Interictal hemodynamic abnormality during motor activation in sporadic hemiplegic migraine: An explorative study

Lo, Yew Long; Wee, Say Li; Zhao, Yi; Narasimhalu, Kaavya

doi:10.1016/j.jns.2020.117148

Cited by 1 publication

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“…This stands in line with a previous experimental observation that the CBF response to neuronal activation achieved with transcallosal electric stimulation declined (Piilgaard & Lauritzen, 2009), and the amplitude of EVP triggered by infraorbital nerve or transcallosal stimulation decreased after SD (Enager et al, 2004;Piilgaard & Lauritzen, 2009). The weakened hyperemic response observed here may be considered analogous to reduced baseline-to-peak changes of the functional near infrared spectroscopy (fNIRS) signal in sporadic hemiplegic migraine patients during a finger opposition task (Lo et al, 2020). A recent meta-analysis cautiously suggests that neurovascular coupling in migraine patients appears to be impaired, but calls for future confirmatory studies (Dzator et al, 2021).…”

Section: The Efficacy Of Neurovascular Coupling In the Wake Of Spread...supporting

confidence: 92%

Nimodipine accelerates the restoration of functional hyperemia during spreading oligemia

Menyhárt

Bálint

Kozák

et al. 2023

Journal of Neurochemistry

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Spreading depolarization (SD) is assumed to be the pathophysiological correlate of migraine aura, leading to spreading depression of activity and a long‐lasting vasoconstriction known as spreading oligemia. Furthermore, cerebrovascular reactivity is reversibly impaired after SD. Here, we explored the progressive restoration of impaired neurovascular coupling to somatosensory activation during spreading oligemia. Also, we evaluated whether nimodipine treatment accelerated the recovery of impaired neurovascular coupling after SD. Male, 4–9‐month‐old C57BL/6 mice (n = 11) were anesthetized with isoflurane (1%–1.5%), and SD was triggered with KCl through a burr hole made at the caudal parietal bone. EEG and cerebral blood flow (CBF) were recorded minimally invasively with a silver ball electrode and transcranial laser‐Doppler flowmetry, rostral to SD elicitation. The L‐type voltage‐gated Ca2+ channel blocker nimodipine was administered i.p. (10 mg/kg). Whisker stimulation‐related evoked potentials (EVPs) and functional hyperemia were assessed under isoflurane (0.1%)–medetomidine (0.1 mg/kg i.p.) anesthesia before, and repeatedly after SD, at 15‐min intervals for 75 minutes. Nimodipine accelerated the recovery of CBF from spreading oligemia (time to full recovery, 52 ± 13 vs. 70 ± 8 min, nimodipine vs. control) and exhibited a tendency to shorten the duration of the SD‐related EGG depression duration. The amplitudes of EVP and functional hyperemia were markedly reduced after SD, and progressively recovered over an hour post‐SD. Nimodipine exerted no impact on EVP amplitude but consistently increased the absolute level of functional hyperemia from 20 min post‐CSD (93 ± 11% vs. 66 ± 13%, nimodipine vs. control). A linear, positive correlation between EVP and functional hyperemia amplitude was skewed by nimodipine. In conclusion, nimodipine facilitated CBF restoration from spreading oligemia and the recovery of functional hyperemia post‐SD, which were linked to a tendency of an accelerated return of spontaneous neural activity after SD. The use of nimodipine in migraine prophylaxis is suggested to be re‐visited.image

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Section: The Efficacy Of Neurovascular Coupling In the Wake Of Spread...supporting

confidence: 92%

Nimodipine accelerates the restoration of functional hyperemia during spreading oligemia

Menyhárt

Bálint

Kozák

et al. 2023

Journal of Neurochemistry

View full text Add to dashboard Cite

show abstract

Interictal hemodynamic abnormality during motor activation in sporadic hemiplegic migraine: An explorative study

Cited by 1 publication

References 31 publications

Nimodipine accelerates the restoration of functional hyperemia during spreading oligemia

Nimodipine accelerates the restoration of functional hyperemia during spreading oligemia

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