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L Symon

Publications and source records attributed to L Symon.

At least 289 records · Page 16Linked to original sources
PubMedDate not supplied

Changes in somatosensory evoked potentials following an experimental focal ischaemic lesion in thalamus.

Experiments have been performed to produce localized thalamic ischaemia in baboons anaesthetised with alpha-chloralose. Somatosensory evoked potentials to median nerve stimulation were recorded in the medial lemniscus, VPL of thalamus and the primary somatosensory cortex. Local blood flow was also recorded by the hydrogen clearance technique in these regions. The early potential recorded in thalamus has been shown to be generated from 3 sources: (i) a positivity generated outside the VPL, (ii) local wavelets, most likely from synaptic activity close to the recording electrode, and (iii) a local overall negativity. The first of these potentials alone remains after thalamic ischaemia. It arises below the level of the thalamus, being very likely generated by the afferent volley in the medial lemniscus, and is seen in the surface-recorded response as the early component P8 (corresponding to P15 in the human).

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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.

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PubMedDate not supplied

Early components of transcallosal responses in acute ischaemia of the corpus callosum.

In 8 baboons maintained under propofol anaesthesia, transcallosal evoked responses were recorded from the primary motor cortex following electrical stimulation of the contralateral homotopic cortical surface. The corpus callosum was made ischaemic by transorbital occlusion of the common anterior cerebral artery; blood flow (measured by the hydrogen clearance method) in the stimulating and recording regions was not significantly affected by this procedure. The transcallosal responses from the normally perfused brain contained early positive (P1) and negative (N1) components. As stepwise ischaemia was produced in the corpus callosum, the amplitude of P1 initially increased up to 150% of control and the peak latency of P1 was significantly prolonged. At flows below 8 ml/100 g/min the amplitude rapidly decreased. Wave form changes and flow threshold of N1 were similar to those of P1. These results suggest that measurement of early transcallosal responses could be useful clinically as monitors of the ischaemic level in anterior cerebral artery territory.

Acute Disease↗
PubMedDate not supplied

Ischemic brain edema following middle cerebral artery occlusion in baboons: relationship between regional cerebral water content and blood flow at 1 to 2 hours.

The relationship between increase in water content in ischemic brain and levels of regional blood flow has been studied in 11 primates. Flows were recorded using the method of hydrogen (2-minute) clearance, from a total of 128 electrodes in cortex and white matter, and a gradation of ischemia was produced by middle cerebral occlusion transorbitally. The flows were reduced in the area of densest ischemia from control levels of 12.0 +/- 12.0 ml/100g/min to 7.0 +/- 5.4 ml/100g/min, with lesser decreases over the remainder of the ischemic hemisphere. Water content was measured in cortex and white matter, in regions topographically related to those of flow measurements, by densitometric assessment using precalibrated kerosene/bromobenzine columns. The average water content of cortex in regions remote from ischemia was 797.4 +/- 5.8 mg/gm and in white matter 708.5 +/- 8.2 mg/gm. Significant increases in water content (comparing corresponding regions of the two hemispheres) of up to 11.4 +/- 7.5 mg/gm were demonstrated in the most ischemic cortical areas. A gradient of water increase was evident in the ischemic hemisphere, increases water content being greatest in the opercular zone and least in the parasagittal area. Significant differences in white matter water content between the 2 hemispheres were demonstrated only in the most densely ischemic areas in the current experiments where ischemia was limited to 93 +/- 20 mins in the 11 animals without reperfusion. The relationship between ischemic density and water content increase showed that significant increases in water content occurred in regions where terminal flows had been below 20 ml/100g/min, indicating that accumulation of water in ischemic brain begins at flow values comparable to those associated with the failure of synaptic transmission, higher than those associated with failure of the ionic pump of the cell. Possible pathophysiological mechanisms are discussed.

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Cerebral blood flow and edema following carotid occlusion in the gerbil.

A technique for measuring focal cerebral blood flow (CBF) and brain specific gravity (SG) in gerbils is described; CO2 reactivity and autoregulation were tested. The mean CBF was 29.5 +/- 4.5 ml/100 gm/min and brain SG 1.0500 +/- 0.0004. Unilateral carotid occlusion resulted in a reduction of flow to 12.8 +/- 5.8 ml/100 gm/min in the ipsilateral hemisphere with little change in the contraleteral hemisphere; there was also a decrease in brain SG. One hour after occlusion, brain edema, as judged by decreased SG, developed at CBF less than 20 ml/100 gm/min and reached maximal levels at 7 +/- 2 ml/100 gm/min. The amount of edema appeared to be related chiefly to the residual post-occlusion flow. With bilateral occlusion, CBF was close to zero and there was no change in SG, indicating that in the "no flow" situation, there is no edema.

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PubMedDate not supplied

Central conduction time in primate brain ischemia -- a study in baboons.

The relationship between central conduction time (CCT) and levels of regional blood flow were studied in 9 primates. Flows were recorded in both hemispheres using the method of hydrogen (2 min) clearance. The somatosensory evoked potentials were recorded over the contralateral cortex and the dorsal columns, following median nerve stimulation. The CCT, a measure of the brain's electrical conduction, was determined by the difference in latencies between N10, (the arrival of the afferent volley at the sensory cortex) and N7 (its arrival at the dorsal column). Ischemia was produced by transorbital occlusion of the right middle cerebral artery. In the acute ischemic phase within 5 minute of occlusion, there was a significant correlation between the change in CCT and the decrease in flow. In the later occlusive phase, the CCT was unaltered with flows above 15 ml/100g/min. Below that level smaller decreases in flow resulted in progressively larger changes in CCT until a flow was reached where the N10 disappeared or the entire cortex was electrically silent. Focal ischemia had no effect on the first positive deflection recorded from the cortex (P8) or the first negative peak response from the cervical region (N7). However, the latency of P8 was increased or it was absent with the introduction of hypotension, while N8 was unaltered. From our measurements, it appears that prolongation of CCT can be related to developing ischemia, and that the thresholds for change are not dissimilar to those already recorded for somatosensory evoked responses to the basis of amplitude alterations in the cortex. Below these levels, prolongation of CCT appears to bear a parametric relationship to alteration in blood flow. While the measurement displays only one of the many alterations which are induced by ischemia in the brain, its attraction lies in its simplicity and in the fact that it may be applied with relative ease in the clinical situation. Under these circumstances, it appears to be an adequately sensitive monitor of developing brain ischemia, and deserves further study.

Acute Disease↗
PubMedDate not supplied

Are prostaglandins involved in experimental ischemic edema in gerbils?

Sixty-five male gerbils, divided into 3 groups, were used in this study, in which focal brain specific gravity, taken as a measure of edema, was compared to the corresponding focal cerebral blood flow using the hydrogen washout technique. Extracranial unilateral or bilateral carotid ligation was performed and one hour later the animal was sacrificed. When focal blood flow was less than 20 ml/100 g/min, edema developed and increased with progressive ischemia, reaching maximal values at 5-7 ml/100 g/min. In the zero flow situation there was no edema. Pretreatment of the other 2 groups with indomethacin or dexamethasone, did not prevent edema formation at flows of 20-12 ml/200 g/min, but considerably reduced the edema previously noted at low flows (5-7 ml/100 g/min). The drugs did not affect the decreased flow in the ischemic area. We conclude that prostaglandins, released by membrane disruption, are involved in the development of ischemic edema.

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PubMedDate not supplied

Modulation of the pathophysiology of primate focal cerebral ischaemia by indomethacin.

The effect of indomethacin (3mg/kg IA) preloading on the pathophysiology of a model of acute cerebral ischaemia has been tested. Primates anaesthetised with alpha-chloralose were used. Indomethacin reduced basal blood flow by 39% and reduced CO2 reactivity by 71%. Water content changes of the cerebral cortex and relationships between blood flow and extracellular potassium (Ke), and calcium (Cae) activities have been measured. Indomethacin infusion did not effect the water content of the left side but there was more water in all regions of the right hemisphere which were rendered ischaemic. There water increases were significant for blood flows greater than 5ml/100g/min in exposed areas. There was a significant increase in the flow thresholds for change in Ke and Cae. Possible mechanisms for these changes have been discussed.

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