Treatment options may vary from a single drug that targets several symptoms, or multiple medications that each treats a specific symptom. Despite major advances in our understanding of narcolepsy mechanisms, its current management is only symptomatic. On the other hand, in narcolepsy type 2, cerebrospinal fluid hypocretin-1 levels are normal and cataplexy absent. Narcolepsy type 1 is characterized by excessive daytime sleepiness and cataplexy and is associated with hypocretin-1 deficiency. 2017 114(17):E3526–35.Narcolepsy type 1 and narcolepsy type 2 are central disorders of hypersomnolence. Serotonin neurons in the dorsal raphe mediate the anticataplectic action of orexin neurons by reducing amygdala activity. Hasegawa E, Maejima T, Yoshida T, Masseck OA, Herlitze S, Yoshioka M, et al. Subjective and polysomnographic effects of milnacipran on sleep in depressed patients. Neurochemical and behavioral characterization of milnacipran, a serotonin and noradrenaline reuptake inhibitor in rats. Mochizuki D, Tsujita R, Yamada S, Kawasaki K, Otsuka Y, Hashimoto S, et al. Increase of pineal noradrenaline concentration in rats by desipramine but not fluoxetine: implications concerning the specificity of these uptake inhibitors. Interactions between reserpine and various compounds on the accumulation of 5-hydroxytryptamine and noradrenaline in homogenates from rat hypothalamus. Psychotropic agent: antipsychotics and antidepressants, handbook of experimental pharmacology. Biochemical effects of antidepressants in animals. Differential pharmacology of newer antidepressants. Pharmacological aspects of human and canine narcolepsy. Neuropharmacology and neurochemistry of canine narcolepsy. Further characterization of the alpha-1 receptor subtype involved in the control of cataplexy in canine narcolepsy. Nishino S, Fruhstorfer B, Arrigoni J, Guilleminault C, Dement WC, Mignot E. Pharmacologic management of excessive daytime sleepiness. Desmethyl metabolites of serotonergic uptake inhibitors are more potent for suppressing canine cataplexy than their parent compounds. Nishino S, Arrigoni J, Shelton J, Dement WC, Mignot E. This compound had less side effect than those of tricyclic antidepressant, clomipramine. Our study contributes further to previously reported role of adrenergic uptake inhibition in cataplexy. Milnacipran reduced cataplexy in human patients and REM sleep in healthy human subjects. Milnacipran also significantly reduced cataplexy dose-dependently in the study on canine narcolepsy. The percentage of REM sleep significantly decreased ( p = 0.042) in the subjects with milnacipran (17.5 ± 1.7%) compared to subjects with placebo (21.5 ± 2.3%). Milnacipran significantly reduced cataplexy from 9.3 to 5.5 episodes per month in human patients without much side effects. The food-elicited cataplexy test was used to assess the anticataplectic effect of milnacipran. In the study on canine narcolepsy, four genetically narcoleptic Doberman pinschers were enrolled. To assess milnacipran’s depressant effect on REM sleep, we performed nocturnal polysomnography examinations twice on each eight healthy adult subjects who were administered with milnacipran or placebo. The change in the frequency of cataplexy and side effects before and after drug replacement was investigated. Ten human patients with narcolepsy–cataplexy who changed medication from clomipramine to milnacipran due to side effects were enrolled. We also assessed the effect of milnacipran on REM sleep suppression in nocturnal sleep. We assessed the anticataplectic effect of milnacipran, an SNRI, on human and canine narcolepsy. Even though tricyclic antidepressants are effective in reducing sleep paralysis and hypnagogic hallucinations, they even enhance daytime sleepiness, dizziness, and orthostatic hypotension. Cataplexy has been treated pharmacologically, most often with tricyclic antidepressants. Cataplexy is a sudden drop of antigravity-muscle tone triggered most often by positive emotional factors, which is one of the major symptoms of narcolepsy.
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