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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A literature review and an own case observation of neurological and psychiatrical disturbances in vinyl chloride disease are presented. In acute vinyl chloride intoxication, patients complain of vertigo, nausea and headache. At higher concentrations, vinyl chloride exerts a narcotic effect. In patients with chronic occupational exposure, neurological disturbances include sensory-motor polyneuropathy, trigeminal sensory neuropathy, slight pyramidal signs and cerebellar and extrapyramidal motor disorders. Psychiatric disturbances present as neurasthenic or depressive syndromes. Sleep disorders and disorders of sexual functions are frequently encountered. Pathological EEG alterations can be found in a high proportion of patients. The long term course and prognosis of the neurological and psychiatrical disorders in vinyl chloride disease are obscure. In an own case, a slight sensory polyneuropathy, bilateral hyposmia, a marked neurasthenic syndrome, typical EEG changes and computed tomography signs of cerebral atrophy were found in a 56-years-old patient as late as 16 years after the exposure to vinyl chloride.
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PMID:[Neurologic and psychiatric disorders in vinyl chloride disease]. 227 28

Eighteen professional divers (age range 24-33 yr, mean 28.3) participated in one simulated dive to 360 meters of seawater (msw) in a helium-oxygen (heliox) atmosphere with equal compression and decompression profiles. All divers were given an extensive neurologic examination before diving. Clinical neurologic symptoms observed during the dives were equilibrium disorder, sleep disturbances, fatigue, nausea, loose stools, stomach pain, tremor, mental disturbances, reduced appetite, and headache. Symptoms were scored individually by each diver. The symptoms were analyzed statistically by factor analysis, which grouped them into four factors. These symptoms are presumably related to functional disturbances in the brain stem and the cerebellum. Factor 3 symptoms (tremor, mental disturbances, reduced appetite) correlated significantly to a history of predive decompression sickness (P = 0.006) and to cerebral concussion (P = 0.023). Three divers were periodically unable to work at bottom due to equilibrium disorder, diarrhea, or nausea. One diver with mild polyneuropathy and slight cerebral atrophy as seen by computerized tomography and another diver with abnormal electroencephalography were periodically unable to work due to equilibrium disorder and nausea, respectively. We advocate that divers with signs of central or peripheral nervous system dysfunction should not be selected for deep diving.
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PMID:Analysis of neurologic symptoms in deep diving: implications for selection of divers. 232 22

Fenestration of basilar artery is an uncommon vascular anomaly that is usually an incidental product on autopsy or angiography. None of the cases in the literature had clinical symptoms associated with this anomaly except for subarachnoid hemorrhage when accompanied with saccular aneurysm. We report a rare case of the basilar artery fenestration associated with clinical symptoms without any aneurysm. A 71-years-old male, who had been treated for labile hypertension and had had recurrent attacks of vertigo, nausea, sometimes diplopia or unsteady gait, for 5 years, was referred to our hospital on Sept. 13, 1985. One day prior to admission, he suddenly felt diplopia and vertigo and unsteady gait. His family noticed he was dysarthric. On admission, he was alert and normotensive. He complained of dysesthesia on the right half of the perioral region and his right fingers. A neurological examination showed a mild weakness and hyperactive deep tendon reflexes on his right leg. His motor coordination was almost normal, but he was unsteady when he stood on one foot with his eyes closed. Laboratory examinations were normal except for an elevated serum uric acid level. A chest x-ray film showed a sclerotic change of aorta and mild cardiomegaly. Left ventricular hypertrophy was observed on his ECG. His CT scans showed multiple lacunae and mild brain atrophy. On cerebral angiography, his basilar artery (BA) had a fenestration almost in its total length that divided the BA, like a duplication, into two components with a smaller diameter than normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of basilar artery fenestration with recurrent attacks of vertebrobasilar insufficiency]. 344 54

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

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 clinical trial of intrathecal chemotherapy with FdUrd was performed in sixteen patients with meningeal dissemination of malignant tumors. Twelve of the sixteen patients responded to intrathecal FdUrd chemotherapy (1-5 micrograms/dose) through an Ommaya reservoir placed in the lateral ventricle: complete response, 2; partial response, 10; progressive disease, 4. Only slight nausea was observed in two patients and dull headache in one patient. No other systemic side effects such as myelosuppression or liver dysfunction were observed in any patients. Moreover, no delayed side effects such as marked brain atrophy or leukoencephalopathy developed during the course of this intrathecal chemotherapy despite over thirty consecutive intrathecal administrations. In conclusion, intrathecal FdUrd proved to be safe and effective for the treatment of meningeal dissemination of malignant tumors.
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PMID:[Clinical application of FdUrd to meningeal dissemination of malignant tumors]. 983 91

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

We report a case of neuronal intranuclear inclusion disease (NIID) confirmed by detection of intranuclear inclusions in a skin biopsy specimen. Brain magnetic resonance imaging showed mild cerebral atrophy and linear hyperintensities at the corticomedullary junction on diffusion-weighted images. This patient developed nonconvulsive status epilepticus with generalized periodic discharges on electroencephalography after recurrent symptoms of paroxysmal nausea and slowly progressive cognitive decline. There have been no previous reports of NIID with nonconvulsive status epilepticus to our knowledge. Since adult patients with NIID display a wide variety of clinical manifestations, skin biopsy should be considered in patients who have leukoencephalopathy of unknown origin.
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PMID:Non-convulsive status epilepticus associated with neuronal intranuclear inclusion disease: A case report and literature review. 3089 4