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Narcolepsy is often mistaken for depression, epilepsy, the side effects of medications, poor sleeping habits or recreational drug use, making misdiagnosis likely. [citation needed] While narcolepsy symptoms are often confused with depression, there is a link between the two disorders. Research studies have mixed results on co-occurrence of ...
The diagnosis of narcolepsy and cataplexy is usually made by symptom presentation. Presenting with the tetrad of symptoms (excessive daytime sleepiness, sleep-onset paralysis, hypnagogic hallucinations, and cataplexy symptoms) is strong evidence of the diagnosis of narcolepsy.
Autosomal dominant cerebellar ataxia, deafness, and narcolepsy (ADCADN) is a rare progressive genetic disorder that primarily affects the nervous system and is characterized by sensorineural hearing loss, narcolepsy with cataplexy, and dementia later in life.
Fatal insomnia is an extremely rare neurodegenerative prion disease that results in trouble sleeping as its hallmark symptom. [2] The majority of cases are familial (fatal familial insomnia [FFI]), stemming from a mutation in the PRNP gene, with the remainder of cases occurring sporadically (sporadic fatal insomnia [sFI]).
Pediatric narcolepsy cases are cases when patients are diagnosed or experience symptoms onset for narcolepsy before the age of 18. Of patients who obtain a formal diagnosis for narcolepsy, more than 50% report first experiencing symptoms of narcolepsy more than 10 years before their formal diagnosis, with an average age of symptom onset being at age 15 and symptom onset most likely to occur ...
Patients with narcolepsy are diagnosed as either type 1 or type 2, with only the former presenting cataplexy symptoms. [58] Type 1 narcolepsy results from the loss of approximately 70,000 orexin -releasing neurons in the lateral hypothalamus , leading to significantly reduced cerebrospinal orexin levels; [ 59 ] [ 60 ] this reduction is a ...
The diagnosis and symptom onset of RBD typically precedes the onset of motor or cognitive symptoms of PD by a number of years, typically ranging anywhere from 2 to 15 years prior. Hence, this link could provide an important window of opportunity in the implementation of therapies and treatments, that could prevent or slow the onset of PD. [27]
One factor that could explain this change in sleep architecture is a disruption in the circadian rhythm, which regulates sleep. [19] This disruption can lead to sleep disturbances. [19] Some studies show that people with Alzheimer's disease have a delayed circadian rhythm, whereas in normal aging, an advanced circadian rhythm is present. [19] [20]
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