Abstract:
:To determine the influence of chronic ethanol intake on the central nervous system, we studied 40 asymptomatic, well-nourished, chronic alcoholics (mean age, 42.6 +/- 9.1 years) and 20 age-, sex-, and education-matched control subjects. Studies included neuropsychological testing, visual and short-latency auditory evoked potentials, and morphometric analysis of computed tomography scans. The mean daily ethanol consumption of the alcoholics was 204 gm over an average of 26.4 years. Compared to control subjects, chronic alcoholics exhibited a significant prolongation of the P100 latency of visual evoked potentials, and a prolongation and reduction in the amplitude of the latency of the V wave of short-latency auditory evoked potentials. These abnormalities were related to the lifetime dose of ethanol consumed. Brain morphometric analysis showed that alcoholics had a significantly greater degree of brain shrinkage with age, compared to control subjects. The cortical atrophy index correlated significantly with the lifetime ethanol consumption. Neuropsychological testing in alcoholics compared to controls revealed a significant impairment of frontal skills that was related to age, degree of scholarship, and the presence of frontal atrophy. In conclusion, well-nourished chronic alcoholics exhibited significant brain impairment, as demonstrated by neuropsychological testing, evoked potentials, and brain morphometric analysis, which was correlated with the lifetime dose of ethanol consumed.
journal_name
Ann Neuroljournal_title
Annals of neurologyauthors
Nicolás JM,Estruch R,Salamero M,Orteu N,Fernandez-Solà J,Sacanella E,Urbano-Márquez Adoi
10.1002/ana.410410507subject
Has Abstractpub_date
1997-05-01 00:00:00pages
590-8issue
5eissn
0364-5134issn
1531-8249journal_volume
41pub_type
临床试验,杂志文章abstract::Increased glutamatergic transmission in the basal ganglia is implicated in the pathophysiology of Parkinson's disease. However, the mechanisms by which activation of glutamate receptors produce parkinsonism are unknown. Therefore, we examined whether the glutamate agonists N-methyl-D-aspartate (NMDA), alpha-amino-3-hy...
journal_title:Annals of neurology
pub_type: 杂志文章
doi:10.1002/ana.410340413
更新日期:1993-10-01 00:00:00
abstract::Charcot-Marie-Tooth (CMT) neuropathies are inherited neuromuscular disorders caused by a length-dependent neurodegeneration of peripheral nerves. More than 900 mutations in 60 different genes are causative of the neuropathy. Despite significant progress in therapeutic strategies, the disease remains incurable. The inc...
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pub_type: 杂志文章,评审
doi:10.1002/ana.23987
更新日期:2013-09-01 00:00:00
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journal_title:Annals of neurology
pub_type: 杂志文章
doi:10.1002/ana.21926
更新日期:2010-03-01 00:00:00
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journal_title:Annals of neurology
pub_type: 杂志文章
doi:10.1002/ana.24428
更新日期:2015-08-01 00:00:00
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journal_title:Annals of neurology
pub_type: 杂志文章,评审
doi:
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abstract::Stereotaxic injection of kainic acid into rat striatum produces neuronal degeneration and neurochemical alterations resembling Huntington's disease (HD). Since correction of the deficiency in gamma-aminobutyric acid (GABA) in HD may be of therapeutic value, the efficacy of drugs that inhibit the GABA-degrading enzyme ...
journal_title:Annals of neurology
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journal_title:Annals of neurology
pub_type: 杂志文章
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journal_title:Annals of neurology
pub_type: 杂志文章
doi:10.1002/ana.410430209
更新日期:1998-02-01 00:00:00
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journal_title:Annals of neurology
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journal_title:Annals of neurology
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journal_title:Annals of neurology
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journal_title:Annals of neurology
pub_type: 杂志文章
doi:10.1002/ana.410290318
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journal_title:Annals of neurology
pub_type: 杂志文章
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journal_title:Annals of neurology
pub_type: 杂志文章
doi:10.1002/ana.410350507
更新日期:1994-05-01 00:00:00
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journal_title:Annals of neurology
pub_type: 杂志文章
doi:10.1002/ana.10352
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journal_title:Annals of neurology
pub_type: 杂志文章
doi:10.1002/ana.410430422
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journal_title:Annals of neurology
pub_type: 杂志文章
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journal_title:Annals of neurology
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journal_title:Annals of neurology
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