Effects on specific organ systems - Cocaine abuse in adults

Key points
- Central nervous system — Cocaine euphoria is associated with transient increases in EEG activity followed by longer-lasting increases in activity.
- Craving for cocaine is associated with increased activity in the so-called mesocorticolimbic reward circuit in the brain.
- Cerebral vasoconstriction, cerebrovascular disease, and hemorrhagic and ischemic stroke are increased in cocaine users, even in patients with no other risk factors.
- Impairment of behavioral inhibition in cocaine users has been associated with reduced activity in the anterior cingulate and prefrontal cortices.
Central nervous system — Cocaine euphoria is associated with transient increases in EEG activity followed by longer-lasting increases in activity. Seizures may occur in persons without a seizure history, even with first time use of cocaine. These are usually single, generalized tonic-clonic seizures occurring within 90 minutes of cocaine use.
Craving for cocaine is associated with increased activity in the so-called mesocorticolimbic reward circuit in the brain. This includes the inferior frontal-orbitofrontal gyrus, amygdala (thought to mediate stimulus-reward association), anterior cingulate (mediating anticipation of reward), and nucleus accumbens/subcalllosal gyrus (mediating incentive motivation).
Cerebral vasoconstriction, cerebrovascular disease, and hemorrhagic and ischemic stroke are increased in cocaine users, even in patients with no other risk factors. Etiologic mechanisms include tachycardia and increased blood pressure from sympathetic activation, vasoconstriction, vasospasm, and intravascular thrombosis due to increased platelet aggregation.
MRI, SPECT, and PET imaging in chronic cocaine users demonstrate structural and functional brain abnormalities: cerebral gray matter atrophy and decreased glucose metabolism in the frontal and temporal lobes, small cerebral perfusion defects, increased creatine concentration in parietal white matter (suggesting abnormal energy metabolism), and decreased D2 dopamine receptors in the striatum. Impairment of behavioral inhibition in cocaine users has been associated with reduced activity in the anterior cingulate and prefrontal cortices.
Cocaine use is associated with a variety of movement disorders, including stereotyped behaviors, acute dystonic reactions, choreoathetosis and akathisia (so-called "crack dancers"), buccolingual dyskinesias ("twisted mouth" or "boca torcida"), and exacerbation of Tourette's syndrome and tardive dyskinesia. Cocaine users are at increased risk of acute dystonic reactions from neuroleptic (antipsychotic) medications.
Cardiovascular system — Cocaine acutely increases heart rate, blood pressure, and systemic vascular resistance by increasing adrenergic activity in the heart, and indirectly via the CNS. The increased myocardial oxygen demand, coupled with decreased coronary blood flow from vasospasm and vasoconstriction, can cause acute myocardial infarction, even in young persons without atherosclerosis. Cocaine use is a factor in about one-quarter of nonfatal heart attacks in persons younger than 45 years. Frequent cocaine users are up to seven times more likely to have a nonfatal heart attack than are nonusers. Cocaine use is not usually associated with chronic hypertension, but may be more prevalent among patients with severe hypertension than among the general population. Cocaine use appears to enhance the progression of renal disease in patients with hypertension.
Written and revised by
David Cohen, M.D.
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