Monday, March 6, 2017

Hyperthermia in Pontine Haemorrhage

Hey guys!

This post will be focused on the pathophysiology of Hyperthermia in Pontine Haemorrhage( which may manifest as the Locked-in Syndrome, remember that super-awesome House episode? <3 )

1. First try the easy simple reason. Hypothalamus has been basically cut off from the body below pons and there has been Haemorrhage. Therefore, there will be a Sympathetic outflow causing peripheral vasoconstriction. Meanwhile the internal visceral organs are still functioning and consequently producing heat. So without hypothalamus, the body's ability to produce heat has transcended it's ability to lose heat.

2. The next reason is a bit "cooler", literally. Our body hates Hypothermia more than Hyperthermia, thanks to evolution. (Ice Age!!!) Now there is no central thermoregulation but peripheral one is still intact. And the peripheral thermoreceptors are much more sensitive to lower temperatures or basically cold environment. Once again, without the Hypothalamus, the body is defending itself too vigorously against Hypothermia as to contribute ironically to Hyperthermia.

3. This reason is the only one which you should know since this will explain how Baclofen, a GABA-B Agonist works to treat this Hyperthermia. Remember the Medial Forebrain Bundle, it connects Hypothalamus to a lot of structures, one of them being Nucleus Raphe in the Pontine reticular formation. This is a very crucial portal in control of Sympathetic nervous system outflow by Hypothalamus. Simply speaking, if the body is hot, Hypothalamus will send inhibitory (GABAergic and Dopaminergic) signals to this nucleus and if the body is cold, it will send excitatory (Glutaminergic and Serotonergic) signals. And apparently this connection is lost in Pontine Haemorrhage, so we substitute it with a drug.

P.S. Now you can guess how Bromocriptine and Apomorphine cause Hypothermia. :)


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