Insufficient sleep may alter cortical excitability near the migraine attack: A blinded TMS crossover study

Mykland, Martin Syvertsen; Uglem, Martin; Stovner, Lars Jacob; Brenner, Eiliv; Snoen, Mari Storli; Gravdahl, Gøril Bruvik; Sand, Trond; Omland, Petter Moe

doi:10.1177/03331024221148391

Cited by 7 publications

(6 citation statements)

References 46 publications

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“…Increased ERD during motor imagery has been associated with reduced short interval intracortical inhibition (SICI) (30). Reduced SICI has also been described after sleep restriction closely after the end of a migraine attack by our group (31). This cortical inhibitory effect is thought to mainly represent post synaptic inhibitory potentials from a2 or a3 subtype GABA-A receptor activation (32).…”

Section: Discussionmentioning

confidence: 76%

Effects of insufficient sleep on sensorimotor processing in migraine: A randomised, blinded crossover study of event related beta oscillations

et al. 2023

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Background Migraine has a largely unexplained connection with sleep and is possibly related to a dysfunction of thalamocortical systems and cortical inhibition. In this study we investigate the effect of insufficient sleep on cortical sensorimotor processing in migraine. Methods We recorded electroencephalography during a sensorimotor task from 46 interictal migraineurs and 28 controls after two nights of eight-hour habitual sleep and after two nights of four-hour restricted sleep. We compared changes in beta oscillations of the sensorimotor cortex after the two sleep conditions between migraineurs, controls and subgroups differentiating migraine subjects usually having attacks starting during sleep and not during sleep. We included preictal and postictal recordings in a secondary analysis of temporal changes in relation to attacks. Results Interictally, we discovered lower beta synchronisation after sleep restriction in sleep related migraine compared to non-sleep related migraine (p=0.006) and controls (p=0.01). No differences were seen between controls and the total migraine group in the interictal phase. After migraine attacks, we observed lower beta synchronisation (p<0.001) and higher beta desynchronisation (p=0.002) after sleep restriction closer to the end of the attack compared to later after the attack. Conclusion The subgroup with sleep related migraine had lower sensorimotor beta synchronisation after sleep restriction, possibly related to dysfunctional GABAergic inhibitory systems. Sufficient sleep during or immediately after migraine attacks may be of importance for maintaining normal cortical excitability.

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Section: Discussionmentioning

confidence: 76%

Effects of insufficient sleep on sensorimotor processing in migraine: A randomised, blinded crossover study of event related beta oscillations

et al. 2023

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“…Reduced sleep quantity, more than other sleep-related issues, has been associated with central sensitization in migraine patients, with a strong correlation with both allodynia and pericranial tenderness. 56 Sleep deprivation has also been reported to increase cortical excitability in migraine patients, 58 , 59 and preclinical studies have shown that sleep deprivation can enhance cortical spreading depolarization, 60 suggesting the possibility that migraine aura could serve as a potential trigger for migraine attack in patients with disrupted sleep. 61 …”

Section: Discussionmentioning

confidence: 99%

Unraveling the directional relationship of sleep and migraine-like pain

Lillo Vizin,

Kopruszinski,

Redman

et al. 2024

Brain Communications

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Migraine and sleep disorders are common comorbidities. Patients frequently link their sleep to migraine attacks suggesting a potential causal relationship between these conditions. However, whether migraine pain promotes or disrupts sleep or whether sleep disruption can increase the risk of migraine remains unknown. We assessed the potential impact of periorbital allodynia, a measure consistent with migraine-like pain, from multiple preclinical models on sleep quantity and quality. Additionally, we evaluated the possible consequences of sleep deprivation in promoting susceptibility to migraine-like pain. Following implantation of EEG/EMG electrodes to record sleep, mice were treated with either single or repeated systemic injections of nitroglycerin at the onset of their active phase (i.e., nocturnal awake period). Neither single nor repeated nitroglycerin affected total sleep time, non-rapid eye movement sleep, rapid-eye movement sleep, sleep depth, or other measures of sleep architecture. To account for the possible disruptive effects of the surgical implantation of EEG/EMG electrodes, we used immobility recordings as a non-invasive method for assessing sleep-wake behavior. Neither single nor repeated nitroglycerin administration during either the mouse sleep (i.e., daylight) or active (i.e., night) periods influenced immobility-defined sleep time. Administration of an inflammatory mediator mixture onto the dura mater at either sleep or active phases also did not affect immobility-defined sleep time. Additionally, inhalational umbellulone-induced migraine-like pain in restraint-stressed primed mice did not alter immobility-defined sleep time. The possible influence of sleep disruption on susceptibility to migraine-like pain was evaluated by depriving female mice of sleep over 6 h with novel objects, a method that does not increase circulating stress hormones. Migraine-like pain was not observed following acute sleep deprivation. However, in sleep-deprived mice, subthreshold doses of systemic nitroglycerin or dural calcitonin gene-related peptide induced periorbital cutaneous allodynia consistent with migraine-like pain. Our data reveal that while migraine-like pain does not significantly disrupt sleep, sleep disruption increases vulnerability to migraine-like pain suggesting that a therapeutic strategy focused on improving sleep may diminish migraine attacks.

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“…a defective inhibition (19,(25)(26)(27)(28)(29). Other studies, however, including patients with aura (16), familial hemiplegic migraine (30) or pediatric patients (31), failed to detect any abnormalities in the CSP (32)(33)(34)(35).…”

Section: Motor and Occipital Cortex Stimulationmentioning

confidence: 98%

Electrophysiological findings in migraine may reflect abnormal synaptic plasticity mechanisms: A narrative review

Puledda,

Viganò,

Sebastianelli

et al. 2023

Cephalalgia

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Background The cyclical brain disorder of sensory processing accompanying migraine phases lacks an explanatory unified theory. Methods We searched Pubmed for non-invasive neurophysiological studies on migraine and related conditions using transcranial magnetic stimulation, electroencephalography, visual and somatosensory evoked potentials. We summarized the literature, reviewed methods, and proposed a unified theory for the pathophysiology of electrophysiological abnormalities underlying migraine recurrence. Results All electrophysiological modalities have determined specific changes in brain dynamics across the different phases of the migraine cycle. Transcranial magnetic stimulation studies show unbalanced recruitment of inhibitory and excitatory circuits, more consistently in aura, which ultimately results in a substantially distorted response to neuromodulation protocols. Electroencephalography investigations highlight a steady pattern of reduced alpha and increased slow rhythms, largely located in posterior brain regions, which tends to normalize closer to the attacks. Finally, non-painful evoked potentials suggest dysfunctions in habituation mechanisms of sensory cortices that revert during ictal phases. Conclusion Electrophysiology shows dynamic and recurrent functional alterations within the brainstem-thalamus-cortex loop varies continuously and recurrently in migraineurs. Given the central role of these structures in the selection, elaboration, and learning of sensory information, these functional alterations suggest chronic, probably genetically determined dysfunctions of the synaptic short- and long-term learning mechanisms.

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Insufficient sleep may alter cortical excitability near the migraine attack: A blinded TMS crossover study

Cited by 7 publications

References 46 publications

Effects of insufficient sleep on sensorimotor processing in migraine: A randomised, blinded crossover study of event related beta oscillations

Effects of insufficient sleep on sensorimotor processing in migraine: A randomised, blinded crossover study of event related beta oscillations

Unraveling the directional relationship of sleep and migraine-like pain

Electrophysiological findings in migraine may reflect abnormal synaptic plasticity mechanisms: A narrative review

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