The possibility of measuring cerebral blood flow by mobile bedside uni
ts with the intravenous 133-Xenon technique increased the interest to
monitor haemodynamic changes after head injury and subarachnoid haemor
rhage in intensive care.Time course of resting CBF after trauma is var
iable (reduced CBF, hyperemia) and there is no strong correlation to c
linical outcome. Additional studies of CBF/CO2 reactivity show normal
and impaired CO2 response in the acute stage after trauma (day 1-8). A
permanently impaired CO2 reactivity correlates with severe brain dama
ge and bad outcome (GOS 1,2). A normal or improving CO2 reactivity ind
icates a favourable outcome (GOS 3-5). There was no significant correl
ation between CBF and ICP, nor between CBF and CPP. A CPP of more than
70 mmHg did not guarantee a sufficient CBF in every case indicating t
he variability of the limits of autoregulation. As therapeutic hyperve
ntilation may lead to ischemia, mannitol was preferred to reduce ICP a
nd increased low CBF to normal values. This fact should be considered
in the treatment of patients with low CBF and normal CO2 reactivity. D
elayed ischemic neurological deficits (''vasospasm'') are well - known
as significant complications of the clinical course following SAH. Im
mediately postoperatively performed CBF measurements enable to detect
ischemia and allow to start early antiischemic therapy. During ''vasos
pasm'' CBF showed a better correlation to the neurological status than
blood flow velocity in the basal arteries measured by transcranial do
ppler sonography. Futhermore hyperemia after SAH could only be verifie
d by CBF measurements.