SUMMARY Sudden death may follow subarachnoid hemorrhage which indicates involvement of neural mechanisms connected with the cardiovascular system. Since various regions of the brain mediate blood pressure and heart rate changes, these parameters and heart rhythm could be affected due to a subarachnoid hemorrhage near the circle of Willis which surrounds the hypothalamus, the highest center for autonomic control. To investigate this in the control group, intracranial pressure, blood pressure, and electrocardiogram were measured before and after a simulated subarachnoid hemorrhage; blood pressure and electrocardiogram were measured following midcollicular lesions in the decerebrate group both before and after a subarachnoid hemorrhage. The results demonstrate that an increase in systemic arterial blood pressure and premature ventricular contractions (with respect to unlesioned group, p < 0.04) are mediated by forebrain areas and require the integrity of neuroanatomical connections with structures that are caudal to the midbrain. Since bradycardia and other electrocardiographic abnormalities could still be produced after midcollicular lesioning it is suggested that they can be mediated via the brainstem only without involvement of more rostral areas and may occur due to increased intracranial pressure.Stroke Vol 16, No 6, 1985
INCREASE IN INTRACRANIAL PRESSURE (ICP), and arterial blood pressure (BP) accompanied by electrocardiographic (ECG) abnormalities are often observed in patients after a subarachnoid hemorrhage (SAH). 14 Sudden death after a SAH has also been reported from time to time, more recently by Doshi and Neil-Dwyer, 9 which may be due to cardiac arrhythmias. 33 Such observations indicate that neural mechanisms and functional neuroanatomical connections between different areas of the central nervous system (CNS) and the heart may be involved.This study was undertaken because to our knowledge no information is available regarding the role of the forebrain and brainstem in producing different ECG abnormalities, BP and heart rate changes after SAH near the circle of Willis which surrounds the hypothalamus. We hypothesized that interruption of the cardiovascular connections within the CNS between the forebrain and the brainstem could reveal the role that these regions play in producing different kinds of arrhythmias e.g., atrial versus ventricular arrhythmias and in control of blood pressure following SAH. To investigate this, we decided an appropriate region to interrupt the cardiovascular neuroanatomical connections without damage to cardiovascular nuclei of the brainstem would be at the level of the midbrain between the superior colliculi and the inferior colliculi via midcollicular lesions. In this study, midcollicular lesions were made dorsoventrally through all structures except the base of the brain which to our knowledge is not known to contain fibers related to the cardiovascular system. This study therefore investigated
