Fluphenazine adverse effects

Case Example Because of a patient s partial response to 5 months of clozapine therapy at 600 mg/day, risperidone was added for augmentation (started with 0.5 mg b.i.d. and increased to 1 mg b.i.d. after 1 week). Before this addition, the clozapine plasma level was 344 ng/mL, but after 2 weeks of risperidone augmentation, the level was elevated to 598 ng/mL with no adverse effects and substantial clinical benefit. In another report, there was an increase in the steady-state plasma levels of clozapine (675 mg/day) and its active metabolite norclozapine after the addition of risperidone 2 mg/day in a patient treated for 2 years. Before the addition of risperidone, her clozapine and norclozapine levels were 829 and 1,384 ng/mL, respectively. Two days after risperidone was added, these levels rose to 980 and 1,800 ng/mL. Clozapine dosage was reduced to 500 mg/day, and after 5 days of combined treatment with 4 mg/day of risperidone, the clozapine and norclozapine levels were 110 and 760 ng/mL, respectively. Aside from some mild oculogyric crises, she had no symptoms of clozapine toxicity or clinical changes during the period of cross-tapering. In another case, risperidone was added to clozapine because the patient had relapsed after discontinuation of fluphenazine and had not responded to clozapine. The addition of risperidone resulted in an acute remission of psychosis ( 100). 

Fluphenazine enanthate and decanoate are similar in potency, efficacy, and adverse effects. They differ only in that the decanoate preparation is slightly more potent and slightly longer acting, requiring lower doses and less frequent administrations. Because the decanoate form manifests marginally fewer adverse effects, it is probably preferable. 

Kissling et al. (27,9) evaluated both fluphenazine and haloperidol decanoate in a 6-month double-blind study involving 31 schizophrenic patients. These authors found both were equally effective in preventing relapse, with a slight advantage for haloperidol decanoate as reflected by fewer adverse effect-related dropouts and a decreased need for antiparkinsonian medications with this latter agent. Wistedt ( 280) compared fluphenazine decanoate with haloperidol decanoate in a double-blind... 

Kissling W, Moller HJ, Walter K, et al. Double-blind comparison of haloperidol decanoate and fluphenazine decanoate effectiveness, adverse effects, dosage and serum levels during a six months treatment for relapse prevention. Pharmacopsychiatry 1985 18 240-245. 

If these measures fail, clonidine, fluphenazine, clonazepam, or carbamazepine should be tried. The pharmacologic properties of these drugs are discussed elsewhere in this book. Clonidine reduces motor or vocal tics in about 50% of children so treated. It may act by reducing activity in noradrenergic neurons in the locus coeruleus. It is introduced at a dose of 2-3 mcg/kg/d, increasing after 2 weeks to 4 mcg/kg/d and then, if required, to 5 mcg/kg/d. It may cause an initial transient fall in blood pressure. The most common adverse effect is sedation other adverse effects include reduced or excessive salivation and diarrhea. Phenothiazines such as fluphenazine sometimes help the tics, as do dopamine... 

After a baseline period of treatment with fluphenazine for a minimum of 2 weeks, 29 patients with chronic schizophrenia participated in a randomized, double-blind, 6-week comparison of clozapine and risperidone (15). Clozapine was superior to risperidone for positive symptoms and parkinsonian adverse effects. In addition, clozapine produced fewer effects on plasma prolactin than risperidone. The mean daily doses during week 6 of the trial were 404 mg of clozapine and 5.9 mg of risperidone. 

There was a different adverse effects profile in a 16-week, double-blind study in 63 out-patients with schizophrenia, who had previously been receiving fluphenazine, when comparing olanzapine (n = 29 mean age 42 years 22 men) and haloperidol (n = 34 mean age 46 years 24 men) (57). Patients taking olanzapine had significantly... 

The typical antipsychotic drugs (e.g., chlorpromazine, thioridazine, fluphenazine, and haloperidol) act primarily as DA antagonists, blocking Dj receptors. Side effects include the induction of pseudo-Parkinsonism, akathisia, and/or acute dystonic effects. Their use and symptom management are discussed, as are other adverse effects including toxicity, tardive dyskinesia, and neuroleptic malignant syndrome. 

The control of the extrapyramidal (parkinsonian) adverse effects of fluphenazine and flupenthixol with procyclidine was lost in two patients when they began to chew areca. 

The manufacturer of moclobemide noted that in 1992 there were data available from 110 patients given moclobemide 150 to 400 mg daily with various antipsychotks, namely acepromazine, aceprometazine, alimemazine, bromperidol, chlorpromazine, chlorprothixene, clothiapine, clozapine, cyamemazine, flupen-thixol, fluphenazine, fluspirilene, haloperidol, levomepromazine, penfluridol, pipamperone, prothipendyl, sulpiride, thioridazine, or zuclopenthixoL There was no evidence of any clinically relevant interactions. There was, however, some evidence that hypotension, tachycardia, sieepiness, tremor and constipation were more common, suggesting synergistic adverse effects. ... 

The atypical neuroleptics also cause less sedation than the low-potency older neuroleptics such as chlorpromazine (Thorazine) and thioridazine (Mellaril), and fewer movement disorders than the older high-potency neuroleptics fluphenazine (Permitil, Prolixin) and haloperidol (Haldol). Although they often improve the symptoms of psychosis more effectively than the older drugs, the atypical neuroleptics are not without adverse side effects. 

Neuroleptics increase the toxicity of the sunlight to human skin, causing discolorations and other adverse dermal reactions. Researchers noted this phenomenon, called phototoxicity, and set out to study its effects on cells loaded with the neuroleptics fluphenazine, perphenazine, or thioridazine (Bastianon et al., 2005). They found that exposure of these cells to light caused abnormalities in both the plasma membrane and mitochondria. 

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