Erratum

The following letter originally appeared in the March 2000 issue of The Canadian Journal of Psychiatry. It contained substantial errors in dosages and was printed without the authors' approval. We apologize to the authors and readers. The corrected text appears here in its entirety. Paroxetine and Tardive Akathisia Dear Editor: There have been several reports of akathisia associated with the use of selective serotonin reuptake inhibitors (SSRIs), usually rapid in onset and occurring within days of drug initiation (1). This report describes the case of a patient who developed delayed-onset or tardive akathisia with paroxetine treatment. Case Report Mr A was a 38-year-old male with obsessive-compulsive disorder (OCD), with compulsions to view morgues and operating rooms. In addition, he suffered from multiple paraphilias, including pedophilia, exhibitionism, and voyeurism. He was born prematurely to a mother who had abused drugs and alcohol throughout the pregnancy, and he had a cleft lip and palate repaired after birth. He also had significant facial dysmorphism. Despite this background, he had a normal to above-average intellect and good insight into his psychiatric problems. He was compliant with his treatment, with few emergency visits and no history of drug-seeking behaviour. He had been treated with paroxetine 70 mg once daily for 2 years for his OCD. In addition, he received leuprolide (Lupron) 7.5 mg intramuscularly (IM) every 4 weeks for 7 years for his paraphilias, and alendronate (Fosamax)5 mg once daily for 3 years for osteoporosis. Previously, a trial of clomipramine had also been used for his OCD. In addition, a diagnosis of Tourette syndrome had been considered in his past because of the presence of motor tics, which resulted in the trial of pimozide 3 years ago. However, this medication was stopped shortly thereafter because the patient developed an acute akathisia. At this time, Mr A presented with a subjective inner restlessness, which he described as being identical to his reaction to pimozide 3 years previously. Objectively, he was noted to have restless leg movements. There had been no change to his medication regimen for 2 years. He was started on lorazepam 1 mg 3 times daily as needed, and all complaints of restlessness disappeared after 4 days. No further treatment or medication change was required. Discussion Tardive akathisia is defined as an akathisia of delayed onset, in the absence of a change of drug dose or type within 3 months (2). The incidence of acute akathisia with neuroleptics is in the range of 20% to 30% (3), compared with 9.8% to 25% for SSRIs (1). The incidence of tardive akathisia with neuroleptics has been reported to be between 18% and 41% (2). Tardive akathisia has not been reported previously in relation to drugs other than antipsychotics (2). While the differential diagnosis for this case could include anxiety related to the patient's OCD, or the combination of medications, the subjective similarityto the previous akathisia and its quick resolution with lorazepam led to a diagnosis of tardive akathisia. Of his 3 medications, paroxetine was the only psychoactive substance and, thus, was the most likely cause of this reaction. Given this patient's complex medical history, there may have been a genetic predisposition to the development of akathisia in this particular case. It has been suggested that SSRIs may inhibit dopaminergic neuronal activity in the ventral tegmental area to produce akathisia (4). While previous reports have indicated that the clinician must be aware of the possibility of akathisia when initiating an SSRI, this case illustrates that this side effect may occur without a recent change in the medication.

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