Cranioplasty with autologous cryopreserved bone after decompressive craniectomy: complications and risk factors for developing surgical site infection.

BACKGROUND: Renewed interest has developed in decompressive craniectomy, and improved survival is shown when this treatment is used after malignant middle cerebral artery infarction. The aim of this study was to investigate the frequency and possible risk factors for developing surgical site infection (SSI) after delayed cranioplasty using autologous, cryopreserved bone. METHODS: This retrospective study included 74 consecutive patients treated with decompressive craniectomy during the time period May 1998 to October 2010 for various non-traumatic conditions causing increased intracranial pressure due to brain swelling. Complications were registered and patient data was analyzed in a search for predictive factors. RESULTS: Fifty out of the 74 patients (67.6 %) survived and underwent delayed cranioplasty. Of these, 47 were eligible for analysis. Six patients (12.8 %) developed SSI following the replacement of autologous cryopreserved bone, whereas bone resorption occurred in two patients (4.3 %). No factors predicted a statistically significant rate of SSI, however, prolonged procedural time and cardiovascular comorbidity tended to increase the risk of SSI. CONCLUSIONS: SSI and bone flap resorption are the most frequent complications associated with the reimplantation of autologous cryopreserved bone after decompressive craniectomy. Prolonged procedural time and cardiovascular comorbidity tend to increase the risk of SSI.

[Resection of malignant tumors involving the anterior cranial fossa]. / Reseksjon av maligne svulster med relasjon til fremre skallgrop.

BACKGROUND: The craniofacial approach has greatly facilitated resections of tumours involving the base of the anterior cranial fossa when compared to either the transcranial or transfacial approach alone. MATERIAL AND METHODS: This approach was used in 11 patients with malignant tumours localized to the ethmoid sinus, orbit and bone or soft tissue of the base of the anterior part of the skull. By combining a low frontal or frontolateral craniotomy with resection of the facial skull, en bloc resections were accomplished. A frontogaleal periostal flap or a muscle flap from the temporal muscle was used to replace resected bone and to seal the skull base. RESULTS: There were no peri- or postoperative deaths. One patient died due to local recurrence, one patient is alive with residual tumour six years after surgery, and one is reoperated due to local recurrence. In addition one patient developed recurrence of a previously treated tumour of the maxillary sinus. Two patients developed meningitis and one pneumocephalus postoperatively. One patient has partial loss of vision and two patients underwent dacryocystorhinostomy due to epiphora. INTERPRETATION: The planning and execution of this type of surgery requires close interaction in an interdisciplinary team, in particular between neurosurgeon and head and neck surgeon.

Transcranial Doppler ultrasonography-guided management of internal carotid artery closure.

OBJECTIVE: To emphasize the integrated use of transcranial Doppler ultrasonography (TCD) in the management of internal carotid artery (ICA) closure. METHODS: Thirty-three patients being considered for ICA closure underwent TCD assessment, vasomotor reserve testing/estimation, and carotid artery test occlusion with concomitant middle cerebral artery (MCA) blood velocity (V(MCA)) monitoring, including calculation of the MCA pulsatility index. Twelve of these patients proceeded to undergo ICA sacrifice. Sequential TCD sonograms guided their postoperative treatment. RESULTS: ICA aneurysms and neck neoplasms affected the TCD results and vasomotor reserve insignificantly, whereas carotid-cavernous fistulae induced characteristic circulatory alterations. The 10 subjects who tolerated ICA sacrifice hemodynamically all showed an initial decrease in the ipsilateral V(MCA) to > or =60% of the preocclusion value and a progressively decreasing MCA pulsatility index during carotid artery test occlusion. The two patients who developed hemodynamic cerebral infarctions exhibited a decrease in V(MCA) to <60% and a MCA pulsatility index that remained stable after a vast initial reduction. Postoperative hypervolemic and hypertensive support was safely titrated in all patients who received postoperative TCD surveillance, providing an ipsilateral V(MCA) of > or =80% of the preocclusion value. ICA closure permanently altered the cerebral circulatory pattern. CONCLUSION: The hemodynamic outcome of ICA sacrifice can be correctly predicted by using the TCD occlusion test. TCD provides the means to titrate the extent of postoperative hypervolemic/hypertensive support.

Cerebral artery blood velocity in normal subjects during acute decreases in barometric pressure.

To investigate the effect of acute changes in barometric pressure on regional cerebral perfusion we studied the middle cerebral artery (MCA) blood velocity in five healthy male volunteers by means of a low-pressure chamber. The MCA blood velocity, arterial blood and respiratory gases were measured at the barometric pressures of 1, 0.8, 0.65, and 0.5 atmospheres. The observed blood velocity (Vo) showed no systematic changes. Decreases in barometric pressure induced hypoxia and hypocapnia. When normalizing the MCA blood velocity (Vn) to a standard P(CO2) (5.3 kPa), thereby correcting for the hypoxic induced hypocapnia, we obtained an inverse relationship between cerebral artery blood velocity and arterial blood oxygen content (CaO2). The oxygen supply to the brain, estimated as the product of Vo and CaO2, decreased with lowering of the barometric pressure. However, the product of Vn and CaO2 remained constant. This suggests the existence of a regulatory mechanism attempting to maintain a constant oxygen supply to the brain during acute changes in CaO2, if the hyperventilation induced decrease in PCO2 can be omitted. In the artificial situation of a low pressure chamber, our findings are quite similar to those obtained at sea level. This indicates that the underlying mechanisms of control of cerebral blood flow do not change during acute exposure to altitude.

The role of transcranial Doppler in the management of patients with subarachnoid haemorrhage--a review.

Introduced 15 years ago, transcranial Doppler (TCD) recordings of blood-velocity in patients with recent subarachnoid haemorrhage (SAH) have two objectives: to detect elevated blood velocities suggesting cerebral vasospasm (VSP) and to identify patients at risk for delayed cerebral ischemic deficits (DID). The pathophysiological cascade causing DID is complex. Discrepancies between blood velocities and DID (presuming that there actually is an "ischemic threshold" for blood velocity in absolute terms, which seems most unlikely) have been demonstrated, particularly in patients with elevated intracranial pressure (ICP) levels. Furthermore, the vessel showing the highest blood velocity is not always the one perfusing the area where ischemic symptoms arise, nor does the site of the greatest subarachnoid blood clot always relate to the ischemic brain region. Moreover, it is probable that the complex haemodynamic changes following SAH and the subsequent development of VSP may be underestimated if only considering the crude intracranial artery blood velocities. Cerebral blood flow measurements combined with TCD to assess both flow and velocity have emphasised this point. Despite these findings and ignoring the basic principles of cerebral haemodynamics, cerebral vasospasm is still being assessed from the intracranial velocity measurement alone. The addition of at least a careful measurement from the extracranial internal carotid artery--using the same TCD equipment and taking only a few short minutes to perform--allows a much more accurate assessment of the degree and the effects of vasospasm. This probably explains why the clinical value of TCD is still debated. There is still uncertainty as to the best method to prevent and to treat VSP, and the overall outcome after SAH depends on so many factors besides VSP. Conclusive evidence may therefore be hard to obtain, and it appears sound to conclude that even with advanced investigation technology available, proper selection, pre- peri- and postoperative care and timing of surgery remain cornerstones in the management of these patients,--equal in importance to their treatment in the operating room or in the interventional angiography suite.

[Life-saving hemicraniectomy in acute massive brain infarction]. / Livreddende hemikraniektomi ved akutt massivt hjerneinfarkt.

Acute occlusion of the middle cerebral artery is an important cause of ischemic stroke. The resulting brain infarction is often very large, leading to massive brain oedema and intracranial hypertension. Despite intensive medical treatment, the mortality rate due to herniation and cerebral circulatory arrest remains very high. A Norwegian left-handed male, 28 years of age, developed signs of impending herniation following an acute right-side middle cerebral artery occlusion. When admitted to neurosurgical care 54 hours after the stroke, he was soporous, had a left-side hemiparalysis, conjugated deviation of the gaze and a mydriatic pupil on the right side. The intracranial pressure level was between 30 and 40 mm Hg. Following a right-side hemicraniectomy, the intracranial pressure fell to levels around 20 mm Hg. The bone flap was replaced four months later. One year after the stroke, the patient is fully independent of others, despite a left-side hemianopia and hemiparesis. Hemicraniectomy may be indicated in selected patients with impending herniation due to brain infarction. Intracranial pressure recordings are useful as an adjunct in the management of these patients. Our report seems to be the first account of decompressive hemicraniectomy performed in Norway for acute massive brain infarction.

Varying impact of common carotid artery digital compression and internal carotid artery balloon test occlusion on cerebral hemodynamics.

BACKGROUND: The purpose of this study was to compare the cerebral hemodynamic changes brought about by common carotid artery (CCA) digital compression and angiographic internal carotid artery (ICA) balloon occlusion. METHODS: Bilateral transcranial Doppler ultrasonographic monitoring of the middle cerebral artery blood velocity (VMCA) was performed in 12 subjects with neck neoplasms or traumatic carotid-cavernous fistulas. The MCA pulsatility index (PIMCA) and hemodynamic tension (Uhem MCA) were calculated. RESULTS: Common carotid artery compression provoked the largest drop in ipsilateral VMCA, PIMCA, and Uhem MCA. Common carotid artery compression caused a steal of blood from the intra- to the extracranial circulation, with the discrepancy in hemodynamic findings between CCA and ICA test occlusions being dependent on the quantity of reversed ipsilateral ICA blood flow. CONCLUSION: If the carotid artery is to be sacrificed, permanent ICA closure is the procedure of choice with respect to the occurrence of cerebral ischemic lesions in patients with neck neoplasms and ICA flow reversal during CCA compression.

Cerebral haemodynamics in internal carotid artery trial occlusion.

The purpose of this study was to analyse the cerebral haemodynamic changes brought about by trial occlusion of the internal carotid artery (ICA). Sixteen patients with surgically inaccessible cerebral aneurysms, carotid cavernous fistulas or neck neoplasms were monitored with transcranial Doppler ultrasonography (TCD) during 90-120 s angiographic ICA balloon occlusion or ICA closure with a Selverstone clamp. The blood velocity (V) was registered continuously in both middle cerebral arteries (MCA) while the pulsatility index (PIMCA) and haemodynamic tension (Uhem MCA) were calculated. ICA closure led to an instantaneous drop in the ipsilateral VMCA, PIMCA and Uhem MCA. The VMCA thereafter increased gradually until reaching a stable level. The subjects were grouped into those with initial drops in VMCA to > or = 60% of pre-occlusion value (group 1) and those that fell to < 60% (group 2), respectively. In group 1 autoregulatory mechanisms made the PIMCA decline further, while the Uhem MCA remained unaltered during ICA closure. In group 2, however, the PIMCA did not change further, while the Uhem MCA increased slightly. The cerebral haemodynamic features during ICA test occlusion were thus essentially different in the two groups. On re-opening the ICA, there was an overshoot in VMCA and Uhem MCA. Contralaterally, the VMCA was increased during ICA occlusion. Seven of the patients later had their ICA closed permanently. While none of five group 1 patients developed haemodynamic complications, two group 2 individuals experienced haemodynamic stroke. Assuming ICA sacrifice is feasible when test occlusion results in an ipsilateral initial reduction in VMCA to > or = 60% of pre-occlusion value, the corresponding limit for the Uhem MCA is > or = 40%. In the pre-operative evaluation of the haemodynamic risk related to ICA loss, TCD emerges as a reliable method. It also seems to allow for the reduction of test occlusion time to 90-120 s.

Haemodynamic classification of symptomatic obstructive carotid artery disease.

63 subjects with symptomatic obstructive carotid artery disease were investigated with transcranial Doppler ultrasonography. Their blood velocities at rest (V) in the middle and posterior cerebral artery (MCA and PCA) and in the extracranial internal carotid artery were measured and the pulsatility index (PI) and Uhem index (VMCA.PIMCA/VPCA.PIPCA) calculated. The vasomotor responses in both MCAs were also tested. The subjects were divided into groups based on the findings on physical examination and cerebral computed tomography. In the patient group with lacunar/territorial infarction we found in the stroke hemisphere: VMCA > VPCA, PIMCA = PIPCA and normal values for the Uhem index and total vasomotor reactivity. In the patient group with watershed infarction this hemisphere was characterized by: VMCA < VPCA, PIMCA < PIPCA and subnormal scores for the Uhem index and total vasomotor reactivity. Displaying features from both stroke groups, we obtained in the hemisphere of interest in patients with transient ischaemic attacks: VMCA = VPCA, PIMCA < PIPCA and normal values for the Uhem index and total vasomotor reactivity. Five patients with clinical evidence of stroke but with negative cerebral computed tomography findings had scores similar to those of the watershed group of patients. For the stroke patients, individual measurements of V, PI and total vasomotor reactivity failed to clearly identify to which stroke group a subject might belong. However, such an identification was achieved in all subjects when using the Uhem index. The Uhem index data in patients with transient ischaemic attacks suggest two subgroups with different pathogenesis underlying, the ischaemic events.

Cerebral haemodynamic considerations in obstructive carotid artery disease.

46 subjects with obstructive carotid artery disease were investigated with transcranial Doppler ultrasonography. Their baseline blood velocities (V) in the middle, anterior and posterior cerebral artery (MCA, ACA and PCA) and in the extracranial internal carotid artery (ICA) were measured and the pulsatility index (PI) calculated for each vessel. Thereafter the vasomotor reserve in both MCAs was tested. Typical patterns of V, PI and vasomotor reactivity are presented. Arterial collaterals were recognized by their relatively increased velocities. We demonstrated a close association of the baseline variables V and PI and the total vasomotor reactivity (hypocapnic plus no, hypercapnic response) by calculating an index of Uhem related to the cerebrovascular tone. The Uhem index is expressed by: Uhem index = VMCA.PIMCA/VPCA.PIPCA The relationship between Uhem index and the total vasomotor reactivity seemed to correspond to a hyperbolic curve. The hyperbolic tangent of Uhem index and total vasomotor reactivity correlated highly significantly, r = 0.8203, p < 0.0001, n = 49, the best fit for the regression line was Y = -0.005 + Uhem index 51.3. On the 99% significance level an Uhem index > or = 0.94 indicated normal total cerebral vasomotor reactivity in contrast to an impaired reactivity when < or = 0.81. Findings in 20 patients investigated post hoc supported the validity of our concept.

Transcranial Doppler in neurosurgery.

This chapter describes the use of the transcranial Doppler apparatus in neurosurgery. The principles of Doppler insonation, the techniques of recording and the use of activation techniques is described. The relationship between blood flow and blood velocity is discussed, and the interaction of various pharmacological agents. The establishment of normal values for the laboratory and various vessels insonated is emphasised. The use of indices particularly the pulsatility index is described together with its variations. Cerebral vascular reactivity measurements and the interaction of Doppler recordings with raised intracranial pressure, useful in assessment of cerebral perfusion pressure as in head injury and in terminal cases, is documented. The use of transcranial Doppler in management of head injury and subarachnoid haemorrhage is described. The latter is probably the most useful routine place for Doppler measurement in neurosurgical practice and the documentation of the onset and progress of vasospasm is the final portion of the chapter.

Long-term results after percutaneous retrogasserian glycerol rhizotomy in patients with trigeminal neuralgia.

We have evaluated the long-term results of percutaneous retrogasserian glycerol rhizotomy (PRGR) in 60 patients with classical trigeminal neuralgia. Complete initial pain relief was achieved in 93% of the patients. Numbness was initially reported by 3/4 of the patients and at follow-up by 1/3, while long-lasting dysaesthesias were an important side effect in 38% of previously untreated patients. The half-life of the method was 47 months in our material, and this figure compares favourably with other previously reported series. The method carries a significant risk of long-lasting and troublesome sensory disturbances. Another disadvantage of the method, reported in the present long-term study, was the high incidence of recurrent neuralgia. We are unable to identify predictors of recurrent neuralgia after PRGR, although major recurrences were more common in patients with unchanged facial sensation postoperatively. In conclusion, PRGR offers safe and reliable relief of pain in patients with trigeminal neuralgia. In spite of the high incidence of recurrence and of long-lasting dysaesthesias it is, in our opinion, the method of choice in the elderly, and particularly suitable for patients at high risk.

A comparison of transcranial Doppler and cerebral blood flow studies to assess cerebral vasoreactivity.

BACKGROUND AND PURPOSE: The aim of this study was to determine the ability of transcranial Doppler ultrasonography when used to assess cerebral vasoreactivity. The results of this method were compared with regional cerebral blood flow measurements. METHODS: Forty-three patients with symptoms suggesting cerebrovascular disease took part. Transcranial Doppler findings in the middle cerebral arteries were compared with regional cerebral blood flow in the corresponding perfusion territories before and after acetazolamide administration. RESULTS: There was a significant positive correlation between the absolute increase in cerebral blood flow in milliliters per 100 g per minute and the percent increase in velocity (r = 0.63). The right-left, side-to-side difference of the acetazolamide response obtained by the two methods also showed a positive correlation (r = 0.80). Control limits obtained from healthy subjects were used for both the blood flow increase (absolute values and asymmetry in absolute values) and the velocity increase (percent increase and asymmetry in percent increase). The two methods then agreed in their evaluation of vasoreactivity in 74 (86%) of the 86 middle cerebral artery perfusion territories; 20 (23%) were assessed by both methods as having a reduced vasodilatory reserve. Eleven hemispheres with a slightly reduced regional cerebral blood flow response to acetazolamide were not detected by transcranial Doppler, whereas all territories with a marked reduction were identified by Doppler. Only one hemisphere with a normal cerebral blood flow increase after acetazolamide administration was assessed by Doppler as having reduced vasoreactivity. CONCLUSIONS: Transcranial Doppler and the acetazolamide test may be used in clinical situations to assess cerebral vasoreactivity.

Assessment of cerebral autoregulation dynamics from simultaneous arterial and venous transcranial Doppler recordings in humans.

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 normocapnia and 36% during hypocapnia. After 5 seconds, the flow index demonstrated a clear oscillatory response during hypocapnia that was not seen during normocapnia. These results suggest that the intact human cerebral circulation in the absence of pharmacological influences does not function as predicted from pial vessel observations in animals.

Side-to-side differences and day-to-day variations of transcranial Doppler parameters in normal subjects.

We investigated 35 normal adults to assess variations in cerebral artery blood velocities, hemispheric blood velocity ratios, and pulsatility indices, both with regard to changes between the sides and between days. We found no significant variations between sides or days. Changes from one day to the next exceeding 20% in blood velocity in the middle cerebral artery (VMCA), the anterior cerebral artery (VACA), the distal extracranial internal carotid artery (VICA), and in the hemispheric VMCA/VICA, VACA/VICA, or VACA/VMCA ratios, may be considered significant at the 95% level.

Continuous recording of middle cerebral artery blood velocity in clinical neurosurgery.

Intracranial pressure, arterial blood pressure, and middle cerebral artery blood velocity were monitored for periods from 1 to 10 days in 30 neurosurgical intensive care patients. The recordings revealed rapid changes in the cerebral perfusion and gave insight into individual cerebral haemodynamic states. Twenty patients consistently showed CO2 reactivity within normal limits, between 2.5 and 5% per mm Hg (19-38% per kPa). Severely impaired CO2 reactivity, considerably below 1% per mm Hg (7.5% per kPa) was observed in four patients. Three of these patients died, while the fourth patient survived in a persistent vegetative state. Seven patients demonstrated pressure-passive blood velocity changes throughout the observed CPP range. The four patients with severely impaired CO2 reactivity all belonged to this group. The recordings from three of the remaining 23 patients showed signs of MCA blood velocity autoregulation with a lower regulatory limit of about 40-45 mm Hg. This observation is in keeping with findings from electromagnetic flowmetry on brain arteries in the neurosurgical operating field, and supports blood velocity measurements as a relevant index of brain perfusion in clinical neurosurgery and neuro-intensive care settings.

Haemodynamic aspects of clinical cerebral angiography. Concurrent two vessel monitoring using transcranial Doppler ultrasound.

To overcome the technical limitations which have precluded noninvasive Doppler ultrasound in investigation of rapid cerebral haemodynamic responses in two cerebrovascular beds at the same time, we have modified a commercial 2 MHz pulsed Doppler instrument with online spectrum analysis. Two probes are activated intermittently, recording eight averaged Doppler-shifted spectra from each probe sequentially. Concurrent recordings of blood velocity in both middle cerebral arteries were performed during 25 selective iohexol carotid angiography runs in 13 patients with near normal cerebral vasculature. The technique permitted the differentiation between the specific responses confined to the recipient vascular bed, and the general responses occurring in remote brain areas as well. The specific response to iohexol was biphasic; a significant decrease in blood velocity occurred less than 4 s after the bolus entry, probably due to the high viscocity of iohexol. Between 4 and 12 s. blood velocity was significantly increased, reflecting the cerebrovascular response to hypertonic solutions. The blood velocity on the opposite side increased from less than 4 s through 45 s after iohexol. This concurs with studies using electromagnetic flowmetry, and suggests that these general responses are elicited by anxiety, discomfort and pain. Thus, no general responses were seen during angiography under general anaesthesia. Eight patients investigated during catheter flushing with normal saline showed a biphasic specific response reciprocal to that due to iohexol. A significant blood velocity peak occurred less than 4 s after the bolus entry, followed by a decrease between 4 and 60 s. The saline injections produced no pain and evoked no significant general response.

Cerebral autoregulation dynamics in humans.

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 PaCO2 (p less than 0.001), indicating that the response rate of cerebral autoregulation in awake normal humans is profoundly dependent on vascular tone.

Cerebral vasospasm diagnosis by means of angiography and blood velocity measurements.

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)

Blood velocity and regional blood flow in defined cerebral artery systems.

Cerebral artery blood velocity and regional blood flow (rCBF) were investigated in 17 normal subjects. Blood velocity was measured with 2 MHz pulsed Doppler ultrasound in the proximal segments of the middle, anterior and posterior cerebral artery (MCA, ACA, and PCA) and in the distal extracranial internal carotid artery (ICA). The rCBF in the regions of interest tentatively corresponding to the perfusion territories of these vessels was estimated using 133Xe inhalation and a rapidly rotating single photon emission computer tomograph. Concomitant capnograph recordings showed that the end-expiratory pCO2 was higher during the rCBF than during the blood velocity examinations. This differences was highly significant. While there was no significant correlation between blood velocity and rCBF when these clear differences in pCO2 were disregarded, we did find significant positive correlations when the data were normalized to a standard pCO2 (5.3 kPa) using accepted formulas. The best correlation was found for the MCA (r = 0.630, p less than 0.001) and the PCA (r = 0.73, p less than 0.001), with a lower correlation in the ACA (r = 0.49, p less than 0.01) and the ICA (r = 0.41, p less than 0.05). The estimated blood velocity (V) given rCBF = 0 was not significantly different from 0. The results support the validity of expressing the relationship between blood velocity (V) and rCBF in defined cerebral artery systems as: V = 1/60 (rCBF) T (A)-1, where A represents the area of the lumen of the vessel segment where the velocity is being measured, and T denotes the size of the brain region being perfused from this artery.