Functional impairment due to white matter ischemia after middle cerebral artery occlusion in cats

We recorded regional cerebral blood flow, somatosensory evoked potentials, and auditory evoked potentials in the thalamic relay nuclei (ventral posterior lateral nucleus and medial geniculate body) and in the somatosensory and auditory cortices during and after 1 hour of transient left middle cerebral artery occlusion in nine cats. Regional cerebral blood flow was also measured in the thalamocortical tracts of five of these cats. Additionally, the integrity of thalamocortical connections was tested by retrograde labeling of the thalamic nuclei with horseradish peroxidase in eight cats (three of which experienced no ischemia). Regional cerebral blood flow was severely reduced during middle cerebral artery occlusion in the left primary auditory cortex (8.5 ml/100 g/min) and in white matter pathways (6.4-7.6 ml/100 g/min). In contrast, regional cerebral blood flow did not change significantly in the somatosensory cortex or in either thalamic nucleus. Evoked potentials were abolished in both cortices but remained unchanged in the thalamic nuclei. Cortical somatosensory evoked potentials disappeared 5-8 minutes later than auditory evoked potentials. Recirculation after 1 hour of ischemia resulted in rapid and almost complete recovery (94%) of somatosensory evoked potentials and little recovery (18.4%) of auditory evoked potentials. We conclude that in the auditory pathway both cortical and fiber tract ischemia are (perhaps synergistically) responsible for dysfunction, while in the somatosensory cortex evoked potentials are abolished due to white matter ischemia. The delayed disappearance and better recovery of somatosensory than of auditory evoked potentials indicate that ischemic tolerance is higher in fiber tracts than in cortex.     

Deafferentation versus cortical ischemia in a rabbit model of middle cerebral artery occlusion

A two-site middle cerebral artery occlusion model in rabbits was developed. Platinum electrodes served for simultaneous recordings of regional cerebral blood flow, auditory evoked potentials, and electroencephalogram in the left and right auditory cortex and in the left medial geniculate body. Auditory evoked potentials and regional cerebral blood flow were also recorded in the subcortical white matter, and regional cerebral blood flow was recorded in the internal capsule. Distal segment occlusion of the middle cerebral artery caused severe cortical ischemia in four of 11 rabbits (Group I), accompanied by abolition of the auditory evoked potential in the left auditory cortex and white matter and severe reduction of the left electrocorticogram. Deep subcortical regions were affected either little or not at all. In the remaining seven rabbits (Group II) with only mild disturbance of cortical perfusion after distal middle cerebral artery occlusion, additional clamping of the proximal middle cerebral artery stem reduced thalamocortical tract blood flow and abolished cortical auditory evoked potentials. Spontaneous electrocorticogram was less affected in Group II than in Group I; thalamic regional cerebral blood flow and auditory evoked potentials were not altered. Histologically, ischemic lesions predominated in the cortex of Group I and in the subcortical structures of Group II rabbits. While correlated reductions in regional cerebral blood flow and auditory evoked potentials indicate effective cortical ischemia, the impairment of auditory evoked potentials in Group II rabbits must be due to cortical deafferentation by ischemia in the afferent tract. This model permits the investigation of the effects of predominantly cortical or subcortical ischemia in one functional system.     

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)     

Differences in ischemia-induced accumulation of amino acids in the cat cortex

It is well established that excitatory amino acid neurotransmitters are extensively liberated during ischemia and that they have neurotoxic properties contributing to neuronal injury. To study changes in the liberation of excitatory and other amino acids during cerebral ischemia, we measured their extracellular concentrations and related them to blood flow levels and electrophysiologic activity (electrocorticogram and auditory evoked potentials) before and for up to 2 hours after multiple cerebral vessel occlusion in 14 anesthetized cats. Blood flow levels between 0 and 43 ml/100 g/min were reached. Concentrations of the excitatory amino acid neurotransmitters increased most (aspartate 10-fold, glutamate 30-fold, and gamma-aminobutyric acid 300-fold compared with control values) below a blood flow threshold of 20 ml/100 g/min. The total power of the electrocorticogram and the amplitude of the auditory evoked potentials were affected below the same blood flow threshold. In contrast, concentrations of the nontransmitter amino acids taurine, alanine, asparagine, serine, and glutamine increased 1.5-5-fold as blood flow decreased, while concentrations of the essential amino acids phenylalanine, valine, leucine, and isoleucine did not change during cerebral ischemia. The great increases in concentrations of the excitatory amino acid neurotransmitters below a blood flow threshold close to that for functional disturbance is in accordance with the role of these amino acids in ischemic cell damage. Their release at blood flow levels compatible with cell survival and the increase in their concentrations with severity and duration of cerebral ischemia imply that excitotoxic antagonists may have potential as therapeutic agents.     

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.     

Experimental study of brain stem infarction in dogs--effect on BAEP, SSEP, blink reflex and EEG of perforator occlusion

Assessment of the lesion in the brain stem by evoked potentials has not been well established. We have already developed a model of brain stem ischemia by occluding the perforators of the posterior cerebral arteries of the dog. The ischemic lesions locates mainly in the ventral side of the midbrain. Using this model, we assessed brain stem function by brain stem auditory evoked potential (BAEP), surface- and depth-recorded (in medial lemniscus) short latency somatosensory evoked potential (SSEP), blink reflex (BR) and electroencephalography (EEG), and investigated the correlation between the electrophysiological abnormalities and the lesion in the brain stem. The studies were performed for 6 hours after perforator occlusion. Furthermore, depth-recorded SSEP and regional cerebral blood flow (rCBF) were measured under induced hypotension by withdrawal of arterial blood. BAEP did not change in 13 of 16 animals. Surface-recorded SSEP remained unchanged in all 6 animals. The results are probably due to the fact that the lesion does not involve the auditory and somatosensory pathways and the accompanying events such as edema does not affect the both pathways. Depth-recorded SSEP remained unchanged after occlusion and did not disappear even when rCBF fell below 10 ml/100 g/min. It may be suggested that the threshold for electrical failure in the brain stem is much lower than that in the cortex. In BR, R1 did not change but ipsilateral R2 became nearly invisible immediately after perforator occlusion in all animals. The fact that the ischemic lesion did not involve the pons and disturbed reticular formation in the midbrain may probably account for the remaining of R1 and the disappearance of ipsilateral R2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Delayed recovery of auditory cortical evoked potentials is correlated with cortical neuronal death after transient cerebral ischemia in awake gerbils

Early detection of irreversible neuronal change after transient cerebral ischemia is important so that adequate treatment can be initiated within the therapeutic window. We have examined the correlation between changes in middle-latency auditory evoked potentials (MAEPs) and histological changes in the auditory cortex of awake Mongolian gerbils subjected to 4 min or 12 min of transient cerebral ischemia. Post-ischemic MAEPs were characterized by the appearance of a markedly large negative and positive component at approximately 17–22 ms latency in both groups. Delay in the appearance of the high amplitude (maximal amplitude at 45 min after recirculation in the 12-min ischemia group) precedes the slowly developing death of neurons in the auditory cortex that results from transient cerebral ischemia.     

Effect of intravenous administration of diltiazem on cerebral blood flow and brain function

The effect of intravenous administration of diltiazem on cerebral circulation and brain function were studied in animals. Diltiazem, at a dose of 150 micrograms/kg BW, was administered intravenously over a period of 5 minutes beginning 30 minutes after ligation of the right brachiocephalic artery in 9 cats in order to investigate its effects in the acute stage of cerebral ischemia. In 5 animals, mean arterial blood pressure was recorded and blood flow in the basilar artery was measured transdurally by use of an ultrasonic Doppler flow-meter. Mean arterial blood pressure began to elevate immediately after ligation of the right brachiocephalic artery, but the degree of elevation was minimal. It began to fall during diltiazem injection and returned to the preadministration value 30 minutes after injection. Basilar artery flow decreased slightly during injection of diltiazem, but began to increase after completion of injection. The increase relative to the preadministration value was 62 +/- 31% 10 minutes after injection, 88 +/- 38% 20 minutes after, and 24 +/- 53% 30 minutes after. The short latency somatosensory evoked potentials (short latency SEP) recorded in the other 2 animals showed no noticeable change either in amplitude or latency during the same procedures. In 1 of 2 animals in which brainstem auditory evoked potentials (BAEP) were monitored, the latency of peak IV increased after ligation of the right brachiocephalic artery, and decreased 20 minutes after injection of diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)     

Polysensory evoked potentials in rat parietotemporal cortex: combined auditory and somatosensory responses

A 64 channel microelectrode array was used to map auditory evoked potentials (AEP), somatosensory evoked potentials (SEP) as well as combined auditory and somatosensory evoked potentials (ASEP) from a 7 × mm² area in rat parietotemporal neocortex. Cytochrome oxidase (CO) stained sections of layer IV were obtained in the same animals to provide anatomical information underlying epicortical field potentials. Epicortical responses evoked by click or vibrissa stimuli replicated earlier findings from our laboratory, and appeared as a family of waveforms centered on primary auditory (AI) or somatosensory (SI) cortical areas as determined from CO histology. Selective microinjections of HRP to AI and SI further confirmed their specific sensory relay nuclei in the thalamus. A small polysensory area between AI and SI, responded uniquely with an enhanced negative sharp wave to combined auditory and somatosensory stimuli. HRP retrograde labeling revealed that the thalamocortical projections to this area were from the posterior nuclear group (Po) and medial division of the medial geniculate (MGm). These data establish close relationships between epicortical AEP, SEP, and especially ASEP and corresponding cortical structures and thalamocortical projections. The neurogenesis of unimodal and polysensory evoked potentials is discussed in terms of specific and non-specific systems.     

支架置入术对椎基底动脉系统短暂性脑缺血发作患者诱发电位的影响

目的 观察支架置入术能否改善椎基底动脉系统短暂性脑缺血发作（TIA）患者的亚临床症状。方法 11例症状性椎基底动脉狭窄的椎基底动脉系统TIA患者,支架置入术前后分别检测体感诱发电位（SEP）、脑干听觉诱发电位（BAEP）、视觉诱发电位（VEP）,记录各诱发电位的潜伏期及波幅。结果 （1）术前诱发电位均异常,主要表现为SEP N20及P40潜伏期异常,BAEPⅠ、Ⅲ、Ⅴ波潜伏期延长,VEP P100潜伏期延长。（2）与术前相比,术后1周BAEP表现为Ⅰ～Ⅲ波潜伏期缩短（P =0.046）、Ⅲ波幅升高（P =0.05）;SEP表现为N20潜伏期缩短（P =0.012）,N13～N20间期缩短（P =0.013）,P14～N20间期缩短（P =0.005）;VEP表现为 P100潜伏期缩短（P =0.022）。结论 支架置入术后,椎基底动脉系统TIA患者的SEP、BAEP、VEP好转,提示患者的亚临床症状恢复。     

Changes in subcortical visual and auditory evoked potentials following amygdaloid kindling in cats

In this study we dealt with the changes in visual and auditory evoked potentials following kindling, to reveal the distant effects of epileptic activity. The experiments were performed using cats. Visual and auditory evoked potentials were obtained initially. Daily stimulation of 60 Hz (rectangular wave, 1 ms in duration, 500 microA in peak current, 2-s train) was given to the right amygdala, for kindling. After the completion of kindling, evoked responses were recorded again. In the auditory system the changes of responses in the cortex, medial geniculate nucleus, and cochlear nucleus were distinguished. The changes of potentials in the subcortex were larger than those at the cortical level. For visual evoked potentials there was a discrepancy between stimulation with light and electrical stimulation of the optic chiasm. There was no significant change in amplitude of visual evoked potentials by flash. In the case of optic chiasm stimulation, an enlargement of evoked responses was obtained. These results indicate modality-specific change of the auditory system and widespread subcortical change. These results might be caused by some vulnerability of the auditory system in the case of amygdaloid kindling, as a result of the epileptogenic process.     

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.     

Selective regulation of thalamic sensory relay nuclei by nucleus reticularis thalami.

Stimulation in the segment of nucleus reticularis thalami adjacent to the lateral geniculate body (RLG), abolished visual evoked potentials for up to 150 msec. Both photic stimulation in the contralateral visual field and electric stimulation in the ipsilateral optic tract elicited primary cortical responses that were markedly reduced or abolished by prior conditioning stimulation in RLG. Stimulation of the segments of nucleus reticularis thalami adjacent to the medial geniculate (RMG) or the ventrobasal complex (RVBC) had the effect of markedly reducing or abolishing unilaterally projected primary evoked responses in the auditory and cutaneous systems, respectively. Only the sensory evoked potentials mediated by the relay nucleus adjacent to the region of R stimulated were affected. The reduction of the cortical evoked potentials was not due to the processes underlying the cortical recovery cycle, because conditioning stimulation on either side of RLG stimulated the primary geniculocortical fibers, but had a minimal or no effect on the visual test evoked response. These results suggest that R functions as a topographically organized inhibitory gate which can regulate the patterns of sensory input from the thalamus to the cortex. The regulatory effects on R by the mesencephalic reticular formation and the mediothalamic-frontocortical system may mediate both generalized and selective control of cortical sensory evoked potentials.     

Middle- and long-latency auditory evoked responses recorded from the vertex of normal and chronically lesioned cats

A prolonged sequence of auditory evoked potentials with latencies ranging from 1 to 250 msec was recorded from the vertex of the awake restrained cat. This sequence was reproduceable within and across subjects and was not altered by complete neuromuscular paralysis. The effects of click rate, pentobarbital, and chronic lesions of a number of different brain areas were evaluated for each of the potentials. Vertex waves 1–5, previously shown to originate from generators in the primary auditory pathway of the brain stem, were followed by smaller and less well defined waves 6 and 7, with peak latencies in the 6–8 msec and 10–12 msec range respectively. These potentials were not abolished by fast click rates (i.e. up to 50/sec) nor by moderate levels of pentobarbital. Correlative extra- and intracranial studies indicated that wave 6 occurred in the same latency range as the medial geniculate body, pars principalis potential, and that wave 7 occurred in the same latency range as the primary ectosylvian cortical potential. The intracranial potentials showed click recovery functions and barbiturate resistance which were similar to those of waves 6 and 7, and wave 7 disappeared following aspiration of ectosylvian cortex. These data suggest that waves 6 and 7 reflec generators in medial geniculate body and ectosylvian gyrus.In contrast to the stability of potentials 1 through 7, the longer latency waves were relatively unstable. Wave A occurred in a latency range of 17–25 msec, wave B, 35–45 msec, wave C, 50–75 msec, and wave D, 150–200 msec. All of these waves showed marked amplitude fluctuations, disappeared as click rates increased to 10/sec, and were abolished by moderate levels of pentobarbital. After bilateral aspiration of middle suprasylvian gyrus, ectosylvian gyrus, or frontal lobes, wave A continued to appear. After hemispherectomy, which removed all cortex, basal ganglia and limbic lobes, wave A was not abolished and appeared enhanced in one animal. Thus, the generator system of wave A appears to be largely independent of auditory cortex and adjacent association cortex, but may be modulated by other forebrain systems. Wave C continued to appear after aspiration of suprasylvian and ectosylvian gyri and after frontal lobectomy, but disappeared after hemispherectomy. Thus, wave C reflects a generator system which differs from that of wave A, but which also appears to be largely independent of the primary geniculo-cortical auditory pathway.These data suggest the following conclusions: waves 1 through 7, which show high fidelity, rate-resistant, barbiturate-insensitive acoustic transmission, appear to reflect activation of the primary auditory system from acoustic nerve to auditory cortex. Subsequent, longer-latency vertex potentials seem to be generated through other forebrain systems which receive auditory information in parallel from the brain stem, rather than serially from the primary geniculo-cortical pathway and association cortex relays. The relevance of data in the cat model to the human vertex potentials is discussed.     

Analysis of central nervous system involvement in the microwave auditory effect

Nine cats were prepared for the recording of potentials in 3 brain sites evoked by acoustic and microwave stimuli. Loci in which potentials were observed were eighth cranial nerve, medial geniculate nucleus and primary auditory cortex. The effect of cochlear disablement on these potentials was evaluated.Potentials at all sites were abolished by cochlear damage. There were no differences between acoustic and microwave stimuli in this regard. Data are interpreted as supporting the contention that the microwave auditory effect is mediated at the periphery as are the effects of conventional acoustic stimuli.     

Somatosensory evoked potentials in rat cerebral cortex before and after middle cerebral artery occlusion

We recorded somatosensory evoked potentials in pentobarbital-anesthetized rats before and after middle cerebral artery occlusion. Trigeminal (vibrissae), median (forelimb), and sciatic (hind limb) nerve stimuli produced consistent, robust, and sharply localized responses in the trigeminal, forelimb, and hind limb regions of the somatosensory cortex of 18 rats. These regions are situated at sequentially greater distances from the center of infarcts produced by middle cerebral artery occlusion. In eight rats, occlusion 1-2 mm below the rhinal fissure abolished somatosensory evoked potentials in all three cortical region within minutes. Positive wavelets preceding the primary cortical response were also diminished by the occlusion, suggesting that ischemia affected the thalamocortical white matter. Four of these eight rats did not show histologically apparent ischemic involvement of the hind limb cortical region at 3 hours after occlusion; sciatic nerve evoked potentials recovered substantially in all four rats, and the amplitudes exceeded baseline (129 +/- 30% at 1 hour, 173 +/- 33% at 3 hours) in three of the four rats. Three of the eight rats did not have gross ischemic involvement of the forelimb cortical region; median nerve evoked potentials recovered fully in all eight rats, but the amplitudes did not exceed baseline. All eight rats had evidence of ischemic damage in the trigeminal cortex; no rat showed full recovery in this region, and all but one had trigeminal evoked potentials that were less than 20% of baseline amplitudes by 3 hours after occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ischemia changes and tolerance ratio of evoked potential monitoring in intracranial aneurysm surgery

Objective

We assessed the relationship between cerebral ischemia-induced changes in evoked potentials and the degree of ischemia tolerance.

Methods

47 patients underwent somatosensory evoked potential (SEP) and motor evoked potential (MEP) monitoring in intracranial aneurysm surgery. Three duration parameters (time) were recorded: Time 1, from the starting of temporary occlusion unavoidable in aneurysm surgery to the time the evoked potentials decrease from basal level to reaching the warning criterion; Time 2, from evoked potentials reaching the warning criterion to the time the blood flow was resumed; Time 3, after resuming the blood flow, the time it took the evoked potentials to recover to baseline. All three times can be reliably calculated in the SEP recording, but not in the MEP recording which consisted of either unchanged amplitudes or abruptly changing amplitudes, making it impossible to obtain Time 1. The ischemic tolerance ratio (ITR) was calculated as ITR = time 2/time 1 × 100%. New decreasing myodynamia and fresh infarction after the surgery were employed for evaluating neurological deficits postoperatively, and their correlations with the ischemia-induced changes of evoked potentials recorded during the surgery were analyzed.

Results

We found a change in SEPs in 12 patients whose cerebral ischemia was induced by temporary occlusion of the aneurysm's parent artery. We also found the development of postoperative neurological deficits in 4 patients whose ischemic tolerance ratio (ITR) reached over 80%, while no deficits were found in the other 8 patients whose ITR was less than 50%. MEP changes were seen in 4 patients whose cerebral ischemia was caused by accidentally clamping the perforating branches, causing the development of postoperative neurological deficits but not necessarily leading to significant SEP changes.

Conclusion

The Ischemia tolerance ratio (ITR) in SEP recordings is valuable to predicting postoperative neurological deficits caused by temporary occlusion of aneurysm's parent artery. Maintaining the ITR under 50% during operation can effectively avoid postoperative neurological deficits, while an ITR above 80% reliably forecasts postoperative neurological deficits. Complementary to SEPs, MEP recordings are particularly valuable in monitoring ischemic effects caused by accidentally clamping perforating branches. Taken together, this system of monitoring makes it possible to promptly adjust surgery procedures and minimize postoperative neurological deficits.     

Short latency somatosensory evoked potentials in patients with neurological lesions

Short latency somatosensory potentials following median nerve stimulation were recorded in patients grouped according to anatomic location of neurological lesion. Patients with cerebral lesions causing severe sensory deficit lacked a major positive wave of cortical origin that in normal subjects peaked at a mean latency of 20.5 ms. Patients with severe cervical spinal cord disease lacked all of the normal somatosensory response except for the earliest component attributed to peripheral nerve activity. Patients with brain-stem lesions showed delayed latencies of later waves and prolonged interwave latencies. However, auditory evoked potentials measured in the group with brain-stem lesions were more helpful in localization. Analysis of short latency somatosensory potentials can discriminate between peripheral nerve, spinal cord, brain-stem, and cerebral lesions. Further experience and refinement of technique of measurement should increase the value of this procedure.     

Consistency of cerebral blood flow and evoked potential alterations with reversible focal ischemia in cats

To enhance the consistency of the ischemic insult caused by reversible transorbital middle cerebral artery occlusion, we investigated the variability of somatosensory evoked potential amplitudes and regional cerebral blood flow in 26 anesthetized cats using four procedures to induce transient ischemia. These procedures included 60 minutes of left middle cerebral artery occlusion with or without left common carotid artery occlusion and 120 minutes of left middle cerebral artery occlusion with or without bilateral common carotid artery occlusion. Blood flow in the left middle cerebral artery territory was markedly and consistently reduced to less than 20 ml/min/100 g with simultaneous occlusion of the left middle cerebral artery and both common carotid arteries. The standard deviation of blood flow with this procedure (5.4) was less than that with the other three procedures (13-25). The amplitudes of ipsilateral somatosensory evoked potentials were decreased to approximately 20% of control during ischemia with all four procedures. During reperfusion, amplitudes recovered more slowly, to half of control, after both procedures involving 120 minutes of ischemia. After 120 minutes of reperfusion, the range of amplitudes was smallest in the group exposed to middle cerebral artery occlusion with bilateral common carotid artery occlusion. The degree of recovery of the somatosensory evoked potentials correlated with residual blood flow in both the ipsilateral middle cerebral artery territory and in the white matter during ischemia. We conclude that the most consistent model of focal ischemia and reperfusion in cats in which there is partial recovery of somatosensory evoked potentials is occlusion of one middle cerebral artery and both common carotid arteries for 120 minutes.     

Electrophysiologic recordings in a patient with a discrete unilateral thalamic infarction

The electroencephalogram, and somatosensory and auditory evoked potentials were recorded from a patient, who, at necropsy, showed a restricted unilateral thalmic infarct involving predominantly the anterior and lateral thalamus. The electroencephalogram showed distinct monomorphic delta activity and a suppression of the alpha rhythm over the side of the lesion. Short latency somatosensory evoked potentials were present bilaterally; mid-latency somatosensory evoked potentials were absent ipsilateral to the lesion. Both mid-latency and long latency auditory evoked potentials were normal.