Examples of cataplexy tv#

For example, he reported waking up and petting an imaginary dog that he had been dreaming of.Īpproximately 2 months after EDS onset, the patient started experiencing symmetrical muscle tone weakness triggered by emotion. He made a few complaints about disturbed nocturnal sleep, especially frequent vivid dreams and dream enactment behavior. Being already retired, the sleepiness did not present important difficulties in his life. He tried to avoid falling asleep unexpectedly by taking a short nap in advance. However, sleep attacks while he was physically active did not occur.

Examples of cataplexy tv#

He fell asleep while engaged in monotonous activities, such as TV watching, reading, or using an iPad. The patient described a sudden onset of disturbing daytime sleepiness and required several 5- to 10-min naps throughout the day. Within 2 or 3 months, his symptoms got more severe so that he contacted a sleep disorder center and was sent to our clinic, where he was completely examined and diagnosed (just after his 70th anniversary). No possible trigger, such as trauma, infectious disease, vaccination, or other serious health or social event, preceded the manifestation of his symptoms. The patient started to suffer from EDS at the age of 69 years. He lives with his wife and likes fishing. Our patient has already been retired for several years from his previous occupation as a tiler. He smokes about 20 cigarettes a day and occasionally likes to drink a couple of beers. Our patient was previously treated for chronic obstructive pulmonary disease, arterial hypertension, and dyslipidemia, with a history of deep vein thrombosis. We would like to present an undoubtedly diagnosed late-onset NT1 in a 69-year-old male subject. To our knowledge, only 3 cases of NC onset at around age 70 years have been described: all of them are not clinically clear. Possible later onset is indicated as rare throughout studies in Roth, only 4 out of 288 cases had onset after 50 years. The typical age at onset is in the second decade and another smaller peak in the fourth decade. The disappearance of hypocretin neurons is suggested to have an autoimmune etiology. The disease is caused by the loss of hypocretin neurons in the lateral hypothalamus. It is often accompanied by hypnagogic hallucinations and sleep paralysis. Narcolepsy type 1 (NT1 older name: narcolepsy with cataplexy ) is a life-long neurological disease characterized by excessive daytime sleepiness (EDS), disrupted nocturnal sleep, and cataplexy. Our unique case demonstrates that even elderly subjects can develop narcolepsy type 1. Bilevel Positive Airway Pressure improved the apnea-hypopnea index without important influence on sleepiness. The administration of 0.25 mg of clonazepam subjectively improved REM sleep behavior disorder. A treatment with 50 mg clomipramine controlled the cataplexy excessive daytime sleepiness was sufficiently managed by repeated naps. HLA DQB1*06:02 was positive and hypocretin-1 in cerebrospinal fluid unmeasurable.

Multiple Sleep Latency Test showed a mean sleep latency of 2.1 min and REM sleep in 3 tests. Nocturnal polysomnography revealed rapid eye movement (REM) sleep behavior disorder, a apnea-hypopnea index of 25.8 events/h, and no sleep-onset REM.

First, daytime sleepiness occurred, soon followed by cataplexy. A 69-year-old male developed symptoms typical of the diagnosis of narcolepsy type 1 without any previous triggering events.