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PubMed1985

Molindone and haloperidol in tardive dyskinesia.

Preliminary results are described from a study of 11 outpatients manifesting exacerbated tardive dyskinesia after tapering and withdrawal of neuroleptic medications. Patients were randomly assigned to molindone or haloperidol under double-blind placebo-controlled conditions to compare the masking effects of the two drugs. Haloperidol treatment masked withdrawal-exacerbated tardive dyskinesia more than molindone did; this difference (measured by percent change in AIMS scores) was significant (p = .04) when the dose was 200% but not 100% of the prestudy neuroleptic dose. Despite several limitations to the study, the results suggest that molindone may have less dyskinetogenic potential than haloperidol. Further research in the area of site-specificity of molindone is indicated.

Adolescent↗
PubMed1982

Differential dose- and time-dependent effects of molindone on dopamine neurons of rat brain: mediation by irreversible inhibition of monoamine oxidase.

The effects of molindone (2.5, 10 and 40 mg/kg) on striatal tyrosine hydroxylase activity and dopamine (DA), 3,4-dihydroxyphenylacetic acid and homovanillic acid levels were measured as a function of time (0-72 hr). Whereas a dose of 2.5 mg/kg produced effects typical of DA receptor blockade (activation of synaptosomal tyrosine hydroxylase, increased DA metabolite levels and unchanged DA levels), a dose of 40 mg/kg produced opposite effects (decreased tyrosine hydroxylase activity and metabolite concentrations and elevated DA levels). A dose of 10 mg/kg elicited intermediate effects. The atypical effects of both higher doses were long-lasting (less than 72 hr). Molindone at doses of 10 or 40 mg/kg, but nor 2.5 mg/kg, selectively, irreversibly and dose-dependently inhibited type A monoamine oxidase. This inhibition appeared to be due to a metabolite, inasmuch as the drug itself inhibited monoamine oxidase (reversibly) only at high concentrations (less than or equal to 10(-4) M). The heretofore unsuspected inhibition of monoamine oxidase by molindone provided a consistent mechanistic interpretation of the differential dose- and time-dependent effects of the drug on dopaminergic neuronal activity. This mechanism may also serve to explain the reported efficacy of molindone in animal tests for antidepressant activity as well as its inability to produce increased DA receptor binding after chronic treatment.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Differences in the time course of dopaminergic supersensitivity following chronic administration of haloperidol, molindone, or sulpiride.

The onset and persistence of changes in 3H-spiroperidol binding to dopamine (DA) D2 receptors were examined in rat mesolimbic and striatal brain regions following daily administration of haloperidol, molindone, or sulpiride for 3, 7, 14, or 28 days. Neuroleptic dose equivalencies were determined by inhibition of 3H-spiroperidol in vivo binding in several rat brain regions. Changes in locomotor and stereotyped responses to the specific DA D2 agonist quinpirole were examined 3 days after the last treatment dose. Haloperidol or molindone administration increased mean stereotypy scores and striatal DA D2 receptor densities throughout the 28-day treatment period. In contrast, mesolimbic DA D2 receptor densities were transiently increased and returned to control values, after 28 days of haloperidol or molindone treatment. Sulpiride treatment increased mean stereotypy scores and striatal Bmax values, but had no effect on locomotion or mesolimbic dopamine receptor density. Additionally, the magnitude of change in the various measures of brain DA function varied among the three neuroleptic treatment groups. Results from this study suggest that mesolimbic and striatal brain regions differ in their response to long-term neuroleptic administration and that drug choice may influence the magnitude of neuroleptic-induced dopaminergic supersensitivity.

Animals↗
PubMedDate not supplied

Effect of clozapine and molindone on plasma and brain levels of mescaline in mice.

Levels of unchanged mescaline were examined in the plasma and brain of albino Swiss-Webster mice pretreated with various doses of either clozapine or molindone. In clozapine treated mice, the mescaline levels were statistically significantly higher at 2 and 3 h with 7.5 and 15.0 mg/kg and at 1, 2 and 3 h with 30 mg/kg. Molindone at 4.0 and 8.0 mg/kg produced no significant effect; at 16.0 and 48.0 mg/kg, the levels were significantly higher at 1 and 2 h. Elevated brain levels of mescaline by clozapine and molindone indicate an adverse metabolic interaction between a hallucinogen and drugs that are commonly used to treat mescaline-induced psychosis.

Animals↗
PubMed1989

Reinstitution of neuroleptic treatment with molindone in a patient with a history of neuroleptic malignant syndrome.

The decision to reinstitute neuroleptic treatment in patients with a history of neuroleptic treatment is fraught with hazards. A case is reported in which neuroleptic treatment was successfully reintroduced with molindone after previous bouts of neuroleptic malignant syndrome (NMS) with trifluoperazine and thioridazine. Molindone may represent an alternative neuroleptic to consider in patients with a history of NMS, although all neuroleptics including clozapine and molindone may potentially precipitate this syndrome.

Adolescent↗
PubMedDate not supplied

A comparison of masking effects of haloperidol versus molindone in tardive dyskinesia.

An experimental method was utilized to compare the masking effects of two neuroleptic agents--molindone and haloperidol--on 18 neuroleptic-treated schizophrenic patients exhibiting operationally defined withdrawal-exacerbated tardive dyskinesia. After a week on one of these two medications at preestablished doses equivalent to that of the pre-study neuroleptic, molindone-masked total AIMS scores by significantly less (12%) than haloperidol (27%). Similarly, during a second week when the dose of these neuroleptics was equivalent to 200% that of the pre-study dose, molindone masked the total AIMS score significantly less (23%) as compared to haloperidol (53%). Several interpretations of this finding are considered. This study demonstrates the feasibility of a method that may offer a model for understanding pharmacological differences among neuroleptic medications.

Adult↗
PubMed1993

Treatment of clozapine- and molindone-induced agranulocytosis with granulocyte colony-stimulating factor.

OBJECTIVE: To report a case of clozapine- and molindone-induced agranulocytosis and to discuss treatment using filgrastim, a granulocyte colony-stimulating factor. CASE SUMMARY: A 64-year-old woman who had been on long-term clozapine therapy for schizophrenia was hospitalized with presumed drug-induced agranulocytosis. She had also been on short-term molindone therapy. A bone marrow biopsy and the initial white blood cell (WBC) count were consistent with drug-induced agranulocytosis. Following seven days of treatment with subcutaneous filgrastim 300 micrograms/d, her absolute neutrophil count was above 500 x 10(6)/L. DISCUSSION: Reports in the literature discussing antipsychotic drug-induced agranulocytosis are reviewed. A relationship between treatment with filgrastim and WBC response is postulated. CONCLUSIONS: Filgrastim may be useful in ameliorating the effects of clozapine- and molindone-induced agranulocytosis.

Agranulocytosis↗
PubMed1985

Clinical experience with molindone hydrochloride in geriatric patients.

Elderly patients (N = 28) with a variety of psychiatric disorders were treated with molindone in an 8-week open clinical trial. Many patients had concomitant medical illnesses, and many were on other medications in addition to molindone. Molindone appeared to be safe, clinically effective, and well-tolerated. The most common adverse effects were extrapyramidal side effects, but the occurrence of these symptoms was relatively low.

Age Factors↗
PubMed1985

Review of clinical and laboratory experiences with molindone hydrochloride.

The literature concerning the pharmacokinetics, pharmacodynamics, receptor physiology, and clinical use of molindone is reviewed. Unanswered questions about the drug are addressed. Although molindone is reputed to have a short half-life (1.5 hours), clinical observations report a prolonged effect from a once-daily dose. Early in treatment, some patients show intolerance due to akathisia or extrapyramidal symptoms. This may be withdrawal dyskinesia due to discontinuation of another drug or an early adverse effect of molindone. Different effects on dopamine receptors have been described, but the significance of these properties for the development of tardive dyskinesia remains unclear.

Akathisia, Drug-Induced↗
PubMed1983

Selective effects of buspirone and molindone on dopamine metabolism and function in the striatum and frontal cortex of the rat.

The hypothesis that the nerve endings of the dopamine projection of the frontal cortex lack autoreceptors for regulation of tyrosine hydroxylase was tested by using the preferential inhibitors of dopamine autoreceptors, molindole and buspirone. In contrast to haloperidol, which elevates dopamine metabolism in the striatum and frontal cortex, both molindone and buspirone elicited little change in dopamine metabolism in the frontal cortex at doses up to 3.0 mg/kg, which cause the same maximal response in the corpus striatum as does haloperidol. Thus, the lack of autoreceptors in the frontal cortex is of pharmacological importance. That preferential inhibition of striatal dopamine autoreceptors may reverse catalepsy by enhancing synthesis and release of dopamine was tested by first inducing catalepsy with different drugs and then administering molindone or buspirone. Only buspirone (1.0 mg/kg) reversed catalepsy. This effect does not require presynaptic dopamine as catalepsy was reversed by buspirone in the dopamine-depleted rat (with 2.0 mg/kg R04-1284) as well as after postsynaptic dopamine receptor blockade by haloperidol of cis-flupenthixol. Thus, the mechanism for the reversal of catalepsy appears to be located efferent from the dopamine neuron. Buspirone, a non-benzodiazepine anti-anxiety drug, may prove useful for treatment of extrapyramidal motor disorders of either iatrogenic or idiosyncratic origin.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

The use of molindone in the treatment of psychotic and delirious patients infected with the human immunodeficiency virus. Case reports.

Four patients with HIV infection and psychosis from various etiologies, refractory to standard treatments, and suffering from severe extrapyramidal symptoms (EPS), had a marked beneficial response to molindone. There was significant control of neuropsychiatric dysfunction without major adverse side effects. The results suggest that further evaluation is warranted of the use of molindone in treating severely ill, psychotic, or delirious HIV-infected patients.

AIDS Dementia Complex↗
PubMed1977

Weight reduction in schizophrenics by molindone.

The weight-reducing property of molindone, a recently introduced antipsychotic drug, was tested in 9 hospitalized chronic schizophrenic patients. There was an average weight loss of 7.6 kg after 3 months on molindone; most of the loss occurred during the first month. The mechanism producing this weight loss is uncertain, but a central anorexigenic effect may be an important factor.

Adult↗
PubMed1985

Molindone and hepatotoxicity.

An adolescent male with chronic schizophrenic disorder, paranoid type, was treated with molindone. He developed hepatotoxicity in the early treatment phase as evidenced by flu-like symptoms and laboratory abnormalities of liver functions. These symptoms and his hepatic functions improved on discontinuing molindone. Similar liver function trends were seen on reintroduction and subsequent withdrawal of the drug. Hepatic hypersensitivity has not been reported previously with the use of this drug. It is suggested that clinicians should be aware of this association and should assess hepatic functions in patients who develop a prodromal flu-like syndrome with this drug, especially in the early treatment phase.

Adolescent↗
PubMed1991

Neuroleptic malignant syndrome possibly caused by molindone hydrochloride.

The case of a patient who developed neuroleptic malignant syndrome (NMS) on three separate occasions is presented. Her third bout of this syndrome possibly was caused by molindone hydrochloride. This medication has been reported only once previously to cause NMS. The pharmacology of molindone is reviewed and a complicating factor in this case--the recent onset of hypothyroidism--is discussed together with its implication in the development of the clinical manifestations of this syndrome.

Adult↗
PubMed2000

Effects of amantadine on modification of dopamine dependent behaviours by molindone.

Amantadine, a dopamine agonist is reported to act by releasing dopamine from the dopaminergic nerve terminals as an anti-Parkinsonian drug. In the present behavioural study in the rat, molindone-induced catalepsy and ptosis, which are dopamine dependent-behaviors are reversed by amantadine. Amantadine has also revered molindone-induced inhibition of traction response in mice. Our study indicates that amantadine, like other DA agonists, e.g. amphetamine and apomorphine can antagonize or even reverse the neuroleptic induced dopaminergic behaviors.

Amantadine↗
PubMed1986

A case of massive rhabdomyolysis following molindone administration.

Rhabdomyolysis is a potentially lethal syndrome that psychiatric patients seem predisposed to develop. The clinical signs and symptoms, typical laboratory features, and complications of rhabdomyolysis are presented. The case of a schizophrenic patient is reported to illustrate massive rhabdomyolysis and subsequent acute renal failure following molindone administration. Physicians who prescribe molindone should be aware of this reaction.

Acute Kidney Injury↗
PubMed1985

Comparison of injectable molindone and haloperidol followed by oral dosage forms in acutely ill schizophrenics.

The comparative efficacy of molindone and haloperidol, given by injection for the first 2-3 days of hospitalization and then continued orally for up to 4 weeks, is reported from an ongoing double-blind study. Efficacy and side effects were assessed by the Brief Psychiatric Rating Scale, Clinical Global Impressions, Treatment Emergent Symptom Scale, and Target Symptom Ratings. Analyses based on the first 35 patients who entered the study indicate that both drugs were effective and well tolerated. There were slight advantages for molindone early during the injectable phase of treatment and for haloperidol late during the oral portion of the study, but these differences were not clinically significant. No significant differences in side effects were found between the two drugs.

Acute Disease↗
PubMedDate not supplied

Blockade of the dopamine depressor response by molindone, a newly introduced neuroleptic.

Pretreatment with the neuroleptics, haloperidol and molindone, significantly antagonized the dopamine-induced depressor response in the anaesthetized dogs. The depressor response to dopamine was however, not significantly affected by propranolol, atropine or antazoline pretreatment. The results suggest that molindone like haloperidol, is capable of blocking the vascular dopamine receptors responsible for mediating dopamine-induced vasodilatation in the coeliac, mesenteric and renal vascular bed and fall in blood pressure.

Animals↗