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The acute psychomotor stimulant effects of cocaine, amphetamine and methylamphetamine, including restlessness, irritability, talkativeness, anxiety, panic attacks, lability of mood, headache, chills, vomiting and sweating, are principally attributable to increases in CNS catecholamine neurotransmitter activity. Enhanced catecholamine activity occurs through stimulantmediated blockade of the neurotransmitter presynaptic reuptake pumps (cocaine) and by presynaptic release of catecholamines (amphetamine). Behaviourally, disinhibition, hypervigilance, compulsive or stereotyped behaviour, paranoia and acute psychosis may supervene. The occurrence of hyperthermia is associated with misuse of Ecstasy.
In very high doses, an acute organic brain syndrome (delirium) may supervene, characterised by clouding of consciousness and disorientation in time and place, with or without delusional thinking and hallucinations. Such reactions are usually self-limiting and should be treated symptomatically, having excluded
an underlying acute neurological lesion (see below). Chronic, frequent use of stimulant drugs may lead to the development of a chronic paranoid perspective or fully formed psychosis that is difficult to differentiate from schizophrenia.
Medical complications of stimulant intoxication may be serious and life-threatening; cocaine intoxication is the commonest cause of myocardial infarction in young males presenting to A&E departments. The medical aspects of cocaine intoxication can be divided into three phases (Weiss, Greenfield & Mirin, 1994). The first phase presents with the psychological/behavioural effects described above and mild physiological effects, usually not requiring specific treatment. The second phase is characterised by myocardial ischaemia or infarction, seizures, malignant encephalopathy, incontinence and ventricular dysrhythmias. The third (premorbid) phase is characterised by coma, paralysis, and fixed, dilated pupils. Other complications include hyperthermia (which may suggest a more severe prognosis (Weiss, Greenfield & Mirin, 1994)) leading to reversible coagulopathy and renal failure, cerebral and pulmonary oedema, cerebral haemorrhage, rhabdomyoloysis, myoglobinuria, nephrotoxicity and hyperkalaemia (Callaway & Clark 1994).
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