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Biomedical subjects

J D Chick

Publications and source records attributed to J D Chick.

11 recordsLinked to original sources
PubMed1993

Mortality studies in the long-term evaluation of treatment of alcoholics.

Mortality studies demonstrate that, in all the Countries evaluated, alcoholics die twenty years earlier than expected. Causes of death vary according to drinking patterns. Though mortality data seem crude, they can detect changes due to clinical intervention. Alcoholism studies should benefit by improvement of research methodologies as already applied to other chronic diseases.

Alcoholism↗
PubMed1989

The relationship of cerebral atrophy and T1 in alcoholics: an MRI study.

There was a significant correlation between two measures of cerebral atrophy (the ventricle to brain ratio and the relative cerebral volume) and T1 in 19 detoxified alcoholics. This provides further evidence that T1 is a marker of structural damage in alcoholics although the partial volume effect of CSF may contribute to this finding. This has implications for studies comparing alcoholics to normal controls and suggests that better ways of excluding CSF need to be found.

Adult↗
PubMed1989

Magnetic resonance imaging of the brain in alcoholics: cerebral atrophy, lifetime alcohol consumption, and cognitive deficits.

Magnetic resonance imaging of the brain in 69 detoxified alcoholics revealed that relaxation time (T1) in whole brain and in grey matter and parietal white matter was greater than in age-matched controls. In 48 patients, data on cognitive function and lifetime alcohol consumption were available. With age-controlled, lifetime consumption, and impairment on performance in the cognitive test (a Category Sorting Test) correlated positively with T1 whole brain and in selected regions. Impairment in the cognitive test correlated with increased T1 in whole brain and white matter independently of cerebral atrophy. Alcohol consumption patterns in the following 6 months were unrelated to changes in T1. The excess water implied by the elevated T1 values may be intra- or extracellular. It is uncertain whether or not T1 elevation in alcoholics is a marker of neuronal damage. T1 elevation appears to be a marker of one type of alcohol-related cognitive impairment.

Adult↗
PubMed1988

Brain hydration during alcohol withdrawal in alcoholics measured by magnetic resonance imaging.

Twenty-seven patients had a first Magnetic Resonance Imaging (MRI) scan 1-3 days after stopping drinking and a second approximately 2 weeks later with no change in whole brain T1 or T1 in selected brain areas. Six patients whose first scan was over 36 h after the last drink underwent an increase in whole brain T1 in the interval to the second scan. The later the first scan was performed the greater was the increase in T1. These results are compatible with a very early fall in brain water immediately on cessation of drinking (perhaps due to a rebound increase of vasopressin activity) with a return to 'baseline' after two weeks. A third scan after discharge from hospital in 23 individuals who had abstained from alcohol or drank very little did not reveal any further significant change in brain T1.

Adult↗
PubMed1988

An NMR study of cerebral oedema and its biological correlates during withdrawal from alcohol.

Five chronic alcoholic patients admitted for detoxification were studied. During the first 24-48 hr of abstinence raised levels of cerebral water (as measured by NMR), vasopressin, renin and supine aldosterone were recorded. Initial vasopressin concentration was correlated (r = 0.88, P less than 0.05) with alcohol consumption in the week prior to admission and was over three times higher in the patients measured after 24-48 hr as compared to less than 24 hr. After one week only supine aldosterone was still raised (P less than 0.05). The results suggest that cerebral oedema occurs during the early stages of abstinence. The role of these changes in the aetiology of withdrawal symptoms, delirium tremens and brain damage remains to be elucidated.

Adolescent↗