Acute thrombotic infarction suppresses metabolic activation of ipsilateral somatosensory cortex

Evidence for functional diaschisis

Myron Ginsberg, Y. Castella, W. Dalton Dietrich, B. D. Watson, R. Busto

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

To study the effects of focal infarction on the capacity for functional activation of an ipsilateral somatosensory system remote from the lesion, we produced a small thrombotic infarct in the left frontal pole of male Wistar rats by a photochemical method. Five days later, the awake, restrained rats received tactile stimulation of the large whiskers (vibrissae) of the right side of the face, while a double-label 14C-autoradiographic study of local CMR(glc) (lCMR(glc)) and local CBF (lCBF) was performed. Unlesioned and unstimulated animals served as controls. In rats without frontal infarct, vibrissae stimulation led to activation of lCMR(glc) in the three synaptic relay stations of the barrel-field pathway (ipsilateral trigeminal medullary nucleus, contralateral ventrobasal thalamus, and contralateral barrel-field cortex). The mean increment in lCMR(glc) was 42% in lamina IV of barrel-field cortex and 49% in ventrobasal thalamus. Normalized lCBF tended to increase in superficial cortical laminae. In unstimulated animals with frontal infarct, lCMR(glc) was reduced by 20-30% throughout the ipsilateral barrel-field cortex as well as other ipsilateral cortical regions, but not in ventrobasal thalamus or other subcortical areas. In animals with frontal infarct subjected to contralateral vibrissae stimulation, a remarkable suppression of activation was observed throughout the barrel-field cortex so that left-less-than-right hemispheral lCMR(glc) asymmetry persisted despite stimulation. The ventrobasal thalamus, similarly, failed to increment its lCMR(glc) with vibrissae stimulation, whereas activation of the trigeminal nucleus was not suppressed. Similar trends were observed in the normalized lCBF data. These observations, which establish that a small frontal infarct is capable of suppressing normal physiological activation in remote ipsilateral brain structures, may have important implications with respect to suppression and recovery of function in human ischemic stroke.

Original languageEnglish
Pages (from-to)329-341
Number of pages13
JournalJournal of Cerebral Blood Flow and Metabolism
Volume9
Issue number3
StatePublished - Jan 1 1989

Fingerprint

Vibrissae
Somatosensory Cortex
Infarction
Thalamus
Trigeminal Nuclei
Recovery of Function
Touch
Wistar Rats
Stroke
Metabolic Activation
Brain

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Neuroscience(all)

Cite this

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title = "Acute thrombotic infarction suppresses metabolic activation of ipsilateral somatosensory cortex: Evidence for functional diaschisis",
abstract = "To study the effects of focal infarction on the capacity for functional activation of an ipsilateral somatosensory system remote from the lesion, we produced a small thrombotic infarct in the left frontal pole of male Wistar rats by a photochemical method. Five days later, the awake, restrained rats received tactile stimulation of the large whiskers (vibrissae) of the right side of the face, while a double-label 14C-autoradiographic study of local CMR(glc) (lCMR(glc)) and local CBF (lCBF) was performed. Unlesioned and unstimulated animals served as controls. In rats without frontal infarct, vibrissae stimulation led to activation of lCMR(glc) in the three synaptic relay stations of the barrel-field pathway (ipsilateral trigeminal medullary nucleus, contralateral ventrobasal thalamus, and contralateral barrel-field cortex). The mean increment in lCMR(glc) was 42{\%} in lamina IV of barrel-field cortex and 49{\%} in ventrobasal thalamus. Normalized lCBF tended to increase in superficial cortical laminae. In unstimulated animals with frontal infarct, lCMR(glc) was reduced by 20-30{\%} throughout the ipsilateral barrel-field cortex as well as other ipsilateral cortical regions, but not in ventrobasal thalamus or other subcortical areas. In animals with frontal infarct subjected to contralateral vibrissae stimulation, a remarkable suppression of activation was observed throughout the barrel-field cortex so that left-less-than-right hemispheral lCMR(glc) asymmetry persisted despite stimulation. The ventrobasal thalamus, similarly, failed to increment its lCMR(glc) with vibrissae stimulation, whereas activation of the trigeminal nucleus was not suppressed. Similar trends were observed in the normalized lCBF data. These observations, which establish that a small frontal infarct is capable of suppressing normal physiological activation in remote ipsilateral brain structures, may have important implications with respect to suppression and recovery of function in human ischemic stroke.",
author = "Myron Ginsberg and Y. Castella and {Dalton Dietrich}, W. and Watson, {B. D.} and R. Busto",
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T1 - Acute thrombotic infarction suppresses metabolic activation of ipsilateral somatosensory cortex

T2 - Evidence for functional diaschisis

AU - Ginsberg, Myron

AU - Castella, Y.

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AU - Watson, B. D.

AU - Busto, R.

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N2 - To study the effects of focal infarction on the capacity for functional activation of an ipsilateral somatosensory system remote from the lesion, we produced a small thrombotic infarct in the left frontal pole of male Wistar rats by a photochemical method. Five days later, the awake, restrained rats received tactile stimulation of the large whiskers (vibrissae) of the right side of the face, while a double-label 14C-autoradiographic study of local CMR(glc) (lCMR(glc)) and local CBF (lCBF) was performed. Unlesioned and unstimulated animals served as controls. In rats without frontal infarct, vibrissae stimulation led to activation of lCMR(glc) in the three synaptic relay stations of the barrel-field pathway (ipsilateral trigeminal medullary nucleus, contralateral ventrobasal thalamus, and contralateral barrel-field cortex). The mean increment in lCMR(glc) was 42% in lamina IV of barrel-field cortex and 49% in ventrobasal thalamus. Normalized lCBF tended to increase in superficial cortical laminae. In unstimulated animals with frontal infarct, lCMR(glc) was reduced by 20-30% throughout the ipsilateral barrel-field cortex as well as other ipsilateral cortical regions, but not in ventrobasal thalamus or other subcortical areas. In animals with frontal infarct subjected to contralateral vibrissae stimulation, a remarkable suppression of activation was observed throughout the barrel-field cortex so that left-less-than-right hemispheral lCMR(glc) asymmetry persisted despite stimulation. The ventrobasal thalamus, similarly, failed to increment its lCMR(glc) with vibrissae stimulation, whereas activation of the trigeminal nucleus was not suppressed. Similar trends were observed in the normalized lCBF data. These observations, which establish that a small frontal infarct is capable of suppressing normal physiological activation in remote ipsilateral brain structures, may have important implications with respect to suppression and recovery of function in human ischemic stroke.

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