![]() The sudden onset of muscle weakness characterizes cataplexy. In addition to excessive daytime sleepiness, patients with type 1 narcolepsy experience symptoms of disordered regulation of REM sleep (i.e., cataplexy, hypnagogic hallucinations, and sleep paralysis). It is essential to realize that patients with narcolepsy are well-rested following a brief nap or sufficient nights' sleep however, the symptoms of excessive daytime sleepiness occur within hours of awakening. The clinician should perform an investigation of behavioral (i.e., caffeine use, insufficient sleep, poor sleep hygiene, tobacco use, etc.) and alternative diagnoses (i.e., anemia, hypothyroidism, obstructive sleep apnea, etc.) of excessive daytime sleepiness. Obtaining an accurate and detailed history is imperative in the diagnosis of narcolepsy. ![]() Intense emotions transmitted from the medial prefrontal cortex to the amygdala, in conjunction with the loss of orexin-A, decrease inhibitory signals of REM sleep, ultimately inhibiting motor neurons in the pons, leading to muscle paralysis and cataplexy. Neurons located in the lateral hypothalamus produce orexin-A it potentiates the production of the following neurotransmitters: dopamine, histamine, norepinephrine, and serotonin, leading to the suppression of rapid eye movement (REM) sleep. In patients with type 1 narcolepsy, the examination of cerebrospinal fluid demonstrates decreased levels of orexin-A, a wakefulness-promoting peptide neurotransmitter. In addition to the physical feature of cataplexy, type 1 narcolepsy further distinguishes from type 2 narcolepsy on the molecular level. In the U.S., Type 1 narcolepsy affects 1 to 2 in 4000 individuals. Two forms of narcolepsy exist: type 1 is associated with cataplexy while this feature is absent in type 2. Symptom onset most frequently occurs during adolescence however, diagnosis often gets delayed on average by 15 years. In the U.S., narcolepsy affects 1 in 2000 individuals with an equal distribution amongst the sexes. It is worth noting that other neurological deficits are often evident in individuals who develop secondary narcolepsy, as lesions are not typically confined to the lateral hypothalamus. Although rare, lesions secondary to arteriovenous malformations, cerebrovascular accidents, inflammatory processes, and neoplasms result in the destruction of orexin-A-producing neurons. Secondary narcolepsy, on the other hand, is due to the development of lateral hypothalamic lesions. Moreover, there was an increased incidence of narcolepsy following the use of the 2009 European Pandemrix vaccination, suggesting the involvement of molecular mimicry in the development of this disorder. The onset of narcolepsy is seasonal, most often surfacing in the spring, following upper respiratory tract infections that had occurred in the preceding months. There is a near-perfect association of type 1 narcolepsy with HLA-DQB1*06:02, leading to the auto-immune hypothesis, which posits a selective, self-destruction of orexin-A producing neurons as the driving force behind the disorder. Type 1 narcolepsy (historically known as narcolepsy with cataplexy) is due to a deficiency of orexin-A, a wakefulness-promoting peptide neurotransmitter. While 19% of patients diagnosed with narcolepsy also get diagnosed with cataplexy, estimates are that roughly 70% of patients with narcolepsy also have cataplexy. Unfortunately, cataplexy is challenging to identify, often going undetected. Subjective descriptions of cataplexy can assist in the identification of narcolepsy, as this feature is all but unique to the disorder. Review the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by cataplexy.Ĭataplexy, a physical feature of narcolepsy, is characterized by transient episodes of voluntary muscle weakness precipitated by intense emotion.Outline the treatment and management options available for cataplexy.This activity reviews the role of the interprofessional healthcare team in improving care for patients with narcolepsy, by raising awareness of cataplexy. While one-third of patients present with the classic narcolepsy tetrad (cataplexy, excessive daytime sleepiness, hypnagogic hallucinations, and sleep paralysis), two-thirds of patients with narcolepsy patients are affected by cataplexy. Subjective descriptions of cataplexy can assist in the identification of narcolepsy, as this feature is almost unique to the disorder. Cataplexy, a physical feature of narcolepsy, is characterized by transient episodes of voluntary muscle weakness precipitated by intense emotion.
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