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The interplay between CSF dynamics, intracranial pressure (ICP), arterial blood pressure (ABP) and sympathetic nervous system (SNS) remains poorly understood. We know that raised ICP reduces CPP (i.e. ABP-ICP) and blood delivery to the brain. Massive ICP rise is also known to produce an increase in ABP termed the Cushing response, a terminal event occurring in extreme pathological conditions of brainstem ischaemia leading to a sympatho-adrenal response. Hence the Cushing response is not activated in a normal patient and is not involved in the pathophysiology of NPH. However, it is still debated whether the Cushing response is an acute pathological response to brain ischemia or part of an important physiological reflex mechanism. Indeed clinical and experimental studies suggest that modest ICP increase modulates systemic hemodynamics probably via the SNS. We hypothesize that modest ICP changes drive sympathetic activity. Using state-of-the-art technique to measure SNS, we performed two different sets of experiments in humans and mice. In both species during controlled hydrostatic modest ICP increase and decrease, SNS was measured directly by microneurography and indirectly by heart rate variability analysis (HRVA).

Intracranial pressure is a physiological stress that determines sympathetic nervous system activity