right ventricular function, with no sign of pulmonary hypertension. Sodium-restricted diet and diuretics (spironolactone 50 mg, furosemide 20 mg daily) were started, with prompt resolution of edema and ascites. Three months after the end of therapy, HCV viral load was 203 IU/mL, and on repeat 69,900 IU/mL, confirming relapse. Albumin level was 2.6 g/dL, AST 91 U/L, ALT 55 U/L, alkaline phosphatase 348 U/L, total bilirubin 1.1 mg/dL, BUN 12 mg/dL, creatinine 0.6 mg/dL, hemoglobin 13.5 g/dL and platelet count 140,000/μL. Diuretics were tapered, then discontinued at posttreatment week 20 with continued control of ascites. Albumin level remained stable at 2.6 g/dL.

[[61.0, 'year']]

F

{'22384189': 1, '3829877': 1, '7639225': 1, '11870385': 1, '24127561': 1, '18609142': 1, '20196120': 1, '20346533': 1, '13684979': 1, '18397389': 1, '18208570': 1, '23177279': 1, '19231019': 1, '21946021': 1, '23268517': 1, '17544878': 1, '18593587': 1, '20795462': 1, '18059233': 1, '24696626': 2}

{'3953743-1': 2}

3955046-1

noncomm/PMC003xxxxxx/PMC3955046.xml

Sarcomatoid carcinoma of the cervix with foci of malignant melanoma

Mrs. SRD, 42-year-old, P5 L3 D1 A1 , came to our hospital on 16th July 2012 with complaints of irregular bleeding per vaginum since 3 years. She had severe pain in the right lower limb since 1 month, because of which she was unable to walk and restricted to the bed. On examination, her general condition was fair, she was anemic. She had right sided unilateral lower limb edema. There was no evidence of any melanocytic lesion on her body.\nOn local examination, she had proliferative growth on the cervix that bleeds on touch. Both anterior and posterior fornix was involved with infiltration of upper 1/3rd of the vagina. On per rectal examination the right parametrium was involved up to the pelvic side wall and half of the left para was involved; the rectal mucosa was free. A clinical diagnosis of cervical cancer stage III B was made. Cervical biopsy was taken. On cystoscopic examination, proliferative growth was seen on the posterior wall of the bladder. Biopsy was taken from the bladder growth for histopathological confirmation.\nHer hemoglobin was 7.6 g%, liver and renal functions were within the normal limit. Chest X-ray was normal. Contrast enhanced magnetic resonance imaging (MRI) of pelvis showed large T2 hyperintense and T1 isointense cervical mass lesion with right parametrial extension. The mass was abutting the postero-lateral wall of the bladder with invasion of the right ureter, and contiguous bilateral pelvic nodes causing hydroureteronephrosis. There were multiple lesion in the left femur. MRI impression was Ca Cervix International Federation of Gynecology and Obstetrics (FIGO) IV-A with bone mets and bladder invasion [Figures –]. Histopathology was suggestive of sarcomatoid carcinoma of the cervix. Immunohistochemistry was positive for cytokeratin, vimentin, HMB45. Hence the final histo-pathological impression was spindle cell carcinoma with aberrant melanocytic differentiation/malignant melanoma [Figures and –]. The histology of bladder growth was similar to that of cervix.\nThe case was discussed in tumor board meeting with radiation and medical oncologists. In view of advanced stage and poor general condition of the patient, decision of only palliative radiation was taken. Single fraction of pelvic radiation with a dose of 10 Gy was given, covering the soft-tissue tumor and the bony metastasis. The unilateral lower limb edema was managed conservatively by keeping the left lower limb elevated. Patient didn′t respond well to the treatment; she had residual disease and succumbed to her disease after 5 months of the diagnosis of the disease.

[[42.0, 'year']]

F

{'33628550': 2, '33023546': 2, '12090596': 1, '18417901': 1, '31446521': 1, '19132380': 1, '19071254': 1, '12821337': 1, '15512438': 1, '5924009': 1, '17012994': 1, '22871628': 1, '10502448': 1, '3942711': 1, '7306481': 1, '19525876': 1, '24672206': 2}

{'7898279-1': 1, '7542461-1': 1}

3955047-1

noncomm/PMC003xxxxxx/PMC3955047.xml

Bladder neck leiomyoma presenting with acute retention of urine in an elderly female

This was a case report of a 45-year-old female patient presented in the emergency department with painful acute retention of urine. She did not have any history of LUTS prior to this. She was peri-menopausal and had a history of irregular and heavy menstrual period. On examination, urinary bladder was palpable and tender. Pelvic examination did not reveal any pelvic organ prolapse or mass. Ultrasonography was carried out prior to catheterization, which revealed a small growth at the bladder neck []. Growth was about 1.4 cm and had hyper echoic peripheral rim with sonolucent center with fine internal echoes. Results of laboratory investigations were within normal limit. On cystourethroscopy, small mass with smooth urothelial covering was present at the bladder neck extending onto proximal urethra []. Mass was extending from 10 o'clock to 2 o'clock position at the bladder neck. It was resected completely using 26 F continuous flow resectoscope and cutting loop electrode []. It was solid to cut and did not bleed much. Special care was taken to preserve the bladder neck. An 18 F two way Foley's catheter was kept for 2 days. Patient voided with good flow after catheter removal. At 6 months follow-up, patient was symptoms free and ultrasound of the bladder was normal.\nThe pathological findings revealed the proliferation of spindle-shaped cells with eosinophilic cytoplasm, muscular and fibrous tissue with fibrous stoma. The nuclei of the cells were cigar-shaped and centrally located. No evidence of mitotic figures, coagulative T-cell necrosis or atypia was seen. Hence, findings were consistent with a diagnosis of benign leiomyoma [].

[[45.0, 'year']]

F

{'28707097': 1, '9215185': 1, '19671234': 1, '19001649': 1, '14587232': 1, '20684762': 2, '2180171': 1, '20947147': 1, '21656478': 1, '8116123': 1, '1953060': 1, '33088718': 1, '29436249': 2, '16409615': 1, '15018444': 1, '9836573': 1, '24672207': 2}

{'6091827-1': 1, '2924335-1': 1}

3955306-1

noncomm/PMC003xxxxxx/PMC3955306.xml

Mucopyocele of the maxillary sinus

A 26-year-old male patient reported with a chief complaint of swelling in the left buccal vestibule distal to 28 since last 2 months associated with mild pain when the buccal mucosa is stretched while eating. There was no history of paresthesia or numbness present in the region of chief complaint and no aggravating or relieving factors. No relevant past medical history except the patient gave a history of recurrent sinusitis since last 8 months.\nOn extra-oral examination, slight tenderness was present below the left zygomatic buttress region without any evidence of swelling [].\nIntra-oral examination revealed a solitary soft fluctuant swelling in the buccal vestibule in the region of 27, 28 causing slight obliteration of left buccal vestibule in the same region. Borders of the swelling were not well-defined. Overlying mucosa was found to be normal and the temperature of the swelling was not raised [Figures and ]. The swelling was slightly tender on palpation. Interesting findings was firm digital pressure on the intraoral swelling resulted in greenish yellow pus discharge from the nose associated with fetid odor. There was no draining sinus in the region of swelling and 27, 28 were slight tender on percussion with distal periodontal pocket with 28. On the basis of case history and clinical findings, a provisional diagnosis of chronic periodontal abscess in relation with 27, 28 were made. Chronic infected sinusitis of the left maxillary sinus and infected cyst of the left maxillary sinus were considered as differential diagnosis.\nIntra-oral periapical radiograph of 27, 28 region, topographic occlusal view of maxilla (left side) and orthopentamogram(OPG) shows periodontal ligament(PDL) space widening with 27 in the apical 1/3rd, loss of lamina dura in apical 1/3rd of 28 mesially and complete loss of lamina dura distally and also shows rarefaction in adjacent alveolar bone [Figure –]. Postero-anterior(PA) waters view shows complete opacification of the left maxillary sinus []. OPG and PA water's view were less informative to give proper diagnosis and to judge the extent of the pathology thus computer tomography (CT) scan was advised.\nAxial section (soft-tissue window) of CT [] shows complete obliteration of the left maxillary sinus with soft-tissue density mass which is protruding posteriorly and causing complete destruction of the postero-lateral wall of the maxillary sinus, obliteration of pterygomaxillary fissure and intact anterior and medial wall []. The soft-tissue expansile mass, which is protruding from the sinus, is well-defined roughly round having smooth borders without cortication. There is a slight obliteration of left nasal cavity. Coronal section of C.T. [Figure and ] shows complete opacification of the left maxillary sinus with destruction of the floor of the sinus laterally, causing the protrusion of the mass laterally. CT scan diagnosis was suggestive of benign expansile and destructive lesion of left maxillary sinus.\nThe patient underwent an incisional biopsy of the lesion under local anesthesia, which was approached by a mucosal incision in the upper buccal vestibule. The incised lesion was submitted for histopathological examination. Histopathological report suggestive of infected mucocele of maxillary sinus (mucopyocele).\nSurgical excisions of the entire lesion were carried out under local anesthesia. Patient recovery was uneventful and was kept under follow-up for next 6 months and no fresh complaints were observed.

[[26.0, 'year']]

M

{'19415059': 1, '11801943': 1, '12618979': 1, '16301155': 1, '27896530': 1, '1054452': 1, '24688571': 2}

{}

3955307-1

noncomm/PMC003xxxxxx/PMC3955307.xml

Binder's syndrome: Report of two cases

A 19-year-old male patient reported to dental clinics with a chief complaint of facial deformity. On extra-oral examination he presented with a mild Class III skeletal pattern. Mid-face hypoplasia was evident with a reduced fronto-nasal angle reflected in a straight profile. The lips were competent at rest with no obvious facial asymmetry [Figures and ]. No deviation was noticed on opening or closing of jaws.\nIntra-oral examination revealed the absence of permanent left central and lateral incisors (21,22) along with both mandibular canines. The maxillary arch exhibited displaced canines and left lateral incisor whereas mild crowding was evident in the mandibular arch. In addition, reverse overjet and over bite of 3-4 mm was seen [Figures –].\nOn radiological examination, the lateral cephalogram confirmed the clinically apparent Class III skeletal pattern, along with an increased mandibular plane angle and increased lower facial height. Pseudo-mandibular prognathism was also seen due to retrognathic maxilla [].

[[19.0, 'year']]

M

{'13961673': 1, '7440179': 1, '3763744': 1, '7271181': 1, '3771740': 1, '2359101': 1, '3860389': 1, '1066977': 1, '2916471': 1, '18005847': 1, '24688572': 2}

{}

3955308-1

noncomm/PMC003xxxxxx/PMC3955308.xml

Management of multiple intrusive luxative injuries: A case report with 7-year follow-up

An 11-year-old girl was referred to the Emergency Ward of Indira Gandhi Medical College, Shimla in the evening, following traumatic injuries to her teeth caused by a fall from the first floor of her house. Her medical history was unremarkable and all her vaccinations were up to date. On examination, there were no signs of neurological or extra oral injuries. Intra-orally, she presented severe intrusive luxation of 11, 21 and 22 (more than 6 mm) and laceration on the lower lip.\nAt the initial appointment, the intra-oral soft-tissues were cleaned with saline and hydrogen peroxide. Patient was prescribed antibiotics and analgesics, chlorhexidine mouthwash, oral hygiene instructions were given and soft diet was advised. Sutures were placed on the lower lip laceration and patient was referred to the Department of Pediatric Dentistry.\nThe intruded teeth showed no mobility. There was no evidence of traumatic injury to any other teeth. The radiographic examination consisted of one panoramic view and two periapical views. Periapical view revealed closed apices of intruded incisors []. The periodontal space surrounding intruded incisors was diminished and no root or bone fracture was detected.\nSince the teeth presented with mature apices, prophylactic endodontic treatment was planned. Hence, gingivectomy was performed to gain access to the root canal. The access opening was carried out neither bleeding nor consistent pulp was found during the root canal preparation; thus, the diagnosis of necrotic pulp of teeth was confirmed. Then, the root canals were filled with calcium hydroxide (Ca(OH)2) mixed with normal saline and it was decided to allow teeth for spontaneous eruption. At 1 week follow-up, there was no evidence of re-eruption. Subsequent weekly examinations revealed no eruption of the intruded teeth.\nTen weeks following dental injury, a decision was made to reposition the intruded teeth orthodontically. A fixed multi-bracketed appliance was bonded to the intruded teeth and adjacent teeth. The extrusion was carried out with elastic traction. Twenty six weeks after the start of treatment by orthodontic extrusion, the location of the intruded 11, 21 and 22 were restored to their original position. Ca(OH)2 dressing was changed initially after 4 weeks and subsequently after 12 weeks. The teeth were obturated with Gutta-percha after 1 year []. The case was monitored for 7 years and no clinical and radiographic pathology was detected [Figures –].

[[11.0, 'year']]

F

{'16499631': 1, '12848710': 1, '12110105': 1, '19021666': 1, '3867505': 1, '11766095': 1, '15460297': 1, '24688573': 2}

{}

3955309-1

noncomm/PMC003xxxxxx/PMC3955309.xml

Treatment of severe rotations of maxillary central incisors with whip appliance: Report of three cases

A 7-year-old boy was referred to the Pediatric Dentistry Department of Mashhad University of Medical Sciences with the chief complaint of severe rotation of one of his maxillary central incisor and a wound in the maxillary anterior labial mucosa caused by the continuous irritation of the incisal edge of rotated tooth. The medical history of the patient revealed no problems. In the extra oral examination, regarding lateral view, patient was mild convex and lip competent and in frontal view he was mesoprosopic. In the intraoral examination, there was Class I molar relationship with about 70° rotation of right maxillary central incisor []. Skeletal relationship of the patient was Class I and he did not have vertical problem. In the radiographic examination, pathologic problems such as supernumerary teeth or odontoma were not discovered, and revealed that 3/4 root was completed. After taking an alginate impression to fabricate study model, space analysis on study models did not show any space deficiency. The parents rejected any traumatic injury to the upper jaw in the past, but the history of intensive finger sucking habit was reported. At the first step, because of severe dental plaque accumulation due to inadequate oral hygiene, 1 week time was given to the patient to correct his oral hygiene. During this period, the parents were instructed to cover the incisal edge of rotated central incisor with wax to prevent continuous irritation of labial mucosa and to change it after each meal. In despite of the existence of dental caries in deciduous teeth of patient, the parents did not agree with restoring these teeth. After a week, an alginate impression was taken of the upper jaw in order to construct a removable appliance. This appliance was made of acrylic base plate, circumferential clasps on the maxillary primary canines and Adams clasp on the maxillary permanent first molars. In the later appointment, a mandibular first molar buccal tube (Dentarum, Germany) was bonded directly on the labial surface of the rotated central incisor with light cured composite resin (Trans Bond XT, 3M Unitek, USA). Whip spring was built with a segment of 0.4 mm stainless steel orthodontic wire (0.0016 inches) (Dentaurum, Germany), in which the distal end of the wire was bended to form vertical loop facing upward and immediately a vertical loop facing downward [Figures –]. The mesial end of the spring was inserted into the slot of the tube and to prevent damage to the gingival tissue, the outer end of the wire from the buccal tube was bent toward the incisal edge. The hook created in the distal end of the spring was engaged into the bridge portion of the right Adams clasp. The patient was instructed to remove the appliance only for tooth brushing after eating and in the rest of the time to wear the appliance for prevention of damage to gingival and buccal mucosa by the whip spring. After a few days, the patient returned with the complaint of a painful wound caused by whip spring in the mucobuccal fold area. Therefore, in order to deviate the wire from the vestibular mucosa, a vertical bend down and then a horizontal bend to distal was formed. The patient had no problem with the whip spring after this modification.\nAfter 4 weeks, the tooth was derotated very well. [] There was no need to coverthe incisal edge and the wound in labial mucosa completely healed. In every follow-up appointment, with a month interval, the whip spring was replaced by a new one. After 4 times replacement of the spring, rotation was almost corrected []. In order to overcorrect the rotated tooth, another removable appliance with a z-spring that forced the mesial aspect of lingual surface of the tooth was fabricated. At the end of treatment, supracrestal fiberotomy was performed and a segmented arch wire was placed to prevent relapse []. At 1 year follow-up, there were not any pathologic findings in the radiographic view like root resorption [].

[[7.0, 'year']]

M

{'24151406': 1, '11587502': 1, '11887384': 1, '7897011': 1, '17465662': 1, '21545300': 1, '9770106': 1, '22497228': 1, '21712629': 1, '24688574': 2}

{'3955309-2': 2, '3955309-3': 2}

3955309-2

noncomm/PMC003xxxxxx/PMC3955309.xml

Treatment of severe rotations of maxillary central incisors with whip appliance: Report of three cases

A 7-year-old boy was referred to the Pediatric Dentistry Department of Mashhad University of Medical Sciences with the chief complaint of severe rotation of the upper anterior tooth. There was no relevant and remarkable medical history reported. The clinical examination showed good facial symmetry and competent lips at rest. Intraoral examination showed Class П molar relationship with about 90° rotation of left maxillary central incisor. The rotated tooth was not fully erupted [Figure and ]. Class I skeletal pattern with no vertical problems was confirmed by cephalometric analysis and there were no transverse problems. Radiographic examination confirmed severe rotation of left maxillary central incisor and early stage of root development []. Space analysis on the study models shows a lack of space in both jaws. At the first visit, an alginate impression was taken from upper arch and a removable appliance consisting of acrylic base plate, circumferential clasps on the maxillary primary canine and Adams clasp on the maxillary permanent premolar and first molars was made. In the later appointment, a bonded mandibular first molar buccal tube (Dentaurum, Germany) was placed on the labial surface of the rotated central incisor. Whip spring was constructed with a segment of 0.4 mm stainless steel orthodontic wire (0.0016 inches) (Dentaurum, Germany) ligated into place. In order to protect buccal mucosa and gingiva from irritation the patient was instructed to wear the appliance fulltime and only to remove the appliance for tooth brushing after eating.\nIn every follow-up appointment, with a month interval, a new whip spring was fabricated. After 5 times replacement of the spring, rotation was almost corrected []. At the end of treatment, supracrestal fiberotomy was performed and alginate impression was taken of the upper jaw in order to construct a removable appliance for retention. This appliance was made of acrylic base plate, labial bow on anterior segment and Adams clasp on the maxillary permanent first molars []. There were no pathologic findings in the radiographic view [].

[[7.0, 'year']]

M

{'24151406': 1, '11587502': 1, '11887384': 1, '7897011': 1, '17465662': 1, '21545300': 1, '9770106': 1, '22497228': 1, '21712629': 1, '24688574': 2}

{'3955309-1': 2, '3955309-3': 2}

3955309-3

noncomm/PMC003xxxxxx/PMC3955309.xml

Treatment of severe rotations of maxillary central incisors with whip appliance: Report of three cases

A 9-year-old boy was referred to Orthodontics Department of Mashhad University of Medical Sciences. His chief complaint was severe rotation of his left maxillary central incisor. The patient was medically healthy. His dentistry history revealed that he had a supernumerary tooth between two maxillary central incisors and the mesiodens had been extracted before referring to orthodontic department. Before beginning of treatment, the patient was instructed about oral hygiene. Intraoral examination revealed that the tooth had 90° rotation. Radiographic examination showed early stage of root development [Figure –] and there was enough space in the upper arch to derotate it. At first alginate impression was taken of the upper jaw and a removable acrylic appliance with C clasps on the maxillary primary canines and Adams clasps on the maxillary permanent first molars was constructed. In the second appointment, just like the previous cases, buccal tube was bonded and the whip spring was constructed and inserted into its position. The patient was instructed to wear the appliance all the time except brushing and eating periods. After 1 month, the tooth was derotated well []. In this appointment, a new spring was fabricated and this process was repeated 2 times with 1 month interval and rotation was corrected. To over-correct the tooth position, the appliance was used one extra month. At the end of treatment, the removable retainer appliance was constructed and used by patient for 6 months to maintain the corrected tooth position []. Follow-up panoramic radiograph revealed healthy root development [].

[[9.0, 'year']]

M

{'24151406': 1, '11587502': 1, '11887384': 1, '7897011': 1, '17465662': 1, '21545300': 1, '9770106': 1, '22497228': 1, '21712629': 1, '24688574': 2}

{'3955309-1': 2, '3955309-2': 2}

3955425-1

noncomm/PMC003xxxxxx/PMC3955425.xml

Laparoscopic Approach to a Large Ovarian Fibroma: A Case Report

A 24 year old Gravida 1 Para1 (G1P1) lady presented to the gynecology clinic of Rasoul-e-Akram hospital with pelvic discomfort for one year, which was recently exacerbated and dominantly located on right lower quadrant of the abdomen. The patient had no medical or surgical history, except for one Pfannenstiel-kerr cesarean section about 3 years ago. Primary physical examinations revealed a mobile solid mass of nearly 12 − 14 cm in diameter, which couldn't be differentiated from a uterine myoma. Pelvic ultrasonography showed a mixed echo mass of 117×83 mm in right adenexa, with vascular flow and pressure on posterior wall of the uterus. There was no sign of ascites or plural effusion. Preoperatively, tumor markers were assessed, which were within normal range and patient was scheduled for laparoscopic resection of the lesion on December 2012 in Rasoul-e-Akram hospital.\nAbdominal access was achieved by primary puncture with a 10 mm diameter umbilical cannula. Two other 5 mm diameter ancillary cannulas were introduced after creation of pneu-moperitoneum by nearly 2.5 L of carbon dioxide.\nA rigid video laparoscope was entered via umbilical port and two grasping forceps were introduced via two ancillary cannulas. During the procedure, the patient was placed in Trende-lenburg position. Several adhesion bundles were seen between uterus, adnexa, omentum and abdominal wall that were lysed. The right ovary contained a huge (10×15 cm), multiloculated, mobile and well circumscribed mass with laparoscopic features similar to a benign ovarian mass especially an ovarian fibroma or thecoma ().\nWe sent a sample for frozen section examination which proved the benign nature of the tumor, ovarian fibroma. Despite the size of the mass and tight adhesion of the capsule to the ovarian tissue, with a careful dissection and desiccation of the tumor, we could preserve the ovary during complete excision of the fibroma. After the excision of the ovarian fibroma, under direct vision of a 5 mm telescope, it was morcellated and removed through the umbilical port.\nPneumoperitoneum was then deflated and ports were removed under direct vision. Finally, the rectus sheath and skin were closed with vicryl 2/0. Operating time from incision to closure was nearly 50 min, with no intraoperative complication. Postsurgical recovery was uneventful and the patient was discharged on the second day of surgery. There were also no immediate postoperative complications. Histopathologic examination revealed proliferation of spindle cells with blended nucleus in stratiform pattern with no pleomorfism or mitotic activity, which confirmed the diagnosis of ovarian fibroma ().

[[24.0, 'year']]

F

{'21772861': 2, '1977643': 1, '31380131': 2, '16498263': 1, '18164409': 1, '20817576': 1, '18501324': 1, '14584663': 1, '21902936': 1, '32090012': 2, '26175813': 1, '18274181': 1, '12837976': 1, '11387302': 1, '16515612': 1, '11055482': 1, '24696796': 2}

{'6662441-1': 1, '3129069-1': 1, '7008642-1': 1}

3955783-1

noncomm/PMC003xxxxxx/PMC3955783.xml

Superior Vena Cava Syndrome Associated with Right-to-Left Shunt through Systemic-to-Pulmonary Venous Collaterals

A 54-year-old woman presented with intermittent swelling of the face and arms. Her past surgical and medical history included pleurodesis for recurrent left-sided pleural effusions and Factor V Leiden deficiency disorder, for which she was taking warfarin. This was further complicated by recurrent hypercoagulable events including deep venous thrombosis and pulmonary embolisms. On examination, her body temperature was 36.8℃, heart rate was 94 beats per minute, blood pressure was 132/68 mm Hg, and respiratory rate was 18 breaths per minute. Clinical examination also revealed bilateral lung basal crackles, and prominent engorged vasculature in the neck and anterior chest wall.\nMultidetector computed tomographic (MDCT) venography of the chest was performed. Coronal reformation images (), maximum-intensity-projection images (), and volume-rendered images () demonstrated complete chronic SVC obstruction () with numerous resultant paravertebral and chest wall venous collaterals (), representing the involvement of lateral thoracic and paravertebral collateral pathways. In addition, a few patent left-sided pleuro-pulmonary venous collaterals () extending from the chest wall, crossing the pleura and lingular lobe, and finally draining into the left superior pulmonary vein were seen, and this finding was consistent with the presence of systemic-to-pulmonary venous collateral pathway (SPVC) and bridging subpleural pulmonary veins.\nSince our patient had complete chronic SVC occlusion resulting in the formation of right-to-left systemic-to-pulmonary venous collaterals, a coexisting hypercoagulable state, and deep vein thrombosis, subsequent lifelong anticoagulation with warfarin was initiated to reduce the risk of stroke. Angioplasty or stenting of the SVC was not recommended, because the SVC occlusion was secondary to a hypercoagulable state, rather than due to external compression, which in most cases, is due to malignancy. Due to the presence of extensive collaterals, embolization of the venous collaterals was not performed, and the patient was discharged after symptomatic improvement.

[[54.0, 'year']]

F

{'20123198': 1, '14716228': 1, '12797605': 1, '16476534': 1, '20308479': 1, '32518547': 2, '8352099': 1, '20083586': 1, '15239421': 1, '22401618': 1, '24644407': 2}

{'7265738-1': 1}

3955784-1

noncomm/PMC003xxxxxx/PMC3955784.xml

Non-Ischemic Perfusion Defects due to Delayed Arrival of Contrast Material on Stress Perfusion Cardiac Magnetic Resonance Imaging after Coronary Artery Bypass Graft Surgery

A 50-year-old man visited our hospital for a 3 month-follow-up examination after coronary bypass graft surgery. In this surgery a left internal thoracic artery (LITA) graft to the distal left anterior descending artery (LAD), and a right saphenous venous Y graft from the LITA to the diagonal branch and posterior descending artery (PDA) was performed through sequential anastomosis. The cardiac adenosine stress perfusion MR imaging revealed two perfusion defects at the mid-anterior and mid-inferior walls (, Movies I, II). One perfusion defect at the mid-anterior wall was reversible on rest perfusion images. However, the other perfusion defect at the mid-inferior wallwas persistent on rest perfusion images. But later it disappeared on both stress and rest perfusion images. On the myocardial single-photon emission computed tomography, the inferior wall showed a mild degree of perfusion decrease which was considered as due to the diaphragmatic attenuation effect rather than an ischemic perfusion defect while the mid-anterior wall showed a reversible perfusion defect indicating a reversible ischemia (). On cine images no regional wall motion abnormalities and on late gadolinium enhancement images no delayed myocardial enhancement were observed.\nSignal time curve analyses at stress and rest perfusion MR were performed at three different regions: normal myocardium at the mid-lateral wall and two perfusion defects at the mid-anterior and mid-inferior walls (). From the data, the perfusion index and ratio index of each region were calculated using a previously described method (). In brief, a smooth-fit corrected signal-time curve within the time window of the first pass was analyzed using the gamma-variate function after subtraction of the baseline signal intensity (SI) value from the mean SI of each region. The time window of the first pass was determined from the SI curve of the left ventricular cavity. The time window of the first pass in the myocardium at the same level as the left ventricular cavity was determined by shifting the time window determined from the left ventricular cavity to when the SI in the myocardium started to rise. The maximal upslope indicating the perfusion index was computed from the peak value of the time derivatives of the fit function in the myocardial region, normalized by the maximal upslope in the left ventricular cavity. The ratio index, widely accepted to represent myocardial perfusion reserve, was defined as the ratio of maximal upslope at stress to that at rest (). To calculate perfusion parameters an in-house software was developed using MATLAB 2012a (MathWorks, Natick, MA, USA).\nThe corrected signal-time curves demonstrated that the maximal upslope of the anterior wall decreased from 0.089 during rest to 0.022 during stress perfusion with a ratio index of 0.25, indicating typical reversible ischemia (). In contrast, the maximal upslope of the mid-inferior wall was similar to that of normal myocardium during stress and rest perfusion. But the time to delivery and time to peak enhancement were delayed 7 seconds on both stress and rest images approximately (). The maximal upslope of the mid-lateral wall increased with a ratio index by 1.10 from 0.094 during rest perfusion to 0.104 during stress perfusion. Also for the mid-inferior wall the maximal upslope increased with a ratio index by 1.10 from 0.079 during rest to 0.087 during stress perfusion (). Coronary angiography revealed a focal tight stenosis at the anastomosis site between the right saphenous venous graft and diagonal branch, limiting the flow to the diagonal branch. With this can be explained the reversible ischemia at the apical to the mid-anterior wall on perfusion MRI. However, there was no significant stenosis at the right saphenous venous graft to the PDA. The contrast delivery in the right saphenous venous graft was slightly delayed compared to the LITA to distal LAD graft. It may indicate that the early perfusion defect at the mid-inferior wall was a result of delayed contrast media delivery due to the wide and long pathway of the bypass graft (). Six-month follow-up images showed still a persistent perfusion defect without significant stenosis of the saphenous venous Y graft in the mid-inferior myocardial wall ().

[[50.0, 'year']]

M

{'31854146': 1, '11869854': 1, '11771450': 1, '19580726': 1, '12570960': 1, '19909933': 1, '12860910': 1, '11342469': 1, '17578718': 1, '20465836': 1, '34134696': 1, '24644408': 2}

{}

3955786-1

noncomm/PMC003xxxxxx/PMC3955786.xml

Forensic Imaging for Causal Investigation of Death

A 63-year-old man was found in the street after overrun by a car. An emergency physician stated the on-site death. According to the whole setting of the accident and after hearing both the car driver and witnesses, when being overrun, the man was lying on the street already. As usual in such cases, one of the first debated questions was if the death occurred prior or subsequent to the overrun.\nA postmortem CT imaging of the whole body was done prior to the autopsy. The examinations were performed on a 128-slice dual-source CT system (Somatom Definition Flash, Siemens AG, Forchheim, Germany). The examination started with anterior-posterior and lateral scout views. The parameters were for the entire body including the head pitch 0.35, gantry rotation time 1.0 seconds, tube voltage 120 kV, effective tube current time product 550 mAs_eff and field of view 50 cm. Image reconstructions were performed using the filtered backprojection. Reconstructed images where transferred for further processing, reformatting and displaying to the syngo multimodality work place (Syngo MMWP, Siemens AG, Forchheim, Germany). The subsequent consensus report of two radiologists (one board-certified radiologist with substantial experiences of clinical CT reporting for more than 20 years and one resident with 2 years experiences of clinical CT reporting as well as each with one year experience in postmortem imaging), revealed as the main findings multiple bone fractures of the skull, ribs, vertebrae and extremities as well as a distinct laceration of the spleen. All this lesions were without any relevant surrounding hemorrhage which would have been expected under these circumstances. In the duodenum, a round radiopaque formation was found which was reminiscent of a conglomeration of ingested tablets which indicates medication intake before death (). The radiologic report concluded that the man was overrun postmortem, after having died shortly before due to another reason, presumably as a consequence of intoxication.\nThe subsequent autopsy was done on the following day by two forensic pathologists being unaware of the radiologic report. In the autopsy report, the stomach and duodenum were documented to contain a brownish friable mass. However, a blister of zopiclone tablets was found in the personal belongings of the man (zopiclone AbZ, 7.5 mg), containing altogether fourteen tablets, nine of them having been removed. Indeed, zopiclone could be identified with the toxicological analysis of the stomach content and urine. Additionally, blood samples were collected from the saphenous vein. The blood concentration of zopiclone was 507 ng/mL and with regard to products of decomposition which might influence the result, the blood concentration of zopiclone was estimated to approximately 660 ng/mL at the time of death (therapeutic concentration in the serum is considered 10 to 50 ng/mL). In addition, a blood alcohol concentration of 1.39‰ was measured. A laceration of the spleen as well as multiple fractures in various regions of the body were also documented, however all with almost no surrounding hemorrhage. Zopiclone and alcohol intoxication were concluded as cause of death, followed by a subsequent overrun accident.\nAfter autopsy, the forensic pathologists got access to the radiological report.\nComputed tomography images were consulted for second reading as a radiopaque formation, which was described in the radiological report, had not been found during the autopsy. Both radiologists independently considered the radiopaque formation to be located within the duodenum, most probably within a duodenal diverticulum. The density of the formation was documented with 90 Hounsfield units (HU).\nTo further examine the observed finding, zopiclone tablets were scanned with the same CT scanner which was used for the postmortem imaging. First, one tablet was put in a bottle, filled with water, and scanned directly, the same procedure was repeated with an aggregate of five tablets, scanned directly and after one hour. In vitro imaging of these tablets revealed nearly the same density (88 HU) as above measured within the radiopaque formation (). This was true for both, the scans of the single tablet and the aggregate of five tablets.\nThe final forensic report revealed zopiclone in combination with alcohol intoxication as the cause of death followed by an overrun accident based on the autopsy results, including toxicological analysis and supported by the CT findings in combination with the in vitro scans of zopiclone.

[[63.0, 'year']]

M

{'20615643': 1, '10981957': 1, '7303462': 1, '17517939': 1, '22673707': 1, '20630787': 1, '28584475': 1, '23169707': 1, '22112684': 1, '20211459': 1, '28635931': 1, '12665000': 1, '12774892': 1, '15657832': 1, '8179737': 1, '8868406': 1, '14519173': 1, '24644410': 2}

{}

3955791-1

noncomm/PMC003xxxxxx/PMC3955791.xml

Myxoid Adrenocortical Adenoma: Magnetic Resonance Imaging and Pathology Correlation

A 74-year-old female was admitted to our hospital for an evaluation of diffuse abdominal pain. She had a history of hypertension with antihypertensive treatment medication. The results of a physical examination were unremarkable. Laboratory tests, including a full blood count, urea and electrolyte measurements, were within normal ranges.\nA contrast-enhanced CT scan of the abdomen during the portal venous phase demonstrated a well-circumscribed, 6-cm, ovoid-shaped, heterogeneously enhancing mass in the right adrenal gland. Thereafter a MR imaging was performed and a smooth, ovoid-shaped mass in the right adrenal gland with low signal intensity on T1-weighted images and high signal intensity on T2-weighted images similar to that of fluid was revealed (). Signal loss on out-of-phase images compared with that on in-phase images were not observed in the tumor (). The enhancement pattern was early heterogeneous and showed a delayed progressive enhancement (). The mass showed hyperintensity on high b-value (1000 s/mm2) diffusion weighted MR images, but the corresponding high apparent diffusion coefficient value confirmed that the hyperintensity on diffusion-weighted MR images represented T2 shine-through rather than restricted diffusion ().\nThe serum and urine marker levels, including those of metanephrines, cortisol, aldosterone and catecholamine, as well as the results of the 24-hour urine collection for vanillylmandelic acid for the detection of a hormonally active tumor were in the normal range.\nThe patient underwent a right adrenalectomy in the operating room.\nOn the cut section, the tumor measured 6.0 × 4.7 × 1.6 cm, was well-circumscribed, a yellow-greenish mass and had a gelatinous consistency (). Microscopically, more than 90% of the tumor mass were characterized by a myxoid background containing anastomosing cords and tubules of tumor cells (). Most of the tumor cells had a uniform polygonal shape with a distinct cell border. Neither mitotic figures nor necrosis were observed as well as no evidence of vascular or capsular invasion. The final pathologic diagnosis was myxoid adrenocortical adenoma.

[[74.0, 'year']]

F

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{}

3955792-1

noncomm/PMC003xxxxxx/PMC3955792.xml

N-Butyl Cyanoacrylate Embolization with Blood Flow Control of an Arterioportal Shunt That Developed after Radiofrequency Ablation of Hepatocellular Carcinoma

A 70-year-old male with liver cirrhosis caused by hepatitis C virus was being followed up at our institution. As contrast-enhanced computed tomography (CE-CT) revealed three HCC lesions of < 15 mm in diameter in segments 1, 2, and 4; RFA of each lesion was performed. However, esophageal varices rapidly deteriorated at 3 months after RFA. Although endoscopic injection sclerotherapy was performed, the esophageal varices deteriorated further, and endoscopy showed greatly enlarged varices (F3) that were red in color (). According to Idezuki (), varices can be classified into three types based on their size: F1 varices are straight small caliber varices; F2 varices are larger with a bead-like appearance; and F3 varices are the largest, with a nodular or tumor-like shape. Red color signs indicate a high risk of bleeding from varices. Arterial phase CE-CT images revealed a marked arterioportal shunt in the left lateral segment of the liver () and portal thrombosis. Therefore, embolization of the arterioportal shunt was planned.\nAngiography of the common hepatic artery before embolization revealed a large arterioportal shunt, but the precise site and size of the shunt were unclear (). Volume-rendered images from CT during angiography revealed the precise site and size (5 mm) of the arterioportal shunt (). A 5.2-Fr balloon catheter (Selecon MP Catheter II, Cobra type; Terumo Clinical Supply, Gifu, Japan) was inserted into the proper hepatic artery via the right femoral artery. A 2-Fr microcatheter (Cerisier; Medikit, Tokyo, Japan) was then advanced as close as possible to the shunt site. NBCA was mixed with iodized oil (lipiodol) at a ratio of 1:2 to control its polymerization time and to make it radiopaque. The NBCA mixture (0.5 mL) was infused through the microcatheter during flow control in the hepatic artery with a balloon catheter. The hepatic artery was incompletely occluded using a balloon to maintain antegrade blood flow in the hepatic artery (). A small amount of the NBCA mixture leaked into a portal vein during embolization. The arterioportal shunt had completely disappeared after embolization, and the NBCA mixture was found at the shunt site (). Arterial phase CE-CT images obtained after embolization confirmed that the arterioportal shunt had disappeared ().\nAfter embolization of the arterioportal shunt, the esophageal varices decreased in size from F3 to F1. However, the varices were still red in color. Therefore, endoscopic injection sclerotherapy was performed again. Endoscopy performed at 4 months after embolization confirmed that the varices had decreased in size from F3 to F1, and the red color had disappeared (). CE-CT performed at 6 months after embolization showed no evidence of recurrence of an arterioportal shunt, the presence of NBCA mixture at the shunt site in segment 3 of the liver and in the left portal vein, and necrotic lesions caused by RFA ().

[[70.0, 'year']]

M

{'7638999': 1, '32884569': 1, '17497067': 1, '8186610': 1, '9696503': 1, '22247646': 2, '34198478': 1, '11487670': 1, '34178070': 1, '3107829': 1, '12563138': 1, '3555408': 1, '6627261': 1, '24643464': 2}

{'3253396-1': 1}

3955798-1

noncomm/PMC003xxxxxx/PMC3955798.xml

A Rare Case of Diffuse Pulmonary Lymphangiomatosis in a Middle-Aged Woman

A 52-year-old woman with abnormal chest radiographs was referred to our hospital. She was asymptomatic and denied having any cough, wheezing, or hemoptysis. Her past medical history was unremarkable. The findings of a physical examination were normal. Laboratory examination revealed a hemoglobin level of 14.1 g/dL, a white blood cell count of 8160/µL (61.7% neutrophils, 31.1% lymphocytes, 2.6% eosinophils, 4.4% monocytes, and 0.2% basophils), and a platelet count of 209000/µL. Urine analysis findings, blood chemistry findings, and erythrocyte sedimentation rates were normal.\nPosteroanterior chest radiograph showed increased interstitial markings in both lungs (). Diffuse, smooth, and nodular interlobular septal thickening, and minimal amounts of bilateral pleural effusion were demonstrated on CT scan (). Low-density infiltration of mediastinal fat and lymph node enlargement were noted in the right anterior diaphragmatic area of a mediastinal window (). Although the patient was asymptomatic, these imaging findings persisted on the follow-up CT scan taken one month later. Our primary radiologic impression was that this was a case of lymphangitic carcinomatosis. Pulmonary edema, sarcoidosis, and lymphoma were included in the differential diagnosis.\nA pulmonary function test showed mild restrictive patterns. The patient underwent bronchoscopy, and no endobronchial lesion was found. Bronchoalveolar lavage results were negative for malignant cells. Thick varicose septal veins and intraalveolar macrophages were identified on transbronchial lung biopsy.\nAfter seven months, a follow-up chest CT scan revealed increased interstitial septal thickening (), new peribronchovascular cuffing, and small amounts of bilateral pleural effusion (). Finally, the patient underwent video-assisted thoracoscopic surgery wedge resection of the right, middle, and lower lobes. In the surgical field, abnormal hypervascularity was noted on the lung surface ().\nMicroscopic examination showed proliferation of thinwalled, anastomosing vascular spaces lined by a single layer of endothelial cells lacking cytological atypia (). Theses lesions were located along the lymphatic distribution and were highlighted by D2-40 (1:100, Dako, Glostrup, Denmark) immunohistochemical stain (), characteristic of DPL. Presently, the patient is alive without any symptoms and being observed without specific treatment such as low fat medium chain fat.

[[52.0, 'year']]

F

{'10658741': 1, '8276379': 1, '29263942': 1, '21518582': 1, '22982897': 1, '32550956': 1, '7790540': 1, '14712135': 1, '32071853': 1, '29245295': 1, '16039928': 1, '26512334': 2, '31531617': 1, '15208112': 1, '10789787': 1, '24642766': 2}

{'4622182-1': 1}

3955799-1

noncomm/PMC003xxxxxx/PMC3955799.xml

Progressive Multiple Cystic Changes in Both Lungs in a Patient Treated with Gefitinib for Lung Adenocarcinoma with Multiple Lung Metastases

A 56-year-old female never-smoker initially developed persistent cough, sputum and progressive dyspnea approximately 1 month before the diagnose NSCLC stage IV. The radiograph and computed tomography (CT) of the chest showed a 2.2-cm soft tissue mass in the right upper lobe with multiple small nodules in the bilateral lungs. A case of lung adenocarcinoma with bilateral intrapulmonary metastases was diagnosed. The patient received two courses of systemic chemotherapy with paclitaxel and cisplatin. However, the chemotherapy had to be discontinued due to paclitaxel-induced hypersensitivity reaction. Thereafter the patient refused further chemotherapy. One year later, after receiving two cycles of first-line chemotherapy, the patient visited the emergency room with an abrupt onset of stuttering, quadriparesis and dyspnea. A spontaneous pneumothorax in the left lung and multiple brain metastases were noted. After a chest tube insertion in the left lung and a 30-Gy whole brain irradiation for brain metastases, the treatment with gefitinib was started with a 250-mg daily dosage and continued for the following 15 months because the patient showed an improvement of symptoms and pulmonary function. Although the primary mass in the right upper lobe with multiple metastatic nodules slightly decreased in size after one month gefitinib treatment, the development of new multiple cystic changes was detected on the follow-up high-resolution CT (HRCT) scan. The pulmonary function 9 months after the initiation of gefitinib therapy showed combined severe obstructive and restrictive ventilatory disturbances (predicted forced expiratory volume at timed interval of 1 second [FEV1] 36%, predicted forced vital capacity [FVC] 31%). Due to a poor performance status neither bronchoalveolar lavages nor histological evaluations were available. In contrast to the gradual progression of parenchymal cystic changes in both lungs were on the follow-up chest CT scan a radiographic regression of the main lesion of NSCLC and metastatic nodules noted (). Simple chest radiographs showed diffuse multiple various sized thin walled cysts and illdefined nodules in bilateral hemi-thorax after the gefitinib therapy. A fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography scan taken 7 months after the use of gefitinib demonstrated a significant increased FDG uptake in the primary lesion only. No uptake was seen in other areas of both lungs, suggesting an interval improvement of metastatic lesions (). Because the patient's condition was tolerable with improved respiratory symptoms, the therapy with gefitinib was continued for 15 months with the patient's approval, despite of the air cystic changes in both lungs. During the follow-up period, neurologic recovery was noted and the patient underwent pulmonary and physical rehabilitation therapies. A follow-up pulmonary function was performed 13 months after the initiation of gefitinib therapy and more improvement was shown than after 9 months (FEV1, 56%; FVC, 53% vs. FEV1, 36%; FVC, 31%) respectively.

[[56.0, 'year']]

F

{'18827433': 1, '15800334': 1, '19667265': 1, '15118125': 1, '16291774': 1, '15554744': 1, '12801775': 1, '16259873': 1, '12897327': 1, '29977544': 1, '15691221': 1, '24642811': 2}

{}

3955819-1

noncomm/PMC003xxxxxx/PMC3955819.xml

Mechanical Thrombectomy Using the Solitaire FR system for Occlusion of the Top of the Basilar Artery: Intentional Detachment of the Device after Partial Retrieval

A 67-year-old male presented in our emergency department complaining sudden, severe dizziness and left ptosis of an hour's duration. On admission, his symptoms gradually worsened, showing left-side facial palsy, severe dysarthria, and left-limb ataxia. He was on oral anticoagulation with a daily aspirin since he had a mechanical aortic valve replaced more than a year previously. However, his international normalization ratio (INR) on admission turned out to be only 1.4.\nSubsequent, acute stroke MR imaging showed occlusion of the basilar artery with a focal infarction in the left superior cerebellar artery territory (). Systemic tissue plasminogen activator (Actylase, Boehringer Ingelheim, Germany) was given at a dose of 0.6 mg/kg as the patient was still within the time window of intravenous thrombolytic therapy. Because the patient did not show any symptomatic improvement, our endovascular treatment team was called in per our institutional acute stroke bridging therapy protocol.\nRight vertebral angiogram showed a typical pattern of BAO. The lesion showed antegrade flow directly after placement of the SFR (). However, the f irst retrieval was unsuccessful and only showed a slight change in the shape of the filling defect. The pattern repeated during several, following trials. Eventually, the clot migrated further distally into the left posterior cerebral artery ().\nAt the time of the final device retrieval, we obtained a control angiogram while the device was still in the midportion of the basilar trunk (). We were able to retract the filling defect proximally into the mid portion of the basilar trunk. However, it was attached at the distal tip of the device. Eventually we could pull down the device to the distal vertebral artery (VA) level proximal to the ipsilateral posterior inferior cerebellar artery (PICA) origin.\nOn the control angiogram we noted that half of the filling defect had migrated into the right PCA and half of it was still within the device mesh as we thought that further manipulation of the device would result in additional distal migration of the clot, we decided to purposely detach the device at the current position in order to avoid the risk of another distal migration ().\nA loading dose of tirofiban (Aggrastat, Iroko Cardio Australia Pty Ltd, Australia) was given systemically on the table. On the following day, the patient's symptoms improved significantly and only showed mild residual diplopia on the left lateral gaze. A dual antiplatelet regimen was initiated on top of oral anticoagulation.\nFollow-up MR showed no new infarcts even in the right PCA territory. There was also no evidence of any hemorrhagic transformation. The patient was discharged with instructions to take both aspirin and warfarin after adjustment of the INR.

[[67.0, 'year']]

M

{'19590057': 1, '18309168': 1, '23645572': 1, '23124642': 1, '22120391': 1, '23835465': 1, '21221560': 1, '22464302': 1, '22723058': 1, '28202431': 1, '24642915': 2}

{'3955819-2': 2}

3955819-2

noncomm/PMC003xxxxxx/PMC3955819.xml

Mechanical Thrombectomy Using the Solitaire FR system for Occlusion of the Top of the Basilar Artery: Intentional Detachment of the Device after Partial Retrieval

A 64-year-old male presented with altered mental status. He was found unconscious and his last known normal time period was four hours previously. His initial NIHSS stroke score was 18. He did not have any known stroke risk factors. However, atrial fibrillation was seen at the time of his admission. Acute stroke MR revealed multi-territorial, wedge-shaped infarcts involving both cerebellar hemispheres and the left PCA territory. Subtle signal changes were also noted in the pons.\nAn urgent, right vertebral angiogram showed distal BAO with a filling defect showing a meniscus sign. () An oval-shaped filling defect was noted along the open arterial lumen when the SFR was placed (). We could pull down the device with the filling defect down to the distal VA level below the origin of the PICA without any fragmentation and/or migration of the clot distally. We decided to detach the stent part at that level ().\nAs the volume of the initial infarct was significant, aspirin monotherapy was started without anti-coagulation which could not be initiated due to combined gastro-intestinal tract bleeding during the acute phase. On his discharge from the intensive care unit, the patient was placed on aspirin and warfarin. After rehabilitation, he could walk with some assistance. His modified Rankin score at 90 days was 3.

[[64.0, 'year']]

M

{'19590057': 1, '18309168': 1, '23645572': 1, '23124642': 1, '22120391': 1, '23835465': 1, '21221560': 1, '22464302': 1, '22723058': 1, '28202431': 1, '24642915': 2}

{'3955819-1': 2}

3955820-1

noncomm/PMC003xxxxxx/PMC3955820.xml

Two Microcatheter Technique for Embolization of Arteriovenous Fistula with Liquid Embolic Agent

A 53-year-old man presented with pain in the neck, both shoulders, and in the upper extremities. A vertebral angiogram showed SDAVF at the level of C1, supplied by the left C1 segmental artery and draining into the perimedullary and perimesencephalic veins (). Under general anesthesia a 6F guide catheter was placed into the left vertebral artery. At first, we considered two flow-control strategies: (1) temporary vertebral artery occlusion by a balloon placed at the origin of the C1 feeder; and (2) temporary balloon occlusion by a small balloon catheter placed in the C1 feeder. However, it was not possible to use either of these techniques because the VA at the curved angle was not fitted by a 4- or 5-mm compliant balloon and a small balloon catheter could not be introduced into the C1 feeder. Finally we decided to use the two catheter technique.\nTwo microcatheters were introduced into the site of the AVF and were positioned with approximately a 5-mm tip distance between them. A repeat angiogram of the glue embolization microcatheter indicated a significant decrease of the AVF flow after a 1.5-mm × 6-cm coil was introduced without detachment into the feeding artery. After obtaining a selected angiogram of C1 artery to make sure that the glue embolization was safe, a 33% glue lipiodol mixture was infused into the AVF. The reflux of the glue filled only a portion of the area between the AVF and the coil which allowed the glue to have good penetration into the vein through the AVF. When the glue embolization was finished, the control angiogram using the guiding catheter showed complete occlusion of the AVF. The coil was then detached and the coil embolization microcatheter was retrieved ().

[[53.0, 'year']]

M

{'17493539': 1, '22454779': 1, '17960371': 1, '20465916': 1, '31339016': 1, '16284566': 1, '10588136': 1, '14729531': 1, '12650420': 1, '9763395': 1, '13679265': 1, '23146212': 1, '22591733': 1, '16570575': 1, '24077579': 1, '34425638': 1, '11110083': 1, '21177391': 1, '20673392': 1, '18958391': 1, '22125741': 1, '24642961': 2}

{}

3955821-1

noncomm/PMC003xxxxxx/PMC3955821.xml

Aneurysm Coil Embolization Using a 1.5-Fr Distal Outer Diameter Microcatheter

A bilobed anterior communicating artery (ACoA) aneurysm in an 80-year-old man with a transient ischemic attack five years prior to presentation was noted to have aneurysm growth up to 7 mm in maximal diameter on serial imaging. During an elective endovascular embolization procedure, severe tortuosity was noted at the femoral iliac junction during guide catheter access, as well as at the origin of the left common carotid artery, which shared an origin with the innominate off the aorta. The f inal guide catheter access consisted of a 90 cm length multipurpose tip shape Neuron Max 088 (Penumbra Inc, Alameda, CA, USA) guide catheter to the left distal common carotid artery over a 115 cm length Navien 058 (Covidien Neurovascular, Irvine, CA, USA) intermediate guide catheter to the left distal cervical internal carotid artery (ICA). Both guide catheters were "hubbed-out" or inserted entirely into the patient. Attempts to advance a 150 cm length SL-10 (Stryker Neurovascular, Fremont, CA) microcatheter over a wire only allowed access to the A1 segment of the left anterior cerebral artery, whereby the hub of the microcatheter was in contact with the hub of the intermediate catheter.\nA 165 cm Marathon microcatheter with a distal inner diameter (ID) of 0.013" instead was advanced over a Synchro 10 guidewire (Stryker Neurovascular, Fremont, CA, USA) and access to the dome of the aneurysm was obtained (). A 5 mm × 13 cm Barricade coil (Blockade Medical, Irvine, CA, USA) was then advanced easily and smoothly through the Marathon microcatheter. The pusher wire length was insufficient to completely deploy the coil, necessitating removal of the rotating hemostatic valve (RHV), and therefore the continuous flush to the microcatheter. This shorter length was sufficient to completely deploy the coil with enough pusher wire length to attach a circuit clip to electrolytically detach the coil. Detachment was also complicated by the lack of a proximal radio-opaque marker on the distal aspect of the Marathon microcatheter which by convention is located 3 cm from the most distal tip of other catheters used to deploy coils. This required additional time to slowly and carefully advance the pusher wire until detachment zone was out of the microcatheter and detachment actually occurred. Five coils in total were deployed, including a 5 mm × 13 cm, 4 mm × 7 cm, 3 mm × 6 cm, 2.5 mm × 6 cm and a 2.5 mm × 4 cm. The f inal coil was able to achieve a satisfactory occlusion grade and the microcatheter was removed without issue (). The patient tolerated the procedure well and was discharged home the next day with a normal neurologic examination.

[[80.0, 'year']]

M

{'22362047': 1, '9763396': 1, '11733309': 1, '17102976': 1, '22993243': 1, '16286410': 1, '27789619': 1, '34919439': 1, '24643022': 2}

{'3955821-2': 2, '3955821-3': 2}

3955821-2

noncomm/PMC003xxxxxx/PMC3955821.xml

Aneurysm Coil Embolization Using a 1.5-Fr Distal Outer Diameter Microcatheter

A 48-year-old man was admitted with a severe headache and subarachnoid hemorrhage in the suprasellar cistern, interhemispheric f issure, and bilateral sylvian fissures. He was found to have a 5 mm bilobed, inferiorly directed ACoA aneurysm (). Using a 6-Fr Neuron guide catheter, access was obtained to the right cervical ICA. A Marathon microcatheter was advanced over a Synchro 10 guidewire to selectively catheterize the aneurysm. Upon withdrawal of the wire, there was some movement of the microcatheter tip that required adjustment of forward tension on the microcatheter. Coil embolization with a 3 mm × 6 cm and 3 mm × 4 cm Barricade coils proceeded with caution. As in the previous case, the RHV and hence continuous flush had to be removed to accommodate the complete deployment of the coils. The lack of a 3 cm distal marker on the Marathon microcatheter prolonged the detachment times since caution was necessary to avoid advancing the pusher wire out of the distal microcatheter tip. Upon placement of a third 2 mm × 4 cm coil, there appeared to be increased resistance within the microcatheter causing buckling of the microcatheter near the carotid siphon. This was presumably because of clot collecting within the microcatheter. The microcatheter was removed, and after straightening out the catheter, the undetached coil was retrieved. The microcatheter was flushed on the back table, and clot emerged from the microcathter (). Another Marathon microcatheter was then advanced into the aneurysm and coil embolization was completed without complication (). The patient tolerated the procedure well and was discharged home after an uneventful hospital stay with a normal neurologic examination.

[[48.0, 'year']]

M

{'22362047': 1, '9763396': 1, '11733309': 1, '17102976': 1, '22993243': 1, '16286410': 1, '27789619': 1, '34919439': 1, '24643022': 2}

{'3955821-1': 2, '3955821-3': 2}

3955821-3

noncomm/PMC003xxxxxx/PMC3955821.xml

Aneurysm Coil Embolization Using a 1.5-Fr Distal Outer Diameter Microcatheter

A 48-year-old female with a strong history of familial cerebral aneurysms was found to have a 4 mm saccular aneurysm with a broad neck at the right ICA terminus on a screening MRA of the brain. The patient was consented for an elective stent-assisted coil embolization of the aneurysm () given the family history a ruptured cerebral aneurysms and patient preference. On the day of the procedure, the right common carotid artery was selected with a 6-Fr Neuron guide catheter through a right common femoral artery access. A 4.5 × 20 mm Neuroform EZ stent (Stryker, Kalamazoo, MI, USA) was deployed from the A1 segment into the ICA. A Marathon microcatheter was used to catheterize the ICA terminus aneurysm through the stent and a 3 mm × 6 cm and 2 mm × 4 cm Target Ultrasoft coils (Stryker, Kalamazoo, MI, USA) were deployed through the Marathon catheter without complication. During deployment of each coil, the RHV and thus continuous flush was temporally removed to accommodate the Styrker electrolytic detachment device (). After the coils were detached from the pusher wire, the electrolytic detachment device was removed and the RHV was replaced restoring the continuous flush before the pusher wire was withdrawn from the catheter to avoid clot formation within the microcatheter. The patient tolerated the procedure well and later discharged home neurologically intact.

[[48.0, 'year']]

F

{'22362047': 1, '9763396': 1, '11733309': 1, '17102976': 1, '22993243': 1, '16286410': 1, '27789619': 1, '34919439': 1, '24643022': 2}

{'3955821-1': 2, '3955821-2': 2}

3955822-1

noncomm/PMC003xxxxxx/PMC3955822.xml

Preoperative Embolization of Cerebellar Hemangioblastoma with Onyx: Report of Three Cases

A 43-year-old man presented with a three day history of progressive headache. Brain MRI revealed a 2.7 × 2.5 cm sized posterior fossa tumor showing significant enhancement with multiple signal void vascular structures within the tumor (). The differential diagnosis included hemangioblastoma, metastasis and high grade glioma. A diagnostic vertebral angiogram demonstrated a significant vascular blush supplied mostly from the right superior cerebellar artery. There was obvious arteriovenous (AV) shunt showing a highly vascular lesion, consistent with a hemangioblastoma (). The patient underwent embolization of core feeder vessel originated off the right superior cerebellar artery using Onyx, resulting near complete resolution of the tumor blush (). Near total resection of the tumor was performed without excessive bleeding or other complication. Post-operative MRI revealed volume reduction over 90% with nearly total regression of the tortuous flow voids. The tumor was pathologically confirmed as hemangioblastoma. Histological examination of the excised tumor revealed that the hemangioblastoma was composed of stromal cells, which showed characteristically large and vacuolated appearance, and abundant vascular cells, such as endothelial cells and pericytes. Nidus vessels were occluded with thrombus and black colored embolic material, Onyx (). After surgical resection, the patient presented gradual regression of the headache.

[[43.0, 'year']]

M

{'29026675': 2, '18824987': 1, '11396304': 1, '22266792': 1, '17564170': 1, '11687669': 1, '8881249': 1, '30574445': 1, '26934897': 1, '21866486': 1, '21237650': 1, '24644530': 2}

{'3955822-2': 2, '3955822-3': 2, '5629862-1': 1}

3955822-2

noncomm/PMC003xxxxxx/PMC3955822.xml

Preoperative Embolization of Cerebellar Hemangioblastoma with Onyx: Report of Three Cases

A 53-year-old man presented with a 15 day history of progressive vertigo and occipital headache. Brain MRI revealed a 3.2 × 2.2 cm cystic tumor with a 1.0 × 0.5 cm sized densely enhancing mural nodule in the right cerebellum (). A diagnostic vertebral angiogram revealed early intense tumor staining in the right cerebellum from the right superior cerebellar artery with AV shunt showing a highly vascular lesion (). The patient underwent Onyx embolization of core feeder vessel originated off the right superior cerebellar artery and tumor blush was complete resolved (). Near total resection of the tumor was performed with minimal blood loss. Post operative MRI revealed volume reduction over 90% of enhancing mural nodule with nearly total regression of the cystic portion. The tumor was pathologically confirmed as hemangioblastoma. After surgical resection, vertigo and occipital headache were gradually resolved.

[[53.0, 'year']]

M

{'29026675': 2, '18824987': 1, '11396304': 1, '22266792': 1, '17564170': 1, '11687669': 1, '8881249': 1, '30574445': 1, '26934897': 1, '21866486': 1, '21237650': 1, '24644530': 2}

{'3955822-1': 2, '3955822-3': 2, '5629862-1': 1}

3955822-3

noncomm/PMC003xxxxxx/PMC3955822.xml

Preoperative Embolization of Cerebellar Hemangioblastoma with Onyx: Report of Three Cases

An 18-year-old man presented with a month history of progressive headache. Brain MRI revealed a 5.3 × 3.8 cm sized large cystic tumor with a 2.0 × 1.6 cm sized heterogeneously enhancing mural nodule in the right cerebellum with tumor effect. Tumor effect was causing effacement and displacement of the fourth ventricle (). A diagnostic vertebral angiogram revealed early intense tumor staining in the right cerebellum from the right superior cerebellar artery with AV shunt showing a highly vascular lesion (). The patient underwent embolization of a pedicle off the hemispheric branch of the right superior cerebellar artery using Onyx, resulting in near complete resolution of the tumor blush (). Near total resection of the tumor was performed with minimal blood loss. Post embolization non-enhanced CT revealed radiopaque embolic agent, Onyx in the mural nodule. Post operative MRI revealed volume reduction over 90% of enhancing mural nodule with nearly total regression of the cystic portion. The tumor was pathologically confirmed as hemangioblastoma. After surgical resection, the patient presented gradual regression of the headache.

[[18.0, 'year']]

M

{'29026675': 2, '18824987': 1, '11396304': 1, '22266792': 1, '17564170': 1, '11687669': 1, '8881249': 1, '30574445': 1, '26934897': 1, '21866486': 1, '21237650': 1, '24644530': 2}

{'3955822-1': 2, '3955822-2': 2, '5629862-1': 1}

3955823-1

noncomm/PMC003xxxxxx/PMC3955823.xml

Conjoined Stent Technique for Radiation Induced Long Segment Carotid Stenosis and Pseudoaneurysm

A 70-year-old man had history of carcinoma larynx (Stage I) treated with conventional radiotherapy with the dose of 70 Gy in the year 2000. In March 2013, he presented with complaint of recurrent transient episodes of left upper limb weakness. He had six such episodes during last three months. Each episode lasted for 2-3 minutes and used to improve on its own. He also complained small swelling in neck in right submandibular area and transient weakness on left side on pressing neck swelling. He had hypertension since 2008. He was nonsmoker and nonalcoholic. He had no known drug allergy. On examination, his left carotid artery was nonpalpable and right carotid artery was less palpable. On auscultation, carotid bruit was present on right side. Neurological examination was normal. Other systemic examination did not reveal any significant abnormality. Magnetic resonance imaging of brain did not reveal acute or old infarcts. Carotid Doppler revealed occlusion of left common carotid artery and significant long segment stenosis of right common and internal carotid artery. Diagnostic cerebral angiography was done which revealed long segment stenosis of right internal carotid artery (70 cms in length and 80-90% stenosis) with a pseudoaneurysm measuring 5.06×3.59 mm (). Left carotid angiogram revealed complete occlusion of left internal carotid artery. Left and right vertebral angiogram revealed good flow in vertebral and basilar arteries.\nIn view of long segment of stenosis, potential clot embolization from pseudoaneurysm and possible rupture of pseudoaneurysm in future, it was planned to cover the whole length of stenosis with stent and apposing distal end of first closed cell design stent (Absolute pro 8×60 mm; Abbott Vascular, Santa Clara, CA, USA) with proximal end of second stent (Acculink 6-8×40 mm; Abbott Vascular, Santa Clara, CA, USA). This was thought to provide extra metal coverage to vessel wall and reducing blood flow inside pseudoaneurysm to promote thrombosis in the aneurysm sac in corollary to flow diverter. After deploying the stent we inflated the balloon up to 10 atm for 10 seconds in each stent (). Post angioplasty right carotid angiogram revealed good flow across the stent with absent flow in pseudoaneurysm with complete circulation in right internal carotid artery territory ().\nOn follow up at three months, patient was asymptomatic with no recurrence of episodes of transient weakness of left upper limb.

[[70.0, 'year']]

M

{'11136925': 1, '8795530': 1, '10587192': 1, '2645540': 1, '7294930': 1, '888060': 1, '10772747': 1, '2650664': 1, '10772307': 1, '21514166': 1, '9882793': 1, '24644531': 2}

{}

3955824-1

noncomm/PMC003xxxxxx/PMC3955824.xml

Cerebral Infarction Caused by a Tortuous Subclavian Artery: a Case Report

A 35-year-old male patient was admitted with headache, visual disturbance and left hemiparesis. He had no history of hypertension, diabetes mellitus or other cardiac disease, and he was currently a 10-pack-per-year smoker. The headache was described as feeling like a tight band around his head. He denied any nausea or vomiting. The neurological examination results were normal, although he complained of numbness in his left side. Upon admission, his vital signs were stable. A chest X-ray and laboratory findings were normal. Brain magnetic resonance image (MRI) revealed an acute infarction in the right lateral thalamus (). Brain CT angiography indicated a severe tortuosity with elongation at the right subclavian artery and stenosis at the right posterior cerebral artery. Negative transthoracic and transesophageal echocardiogram and Holter monitoring ruled out a cardiac source of the embolus. Hypercoagulation tests for antinuclear antibody, anticardiolipin, antithrombin III, protein C, protein S and lupus anticoagulant were all negative.\nDigital subtraction angiography demonstrated a severe tortuosity with elongation of the right subclavian artery (). The carotid vessels on both sides were normal. On hospital day 4, he underwent a right subclavian exposure through a supraclavicular approach. The wall of the proximal right subclavian artery was tortuous and enlarged. The abnormal right subclavian artery was resected after clamping the diseased portion at both ends. The proximal right subclavian artery was then anastomosed directly at the right common carotid artery directly. After an end to end anastomosis, magnetic resonance angiography (MRA) revealed recanalization of the subclavian artery (). The histopathological findings revealed tortuous lumen and myxoid degeneration of the wall without evidence of vasculitis ().

[[35.0, 'year']]

M

{'12011548': 1, '16864843': 1, '8526472': 1, '32291404': 1, '22433458': 1, '17935213': 1, '12820762': 1, '19356510': 1, '10947875': 1, '24644532': 2}

{}

3956491-1

noncomm/PMC003xxxxxx/PMC3956491.xml

Amyloid arthropathy associated with multiple myeloma: polyarthritis without synovial infiltration of CD20+ or CD38+ cells

Patient 1 was a 58-year-old male with MM complicated by transfusion-dependent anemia, lytic bone lesions, and myeloma kidney requiring dialysis. He presented with left shoulder pain and swelling two months after diagnosis of MM, followed by bilateral hand and shoulder swelling with morning stiffness lasting hours. Examination demonstrated left second metacarpophalangeal (MCP) joint swelling, right flexor tenosynovitis, bilateral shoulder effusions, flexion contractures of both elbows, and decreased range of motion in the cervical spine. Joint aspiration revealed a synovial fluid cell count of 2500 cells/mm3 (6% PMN, 17% lymphocytes, 77% synovial lining cells). Repeat aspiration one week later revealed a cell count of 1050 cells/mm3 and amyloid in the synovial fluid sediment by Congo Red staining. There were no crystals in either aspirate. A synovial biopsy of the right shoulder joint was performed after another week. MM therapy, which had been initiated prior to the biopsy, included one cycle of melphalan (12 mg/d × 4 days), prednisone (60 mg/d × 4 days), and apheresis to treat renal failure suspected to have resulted from free Ig light chains. Joint symptoms improved with this treatment, but therapy was eventually halted due to nausea. The patient died four months after the biopsy.

[[58.0, 'year']]

M

{'33467968': 2, '19916737': 1, '8336318': 1, '20840673': 1, '19181644': 1, '21376667': 1, '18414968': 1, '4722853': 1, '14437851': 1, '17907214': 1, '23951325': 1, '21173013': 1, '23113696': 1, '31956619': 1, '31645392': 1, '17686051': 1, '22096352': 1, '8484132': 1, '22855296': 1, '12092767': 1, '5069952': 1, '23040361': 1, '23992800': 1, '24286442': 2}

{'3956491-2': 2, '7960901-1': 1}

3956491-2

noncomm/PMC003xxxxxx/PMC3956491.xml

Amyloid arthropathy associated with multiple myeloma: polyarthritis without synovial infiltration of CD20+ or CD38+ cells

Patient 2 was a 77-year-old male with a history of coronary artery disease, non-insulin dependent diabetes, hypertension, chronic renal insufficiency and MM. Complications of MM included anemia, painful lytic bone lesions, a paraspinal extramedullary plasmacytoma, and worsening kidney disease requiring dialysis. Three months after the diagnosis, the patient presented with right shoulder, right knee and bilateral MCP pain. Examination showed swollen and tender knees in addition to warmth, erythema and tenderness in MCP joints bilaterally. A synovial biopsy of the right knee was performed. Cytologic examination of synovial fluid was reported as “few mononuclear cells”, but absolute or differential synovial fluid leukocyte counts were not enumerated. There were no crystals. Amyloid was demonstrated in synovial fluid sediment by Congo red staining. Treatment prior to the biopsy included two cycles of melphalan (8 mg/m2/day × 4 days) and prednisone (100 mg/day × 4 days) followed by palliative radiation therapy for bone lesions. The patient was taking prednisone 10 mg daily at the time of the biopsy. He passed away 3 months after the biopsy.

[[77.0, 'year']]

M

{'33467968': 2, '19916737': 1, '8336318': 1, '20840673': 1, '19181644': 1, '21376667': 1, '18414968': 1, '4722853': 1, '14437851': 1, '17907214': 1, '23951325': 1, '21173013': 1, '23113696': 1, '31956619': 1, '31645392': 1, '17686051': 1, '22096352': 1, '8484132': 1, '22855296': 1, '12092767': 1, '5069952': 1, '23040361': 1, '23992800': 1, '24286442': 2}

{'3956491-1': 2, '7960901-1': 1}

3956695-1

noncomm/PMC003xxxxxx/PMC3956695.xml

Inflammatory response following neutrophil recovery postchemotherapy in acute myeloid leukemia cases without evidence of infection: role of homing of neutrophils

A 32-year-old woman with remote history of pilonidal abscess presented with easy bruising, fatigue, generalized bony pain, and heavy menses. She was found to have acute myeloid leukemia (AML) with 34% bone marrow blasts and t(8;21) (q22;q22). She was placed on levaquin, acyclovir, and posaconazole for prophylaxis, and induction chemotherapy with standard daunorubicin and cytarabine was initiated for a total of 7 days. While neutropenic, she developed an area of tenderness and erythema around her sacrum in the previous site of a pilonidal cyst and then became febrile. Cefepime was initiated, and was later changed to vancomycin and piperacillin/tazobactam because of suspected rash from cefepime. She remained febrile for 3 days after initiating antibiotic therapy. Blood cultures were drawn and remained negative. Computed tomography (CT) of the pelvis revealed ill-defined soft-tissue thickening in the mid-lower back from the lumbar spine to the sacrum within the deep subcutaneous fat to the gluteal crease without any evidence of muscular involvement. There was also a well-defined fluid collection measuring approximately 2.9 × 0.8 cm within the subcutaneous tissues, superficial to the lower sacrum and to the right of the midline (). Erythema and fever resolved, and tenderness improved with antibiotics. Vancomycin was discontinued after 48 hours, but piperacillin/tazobactam was continued until her neutrophil count became >500 neutrophils/μL. The total duration of antibiotic therapy was 11 days. A postinduction bone marrow evaluation revealed no residual leukemia.\nAfter 48 hours off antibiotics, the presacral tenderness and redness returned. Examination revealed an area of fluctuance, erythema, and tenderness in the same location of her previous pilonidal cystectomy. At this time, her absolute neutrophil count (ANC) was 2,500/μL. CT of the pelvis showed an increase in size of well-defined fluid collection, measuring 1.3 × 2.2 × 6.4 cm (). She was off antibiotics for 48–72 hours before aspiration, and drainage was performed. Foul, cloudy, purulent fluid was aspirated and sent for analysis. This showed many neutrophils with no organisms, and cultures were negative. The patient was placed on ertapenem, and her symptoms improved primarily after initial drainage. Follow-up sonogram, done after 3 days, showed a mild complex fluid collection within the subcutaneous tissues. She underwent incision and drainage of the area of greatest redness. Retrieved tissue and fluid were sent for cultures and remained negative again. Gram stain of the swabbed fluid showed rare neutrophils, and no organisms were seen. The area healed well, and after 12 days she proceeded with treatment for her AML with a matched-sibling donor stem cell transplant without complications.\nThe second case was a 52-year-old male patient who presented with pancytopenia, 35% myeloid blasts in the bone marrow, fever, chills, and tachycardia, with redness, swelling, and pain involving the medial posterior left thigh, and mild redness and swelling but no pain of the lateral aspect of the right thigh. Magnetic resonance imaging (MRI) of the left thigh showed pyomyositis with extensive edema throughout quadriceps musculature, with focal areas of myonecrosis and intercommunicating pockets of fluid. Creatine phosphokinase was 905 U/L. There was also subcutaneous edema suggestive of cellulitis. He was diagnosed with AML and sepsis. Peripheral blood, bone marrow, and urine cultures obtained initially showed no bacterial or fungal infection. He was started on vancomycin, cefepime, and clindamycin, and then changed to vancomycin and piperacillin/tazobactam after 8 days. AML induction therapy with daunorubicin and cytarabine was initiated for a total of 7 days. Surgical intervention was considered but not done, due to clinical improvement while on antibiotics.\nWith antibiotic therapy, the patient became afebrile with decreased pain, swelling, and redness of the left upper thigh and stabilization of the right thigh. On postinduction day 21, the ANC was 80/μL, and while on piperacillin/tazobactam, the patient developed fever. A repeat MRI showed progressively evolving areas of myonecrosis/abscess in the left thigh, predominately in the abductor brevis and magnus, and unchanged to slightly decreased area of myonecrosis/abscess in the proximal right thigh, with slightly increased enhancement and edema in the adductor magnus (). Orthopedic surgery was reconsidered, and it was thought that overall the abscesses were unchanged. Blood cultures were drawn and were negative. Slowly, his symptoms improved with antibiotics, and he was discharged off antibiotics after he became afebrile and had recovered his neutrophil count (ANC was 666/μL upon discontinuation of antibiotics).\nThree days later, he presented with severe pain and increased swelling in his left thigh. His white blood cell count was 8,800/μL at that point. On examination, his left thigh was swollen and painful to the touch without any fuctuation. A repeat MRI showed marked progression and enlargement of multiple fluid collections in the left thigh consistent with worsening areas of myonecrosis/abscess (). Routine blood cultures and one fungal blood culture were obtained, and showed no growth. Prior to reinitiation of antibiotic therapy, a CT-guided aspiration was done and a drain placed. The recovered fluid showed no bacteria, fungus, or mycobacteria. Gram stain, however, showed many neutrophils and red blood cells, but no organisms. Following the procedure, his left thigh pain improved; however, his pain dramatically improved with anti-inflammatory agents. Vancomycin and piperacillin/tazobactam were started, and later changed to ertapenem. The drain output slowed down and became insignificant 15 days post-drain placement. Ertapenem was stopped 20 days after drain placement. The patient remained afebrile and proceeded with subsequent chemotherapy.

[[32.0, 'year']]

F

{'16259636': 1, '15840024': 1, '18716065': 1, '20035633': 1, '17548653': 1, '16148869': 1, '16729305': 1, '1519296': 1, '10897669': 1, '15563869': 1, '20965212': 1, '22751460': 1, '23382785': 1, '14563322': 1, '23168453': 1, '18552407': 1, '21067040': 1, '14748564': 1, '25253631': 1, '11927659': 1, '21460863': 1, '21690321': 1, '15054039': 1, '20813109': 1, '22280231': 1, '20813010': 1, '24648782': 2}

{}

3956773-1

noncomm/PMC003xxxxxx/PMC3956773.xml

Elastosis Perforans Serpiginosa

A 35-year-old healthy man visited Gangnam Severance Hospital with hyperkeratotic papules on his anterior neck. These papules first appeared 2 years ago and slowly increased in number. Over time, the skin lesions had spread peripherally with some central clearing. The patient stated that the skin lesions had developed after a skin injury. Previous treatments with topical antifungal and topical steroid were ineffective. The patient's medical and family history was also negative for EPS or any other connective tissue diseases. On examination, multiple crusted erythematous papules (2 to 5 mm in size) were arranged in an annular and serpiginous pattern (). A potassium hydroxide preparation obtained from the skin lesion was negative for fungal elements. A punch biopsy specimen revealed focal epidermal hyperplasia with the formation of a narrow vertical transepidermal channel containing nuclear debris and eosinophilic degenerated elastic fibers (). The amount and thickness of the elastic fibers in the papillary dermis had increased markedly. It looked like entering the canals toward the outside of the skin (). The papillary dermis and superficial reticular dermis were infiltrated by numerous inflammatory cells, including lymphocytes and histiocytes (). Verhoeff-van Gieson staining showed a markedly increased number of altered elastic fibers forming dense clumps in the upper dermis (). Gomori methenamine silver stain and D-PAS stain were both negative for fungal elements. A diagnosis of EPS was made based on these clinical and histopathological findings. Despite treatment with topical 0.05% tretinoin nightly for 6 months, no improvement was observed.

[[35.0, 'year']]

M

{'15243519': 1, '21388484': 1, '2523911': 1, '12786719': 1, '11678881': 1, '11843635': 1, '21165224': 1, '7679569': 1, '6216862': 1, '27881947': 1, '34632026': 1, '15604549': 1, '31934466': 2, '11096396': 1, '4230639': 1, '3160676': 1, '8125690': 1, '2272739': 1, '3372794': 1, '16847197': 1, '24648695': 2}

{'6942716-1': 1}

3956774-1

noncomm/PMC003xxxxxx/PMC3956774.xml

Four Cases of Successfully Treated Chronic Expanding Soft Tissue Hematoma

Case 1 was a 40-year-old man who presented with painless swelling of the right sole that increased gradually in size for 4 months. An examination revealed a firm, skin-colored, subcutaneous tumor adhering to the skin (). There was no recent history of trauma or anticoagulant medication. A laboratory examination, including a coagulation profile, was within normal limits. A magnetic resonance imaging (MRI) examination revealed a 2.5×2.5 cm well-encapsulated mass, which was removed completely by surgery (). A histopathological examination revealed a fibrotic capsule, inflammatory cellular infiltration, and organized blood (, ); the lesion was diagnosed as CEH. The patient's postoperative course was uneventful and his tumor has not recurred after 2 years.

[[40.0, 'year']]

M

{'12665946': 1, '21497371': 1, '29844806': 1, '27904289': 1, '27917326': 2, '28442862': 1, '6448929': 1, '5675406': 1, '956874': 1, '24648696': 2}

{'3956774-2': 2, '5133135-1': 1}

3956774-2

noncomm/PMC003xxxxxx/PMC3956774.xml

Four Cases of Successfully Treated Chronic Expanding Soft Tissue Hematoma

Case 2 was a 54-year-old man who presented with a 10-year history of a large mass in the left thigh. The surface was dark-reddish, soft, fluctuant, and painless when palpitated. A firm subcutaneous tumor was situated lateral to the lesion. The patient had had an injection (detailed information was not available) in his left thigh during childhood, and a large hematoma initially appeared at the injection site. The hematoma resolved immediately, leaving a small induration that increased rapidly in size 1 year ago. His medical and family history was otherwise unremarkable except for having hepatitis B carrier status. Blood biochemistry, coagulation profile, and platelet counts were normal. An MRI scan demonstrated a well-circumscribed, subcutaneous, 4×4×5 cm cystic mass (). The patient underwent complete resection of the mass including the fibrous capsule, which had partly adhered to the fascia (). The lesion was removed surgically, and microscopically, the resection revealed a hematoma surrounded by a hyalinized fibrous capsule. No recurrence was detected within 2 years.\nA 66-year-old woman (Case 3) presented with a painful 6 months old and increasingly large swelling on the buttock. She had no history of trauma. Clinical and MRI findings revealed a tender 10×10 cm cystic swelling in the subcutaneous tissue. An incision biopsy confirmed that the swelling was a hematoma. Because the patient was receiving anticoagulant therapy including 2 mg/day warfarin potassium and 100 mg/day aspirin for anti-phospholipid antibody syndrome, the hematoma was aspirated rather than complete dissection. The mass has not recurred after 3 years.\nA 14-year-old girl (Case 4) noted a cystic, slightly tender, 1.5×1.5 cm swelling on the right upper arm 3 months prior to consultation. No inducible cause could be discovered and her history was unremarkable. She successfully underwent enucleation of the lesion at Kyushu University Hospital. Her condition was histopathologically diagnosed as CEH. The swelling has not recurred after 2 years.

[[54.0, 'year']]

M

{'12665946': 1, '21497371': 1, '29844806': 1, '27904289': 1, '27917326': 2, '28442862': 1, '6448929': 1, '5675406': 1, '956874': 1, '24648696': 2}

{'3956774-1': 2, '5133135-1': 1}

3956801-1

noncomm/PMC003xxxxxx/PMC3956801.xml

Cutaneous Mycobacterium massiliense Infection of the Sole of the Feet

In February 2011, a 45-year-old male visited our hospital with a painful nodule on his left sole that had appeared four weeks ago. Before visiting our outpatient clinic, he had undergone acupuncture on his back and both extremities including the soles and palms to alleviate chronic back pain. The skin lesion on his left sole developed after a few weeks of receiving acupuncture. On physical examination, the patient showed an erythematous subcutaneous nodule with local tenderness and heat on the sole of his left foot (). There was no discharge or fluctuation. No systemic symptoms including fever were detected.\nHistological examination of a biopsy obtained from the lesion on his sole showed granulomatous inflammation with neutrophilic microabscesses in the dermis and subcutaneous fat tissue. No special staining was performed ().\nA Gram stain and a culture of the tissue specimens to identify the bacterial infection revealed negative results. Acid-fast bacili culture of the tissue specimen on liquid media (Mycobacterium growth indicator tube: middle block 7H9 broth agar) and 3% Ogawa solid media at 25℃ to 30℃ and 37℃ was done. Numerous colonies were observed after 1 week of culture on liquid media at 37℃ (). For identification of the mycobacterium species, polymerase chain reaction-hybridization (REBA Myco-ID®, M&D Inc., Wonju, Korea) was performed. We used a molecular diagnostic kit designed to identify 19 species of NTM by binding the amplifying rpo B gene product to a species-specific probe. Then the culture was identified as M. massiliense (). Susceptibility testing for antibiotics was done using the broth microdilution method according to the criteria of the Clinical and Laboratory Standards Institute. The isolate was susceptible to clarithromycin (minimum inhibitory concentration≤0.5µg/ml) and it showed intermediate susceptibility to amikacin and cefoxitin. However, the isolate was resistant to ciprofloxacin and doxycycline.\nBecause we at first considered his cutaneous lesion to be an abscess or inflammation due to a ruptured epidermal cyst, he received empirical antibiotic treatment with cefadroxil for 2 weeks. And then, based on the susceptibility results, we treated the patient with clarithromycin 100 mg a day for 4 months, and he showed improvement of both his subjective symptoms and his cutaneous lesion.

[[45.0, 'year']]

M

{'21159943': 1, '10325313': 1, '20833823': 1, '15583272': 1, '26612992': 1, '17626174': 1, '34858010': 2, '18753344': 1, '29062643': 1, '20548899': 1, '15571497': 1, '24648692': 2}

{'8577914-1': 1}

3956802-1

noncomm/PMC003xxxxxx/PMC3956802.xml

Warfarin-Induced Skin Necrosis

A 62-year-old woman was referred for skin necrosis on the lateral aspect of the right thigh (), 12 days after admission for refractory atrial fibrillation secondary to mitral valve stenosis and insufficiency. Her ventricular rate had been controlled by isoprolol and the patient had been started immediately on 5 mg warfarin per day without simultaneous administration of heparin. On day 4, she developed painful ecchymosis of the lateral surface of the right thigh, initially misinterpreted as a hematoma, and the warfarin was reduced to 2 mg daily. On day 6, skin necrosis with eschar formation developed, and warfarin therapy was resumed to 1 mg per day. On day 12, the patient presented with a full thickness cutaneous necrosis. A laboratory workup indicated a normal clotting profile (). A histopathologic examination of incisional cutaneous biopsy was suggestive of warfarin-induced skin necrosis ().\nAccordingly, warfarin was discontinued and intravenous unfractionated heparin therapy was initiated. As the patient refused surgery, conservative autolytic debridement with hydrogel and hydrocolloid dressings was achieved, and the cutaneous deficit was healed by secondary intention. Unfractionated heparin was replaced with low-molecular weight (LMW) heparin for 17 days. Subsequently, warfarin was re-introduced at a daily dose of 2 mg with continuation of heparin, until international normalized ratio (INR) was within the therapeutic range. The cutaneous lesion healed with a scar and the patient developed no further skin necrosis during 15 months of follow-up.

[[62.0, 'year']]

F

{'11601930': 1, '27069859': 1, '34361773': 1, '29924250': 1, '33883776': 2, '2527005': 1, '29844641': 1, '8294318': 1, '8024618': 1, '6688309': 1, '33493142': 1, '30923407': 1, '19615543': 1, '29201953': 2, '31911909': 2, '1833851': 1, '34684165': 1, '24648693': 2}

{'5703748-1': 1, '6940348-1': 1, '8042803-1': 1}

3956803-1

noncomm/PMC003xxxxxx/PMC3956803.xml

Subdermal Coagulation Treatment of Axillary Bromhidrosis by 1,444 nm Nd:YAG Laser: A Comparison with Surgical Treatment

A 25-year-old female presented with malodor in both axillae aggravated since adolescence. She had no medical history, but a maternal family history of axillary bromhidrosis was present. On examination, wet earwax in both ears was noted. Serious hyperhidrosis was diagnosed based on the clinical findings.\nWe decided to treat the left axilla with the 1,444 nm Nd:YAG laser (Accusculpt™; Lutronic Corp., Seoul, Korea), and the right axilla with a modified Inaba's method and compared the effectiveness and complications of each modality.\nBoth axillary areas were anesthetized with 24 ml of 0.5% lidocaine mixed with 1:100,000 epinephrine. As the 1,444 nm Nd:YAG laser is highly absorbed by water which becomes heat energy, tumescent anesthesia was not used to avoid unwanted thermal damage via heated tumescence.\nLaser irradiation areas of 10×5 cm in size were marked on the left axilla. Apocrine glands in the subcutaneous and dermal layers were destroyed by irradiating 1,254 J of laser at 1,444 nm with 175 mJ of pulse energy at a pulse rate of 40 Hz (power 7 W) using a fiber type internal probe via 18-G needle puncture sites (). The amount of energy applied was based on the surface temperature elevation and the extent of fat dissolution assessed by the operator's hands. No liposuction was performed. The 18-G needle puncture sites were not sutured, and the operative area was not compressed.\nModified Inaba's surgery was performed on the right side. After local anesthesia, a 2-cm long single incision line was made, and subdermal dissection was done. Subdermal apocrine glands were manually shaved with a modified Inaba's shaver, and a compression dressing was applied to avoid hematoma or seroma formation.\nThe patient revisited our hospital on postoperative days 3 and 10 and after 6 and 12 months. Relatively less ecchymosis and scars were observed on the left axilla treated with the laser (). The right and left axillae, including acute complications, were compared at long-term follow-up (). Other than a serious bruise in the right axilla lasting about 2 weeks and a mild bruise in the left axilla lasting less than 1 week, no major complications were noted. Pain score was measured on a scale of 0 to 10, and the patient experienced no pain in the left axilla. However, the patient experienced moderate to severe pain (7 to 8 out of 10) with activity limitations on the modified Inaba's operation side. As the postoperative compression dressing had to be applied for 2 weeks, activity limitations continued for 2 weeks on the right side. Additionally, postoperative pain continued for 7 to 10 days. The remnant malodor in the left axilla was deemed 'tolerable' (scale 3) and the right axilla was deemed 'none' (scale 0). After the 1 year follow-up, the remaining odor was <10% to 15% compared with the initial grade. Other complications, such as restriction of movement and pain, were completely cleared. The patient's level of satisfaction with the left, laser treated side, was generally high in terms of quality of life.\nHistological examinations were also done on the subcutaneous fat layer of the laser-irradiated side immediately after the procedure and at 6 months postoperatively (). Immediately after the procedure, the exam showed ablated adipose tissue and apocrine glands. The 6 month histologic examination showed more ablated apocrine glands than previously, which resulted in decrease in malodor.

[[25.0, 'year']]

F

{'19240525': 1, '10594601': 1, '17214695': 1, '20014250': 1, '18649385': 1, '29386831': 1, '24648694': 2}

{}

3956953-1

noncomm/PMC003xxxxxx/PMC3956953.xml

Schwannoma of the Scrotum: Case Report and Review of the Literature

A 45-year-old male presented with a history of gradually increasing, painless, left-sided testicular swelling lasting 6 months. On physical examination, a firm mass measuring 9.5 cm×9.5 cm was observed at the root of the scrotum, close to the testis. The patient had no neurological symptoms and careful evaluation for neurofibromatosis was negative. No lymphadenopathy was detected. The patient also had a friction ulcer over the scrotal skin and a provisional clinical diagnosis of an epididymal or testicular tumor was made.\nUltrasonographic examination revealed a well-circumscribed heterogeneous scrotal mass that was well separated from the epididymis and testis and isoechoic in echotexture (). Preoperative evaluation for tumor markers of testicular tumors, which included alpha-fetoprotein, beta-hCG, and lactate dehydrogenase, were all negative. Curative surgical excision of the left scrotal mass was undertaken for removal of the tumor and a definitive diagnosis. Partial scrotectomy was done, which revealed a firm, nodular whitish lesion attached to the scrotal sac not involving the testis. The testis was spared and the scrotal mass was excised. The specimen submitted for histopathological examination consisted of an oblong, firm scrotal mass that measured 8.5 cm×8.5 cm×6.0 cm. The cut surface was whitish, lobulated, and glistening, with central yellow-brown areas (). Microscopic examination showed two different patterns: Antoni type A and Antoni type B areas. Antoni A areas are quite cellular and are composed of spindle cells that are often arranged in a palisading pattern or in an organoid pattern representing Verocay bodies. Antoni B areas are hypocellular with abundant edematous fluid-forming cystic spaces (, ).

[[45.0, 'year']]

M

{'17244372': 2, '29992916': 1, '9644798': 1, '12692434': 1, '9494170': 1, '12613010': 1, '12937811': 1, '31801392': 2, '27169021': 1, '14665342': 1, '15269020': 1, '12350506': 1, '24648879': 2}

{'7607288-1': 1, '1783662-1': 1}

3956954-1

noncomm/PMC003xxxxxx/PMC3956954.xml

Metastasis of Non-Muscle-Invasive Bladder Cancer Into the Thyroid Gland: A Literature Review Accompanied by a Rare Case

An 83-year-old male patient visited the Urology Department with complaints of macroscopic hematuria at intervals over 9 months. Transurethral resection of the bladder (TUR-B) was performed on the patient when a 17-mm×14-mm mass was found in the ultrasound examination. The pathological result was a high-grade superficial papillary urothelial carcinoma (). Repeat TUR was applied to the patient 4 weeks later and high-grade urothelial carcinoma with lamina propria invasion was found, whereas muscularis propria invasion did not exist. Positron emission tomography (PET) was performed during the second month because the patient had chest pain in the postoperative period, and multiple metastatic bone lesions, metastatic lymphadenopathies on the mediastinum and right external iliac area, a hypermetabolic lesion on the left thyroid lobe, and a hypermetabolic lesion on the left adrenal gland were found. Incisional biopsy performed on the fifth rib of the patient was evaluated as urothelial carcinoma metastasis and radiotherapy was applied to the patient for these lesions ().\nIn the physical examination of the patient, a fixed, 3-cm mass was palpated on the left lobe of the thyroid. Then, in the neck computed tomography (CT) with contrast, a 40 mm×34 mm nodular mass was found on the left lobe of the thyroid gland, which caused left-sided destruction of the thyroid cartilage. The mass was evaluated as a hypoactive nodule in thyroid scintigraphy. A hypermetabolic nodular lesion was seen on the left thyroid lobe by PET. Malignant tumor cells were observed in the fine-needle aspiration sample taken from the hypermetabolic lesion on the left lobe of the thyroid. Owing to the patient's clinical history, primary thyroid carcinomas were considered in the differential diagnosis, because metastatic carcinoma and anaplastic and medullar carcinomas are of first priority. The immunohistochemical panel included thyroid transcription factor-1 (TTF-1) and thyroglobulin in terms of thyroid tumors; calcitonin, carcinoembryonic antigen (CEA), chromogranin A, and synaptophysin in terms of medullar carcinoma; and cytokeratins (CK) 7 and CK 20 antibodies in terms of urothelial carcinoma. No reaction was observed with neuroendocrine markers (synaptophysin and chromogranin), calcitonin, thyroglobulin, or TTF-1 in tumoral cells. Positivity was established in some cells by CEA and CK 20. The tumor was evaluated as a urothelial carcinoma metastasis owing to the clinical history of the patient, the existence of other metastases, the morphological similarity of the tumor cells with the primary tumor, and CK 20 positivity in some cases immunohistochemically (). Because the general condition of the patient worsened while planning chemotherapy, no systematic chemotherapy was applied. After 6 months, the patient died.

[[83.0, 'year']]

M

{'18372021': 1, '14734003': 1, '21458150': 1, '9082363': 1, '9561583': 1, '18446450': 1, '11458053': 1, '29359114': 1, '2106210': 1, '34527518': 1, '17971176': 1, '16552241': 1, '24648880': 2}

{}

3956994-1

noncomm/PMC003xxxxxx/PMC3956994.xml

Dermatomyositis associated with hepatitis B virus-related hepatocellular carcinoma

A 55-year-old male visited our hospital complaining of progressive weakness in his bilateral arms, hips, and thighs. He had difficulty combing his hair and was experiencing dysphagia and erythematous changes in the skin (his face and a 'V' on his upper chest and neck that had developed 3 weeks earlier) ().\nA physical examination revealed a heliotrope rash with bilateral periorbital edema and poikiloderma on the upper chest and neck. A musculoskeletal examination showed marked weakness of all proximal muscles in the symmetric extremities. Serum laboratory tests revealed the following: white blood cells 9,720/mm3, hemoglobin 13.6 g/dL, platelets 98,000/mm3, creatine kinase 16,440 IU/L (normal range, 0 to 190), lactate dehydrogenase 994 IU/L, aspartate aminotransferase 717 IU/L, alanine transaminase 139 IU/L, total bilirubin 1.4 mg/dL, albumin 2.2 g/dL, alkaline phosphatase 119 IU/L, and prothrombin time (activity) 55%. HBV surface antigen was detected, and the HBV DNA level was 7,380 IU/mL. No antibodies against hepatitis C virus were detected.\nIgM antibodies against Epstein-Barr virus, cytomegalovirus, and herpes simplex virus were not detected. There was no other evidence of infectious mononucleosis. Antinuclear antibody and anti-SS-Ro tests were both positive. Tests for other autoantibodies, including anti-dsDNA, anti-ribonucleoprotein, anti-Sm, anti-Jo-1, and anti-Scl70, were all negative. Electromyography showed a small number of polyphasic waves with a normal interference pattern in all muscles tested. A muscle biopsy of the right upper arm showed a sparse lymphocytic infiltrate around the blood vessels and negative immunofluorescence pathologic findings, compatible with DM (). The patient's levels of carcinoembryonic antigen, carbohydrate antigen 19-9, and prostate-specific antigen were normal, but he had elevated levels of α-fetoprotein (AFP; 448.8 ng/mL) and proteins induced by vitamin K absence-II (> 500 mAU/mL). Liver dynamic computed tomography (CT) revealed a 6.5-cm sized arterial enhancing mass in hepatic segment 7/6 ().\nWe diagnosed the patient with HBV-related HCC based on his status as an HBV carrier, elevated AFP level (> 200 ng/mL), and typical radiographic findings (e.g., arterial enhancing features on liver dynamic CT).\nOptimal management procedures for HCC such as transcatheter arterial chemoembolization could not be performed because of the patient's poor general condition. We started prophylactic antiviral therapy with lamivudine for the prevention of viral reactivation. A total of 60 mg of oral prednisolone was administered daily. After steroid therapy, the patient's skin rash, muscle strength, and dysphagia showed slight improvement, and his elevated muscle enzyme levels returned to the near-normal range. However, his underlying HCC progressed rapidly: the size of the cancer grew up to 11 cm with portal vein thrombosis and multiple lymph node metastasis. The patient ultimately died due to hepatic failure after 4 months.

[[55.0, 'year']]

M

{'16570363': 1, '30227596': 1, '28717078': 1, '9041958': 1, '31183354': 2, '18203322': 1, '32743506': 1, '17053509': 1, '32274435': 1, '33842655': 1, '12453288': 1, '16410528': 1, '18423790': 1, '15796260': 1, '18802699': 1, '11251586': 1, '30113453': 1, '24648807': 2}

{'6547324-1': 1}

3956995-1

noncomm/PMC003xxxxxx/PMC3956995.xml

Hypersensitivity myocarditis confirmed by cardiac magnetic resonance imaging and endomyocardial biopsy

A 68-year-old woman presented with constrictive chest pain lasting for 2 hours. She had a history of hypertension, transient cerebral ischemic attack, and osteoarthritis in both knees. Her blood pressure was 91/53 mmHg, pulse rate was 63 beats per minute, respiration rate was 20 breaths per minute, and body temperature was 37℃. Upon physical examination, heart sounds were normal without murmur. Pulmonary auscultation revealed coarse vesicular sounds with crackles on both lower lung fields. Multiple itchy erythematous lesions were present on the hands, buttocks, abdomen, and trunk ().\nThe results of laboratory examinations were as follows: white blood cell count, 9,140/mm3; eosinophil count, 1,380/mm3; hemoglobin, 10.3 g/dL; platelet count, 123,000/mm3; C-reactive protein level, 1.7 mg/dL; and erythrocyte sedimentation rate, 72 mm/sec. The levels of brain natriuretic peptide, creatine kinase-MB (CK-MB), and troponin-I were 944 pg/mL, 56.73 ng/mL, and 38.85 ng/mL, respectively.\nInitial electrocardiography showed ST segment elevation ≥ 1 mm in leads II, III, aVF, V5, and V6 (). Emergency coronary angiography was performed under the assumption of acute ST segment elevation myocardial infarction at the inferolateral wall, but coronary atherosclerosis was not evident. Echocardiography showed the "sparkling" appearance of the left ventricular (LV) myocardium, concentric LV hypertrophy, and mild hypokinesia on the anterior, anterolateral, and posterior walls from the mid-LV to the apex with 50% LV ejection fraction. Peripheral blood eosinophilia, skin rash, and a history of taking multiple medications suggested hypersensitivity myocarditis. The medications taken recently by the patient are shown in . Management of heart failure using aldosterone and furosemide was initiated promptly.\nOn the second day of hospital admission, however, dyspnea worsened, and newly developed bilateral pulmonary congestion was noted on chest radiography. The level of troponin I peaked at > 50.00 ng/mL. Therefore, CMR and EMB were carried out to confirm the diagnosis of hypersensitivity myocarditis. Prednisolone (60 mg, orally) treatment was initiated. Contrast-enhanced CMR (CE-CMR) showed high signal intensities in circular and nodular patterns mainly in the epicardium and septum of the left ventricle (). These patterns suggested infiltrative myocarditis, such as amyloidosis, sarcoidosis, or eosinophilic myocarditis. EMB obtained from the septum of the right ventricle revealed lymphocytic and eosinophilic infiltration in the interstitium and perivascular area, findings that were consistent with a diagnosis of hypersensitivity myocarditis ().\nThe dyspnea improved upon treatment with prednisolone and diuretics. Levels of CK-MB and troponin-I were normalized on days 6 and 9, respectively. The peripheral eosinophil count decreased from 1,380/mm3 to 620/mm3 on day 2 and was normalized (50/mm3) on day 4. The skin rash disappeared almost completely after use of 5 mg prednisolone, and the patient was discharged from the hospital on day 12. Echocardiography at the 6-month follow-up showed normalized regional wall motion abnormalities and improved LV systolic function from 50% to 70% of the ejection fraction. At the 6-month follow-up, CE-CMR showed that previously high signal intensities in circular patterns in the epicardium of the left ventricle had disappeared and the oval-shaped area of high signal intensity in the LV septum had decreased in size (). The patient remained asymptomatic without the need for prednisolone or diuretics.

[[68.0, 'year']]

F

{'25990281': 1, '19356546': 1, '24926359': 2, '29367574': 1, '22361396': 1, '22065913': 2, '27583870': 1, '30122752': 1, '16476862': 1, '28210568': 2, '19440116': 1, '22185868': 1, '30546573': 1, '34900557': 2, '19630574': 1, '24648808': 2}

{'5304556-1': 1, '3207060-1': 1, '4043629-1': 1, '8603774-1': 1}

3956996-1

noncomm/PMC003xxxxxx/PMC3956996.xml

Isolated dilatation of the inferior vena cava

A 46-year-old female underwent abdominal computed tomography (CT) imaging at a private clinic due to mild right upper quadrant abdominal discomfort and back pain during the previous 2 weeks. She was referred to our hospital to evaluate the cause of IVC dilatation shown by abdominal CT (). The patient had no history of hypertension or diabetes mellitus and no family history of aortic, collagen, vascular or congenital heart disease. She had latent hepatitis B virus infection and her mother died of hepatocellular carcinoma. Ultrasonography of the liver showed hepatic vein dilatation without obstruction or thrombus in either the hepatic vein or IVC. The abdominal CT showed prominent dilatation of the IVC and hepatic vein with no evidence of liver disease such as cirrhosis, hepatocellular carcinoma or Budd-Chiari syndrome. Her vital signs included blood pressure of 107/64 mmHg, pulse of 60 beats per minute, respiration of 20 breaths per minute, and body temperature of 36.5℃. During the physical examination, cardiac auscultation revealed no definite murmurs and her electrocardiography demonstrated no apparent ST segment or T wave abnormalities. The blood chemistry analyses were within normal limits, including N-terminal pro-B natriuretic peptide, coagulation studies with fibrinogen, antinuclear antibody, complete blood cell count, and liver enzymes. Her heart size was normal on chest X-ray. Transthoracic echocardiography was performed to evaluate right side heart abnormalities. Dilated IVC with diminished inspiratory collapse was observed (expiration 24.3 mm, inspiration 21.4 mm) using a subxiphoid approach to view the IVC along the longitudinal axis (). Spontaneous echo contrast was present in the dilated IVC without flow obstruction including the entry from the RA. The hepatic vein was dilated mildly (13.2 mm), but the flow through the hepatic vein was normal (). Tricuspid regurgitation (TR) was mild and showed normal right ventricular (RV) systolic pressure (). Normal pulmonary artery (PA) pressure without regurgitation or stenosis () and normal flow of the superior vena cava were observed. The RV size and its contractility were normal with a normal degree of tricuspid annulus displacement toward the apex in the systole (1.75 cm). Additionally, we observed normal left ventricle (LV) size and LV systolic function (ejection fraction = 68%) without regional wall motion abnormalities. Normal RA pressure, RV pressure, and PA pressure were observed (), and the RA pressure was decreased with an inspiratory effort (-2 mmHg). As the patient had no symptoms or abnormal signs, we observed her and plan to follow-up annually with echocardiography.

[[46.0, 'year']]

F

{'19786685': 1, '9416951': 1, '22715560': 1, '21906159': 1, '2386120': 1, '10552361': 1, '30627450': 2, '14762185': 1, '6773338': 1, '6695787': 1, '17617312': 1, '24648809': 2}

{'6304925-1': 1}

3956997-1

noncomm/PMC003xxxxxx/PMC3956997.xml

Ifosfamide-induced Fanconi syndrome with diabetes insipidus

A 61-year-old Russian man was admitted to the clinic for evaluation of a 5-cm axillary mass that had invaded the adjacent bony structures. He was diagnosed with inflammatory malignant fibrous histiocytoma. Neoadjuvant chemotherapy with adriamycin (25 mg/m2) and ifosfamide (2.5 g/m2) was administered on days 1 to 3 following mesna prophylaxis. On day 3 of chemotherapy, the patient showed general weakness, polyuria, and dehydration. Laboratory findings included hypernatremia (serum sodium, 150 mmol/L), hypokalemia (serum potassium, 1.7 mmol/L), hypercalcemia (serum calcium, 10.6 mg/dL), and hypophosphatemia (serum phosphate, 2.1 mg/dL). The combination of hypernatremia, hyperosmolarity, polydipsia, and polyuria were consistent with nephrogenic diabetes insipidus (). The patient was thus treated with electrolyte replacement and dichlozid. However, his electrolyte imbalances were aggravated by this treatment, and his mental status deteriorated to a stupor. Six days after chemotherapy, his serum blood urea nitrogen and creatinine levels increased to 49.5 mg/dL (normal, 5.0 to 25.0) and 1.81 mg/dL (normal, 0.5 to 1.4), respectively. A 24-hour urinalysis revealed urinary loss of glucose, amino acids, uric acid, and potassium. The presence of these multiple defects in renal proximal tubular reabsorption, including glycosuria, hypophosphatemia, and proteinuria, were suggestive of Fanconi syndrome (). Treatment of isotonic saline with electrolyte replacement was maintained. However, the electrolyte imbalance was not corrected, and the metabolic acidosis was aggravated by this treatment. Nine days after chemotherapy, the patient died of uncorrected metabolic acidosis.

[[61.0, 'year']]

M

{'19309244': 1, '34235046': 2, '26918138': 1, '1503924': 1, '2386379': 1, '18214444': 1, '18278066': 1, '9641191': 1, '7974492': 1, '33990157': 2, '34484686': 1, '32509580': 1, '8270973': 1, '22392832': 1, '4552918': 1, '24648810': 2}

{'8685724-1': 1, '8259464-1': 1}

3957044-1

noncomm/PMC003xxxxxx/PMC3957044.xml

Adalimumab for Treatment of Idiopathic Frosted Branch Angiitis: A Case Report

A 14-year-old boy, who was otherwise healthy, was referred to the uveitis clinic for progressive blurring of vision in both eyes since 1 month before.\nOn examination, visual acuity was 20/400 in both eyes. Anterior segment examination revealed mild ciliary injection and anterior chamber reaction (2+ cells) but no keratic precipitates or posterior synechiae. Both eyes had inflammatory reaction in the vitreous (2+ cells) but there were no snow balls or snow bank formation. Fundus examination disclosed extensive retinal vascular sheathing and scattered intraretinal hemorrhages with severe macular edema in both eyes ().\nSystemic work-up and investigations, including a complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) titer, angiotensin converting enzyme (ACE) titer, tuberculin skin test (TST), urine analysis and chest X-ray were unremarkable. Rheumatologic tests including antinuclear antibodies (ANA), anti double strand DNA antibody (anti ds-DNA), rheumatic factor (RF), antiphospholipid antibody, anti-neutrophil cytoplasmic antibodies (ANCAs), and cryoglobulin assay were all negative. Blood CD4 and CD8 counts were within normal range and serology for the human immunodeficiency virus was also negative. Brain magnetic resonance imaging (MRI) did not show any abnormality. Blood serology for possible infectious causes including herpes family viruses, i.e. herpes simplex virus (HSV) type 1 and 2, varicella zoster virus (VZV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV), hepatitis B and C viruses, treponema, borrelia, and toxoplasma were checked. Immunoglobulin G (IgG) levels against HSV type 2 and CMV (but not IgM) were elevated. We tested the aqueous specimen after an anterior chamber paracentesis to investigate the presence of deoxyribonucleic acid (DNA) of HSV type 1 and CMV viruses. The result of polymerase chain reaction (PCR) on aqueous samples was negative for both viruses.\nUntil the results of blood tests and aqueous PCR became ready, vision continued to deteriorate down to 20/1000 and 20/800 in the right and left eyes, respectively.\nBased on the inconclusive work-up a diagnosis of idiopathic FBA was entertained and a course of systemic steroids was suggested. At this time, the patient’s parents mentioned that two years ago, for treatment of a similar condition, oral prednisolone 1 mg/kg had been commenced but soon after initiation, the patient developed severe mood changes which persisted long after discontinuation of treatment. The parents therefore rejected corticosteroid treatment. The progressive nature of the condition mandated considering other therapeutic measures to prevent macular scarring. Due to the safety profile of anti-tumor necrosis factor (TNF) agents and their rapid onset of effect, adalimumab was considered as an alternative to conventional treatment for which the parents provided written informed consent. A single dose of 40 mg pre-filled adalimumab (HUMIRA®, Abbott Laboratories, North Chicago, IL, USA) was injected subcutaneously in the patient’s right thigh. No local or systemic adverse effect was noted at the time of injection or later on.\nThree weeks after injection, visual acuity improved to 20/200 and 20/120 in the right and left eyes, respectively. Anterior chamber and vitreous reaction decreased to 1+ cell, and vascular sheathing and macular edema resolved dramatically. Repeat fluorescein angiography and optical coherence tomography (OCT) confirmed the improvement (Figs. and ).\n10 weeks after injection, visual acuity improved to 20/40 and 20/30 in the right and left eyes, respectively. In both eyes, the anterior chambers were quiet and the vitreous had only trace cellular reaction. Clinical improvement continued up to the last visit (6 months after the injection) when visual acuity reached 20/25 in both eyes with no sign of active inflammation.

[[14.0, 'year']]

M

{'29090058': 2, '22034564': 1, '1550190': 1, '9355182': 1, '3651369': 1, '17035274': 1, '17556427': 1, '15131687': 1, '24653825': 2}

{'5644415-1': 1}

3957045-1

noncomm/PMC003xxxxxx/PMC3957045.xml

Granular Cell Tumor of the Orbit

A 50-year-old woman presented with a 4-year history of vertical diplopia and painless superior displacement of the right eye. She had no history of ocular discharge or thyroid eye disease. Biopsy of the right orbital mass three years before had yielded a non-specific diagnosis.\nOn admission, best corrected visual acuity (BCVA) was 20/30 and 20/20 in the right and left eyes, respectively; a mild afferent pupillary defect was also noted in the right eye. There was a firm non-tender mass palpable through the right lower lid producing a small amount of proptosis and upward displacement. Exophthalmometric values were 18 mm and 14 mm on the right and left sides, respectively (). A significant reduction in ocular abduction and depression was noted without orbital bruits or pulsation. Slit lamp biomicroscopic examination was unremarkable but funduscopy disclosed right optic disc swelling nasally. Ishihara test revealed red-green color deficiency and visual field testing demonstrated a cecocentral scotoma in the right eye. Intraocular pressure was 15 mmHg bilaterally.\nOrbital computed tomography (CT) scan showed enlargement of the right inferior rectus muscle which was infiltrated by a muscle-density mass displacing the globe upward; maxillary sinus involvement and bone erosions were not observed ().\nDue to close proximity of the tumor with inferior orbital muscles, a subciliary approach was employed to excise the tumor. Under general anesthesia, the anterior portion of the mass was excised as much as possible and sent in 10% formalin solution for histopathologic evaluation. Complete excision of the mass was not feasible due to infiltration of the tumor within the rectus muscle and other orbital structures.\nGross examination revealed a cream-colored to brownish firm mass measuring 20Í16Í12mm. After tissue processing and embedding in paraffin blocks, thin sections were stained with hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS). Microscopic examination disclosed a partially encapsulated mass composed of lobules and cords of polyhedral and spindle-shaped cells with bland nuclei and intracytoplasmic PAS-reactive granules (A and B); however, mitosis was not a feature. The tumor cells were strongly immunoreactive for S100 in both nuclear and cytoplasmic areas but not for HMB45 and pan-cytokeratin immunostaining (C and D). These histopathologic features were consistent with GCT.\nDuring a six-month postoperative course, BCVA of the right eye decreased gradually and multiple sessions of radiotherapy, summing to 40 Gy in 2 Gy fractions, failed to control the growth of the residual tumor. Eventually vision dropped to no light perception and exenteration of the right orbit was performed to prevent extension of the tumor to the optic canal.

[[50.0, 'year']]

F

{'27176551': 2, '1749468': 1, '6192721': 1, '29755264': 1, '3028469': 1, '5279444': 1, '26090251': 2, '34898922': 2, '21464781': 1, '6302618': 1, '10711894': 1, '30320087': 1, '26742863': 1, '3039674': 1, '26637199': 1, '10503740': 1, '28639585': 1, '19337479': 2, '24653826': 2}

{'4451783-1': 1, '2655740-1': 1, '8603796-1': 1, '4866422-1': 1}

3957046-1

noncomm/PMC003xxxxxx/PMC3957046.xml

Acute Myelogenous Leukemia Mimicking Fulminant Periorbital Cellulitis

A 17-year-old boy presented with fever, progressive swelling and erythema of the right upper and lower lids and periorbital soft tissues of 5 days’ duration (A). He had received intramuscular gentamicin and oral ciprofloxacin over the last 5 days. He had no history of trauma, systemic disease or insect bites. No abnormal findings such as lymphadenopathy or hepatosplenomegaly were noted on systemic physical examination. He was ill and had high grade fever. Visual acuity was 8/10 in both eyes and relative afferent pupillary defect was negative. Ocular motility was normal but painful in the affected eye. Slit lamp examination and funduscopy were unremarkable and intraocular pressure was within normal limits. The patient had no evidence of dental infections or dacryocystitis. A complete blood count (CBC), blood culture, and other laboratory tests were requested.\nThe patient was admitted with a clinical impression of preseptal cellulitis and impending orbital involvement; intravenous ceftriaxone 1 gm every 12 hours was initiated empirically. The swelling and erythema progressed throughout the right facial and left periorbital area, and some blisters appeared on the right upper eyelid the day after admission (B). Orbital and paranasal sinus computed tomography (CT) images showed right periorbital soft tissue swelling without sinus involvement (). Laboratory tests revealed leukocytosis (120,000/ml) with a predominance of immature blast cells (>90%), anemia (hemoglobin level 10.9 gm/dl) and thrombocytopenia (54,000/ml).\nThe patient was referred to a hematologist with a presumptive diagnosis of acute leukemia and underwent bone marrow aspiration (BMA) and flow cytometry which confirmed type M4-M5 AML (). Chemotherapy including cytarabine 100 mg/m2 and idarubicin 12 mg/m2 together with broad spectrum antibiotics including vancomycin 1 gm every 12 hours, ceftazidime 1 gm every 8 hours and imipenem 500 mg every 6 hours were initiated. Signs and symptoms regressed after two courses of chemotherapy over 2 months and he was relapse free for 2 years (C).

[[17.0, 'year']]

M

{'7953914': 1, '15002029': 1, '8948669': 1, '1060381': 1, '11965121': 1, '31456931': 1, '9881556': 1, '205341': 1, '2778482': 1, '9116554': 1, '14573980': 1, '28868277': 1, '16085011': 1, '24653827': 2}

{}

3957175-1

noncomm/PMC003xxxxxx/PMC3957175.xml

Paraquat poisoning: A case report and review of literature

An 18-year-old female was admitted to the emergency room with an alleged history of attempted suicide in which an unknown quantity of paraquat (liquid form) was consumed at her residence. The patient was managed at local hospital with (intravenous (IV) fluids, antiemetic, and H2 blockers) and brought to our hospital for further treatment after 24 h. She had difficulty in opening her mouth and a decreased urine output. There was no history of vomiting, loose stools, abdominal pain, seizures, or fever. At the time of examination, the patient was conscious and oriented. There was neck edema. Examination of the oral cavity showed mucosal erosion of tongue, palate, and lips with oral bleeding []. On clinical examination, the pulse rate was 98 beats per min, regular, blood pressure (BP) was 130/80 mmHg, with respiratory rate of 22 per min. Cardiovascular system was normal. There was difficulty in breathing, but there were no added sounds on examination of the respiratory system. Pupils were bilaterally equal and reactive to light. The patient was intubated as there was associated laryngeal edema and difficulty in breathing. Gastric lavage was performed and charcoal was given in the emergency department. She was kept on elective ventilation. In the intensive care unit (ICU), she received IV fluids and an antiemetic as a supportive measure. Her initial chest X-ray showed a left lower zone infiltrate []. She had high serum urea (221 mg/dL) and creatinine (8.78 mg/dL) on the day of admission that gradually reduced to normal after two sessions of dialysis. Blood and urine cultures were sterile. Other blood investigations including thyroid and liver functions were normal. Urine examination was normal. Ultrasound of the abdomen showed bilateral grade I changes in the kidneys. Two-dimensional (2D) echo and electrocardiogram (ECG) were normal. upper gastrointestinal (GI) endoscopy showed corrosive injury to the esophagus and proximal stomach. Endotracheal culture showed Klebsiella pneumoniae. She received intravenous methylprednisolone 1 g in 200 ml normal saline every 2 h daily for 3 days, IV cyclophosphomide 750 mg (15 mg/kg/day) in three divided doses (in 200 ml of N-saline over 2 h) for 2 days followed by IV dexamethasone 5 mg 6 hourly, injection N-acetylcysteine 2 g stat followed 1 gm TID for 5 days, vitamin C (500 mg/amp) 6 g/day IV, vitamin E (400 i.u./tab) 2 tabs QID. The patient did not respond to treatment and expired on the 12th day post injury as a result of septicemia and respiratory failure.

[[18.0, 'year']]

F

{'17139398': 1, '4877735': 1, '15779152': 1, '10773838': 1, '31083174': 1, '7015857': 1, '4141727': 1, '9018188': 1, '15266931': 1, '6055745': 1, '1325624': 1, '687937': 1, '24826339': 1, '11926615': 1, '7175991': 1, '1892020': 1, '3285127': 1, '5812101': 1, '2198050': 1, '12974543': 1, '171945': 1, '5939816': 1, '5017564': 1, '5809560': 1, '3546085': 1, '1248304': 1, '2591987': 1, '12194161': 1, '6038370': 1, '1987360': 1, '29862459': 1, '11179138': 1, '5929686': 1, '9927343': 1, '12324200': 1, '29234027': 1, '11774102': 1, '10778636': 1, '24672279': 2}

{}

3957312-1

noncomm/PMC003xxxxxx/PMC3957312.xml

Relapsed Herpes Simplex Virus Encephalitis after Epilepsy Surgery

An 11-year-old boy with a past medical history of HSV encephalitis at the age of five presented to Severance Children’s Hospital with a history of intractable seizures for the past six years. He had been healthy with normal neuropsychological development until the onset of the encephalitis. Magnetic resonance imaging (MRI) demonstrated focal encephalomalacia in the right temporal and left parietal lobes, suggestive of sequelae of previous insult (). He had suffered from daily convulsive seizures, which were sometimes provoked by auditory stimulation. His electroencephalogram (EEG) showed diffuse slowing in both hemispheres; frequent generalized slow sharp and wave discharges; frequent generalized paroxysmal fast activities; and frequent sharp waves from multifocal areas with ictal episodes originating from the left parietal area. He underwent left parietal cortisectomy after an extensive presurgical evaluation. Five days after the operation, he presented with a high fever, lethargy and recurrent seizures. Cerebrospinal fluid (CSF) examination by lumbar puncture showed 5/mm3 red blood cells, 105/mm3 white blood cells (99% lymphocytes), 90.1 mg/dL protein, and 60 mg/dL glucose. CSF HSV type 1 PCR was positive, and CSF HSV culture was not available. Brain tissue pathology from cortisectomy revealed focal cortical dyslamination with giant and dysmorphic neurons, accompanied by focal microglial cell nodules (CD 68 positive) with perivascular lymphocytic infiltrations that implied an old viral infection which is consistent with focal cortical dysplasia (FCD) type IIId. Brain MRI showed swelling and hyperintensity in the left temporoparietal region on T2-weighted images that were widely distributed from the surgical resection margin, suggesting the possibility of ischemic insult or infection (). EEG showed excessive delta activity, generalized rhythmic sharp wave discharges, and occasional subclinical seizures from the left occipital area. Intravenous acyclovir 45 mg/kg/day was initiated after relapsed HSV encephalitis was suspected based on these results. High spiking fever and altered mental status improved during the three-week intravenous acyclovir treatment. When he visited the outpatient clinic one month later, our patient’s neurological function had returned to baseline status, including cognition, mental, speech, and motor functions.

[[11.0, 'year']]

M

{'15627947': 1, '8385702': 1, '16275548': 1, '10069600': 1, '20951065': 1, '17554701': 1, '29846779': 1, '31468470': 1, '30405395': 1, '27216026': 2, '6148470': 1, '18230840': 1, '7706811': 1, '21219302': 1, '25883839': 2, '21867861': 1, '31386089': 1, '28251511': 1, '24649468': 2}

{'4877812-1': 1, '4877812-2': 1, '4392527-1': 1}

3957313-1

noncomm/PMC003xxxxxx/PMC3957313.xml

Cefepime- Induced Non-Convulsive Status Epilepticus (NCSE)

A 71-year-old woman with a history of diabetes mellitus and liver cirrhosis associated with hepatitis B viral infection was hospitalized for right lower lobe lobectomy after diagnosis of lung cancer. Although she had successful lobectomy, she underwent several post-operative complication including operation site bleeding, acute renal failure, acute respiratory distress syndrome, and atypical pneumonia. Her renal failure was prerenal type after massive operation site bleeding, and continuous renal replacement therapy (CRRT) were started for renal replacement treatment. Post operation (OP) day 9, she experienced confusion, and disorientation and started on quetiapine with diagnoses of delirium. Post OP day 13, she had antibiotic resistance for atypical pneumonia, which had to switch from imipenem and vancomycin to cefepime. Although her serum creatinine level was much improved from 2.7 mg/dL to 1.87 mg/dL, after 5 days of renal replacement therapy, she was started on cefepime renal dose of 2 g every 12h. Plasma concentration of cefepime was not measured because the analytical technique was not available in our hospital. After 5th day of cefepime use, the patient became stupor and developed one episode of brief generalized myoclonic seizure. The neurologic examination revealed change in mental status, and minimal response to noxious pain stimulation. There was no focal neurological sign, pathologic reflex, and neck stiffness. Temperature, vital signs and the rest of the physical examination were normal. The brain magnetic resonance imaging (MRI) including diffusion and gradient echo images revealed no acute lesions which can explain sudden mental status change. Serum blood cell counts, glucose, ammonia and electrolytes were within the normal range. Renal profile showed blood urea nitrogen (BUN) of 27 mg/dL (normal range: 7–25 mg/dL), creatinine of 1.33 mg/dL, creatinine clearance (Ccr) of 25.35 mL/min/1.73m2. The electroencephalograph (EEG) revealed continuous 2–3 Hz generalized sharp and wave (). NCSE was diagnosed and administered lorazepam 4 mg intravenous injection with continuous EEG monitoring were started. She was than further treated with levetiracetam 500 mg and valproic acid 900 mg intravenously. She stay on maintenance doses of valproic acid (900 mg/day) and phenytoin (300 mg/day), clonazepam (1.5 mg/day). Repeated EEG revealed improved after anti-epileptic treatment (). As we discontinued cefepime, considering as a causative agent for NCSE, clinical symptoms improved 3 days after discontinuation of cefepime. She was than diagnosed with cefepime induced non convulsive status epilepticus. Anti-epileptic treatment was than discontinued uneventfully. No relapse occurred.

[[71.0, 'year']]

F

{'19034700': 1, '30915188': 1, '27298247': 1, '30756319': 1, '11498064': 1, '7514976': 1, '3284342': 1, '16278098': 1, '14984909': 1, '32357511': 1, '14690782': 1, '27408805': 1, '14982986': 1, '12871648': 1, '21720898': 1, '29081627': 2, '16162436': 1, '28755095': 1, '19033476': 1, '29137682': 1, '2401125': 1, '33614301': 2, '15616309': 1, '24649471': 2}

{'7883526-1': 1, '5642132-1': 1}

3957314-1

noncomm/PMC003xxxxxx/PMC3957314.xml

Thalamic Hyperintensity on Diffusion-Weighted MRI in a Patient with Nonconvulsive Status Epilepticus

A 70-year-old woman with altered mentality and unresponsiveness arrived at our emergency room. She had a medical history of Alzheimer’s disease, hypertension and chronic obstructive pulmonary disease, but no seizure or stroke. Her vital signs were stable. On the initial neurologic examination, she was drowsy and mute. She had left homonymous hemianopsia and right gaze preponderance. She showed symmetric withdrawal response to noxious stimuli. Electrocardiogram revealed atrial fibrillation and the cardiac enzymes were normal. Since eight hours before arrival, she had a cluster of generalized tonic clonic seizures at an interval of about ten minutes without full recovery of consciousness for just prior two hours. The convulsive seizure subsided with intravenous lorazepam injection. However, her drowsiness and unresponsiveness did not return to the baseline normal status. We took the DWI and the EEG to identify the cause of sustained abnormal mentality. The DWI revealed an ill-defined high signal intensity in the right thalamus and subtly in the right temporal area, in which the values of apparent diffusion coefficient (ADC) were reduced (). In the MR angiography, there was no significant steno-occlusive lesion. These DWI findings suggested a possibility of a clustered seizure-related change or an acute ischemic stroke. EEG recording showed a right temporal ictal onset zone with persisting ictal discharges with rhythmic alpha to theta activity ().\nAfter the confirmation of ictal EEG, we applied intravenous phenytoin to control the NCSE. Oral topiramate and intravenous levetiracetam were added to suppress remnant ictal discharges. Finally, ictal discharges disappeared (). Though she was gaining alertness, her mutism sustained. Follow-up DWI at the 5th day clarified a brighter lesion localized to the pulvinar (). Transthoracic and transesophageal echocardiographies revealed a small echogenic nodular mass (7.5 × 3.5 mm sized) attached to the posterior mitral valve leaflet and a severely dilated left atrium. Other studies including CSF examination and serologic markers for autoimmune and paraneoplastic diseases were normal. The cause of status epilepticus remained unknown despite extensive work-ups. We suspected a ringt posterior cerebral artery (PCA) infarction when we took her atrial fibrillation and the infarction territory into account. As CHA2DS2-VASc score was 3, it was reasonable to start anticoagulation irrespective of the feasible mechanism of the seizure. Altered mentality with global aphasia persisted despite the adequate treatment.

[[70.0, 'year']]

F

{'17362837': 1, '21984190': 1, '7707917': 1, '11340227': 1, '33276270': 1, '15743871': 1, '18717714': 1, '15158702': 1, '25625092': 2, '11405815': 1, '9738086': 1, '24649469': 2}

{'4295057-1': 1, '4295057-2': 1}

3957316-1

noncomm/PMC003xxxxxx/PMC3957316.xml

Surgical Treatment of Mesial Temporal Lobe Epilepsy in a Patient with Neurofibromatosis Type 1

A 32-year-old lady had developed seizures 5 years before visiting our hospital. She was a right handed postgraduate student. Her mom reported that she fumbled her fingers and showed lip smacking during her seizures and did not respond to questions. She reported only one episode of secondarily generalized seizures, which occurred before taking any antiepileptic drugs. The auras were the most frequently abdominal, but rarely vertiginous or psychic. The initial brain MRI had showed unusual multifocal lesions. Stereotaxic biopsy did not confirm the etiologic diagnosis.\nAfter the biopsy, she had been transferred and followed-up at our epilepsy outpatient clinic for seizure control. On family history, her grandmother had seizures. Physical examination showed apparent axillary pigmentation and freckling, seven café-au-lait spots which are more than 15 mm on back. Neurological examination, including visual, and auditory and somatosensory systems, did not reveal any focal deficit. Serial brain MRI showed multifocal lesions in right temporal area, left tectum, right cerebellar peduncle thalamus, basal ganglion, and intraventricular cyst in left trigon of the ventricle (). Those lesions were well localized and not enhanced, and were not accompanied by surrounding edema, which were compatible with CNS hamartomas. The right mesial temporal area showed increased signal changes and increased volume, prominently in the head of hippocampus. The volumetric study of hippocampi demonstrated that the total volume of right hippocampus was slightly bigger than that of left hippocampus [right hippocampus: 4,105 mm3 (normal range: 2,563–4,195 mm3), left hippocampus 3,659 mm3 (normal range: 2,476–3,973 mm3)]. The difference of right to left hippocampal volume was 446.14 mm3, which was in the normal range (−38.3–531.3 mm3). Those lesions were suggestive of multifocal infiltrative glioma, pleomorphic xanthoastrocytoma with multifocal involvement, other CNS lymphoma, vasculitis, and etc. However the enhanced MRI demonstrated multiple small lesions mainly in the scalp areas, indicating neurofibromas in skin, even though those lesions did not show clinical features (). Those skin manifestations and scalp MRI findings suggested neurofibromatosis type 1.\nAfter the polytherapy of antiepileptic drugs, the intensity of her seizures was milder, but the frequency of her seizures was not changed. During the hospital course, she had simple partial seizures monthly and, complex partial seizures twice per year, when she had been on oxcarbazepine 1,500 mg, topiramate 400 mg, levetiracetam 3,000 mg, clobazam 10 mg, and pregabalin 150 mg per day.\nIntellectual assessment revealed that the score of full scale IQ was 85, that of verbal IQ score 87, and that of performance IQ 84 which was estimated to be between 14.2–19.2 percentile. Her neuropsychological tests showed diffuse cerebral dysfunction. Beck’s depression inventory score was normal.\nFor treating intractable seizures and obtaining the pathologic tissues, presurgical evaluation of epilepsy surgery was performed, including video-EEG monitoring, Wada test, and detailed neuro-imaging studies.\nShe underwent three day video-EEG monitoring. During the stay, 10 complex partial seizures and 1 simple partial seizure were recorded. The one simple partial seizure was only abdominal aura. The complex partial seizures were consisted of abdominal aura, lip smacking, leaning backward, often with right or both hand fumbling, but, not accompanied by generalized seizures.\nThe interictal epileptiform discharges were frequently seen on right mid-temporal area about once per minute. The 11 ictal epileptiform discharges started with semi-rhythmic theta waves in right temporal area, and then delta waves in the same area, spreading into whole leads ().\nShe underwent ictal and interictal 99m-Tc HMPAO SPECT. The radiotracer for ictal SPECT was injected at 40 seconds from the onset of 102 second duration habitual complex partial seizure. The hyperperfusion was localized to right anterior mesial temporal area. Interictal SPECT, taken after 24 hour seizure freedom, showed focal hypoperfusion in right mesial temporal area. Subtracted ictal SPECT co-registered to MRI demonstrated definitely hyperperfused areas in right mesial temporal regions, which are concordant to the localization of ictal EEG onset (). Other lesions did not show any perfusion changes in SPECT studies. Brain 18F-FDG PET showed right temporal hypometabolism. Other brain and scalp lesions, which were confirmed on brain MRI, did not reveal any metabolic changes in PET study. Wada test demonstrated that her left hemisphere were both dominant for speech and memory, predicting good surgical outcome of right anteromesiotemporal resection.\nAfter the removal of right anteromesial temporal area, her seizures became free. The pathologic tests showed mild neuronal loss at hippocampus, and dysplastic changes in the specimen of lesion tissue without any evidence of neoplasm.

[[32.0, 'year']]

F

{'17105749': 1, '1946382': 1, '8330570': 1, '19117870': 1, '23602237': 1, '14694053': 1, '9880138': 1, '21344624': 1, '29566708': 1, '23597854': 1, '32613422': 1, '10469430': 1, '24649470': 2}

{}

3957446-1

noncomm/PMC003xxxxxx/PMC3957446.xml

Double-outlet left atrium: Ventriculo-atrial malalignment defect

A four-month-old, female infant, weighing two kilograms, presented to us with failure to thrive and easy fatigability during feeding, since birth. She had two episodes of lower respiratory tract infection in the past and had a history of mild cyanosis on crying. The physical examination revealed a heart rate of 124 beats/minute, blood pressure of 84/52 mmHg, respiratory rate of 32/minute with oxygen saturation (SaO2) of 92% in room air. A pansystolic murmur at the left lower sternal border and a split second heart sound were heard on auscultation. Mild hepatomegaly was noted. The electrocardiogram (EKG) showed left atrial enlargement, with left axis deviation, without ventricular hypertrophy. The chest radiograph showed cardiomegaly and increased pulmonary vascularity. A transthoracic echocardiography [ and ] revealed situs solitus, levocardia, and d-loop ventricles, with normal pulmonary and systemic venous drainage. Well-defined right and left atria were present. There was right atrial outlet Atresia, with the only outlet for the right atrium being a secundum ASD. The left atrium emptied into the right and left ventricles through two AV valves. The right-sided AV valve had septal attachments and opened into the trabeculated right ventricle, while the left AV valve opened into a smooth-walled left ventricle. Thus, morphologically the right and left AV valves resembled the tricuspid and mitral valves, respectively. There was no significant AV regurgitation. There was a restrictive inlet ventricular septal defect (VSD) shunting left to right with a gradient of 40 mmHg [ and ]. The great vessels were normal in origin and position. There was no right ventricular outflow obstruction. The left ventricular outflow tract (LVOT) was somewhat elongated []. The coronary sinus and aortic arch anatomy were normal.\nShe was planned for an initial pulmonary artery banding followed by total repair at a later date. However, she died at home from a possible chest infection few weeks after presentation to the hospital.

[[4.0, 'month']]

F

{'9358668': 1, '24688232': 1, '1262385': 1, '23804724': 1, '3945088': 1, '7470345': 1, '19910160': 1, '29922021': 2, '26556972': 2, '17198818': 1, '22423064': 1, '32295626': 1, '7471829': 1, '25419523': 1, '24688233': 1, '3348706': 1, '11781560': 1, '24688234': 2}

{'4608203-1': 1, '5963238-1': 1}

3957447-1

noncomm/PMC003xxxxxx/PMC3957447.xml

An unusual example of isolated double-orifice tricuspid valve

A 12-year-old girl presented with palpitation of recent onset. She was previously identified to have a restrictive perimembranous ventricular septal defect (VSD) (restricted by the septal tricuspid leaflet) during infancy. She remained asymptomatic throughout childhood and presented 12 years later with a history of palpitation of one-month duration. On examination, there was left parasternal heave with epigastric pulsations, a wide variably split second heart sound and a pansystolic murmur at the left lower sternal border. There was no cyanosis. The electrocardiogram showed ectopic atrial rhythm with low atrial focus and incomplete right bundle branch block. Transthoracic echocardiography showed dilated right atrium (RA) and right ventricle (RV). An accessory opening of the tricuspid valve (TV) into the left ventricle (LV) was found to be situated in the posterior plane with a separate tensor apparatus [Figure and ]. The atrioventricular junction was overriding the ventricular septum. A large LV-to-RA shunt was noticed through the regurgitant accessory tricuspid orifice during systole. There was unobstructed flow from RA to LV during diastole. The other orifice (RA to RV) was unobstructed and competent. No VSD was seen.\nSurgical findings showed two tricuspid valves. The additional valve orifice with separate tensor apparatus with ruptured chordae was situated posterior and inferior to the normal valve orifice [Figure and ]. On testing with saline, an LV-to-RA shunt was found. Under cardiopulmonary bypass through RA, the abnormal TV leaflets were sutured together and the additional orifice was further closed with a tanned pericardial patch, sutured along the annulus, safeguarding the conduction tissue. There was no residual shunt on postoperative echocardiography.

[[12.0, 'year']]

F

{'24688232': 1, '22889648': 1, '21504473': 1, '25684896': 1, '17944123': 1, '6058827': 1, '24688233': 1, '12691297': 1, '32703195': 2, '26556972': 2, '24688235': 2}

{'4608203-1': 1, '7379346-1': 1}

3957448-1

noncomm/PMC003xxxxxx/PMC3957448.xml

Submitral aneurysm: An antenatal diagnosis

A 26-year-old primigravida with gestation of 26 weeks presented for fetal echocardiography with fetal tachycardia on antenatal ultrasound. Fetal echocardiography showed large aneurysm arising from the submitral region, protruding predominantly into the right atrium (8 × 7 mm) and partly into the left atrium [Figure and , ]. The aneurysm expanded with ventricular systole and decompressed with ventricular diastole. Considering this characteristic feature, the possibility of a submitral aneurysm was considered. The differential diagnosis of atrial septal aneurysm was considered, but as the aneurysm projected predominantly into the right atrium and expanded in systole, this diagnosis was excluded. There was no inflow obstruction with normal tricuspid and mitral valve inflow velocities. There was no mitral regurgitation. There was no other intracardiac abnormality []. The characteristic movement of the aneurysm, i.e., the expansion with ventricular systole and its collapse with ventricular diastole was seen. There was transient fetal tachycardia (heart rate of 210/min) with PR interval of 70 m sec and 1:1 atrioventricular (AV) conduction. During the rest of the study, the heart rates varied from 140 to 160/min with 1:1 AV conduction. Ventricular contractility was normal and there was no pericardial effusion. The baby was delivered at term through normal vaginal delivery. The birth weight was 3 kg. Postnatal evaluation confirmed the diagnosis of submitral aneurysm [Figures and , , ]. The child is asymptomatic after birth with sinus rhythm and is under close follow-up for the size of the aneurysm and any other hemodynamic compromise. The child is planned for an elective surgery.

[[26.0, 'year']]

F

{'27081448': 2, '967588': 1, '13859018': 1, '8680275': 1, '9263558': 1, '7668941': 1, '17670119': 1, '33738423': 2, '27751280': 1, '7225261': 1, '34567801': 1, '3609038': 1, '9047060': 1, '24688236': 2}

{'7954274-1': 1, '7954274-2': 1, '7954274-3': 1, '7954274-4': 1, '4828418-1': 1}

3957450-1

noncomm/PMC003xxxxxx/PMC3957450.xml

Off-pump atrial septostomy with thoracoscopic scissors under transesophageal echocardiography guidance

An 8-month-old female child with single ventricle physiology (double-inlet left ventricle) with hypoplastic mitral valve (9 mm, Z score = −2.44) and intact atrial septum and unobstructed pulmonary blood flow needed PA banding and creation of an inter-atrial communication.\nAfter detailed evaluation of the child and taking informed consent from her parents, the child was prepared under anesthesia as for open-heart surgery and the procedure was carried out through a median sternotomy. The patient was heparinized. A purse-string suture was made on the right atrial (RA) appendage. A stab was made within the purse string, and through this, thoracoscopy scissors [] was introduced in the RA. Under TEE guidance, the closed tip of the instrument was used to tent the fossa ovalis below the limbus [] and a small perforation was created. It was then dilated by stretching with the opening of the blades of the scissors []. The orifice was assessed and found to be restrictive with a peak gradient of 4 mmHg and a mean gradient of 2 mmHg.\nThe scissors was then rotated to face inferiorly with one blade on either side of the inter-atrial septum, and two cuts were made in the inferior and lateral directions, away from the AV valves and conduction tissue, creating an orifice of maximum size 9 mm with free laminar flow across the resulting defect []. PA banding was done as per Trussler's formula to 27mm.\nThe child recovered uneventfully and was discharged from the hospital on the 6th postoperative day. The PA band gradient on the pre-discharge echo was 60 mm Hg. At 1 month follow-up, the child was well and symptom free with an oxygen saturation of 92%. The child had gained 0.5 kg in the 1 month following discharge. The follow-up echo at 1 month showed a band gradient of 50 mm Hg. The atrial septal opening measured 9 mm with laminar flows across the defect. A bidirectional Glenn shunt is planned in the subsequent 3-6 months.

[[8.0, 'month']]

F

{'8619678': 1, '18377559': 1, '18942130': 1, '8787484': 1, '4553415': 1, '24688238': 2}

{}