Treatment Of Drug-induced Psychosis Research Articles

Effect of quetiapine in psychotic Parkinson's disease patients: A double‐blind labeled study of 3 months' duration

This double-blind randomized study examined the effect of quetiapine (QTP) on drug-induced psychosis (DIP) in Parkinson's disease (PD). Conventional antipsychotic drugs are associated with adverse extrapyramidal effects. QTP is a new atypical antipsychotic drug used in the treatment of psychosis in PD. A total of 58 consecutive psychotic PD patients (mean age, 75 +/- 8.3 years; mean disease duration, 10.5 +/- 6.4 years; 29 with dementia) were randomly assigned to 2 groups: 30 were treated with QTP (mean dose, 119.2 +/- 56.4 mg) and 28 received placebo for 3 months. The motor part of the Unified Parkinson's Disease Rating Scale, the Brief Psychiatric Rating Scale, the Mini-Mental State Examination, the Hamilton Rating Scale for Depression, the Epworth Sleepiness Score, and the Clinical Global Impression Scale were administered before and during the study. No significant difference was found between the groups in all parameters. There were 32 PD patients (55%) completed the 3-month study (15 [26%] QTP and 17 [29%] placebo). Treatment was interrupted in 15 patients in the QTP and 11 in the placebo groups. This double-blind study did not show a beneficial effect of QTP for the treatment of DIP in PD. The high rate of withdrawal probably influenced the results. Larger double-blind studies are required.

Treatment of drug-induced psychosis in Parkinson's disease with ziprasidone can induce severe dose-dependent off-periods and pathological laughing

“Atypical anti-psychotics” are substances of choice in treating drug-induced psychosis (DP) in Parkinson's disease (PD). We report on four patients with DP who received treatment with ziprasidone after previously applied clozapine and quetiapine had failed. Three patients showed a significant improvement of DP, without deterioration of motor function. In one case, ziprasidone considerably increased decline in off-periods. Two patients developed pathological laughing as a possible side-effect of ziprasidone. Ziprasidone may serve as an additional “atypical anti-psychotic” for the treatment of DP in PD but can also induce deterioration of motor function.

For the treatment of drug-induced psychosis in Parkinson's disease (PD) "preliminary experience with aripiprazole is mixed

For the treatment of drug-induced psychosis in Parkinson's disease (PD) "preliminary experience with aripiprazole is mixed

For the treatment of drug-induced psychosis in Parkinson's disease (PD) "preliminary experience with aripiprazole is mixed

For the treatment of drug-induced psychosis in Parkinson's disease (PD) "preliminary experience with aripiprazole is mixed

Optimizing the duration of prophylactic use of anti-psychotics after a first psychotic episode in patients with schizophrenia; A decision analytic approach

“Atypical anti-psychotics” are substances of choice in treating drug-induced psychosis (DP) in Parkinson's disease (PD).We report on four patients with DP who received treatment with ziprasidone after previously applied clozapine and quetiapine had failed. Three patients showed a significant improvement of DP, without deterioration of motor function. In one case, ziprasidone considerably increased decline in off-periods. Two patients developed pathological laughing as a possible side-effect of ziprasidone.Ziprasidone may serve as an additional “atypical anti-psychotic” for the treatment of DP in PD but can also induce deterioration of motor function.

Clinicial outcome, service use and costs of care-follow-up data from the Australian scap

“Atypical anti-psychotics” are substances of choice in treating drug-induced psychosis (DP) in Parkinson's disease (PD).We report on four patients with DP who received treatment with ziprasidone after previously applied clozapine and quetiapine had failed. Three patients showed a significant improvement of DP, without deterioration of motor function. In one case, ziprasidone considerably increased decline in off-periods. Two patients developed pathological laughing as a possible side-effect of ziprasidone.Ziprasidone may serve as an additional “atypical anti-psychotic” for the treatment of DP in PD but can also induce deterioration of motor function.

Treatment of drug-induced psychosis and clozapine with quetiapine and clozapine in Parkinson’s disease

In the Letter to the Editor, “Treatment of drug-induced psychosis with quetiapine and clozapine in Parkinson’s …

Treatment of drug-induced psychosis with quetiapine and clozapine in Parkinson's disease.

Drug-induced psychosis is a major problem that complicates the treatment of PD, and occurs in up to 22% of patients.1 Because conventional neuroleptics are poorly tolerated in patients with PD, most authors recommend a two-step approach, consisting first of a reduction of dopaminergic drugs to the minimum level required, followed by the initiation of an atypical antipsychotic drug if necessary.2 Clozapine has been shown to significantly improve psychosis without worsening motor symptoms of parkinsonism.3 However, frequent monitoring of the white blood cell count makes the use of this drug cumbersome and expensive. Risperidone and olanzapine have been shown to worsen PD symptoms.4,5⇓ Quetiapine has been recently suggested as a possible treatment for PD because it reduces psychosis without worsening motor symptoms, and because its use does not require blood monitoring.6,7⇓ We performed a retrospective review of our own use of quetiapine in drug-induced psychosis of PD to evaluate its …

Atypical antipsychotics in the treatment of drug-induced psychosis in Parkinson's disease.

Our experience with atypical antipsychotics in patients with PD is that their motor effects are not predictable. The multiple reports concerning clozapine's beneficial effects on tremor, dystonia, nocturnal akathisia, and dyskinesias all underscore this observation. However, the appearance of even minor degrees of parkinsonism in normal volunteers or schizophrenics should suggest that an antipsychotic will not be well-tolerated in patients with PD. The treatment of PD is probably the most stringent test of a drug's freedom from parkinsonian side effects. The data from trials in schizophrenia concerning parkinsonian effects cannot always be confidently interpreted. Virtually all subjects in these trials have been treated with typical neuroleptics until shortly before study entry. Because the parkinsonian side effects of these drugs may persist for several months, patients may still show declining levels of parkinsonism even when placed on a drug that induces it if this effect is milder than that induced by the pre-study neuroleptic. Depending on the pre-study drug used and the duration of the study, distinguishing placebo from a low-potency neuroleptic may be impossible. Furthermore, the standard measure of parkinsonism in psychiatric studies is the Simpson-Angus scale which is heavily weighted toward rigidity and may underscore bradykinesia, gait, and posture abnormalities. The prolactin response to an antipsychotic drug may turn out to be a good predictor of its freedom from parkinsonian side effects. That would fit with the data presented above of clozapine and quetiapine having less parkinsonian effects, olanzapine having more but variable effects and risperidone being poorly tolerated. With the data presented above, comprising a current review of all reports of the use of atypical antipsychotics in PD that we could locate, we can say little with certainty. The only drug with confirmed benefit without worsening parkinsonism is clozapine. Open-label trials involving over 400 patients and two multicenter, placebo-controlled, double-blind trials have demonstrated that it is effective in treating the psychosis. It improves tremor, does not worsen other motor functions to any significant extent, and is safe at low doses. Limited data provide conflicting information on both risperidone and olanzapine. Quetiapine seems to be well-tolerated with some, but definitely less, worsening of PD motor features than risperidone and olanzapine. Based on the current literature, our personal experience, and anecdotal experience of other PD specialists which we solicited, we will venture our own interpretation and recommendations. We think risperidone is poorly tolerated and should be used only as a last resort; that olanzapine is better than risperidone but will, in a majority of patients with PD, worsen motor function. We are optimistic, but not yet convinced, that quetiapine may prove to be as effective and better tolerated than clozapine. It will not require cumbersome monitoring because it does not induce a blood dyscrasia. We therefore recommend that DP be treated in the following manner. First, the anti-PD medications should be simplified and reduced as much as tolerated. We think, in general, side effects multiply more with increasing numbers of drugs than with drug dose, so that patients are more likely to tolerate a higher dose of levodopa than a lower dose of levodopa combined with other adjunctive anti-PD medications. In reducing anti-PD medications, we recommend tapering and stopping, if necessary, the drugs with the highest risk-to-benefit ratio first. Anticholinergics are stopped first, then selegiline, dopamine agonists, amantadine, and finally COMT inhibitors, which have no psychotomimetic action of their own. Finally, levodopa is reduced. Generally, a point is reached at which the anti-PD medications cannot be reduced without jeopardizing motor function. If psychosis persists at this point, then an antipsychotic is added. (ABS

Neuropsychiatric adverse effects of antiparkinsonian drugs. Characteristics, evaluation and treatment.

Parkinson's disease (PD) is a progressive neurological condition that causes considerable disability in the elderly. Drugs used to treat PD, such as levodopa, offer symptomatic relief but often have neuropsychiatric adverse effects, most prominently psychosis and delirium. Aged patients and those with dementia are particularly vulnerable to these adverse effects. Evaluating PD patients with drug-induced neuropsychiatric adverse effects is made difficult by their complex clinical presentations. The treatment of drug-induced psychosis and delirium begins with manipulating the antiparkinsonian drug regimen, but this frequently worsens motor function. Atypical antipsychotics such as clozapine have been successfully employed to treat the psychosis without worsening the motor disability. Patient intolerance of clozapine therapy has prompted open-label studies with newer agents such as risperidone, remoxipride, zotepine, mianserin and ondansetron.

The D1 receptor-mediated effects of the ergoline derivative LEK-8829 in rats with unilateral 6-hydroxydopamine lesions.

1. Previous experiments have suggested a potential atypical antipsychotic activity of the ergoline derivative LEK-8829. In vitro experiments showed a high affinity to 5-HT1A, 5-HT2 and D2 receptors (the ratio of pKi values 5-HT2/D2 = 1.11) and a moderate affinity to D1 receptors. In vivo experiments showed antagonism of dopamine and 5-hydroxytryptamine (5-HT) receptor-linked behaviours. 2. In the present study, the rats with unilateral dopaminergic deafferentation of the striatum, induced by the lesion of the median forebrain bundle with 6-hydroxydopamine (6-OHDA), were used to determine the effects of LEK-8829 on turning behaviour and on striatal c-fos mRNA levels. 3. The administration of LEK-8829 induced a long lasting contralateral turning behaviour that was dose-dependent. It was found that the specific D1 receptor antagonist SCH-23390 but not the D2 receptor antagonist haloperidol or 5-HT1A antagonist pindolol, dose-dependently inhibited the turning behaviour induced by LEK-8829. 4. In an attempt to clarify the D1:D2 receptor interactions involved in the action of LEK-8829 in the 6OHDA model, we used in situ hybridization histochemistry to compare the effect of SCH-23390 pretreatment on striatal c-fos mRNA expression induced either by LEK-8829 or by the typical antipsychotic haloperidol. 5. LEK-8829 induced a bilateral striatal c-fos mRNA expression that was significantly higher in the denervated striatum as compared to the intact striatum and was completely blocked on both sides by pretreatment with SCH-23390. In contrast, haloperidol-induced striatal c-fos mRNA expression was limited to the innervated striatum and was not blocked by SCH-23390. 6. Our data demonstrate an intrinsic activity of LEK-8829 on D1 receptors that is potentiated in the dopamine-depleted striatum. We conclude, therefore, that the putative atypical antipsychotic LEK-8829 may prove useful as an experimental tool for the study of D1:D2 receptor interactions and could have beneficial effects in the treatment of drug-induced psychosis in patients with Parkinson's disease.

Mianserin treatment of patients with psychosis induced by antiparkinsonian drugs.

We evaluated the effects of mianserin, a relatively selective 5-HT2 receptor antagonist, on symptoms related to drug-induced psychosis in patients with Parkinson's disease (PD). A total of 12 patients with PD who had developed drug-induced psychosis showed delirium (DSM-III-R criteria; n = 10) and pure visual hallucinations (n = 2). The antiparkinsonian drugs involved in the drug-induced psychosis were L-DOPA/carbidopa, bromocriptine, trihexyphenidyl, and amantadine. They received mianserin (mean 36.7 mg, range 20-60 mg) given orally for 8 weeks. Complete relief or marked improvement in psychotic symptoms was noted in 8 patients, moderate improvement in 2 patients, and no effect in 2 patients. The parkinsonian disability also decreased slightly in 8 patients. These results suggest that serotonin antagonism at 5-HT2 receptors may not only play an important role in the treatment of drug-induced psychosis in PD, but may also ameliorate the symptoms of parkinsonism.

Treatment of Drug-Induced Psychosis with Diphenylhydantoin†

Summary This paper introduces an alternative to the major tranquilizers in the treatment of acute psychotic breakdown following multiple drug abuse. All the patients described had been taking hallucinogenic drugs for over five years. Only three of several successfully treated cases are described. Two of these cases were followed by EEG recordings, which did not show any localized epileptiform activity. The response to diphenylhydantoin is described both clinically and as recorded by EEG. An initial two-week period is necessary in order that the effects of the drugs can be demonstrated clinically or on EEG tracing. It cannot be concluded from this that the antiepileptic drugs are the drugs of choice in drug-induced psychosis; but, diphenylhydantoin has shown dramatic effectiveness in these previously refractory cases. In view of the response, some abnormal cerebral discharge from an as yet undiscovered locus may be involved in the pathogenesis of drug-induced hallucinations.