Abstract
Sir: Antidepressants have been noted to cause hallucinations, often with drug overdose, but also in rare instances as a side effect at therapeutic dose.1 Bupropion, tricyclics, and selective serotonin reuptake inhibitors (SSRIs) have most often been cited as the causative agents.1 We present a case of transient complex visual hallucinations following the initiation of venlafaxine for major depressive disorder. Case report. Mr. A was a 44-year-old man recovering from alcohol dependence in an outpatient partial hospitalization program. He had been recently hospitalized for delirium tremens and was discharged 3 days before admission to our outpatient program in December 2007. He began venlafaxine treatment, 75 mg daily, for depression 2 weeks after his last drink. Before initiation of treatment, he had had no auditory or visual hallucinations for 10 days and no history of psychotic disorders or manic symptoms. He was diagnosed according to DSM-IV-TR with alcohol dependence and recurrent major depressive disorder without psychosis. Mr. A had been 3 weeks' sober when, after 1 week of venlafaxine treatment, he reported having visual hallucinations during daytime group sessions: seeing an acetylene torch in his hand and trying to strike it against his desk to light it as well as nodding his head to drop a welding shield over his face, as he did when he worked as a welder. He had insight that these were hallucinations. He had no delusions or hallucinations in other modalities, no manic symptoms, and no altered mental status. The only other side effect noted was increased vividness to his dreams. The only other medication changes were the addition of lactulose for mildly elevated ammonia, 41 μmol/L at the onset of hallucinations. After 1 week, his hallucinations resolved, and he had no repeat episodes. The venlafaxine dose was maintained throughout his treatment. He completed the outpatient program and was discharged without further incidents 3 weeks later, and at 2 monthly follow-up appointments he reported no additional hallucinations. Antidepressants have been cited as inducing hallucinations in rare cases. There have been 2 reports of venlafaxine-induced hallucinations, in an adolescent patient and an adult patient.2,3 Given that Mr. A's dose was low (75 mg daily), the assumed mechanism of action for hallucinosis is serotonergic, not norepinephrinergic. Some studies have suggested that SSRIs may induce psychotic symptoms by 5-HT2– and 5-HT3–mediated dopamine release in the ventral striatum.4 Venlafaxine may have produced visual hallucinations via dopamine release in the mesolimbic pathway by stimulation of 5-HT2 and 5-HT3 receptors. A possible interaction could have been reactivation of alcoholic hallucinosis with venlafaxine, which was reported with sertraline in 1 case by Hermann et al.5 However, the causative mechanism in that case was felt to be due to increased dopamine availability. Sertraline shows the greatest amount of dopamine reuptake inhibition of all SSRIs, while venlafaxine shows no inhibition of the dopamine reuptake transporter. Lastly, our patient's ammonia was mildly elevated, and treatment could have exacerbated a subclinical hepatic encephalopathy, although no altered mental status or other signs of delirium were observed during his partial hospitalization. Adam C. Tripp, M.D., Ph.D. Western Psychiatric Institute & Clinic, University of Pittsburgh Medical Center Scott A. Golden, M.D. Behavioral Health Division, Veterans Hospital at Highland Drive, Pittsburgh, Pennsylvania
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