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Other drugs which are less effective stimulants but have lower abuse potentials include atomoxetine which inhibits the reuptake of noradrenalin allowing it to persist allowing its effects such as increasing heart rate, promotion of glucose release from the muscles and increasing blood flow to the brain to persist.Ĭataplexy on the other hand needs its own special attention. For this reason both –dafinals are monitored for potential abuse and addiction. Exactly how these drugs work is not known but what we do know is they work differently to amphetamines and some attributes are shared, such as the effects of the drugs on dopamine levels in the brain. Amphetamine based drugs were favoured but new drugs like Modafinil and Armodafinil are now used instead.
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Initially central nervous system (CNS) stimulants are given. Treating such an unusual disease necessarily takes an individual by individual response but certain guidelines are followed. What is orexin? Orexin is a fundamental controller of both appetite and sleep-patterning suggesting that some forms of narcolepsy are in fact an autoimmune disease! Some, not all, narcoleptics show a number of important variations in their HLA’s that increase their ability to target orexin-producing neurons in the brain. I won't go into it here but the HLA is related to antibodies, which the body uses to identify things that shouldn’t be in the body and target them for removal. Despite the neurological trigger it is predicted that both conditions share a level of genetic involvement as well as both conditions have been shown to run in families.Īn interesting discovery in narcolepsy research is the involvement of a region of DNA on chromosome 6 involved in the production of human leukocyte antigen ( HLA, a.k.a Major Histocompatability Complex or MHC in mice). Credit: me.īoth narcolepsy and cataplexy can appear at the same time as both have similar triggers, most notably strong emotional reactions, which can set them off together. I don't think my dogs are narcoleptic, just lazy. The cataplexy and sleep paralysis reflect the encroachment of REM atonia into wakefulness resulting in muscle paralysis when it is not desired. REM sleep is when dreaming occurs which explains the hypnagogic hallucination as there is no non-REM ( NREM) sleep to buffer dreaming from wakefulness (hypnagogic means sleep leading and refers to the transition sleep to awake and vice versa). Essentially this, alongside all the other symptoms suggests the brain does not follow the normal pattern of sleep. Most people take approximately 90 min to achieve this level of sleep and this is a really significant part of the problem. For sufferers this condition is understandably terrifying.Īnother of the defining characteristics of narcolepsy is that its sufferers seem to have the ability to enter deep rapid eye movement ( REM) sleep in as little as 10 min. Some only suffer from weakness in facial muscles that fades quickly but in severe cases the weakness can be felt in all skeletal muscles at the same time causing the sufferer to drop (if you'll mind the use of the word) into a paralysed state while remaining entirely conscious of their surroundings and what is happening to them. Cataplexy, like narcolepsy, has varying degrees of severity. Narcolepsy is characterised by four basic symptoms known as the ‘tetrad of narcolepsy’, cataplexy, sleep paralysis, hypnagogic hallucinations (hallucinations associated with the transition between asleep and awake) and excessive daytime sleepiness (EDS).Ĭataplexy is simply one of the characteristics of narcolepsy and refers to a sudden onset muscle weakness, which can be experienced alongside or independently from narcolepsy. So what’s the difference and what’s the deal with narcolepsy? Credit: įurthermore narcolepsy is often confused with cataplexy, a related yet very distinct condition.