Department of Neuromedicine and Movement Science, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway; Department of Neurology and Clinical Neurophysiology, St. Olavs Hospital, Trondheim, Norway.
Department of Neuromedicine and Movement Science, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway; Department of Neurology and Clinical Neurophysiology, St. Olavs Hospital, Trondheim, Norway.
Clin Neurophysiol. 2022 Jul;139:28-42. doi: 10.1016/j.clinph.2022.04.004. Epub 2022 Apr 20.
Migraine is a primary headache disorder with a well-known association with insufficient sleep. However, both the underlying pathophysiology of the disease and the relationship with sleep is still unexplained. In this study, we apply transcranial magnetic stimulation to investigate possible mechanisms of insufficient sleep in migraine.
We used a randomised, blinded crossover design to examine 46 subjects with migraine during the interictal period and 29 healthy controls. Each subject underwent recordings of cortical silent period, short- and long-interval intracortical inhibition, intracortical facilitation and short-latency afferent inhibition after both two nights of habitual eight-hour sleep and two nights of restricted four-hour sleep.
We found reduced cortical silent period duration after sleep restriction in interictal migraineurs compared to controls (p = 0.046). This effect was more pronounced for non-sleep related migraine (p = 0.002) and migraine with aura (p = 0.017). The sleep restriction effect was associated with ictal symptoms of hypersensitivity such as photophobia (p = 0.017) and overall silent period was associated with premonitory dopaminergic symptoms such as yawning (p = 0.034).
Sleep restriction reduces GABAergic cortical inhibition during the interictal period in individuals with migraine.
Sleep related mechanisms appear to affect the pathophysiology of migraine and may differentiate between migraine subgroups.
偏头痛是一种原发性头痛障碍，与睡眠不足有明显关联。然而，该疾病的潜在病理生理学及其与睡眠的关系仍未得到解释。在这项研究中，我们应用经颅磁刺激来研究偏头痛患者睡眠不足的可能机制。
我们采用随机、双盲交叉设计，在发作间期检查了 46 名偏头痛患者和 29 名健康对照者。每位受试者均接受了两种睡眠习惯（8 小时/夜）和两种限制睡眠（4 小时/夜）后的皮质静息期、短程和长程皮质内抑制、皮质内易化和短潜伏期传入抑制的记录。
与对照组相比，发作间期偏头痛患者在睡眠限制后皮质静息期持续时间缩短（p=0.046）。这种影响在非睡眠相关偏头痛（p=0.002）和偏头痛伴先兆（p=0.017）中更为明显。睡眠限制效应与光过敏等发作性敏感性症状相关（p=0.017），总体静息期与哈欠等前驱性多巴胺能症状相关（p=0.034）。
睡眠限制会降低偏头痛患者发作间期的 GABA 能皮质抑制。
睡眠相关机制似乎会影响偏头痛的病理生理学，并可能区分偏头痛亚组。
