A brain scan of narcolepsy cataplexy11/18/2023 Subsequently, he manifested the classic tetrad of narcolepsy: cataplexy, excessive. ![]() 6 In addition, a previous study has revealed loss of hypocretin neurons following post-traumatic brain injury on postmortem examination. This patient sustained moderate brain injury from a motorcycle accident. 8 While the etiology of post-traumatic narcolepsy remains unknown, blunt injury may cause hypothalamic injury leading to an impaired hypocretin system. 6 There has been only one previously reported case of post-traumatic narcolepsy with a documented brain lesion and surgical treatment. We used MEDLINE to retrieve neuroimaging studies to compare patients with narcolepsy and healthy controls. Most post-traumatic narcolepsy patients experience mild to moderate head injury but with no specific brain injury area determined. Abstract Recent developments in neuroimaging techniques have advanced our understanding of biological mechanisms underpinning narcolepsy. 2 In our current case, obvious injury of the hypothalamus was observed, and the patient’s symptoms gradually resolved over time with improvements in his narcolepsy symptoms. 6 Narcolepsy can occur after hypothalamic lesions that are related to hypocretin neurotransmission. 5 About 20 cases were reported of post-traumatic narcolepsy with heterogeneous manifestations from clinical presentation, severity of injury, symptoms onset time, and HLA typing. He scored 15 on the Epworth Sleepiness Scale (ESS) when he underwent a nocturnal polysomnography.Īlthough traumatic narcolepsy was first reported more than 70 years ago, distinction from other sleep disorders such as sleep apnea or post-traumatic hypersomnia has remained unclear. He didn’t show mood or psychotic symptoms when he was interviewed by a psychiatrist (S.C.). He did not consume alcohol or tobacco and he drank three cups of coffee a day. He had no history of cataplexy, hypnogogic hallucinations, or sleep paralysis. During the day, he would nod off and become tired, with excessive sleepiness lasting nearly all day. Middle-of-the-night awakenings were rare, and he had no history of snoring, sleep apnea, or restless legs syndrome. In patients with secondary narcolepsy, MRI of the brain may show various abnormalities that correspond to the underlying cause. Structural abnormalities of the brain stem and diencephalon may present as idiopathic narcolepsy. History taking revealed that before the accident, he had mild daytime sleepiness but no functional impairment and a relatively regular sleep pattern (asleep at 11 pm–12 am and waking up at 6 am). Imaging studies such as MRI are useful for excluding rare causes of symptomatic narcolepsy. He had developed daytime sleepiness following the accident that impaired his daytime activities. Cardiovascular changes can occur in association with narcolepsy/cataplexy and should be considered when dealing with patients presenting with these specific clinical signs.A 37-year-old man was referred to our hospital due to excessive daytime somnolence and with a history of a trauma resulting from a car accident, in which he lost consciousness, 6 months prior. Although very rare, symptomatic narcolepsy/cataplexy can occur in dogs and can be secondary to brainstem encephalitis. narcolepsy-cataplexy and limbic encephalitis with Ma-2/Ta antibodies and MRI axial FLAIR image revealing bilateral T2-hyperintensity in the hypothalamus (B). ![]() Repeated MRI revealed marked reduction in the lesion size cerebrospinal fluid analysis revealed no abnormalities. No relapse occurred over a 32 mo follow-up period from the diagnosis. ![]() Narcolepsy-cataplexy episodes could initially still be triggered by offering food however, they gradually became shorter and less frequent until they completely subsided along with all other clinical signs after 3 wk. The dog was started on immunosuppressive treatment with prednisolone and cytosine arabinoside, which was subsequently switched to cyclosporine. MRI of the brain and cerebrospinal fluid analysis were compatible with meningoencephalitis of unknown origin affecting the mesencephalon, pons and rostral medulla oblongata. Hematology, serum biochemistry, and thoracic and abdominal imaging were unremarkable. There was no evidence of arrhythmia on electrocardiography during the episode. A narcolepsy-cataplexy episode with associated hypertension and bradycardia was triggered during examination. A 4 yr old, intact female cocker spaniel was presented for investigation of acute, progressive lethargy/hypersomnia vestibular signs and cataplexy.
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