Cataplexy is treated with medications. Treatment for<unk>  and cataplexy can be divided to those that act on the excessive daytime sleepiness (EDS) and those that improve cataplexy. For most of the patients, this represents lifelong use of medications. Nevertheless, most of the treatments in humans will act only symptomatically and do not target the loss of the orexin producing neurons. When treating cataplexy, all three systems: adrenergic, cholinergic and dopaminergic must be considered. In the studies made both in vitro and in vivo, it was proven that the adrenergic system can be inhibited by the antidepressants. In mouse models, cataplexy is regulated by the dopaminergic system via the D2-like receptor, which when blocked decreases cataplectic attacks . The role of the cholinergic system was also observed in canine models, where it was suggested that stimulation of this system led to severe cataplexy episodes. There are no behavioral treatments. People with<unk>  will often try to avoid thoughts and situations that they know are likely to evoke strong emotions because they know that these emotions are likely to trigger cataplectic attacks. Gamma-hydroxybutyrate Gamma-hydroxybutyrate (GHB, also known as sodium oxybate) has been found to be effective at reducing the number of cataplexy episodes. Sodium oxybate is generally safe and is typically the recommended treatment. Sodium oxybate (GHB) is a natural metabolite of GABA. Its main target is the dopaminergic system because at pharmacological concentration it acts as an agonist and modulates the dopamine neurotransmitters and dopaminergic signalling. GHB was used to treat<unk>  and cataplexy for more than 15 years and it is the only drug authorised by the EMA to treat the whole disease in adults, and by the FDA to treat patients who suffer from cataplexy with the indication to be used for combating excessive daytime sleepiness. This drug helps to normalise the sleep architecture, pushing the REM sleep toward its normal setting, and inhibits the intrusion during the day of its elements like the paralysis in cataplexy. Antidepressants If the above treatment is not possible venlafaxine is recommended. Evidence for benefit is not as good . Previous treatments include tricyclic antidepressants such as imipramine, clomipramine or protriptyline. Monoamine oxidase inhibitors may be used to manage both cataplexy and the REM sleep-onset symptoms of sleep paralysis and hypnagogic hallucinations. In clinical practice, venlafaxine (doses 75–225 mg daily) or clomipramine (25–100 mg daily) are the most common antidepressants used to treat cataplexy. If the patient wishes to have a sedative effect then clomipramine is prescribed. The effect of these drugs is to suppress the REM component and to increase the brainstem monoaminergic levels. Venlafaxine is a norepinephrine and serotonin reuptake inhibitor whereas clomipramine is a tricyclic antidepressant. Their effects can be seen within 48 hours after the drug is administrated and at doses smaller than the ones used in depression. Nonetheless, antidepressants are not approved by the FDA for the treatment of cataplexy; some jurisdictions have approved clomipramine for this use, however. Frequently, tolerance is developed by the patients and typically the risk of cataplexy rebound or “status cataplecticus” appears when their intake is abruptly interrupted. Future treatments for cataplexy Immune-based therapies<unk>  with cataplexy is considered an autoimmune-mediated disorder, so some therapies based on this hypothesis were developed. The immune-based therapies developed were more or less effective and include: * Corticosteroid: after testing in 1 human and 1 canine case it proved to be ineffective so is less likely to be further used. * Intravenous immunoglobulins (IVIgs): it may decrease the symptoms but its effectiveness is still subjective and unconfirmed by the placebo-controlled trials. It was also suggested that sometimes it might have life-threatening side effects. Nevertheless, after giving this treatment to a patient with undetectable orexin levels in the cerebrospinal fluid after only 15 days after the disease onset, the cataplexy was improved and the orexin levels started to normalise. * Plasmapheresis: should be similar with IVIgs but it is more invasive and for it even less data is available. * Immunoadsorption * Alemtuzumab Histaminergic H3 receptor inverse agonist The histaminergic neurons have a very important role in preserving consciousness and in helping maintain wakefulness and remain active during cataplexy. In<unk> , there seems to be an increase in these neurons, possibly to compensate for hypocretin loss. A promising therapy would be to increase the activation of histaminergic neurons by an inverse agonist of the histamine H3 receptor, which enhances histamine release in hypothalamus. An inverse agonist of the histamine H3 is Pitolisant. Results after testing on animals have indicated increased wakefulness in normal animals, decreased sleepiness and blocked the abnormal transitions from REM sleep to awake state in the hypocretin knock-out mice. Also placebo-controlled studies suggest some positive effects of Pitolisant on cataplexy symptoms increasing the levels of alertness and wakefulness.
symptom of Narcolepsy
symptom of Delirium
symptom of Botulism
symptom of Alcohol intoxication
symptom of Opioid use disorder
symptom of Delirium tremens
symptom of Insomnia
symptom of Progeria