一例视神经胶质瘤导致的嗜睡症的脑电图特征

Azusa Shinozaki , Norimichi Higurashi , Haruka Takami , Takaya Honda , Erika Hiwatari , Takaaki Yanagisawa , Takashi Kanbayashi
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摘要

背景奥曲肽在下丘脑外侧区域分泌,对觉醒至关重要。下丘脑病变患者的奥曲肽分泌受损会导致继发性嗜睡症。病例介绍 一名 16 岁男孩在接受视神经胶质瘤(累及视交叉)的维持治疗期间出现嗜睡、认知功能障碍和记忆力减退。脑部核磁共振成像显示,肿瘤已扩大到鞍上区域以外,并压迫了下丘脑、中脑、鞍上核和基底前脑。嗜睡症期间的脑电图记录显示,无论患者是睡着还是醒着,都会出现重复的高电压、前额占主导地位的德尔塔波爆发,睡眠驼峰和棘波模糊不清,睡眠结构紊乱。额外的化疗缓解了嗜睡症,脑电图上也不再出现德尔塔波阵。入院时脑脊液中的奥曲肽水平极低,但嗜睡症消失后奥曲肽水平有所上升。讨论与结论该病例的嗜睡症可能不仅与下丘脑病变导致的奥曲肽分泌受损有关,还与包括基底前脑和脑干在内的其他唤醒网络功能障碍有关。脑电图上重复出现的高压三角波阵列与继发性嗜睡症之间的联系以前从未描述过。虽然其病理生理基础尚不清楚,但这种多重唤醒促进网络的损伤可能与特征性脑电图发现有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Electroencephalographic features in a case of hypersomnia due to an optic nerve glioma

Background

Orexin is secreted in the lateral hypothalamic area and is essential for wakefulness. Impaired secretion of orexin in patients with hypothalamic lesions results in secondary hypersomnia. However, reports on the EEG features of secondary hypersomnia are limited.

Case presentation

A 16-year-old boy experienced hypersomnia, cognitive impairment, and memory deficits during maintenance treatment for an optic nerve glioma involving the optic chiasm. Brain MRI revealed that the tumor had enlarged beyond the suprasellar region and compressed the hypothalamus, midbrain, suprasellar nucleus, and basal forebrain. EEG recording during hypersomnia showed repetitive high-voltage, frontal dominant delta wave bursts regardless of whether the patient was sleeping or awake, indistinct sleep humps and spindles, and disruption of sleep architecture. Additional chemotherapy alleviated the hypersomnia, and delta wave bursts were no longer observed on EEG. Orexin levels in the cerebrospinal fluid were extremely low on admission but increased after the disappearance of hypersomnia.

Discussion and Conclusion

Hypersomnia in this case may be associated not only with impaired orexin production due to hypothalamic lesions, but also with dysfunction of the other arousal networks, including the basal forebrain and brainstem. The association between repetitive high-voltage delta wave bursts on EEG and secondary hypersomnia has not been previously described. Although the pathophysiological basis remains unclear, the damage to such multiple wake-promoting networks may be involved in the characteristic EEG finding.

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