Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 45-year-old Japanese man, who had had bilateral visual disturbance due to Vogt-Koyanagi-Harada (VKH) disease 17 years before entry, was admitted to this hospital because of headache, vertigo and vomiting. On examination at entry, no abnormalities except for poliosis, patches of vitiligo on his left shin, sunset glow fundus, and positional nystagmus with Frenzel glasses were found. Laboratory data other than leukocytosis and elevated level of gamma-GTP were normal and the results of brain CT scan were within normal limits. On the following day, diplopia was developed and the neurological symptoms including loss of bilateral visual acuity, Horner's syndrome on the right side, right facial palsy, bilateral sensorineural hearing disturbance, palsy of the soft palate on the right side with swallowing difficulty, and dissociated sensory disturbance on the right face and the upper and lower extremities on the left side appeared with a few days. He couldn't get up. The cerebrospinal fluid (CSF) was clear and had pleocytosis with normal sugar content. The protein, immunoglobulin G and myelin basic protein (MBP) were elevated but the tests for oligoclonal band and antiviral antibodies were negative. Brain CT scan showed low density areas in right cerebellar hemisphere and in left putamen without abnormality with contrast material and evoked potentials were normal. Prednisolone was prescribed and his symptoms were subsided but his gait remained ataxic. Magnetic resonance imaging (MRI) 4 months later showed an atrophy of the lower half of bilateral cerebellar hemisphere supplied by posterior inferior cerebellar artery, suggesting cerebellar infarction, and high intensity areas on T2 image in bilateral cerebral white matters, basal ganglia, and left cerebral peduncle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Wallenberg's syndrome in a case of Vogt-Koyanagi-Harada disease]. 261 5

Three children ranging in age from 2 to 5 years with acute disseminated encephalomyelitis (ADEM) were successfully treated with high-dose intravenous immunoglobulin (IVIG). Their symptoms were somnolence, fever, headache, vomiting, and resting tremor. In all of these patients, it was difficult to distinguish the condition from viral encephalitis before analyzing the myelin basic protein. ADEM was diagnosed because of increased levels of myelin basic protein in their cerebrospinal fluid and abnormal high-signal intensity on T2-weighted magnetic resonance imaging. All patients were given IVIG at a dose of 400 mg/kg/day for 5 consecutive days. The patients rapidly regained consciousness in 14 hours, 2 days, and 4 days and demonstrated a complete clinical improvement within 18 days, 10 days, and 7 days of the initiation of the treatment, respectively. IVIG may prove useful as an alternative treatment to corticosteroids for ADEM.
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PMID:Intravenous immunoglobulin therapy in acute disseminated encephalomyelitis. 1046 50

Acute disseminated encephalomyelitis (ADEM) is a demyelinating disease showing multifocal central nervous system lesions due to an autoimmune disorder. We reported a 3-month-old girl with ADEM. One week after having a cold, she presented with somnolence, poor feeding and vomiting. When she was admitted three days after the onset, she could neither fix or follow objects with her eyes nor respond to sound. Her muscle tone was decreased. Cerebrospinal fluid examination revealed pleocytosis, elevated protein concentration and positive myelin basic protein. No oligoclonal band was detected. Diffuse monomorphic slow wave activity was noted on the electroencephalogram. Only wave I was present bilaterally on the auditory brainstem response. T2 weighted images of magnetic resonance imaging revealed multiple areas of high signal in the right posterior limb of the internal capsule, white matter of the cerebellum and brainstem. She was diagnosed as having ADEM, and underwent high dose gamma-globulin therapy. Corticosteroids were not given because of her high blood pressure. The clinical symptoms improved continuously before and after the administration. Two years after the onset, she showed normal growth and development without reoccurrence. The age at onset of childhood ADEM is usually 3 or 4 years. ADEM before one year of age is very rare. The demyelinating lesions of this case corresponded to the regions which normally become myelinated by 3 months. Although ADEM is usually treated with corticosteroids, high dose gamma 1-globulin therapy can be considered if patients are very young or have a high risk for corticosteroid, or respond poorly to corticosteroids.
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PMID:[Acute disseminated encephalomyelitis in a 3-month-old infant]. 1126 Sep 21

Intraventricular hamartomas are extremely uncommon lesions outside of a setting of tuberous sclerosis. The second case of its kind in medical literature is presented and its possible aetiopathogenesis, imaging characteristics, pathognomonic magnetic resonance spectroscopy (MRS) and histopathology are discussed. An 11-year-old male presented with a seizure disorder for one year, with headache and vomiting for 15 days. Computerized tomography (CT) revealed a non-enhancing, heterogeneous, left-sided, trigonal lesion with areas of calcification trapping the left frontal horn. Magnetic resonance imaging (MRI) indicated that the lesion was iso to hypointense on T1 weighted images (T1WI) and iso to hyperintense on T2 weighted images (T2WI). A pathognomonic neurochemical signature was elicited on (1)H MRS showing low N-acetylaspartate resonance and normal creatine:choline ratios. Radical decompression of the tumor resulted in an excellent outcome. The diagnosis was established by positive immunohistochemical reactivity for synaptophysin, glial fibrillary acidic protein (GFAP) and myelin basic protein. This is the first case report in existing medical literature in which a histopathological correlation is available for a hamartoma with an unequivocal MRS signal. The authors advocate the use of MRS in patients with tuberous sclerosis or neurofibromatosis with suspected hamartomas to distinguish these benign lesions from gliomas prior to a surgical exploration.
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PMID:Intraventricular glioneuronal hamartoma: histopathological correlation with magnetic resonance spectroscopy. 1613 21

A 9-year-old girl was admitted for the treatment of hyper-natremic dehydration. Her history was significant for psychogenic polydipsia, hyponatremia, and a renal concentrating defect. She presented with a 2-day history of altered mental status, ataxia, lethargy, fever, nausea, vomiting, and diarrhea. Meningitis was ruled out. Over the course of her illness, slow rehydration was maintained with a gradual decrease (10 mEq per 24 hours) of the serum sodium. Despite this care, she developed quadriparesis, and magnetic resonance imaging performed on day 6 of her illness was consistent with osmotic demyelination (central pontine myelinolysis). To rule out an excessively rapid correction of hypernatremia as the etiology of the problem, a myelin basic protein was measured in the cerebrospinal fluid that had been obtained on hospital day 1. The myelin basic protein was 649.50 ng/mL (normal, 0.07-4.10 ng/mL). The current literature is presented regarding the postulated pathogenesis of central pontine myelinolysis and suggested therapies, previous reports of central pontine myelinolysis in children are reviewed, and the potential role of myelin basic protein in its diagnosis is discussed.
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PMID:Osmotic demyelination and hypertonic dehydration in a 9-year-old girl: changes in cerebrospinal fluid myelin basic protein. 1709 2