In patients with pre-existing enhanced risk of seizures (for example, those with epilepsy or taking other epileptogenic drugs), intranasal cocaine may apparently precipitate fits. Seizures may occur, particularly with the more rapid and higher levels achieved when cocaine is injected or smoked as “crack”. However, several potential mechanisms may apply in individual patients, and it may be impossible to disentangle the many possibilities, particularly in infarction. The association is temporal, often very close, and this is the main evidence for a causal link, though there are also very plausible mechanisms for causation. Headache and/or seizures may accompany onset.

Stroke is the most common lasting adverse neurological event associated with the use of these stimulant drugs. In the case of cocaine, at least, there is an interaction with alcohol that increases risk of sudden death.Īcute abstinence from these stimulants is not associated with the autonomic or life threatening problems seen with alcohol and opiate dependence, but rather with disturbances of sleep, low mood and anxiety, and a craving for the drug. Temperature and blood pressure rise, and cardiac arrhythmias and/or sudden death may occur. The motor manifestations of excess include tremor, myoclonus, and seizures, while the neuropsychiatric manifestations include restlessness, irritability, violence, and a psychotic state, which is often paranoid. Those with greatest central action produce elation and increased alertness, with increased motor activity in the short and longer term (increased endurance).

These drugs share the ability to enhance transmission at the catecholaminergic (including dopaminergic) synapses and so share some common pharmacological effects and adverse effects in excess. Examples of the stimulants include cocaine/crack, amphetamine, 3,4-methylene, dioxymethylamphetamine (“Ecstasy”), ephedrine, phenylpropanolamine, and methylphenidate.

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