Effect of preexisting brain ischemia on sympathetic nerve response to intracranial hypertension

Abstract

The performance of the sympathetic nervous system during sustained moderate cerebral ischemia (CI) was examined in the present study. For this purpose, a Cushing response was elicited repeatedly during incomplete global CI in anesthetized artificially ventilated cats after vagotomy and baroreceptor denervation. In control animals without CI, sympathetic activity in response to brief elevation of intracranial pressure (ICP) showed a well-repeatable two-phase reaction. During CI there was a progressive deterioration of background sympathetic nerve discharge (SND) over a period of 30 min. SND response to repeated elevation of ICP was initially similar to control response but later with progression of CI was seriously changed. 1) Instead of the usual hyperactivation, sympathetic nerve activity was depressed during intracranial hypertension. 2) The characteristic desynchronized activity either appeared later during the reperfusion period or remained absent. The progressive loss of SND response to raised ICP in developed CI was compared with the changes seen in experiments in which repeated ICP elevations were superimposed on asphyxia. These findings suggest that the sympathetic component of the Cushing reaction strongly depends on the actual state of brain stem autonomic circuits and may be seriously altered in pathological situations involving ischemic brain injury.

Differential sympathetic reactions during cerebral ischaemia in cats: the role of desynchronized nerve discharge.

“…After some time the SND desynchronized and high-frequency components started to dominate the nerve signals. These changes were reversible and could be repeated many times in the same animal (Kocsis, Fedina & Pasztor, 1991 a).…”

Changes in Blood Pressure and Heart Rate during Decompressive Craniectomy

“…Several animal, pathophysiological and clinical observational studies have reported elevated blood pressure in subjects with severely increased ICP. This increase can result from an autoregulation response to maintain cerebral perfusion pressure and cerebral blood flow [ 1 , 6 , 10 , 11 , 18 , 20 - 22 , 29 , 31 ], which may be associated with paroxysmal sympathetic hyperactivity [ 7 , 10 , 18 , 21 - 23 , 25 ]. The respiratory irregularity, characterized by Harvey Cushing, is believed to be a phenomenon caused by tonsillar herniation [ 1 , 6 , 11 , 31 ], which is better known as the Cushing reflex, the Cushing reaction, the Cushing phenomenon, the Cushing response, and Cushing’s law [ 1 , 6 , 11 , 18 , 31 , 38 ].…”

“…Several pathophysiological studies refined Cushing's findings by showing an initial tachycardia associated with hypertension followed by bradycardia. The initial hypertensive and tachycardia symptoms were due to the elevated activity of the sympathetic nervous system and late bradycardia was mediated by parasympathetic nerve activation 1,6,7,10,11,[20][21][22][23]29,31) .…”

Systemic complications after head injury: a clinical review

“…The initial catecholamine response after TBI results in a hyperdynamic circulation usually characterised by tachycardia and hypertension, although a marked sinus bradycardia, due to a baroreceptor reflex, is also classically described (the Cushing response). Raised intracranial pressure (ICP) causes depression of sympathetic activity because of disruption of brainstem autonomic pathways by a variety of causes including direct injury, cerebral swelling and diffuse axonal injury [21]. Conventional teaching suggests that isolated head injury does not result in hypotension in adults and, whilst this wisdom reinforces the importance of identifying and treating active bleeding, there is evidence to support a neurogenic aetiology of hypotension in some cases.…”