Of course, there are often other confounders in the lifestyles of these individuals which may also be implicated, not just the drug.Ĭhronic amphetamine (and to a lesser extent cocaine) use may be complicated by a psychosis with visual and auditory hallucinations, often with paranoia, though without the sympathomimetic effects of these drugs. These effects may all persist despite abstinence. Long term cocaine abuse has been associated with cognitive dysfunction and cerebral atrophy, and with multiple focal perfusion defects on single photon emission computed tomography (SPECT) and positron emission tomography (PET) studies. Movement disorders have been reported with these drugs-for example, tics and acute dystonic reactions with cocaine and acute chorea with metamphetamine. These problems have been emphasised in patients dying after the use of Ecstasy. In addition, cocaine may have a direct toxic effect on skeletal muscle (as it does on cardiac muscle). These may contribute along with muscle vasoconstriction, central rigidity, and seizures to the rhabdomyolysis that sometimes occurs in more sick patients. Hyperpyrexia may develop because of direct effects on the hypothalamus and also the agitation and hyperactivity that these stimulant drugs tend to produce. When they do occur, seizures may be prolonged and fatal, not only through the secondary consequences of prolonged seizures but also perhaps through the direct effect of the high drug levels. 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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