An “Eye-Closing” Experience: A Rare Case of Hypersomnia Occurring Two Years After COVID-19

Article information

J Sleep Med. 2026;23(1):28-31

Publication date (electronic) : 2026 April 30

doi : https://doi.org/10.13078/jsm.250031

Mariam Mirza^,1,*, Celina R. Bou Jaoude^2,*, Efeose Airewele³, Hrayr Attarian³

¹Sleep Disorders Center, Department of Neurology, Cleveland Clinic Foundation, Cleveland, OH, USA

²Faculty of Medicine, American University of Beirut, Beirut, Lebanon

³Department of Neurology, Northwestern Memorial Hospital, Chicago, IL, USA

Address for correspondence Mariam Mirza, MD Sleep Disorders Center, Department of Neurology, Cleveland Clinic Foundation, 17840 Bagley Rd, Middleburg Heights, OH 44130, USA Tel: +1-216-444-2165x5 Fax: +1-216-636-0090 E-mail: marmirza4@gmail.com

^*

These authors contributed equally to this work.

Received 2025 December 10; Revised 2026 February 11; Accepted 2026 March 18.

Trans Abstract

INTRODUCTION

Idiopathic hypersomnia (IH) is a central hypersomnolence disorder characterized by excessive daytime sleepiness (EDS), commonly accompanied by long, unrefreshing naps and morning inertia [1]. Although a genetic predisposition has been suggested, the exact pathophysiology of IH remains unknown [2]. Potential triggers, including sleep cycle changes, viral illnesses, general anesthesia, and head trauma, have been identified. This disease usually begins during adolescence or early adulthood, with a mean age of 30 years at diagnosis [1]. Many patients with IH are refractory to treatment, and even if treatments are beneficial, their quality of life and safety may remain chronically impaired [2]. COVID-19 is associated with a wide spectrum of neurological sequelae ranging from cognitive impairment to sleep disturbances and fatigue [3]. While the latter is commonly reported as a persistent symptom following COVID-19 infection, a true sleeping disorder causing EDS is rare. For instance, insomnia has been reported in up to a quarter (22%) of long COVID patients, whereas hypersomnia disorders are much less frequent (3.17%) [4]. To date, only a few cases of new-onset IH following COVID-19 have been documented. Reported cases of post-COVID IH have occurred shortly after resolution of infection in young adults under the age of 35 years [3]. Here, we present a unique case of a 54-year-old man with late-onset IH emerging two years after COVID-19 infection, representing an uncommon potential manifestation within the long COVID spectrum.

CASE REPORT

A 54-year-old man with a history of hyperlipidemia presented for evaluation of persistent and progressive daytime sleepiness that began in early 2022. In 2020, he contracted COVID-19, after which he experienced cognitive difficulties, including word-finding difficulties, trouble remembering names, and loss of verbal fluency. Approximately 18–24 months later, he gradually developed daytime drowsiness and “sleep attacks.” He dozed off unintentionally while engaging in sedentary activities, including driving, and took 2–3-hour naps that were unrefreshing. The patient’s Epworth Sleepiness Scale score was 20/24, consistent with his subjective report of profound daytime sleepiness (a score of >10 is considered significant sleepiness). The patient had no history of sleep disorders.

His medical history was unremarkable, except for hyperlipidemia. His family history was negative for sleep disorders. The patient was overweight with a body mass index of 25 kg/m². Shortly before sleepiness began, in late 2021, he received the shingles vaccine.

A thorough evaluation of his hypersomnolence was performed. His consistent 9 PM bedtime and 5–6 AM waking time did not change with onset of hypersomnia. His total sleep duration was 8–9 hours. Prior to the onset of symptoms, the patient awakened easily at 5 AM. His physical and neurological examination results were unremarkable. Standard laboratory workup results, including complete blood count, comprehensive metabolic panel, thyroid function, vitamins B1 and B12, methylmalonic acid, homocysteine, folic acid, and ANA, were normal. Neuropsychiatric testing, brain magnetic resonance imaging, and positron emission tomography scans were unremarkable.

Polysomnography showed adequate total sleep time with normal architecture, as shown in Fig. 1. No significant sleepdisordered breathing was present. His apnea–hypopnea index was 3.2 events/hour, respiratory disturbance index was 3.2, sleep efficiency was 90.9%, and oxygen saturation remained high throughout the night, with the lowest recorded oxygen saturation being 88.6%. On the following day, a standard multiple-sleep latency test (MSLT) was performed. The patient had a mean sleep latency of 2.6 minutes as shown in Fig. 2, confirming marked hypersomnolence compared with normal reference values (>8 min). No sleep-onset REM periods (SOREMPs) were observed during any MSLT naps. His combined total sleep duration, including overnight polysomnography, was 456.2 minutes. He was not taking any medications prior to testing and stopped his daily 1 cup caffeine intake on the day of testing. In the weeks prior to testing, the patient reported a consistent sleep–wake schedule with a bedtime of 9 PM and waking time of 6 AM. Lack of sleep diary records or wrist actigraphy leading up to the sleep studies is a limitation.

Fig. 1.

Diagnostic polysomnography results. A: Table outlining key study findings. B: Time-synchronized graphs depicting the hypnogram (sleep stages), body position, oxygen saturation, hypopneas, and obstructive apneas during the study. AHI, apnea–hypopnea index; PLM, periodic limb movement; RERA, respiratory effort-related arousal; RDI, respiratory disturbance index.

Fig. 2.

Multiple sleep latency test results. A: Table outlining detailed study characteristics including sleep latency. B: Hypnogram showing sleep stages during the study.

Based on a combination of EDS, unrefreshing long naps, normal overnight sleep, pathological MSLT findings, and no alternative medical or psychiatric explanation, the patient was cautiously diagnosed with IH. Given his prior COVID-19 infection and the temporal sequence, hypersomnia was suspected to be a post-COVID manifestation. This diagnosis remains tentative due to the unavailability of sleep diary and wrist actigraphy data.

DISCUSSION

IH most commonly arises in young adults with a positive family history of IH or other central hypersomnolence disorders such as narcolepsy. The case described above is an unusual presentation of hypersomnia in a 54-year-old man with no family history of sleep disorders two years after COVID-19 infection. To our knowledge, post-COVID hypersomnia with such a delayed onset in someone over 35 has never been reported in the literature, highlighting the unique nature of this case. Morelli-Zaher et al. [3] published in 2024 four cases of post-COVID central hypersomnia with three cases fulfilling the criteria of the 3rd International Classification of Sleep Disorders for IH and one case of type II narcolepsy. All three IH cases in that series were under 35 years of age and developed hypersomnia soon after their COVID-19 infection [3]. In contrast, our patient was a 54-year-old man whose hypersomnolence began approximately 24 months after his COVID-19 infection, which is an unusually prolonged interval. Given that an extensive workup failed to reveal another cause, it is reasonable to conclude that his hypersomnolence was potentially related to his previous SARS-CoV-2 infection. The narcolepsy type 2 case involved a 54-year-old man with a history of hypertension and obstructive sleep apnea who reportedly showed improvement 20 months after COVID-19 infection [3].

Several potential triggers contribute to hypersomnia development, including infections and vaccines [1]. Multiple pathophysiological pathways could link prior SARS-CoV-2 infection with subsequent hypersomnia. SARS-CoV-2 is a neuroinvasive virus that can trigger widespread neuroinflammation. Acute COVID-19–associated encephalitis may result in EDS due to direct neuronal damage within key sleep–wake regulatory regions, such as the hypothalamus, hippocampus, temporal lobes, and brainstem [5]. Other infections, including Epstein-Barr virus, have been linked to development of hypersomnia. Sforza et al. [6] demonstrated that prior infectious mononucleosis may increase susceptibility to IH, further emphasizing the contribution of inflammatory and immune-mediated processes to this disorder. Biologically active agents, including vaccines, have been implicated in triggering narcolepsy and hypersomnia in vulnerable individuals. The best-known example is the sudden increase in reported narcolepsy incidence in several European countries following the influenza A (H1N1) vaccination campaign by Pandemrix [7]. Emerging evidence suggests that COVID-19 vaccination may be associated with transient sleepiness. Previous studies have reported that up to 50% of recipients experience increased sleepiness after vaccination [5]. Similar findings have been observed in other studies, where sleepiness was identified as the second most common systemic side effect after COVID-19 vaccination, occurring in approximately 15% of recipients after the first dose and 10% after the booster dose [8]. One case has been reported in which a 19-year-old woman developed a relapse of hypersomnia 10 days after receiving the first dose of the CoronaVac vaccine, raising the possibility of immune-mediated reactivation of a pre-existing sleep–wake disorder [9]. Vaccination-induced immune activation may thus theoretically act as an environmental trigger. In our patient’s case, the shingle vaccination in late 2021 may have provoked an immune response that, in the setting of prior SARS-CoV-2 infection, contributed to the onset of hypersomnia, perhaps as a “second hit” to the immune system. This remains speculative and causality cannot be established, as no cases of IH following the shingles vaccine have been reported to date. Our patient’s hypersomnia seems more consistent with delayed post-COVID manifestation, although a rare vaccine-related immune response cannot be definitively ruled out.

This case expands the recognized spectrum of post-COVID neurological complications to include a primary hypersomnolence disorder with a prolonged delay between infection and symptom onset. Clinicians should be aware of the possibility of central hypersomnolence disorders, such as IH or narcolepsy, in patients with persistent excessive sleepiness following COVID-19, as these conditions are often treatable. Research is warranted to elucidate the pathophysiological links between vaccination and viral illnesses including COVID-19, and sleep-wake regulation. This case highlights a need for long-term follow-up of COVID-19 survivors to detect lateemergent sequelae. By reporting this patient’s case, we hope to increase awareness of post-COVID IH and encourage vigilance for similar cases in clinical practice.

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