Differential effects of hyperventillation on the excitability of intact and isolated cortex

Sherwin, Ira

doi:10.1016/0013-4694(65)90077-5

Cited by 21 publications

(16 citation statements)

References 17 publications

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“…Because cortical rhythmic activity arises from an interplay between thalamic relay cells with cells in the reticular nuclei and cortico-cortical reverberant loops [30, 31], the VEP changes we recorded after deep-breathing-induced HV could plausibly depend on thalamic neuronal hyperpolarization. This neural mechanism accords perfectly with early evidence that lesions involving the anterior pole of the thalamus (nucleus centralis lateralis) abolish the cortical response to HV [32, 33]. Another major brain nervous structure involved in HV-induced EEG changes is the reticular formation.…”

Section: Discussionsupporting

confidence: 87%

Changes in visual-evoked potential habituation induced by hyperventilation in migraine

et al. 2010

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Hyperventilation is often associated with stress, an established trigger factor for migraine. Between attacks, migraine is associated with a deficit in habituation to visual-evoked potentials (VEP) that worsens just before the attack. Hyperventilation slows electroencephalographic (EEG) activity and decreases the functional response in the occipital cortex during visual stimulation. The neural mechanisms underlying deficient-evoked potential habituation in migraineurs remain unclear. To find out whether hyperventilation alters VEP habituation, we recorded VEPs before and after experimentally induced hyperventilation lasting 3 min in 18 healthy subjects and 18 migraine patients between attacks. We measured VEP P100 amplitudes in six sequential blocks of 100 sweeps and habituation as the change in amplitude over the six blocks. In healthy subjects, hyperventilation decreased VEP amplitude in block 1 and abolished the normal VEP habituation. In migraine patients, hyperventilation further decreased the already low block 1 amplitude and worsened the interictal habituation deficit. Hyperventilation worsens the habituation deficit in migraineurs possibly by increasing dysrhythmia in the brainstem-thalamo-cortical network.

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Section: Discussionsupporting

confidence: 87%

Changes in visual-evoked potential habituation induced by hyperventilation in migraine

et al. 2010

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“…In the first study we discuss (Sherwin, 1965), Sherwin demonstrated that hyperventilating a cat elicits high amplitude, rhythmic slowing in the cortical EEG comparable to activity observed during HIHARS (Fig. 6).…”

Section: A Basic Modulation Of the Thalamusmentioning

confidence: 84%

“…Experiments performed by Ira Sherwin in the 1960s represent some of the few attempts to do so. Sherwin posed two key questions in his experiments: (1) what brain structures are recruited by hyperventilation to increase the occurrence of SWDs (Sherwin, 1965, 1967), and (2) do these structures possess a specific, element that is responsive to respiratory-induced changes in pH?…”

Section: A Basic Modulation Of the Thalamusmentioning

confidence: 99%

Out of thin air: Hyperventilation-triggered seizures

Salvati

Beenhakker

2019

Brain Research

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“…A simi¬ lar pattern of response to hyperventilation has been reported for a unilateral focus in the intact cortex compared to isolated cor¬ tex. 45 Hyperventilation markedly decreased the spontaneous activity of large blocks of isolated cerebral cortex.40 Whether this spike discharge enhancement effect of hyperventi¬ lation in the intact brain may be mediated by the nonspecific diffuse systems of thala¬ mus and brain stem45 would not be certain.…”

Section: Significant Regional Differences Were Evidentmentioning

confidence: 99%

Symmetrical Epileptogenic Foci in Monkey Cerebral Cortex

Marcus¹,

Watson²

1968

Arch Neurol

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WE HAVE previously reported the results of a series of experiments in the cat concerning the interaction of acute relatively large bilateral epileptogenic foci in homologous areas of cerebral cortex1,2 (predominantly posterior sigmoid and suprasylvian gyri). In the intact animal, this interaction often resulted in the rapid production of persistent synchronous and symmetrical patterns of bilateral discharge including 21/2 to 31/2 cycles per second (cps) spike-slow wave complexes. Relevant behavioral concomitants of these bilateral discharges resembled some of the clinical phenomena observed in patients with idiopathic petit mal or grand mal seizures during similar bilater-$ al discharges: bilateral facial muscle and forelimb myoclonus, transient suspension or imperfect continuation of a repetitive act, and occasional generalized convulsive seizures.Investigations of the underlying anatomical pathways involved in this interaction of bilateral cortical foci indicated the significant role of the corpus callosum. Synchrony of bilateral discharge failed to occur after total section of corpus callosum. On the other hand, depth recordings indicated little involvement of medial thalamic structures.Moreover, the production of bilateral foci in preparations in whom all diencephalic, ros¬ tral mesencephalic, and most of dorsal hippocampal structures had been ablated did result in these synchronous patterns of bilat¬ eral discharge. A similar interaction occurred in preparations in which large bilateral blocks of cerebral cortex had been isolated from subcortical structures but remained connected by the corpus callosum.From a clinical standpoint, it is evident that the bilateral discharges of the patient with petit mal seizures are not equally dis¬ tributed throughout all recording areas over¬ lying cerebral cortex. Thus the "larval" bi¬ lateral discharges of spike and slow waves occur most prominently in frontal central areas.3 From an anatomical standpoint, it is evident that any conclusions based on the cat brain may not be entirely applicable to all areas of human cerebral cortex in view of (1) the marked evolution of neocortical areas.3 From an anatomical standpoint, it is evident that any conclusions based on the cat brain may not be entirely applicable to all areas of human cerebral cortex in view of (1) the marked evolution of neocortical areas, particularly frontal lobes in the pri¬ mates, (2) phylogenetic differences in callosal, cortical, and subcortical projections pathways of various neocortical areas,46 and (3) the regional differences in density of callosal pathways which occur in primates.5

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Differential effects of hyperventillation on the excitability of intact and isolated cortex

Cited by 21 publications

References 17 publications

Changes in visual-evoked potential habituation induced by hyperventilation in migraine

Changes in visual-evoked potential habituation induced by hyperventilation in migraine

Out of thin air: Hyperventilation-triggered seizures

Symmetrical Epileptogenic Foci in Monkey Cerebral Cortex

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