Cataplexy is treatable and there are currently approved treatment options, but additional therapies are needed. While most attacks are brief, some can last several minutes. Cataplexy occurs in 60-70% of people with narcolepsy. Sometimes the attack could be severe and cause a total body collapse. Sometimes there may be mild weakness, such as a drooping of the eyelids. EDS can affect normal sleep-wake cycles, causing people to fall asleep at unexpected times throughout the day.Ĭataplexy is a sudden loss of muscle tone or weakness brought on by strong emotions like laughter, embarrassment, frustration or surprise. What is Excessive Daytime Sleepiness (EDS)?Įxcessive daytime sleepiness (EDS) is a persistent feeling of sleepiness commonly found in people with narcolepsy. The SYMPHONY Study is evaluating AXS-12 (reboxetine) as an investigational oral medication to improve wakefulness and reduce occurrence of cataplexy. The study is for people with narcolepsy who are experiencing excessive daytime sleepiness (EDS) and cataplexy (sudden muscle weakness).
Eds and cataplexy trial#
The existence of co-occurring symptoms supports the hypothesis of a distinct pathophysiology of single narcoleptic symptoms.The SYMPHONY Study is a clinical research trial currently being conducted at select centers in the US and Canada. Specific questions on severity of EDS (SPAS score) and characteristics of cataplexy allow the recognition of subgroups of narcoleptics and their differentiation from non-narcoleptic EDS patients, including those reporting cataplexy-like episodes.
Low/undetectable cerebrospinal fluid hypocretin-1 levels and a history of definite cataplexy identify similar subgroups of narcoleptics. Analysis of co-occurring symptoms in narcolepsy revealed two symptom complexes: EDS, cataplexy, automatic behaviors and sleep paralysis, hallucinations, parasomnias. Our narcolepsy score had a similar sensitivity (96% versus 98%) but a higher specificity (98% versus 56%) than the UNS. Cataplexy-like symptoms in H (18%) and No (8%) could be discriminated from 'true' cataplexy in N on the basis of topography of motor effects, triggering emotions and triggering situations (P < 0.001). A score of sleep propensity during active situations (SPAS) and the frequency of sleep paralysis/hallucinations at sleep onset, dreams of flying, and history of sleep shouting discriminated N from H and No (P < 0.001). There were significant differences between N and NpC (including mean sleep latency on MSLT), but none between N and N-hd. The clinical features are excessive daytime sleepiness (EDS), cataplexy. Data were compared with those of 12 hypocretin-deficient narcoleptics (N-hd). Fluoxetine did not control cataplexy satisfactorily and the patient was still. A new narcolepsy score based on five questions was developed. Assessment consisted of questionnaires, polysomnography (all patients), multiple sleep latency test (MSLT) and human leukocyte antigen typing (in most narcoleptics).
Based on suggested and published criteria, we differentiated between narcoleptics with definite cataplexy (N) and narcoleptics without definite cataplexy (possible cataplexy, NpC). We prospectively studied 57 narcoleptics with cataplexy, 56 patients with non-narcoleptic hypersomnia (H), and 40 normal controls (No). The aims of this study were (1) to determine frequency and characteristics of sleep-wake symptoms in patients with narcolepsy with cataplexy, (2) to compare clinical characteristics with results of ancillary tests, and (3) to identify factors that discriminate narcolepsy from other conditions with excessive daytime sleepiness (EDS). In the absence of a golden standard for the diagnosis of narcolepsy, the clinical spectrum of disorder remains controversial.
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