Indian J. Psychiat., 1992,34(3), 27S-279 FLUOXETINE INDUCED AKATHISIA - A CASE REPORT VINAY GUPTA1 Akathisia is a common side-effect of the amitriptyline, nitroxazepine given along with neuroleptic drugs and occurs in about 5% to lithium, low doses of haloperidol and 75% cases treated with these compounds (Bar­ thioridazine, in different combinations. How­ nes et al., 1985; Van Putten et at., 1984). In ever not all drugs were precribed in adequate addition, akathisia like syndromes are doses and for sufficient length of time to actual­ produced with conditions such as uremia, ly call him resistant to treatment with these idiopathic restless legs syndrome, congestive compounds. He was prescribed fluoxetine in heart failure, idiopathic parkinsonism, and with view of its established efficacy in OCD and also drugs such as reserpine, .trycyclic antidepres­ in depressive illness. sants (Gibb et al., 1986; Zubenko et al., 1987) and diltiazem. Two weeks later when he came for his scheduled follow up, he was not taking In 1978, Zitrin et alreported that 18% of fluoxetine, as he reported to have their cases in a series of patients with phobias, developed marked restlessnes, anxiety, in­ treated with imipramine developed a syndrome somnia, inability to sit still on the 5th day of characterised by "insomnia, jitteriness ir­ medication with 20mg/day morning dose of ritability and unusual energy" on dosage ranging fluoxetine. He was prescribed phenargan 25 from 5-75mg/day. This is quite similar to mg thrice a day by a local psychiatrist in his akathisia, a side-effect also reported with the city, whom he contacted with these com­ antidepressant fluoxetine by Lipinski et al. plaints, and he felt relieved of these (1989). symptoms within two days. A single case report of akathisia as a. On this follow up visit he had no such side-effect with fluoxetine is being discussed complaints and he had been off medicines for below. almost 8 days. He was reassured and advised to restart fluoxetine 20mg/day, considering his CASE HISTORY complaints to be temporary side-effects with the drug, which would pass off after a few days. A 22 year old unmarried, north Indian On the 6th day, he was back in the hospital, very male, visited our hospital clinic, with 3 year anxious, restless, jittery, and unable to keep his illness history, diagnosed as obsessive com­ legs still, and unable to sit still, with an urge to pulsive disorder (OCD) with secondary move about with which he felt better. The sub­ depression. He was put on Fluoxetine, start­ jective experience and his appearance sug­ ing with 20mg/day along with bed time gested the possibility of akathisia which is not diazepam 5mg. He had been drug free for mentioned as a side-effect in the product almost 15 days, and prior to this he had been monograph of fluoxetine, but anxiety, nervous­ treated with a variety of antidepressants, ness and insomnia is reported in about 10%- alone and in combination with other 15% of treated patients (Stark et al., 1985). psychopharmacological agents. He seemed to There was no sign of parkinsonism or dystonia have been unresponsive to imipramine, or any other finding on examination. 1 Lecturer, Department of Psychiatry, Christian Medical College, Ludhiana -141001. FLUOXETINE INDUCED AKATHISIA 279 He was then advised diazepam Lipinski et al., have suggested the prob­ lOmg/day along with propranolol 40mg/day ad­ able patho-physiology of fluoxetine induced ditionally, both in three divided doses, with akathisia. Akathisia follows the inhibition of which he felt better around 2nd & 3rd day, with dopaminergic neilrone in the Ventral tegmental symptoms reappearing on discontinuation of area (VTA). Fluoxetine and other compounds these. He was later shifted to imipramine that enhance serotonergic transmission (in­ therapy and fluoxetine was totally discontinued cluding Tricyclic anti-depressants (TCA'S) and because the patient refused to continue to take Mono-amine Oxidase Inhibitor's (MAOI'S)) it. produce akathisia, by enhancing serotonergi- cally mediated inhibition of Dopamine (DA) cells in the VTA, producing DA defiency and thus akathisia (Lipinski et al., 1989). DISCUSSION The case report is relevant because of Review of the literature on fluoxetine the recent introduction of fluoxetine in the In­ brought to light a paper by Lipinski et al. (1989), dian market. Combination of fluoxetine with a reporting 5 cases of akathisia induced by neuroleptic compound may increase the risk of fluoxetine. Three out of these five cases developing akathisia with fluoxetine. Moreover developed akathisia on the 5th day on 60 mg/day controlled prospective studies to determine its of fluoxetine, one within 12 hours on 20mg/day true incidence can be carried out. and the 5th after hours on a dose of 40mg/day. Fluoxetine induced akathisia is indistin­ guishable from neuroleptic akathisia, but is REFERENCES milder, and usually comes around the 5th day. Tolerance may develop to it, but it is relieved by Barnes, T.R.F. and Braudc, W.M. (1985). Akathisis variant either decreasing the dose of fluoxetine or ad­ and tardive dyskinesia. Arch Gen. Psychiatry, 42,874-878. ministration of propranolol, an adnergic recep­ Glbb, W.R.G. and Lees, AJ. (1986). The restless leg tor antogonist. Akathisia in these cases is not syndrome. Post. Grad. Med. J., 62,329-333. associated with signs and symptoms of parkin­ Lipinski, J.F.; Keck, P.F. and McElory, S.L. (1988). 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