Status Cataplecticus Precipitated by Abrupt Withdrawal of Venlafaxine

Wang, Janice; Greenberg, Harly

doi:10.5664/jcsm.2848

Cited by 41 publications

(18 citation statements)

References 4 publications

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“…Typical side effects of SNRIs include sweating, tachycardia, and hypertension. In both, SSRI and SNRI, status cataplecticus can emerge with a fast withdrawal [53]. Interestingly, the efficacy of SSRIs and SNRIs for cataplexy treatment has not been investigated in randomized placebo-controlled trials.…”

Section: Antidepressantsmentioning

confidence: 99%

Therapy for Cataplexy

Heidbreder

Dirks

Ramm

2020

Curr Treat Options Neurol

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Purpose of the review Cataplexy, an involuntary loss of muscle activity triggered by strong emotions is the most impressive symptom in narcolepsy. This review gives an overview of the current understanding of cataplexy and its available treatment options. Recent findings With the discovery of hypocretin/orexin, the understanding of the pathophysiology of cataplexy advanced in the past decades. In the recent years, with the development of new anticataplectic agents (e.g., Pitolisant) symptomatic treatment of cataplexy has further improved. Abrupt cessation of anticataplectic medication especially antidepressants increase the risk of status cataplecticus, a virtually continuous series of long-lasting cataplectic attacks. Summary Cataplexies still remain an under-recognized phenomenon due to missing diagnostic measures. Treatment for cataplexy still remains symptomatic but new agents with better tolerability and usability are continuously developed. New therapeutic actions either targeting the autoimmune mechanisms underlying orexin cell death or substituting orexin action are promising treatments for the near future.

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Section: Antidepressantsmentioning

confidence: 99%

Therapy for Cataplexy

Heidbreder

Dirks

Ramm

2020

Curr Treat Options Neurol

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“…Any positive effect occurs fairly soon after starting treatment, in contrast to the expected delay when using such agents for depression. Once established on treatment, patients are encouraged to adhere strictly to the medication, as suddenly stopping it commonly leads to severe rebound cataplexy 27. From animal studies, cataplexy can be exaggerated by agents such as prazosin that enhance or promote REM sleep,28 implying that such drugs should be avoided in narcolepsy.…”

Section: Treatmentmentioning

confidence: 99%

Cataplexy

Reading

2018

Pract Neurol

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Remarkably and almost invariably, the clinical phenomenon of cataplexy results from the loss of around 40 000 hypocretin-containing neurones in the lateral hypothalamus in the context of narcolepsy type 1. Cataplexy reflects the dysregulation of rapid-eye-movement (REM) sleep, such that REM-sleep atonia intrudes inappropriately into wakefulness as brief episodes of either focal or total paralysis of voluntary muscle. The semiology of cataplexy differs between adults and children. A defining and enigmatic aspect is that certain emotional stimuli usually trigger the episodes. Cataplexy can be the most disabling symptom of the narcolepsy syndrome, severely limiting normal activities of daily living. Antidepressant drug therapy at relatively low doses is the traditional treatment; these most likely work through inhibiting REM sleep, predominantly by increasing brain monoamine concentrations. Sodium oxybate is probably the most effective drug for severe cataplexy, taken before overnight sleep and once through the night; its precise mechanism of action remains obscure. Pitolisant is a new agent for treating the excessive daytime sleepiness of narcolepsy that also helps cataplexy control by increasing histamine concentrations in the hypothalamus. Further understanding of the neurobiology of cataplexy and how it relates to hypocretin deficiency should improve our understanding of the brain’s emotional processing and provide insights into REM sleep and its control.

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“…SNRIs are advantageous over tricyclic antidepressants because, unlike the latter, they do not block muscarinic cholinergic, H 1 histaminergic, nor α1-adrenergic receptors, thereby resulting in fewer side effects (Dauvilliers et al, 2014b; Guilleminault and Cao, 2011). However, similar to tricyclic antidepressants, SNRIs are associated with an increase in the number and severity of cataplexy attacks after withdrawal, even with gradual tapering of the drugs (Ristanovic et al, 2009; Wang and Greenberg, 2013). Antidepressants have also been linked to the development of REM behavior disorder (Ju et al, 2011), although it is not clear if narcolepsy predisposes for this risk.…”

Section: Therapeuticsmentioning

confidence: 99%

Challenges in the development of therapeutics for narcolepsy

Black

Yamanaka

Kilduff

2017

Progress in Neurobiology

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Narcolepsy is a neurological disorder that afflicts 1 in 2000 individuals and is characterized by excessive daytime sleepiness and cataplexy—a sudden loss of muscle tone triggered by positive emotions. Features of narcolepsy include dysregulation of arousal state boundaries as well as autonomic and metabolic disturbances. Disruption of neurotransmission through the hypocretin/orexin (Hcrt) system, usually by degeneration of the HCRT-producing neurons in the posterior hypothalamus, results in narcolepsy. The cause of Hcrt neurodegeneration is unknown but thought to be related to autoimmune processes. Current treatments for narcolepsy are symptomatic, including wake-promoting therapeutics that increase presynaptic dopamine release and anticataplectic agents that activate monoaminergic neurotransmission. Sodium oxybate is the only medication approved by the US Food and Drug Administration that alleviates both sleep/wake disturbances and cataplexy. Development of therapeutics for narcolepsy has been challenged by historical misunderstanding of the disease, its many disparate symptoms and, until recently, its unknown etiology. Animal models have been essential to elucidating the neuropathology underlying narcolepsy. These models have also aided understanding the neurobiology of the Hcrt system, mechanisms of cataplexy, and the pharmacology of narcolepsy medications. Transgenic rodent models will be critical in the development of novel therapeutics for the treatment of narcolepsy, particularly efforts directed to overcome challenges in the development of hypocretin replacement therapy.

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Status Cataplecticus Precipitated by Abrupt Withdrawal of Venlafaxine

Cited by 41 publications

References 4 publications

Therapy for Cataplexy

Therapy for Cataplexy

Cataplexy

Challenges in the development of therapeutics for narcolepsy

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