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Neurological Aspects of Substance Abuse

John C.M. Brust, M.D.

Abused substances in the United States are broadly categorized as opiates (eg., heroin), psychostimulants (eg., methamphetamine, cocaine), sedatives (eg., barbiturates, benzodiazepines), hallucinogens (eg., LSD), inhalants (eg., glues, gasoline), cannabis (marijuana), phencyclidine ("angel dust"), anticholinergics, ethanol, and tobacco. Intended effects and symptoms of overdose and withdrawal vary markedly among different agents. For example, ethanol or sedative withdrawal can cause fatal delirium tremens, whereas opiate withdrawal causes an unpleasant but not dangerous flu-like syndrome, and psychostimulant withdrawal causes depression but little in the way of measurable signs.

Neurological complications of substance abuse also vary with the agent. (1) Trauma in the case of ethanol or sedatives is usually the result of intoxication, whereas with other drugs is more likely the consequence of the drug's illegality. (2) Infection, a major risk for any parenteral drug abuser, includes HIV, endocarditis, hepatitis, tetanus, botulism, and a plethora of exotic organisms. (3) Seizures can be a feature of intoxication (eg., cocaine), of withdrawal (eg., ethanol) or of brain lesions consequent to drug use (eg., cerebral toxoplasmosis). (4) Parenteral drug use predisposes to ischemic and hemorrhagic stroke. Some drugs, eg., ethanol, cocaine, and tobacco, are risk factors for stroke by less wellunderstood mechanisms. (5) Persistently altered mentation is common among alcoholics, probably the result of both nutritional deficiency and direct toxicity. More controversial are the contributions of illicit drugs such as cocaine, marijuana, phencyclidine, and LSD to lasting cognitive impairment, for such studies tend to lack pre-drug use baselines. (6) Ethanol is an established teratogen, and animal studies demonstrate that other drugs (eg, cocaine) are harmful to fetuses, but in humans the effects are difficult to separate from inadequate prenatal care, ethanol, and tobacco. (7) Heroin users are at risk for acute transverse myelopathy, and nitrous oxide sniffers develop myeloneuropathy resembling that caused by cobalamin deficiency. (8) Alcoholic polyneuropathy is probably nutritional in origin. Heroin users have developed Guillain-Barre neuropathy and brachial plexopathy. Severe polyneuropathy affects sniffers of glues containing n-hexane. (9) Acute rhabdomyolysis is associated with use of opiates, psychostimulants, phencyclidine, and ethanol. (10) Miscellaneous neurological complications include quinine amblyopia, spongiform encephalopathy, and methylphenyltetrahydropyridine (MPTP)-induced parkinsonism in opiate users; dyskinesias in psychostimulant users, hypogonadism in marijuana users, and cerebellar ataxia in sniffers of products containing toluene.


  1. Brust JCM, Neurological Aspects of Substance Abuse. Boston, Butterworth- Heinemann, 1993.

  2. Brust JCM (ed). Neurologic complications of drug and alcohol abuse. Neurologic Clinics, Vol. 11, August 1993.

  3. Brust JCM, Drug dependence, In: Joynt R, Griggs R (eds). Clinical Neurology, Vol. 2, Chapter 21, Philadelphia, JP Lippincott Co., 1999, pp. 1-130.

  4. Brust JCM, Stroke and substance abuse. In: Barnett HJM, Mohr JP, Yatsu F, Stein BM (eds). Stroke: Pathophysiology, Diagnosis, and Management, Third Edition, New York, Churchill Livingstone, 1999, pp. 979-1000.

  5. Chiriboga CA, Brust JCM, Bateman D, Hauser WA. Dose-response effect of fetal cocaine exposure on newborn neurologic function. Pediatrics 103: 79-85, 1999.

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