Venlafaxine-Induced Complex Visual Hallucinations in a 17-Year-Old Boy

Jacob, Maryann; Ash, Peter

doi:10.4088/jcp.08l04627

Cited by 7 publications

(6 citation statements)

References 8 publications

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“…Such clinical judgement would justify the prescription of a medication class (i.e. ADs) that otherwise, is well-known to increase the risk of a manic switch (Fava, 2020) and may rarely induce isolated symptoms of psychosis in young people (Capaldi & Carr, 2010; Jacob & Ash, 2009).…”

Section: Discussionmentioning

confidence: 99%

Do antidepressants prevent transition to psychosis in individuals at clinical high-risk (CHR-P)? Systematic review and meta-analysis

2022

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Background Emerging meta-analytical evidence indicates that baseline exposure to antipsychotics in individuals at clinical high-risk for psychosis (CHR-P) is associated with a higher risk of an imminent transition to psychosis. Despite their tolerability profile and potential beneficial effects, baseline exposure to antidepressants (AD) in CHR-P has surprisingly received far less attention as a potential risk modulator for transition to psychosis. The current systematic review and meta-analysis were performed to fix such a knowledge gap. Methods Systematic scrutiny of Medline and Cochrane library, performed up to 1 August 2021, searching for English-language studies on CHR-P reporting numeric data about the sample, the transition outcome at a predefined follow-up time and raw data on AD baseline exposure in relation to such outcome. Results Of 1942 identified records, 16 studies were included in the systematic review and meta-analysis. 26% of the participants were already exposed to AD at baseline; at the end of the follow-up 13.5% (95% CI 10.2–17.1%) of them (n = 448) transitioned to psychosis against 21.0% (18.9 to 23.3%) of non-AD exposed CHR-P (n = 1371). CHR-P participants who were already under AD treatment at baseline had a lower risk of transition than non-AD exposed CHR-P. The RR was 0.71 (95% CI 0.56–0.90) in the fixed-effects model (z = −2.79; p = 0.005), and 0.78 (0.58–1.05) in the random-effects model (z = −1.77; p = 0.096; tau-squared = 0.059). There was no relevant heterogeneity (Cochran's Q = 18.45; df = 15; p = 0.239; I2 = 18.7%). Conclusions Ongoing AD exposure at inception in CHR-P is associated to a reduced risk of transition to psychosis at follow up.

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Section: Discussionmentioning

confidence: 99%

Do antidepressants prevent transition to psychosis in individuals at clinical high-risk (CHR-P)? Systematic review and meta-analysis

2022

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“…We cannot definitively conclude that this patient's visual hallucinations were entirely induced by pregabalin, although similar rare occurrences have been reported in the literature. Venlafaxine has been associated with hallucinations and psychotic symptoms previously and so the potential for a synergistic effect with pregabalin cannot be ruled out and further research is needed [26,27]. We have performed a formal assessment of the likelihood the adverse event was caused by pregabalin, using the Naranjo algorithm and the score was 7, which shows that this is a probable adverse drug reaction due to pregabalin.…”

Section: Discussionmentioning

confidence: 99%

Pregabalin induced visual hallucinations – a rare adverse reaction

Mousailidis

Papanna

Salmon

et al. 2020

BMC Pharmacol Toxicol

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Background: Pregabalin is an anticonvulsive, analgesic and anxiolytic medication. The typical side effects include dizziness, somnolence and weight gain. Few studies or case reports have demonstrated psychiatric side effects resulting from its use. Case presentation: We present a patient who suffered visual hallucinations and agitation associated with an increase in pregabalin dose, resolving completely after pregabalin discontinuation.Conclusions: Acute visual hallucinations should be considered in the clinical spectrum of very rare side effects of pregabalin use, especially at higher doses. Tapered discontinuation of the medication can improve and resolve symptoms.

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“…Since DAT is not very high in the prefrontal cortex, dopamine is removed from the synaptic space via NET [14]. It is thought that, increased dopamine in the synaptic range, alongside the NET inhibition of SNRIs, may cause hallucinations [15]. It is also emphasized that serotonin may cause hallucinations as a result of increased dopamine in the ventral striatum via 5HT2 and 5HT3 receptors, as a consequence of the inhibition reuptake [16][17][18].…”

Section: Discussionmentioning

confidence: 99%