Responses of Cerebral Blood Flow Regulation to Activation of the Primary Somatosensory Cortex During Electrical Stimulation of the Forearm

Ichimi, Kazuyoshi; Kuchiwaki, Hiroji; Inao, Suguru; Shibayama, Mikine; Yoshida, Jun

doi:10.1007/978-3-7091-6837-0_90

Cited by 3 publications

(4 citation statements)

References 3 publications

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“…Ischemic changes are found in the brains of patients who died at various time intervals starting 10 minutes after SAH [8]. Experimental studies demonstrate that brain cells express stress signals such as the immediate early genes c-jun and c-fos, hemeoxygenase-1, and heat shock protein within minutes to hours after SAH [10, 12]. Cells expressing stress signals after SAH include neurons, glia and endothelium [10, 12].…”

mentioning

confidence: 99%

“…Experimental studies demonstrate that brain cells express stress signals such as the immediate early genes c-jun and c-fos, hemeoxygenase-1, and heat shock protein within minutes to hours after SAH [10, 12]. Cells expressing stress signals after SAH include neurons, glia and endothelium [10, 12]. Death of brain cells is found 24 hours after SAH and involves apoptosis, necrosis and autophagy [3, 14, 16, 26].…”

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confidence: 99%

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Cell death starts early after subarachnoid hemorrhage

Friedrich

Flores²,

Sehba

2012

Neuroscience Letters

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Brain injury begins early after aneurysmal subarachnoid hemorrhage (SAH). Although cell death via apoptosis and necrosis is known to be present in brain 24 hours after SAH, it is not known how soon after SAH cell death begins. We have previously described structural changes in rat brain microvessels 10 minutes after induction of SAH by endovascular puncture. This study examined brain for evidence of cell death beginning 10 minutes after induction of SAH. Cleaved caspase-3 (cl-caspase-3) staining was evident in vascular and parenchymal cells at 10 minutes after SAH and was significantly greater than in time-matched, sham-operated controls. The number of cl-caspase-3 positive cells was increased further at 24 hour after SAH. TUNEL assay revealed apoptotic cells present at 10 minutes, with substantially more at 24 hours after SAH. Scattered Fluoro-Jade positive neurons appeared at 1 hour after SAH and their number increased with time. At 1 hour Fluoro-Jade positive neurons were present in cortical and subcortical regions but not in hippocampus; at 24 hours they were also present in hippocampus and were significantly greater in the hemisphere ipsilateral to the vascular puncture. No Fluoro-Jade staining was present in shams. These data demonstrate an early activation of endothelial and parenchymal cells apoptosis and neuronal necrosis after SAH and identifies endpoints that can be targeted to reduce early brain injury after SAH.

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confidence: 99%

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confidence: 99%

Cell death starts early after subarachnoid hemorrhage

Friedrich

Flores²,

Sehba

2012

Neuroscience Letters

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“…Similarly, a microballoon inserted into the ventral posterolateral nucleus of the thalamus in cat caused a rapid reduction in CBF following gradual balloon inflation. 60 AuTologous wHole blood InjeCTIon models Anatomically localised haematomas may be realised by this method without artificial agents. 48 49 61 Except for needle insertion, autologous blood injection may closely mimic clinical ICH.…”

Section: Microballoon Insertion Modelsmentioning

confidence: 99%

Intracerebral haemorrhage: from clinical settings to animal models

et al. 2020

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Spontaneous intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity and for which no effective treatments are available to date. Much experimental and clinical research have been performed to explore its mechanisms regard the subsequent inflammatory cascade and to seek the potential therapeutic strategies. The aim of this review is to discuss insights from clinical settings that have led to the development of numerous animal models of ICH. Some of the current and future challenges for clinicians to understand ICH are also surveyed.

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“…Unlike many other studies on the role of sensory nuclei of the thalamus in sensation, we did not use simple sensory stimuli like median nerve or finger electrical stimulation [5,6,[8][9][10][11], but relied on more cognitive tasks to test the patients' performance under thalamic stimulation. Moreover, the stimuli were designed so that the subjects could not use a three-dimensional shape and could not use stereognosis, but had to rely mostly on fine touch.…”

Section: Discussionmentioning

confidence: 99%

Tactile Discrimination Task Not Disturbed by Thalamic Stimulation

Abbassian¹,

Shahzadi

Afraz³

et al. 2001

Stereotact Funct Neurosurg

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The major pathway of human somatosensation passes through the ventrocaudal nucleus (Vc) of the thalamus. We tested the effect of direct electrical stimulation of the Vc on tactile discrimination in 5 Parkinson patients undergoing stereotactic thalamotomy. Raised gratings with lines 3, 4, or 6 mm apart were used. Patients had to actively touch test patterns placed in the hand contralateral to the thalamus under operation and compare it with a reference 3-mm grating held continuously in their other hand. Their performance was best for 6-mm, followed by 3-mm and then by 4-mm patterns regardless of electrical stimulation. Under Vc stimulation, patients recognized the 4-mm gratings slightly better. This can be explained either by the nature of thalamocortical interaction, which makes it resistant to external noise, or by the involvement of other pathways that circumvent the effect of thalamic stimulation.

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Responses of Cerebral Blood Flow Regulation to Activation of the Primary Somatosensory Cortex During Electrical Stimulation of the Forearm

Cited by 3 publications

References 3 publications

Cell death starts early after subarachnoid hemorrhage

Cell death starts early after subarachnoid hemorrhage

Intracerebral haemorrhage: from clinical settings to animal models

Tactile Discrimination Task Not Disturbed by Thalamic Stimulation

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