Related Experiment Video
Updated: Jul 18, 2026
08:22
Stereotaxic Microinjection of Viral Vectors Expressing Cre Recombinase to Study the Role of Target Genes in Cocaine Conditioned Place Preference
Published on: July 30, 2013
Neurologic consequences of cocaine use.
M C Rowbotham1, D H Lowenstein
1Department of Neurology, University of California, San Francisco 94143.
Annual Review of Medicine
|January 1, 1990
Summary
Cocaine use causes serious neurologic emergencies like stroke and seizures, especially in young adults. Effective treatment requires abstinence, but the underlying causes of these cocaine-related brain conditions are still not fully understood.
Area of Science:
- Neurology
- Toxicology
- Public Health
Background:
- Cocaine use is increasingly recognized as a cause of severe neurologic emergencies.
- Neurologic syndromes associated with cocaine are often fatal or disabling.
- These conditions include stroke, seizures, encephalopathy, headache, and transient deficits.
Purpose of the Study:
- To summarize the current understanding of neurologic consequences of cocaine use.
- To highlight the significance of cocaine as a cause of stroke in young adults.
- To underscore the limited treatment options and understanding of pathophysiology.
Main Methods:
- Literature review of documented cases and studies on cocaine-induced neurologic illness.
- Analysis of reported neurologic emergencies linked to recreational cocaine consumption.
- Examination of existing research on the pathophysiology and treatment of these conditions.
Main Results:
- Cocaine use is a major cause of stroke in young adults.
- Neurologic emergencies include stroke, seizures, encephalopathy, headache, and transient deficits.
- Long-term effects of maternal cocaine use on fetuses are still unknown.
Conclusions:
- Abstinence is the primary recommendation for managing cocaine-associated neurologic illness.
- The pathophysiology of these neurologic conditions remains poorly understood.
- Further research is needed to elucidate the mechanisms and develop effective treatments.
Related Concept Videos
01:23Drugs Acting on Autonomic Ganglia: Stimulants
Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
01:21Drugs Affecting Neurotransmitter Release or Uptake
Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
01:12Local Anesthetics: Adverse Effects
While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
01:29Drugs Affecting Neurotransmitter Synthesis
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
01:24CNS Stimulants: Cocaine, Amphetamines and Cannabinoids
CNS stimulants, such as cocaine, amphetamines, and cannabinoids, have varying structures and mechanisms of action that lead to different therapeutic effects and side effects. Cocaine, with its molecular formula C17H21NO4, is a tropane alkaloid and a tertiary amino compound. It has two chemical forms: the hydrochloride salt and the "freebase." The former is in powder form, while the latter involves removing the hydrochloride salt to create a form that can be smoked. Cocaine exerts its effects by...
01:29Hepatic Encephalopathy
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...