Mechanisms of cerebral autoregulation, assessment and interpretation by means of transcranial Doppler sonography

Cerebrovascular autoregulation assures constancy of cerebral perfusion desp ite blood pressure changes, as long as mean blood pressure remains in a ran ge between 50-170 mmHg. Static and dynamic myogenic mechanisms dampen sudde n blood pressure changes. Neurogenic influences of sympathetic, noradrenerg ic fibers modulate primarily proximal, large diameter segments of cerebral arteries, but also small 15-20 mu m diameter vessels. Parasympathetic, vaso dilating impulses are of less influence. Monoaminergic brainstem centers su ch as the dorsal raphe nucleus, locus coeruleus or nucleus reticularis pont is oralis also influence Vessel tone. Metabolic, local parenchymal and endo thelial substances have major impact on cerebral vessel tone. Particularly important are nitric oxide, calcitonin gene related peptide, substance P, e ndothelin, potassium channels and autocoids such as histamine, bradykinin, arachidonic acid, prostanoids, leucotrienes, free radicals or serotonin. Th e clinical examination of autoregulation is mostly based on brief blood pre ssure changes induced by drugs such as angiotensin, phenylephrine or sodium nitroprusside, or by challenge maneuvers. Frequently, blood pressure is ch allenged by a tilt-table maneuver, the "leg-cuff"-method according to Aasli d, or a Valsalva maneuver. The analysis of coherence and phase relation bet ween spontaneous or metronomic breathing modulation of blood pressure and b rain perfusion also assesses autoregulatory function. Cerebral blood flow i s determined by means of transcranial Doppler sonography, mostly of the pro ximal segment of the mid-cerebral artery. There is some controversy whether a decrease of cerebral blood flow velocity measured at this segment indica tes vasodilatation at the insonated segment or reflects blood flow reductio n due to decreased perfusion of down-stream vessel segments. Various clinic al and animal studies are presented demonstrating diameter constancy of the insonated mid-cerebral artery segment and thus indicating that slowing of mid cerebral artery brood flow velocity as assessed by transcranial Doppler sonography is due to a decrease of down-stream perfusion. Direct, intraope rative measurements of vessel diameter confirm this conclusion.