V. BOZIKAS ET AL.: URINARY RETENTION AFTER FLUOXETINE-RISPERIDONE COMBINATION
143
patient showed improvement in psychopathology without
parkinsonism (Simpson-Angus Scale 5) or anticholinergic side-
effects. Amantadine was tapered off.
Address for correspondence
Vasilis Bozikas
1
5
9 Iatrou Magou Street
8100 Giannitsa
Greece
Discussion
Our patient developed severe extrapyramidal effects and urinary
retention 15 days after the addition of fluoxetine to a previous
treatment with risperidone. Risperidone alone had been
administered for 1 month without any of these side-effects. EPS re-
emerged even when 2 mg/day of risperidone was reintroduced in
combination with amantadine. Despite the administration of
olanzapine, which is a drug with peripheral anticholinergic activity
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(
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Risperidone is metabolized to 9-hydroxyrisperidone in the liver
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(He and Richardson, 1995; Scordo et al., 1999). It was found that
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our patient may be due to the increase of the active moiety of
risperidone’s plasma concentration and/or the intrinsic propensity
of fluoxetine to produce EPS.
Odou P, Levron
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(1999) Cythochrome P450 2D6 genotype and steady state plasma
Urinary retention cannot be attributed to the cumulative impact
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(Collaborative Working Group, 1998) and fluoxetine (Tollefson
and Rosenbaum, 1998). Many central nervous system (CNS)
regions and several CNS transmitter systems are involved in the
control of micturition (Andersson, 2000). Descending serotonin
pathways from the raphe nuclei inhibit bladder contractions and
this may explain the efficacy of serotonergic-based antidepressants
in the treatment of urge incontinence (Zorn et al., 1999).
Stahl S M (1996) Essential psychopharmacology. Cambridge
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Furthermore, it was found that agonists of D receptors suppress an
1
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Neuro-
overactive bladder (in 1-methyl-4-phenyl-1,2,3,-tetrahydropyridine-
pharmacology 32: 315–321
treated monkeys) and agonists of D receptors stimulate bladder
2
Zorn B H, Montgomery H, Pieper K, Gray M, Steers W D (1999)
Urinary incontinence and depression. J Urol 162: 82–84
overactivity (in MPTP-treated and normal monkeys) (Yoshimura et
al., 1993). As a result, stimulation of central D1 receptors and
blockade of central receptors have been proposed as possible
therapeutic mechanisms for the treatment of an overactive bladder
(
Andersson, 2000). Urinary retention in the patient may have been
the consequence of central serotoninergic mechanism, in or
without combination with central D blockade.
2