Comparison of the effects of ischaemia on early components of the somatosensory evoked potential in brainstem, thalamus, and cerebral cortex

In 14 ventilated, normocapnic baboons anaesthetised with alpha-chloralose, local CBF (hydrogen clearance) and the amplitude and latency of local components of the somatosensory evoked potential (SEP, median nerve stimulation) were measured bilaterally in ventrobasal thalamus (VPL), medial lemniscus (ML), and cerebral cortex before and during progressive ischaemia, produced by occlusion of the right middle cerebral artery and subsequent controlled reductions in mean systemic blood pressure (MSBP). The first significant reduction from control of the left cortical SEP amplitude occurred in the range of 30-40 mm Hg MSBP, but those of the VPL and ML responses only below 30 mm Hg; in the range of 20-30 mm Hg, the average SEP amplitudes in cortex, VPL, and ML were 8.6, 72.6, and 90.7% of control, respectively. In terms of local CBF, the cortical SEP threshold was in the range of 15-20 ml/100 g/min (as in previous work), that of VPL in the range of 10-15 ml/100 g/min, but the ML response was only markedly reduced below 10 ml/100 g/min. Thus, the differential ischaemic sensitivity of the SEP between the three regions was clearly demonstrated. These results indicate that as one descends the neuraxis, there is an increasing resistance of electrophysiological function to systemic hypotension, together with a decreasing threshold for local ischaemia.     

Changes in the somatosensory evoked potential during and immediately following temporary middle cerebral artery occlusion predict somatosensory cortex ischemic lesions in monkeys

Somatosensory evoked potentials (SEP) were recorded during and immediately following temporary middle cerebral artery (MCA) occlusion to determine whether they can be used to predict ischemic lesions to the somatosensory cortex (SI). Twenty-one cynomolgus female monkeys were subjected to four different MCA occlusion durations (15-60 min) during hypotension (45-50 mm Hg mean arterial blood pressure). The amplitude and central conduction time (CCT) of the median nerve SEP were recorded preceding, during, and following occlusion. Two groups were established based on the development of SI ischemic lesions: animals developing SI lesions formed the SI-lesion group (n = 9), and animals without ischemic lesions or with lesions outside the SI cortex formed the SI-spared group (n = 12). Changes in the SEP during and following MCA occlusion under conditions of hypotension were similar to those reported by others. The SEP disappeared in all animals within 15 min of occlusion and reappeared 5 min following reperfusion. Several differences were observed between the SI-lesion and SI-spared groups. The SI-lesion group had a more rapid decrease in SEP amplitude during the first 5 min of occlusion and had smaller SEP amplitudes and longer CCTs during reperfusion. These results suggest that changes in SEP amplitude and latency during and immediately following temporary MCA occlusion predict development of SI ischemic lesions.     

Functional changes in thalamic relay neurons after focal cerebral infarct: a study of unit recordings from VPL neurons after MCA occlusion in rats.

We evaluated neuronal and histological changes of thalamic neurons 1, 4, 7, and 14 days after middle cerebral artery (MCA) occlusion in rats. After the somatosensory evoked potentials (SEPs) were measured from the cerebral cortex, the thalamic relay neuronal activities were recorded with a glass microelectrode following repetitive electrical stimulation of the contralateral forepaw at frequencies ranging from 1 to 50 Hz. In approximately 95% of the occluded rats, the ipsilateral somatosensory cortex and/or the subcortical somatosensory pathway developed infarct, resulting in SEP loss. We evaluated unit data from rats with abolished SEPs. The average firing rate of the nucleus ventralis posterolateralis (VPL) neurons in response to 25 stimulations at 30 Hz was significantly reduced to 0.1 spike/stimulus 1 day after MCA occlusion. In sham-operated rats, the same stimulation produced 0.7 spike/stimulus. The firing rate recovered to 0.4 spike/stimulus at 30-Hz stimulation 4 and 7 days after occlusion. This was followed by resuppression (0.1 spike/stimulus) 14 days after occlusion. Histological study revealed some abnormal neurons in the ipsilateral thalamus 7 days after occlusion. We were unable to find normal-shaped neurons in the VPL 14 days after occlusion. The present study demonstrates that cortical infarct produces functional and morphologic changes that gradually and progressively affect the ipsilateral thalamus, although incomplete transient recovery of somatosensory transmission may occur.     

Correlation between somatosensory evoked potentials and neuronal ischemic changes following middle cerebral artery occlusion

In an attempt to determine the usefulness of evoked potentials as a measure of focal cerebral ischemia, we examined somatosensory evoked potentials (SEP's) and morphological neuronal changes in cats following unilateral middle cerebral artery (MCA) occlusion. Fifteen adult cats underwent transorbital occlusion of the MCA under halothane anesthesia. In seven cats the ipsilateral SEP's were abolished after middle cerebral artery occlusion, and did not show any recovery after 6 hours. The same seven cats showed the greatest area of moderate and severe ischemic neuronal changes, ranging from 21 to 64% (mean 39 +/- 14%) of the total ipsilateral cortical area. The remaining eight cats showed a complete flattening or decreased amplitude of the SEP after occlusion, but demonstrated a considerable recovery in the amplitude of the primary cortical potential during the six hours of the study. All these cats had ischemic areas of less than 15% (mean 9 +/- 3%) of the total ipsilateral cortex. These results demonstrate that the disappearance of the SEP and their failure to recover correlate with the extent and degree of histological cerebral ischemia.     

Autoradiographic analysis on second-messenger systems and local cerebral blood flow in ischemic gerbil brain

Alterations of the second-messenger systems, adenylate cyclase (AC) and protein kinase C (PKC), and local cerebral blood flow (lCBF) were evaluated during experimental cerebral ischemia in gerbils employing a quantitative autoradiographic method, which permitted these three parameters to be measured in the same brain. Ischemia was induced by occlusion of the right common carotid artery for 6 h. Animals attaining more than 5 in their ischemic scores were utilized for further experiments. At the end of ischemia, lCBF was measured by the [14C]iodoantipyrine method. The AC and PKC activities were estimated by the autoradiographic technique developed in our laboratory using [3H]forskolin (FK) and [3H]phorbol-12,13-dibutyrate (PDBu), respectively. The lCBF fell below 10 ml/100 g/min in most cerebral regions on the ligated side. The greatest reduction in FK binding was noted in the olfactory tubercle, caudate-putamen, and globus pallidus, followed by the hippocampus and cerebral cortices. The FK binding tended to be low at lCBF less than 20 ml/100 g/min in the cerebral cortices. However, the PDBu binding was relatively well preserved in each cerebral structure, and no significant correlation between lCBF and PDBu binding was noted in the cerebral cortices. The AC system may thus be vulnerable to ischemic insult over extensive brain regions, while the PKC system may be relatively resistant to ischemia.     

Role of a hydrostatic pressure gradient in the formation of early ischemic brain edema

We studied whether a hydrostatic pressure gradient between arterial blood and brain tissue plays a role in the formation of early ischemic cerebral edema after middle cerebral artery (MCA) occlusion in cats. Tissue pressure, regional CBF, and water content were measured from the cortex in the core and the peripheral zone of brain normally perfused by the MCA. Intraluminal arterial pressure was altered at intervals by inflation of an aortic balloon to vary the blood-tissue pressure gradient in the ischemic zone. Brain water content in the ischemic core, where flow fell to 5.5 ml/100 g/min, increased within 1 h of occlusion. After occlusion tissue pressure rose from 7.95 +/- 0.72 mm Hg at 1 h to 13.16 +/- 1.13 mm Hg at 3 h. When intraluminal pressure was increased, water content increased further, but only at 1 h after occlusion. In the periphery where flow was 18.9 ml/100 g/min during normotension, neither water content nor tissue pressure rose within 3 h of occlusion. Increased intraluminal pressure was accompanied by increased water content only at 3 h. This study indicates that a hydrostatic pressure gradient is an important element in the development of ischemic brain edema, exerting its major effect during the initial phase of the edema process.     

Neurofunctional disturbances as related to cortical ischemia and white matter ischemia

We evaluated regional cerebral blood flow (rCBF) by means of hydrogen clearance method as well as [14C]-iodoantipyrine autoradiographic method, cortical auditory evoked potentials (AEP), somatosensory evoked potentials (SEP) induced by forelimb (median nerve) stimulation (SEP-F), and SEP induced by hindlimb (tibial nerve) stimulation (SEP-H) in cats after occlusion of the left middle cerebral artery (MCA) under alpha-chloralose anesthesia. According to the degree of ischemia, the experimental animals were divided into two groups. One was the critical ischemia which was defined as permanent total suppression of AEP, and low residual blood flow in the auditory cortex. And the other was the non-critical ischemia which included transient suppression and spontaneous recovery of the cortical sensory evoked potentials, and high residual blood flow (greater than 15 ml/100 g/min). In one cat with transient suppression of three kinds of sensory evoked potentials, the [14C]-iodoantipyrine (IAP) autoradiograph revealed only a limited ischemic area of subcortical white matter. In the critical ischemia group, ischemia of the primary sensory cortex ranged from the mostly affected primary auditory cortex (supplied by the MCA) to the least affected hindlimb projection area within primary somatosensory cortex (supplied by the ACA). The forelimb projection area of the primary somatosensory cortex (supplied by both ACA and MCA) showed a mild or moderate reduction of rCBF after occlusion. The [14C]-IAP autoradiograph showed severe reduction of the white matter including the somatosensory pathway in the wide range. However, rCBF in the thalamus and hindlimb projection area within somatosensory cortex was almost intact in the cat with ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cortical tissue pressure gradients in early ischemic brain edema

We examined the role of ischemic brain edema, tissue pressure gradients, and regional CBF (rCBF) in adjacent regions of cerebral cortex in cats with middle cerebral artery (MCA) occlusion (MCAO). Tissue pressure, rCBF, and water content were measured from gray matter in the central core and the peripheral margin of the MCA territory over 6 h after MCAO. Ventricular fluid pressure and CSF pressure were recorded. Tissue pressure in the ischemic core, with a flow of approximately 5 ml/100 g/min, increased more than that in the periphery where flow was approximately 19 ml/100 g/min. Tissue pressure rose progressively to 14.8 +/- 1.0 mm Hg in the core over 6 h after MCAO, establishing a significant pressure gradient between that tissue and the lateral ventricle nearby or the subarachnoid space in the middle fossa within the first 3 h. The increase in tissue pressure was linearly related to the amount of edema fluid that developed until the edema reached a severe degree. This study shows that a hydrostatic tissue pressure gradient within ischemic cortex is associated with ischemic brain edema. The magnitude of the gradient that develops is related to the severity of ischemic edema in that tissue.     

A comparison of the functional vulnerability of the cerebral cortex and thalamus to acute ischemia

Using cerebral cortical and thalamic ischemia models produced in mongrel dogs, the reversibility of short-latency somatosensory-evoked potentials (SSEPs) and the effects of ischemic brain edema on reversibility were compared. The mean systemic blood pressure (MSBP) of animals was reduced by exsanguination until cortical SSEPs disappeared, and was held constant at that level. The MSBP was recovered by autogenous blood transfusion at 30 minutes (subgroup A), 60 minutes (subgroup B) and 90 minutes (subgroup C) after SSEP disappearance in the cortical ischemia group; and at 15 minutes (subgroup D) and 30 minutes (subgroup E) after SSEP disappearance in the thalamic ischemia group. Local cerebral blood flows (lCBF) were measured and SSEPs were monitored serially up to 2 hours after blood transfusion. At the end of measurement, the leakage of Evans blue was evaluated and brain tissue water content was measured. Cortical SSEPs disappeared when lCBF in the right cerebral cortex, measured by hydrogen clearance method decreased to 18.4 +/- 5.4 ml/100 g/min (mean +/- SD) and neuronal transmission failure in thalamus occurred when thalamic blood flow decreased to 10.0 +/- 3.3 ml/100 g/min. After blood transfusion. SSEP reappeared in all 12 animals in subgroup A, but did not appear in 2 of 9 animals in subgroup B and in all of 7 animals in subgroup C.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of ulinastatin on postischemic brain edema in cats]

The effect of ulinastatin on postischemic brain edema was investigated in adult mongrel cats. Focal brain ischemia was produced by occlusion of the left middle cerebral artery (MCA) through the transorbital approach. Following two hours of occlusion, the brain was reperfused for two hours. In all seven animals of the ulinastatin-treated group, ulinastatin was administered intravenously at a dose of 50000 U/kg before and after occlusion. In the control group, six animals were given only vehicle. Measurements of regional cerebral blood flow (rCBF) were performed before MCA occlusion by the hydrogen clearance method, and then repeated every 30 minutes during and after occlusion. Following two-hour reperfusion, the animals were sacrificed by intravenous KCl injection. Specific gravity of the cortex, where rCBF was measured, was determined by microgravimetric method. In the analysis of specific gravity of the cortex, in which mean rCBF during ischemia was above 15ml/100g/min, no significant difference was found between the ulinastatin-treated and control groups. In the specimen with mean rCBF below 15ml/100g/min during ischemia, cortical specific gravity was reduced remarkably in the control group, while not decreased in the ulinastatin-treated group. The difference was statistically significant between two groups (p less than 0.001). These findings suggest antiedema effect of ulinastatin.     

Somatosensory evoked potentials in cerebral ischemia of rabbits

Twenty-one rabbits were used in the ischemic group and six in the control group. Cerebral ischemia of variable degree was induced by Fe particle injection method. Somatosensory evoked potentials (SEPs) and cerebral blood flow (CBF) were compared when the CBF levels decreased to their minimum. The latency of the SEPs increased along with the decrease of the CBF when it was lower than 20 ml/100 g/min (68% of the pre-ischemic control level). This may be related to the ischemic change of the white matter. The amplitude showed diphasic changes. When the CBF decreased below 20 ml/100 g/min, the amplitude increased; when the CBF was lower than 11 ml/100 g/min (38% of the pre-ischemic level), it decreased. These results indicate that the functions of the cerebral cortex might be excited in mild ischemia, and be suppressed in severe ischemia.     

The temporary occlusion of middle cerebral artery in cats--the correlation between the rCBF and the histological changes (author's transl)

The correlation between the changes of regional cerebral blood flow (rCBF) and the histological changes were examined using the middle cerebral arterial (MCA) occlusion model in cats. A total of 24 adult cats were tracheostomized and anesthetized by inhalation of halothane. The right MCA was clipped by the transorbital approach. Two hours after the application, the clip was removed and the brain was recirculated for two hours. Then, the brain was perfusion-fixated and the histological studies were carried out. The animals were separated into two groups according to the severity of histological damages using light and electron microscope. Severe cortical damage was present in 8 cats (Group A). In the remaining 16 cats, little or no cortical damage was found (Group B). The averaged rCBF values before occlusion were 45.4 +/- 2.3 ml/100 gm/min in group A and 46.5 +/- 1.6 in group B, showing no statistically significant difference. Between these two groups, however, there was a statistically significant difference in the averaged rCBF values during the ischemic period. In group A, the averaged rCBF values during MCA occlusion was only 6.8 +/- 0.9 and in group B, it was 25.3 +/- 0.8. In the recirculation period, there was a prompt and uniform recovery of rCBF in group B. Whereas in group A, a marked diversity of rCBF ranging from oligemia to hyperemia ensued. This is presumably a reflection of inhomogeneous blood flow, or patchy non-filling of the cerebral cortex. The critical values of rCBF as to the occurrence of severe cortical damage in two-hours MCA occlusion is considered to lie between the lowest value of group B and the highest value of group A, i.e., around 12--15 ml/100 gm/min.     

Autoradiographic evaluation of forskolin and D1 dopamine receptor binding in a rat model of focal cerebral ischaemia.

Post-ischaemic changes in forskolin and D1 dopamine receptor (labelled with SCH23390) binding sites were evaluated in a rat unilateral middle cerebral artery occlusion (MCA) model. The changes in binding were assessed acutely (2 h post-MCA occlusion) in relation to local cerebral blood flow (lCBF) and chronically (24 h post-MCA occlusion) in relation to histopathological alterations. Two hours following occlusion lCBF was significantly reduced throughout the territory of the MCA. Despite the widespread hypoperfusion, significant reductions in binding were only observed in the dorsolateral caudate nucleus--the region with the most profound reduction in blood flow (6% of the control contralateral lCBF value). Forskolin binding sites were reduced to 40% of the contralateral value while D1 binding sites were reduced to 80% of the contralateral value. Analysis of the relationship between forskolin binding and CBF in the caudate nucleus revealed that the ischaemic threshold for alteration in forskolin binding sites 2 h after MCA occlusion was approximately 34 ml/100 g/min. Twenty-four h post-occlusion forskolin binding sites were further reduced in the dorsolateral caudate nucleus (to 6% of contralateral) while D1 binding showed minimal reduction from that observed at 2 h. The areas of reduced binding corresponded to the area of histopathological change in the caudate nucleus and rostral neocortex. In conclusion, reduction in forskolin binding progresses further than reduction in D1 binding within the first 24 h following focal cerebral ischaemia. For both forskolin and D1 binding sites, the areas of reduced binding 24 h post-MCA occlusion predicted the area of histopathological change.     

Short- and long-latency tibial somatosensory evoked potentials in cerebral lesions affecting rolandic leg areas

Summary Short- and long-latency tibial somatosensory evoked potentials (SEPs) were studied in nine patients with clinical presentation primarily involving one lower extremity. In group 1, with extensive infarcts in the territory of anterior cerebral artery, tibial cortical SEPs were uniformly absent. In group 2, with small infarcts involving Rolandic leg areas, tibial SEPs showed a decrease in overall response amplitude and attenuation of P40. In group 3, with discrete mass lesions compressing Rolandic leg areas, P40 was preserved but might be delayed. Late SEP components (N75, P100 and N135) tended to be preserved in the patients of group 2 and 3. The data suggest that Rolandic leg areas and the neighboring cortex are crucial for short- and long-latency tibial cortical SEPs and that small lesions affecting Rolandic leg areas tend to affect short-and mid-latency SEP components.     

Brain tissue oxygenation monitoring supplementary to somatosensory evoked potential monitoring for aneurysm surgery. Initial clinical experience

The object of the study was to evaluate brain tissue oxygenation (p(ti)O2) for intra-operative monitoring of critical ischemic events during early cerebral aneurysm surgery of the anterior circulation supplementary to somatosensory evoked potentials (SEPs). P(ti)O2 was continuously evaluated during surgery for an intracranial aneurysm in 28 patients. Standard cortical SEP monitoring was simultaneously performed. The two monitoring methods were compared by evaluating their respective responses to intra-operative events (particularly temporary vessel occlusion), clinical and neuroradiological outcome. P(ti)O2 and SEPs were reliably used for monitoring in 16 patients. Seven patients were excluded due to too high or too low p(ti)O2 readings or initial absence of SEPs (six patients). Of 64 intra-operative events 19 events (eight patients) were associated with a significant decrease in p(ti)O2 (below 10 mmHg), 22 events (13 patients) were associated with a significant change in SEP amplitude (< 50% decrease related to baseline). Temporary vessel occlusion (six SEP andp(ti)O2 changes each in eightpatients) and surgical dissection were most likely to be followed by significant changes in a monitoring method. Intra-operative p(ti)O2 was found to be a safe, rapid method for documenting ischemic events. P(ti)O2 was found to supplement SEP monitoring. The use of p(ti)O2 measurement as a routine monitoring method in aneurysm surgery is limited by its focal spatial resolution. Nevertheless, it might be helpful as an adjunct in situations when SEPs are absent at baseline, in aneurysms when parent vessel anatomy is complex or if temporary vessel occlusion is planned.     

The biphasic opening of the blood-brain barrier to proteins following temporary middle cerebral artery occlusion

Summary The behavior of the blood-brain barrier (BBB) was studied in cats following release after 1-h middle cerebral artery (MCA) occlusion. The regional cerebral blood flow (rCBF) was determined by hydrogen clearance method in the caudate nucleus and the cerebral cortex. The BBB was assayed with Evans blue (EB) tracer and by immunohistochemical peroxidaseantiperoxidase (PAP) method. Following release of MCA occlusion, there were two openings of the BBB, separated by a refractory period. The first opening, occurred shortly after recirculation; this was associated with rCBF below 15 ml/100 g/min during the ischemic period and a pronounced reactive hyperemia promptly following release of MCA occlusion. A refractory period of the BBB was indicated by the absence of EB leakage in cats injected with the tracer 30 min before killing at 3 h after recirculation, although the rCBF values in these animals were even lower (6±1 ml/100 g/min) during occlusion, and all of them showed a pronounced hyperemia after recirculation. The occurrence of the previous BBB opening in these animals was confirmed by the PAP staining. The second opening of the BBB was observed at 5 and 72 h after recirculation in cats which were injected with EB 30 min before killing, and which showed rCBF below 15 ml/100 g/min during occlusion, followed by a pronounced reactive hyperemia. No EB extravasations were observed at any time in cats in which the rCBF during occlusion was above 15 ml/100 g/min and which failed to show a marked reactive hyperemia.     

A nonNMDA antagonist, GYKI 52466 improves microscopic O2 balance in the cortex during focal cerebral ischemia.

This study was performed to test whether GYKI 52466, a nonNMDA receptor antagonist, would improve microregional oxygen supply and consumption balance in the focal cerebral ischemic area. Rats were anesthetized with 1.4% isoflurane. For the GYKI Group (n = 8), 10 min before middle cerebral artery (MCA) occlusion, a bolus of 5 mg kg-1 of GYKI 52466 i.v. was administered and was followed by an infusion of 5 mg kg-1 h-1. For the Control Group (n = 8), the same volume of the vehicle was administered. One hour after MCA occlusion, regional cerebral blood flow (rCBF) was measured using the 14C-iodoantipyrine autoradiographic technique. Microscopic arterial and venous oxygen saturations were determined using microspectrophotometry. In the cortex contralateral to MCA occlusion, the average rCBF and the average O2 consumption were lower in the GYKI Group than in the Control Group (rCBF: GYKI 65.5 +/- 24.1 ml 100 g-1 min-1, Control 97.7 +/- 33.4 ml 100 g-1 min-1; O2 consumption: GYKI 3.9 +/- 1.2 ml O2 100 g-1 min-1, Control 6.2 +/- 2.5 ml O2 100 g-1 min-1) without a significant difference in the number of veins with SvO2 < 50%. In the ischemic cortex, the number of veins with SvO2 < 50% was significantly smaller in the GYKI Group (21 veins out of 63) than in the Control Group (45 out of 59) without a significant difference in the average rCBF (GYKI 44.9 +/- 17.7, Control 29.7 +/- 10.4) or regional O2 consumption between these two groups (GYKI 3.3 +/- 1.4, Control 2.7 +/- 1.2). Our data demonstrated that GYKI 52466 was effective in improving microscopic O2 balance in the focal ischemic cortical area of the brain and it decreased O2 consumption in the non-ischemic cortex.     

The novel dihydronaphthyridine Ca2+ channel blocker CI-951 improves CBF, brain pHi, and EEG recovery in focal cerebral ischemia

The effects of the novel dihydronaphthyridine Ca2+ antagonist CI-951 on focal cerebral ischemia were assessed during MCA occlusion in 30 white New Zealand rabbits under 1.0% halothane anesthesia. In vivo brain pHi and focal CBF were measured with umbelliferone fluorescence. Baseline normocapnic brain pHi and CBF were 7.02 +/- 0.02 and 48.4 +/- 2.9 ml/100 g/min, respectively. In the severe ischemic regions, 15 min postocclusion brain pHi and CBF were 6.62 +/- 0.04 and 14.4 +/- 0.7 ml/100 g/min in controls vs. 6.60 +/- 0.02 and 12.9 +/- 2.3 ml/100 g/min, respectively, in animals destined to receive CI-951. Twenty minutes after MCA occlusion, CI-951 was administered at 0.5 microgram/kg/min and brain pHi and CBF were determined in both regions of severe and moderate ischemia for 4 h postocclusion. Control severe ischemic sites demonstrated no significant improvement in brain pHi and only mild increases in CBF over the next 4 h. CI-951 caused significant improvement in both of these parameters. Postocclusion 4 h brain pHi and CBF measured 6.69 +/- 0.04 and 18.5 +/- 3.2 ml/100 g/min in controls vs. 7.01 +/- 0.04 and 41.7 +/- 5.3 ml/100 g/min, respectively, in CI-951 animals (p less than 0.001). Similar improvements were observed in moderate ischemic sites. In animals that demonstrated postocclusion EEG attenuation, 75% of CI-951 animals had EEG recovery as compared to 18% in controls. CI-951 may be a useful therapeutic agent for focal cerebral ischemia if histological and outcome studies verify these data.     

Pathophysiological studies in moyamoya disease by rCBF and cortical artery pressure measurements in comparison to those in ICA or MCA occlusion

The authors measured preoperative rCBF and intraoperative cortical artery pressure (CAP) during STA-MCA anastomosis to investigate cerebral hemodynamics in moyamoya disease. Six of 13 patients including 3 children showed ischemic attack and the remaining presented hemorrhagic attack. rCBF was measured by single photon ECT with Xe-133 inhalation technique. CAP's and rCBF's in moyamoya disease were compared to those in the 22 internal carotid artery (ICA) and 8 middle cerebral artery (MCA) occlusion. Systemic arterial blood pressure (SABP) was obtained at the radial artery. Mean rCBF in the MCA territory in moyamoya disease, ICA occlusion, and MCA occlusion were 39, 37, and 33 ml/100 g/min respectively. Mean SABP and CAP in moyamoya disease were 103 and 28 mmHg, respectively. In ICA occlusion, mean SABP and CAP were 98 and 45 mmHg, respectively. In MCA occlusion, mean SABP and CAP were 89 and 36 mmHg, respectively. To clarify the hemodynamics, vascular resistance was obtained from the following equations: The proximal vascular resistance (Rp), which was produced from the cervical ICA to cortical artery, was obtained by (mean SABP - mean CAP)/(rCBF). And distal vascular resistance (Rd) which was produced from the cortical artery to jugular vein, was obtained by (mean CAP)/(rCBF). Mean Rp in moyamoya disease ICA occlusion and MCA occlusion were 2.01, 1.21 and 1.70, respectively. Rd in moyamoya disease, ICA occlusion and MCA occlusion were 0.79, 1.37 and 1.22, respectively. There were significant differences in Rp and Rd between moyamoya disease and ICA or MCA occlusion. In ischemic group in moyamoya disease, rCBF, SABP, CAP, Rp and Rd were 41 ml/100 g/min, 111 mmHg, 28 mmHg, 1.92 and 0.70, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of experimental ischaemia on the direct cortical response of the motor cortex in primates

We studied the changes in amplitude of the first short latency positive potential (2.3 +/- 0.3 msec, mean +/- S.D.) of the direct cortical response (DCR) elicited by surface electrical stimulation of the motor cortex in anaesthetised baboons. Local cortical blood flow, measured by the hydrogen clearance method, was progressively reduced by acute middle cerebral artery occlusion and subsequent hypotension and was related to the amplitude of this potential. With flow levels greater than 25 ml/100 g/min the DCR was essentially unaffected, but it was lost with flows below 20 ml/100 g/min. These results indicate a threshold relationship between the generation of the electrical activity evoked in the cortical elements and local cortical flow, similar to that previously demonstrated for cortical somatosensory evoked potentials.