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)

Neurological manifestations in infantile osteopetrosis are common and varied, and not always attributable to the skeletal pathology. An unusual association of osteopetrosis with neuronal storage of ceroid lipofuscin is reported in two infant brothers born of nonconsanguinous parents. The first child became symptomatic at age 5 days with weight loss and vomiting. He had poor head control, hypertonia, and persistent fisting, and died at age 2 months. In the second infant, the diagnosis of osteopetrosis was confirmed at age 2 days. His neurological symptoms included blindness, deafness, and recurrent seizures. The infant died at 7 months of age. In both cases, autopsy confirmed the diffuse bony sclerosis with hepatosplenomegaly and extramedullary hematopoiesis. Neuropathological examination revealed cerebral atrophy with ventricular dilation, neuronal loss, and astrogliosis. The most striking finding was widespread accumulation of neuronal ceroid lipofuscin associated with formation of axonal spheroids. The optic nerves were compressed at the optic foramina and showed loss of myelinated axons and gliosis. Rapid Golgi impregnations of neurons from the calcarine cortex in the second infant were analyzed quantitatively, showing a reduction in the total dendritic length and number of branches. The primary defect in osteopetrosis is thought to be a lysosomal dysfunction involving the monocyte cell line from which osteoclasts are derived. Thus, the association in two brothers of osteopetrosis with accumulation of neuronal ceroid lipofuscin may not be fortuitous. The neuronal storage disorder in this instance probably reflects lysosomal dysfunction.
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PMID:The association of infantile osteopetrosis and neuronal storage disease in two brothers. 334 81

A 67-year-old man was admitted for status epilepticus, right hemiparesis, repeating vertigo and vomiting. Computed tomography showed no abnormality except for slight brain atrophy. Angiogram demonstrated bilateral vertebral artery stenosis at the origin, especially on the left side, and bilateral cervical internal carotid artery stenosis associated with ulceration. Intracranially, bilateral anterior cerebral artery was filled only by right internal carotid artery. Internal carotid artery on both sides did not fill the posterior cerebral artery. From these findings, we thought that both bilateral internal carotid artery and left vertebral artery should be surgically reconstructed. On June 4, 1986, left vertebral transposition to the common carotid artery and left carotid endarterectomy using double-balloon shunt were performed. Waiting for recovery of the general condition, right carotid endarterectomy was carried out on June 27, 1986. Postoperative angiogram demonstrated disappearance of bilateral internal carotid artery stenosis, and good filling of left vertebral artery through left common carotid artery. Postoperative course was uneventful and right hemiparesis gradually improved. Vertigo and vomiting completely subsided. The method and indication of combined reconstruction for extracranial vertebral and carotid artery were discussed.
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PMID:[A case of combined reconstruction of extracranial vertebral and carotid artery stenosis]. 337 49

A rare case with the episodes of vertebrobasilar TIAs which were caused by carotid ulcerative lesion and by persistence of proatlantal intersegmental artery is reported. This 69-year-old man was admitted on 14th Feb. 1985 with complaints of three attacks of vertigo, diplopia, nausea, vomiting and dysequilibrium lasting about 1 hour. His past history and family history were unremarkable. On admission, physical and neurological examinations revealed nothing particular, except bilateral carotid bruits. On the right side, innocent low pitched bruit was detected, however on the left side, carotid bruit was high pitched and was regarded as pathological. Blood pressure was 180/80 mmHg. Pulse rate was 66/min and cardiac arrhythmia was not detected by EKG. He also had no history of cardiac arrhythmia as mentioned above. CT scans and MRI showed only mild brain atrophy and no brain stem nor cerebellar lesions. Left carotid angiogram revealed ulcerative lesion of the common carotid bifurcation which was compatible with high pitched bruit. And at the level of the C2 vertebra, persistent proatlantal intersegmental artery originated from the left internal carotid artery which, after running upward, joined to the horizontal portion of the left vertebral artery above the atlas. Internal carotid and the vertebrobasilar vasculature beyond the proatlantal intersegmental artery were normal except slight irregularity of carotid siphon. Right carotid and vertebral angiograms revealed no abnormality and basilar artery was opacified clearly again via right vertebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of transient cerebral ischemia of the vertebrobasilar system caused by carotid ulcerative lesion and persistent proatlantal intersegmental artery: a case report]. 360 Sep 93

We studied a 59-year-old woman with dementia, retinitis pigmentosa, sensorimotor neuropathy, and attacks of vomiting associated with blood pressure lability and loss of consciousness. Abnormalities included CT evidence of cerebral atrophy, low IQ, slow central and peripheral nerve conduction velocities, axonal degeneration in sural nerve biopsy, and elevated levels of catecholamines and slow waves in EEG during attacks. Her sister, two brothers, and daughter also had progressive muscle weakness, visual disturbance, and similar vomiting attacks. The hereditary nervous system disorder does not fit any previously described condition.
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PMID:Familial neuropathy with dementia, retinitis pigmentosa, and dysautonomia. 386 Jul 47

A 5-year-old girl was admitted to another clinic because of vomiting and convulsions. She was brought to our clinic after a ventriculoperitoneal shunt was inserted. CT scan on admission in our clinic showed a tumor in the pineal region with tumoral hemorrhage. Tumor markers such as HCG, AFP, CEA, P-LAP were within normal range. A biopsy of the tumor was performed and the histological diagnosis was pineoblastoma. Her recovery was excellent and disseminated metastasis was not recognized. A subtotal removal of the tumor was performed through the occipital transtentorial approach. She had no neurological deficits after surgery. She then received two 5-day cycles of chemotherapy, consisting of intravenous administration of 20 mg/m2/day cisplatin and 60 mg/m2/day etoposide, and craniospinal radiotherapy. After these therapies, the tumor responded and disappeared completely. Follow-up radiographic investigations also demonstrated no abnormal evidence except for brain atrophy. She is attending a primary school without any problems. Pineoblastoma is quite rare and remarkably malignant. Hence, aggressive therapies including surgery, radiotherapy and chemotherapy is indicated for this tumor.
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PMID:[A case of pineoblastoma successfully treated with surgery, combined chemotherapy of cisplatin and etoposide, and radiotherapy]. 747 3

During an 8-year period, fifteen patients with subacute or chronic epidural haematoma were seen among 110 treated cases of extradural haematoma corresponding to a frequency of 13.6%. Increasing headache, nausea, vomiting, mild drowsiness and cranial nerve palsy were the symptoms resulting in the correct diagnosis in most cases. Clinical and pathological findings are described, and the factors influencing the course of events are discussed. The most important factors are cerebral atrophy, age, source of bleeding and location. By means of early CT (computed tomography) diagnosis of haematoma, fatal outcome could be prevented in most of the cases.
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PMID:[Subacute and chronic epidural hematoma after craniocerebral trauma]. 814 52

A previously healthy 16-month-old Korean girl with symptoms of fever, vomiting, and generalized tonic seizure was diagnosed to have Group D non-typhoid Salmonella meningitis. The patient was treated with ceftriaxone (100 mg/kg/day) and amikin (22.5 mg/kg/day) initially and ciprofloxacin (30 mg/kg/day) was added later because of clinical deterioration and disseminated intravascular coagulation. Brain CT performed on the second day showed a well-demarcated low density lesion in the right lentiform nucleus and both caudate nuclei, without evidence of increased intracranial pressure. MRI performed on the 11th day confirmed CT scan findings as well as right subdural fluid collection, brain atrophy, and ventriculomegaly. She underwent subdural drainage and later ventriculo-peritoneal shunt operation. Despite receiving intensive treatment, she still has severe neurologic sequelae. Our case shows that infarctions of basal ganglia and thalami are not specific for tuberculous meningitis and that meningitis complicated by infarction is indicative of grave prognosis.
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PMID:Non-typhoid Salmonella meningitis complicated by a infarction of basal ganglia. 1040 82

The clinical, biochemical, and neuroradiologic findings and clinical follow-up of seven patients with glutaric aciduria type II are reported. Three phenotypes of the disease are encountered: neonatal-onset form with congenital anomalies (two patients) or without congenital anomalies (three patients) and late-onset form (two patients). The neonatal-onset form presents as an overwhelming illness, with severe hypoglycemia and metabolic acidosis leading to rapid death. Frequently it is associated with perinatal energy deprivation, a neonate with low birth weight and prematurity. The late-onset form presents with intermittent episodes of vomiting, hypoglycemia, and acidosis especially after meals rich in fat and/or proteins. All parents are consanguineous and have a first- or second-degree relationship. Initially, in the two phenotypes with neonatal onset and during crisis in the late-onset phenotype, routine laboratory evaluation showed severe metabolic acidosis, with an increased anion gap, hypoglycemia without ketonuria, and disturbed liver function tests. In the majority of patients with neonatal-onset forms, the kidneys, liver, and at times the spleen are enlarged with an increased echogenic pattern; however, no hepatic or renal cysts are detected. Cardiomegaly is observed in most patients. The diagnosis can be easily and rapidly reached through tandem mass spectrometry study of the blood and can further be confirmed by gas chromatography/mass spectrometry analysis of the urine organic acids. In this report, the magnetic resonance imaging/computed tomography brain studies showed brain atrophy, white matter disease, and in one patient, fluid-filled cavities in the periventricular area and putamina. Fluorine-18-labeled 2-fluoro-2-deoxyglucose positron emission tomographic (FDG PET) brain studies in two patients with late-onset disease showed slightly decreased activity in the cerebral cortex in one and in the caudate nuclei in the other. Brain FDG PET scan and magnetic resonance spectroscopy were normal in one patient with neonatal-onset disease. All patients were treated with a diet low in fat and protein, oral riboflavin, and carnitine. The results were promising for the late-onset disease. Intravenous carnitine gave rewarding results in one patient with neonatal-onset disease.
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PMID:Glutaric aciduria type II: observations in seven patients with neonatal- and late-onset disease. 1078 89

A 12-month-old girl presented with fever and vomiting. Cerebrospinal fluid (CSF) examination revealed an increase of mononuclear cells and Mycobacterium tuberculosis. Magnetic resonance imaging (MRI) taken two months after the onset showed cerebral infarction in the left basal ganglia, tuberculoma in the interpeduncular cistern and brain atrophy. The infarction was shown as central cystic lesions with surrounding hyperintensity in the fluid-attenuated inversion-recovery (FLAIR) image. The cystic lesions were not differentiated from surrounding lesions in T2 weighted image (T2WI) because both lesions were demonstrated as hyperintensity areas. The hyperintensity lesion shown in FLAIR image may indicate border zone encephalitis. The FLAIR image is more useful than T1 or T2WI to detect the extension of the infarcted area and circumscribed change.
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PMID:Fluid-attenuated inversion-recovery imaging of cerebral infarction associated with tuberculous meningitis. 1094 Jun 11

We report on seven elderly patients with severe hyponatremia (plasma sodium < 125 meq/l). All were symptomatic for central nervous system disturbances, weakness, nausea/vomiting and met clinical and laboratory criteria for the diagnosis of inappropriate secretion of antidiuretic hormone (SIADH). Investigations performed to determine the etiology of the syndrome gave negative results, so that the form was considered to be idiopathic. TC scans or MNR showed brain atrophy and/or chronic ischemic lesions. According to the scant series found in the literature, we believe that aging itself may be a risk factor for SIADH. Lowering of the osmolal threshold and/or reduced receptors sensitivity to osmotic stimula, induced by ischemic changes in the hypothalamic region, can represent the underlying mechanisms.
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PMID:[Severe idiopathic hyponatremia caused by ADH inappropriate secretion in the elderly]. 1208 17


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