- Email: [email protected]
Propanolol for fluoxetine-induced akathisia
Correspondence
toOL IaS¥CH|ATRY
53 |
t99t ~ 5 2 ~ 532
Table I. Symptom Response of DOP and Side Effects Under Treatment with FluspiriMr~, Fen~ayl, Opiate Receptor Antagonists, and Placebo Drug
Daily doses
Duration of treatment
Symptom respome of DOP
Fluspirilene
Unknown
8 weeks
Tempor'ay Lmpr~,ce~at
Fentanyl
0. i mg IV in 500 mi saline solution 500 mi saline solution 10 mg IV in 500 mi saline solution
! day
Marked deterioration
4 days
No char~ge
5 days
Total remiss~ d ~ n g the first hours ~ter mfus~em thereupon gr~u~ return of DOP-symptems No change Marked improvement Marked ~mpm:,~emem
Placebo Naloxone
Placebo Naloxone Naltrexone
2 tabletsp.o. 2.4 mg IM Up to 200 mg p.o.
I week I week 8[ weeks
Psychiatric Hospital of the University of Munich Nul~baumstral3e 7 8000 Mfinchen 2 Federal Republic of Germany
References
and behavioral responses. 13:397-408.
Sk~ effects Severe exwa.O?rarmdai side effects Anxiety ~ a g i ~ after mfusio~ No s ~ effects Euphoric ~ infuskm
after
No s ~ effects No side effects Slight increase of I,iver e n z y ~ concentrations in blood
Psychoneuroendocrinology
Johnson GC, Antort P,F (1983): Pimozide m ~lmions of parasitosis. J Ctin P~chiat~., 44:233. Naber D, PickaxD, Davis C~, et M( 1981)::Naloxone effects on ~-endorphin, cQrtisoI, protactin, grow~ hormone, HVA and MHPG in plasma of no,,-mal voIunteers. P~¢chophamacology 74:125-128.
Hoehe M, Duka T, Doeniche A (1988): Human studies o n the Ix opiate receptor agonist fentanyl: neur~ndocrine
Propanolol for Fluoxetine-lnduced Akathisia To the Editor: The syndrome of akathisia is a common side effect of the treatment with antipsychotic drugs. Drug-induced akathisia has also been reported following treatment with lithium (Patterson 1988), methysergide (Bemick 1988), tricyclic antidepressants (Zubenko et al 1987), trazodone (Zubenko et al 1987) and fluoxetine (Lipinski et al 1989). In the following we describe a patient with fluoxetine-induced akathisia who responded to treatment with propanolol.
Mrs. R., a 46-year-old w o ~ , suffering from a major depressive episode (DSM-m-R, American Psychia~ic Association 1987) had been treat*~ with various antidepressants over the last l0 years. She had never received a 5 Hydroxytryptamin (HT) reuptake inhibitor before. Because of s i ~ f i c a n t weight gain following treatment with tricyclic antidepressants we attempted to treat her most recent episode with the specific 5 HT reuptake ~ i b i t o r fluoxetine. She was started on 20 mg fluoxetme dmly. The dose was raised to 40 mg after 2 weeks due to insufficient efficacy. On the visit following the dose increment, the patient reported she felt increasingly anxious and
532
BIOLPSYCHIATRY 1991;30:526-532
agitated since her dose was raised. She also experienced an increase in sleep disturbance. Objective evaluation wi~h the Hillside Akathisia Scale (HAS, Fleischhacker et al 1989) revealed significant objective (9) and subjective (6) akathisia with a total score of 15. Objective symptoms were found in legs and arms, the patient constantly moved her feet while sitting and showed fidgety symptoms in her fingers. Propanolol (20 mg rid) was prescribed to counteract akathisia and led to immediate symptom relief, which started on the second day of treatment and reached a maximum by day 3. ~uoxetine dose reduction was not attempted due to the patient's primary symptoms. Stopping propanolol for 2 days was followed by a recurrence of akathisia, treatment had to be taken up again. After 12 weeks of treatment the patient had lost 12 pounds, her depression resolved, and she stopped all medication abruptly without negative consequences. She has s;,".cc ~ , weii for the l~st 4 months. The notion that selective 5-HT reuptake inhibitors induce akathisia is supported by case reports like the one by Lipinski et al (1989) and ours. Inte~stingly, a preliminary analysis of the German drug side effects surveillance study AMUP (Arzneimittelfiberwachung in der Psychiatrie, Grohmann 1989) has also reported the side effect "agitation" to be significantly more frequent following clomipramine, a tricyclic antidepressant with strong antiserotonergic properties, when compared with other tricyclic antidepressant drugs. The fact that Ritanserin, a 5HT2 antagonist, has been shown to be effective in the treatment of NIA can also be seen as an indication of the involvement of the serotonergic system in the pathophysiology of this syndrome. Our patient clearly presented with subjective and objective akathisia during fluoxetine treatment. Whether the dose increase led to akathisia cannot be answered cle~xly; it might also be possible that the late onset cf steady state plasma levels, as reported
Correspondence
for fluoxetine (Sommi et al 1987) resulted in the time course of akathisia observed in this patient. Pmpanolol treatment induced rapid aod complete symptom remission as has been reported for neuroleptic-induced akathisia. The problem of antidepressant ind~ akathisia clearly calls for furfl~x study as neither prevalence nor incidence of this syedrome have so far been systematically investigated. At the same time the treatment of this syndrome needs to be evaluated by controlled clinical ~als. W. Wolfgang Fleischhacker Department o f Psychiatry lnnsbruck University A-6020 Innsbruck, Austria
Refere.ces Amefi~ Psychiatric Association (1987): Diagnostic and Statistical Manual of Mental Disorder.,', 3,d ed, revised.
Washington DC: Americm Psychiamc Association. Bemick C. (1988): Methysergide-induced akathisia. Clin Neuropkannacol ! !:87-89. Fleischhacker W, Be~'gmannKJ, Perovich R et al (1989): The Hillside Akathisia Scale: a new rating insmunent for ~ inctu~e akathim. Psychor~nmc~ a ~ 25:222-226. Grohm.annR (t989): I0 Jahre AMUP---R0ckblickund Ausblick. Plesentationgiven at a workshopof the 16 AGNP Symposium, Nuemberg (Absuact) Lipinski Jr JF, Mallya G, Zimmerman P, Pope G (1989): Fluoxetine-induced akathisia: clinical and theoreti~'~al implications. J Clin Psych~ury 50:339-342. P~tterson J'F (1988): Lithium-inducedakathisia. 1 Clin Psychopharmaco/8:455. Sommi R, Crismon M, Bowden C (1987): Fluoxet~e: a serotonin-specific, second-generation antidepressant. •-,m,m,,,o, nerapy 7:1-15. Zubenko GS, Cohen BM, Lipinski LF (1987): Antidepressant related ~athisia..7 Clin Psychopharmacol 7"254DL
.
.
257.
.
.
.L
. . . .
toOL IaS¥CH|ATRY
53 |
t99t ~ 5 2 ~ 532
Table I. Symptom Response of DOP and Side Effects Under Treatment with FluspiriMr~, Fen~ayl, Opiate Receptor Antagonists, and Placebo Drug
Daily doses
Duration of treatment
Symptom respome of DOP
Fluspirilene
Unknown
8 weeks
Tempor'ay Lmpr~,ce~at
Fentanyl
0. i mg IV in 500 mi saline solution 500 mi saline solution 10 mg IV in 500 mi saline solution
! day
Marked deterioration
4 days
No char~ge
5 days
Total remiss~ d ~ n g the first hours ~ter mfus~em thereupon gr~u~ return of DOP-symptems No change Marked improvement Marked ~mpm:,~emem
Placebo Naloxone
Placebo Naloxone Naltrexone
2 tabletsp.o. 2.4 mg IM Up to 200 mg p.o.
I week I week 8[ weeks
Psychiatric Hospital of the University of Munich Nul~baumstral3e 7 8000 Mfinchen 2 Federal Republic of Germany
References
and behavioral responses. 13:397-408.
Sk~ effects Severe exwa.O?rarmdai side effects Anxiety ~ a g i ~ after mfusio~ No s ~ effects Euphoric ~ infuskm
after
No s ~ effects No side effects Slight increase of I,iver e n z y ~ concentrations in blood
Psychoneuroendocrinology
Johnson GC, Antort P,F (1983): Pimozide m ~lmions of parasitosis. J Ctin P~chiat~., 44:233. Naber D, PickaxD, Davis C~, et M( 1981)::Naloxone effects on ~-endorphin, cQrtisoI, protactin, grow~ hormone, HVA and MHPG in plasma of no,,-mal voIunteers. P~¢chophamacology 74:125-128.
Hoehe M, Duka T, Doeniche A (1988): Human studies o n the Ix opiate receptor agonist fentanyl: neur~ndocrine
Propanolol for Fluoxetine-lnduced Akathisia To the Editor: The syndrome of akathisia is a common side effect of the treatment with antipsychotic drugs. Drug-induced akathisia has also been reported following treatment with lithium (Patterson 1988), methysergide (Bemick 1988), tricyclic antidepressants (Zubenko et al 1987), trazodone (Zubenko et al 1987) and fluoxetine (Lipinski et al 1989). In the following we describe a patient with fluoxetine-induced akathisia who responded to treatment with propanolol.
Mrs. R., a 46-year-old w o ~ , suffering from a major depressive episode (DSM-m-R, American Psychia~ic Association 1987) had been treat*~ with various antidepressants over the last l0 years. She had never received a 5 Hydroxytryptamin (HT) reuptake inhibitor before. Because of s i ~ f i c a n t weight gain following treatment with tricyclic antidepressants we attempted to treat her most recent episode with the specific 5 HT reuptake ~ i b i t o r fluoxetine. She was started on 20 mg fluoxetme dmly. The dose was raised to 40 mg after 2 weeks due to insufficient efficacy. On the visit following the dose increment, the patient reported she felt increasingly anxious and
532
BIOLPSYCHIATRY 1991;30:526-532
agitated since her dose was raised. She also experienced an increase in sleep disturbance. Objective evaluation wi~h the Hillside Akathisia Scale (HAS, Fleischhacker et al 1989) revealed significant objective (9) and subjective (6) akathisia with a total score of 15. Objective symptoms were found in legs and arms, the patient constantly moved her feet while sitting and showed fidgety symptoms in her fingers. Propanolol (20 mg rid) was prescribed to counteract akathisia and led to immediate symptom relief, which started on the second day of treatment and reached a maximum by day 3. ~uoxetine dose reduction was not attempted due to the patient's primary symptoms. Stopping propanolol for 2 days was followed by a recurrence of akathisia, treatment had to be taken up again. After 12 weeks of treatment the patient had lost 12 pounds, her depression resolved, and she stopped all medication abruptly without negative consequences. She has s;,".cc ~ , weii for the l~st 4 months. The notion that selective 5-HT reuptake inhibitors induce akathisia is supported by case reports like the one by Lipinski et al (1989) and ours. Inte~stingly, a preliminary analysis of the German drug side effects surveillance study AMUP (Arzneimittelfiberwachung in der Psychiatrie, Grohmann 1989) has also reported the side effect "agitation" to be significantly more frequent following clomipramine, a tricyclic antidepressant with strong antiserotonergic properties, when compared with other tricyclic antidepressant drugs. The fact that Ritanserin, a 5HT2 antagonist, has been shown to be effective in the treatment of NIA can also be seen as an indication of the involvement of the serotonergic system in the pathophysiology of this syndrome. Our patient clearly presented with subjective and objective akathisia during fluoxetine treatment. Whether the dose increase led to akathisia cannot be answered cle~xly; it might also be possible that the late onset cf steady state plasma levels, as reported
Correspondence
for fluoxetine (Sommi et al 1987) resulted in the time course of akathisia observed in this patient. Pmpanolol treatment induced rapid aod complete symptom remission as has been reported for neuroleptic-induced akathisia. The problem of antidepressant ind~ akathisia clearly calls for furfl~x study as neither prevalence nor incidence of this syedrome have so far been systematically investigated. At the same time the treatment of this syndrome needs to be evaluated by controlled clinical ~als. W. Wolfgang Fleischhacker Department o f Psychiatry lnnsbruck University A-6020 Innsbruck, Austria
Refere.ces Amefi~ Psychiatric Association (1987): Diagnostic and Statistical Manual of Mental Disorder.,', 3,d ed, revised.
Washington DC: Americm Psychiamc Association. Bemick C. (1988): Methysergide-induced akathisia. Clin Neuropkannacol ! !:87-89. Fleischhacker W, Be~'gmannKJ, Perovich R et al (1989): The Hillside Akathisia Scale: a new rating insmunent for ~ inctu~e akathim. Psychor~nmc~ a ~ 25:222-226. Grohm.annR (t989): I0 Jahre AMUP---R0ckblickund Ausblick. Plesentationgiven at a workshopof the 16 AGNP Symposium, Nuemberg (Absuact) Lipinski Jr JF, Mallya G, Zimmerman P, Pope G (1989): Fluoxetine-induced akathisia: clinical and theoreti~'~al implications. J Clin Psych~ury 50:339-342. P~tterson J'F (1988): Lithium-inducedakathisia. 1 Clin Psychopharmaco/8:455. Sommi R, Crismon M, Bowden C (1987): Fluoxet~e: a serotonin-specific, second-generation antidepressant. •-,m,m,,,o, nerapy 7:1-15. Zubenko GS, Cohen BM, Lipinski LF (1987): Antidepressant related ~athisia..7 Clin Psychopharmacol 7"254DL
.
.
257.
.
.
.L
. . . .