CNS depression after an acute generalised tonic clinic seizure - “The ghostly calm after the plundering cyclone.”

 An all pervasive, flooding of electrical activity occurs during an episode of generalised tonic clinic seizure. The abnormal electrical disturbances get manifested in the form of sustained, severe, generalised and vigorous contractions of all or most of the group of the muscles of the body. The condition is a medical emergency and unless  intervened promptly with the right medical therapy, is often fatal. In the aftermath of the serious event, the patient goes into an obtunded state. This phase which occurs after the episode of convulsion is known as the post-ictal state. Mostly, the patients sleep for prolonged periods, sometimes with audible snoring. The underlying mechanism of the post-ictal state is not clearly known, but the ‘storm’ that has passed during the episode of GTCS must have ‘inflicted’ a state of ‘refractoriness’ to the neurons. Likely, in such a state, the ‘routine’ transmission of impulses suffer a major ‘setback’ throwing the patient into a state of CNS depression. We can also speculate that there has been depletion of neurotransmitters from the presynaptic neurons during the ‘agitated’ phase of seizure. Collectively, the post-ictal phase is an inactive state of the brain where the higher cognitive functions, the autonomic system and the peripheral nervous system are highly subdued and suppressed.

Cocaine and it’s effect on the cardiovascular physiology

 The direct effect of cocaine on the vagal centre in the brain can cause bradycardia, but the bradycardia is seldom seen clinically. At the usual doses taken by people who abuse cocaine, the peripheral adrenergic actions of the drug dominates over its central vagal response. The phenomenon is explained by the pharmacokinetics of the drug. Cocaine is a low molecular weight tropane alkaloid (Pka=8.6), which is easily transported across the nasal, gut and alveolar membranes. However, it transport into the brain depends upon a proton driven antiporter. The stimulatory action of cocaine is rapid and provides the abuser with the sought for “kick”. At any time point after the intake of the drug, the peripheral cardiovascular effects of the drug dominates over the central vagal action. The peripheral adrenergic action is due to over accumulation of catecholamines in the synaptic cleft of the adrenergic neurones leading to vasoconstriction (blood vessels) and tachycardia (heart). Any reflex bradycardia mediated by central mechanism is overwhelmed by the peripheral adrenergic action. No doubt, subjects abusing cocaine present with accelerated hypertension, tachycardia and agitation in the emergency department. The severe vasoconstriction effect of cocaine may also precipitate coronary vasospasm and myocardial infarction in some drug abusers.