We studied the response of cerebral blood flow to acute step decreases in arterial blood pressure noninvasively and nonpharmacologically in 10 normal volunteers during normocapnia, hypocapnia, and hypercapnia. The step (approximately 20 mm Hg) was induced by rapidly deflating thigh blood pressure cuffs following a 2-minute inflation above systolic blood pressure. Instantaneous arterial blood pressure was measured by a new servo-cuff method, and cerebral blood flow changes were assessed by transcranial Doppler recording of middle cerebral artery blood flow velocity. In hypocapnia, full restoration of blood flow to the pretest level was seen as early as 4.1 seconds after the step decrease in blood pressure, while the response was slower in normocapnia and hypercapnia. The time course of cerebrovascular resistance was calculated from blood pressure and blood flow recordings, and rate of regulation was determined as the normalized change in cerebrovascular resistance per second during 2.5 seconds just after the step decrease in blood pressure. The reference for normalization was the calculated change in cerebrovascular resistance that would have nullified the effects of the step decrease in arterial blood pressure on cerebral blood flow. The rate of regulation was 0.38, 0.20, and 0.11/sec in hypocapnia, normocapnia, and hypercapnia, respectively. There was a highly significant inverse relation between rate of regulation and PacOj (p<0.001), indicating that the response rate of cerebral autoregulation in awake normal humans is profoundly dependent on vascular tone. (Stroke 1989;20:45-52) C erebral autoregulation is a homeostatic mechanism that minimizes deviations in cerebral blood flow (CBF) when cerebral perfusion pressure (CPP) changes. Cerebral autoregulation acts through vasomotor effectors that control cerebrovascular resistance (CVR). Previous studies have convincingly documented the ability of this physiologic system to maintain relatively constant CBF when CPP is within the range 50-170 mm Hg. 1 -6 Because this is a very fast-acting homeostatic mechanism, 7 the method for measuring autoregulatory responses should ideally have good time resolution. Our knowledge about the dynamic response of cerebral autoregulation in humans is limited because most indicator methods permit sampling of regional CBF at intervals of only minutes. Animal experiments 7 -10 indicate that the main autoregulatory response is produced within seconds. Measurement of dynamic response times and response rates to characterize the effectiveness of autoregulation is of interest not only from a physi-

We investigated 76 patients with known subarachnoid haemorrhage (SAH) in order to compare the results of angiography and non-invasive Doppler recordings of cerebral artery blood velocity in the diagnosis of cerebral vasospasm. One radiologist and one neurovascular surgeon assessed angiographic spasm visually on a four-level scale. The radiologist's ratings were the term of reference for the study. When there was angiographic spasm of the middle cerebral artery (MCA), the MCA blood velocity was higher and the blood velocity in the distal extracranical internal carotid artery (ICA) was lower than when MCA spasm was scored as absent. Analysis by Kappa statistics, a measure for the agreement between two independent judges with correction for random coincidence, revealed moderate agreement between angiographic spasm and the absolute MCA blood velocity (Kappa = 0.47). However, there was substantial agreement (Kappa = 0.64) between angiographic spasm and the index calculated from dividing the blood velocity in the MCA (VMCA) by the blood velocity in the ipsilateral ICA (VICA). The results indicate that this VMCA/VICA index gives more appropriate information on MCA spasm. Congenitally asymmetric circles of Willis with one wide dominant ACA showed normal blood velocities. In asymmetry induced by vasospasm, the diameter of the major ACA was normal or even reduced, and the blood velocity was significantly elevated. Hence, the agreement between blood velocity recordings and angiographic findings was substantial (Kappa = 0.64) when considering together the findings from both sides of the anterior circle of Willis.(ABSTRACT TRUNCATED AT 250 WORDS)

The cases of 208 patients with histologically confirmed oligodendrogliomas were studied. The incidence represents 4.2% of all primary brain tumors diagnosed in the Norwegian population over a 25-year period. All of these tumors were cerebral and the majority affected the frontal lobe. The patients' median age at diagnosis was 47 years, with a range from 3 to 76 years; 6% of the oligodendrogliomas occurred in children. The median duration of symptoms before diagnosis was 20.5 months (mean 43 months). Plain skull x-ray films showed calcified deposits in 28% of the tumors. At operation, most of the tumors were poorly defined, without cyst formation, hematoma necrosis, or calcification. The median duration of disease from onset of symptoms until death was 14 months in nine untreated cases. In surgically treated oligodendroglioma patients the median survival time from onset of symptoms was 74 months. The median postoperative survival time was 35 months (mean 52 months). Tumor calcification, as seen on plain skull x-ray films, was associated with a significantly longer survival period. The surgical findings of gross necrosis, gross hypervascularity, and soft tumor consistency were all related to a shorter total duration of disease. Grossly well demarcated lesions were associated with a significantly longer postoperative survival. The length of postoperative survival correlated with the preoperative clinical status. The cumulative proportion of patients surviving 5 years was 0.342. The patient's age and sex did not have a statistically significant influence on survival time. The extent of surgical excision only seemed to play a role when the neurosurgeon considered that he had removed the whole lesion: these patients had a median postoperative survival period 14 months longer than the other oligodendroglioma patients. The ABO blood group of the oligodendroglioma patient was of prognostic value. In particular, patients with blood group A had a distinctly poorer prognosis than patients with O or B blood. The survival data from this unselected series indicate that cerebral oligodendrogliomas have a less favorable prognosis than has generally been believed.

We investigated the validity of transcranial Doppler recordings for the analysis of dynamic responses of cerebral autoregulation. We found no significant differences in percentage changes among maximal (centerline) blood flow velocity, cross-sectional mean blood flow velocity, and signal power-estimated blood flow during 24 -mm Hg stepwise changes in arterial blood pressure. We investigated blood flow propagation delays in the cerebral circulation with simultaneous Doppler recordings from the middle cerebral artery and the straight sinus. The time for a stepwise decrease in blood flow to propagate through the cerebral circulation was only 200 msec Brief (1-37-second) carotid artery compression tests also demonstrated that the volume compliance effects of the cerebral vascular bed were small, only about 2.2% of normal blood flow in 1 second. Furthermore, transients associated with inertial and volume compliance died out after 108 msec We also investigated the hypothesis that autoregulatory responses are influenced by hyperventilation using the same brief carotid artery compressions. One second after release, the flow index increased by 17% during nonnocapnia and 36% during hypocapnia. sudden changes in arterial blood pressure in unanesthetized humans have been found to be extremely rapid, with a latency time (t L ) of <2 seconds.1 In contrast, a much longer delay was observed in cat pial arteriolar diameters after blood pressure changes. 2 We address the possibility that errors in the calculation of CBF from transcranial Doppler (TCD) recordings in humans were responsible for this shorter