Transcorneal stimulation of trigeminal nerve afferents to increase cerebral blood flow in rats with cerebral vasospasm: a noninvasive method to activate the trigeminovascular reflex

Atalay, Başar; Bolay, Hayrünnisa; Dalkara, Turgay; Söylemezoğlu, Figen; Öge, Kamil; Özcan, Osman

doi:10.3171/jns.2002.97.5.1179

Cited by 33 publications

(31 citation statements)

References 22 publications

(34 reference statements)

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“…The cerebrovascular sensory nerves originate in the trigeminal ganglion (Mayberg, Langer, Zervas, & Moskowitz, 1981). The electrical stimulation of the trigeminal ganglion (or its branches) causes an increase in the cerebral blood flow (Atalay et al, 2002;Lambert, Goadsby, Zagami, & Duckworth, 1988;Suzuki et al, 1990). It has been reported that trigeminal stimulation may improve the cerebral ischemic conditions such as cerebrovasospasm (Arbit & DiResta, 1996;Gurelik et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Assessment of the Outcomes of Cerebral Blood Flow Measurements After Electrical Stimulation of Upper Right Incisor Tooth in Rabbits

Gültürk

Gedik

Develıoğlu

et al. 2009

International Journal of Neuroscience

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The cerebral vessels are innervated by sympathetic, parasympathetic, and sensory nerves. A sensory innervation of the cerebral vessels originating in the trigeminal ganglion has been described in a number of species by several investigations. It has been shown that the electrical stimulation of the trigeminal ganglion causes an increase of cerebral cortical blood flow (CCoBF). The aim of the present study was to determine the effects of dental electrical stimulation the CCoBF in rabbits. A stimulating electrode was located in the upper right incisor tooth of rabbits and trigeminal ganglion was stimulated orthodromically via the infraorbital nerve. Variations in the cortical CCoBF were evaluated by laser-Doppler flowmetry. In experiment group, CCoBF increased together with the beginning of electrical stimulation (5 V, 0.5-ms impulse duration, square-shaped, 10-Hz frequency). The right and left hemisphere CCoBF values of stimulation period at 15s, 30s, 45s, 60s, 75s, and 90s were significantly higher than those of baseline and 105 and 120s (p < 0.05). The maximum increase in right and left CCoBF was 15.6% and 15.1% respectively. In post-stimulation period, the right CCoBF decreased gradually and returned to the baseline values at 120 s. In experiment groups, the CCoBF values of right hemisphere were comparable that of left hemisphereL (p > 0.05). This study demonstrated that the electrical stimulation of the trigeminal nerve's infraorbital branch via dental pulp increases the cortical right and left CCoBF under physiological conditions.

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Section: Introductionmentioning

confidence: 99%

Assessment of the Outcomes of Cerebral Blood Flow Measurements After Electrical Stimulation of Upper Right Incisor Tooth in Rabbits

Gültürk

Gedik

Develıoğlu

et al. 2009

International Journal of Neuroscience

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“…Indeed, the trigeminal ganglion is central to the cardiovascular adjustments associated with the mammalian diving reflex upon cold-water facial immersion (19), and releases known potent vasodilators, namely, substance P (309). In animals, trigeminal stimulation increases CBF (23,168,220,243,382). Similarly in humans, stimulation of the trigeminal ganglion by local injection of glycerol (451) or by thermocoagulation (450) yields marked increases in CBF.…”

Section: Neurogenic Regulation Of Cerebral Blood Flowmentioning

confidence: 99%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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“…As well as nitrergic fibres, trigeminal sensory nerves that innervate pial vessels include a subpopulation of peptidergic fibres, some of which contain CCK, often co-localised with substance P or CGRP (Liu-Chen et al, 1985;O'Connor and van der Kooy, 1988). Antidromic activation of trigeminal afferents, either by stimulation of the trigeminal ganglion or via an axon reflex activated by stimulation of extracranial trigeminal sensory nerves, elicits vasodilatation in meningeal vessels (Atalay et al, 2002;Peitl et al, 2004). CCK released from trigeminovascular sensory nerve terminals could therefore contribute to this effect.…”

Section: Meningeal Vesselsmentioning

confidence: 98%

CCK as a modulator of cardiovascular function

Lovick

2009

Journal of Chemical Neuroanatomy

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Transcorneal stimulation of trigeminal nerve afferents to increase cerebral blood flow in rats with cerebral vasospasm: a noninvasive method to activate the trigeminovascular reflex

Abstract: Data from the present study demonstrate that transcorneal stimulation of trigeminal nerve endings induces vasodilation and a robust increase in CBF. The vasodilatory response of cerebral vessels to trigeminal activation is retained after SAH-induced vasospasm.

Cited by 33 publications

References 22 publications

Assessment of the Outcomes of Cerebral Blood Flow Measurements After Electrical Stimulation of Upper Right Incisor Tooth in Rabbits

Assessment of the Outcomes of Cerebral Blood Flow Measurements After Electrical Stimulation of Upper Right Incisor Tooth in Rabbits

Cerebral Vascular Control and Metabolism in Heat Stress

CCK as a modulator of cardiovascular function

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