![]() Monoamine oxidase inhibitors such as phenelzine are effective in suppressing REM sleep and cataplexy but are rarely used because of their side-effects. Fluoxetine(4) and paroxetine have been the most widely used, and some studies have shown them to be almost as effective as clomipramine. The selective nature of these drugs, acting only on 5HT synapses, may be responsible for their slightly lower effectiveness compared with tricyclic anti‑depressants. Rebound cataplexy can be intense if these drugs are suddenly withdrawn for any reason. Common side-effects include weight gain (which is also often a feature of narcolepsy itself), impotence and worsening of daytime sleepiness. It is probably the most effective at suppressing REM sleep,(3) and it blocks 5HT uptake. Their activity presumably reflects their differing profile at noradrenergic and 5HT synapses and their anticholinergic activity.Ĭlomipramine is the only tricyclic antidepressant licensed for cataplexy in the UK. Although antidepressants have been widely used for many years to treat cataplexy, there is surprisingly little data about their effectiveness or the comparative value of each drug. This suggests that the mechanism of action is different in these two situations. Interestingly, antidepressants almost immediately relieve cataplexy, whereas their action in combating depression may take around one to two weeks to appear. The 5HT-promoting effect is important for selective serotonin reuptake inhibitors (SSRIs). The efficacy of tricyclic antidepressants relates to their noradrenergic and anticholinergic activity. Lastly, sodium oxybate is a new and unrelated compound that improves cataplexy and other REM sleep-related phenomena, as well as daytime sleepiness.Ĭataplexy is suppressed by drugs that increase 5HT and noradrenergic activity and is worsened by antagonists of these transmitters, such as prazosin, an alpha1-antagonist, and by cholinergic agents. Secondly, drugs such as amphetamine and related agents, which are usually prescribed to improve daytime alertness but which also have an anticataplectic action. First, antidepressants, which have relatively little effect on the excessive daytime sleepiness of narcolepsy but may relieve some of the other REM sleep-related phenomena such as vivid dreams and sleep paralysis as well as cataplexy. Several agents are available for treating cataplexy.(2) These can be divided into three groups. During wakefulness, the pontine REM sleep centres are inhibited by noradrenaline and serotonin (5HT) released by activity in the locus coeuruleus and raphe nuclei, but in REM sleep and during cataplexy this inhibition ceases. This causes glycine-mediated inhibition of the alpha motor neurones in the spinal cord with loss of muscle activity. Emotional activity in the limbic system activates the pontine REM sleep centres and nearby regions to increase the activity in the medullary motor centres. The neurological mechanisms underlying cataplexy are complicated. Attention to sleep hygiene, particularly avoiding sleep deprivation, may help, but nevertheless most subjects require drug treatment, usually in the long term. Episodes can sometimes be aborted by tensing the muscles at the onset of an attack. Patients tend to avoid situations in which sudden or intense emotions may be felt and develop coping techniques of controlling the emotions in order to prevent cataplexy. Each episode usually lasts for a few seconds or up to two minutes. It is a specific feature of narcolepsy, a condition characterised by fragmentation and instability of rapid eye movement (REM) sleep, such that the muscle atonia which is normal in REM sleep can appear during wakefulness.Ĭataplexy may be mild and only cause, for instance, twitching of the face or the upper limbs, but it can lead to generalised muscle weakness in which the subject falls to the ground. Cataplexy is the sudden onset of muscle weakness during wakefulness.(1) It is almost always triggered by sudden or intense emotion, usually laughter. ![]()
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