Withdrawal syndrome after discontinuation of venlafaxine
Available from: Brian H Harvey
- "The pharmacological and pharmacokinetic profile of the prescribed antidepressant is a reliable predictor of ADS risk. For most, ADS symptoms are more common after the sudden discontinuation of antidepressants (Baldwin et al., 2007), especially SRIs, for example paroxetine and sertraline (Thompson, 1998), and SNRIs, for example venlafaxine (Agelink et al., 1997) and duloxetine (Warner et al., 2006), but also atypical agents such as mirtazapine (Berigan, 2001) and trazodone (Peabody, 1987). Clinical experience strongly suggests that a short T½ provides added risk (e.g. "
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Antidepressants are at best 50–55% effective. Non-compliance and the antidepressant discontinuation syndrome (ADS) are causally related yet poorly appreciated. While ADS is associated with most antidepressants, agomelatine seems to be devoid of such risk. We review the neurobiology and clinical consequences of antidepressant non-compliance and the ADS. Agomelatine is presented as a counterpoint to learn more on how ADS risk is determined by pharmacokinetics and pharmacology.DesignThe relevant literature is reviewed through a MEDLINE search via PubMed, focusing on agomelatine and clinical and preclinical research on ADS.ResultsAltered serotonergic dysfunction appears central to ADS so that how an antidepressant targets serotonin will determine its relative risk for inducing ADS and thereby affect later treatment outcome. Low ADS risk with agomelatine versus other antidepressants can be ascribed to its unique pharmacokinetic characteristics as well as its distinctive actions on serotonin, including melatonergic, monoaminergic and glutamatergic-nitrergic systems.Conclusions
This review raises awareness of the long-term negative aspects of non-compliance and inappropriate antidepressant discontinuation, and suggests possible approaches to “design-out” a risk for ADS. It reveals intuitive and rational ideas for antidepressant drug design, and provides new thoughts on antidepressant pharmacology, ADS risk and how these affect long-term outcome. Copyright © 2014 John Wiley & Sons, Ltd.
Human Psychopharmacology Clinical and Experimental 11/2014; 29(6). DOI:10.1002/hup.2429 · 2.19 Impact Factor
Available from: Dieter Riemann
- "Various withdrawal symptoms have been repeatedly described for all subclasses of antidepressants and include mainly mild changes in mood, vegetative functions and sleep (Lejoyeux and Ades, 1997). Venlafaxine, as a potent serotonine and noradrenaline reuptake inhibitor with a relatively short half-life of about 5 h (11 h for its main metabolite O-desmethyl-venlafaxine) seems to cause a particularly strong REM sleep suppression (Salin- Pascual et al., 1997) and may be especially potent to induce withdrawal reactions including a marked REM rebound after discontinuation (Agelnik et al., 1997). The high REM sleep pressure may result in SOREMPs during sleep and even multiple cataplectic attacks during waking caused by short REM sleep episodes with the REM typical inhibition of alphamotoneurons and muscle atonia. "
Journal of Sleep Research 07/2005; 14(2):207-8. DOI:10.1111/j.1365-2869.2005.00447.x · 3.35 Impact Factor
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Venlafaxine is an antidepressant that selectively inhibits serotonin reuptake and is a norepinephrine inhibitor. Withdrawal syndromes can occur after abrupt drug discontinuation of long-term regimens.
We report six cases of withdrawal symptoms after venlafaxine discontinuation.
Physicians must be aware of the frequency, rapidity and potent severity of these withdrawal syndromes.
La Revue de Médecine Interne 03/2000; 21(3):282-284. DOI:10.1016/S0248-8663(00)80048-X · 1.07 Impact Factor
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