cocaine/atrophy

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Cocaine, in contrast to D-amphetamine, does not cause axonal terminal degeneration in neostriatum and agranular frontal cortex of Long-Evans rats.

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Continuous three day administration via implanted minipumps of cocaine hydrochloride (50-450 mg/kg/day, sc and 100-250 mg/kg/day, iv) did not produce axonal degeneration in frontal agranular cortex or neostriatum that was detectable by Fink-Heimer silver staining or tyrosine hydroxylase

Cerebral atrophy in habitual cocaine abusers: a planimetric CT study.

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We compared cranial CTs of 35 habitual cocaine abusers, 16 self-reported 1st-time users, and 54 headache patients using linear planimetric measures. All patients met the following criteria: age 20 to 40 years, no polydrug abuse (including alcohol), HIV seronegativity, normal albumin level, and no

Pseudosclerodermatous triad of perniosis, pulp atrophy and 'parrot-beaked' clawing of the nails--a newly recognized syndrome of chronic crack cocaine use.

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The number of people dependent on crack-cocaine in the UK has increased substantially in recent years. Some crack-cocaine users develop coarsening changes in the appearance of their hands after prolonged use of the drug. These changes have most often been recognized in females and include: (i)

Cocaine neurotoxicity and altered neuropeptide Y immunoreactivity in the rat hippocampus; a silver degeneration and immunocytochemical study.

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Neuroanatomical methods were used to determine if cocaine irreversibly injures neurons. Despite acute and chronic high-dose treatments for months that produced stereotyped behavior and seizures, and the use of a sensitive silver impregnation method, we were unable to find any evidence of neuronal

Sleep quality deteriorates over a binge--abstinence cycle in chronic smoked cocaine users.

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BACKGROUND In cocaine dependent individuals, changes in subjective and objective sleep quality accompany their characteristic binge-abstinence cycle. Preliminary studies suggest that sleep quality may decline with prolonged abstinence. Reported here are results of the most extensive study to date on

Brain atrophy and chronic cocaine abuse: background and work in progress.

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Cocaine and cerebral atrophy.

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Effects of crack cocaine on neurocognitive function.

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Because crack cocaine appears to have a preferential effect on the metabolic and electrophysiological activity of the frontal and temporal regions of the brain (Pascual-Leone et al., 1991a, 1991b; Volkow, 1992), we hypothesized that cognitive measures of those regions would be impaired in crack

Cocaine-Induced Acute Interstitial Nephritis: A Comparative Review of 7 Cases

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Acute interstitial nephritis is a well-known cause of acute kidney injury, but its association with cocaine use is extremely rare. In this article, we chronicle the case of a patient who developed acute interstitial nephritis secondary to cocaine insufflation. Furthermore, we conducted a systematic

Interactive effects of cocaine on HIV infection: implication in HIV-associated neurocognitive disorder and neuroAIDS.

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Substantial epidemiological studies suggest that not only, being one of the reasons for the transmission of the human immunodeficiency virus (HIV), but drug abuse also serves its role in determining the disease progression and severity among the HIV infected population. This article focuses on the

Neuroimaging in drug and substance abuse part I: cocaine, cannabis, and ecstasy.

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Multiple neurological complications of cocaine abuse have been described including both ischemic and hemorrhagic cerebrovascular events, atrophy in the case of chronic abuse, and an increase in incidence of congenital malformations in the setting of maternal use. The abuse of cannabis may cause a

Effects of cocaine on testicular structure in the rat.

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The effects of hourly injections of moderate doses of cocaine hydrochloride (0.5 and 10 mg/kg body weight) over 5 h on testicular structure and testosterone levels were studied in male Wistar rats. Cocaine produced a rapid disruption of spermatogenesis; the number of normal seminiferous tubules

[Progressive hemifacial atrophy with sympathetic nerve dysfunction of central origin].

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A 37-year-old unmarried man was admitted because of gait disturbance and right hemifacial atrophy. Family history was unremarkable. He had an unconscious attack at age 13 and had writer's cramp since age 15. He was thin and lipodystrophic. In reviewing his portraits, hemifacial atrophy was

Protective potential of glutathione peroxidase-1 gene against cocaine-induced acute hepatotoxic consequences in mice.

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Since the cocaine-induced oxidative stress has been established to lead to hepatotoxicity, we examined the role of the glutathione peroxidase (GPx)-1 gene in cocaine-induced hepatotoxicity. Cocaine treatment significantly increased superoxide dismutase activity in as little as 1 hour, with a maximum

Cocaine hepatotoxicity in mice: histologic and enzymatic studies.

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The severity of hepatotoxicity in CF-1 mice given 5 daily doses of 5, 10, and 20 mg cocaine/kg body weight and sacrificed 24 hr after the last injection appeared to be dose-dependent. Using light microscopy, the hallmark of cocaine early toxicity was manifested by pallor and ballooning of the

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