|LETTER TO EDITOR
|Year : 2021 | Volume
| Issue : 1 | Page : 79-80
Coexistence of hypokalemic periodic paralysis with central hypersomnolence: An attack of paralysis in polysomnographic recording
Gulcin Benbir Senel, Derya Karadeniz
Department of Neurology, Division of Clinical Neurophysiology, Sleep and Disorders Unit, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey
|Date of Submission||19-Aug-2020|
|Date of Acceptance||19-Oct-2020|
|Date of Web Publication||26-Mar-2021|
Gulcin Benbir Senel
Department of Neurology, Sleep and Disorders Unit, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul 34098
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Senel GB, Karadeniz D. Coexistence of hypokalemic periodic paralysis with central hypersomnolence: An attack of paralysis in polysomnographic recording. Neurol Sci Neurophysiol 2021;38:79-80
|How to cite this URL:|
Senel GB, Karadeniz D. Coexistence of hypokalemic periodic paralysis with central hypersomnolence: An attack of paralysis in polysomnographic recording. Neurol Sci Neurophysiol [serial online] 2021 [cited 2022 Aug 19];38:79-80. Available from: http://www.nsnjournal.org/text.asp?2021/38/1/79/311964
Disorders of central hypersomnolence are a group of sleep disorders, such as narcolepsy or idiopathic hypersomnia. A variety of medical and neurological conditions have been reported to be associated with central hypersomnolence, including neuromuscular disorders., To the authors' knowledge, there are no data in the literature regarding the association between periodic paralysis and central hypersomnolence.
A 36-year-old female was admitted to our Sleep Disorders Unit complaining of tiredness and excessive daytime sleepiness for >1 year. She regularly sleeps for 8 h during the week and about 12–13 h at weekends. She feels sleepy no matter how many hours she slept. Daytime siestas are unrefreshing, last between 10 min to 2 h, and lack dream content. She denies cataplexy or sleep-related hallucinations. Systemic and neurologic examinations were normal. Her medical history revealed that she had hypokalemic periodic paralysis since her childhood, and she was under potassium replacement therapy.
A full-night polysomnography (PSG) was performed in sleep laboratory (American Academy of Sleep Medicine Type 1) as per the standard criteria. Sleep efficiency was 91.6% with a normal distribution of sleep stages. Indices of abnormal respiratory events and periodic leg movements were within normal limits. During PSG recording, she awakened following an arousal reaction during superficial N2 (non-REM sleep stage 2; nonrapid eye movements sleep) sleep stage, tried to push the alarming button but failed, and then managed to push the button after few attempts [Figure 1]. Simultaneously, our sleep technician noticed her condition, entered the room, and observed that she had difficulty in moving. The attack decreased in severity upon potassium intake (40 mmol). During the attack, no changes in the tonus of chin electromyography (EMG) and bilateral tibialis anterior EMG recordings were observed. Multiple sleep latency test revealed a mean sleep latency of 4.1 min without REM sleep onset. The patient was diagnosed as having central hypersomnolence (probably of idiopathic hypersomnia).
|Figure 1: During polysomnography recording, at 1 am, the patient awakens the following an arousal reaction from (a), tries to push the alarming button but fails (b), and then manages to push the button after few attempts (c). Simultaneously, our sleep technician notices her condition, enters the room, and observes that she has difficulty in moving (d). The attack decreases in severity upon potassium intake (40 mmol), and then, she goes back into sleep|
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Periodic paralyses are characterized by the episodic attacks of focal or generalized muscle weakness caused by the mutations in sodium, calcium, or potassium channels. Although sleep problems have commonly been encountered in neuromuscular disorders, this is the first case in the literature presenting with hypokalemic periodic paralysis and central hypersomnolence. Intriguingly, our patient had an attack of paralysis during PSG recording during superficial N2 sleep stage. Although a detailed EMG recording was not planned, no prominent change was observed in the tonus of recorded muscles that are used to determine REM sleep atonia. Although the patient was not aroused from REM sleep stage, the tonus might give us about the underlying pathophysiologic mechanisms of these paralytic attacks. One may assume that the paralysis resulting from hypokalemia, as in our patient, has different mechanisms from cataplexy, resulting from REM sleep atonia.
In a patient with falls and hypersomnolence, this rare comorbidity should be kept in mind and the differentiation of attacks between periodic paralysis and cataplexy should carefully be made. Quality of sleep, changes in sleep structure, and associated sleep disorders wait to be defined in patients with periodic paralysis.
Financial support and sponsorship
Local support by the Cerrahpasa Faculty of Medicine, Department of Neurology, Sleep and Disorders Unit.
Conflicts of interest
There are no conflicts of interest.
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