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

We evaluated the brain lesions of patients with chronic alcoholism (n = 34) in comparison with age- and sex-matched controls (n = 40) by MR imaging. T1-weighted sagittal and axial images and T2-weighted axial images were obtained with a 0.5 T superconducting MR unit. Various brain measurements were then performed, and the presence of regions of abnormal signal intensity was also compared between the two groups. The brain measurements revealed significant cerebral atrophy (characterized by lateral and 3rd ventricular dilatation, and widening of the interhemispheric fissure) as well as significant cerebellar atrophy (represented by 4th ventricular dilatation) in the alcoholic group. These changes were more prominent in patients in their fifties and sixties than in those aged in the thirties and forties. Focal hypointense lesions were observed in 20.6% of the alcoholics and in 5% of the controls (p less than 0.01), while focal hyperintense lesions were observed in 61.8% of the alcoholics and in 20% of the controls (p less than 0.001). The severity of these MR findings correlated well with the age of the patients. These observations suggest that alcohol is an important promoter of brain aging.
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PMID:MR imaging of chronic alcoholism. 159 Nov 20

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

OBJECTIVE - To describe clinical observations of marked improvement in ventricular dysfunction in a medical office environment under circumstances differing from those in study protocols and multicenter studies performed in hospital or with outpatient cohorts. METHODS - Eleven cardiac failure patients with marked ventricular dysfunction receiving treatment at a doctors office between 1994 and 1999 were studied. Their ages ranged from 20 and 66 years (mean 39.42+/-14.05 years); 7 patients were men, 4 were women. Cardiopathic etiologies were arterial hypertension in 5 patients, peripartum cardiomyopathy in 2, nondefined myocarditis in 2, and alcoholic cardiomyopathy in 4. Initial echocardiograms revealed left ventricular dilatation (average diastolic diameter, 69.45+/-8.15mm), reduced left ventricular ejection fraction (0.38+/-0.08) and left atrial dilatation (43.36+/-5.16mm). The therapeutic approach followed consisted of patient orientation, elimination of etiological or causal factors of cardiac failure, and prescription of digitalis, diuretics, and angiotensinconverting enzyme inhibitors. RESULTS - Following treatment, left ventricular ejection fraction changed to 0.63+/-0.09; left ventricular diameters changed to 57.18+/-8.13mm, and left atrium diameters changed to 37.27+/-8.05mm. Maximum improvement was noted after 16.9+/-8.63 (6 to 36) months. CONCLUSION - Patients with serious cardiac failure and ventricular dysfunction caused by hypertension, alcoholism, or myocarditis can experience marked improvement in ventricular dysfunction after undergoing appropriate therapy within the venue of the doctor's office.
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PMID:Reversibility of ventricular dysfunction. Clinical experience in a medical office. 1179 29

In this article, we reviewed brain damage seen in patients with alcohol dependence briefly focusing on neuroimaging studies. In uncomplicated alcoholic patients, a high incidence of cortical shrinkage and ventricular dilatation were reported using brain CT scans. In older alcoholics, prefrontal gray matter deficits were especially marked when compared with younger alcoholics. Reversibility of brain shrinkage is a common neuroimaging finding in patients with alcohol dependence and a study by Gazdinski et al. reported more rapid brain tissue gain during the first month of sobriety than in the following months. Another MRI study using deformation-based morphometry revealed significant shrinkage in the frontal and temporal lobes within 1 week of abstinence of alcoholic patients. This study followed participants for 8 months longitudinally and revealed that abstaining alcoholics recovered tissue volumes significantly faster than nonalcoholic controls in the parietal and frontal lobes and this study also revealed that when abstaining alcoholics were compared with relapsed alcoholics, additional regions with significantly greater recovery in abstainers were the temporal lobes, thalamus, brainstem, cerebellum, corpus callosum, anterior cingulate, insula, and subcortical white matter. Finally we introduced a MR spectroscopy (MRS) study on alcoholic patients. This study using proton MRS indicated that with short-term abstinence, cerebellar choline and frontomesial N-acetylaspartate (NAA) were significantly increased. Findings showing that a cerebellar choline increase and a frontomesial NAA increase were detected at stable water integrals and creatine concentrations, serum electrolytes and red blood cell indices suggest that early brain recovery through abstinence does not simply reflect rehydration. This might indicate that even the adult brain has capacities for regrowth and further understanding of the mechanisms of recovery of alcoholics' brains may result in a valuable model of brain regeneration with relevance for other disorders.
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PMID:[A review of the neuroimaging studies of alcoholism]. 1824 Jun 49