What are the neurologic complications of cocaine toxicity?

Updated: Sep 01, 2018
  • Author: Lynn Barkley Burnett, MD, EdD, LLB(c); Chief Editor: Sage W Wiener, MD  more...
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Answer

Cocaine users have a 14-fold increase in risk of ischemic or hemorrhagic stroke compared to matched controls. In the study of Darke, Kaye, and Duflou, atherosclerosis of the basal vasculature of the brain was noted in approximately 10% of the cocaine toxicity cases autopsied versus less than 1% noted in either of the comparison groups. [12]

Cocaine acts as a CNS stimulant by inhibiting presynaptic reuptake of norepinephrine, dopamine, and serotonin. It also causes release of epinephrine by the adrenal glands. The intensity and duration of the stimulant effects of cocaine are mediated by the rate at which blood levels of cocaine rise (a function of the route of administration) (see Table 1) and the peak of blood levels.

Table 1. Onset of Effects, Peak Effects, Duration of Euphoria, and Plasma Half-Life by Routes of Administration (Open Table in a new window)

Route

Onset

Peak Effect (min)

Duration (min)

Half-Life (min)

Inhalation

7 s

1-5

20

40-60

Intravenous

15 s

3-5

20-30

40-60

Nasal

3 min

15

45-90

60-90

Oral

10 min

60

60

60-90

Cocaine may cause generalized tonic and clonic convulsions as well as focal seizures. Intense stimulation of sigma and muscarinic receptors by cocaine and increased synaptic concentration of serotonin have been proposed as causal. Cocaine lowers the threshold for seizures and may produce a kindling effect on neurons that promotes convulsions.

Seizure frequency ranges from 1-29%–perhaps reflecting variations in use and concurrent use of other drugs. Of 474 patients with medical complications of cocaine abuse, 8% experienced first-time seizures and, of these, 85% had seizures during administration of the drug.

Cocaine-associated seizures occur in naive users and among long-term users. Seizures are most frequently single tonic-clonic and resolve without intervention. However, status epilepticus may occur. The first stage of status epilepticus is manifested by generalized tonic-clonic seizures associated with hypertension, hyperpyrexia, and diaphoresis. After approximately 30 minutes, the second stage may occur, in which cerebral autoregulation fails, cerebral blood flow diminishes, and systemic hypotension occurs. During this phase, the only clinical manifestations may be minor twitching, though cerebral electrical seizure activity continues.


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