OBJECTIVE: There is a rising debate about the role of inflammation in the 
pathogenesis of complications after aneurysmal subarachnoid hemorrhage (SAH) 
such as intracranial hypertension (intracranial pressure, ICP >20 mmHg). This 
study aimed to analyse the origin of interleukin-6 (IL-6) in respect to ICP and 
cerebral metabolism in SAH patients.
METHODS: Prospectively, IL-6 was measured in three compartments, the 
extracellular fluid (ECF) monitored by cerebral microdialysis (MD), 
cerebrospinal fluid (CSF) and plasma for 10 days after SAH (days 0-4, three 
times daily; days 5-10, two times daily). Patients were classified having 
intracranial hypertension (n=7) or normal ICP (n=17) during 10 days after 
bleeding. Glasgow outcome scale (GOS) was assessed after 3 and 6 months.
RESULTS: Patient groups were comparable for age, WFNS and Fisher grade. 
Intracranial hypertension was associated with an inflammatory response, 
indicating activation of the inflammatory cascade in the brain (ECF) and 
systemic circulation with high IL-6 and C-reactive protein (CRP) plasma levels 
after SAH, the latter associated with unfavourable outcome. The data suggest the 
ECF but not the CSF as main origin of IL-6 in the systemic circulation in the 
presence of intracranial hypertension in SAH.
DISCUSSION: Intracranial hypertension is associated with a strong activation of 
the inflammatory cascade in the brain and systemic circulation, and might be 
underestimated as proinflammmatory trigger in the pathogenesis of complications 
after SAH. Future therapies targeting anti-inflammatory response in plasma may 
help to reduce the inflammatory cascade responsible for development of 
intracranial hypertension.