Cerebral blood flow autoregulation during intracranial hypertension: a simple, purely hydraulic mechanism?

OBJECTIVE: In this paper, we re-propose the role of a hydraulic mechanism, acting where the bridging veins enter the dural sinuses in cerebral blood flow (CBF) autoregulation. MATERIALS AND METHODS: We carried out an intraventricular infusion in ten albino rabbits and increased intracranial pressure (ICP) up to arterial blood pressure (ABP) levels. We measured CBF velocity by an ultrasound probe applied to a by-pass inserted in a carotid artery and recorded ICP by an intraventricular needle. Diastolic and pulsatile ICP and ABP values were analyzed from basal conditions up to brain tamponade and vice versa. CONCLUSIONS: A biphasic pattern of pulsatile intracranial pressure (pICP) was observed in all trials. Initially, until the CBF velocity remained constant, pICP increased (from 1.2 to 5.4 mmHg) following a rise in diastolic intracranial pressure (dICP); thereafter, in spite of a further rise in dICP, pICP decreased (2.87 mmHg) following CBF velocity reduction until intracranial circulation arrest (pICP=1.2 mmHg). A specular pattern was observed when the intraventricular infusion was stopped and CBF velocity returned to basal levels. These findings can be interpreted as indicating a hydraulic mechanism. Initially, when CBF is still constant, pICP rise is due to an increase in venous outflow resistance; subsequently, when CBF decreases following a further increase in venous outflow resistance, the vascular engorgement produces an arteriolar vasodilation. This vasodilation determines an increase in vascular wall stiffness, thus reducing pulse transmission to surrounding subarachnoid spaces.

ICP and CBF regulation: effect of the decompressive craniectomy.

The view of the intracranial system as a rigid and closed box has been criticised by many authors who take into account the possibility of a certain degree of elastic bulk accommodation, mainly in the spinal sac. In nine patients, who underwent decompressive craniectomy for treatment of life-threatening intracranial hypertension, when the clinical conditions improved, just before cranioplasty, the blood flow velocities at middle cerebral artery (MCA) and at superior sagittal sinus (SSS) level were simultaneously recorded. The measurements were repeated after cranioplasty. The blood flow velocity recorded from SSS in craniectomized patients appeared flat, without evident pulsation; after cranioplasty a clear-cut pulsatile wave became again evident. The disappearance of a pulsatile shape in the blood flow velocity recorded from the SSS when the intracranial system was "open" and the reappearance of a pulsatile blood flow waveform after the "closure" of the skull confirm that the venous bed acts as a bulk compensatory system in order to maintain the intracranial volume absolutely constant.

ICP and CBF regulation: a new hypothesis to explain the "windkessel" phenomenon.

The brain tamponade represents the final condition of a progressive intracranial pressure (ICP) increase up to values close to arterial blood pressure (BP) producing a reverberating flow pattern in the cerebral arteries with no net flow. This finding implies intracranial volume changes, therefore a full application of the Monro-Kellie doctrine is impossible. To resolve this contradiction, in eight pigs a reversible condition of brain tamponade was produced by infusing saline into a cerebral ventricle. The following parameters were measured: BP in the common carotid artery, ICP by the same needle utilised for the infusion, arterial and venous blood flow velocity (BFV) at, respectively, internal carotid artery (ICA) and sagittal sinus (SS) site by ultrasound technique. When ICP approached carotid BP values, reverberating BFV waves both at ICA and SS site were simultaneously observed. The arterial and venous reverberating waves appeared to be almost exactly superimposable, with a delay of about 40 msec. This synchronism between the pulsatile arterial and venous BFV indicates that the residual pulsation, still occurring at the arterial proximal level, is compensated by a passive compression-distension of the SS with no blood volume (that is net flow) crossing the intracranial vasculature.