Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nervous system is particularly susceptible to the harmful effects of alcohol. These include Wernicke-Korsakoff syndrome, which is related to thiamine deficiency secondary to chronic alcohol abuse. Other neurotoxic effects of alcohol with cognitive impairments include delirium tremens, alcoholic seizures or "rum fits," and alcoholic neuropathies. It has become recognized in recent years that alcohol and its metabolites directly damage the nervous system even in the absence of nutritional deficiencies. Cerebral blood flow (CBF) measurements provide a noninvasive indirect monitor of cerebral metabolic activity. It has been shown conclusively that CBF measured by the 133Xe inhalation method is decreased in chronic alcoholism, correlating well with the amount of alcohol consumed. With abstinence, CBF returns toward normal levels provided the neurotoxic effects of chronic alcoholism are of recent onset. Clinical and pathological studies show significant loss of brain volume with ventricular dilatation after alcohol abuse even among young "social" drinkers. This toxic effect of alcohol is accompanied by varying degrees of cognitive impairments ranging from slight memory loss to frank dementia. Both the decrease in brain volume and the cognitive impairments, which occur with or without nutritional deficiency, are to a large extent reversible with abstinence and nutritional supplementation. Alcohol appears to accelerate age-related declines in CBF while nutritional deficiencies enhance the neurotoxic effects of alcohol. Measurements of local CBF (LCBF) and partition coefficients (L lambda) in deep cerebral structures, including the hypothalamus, thalamus, forebrain nuclei, and limbic system, can be achieved utilizing three-dimensional methods after inhalation of stable xenon as a contrast medium combined with serial computed tomographic imaging of the brain. Among chronic alcoholics, there are significant and diffuse reductions in cortical and subcortical gray matter CBF that are especially remarkable in hypothalamus and substantia innominata, which includes the nucleus basalis of Meynert, a major source of cholinergic input to neocortex and hippocampus. Reductions in LCBF are measurable in cognitively impaired patients with and without Wernicke-Korsakoff syndrome. Reductions of CBF include white matter and are more severe in patients with Wernicke-Korsakoff syndrome. Both types of encephalopathy improve with treatment, but recovery is usually more rapid and complete if nutritional deficiency is absent. Alcohol also appears to be a risk factor for stroke, possibly by depleting neuronal reserves and unfavorably influencing cardiovascular risks.
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PMID:Cerebral hemodynamic and metabolic effects of chronic alcoholism. 270 68

We report a 85-year-old woman who died after one year history of convulsion, dementia, and consciousness disturbance. She was apparently well until January 6, 1995 when she was 85 year old; on that evening, she suddenly stated that some one was in her room and she became confused. A local MD gave her diazepam and she fell into sleep. At 3 o'clock in the following morning, she developed tonic-clonic convulsion in her right lower extremity which showed a march to her right upper extremity and the left lower extremity. She was admitted to our hospital. On admission, she was comatose with respiratory acidosis. She was intubated and placed on a ventilator. She was treated with intravenous phenytoin. She gradually gained consciousness and became alert. Respiration became normal. Her MRI revealed ventricular dilatation, fronto-parietal cortical atrophy, and a T1-low and T2-high signal intensity lesion in the left occipital lobe. She was discharged for out patient follow-up on February 4, 1995. Since then, she noted loss of memory and small step gait. A follow-up CT scan revealed a mass lesion which showed a ring-shaped enhancement in the left occipital lobe and was admitted again. On admission, she was alert but markedly demented. The optic fundi was unremarkable, but she appeared to have right homonymous hemianopsia. No motor weakness was noted. In Gd-DTPA enhanced MRI, the above tumor showed a ring enhancement. The diagnosis of glioblastoma was entertained, however, considering her age, she was treated with intravenous glycerol and intramuscular steroid. She was discharged for out-patient follow-up on July 15, 1995. Her gait disturbance had progressively become worse and she developed nausea and vomiting and was admitted again on October 2, 1995. On admission, she was somnolent and markedly demented. Brain stem responses were retained normally. She was unable to stand or walk. Deep tendon reflexes were slightly increased in the right upper extremity and the plantar response was extensor on the right. Her hospital course was complicated by respiratory tract infection and respiratory acidosis. She expired on November 2, 1995. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that she had a glioblastoma involving the left occipital lobe and the adjacent areas. Post-mortem examination revealed an infiltrating tumor in the left occipital lobe. On microscopic examination, the tumor was very cellular; nuclear atypism was marked and tumor cells undergoing mitosis were seen. In some areas, capillary proliferation was seen. Histologic characteristics were consistent with glioblastoma.
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PMID:[A 85-year-old woman with one year history of convulsion, dementia, and consciousness disturbance]. 936 96