Alteration of somatosensory evoked potentials in response to global ischemia

Lesnick, James E.; Michele, John J.; Simeone, Frederick A.; DeFeo, Steven; Welsh, Frank A.

doi:10.3171/jns.1984.60.3.0490

Cited by 84 publications

(26 citation statements)

References 14 publications

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“…Second, in some experimental models of global and focal ischemia in mature brain, loss of SEP correlated with reduction in blood :flow, high energy phosphates and edema in subcortical white matter tracts rather than in gray matter (7)(8)(9)(10)(11). Perinatal models of asphyxia often show histologic changes in white matter (41,42).…”

Section: Discussionmentioning

confidence: 99%

“…(Pediatr Res 37: 661-666, 1995) Abbreviation SEP, somatosensory evoked potential white matter conduction. With moderate forebrain ischemia, decreases in white matter blood flow and energy metabolism can precede those in gray matter and affect SEP (7,8). With focal cerebral ischemia, some regions of somatosensory cortex can have near-normal levels of blood flow but have depressed SEP associated with subcortical white matter ischemi a (9)(10)(11).…”

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confidence: 99%

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Somatosensory Evoked Potential and Brain Water Content in Post-Asphyxic Immature Piglets

et al. 1995

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Somatosensory Evoked Potential and Brain Water Content in Post-Asphyxic Immature Piglets

et al. 1995

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“…It corresponds to the early near-field potential previously designated P2-N2, P2-MN, or V and is thought to be generated in somatosensory cortical areas. 6 ' 830 ' 32 The comparable SEP in humans is probably the N20 or P20 potential. 30 In our study, the duration of SEP recording (20 milliseconds) was not long enough to observe later cortical peaks reported in the literature.…”

Section: Discussionmentioning

confidence: 99%

“…29 SEP's in the cat and in humans have been previously characterized. 6 ' 830 " 32 Several short latency far-field components (designated I-IV in cat, N12-N14 in man) are presumed to originate in peripheral nerve, spinal cord, brainstem and possibly cerebellum. 30 " 32 These peaks were not consistently identified in our cats or in other studies.…”

Section: Discussionmentioning

confidence: 99%

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

Steinberg¹,

Gelb²,

Lam³

et al. 1986

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SUMMARYIn 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 histologicai cerebral ischemia.Stroke 4 Recently, SEP's have been applied to canine and feline models to study cerebral ischemia.5 " 8 In an attempt to explore the relationship between evoked potentials and histologicai focal cerebral ischemia, we examined SEP's and ischemic neuronal changes in cats following unilateral middle cerebral artery occlusion. Material and MethodsFifteen adults cats (mean weight 3.2 kg) were studied. The anesthetic technique and method of SEP recording were identical during implantation of the occlusive device and the acute experiment. Anesthetic TechniqueEach animal was sedated with ketamine HC1 (30 mg/kg intraperitoneally) and atropine sulphate (0.2 mg intraperitoneally), intubated, paralyzed with gallamine triethiodide (0.3 mg/kg) and artifically ventilated with air and oxygen (FIO 2 0.6). Anesthesia was maintained with halothane (0.75-1.25%) adjusted to keep the blood pressure constant at approximately 120/80. A cephalic venous catheter was inserted and 0.9% saline infused at 4 ml/hr. A femoral arterial cut-down catheter was placed. Body temperature was measured with

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“…Cerebral blood flow (CBF) was measured by the hydrogen clearance technique. 21 Two holes Vie in. in diameter were drilled at midparietal bone, approximately 1 cm lateral to the sagittal suture on each side, for the placement of the platinum electrodes.…”

Section: Methodsmentioning

confidence: 99%

Comparison of intraluminally versus extraluminally administered nimodipine on serotonin-induced cerebral vascular responses in vitro and in situ.

Vinall¹,

Michele²,

Gordon³

et al. 1989

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The purpose of our study was to compare the ability of intraluminally and extraluminally administered nimodipine to inhibit serotonin-induced cerebral vascular responses in vitro and in situ. No difference was noted in the ability of nimodipine, whether administered intraluminally or extraluminally, to reduce the contractile response of extraluminally administered serotonin in a closed, pressurized, in vitro bovine middle cerebral artery preparation; histologic studies indicated that the tight endothelial junctions normally found in cerebral arteries remained intact in this preparation. In cats, pretreatment with nimodipine did not significantly reduce the ability of intracisternally injected serotonin to decrease cerebral blood flow; however, nimodipine did reduce the changes in cerebral artery diameter normally noted angiographically after serotonin injection. Although minor differences were noted between the intraluminal and extraluminal routes of administration of nimodipine in situ, in general the effects were comparable.

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Alteration of somatosensory evoked potentials in response to global ischemia

Cited by 84 publications

References 14 publications

Somatosensory Evoked Potential and Brain Water Content in Post-Asphyxic Immature Piglets

Somatosensory Evoked Potential and Brain Water Content in Post-Asphyxic Immature Piglets

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

Comparison of intraluminally versus extraluminally administered nimodipine on serotonin-induced cerebral vascular responses in vitro and in situ.

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