benztropine and Dyskinesia--Drug-Induced

Blockade of dopamine D2 receptors remains a common feature of all antipsychotics. It has been hypothesized that the extrastriatal (cortical, thalamic) dopamine D2 receptors may be more critical to antipsychotic response than the striatal dopamine D2 receptors. This is the first double-blind controlled study to examine the relationship between striatal and extrastriatal D2 occupancy and clinical effects. Fourteen patients with recent onset psychosis were assigned to low or high doses of risperidone (1 mg vs 4 mg/day) or olanzapine (2.5 mg vs 15 mg/day) in order to achieve a broad range of D2 occupancy levels across subjects. Clinical response, side effects, striatal ([11C]-raclopride-positron emission tomography (PET)), and extrastriatal ([11C]-FLB 457-PET) D2 receptors were evaluated after treatment. The measured D2 occupancies ranged from 50 to 92% in striatal and 4 to 95% in the different extrastriatal (frontal, temporal, thalamic) regions. Striatal and extrastriatal occupancies were correlated with dose, drug plasma levels, and with each other. Striatal D2 occupancy predicted response in positive psychotic symptoms (r=0.62, p=0.01), but not for negative symptoms (r=0.2, p=0.5). Extrastriatal D2 occupancy did not predict response in positive or negative symptoms. The two subjects who experienced motor side effects had the highest striatal occupancies in the cohort. Striatal D2 blockade predicted antipsychotic response better than frontal, temporal, and thalamic occupancy. These results, when combined with the preclinical data implicating the mesolimbic striatum in antipsychotic response, suggest that dopamine D2 blockade within specific regions of the striatum may be most critical for ameliorating psychosis in schizophrenia.

Topics: Adolescent; Adult; Antipsychotic Agents; Benztropine; Dopamine Antagonists; Double-Blind Method; Dyskinesia, Drug-Induced; Female; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Muscarinic Antagonists; Neostriatum; Positron-Emission Tomography; Prolactin; Prospective Studies; Psychiatric Status Rating Scales; Psychomotor Agitation; Pyrrolidines; Raclopride; Receptors, Dopamine D2; Salicylamides; Schizophrenia; Schizophrenic Psychology

We challenged five patients suffering from tardive akathisia (TA) with intravenous benztropine (2 mg), propranolol (1 mg) and placebo (saline) using a random, double-blind cross-over design to examine the effects of the drugs on the subjective, objective and global manifestations of neuroleptic-induced akathisia. Benztropine produced a marginally significant, and propranolol a significant improvement in the overall manifestations of the disorder. The patients demonstrated a considerable placebo effect and marked variation in their responses to the drugs. The implications of these findings for the pathophysiology of TA in relation to acute akathisia and tardive dyskinesia are discussed.

Topics: Adult; Akathisia, Drug-Induced; Anxiety; Benztropine; Cross-Over Studies; Double-Blind Method; Dyskinesia, Drug-Induced; Humans; Male; Middle Aged; Propranolol; Schizophrenia

Effects of the dihydropyridine calcium channel inhibitor nifedipine on chronic schizophrenia and tardive dyskinesia were studied in an 8-week double-blind crossover trial. Four of the ten patients had tardive dyskinesia, and three of these were not receiving neuroleptics. No effects on symptoms of chronic schizophrenia were found using Psychiatric Symptom Assessment Scale ratings. In the four patients with tardive dyskinesia, an average improvement in total Abnormal Involuntary Movement Scale scores of 57% was observed. These data suggest that dihydropyridine calcium channel inhibitors may be effective in the treatment of tardive dyskinesia in schizophrenic patients.

Topics: Adult; Antipsychotic Agents; Benztropine; Double-Blind Method; Dyskinesia, Drug-Induced; Female; Humans; Male; Nifedipine; Psychiatric Status Rating Scales; Schizophrenia

Twenty-nine inpatients with major psychotic disorders were treated for 14 days with a clinician-determined dose of haloperidol and with either benztropine or placebo given by double-blind random assignment on days 1 through 7. No differences were noted in haloperidol mean dose, haloperidol blood levels, or BPRS scores during the first seven days between benztropine (N = 14) and placebo (N = 15) groups. Benztropine-treated patients demonstrated increased dry mouth and diminished sweat and a non-significantly lower rate of dystonia compared to placebo (14% vs. 33%). Dystonic patients were significantly younger than nondystonic patients, but did not differ in haloperidol mean dose or plasma concentration. The effect of benztropine on the incidence of dystonia was consistent with other studies, which, when analyzed together, demonstrate the efficacy of anticholinergic prophylaxis. The relatively low incidence of anticholinergic side effects, coupled with the lack of effect on haloperidol blood levels or antipsychotic efficacy, suggest that moderate doses of benztropine in conjunction with haloperidol are a rational approach for the treatment of acute psychosis in young patients.

Topics: Adult; Benztropine; Double-Blind Method; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Haloperidol; Humans; Male; Neurologic Examination; Parasympatholytics; Prospective Studies; Psychiatric Status Rating Scales; Psychotic Disorders

A patient with tardive neuroleptic-induced akathisia was investigated with multiple pharmacological challenges. It was noted that the patient responded positively to benztropine, bromocriptine, and propranolol, and negatively to physostigmine, and showed little or no response to discontinuation of neuroleptics and challenges with metoclopramide, metoprolol, atenolol, and clonidine. The implications of this pharmacological characterization for the understanding of the pathophysiology of tardive akathisia in relation to acute akathisia and tardive dyskinesia are discussed.

Topics: Administration, Oral; Aged; Akathisia, Drug-Induced; Antipsychotic Agents; Arousal; Atenolol; Benztropine; Brain; Bromocriptine; Chronic Disease; Clonidine; Dose-Response Relationship, Drug; Double-Blind Method; Drug Administration Schedule; Dyskinesia, Drug-Induced; Humans; Infusions, Intravenous; Male; Metoclopramide; Metoprolol; Physostigmine; Propranolol; Psychomotor Agitation; Schizophrenia, Paranoid

Anticholinergic drugs have been shown to impair new memory acquisition. In a double-blind study, 22 chronically schizophrenic patients had the anticholinergic drugs that they had been taking to control the extrapyramidal side effects (EPSE) of neuroleptic drugs discontinued and were randomly assigned to treatment either with benztropine (an anticholinergic) or with amantadine (which has little or no anticholinergic effect). The EPSE of five of the ten patients assigned to amantadine could not be adequately controlled with that drug alone, and these patients were withdrawn from the study prematurely. The five patients who completed the six-week trial on amantadine showed improved performance on tests of memory acquisition in comparison with patients treated with benztropine. Global inspection of the results showed that only 36% of the patients taking benztropine showed improvement in memory acquisition at the four- and six-week assessments, whereas 80% of the amantadine users showed improvement at the four-week assessment. Analysis of covariance, however, revealed that the performance of the latter group decreased almost to baseline at six weeks, as an additional two of the remaining patients developed distressing EPSE.

Topics: Adult; Amantadine; Antipsychotic Agents; Benztropine; Chronic Disease; Dyskinesia, Drug-Induced; Female; Humans; Male; Memory; Mental Recall; Middle Aged; Schizophrenia; Schizophrenic Psychology; Tropanes; Verbal Learning

Studies on the withdrawal of anticholinergics from patients on antipsychotics have produced conflicting results. This 12-week study employed a double-blind crossover design on 39 adult in-patients selected from a total hospital population of 620. The Colombia Scale was used to determine extrapyramidal side effects (EPS). All patients were stabilised prior to the study on benztropine mesylate 2 mg b.i.d., and gradual withdrawal was employed. Benztropine withdrawal produced a significant increase in overall EPS scores. Ten patients (26%) required reinstatement of benztropine while on placebo. Sialorrhoea, rigidity and postural instability were the most prominent changes. Neither age, sex, nor diagnosis were significantly predictive of EPS. Depot medications and doses greater than 1000 mg/day chlorpromazine-equivalent were related to significant EPS increase. The intrinsic anticholinergic properties of the antipsychotics themselves and concomitant medications, such as antidepressants, appeared protective against development of EPS. Most patients on a combination of antipsychotics and anticholinergics can safely be withdrawn from the latter.

Topics: Adult; Antipsychotic Agents; Benztropine; Clinical Trials as Topic; Double-Blind Method; Dyskinesia, Drug-Induced; Humans; Long-Term Care; Mental Disorders; Middle Aged; Parasympatholytics; Schizophrenia; Substance Withdrawal Syndrome

Benztropine mesylate (intravenous [IV] and oral) challenge was compared with brief neuroleptic withdrawal on dyskinesia ratings and symptom measures. Thirty-six neuroleptic-treated patients underwent a placebo-controlled acute IV challenge with 2 mg benztropine and a placebo-controlled two-week trial of oral benztropine mesylate (2 mg three times a day), followed by a double-blind placebo-controlled neuroleptic withdrawal involving four weeks of dose tapering and six weeks of placebo treatment. Benztropine given IV had no significant effect. Orally administered benztropine, however, led to statistically significant increases in dyskinesia and dysphoric mood. The brief neuroleptic withdrawal significantly increased dyskinesia scores and dysphoria and resulted in early termination of therapy in 12 of 36 patients (33%) due to symptom exacerbation. There was a striking absence of correlation between dyskinesia change measures brought about by benztropine and changes following neuroleptic withdrawal. Therefore anticholinergic challenge does not appear to be a fruitful procedure for identifying patients with covert dyskinesia.

Topics: Administration, Oral; Adult; Aged; Antipsychotic Agents; Benztropine; Chronic Disease; Double-Blind Method; Dyskinesia, Drug-Induced; Female; Humans; Injections, Intravenous; Male; Middle Aged; Placebos; Psychiatric Status Rating Scales; Schizophrenia; Schizophrenic Psychology; Substance Withdrawal Syndrome; Tropanes

Patients receiving fluphenazine decanoate who were switched from adjunctive benztropine to imipramine in a double-blind trial experienced marked exacerbations of extrapyramidal side effects. No substantial increase in anticholinergic side effects occurred, however, when imipramine was added to fluphenazine decanoate and benztropine.

Topics: Adult; Benztropine; Clinical Trials as Topic; Depressive Disorder; Double-Blind Method; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Female; Fluphenazine; Humans; Imipramine; Male; Middle Aged; Tropanes

In a 12-week controlled study ethopropazine was compared to benztropine in the treatment of parkinsonism induced by fluphenazine enanthate in 60 schizophrenic outpatients. Ethopropazine and benztropine were found to be equally effective in controlling parkinsonian symptoms and were as efficacious as procyclidine, their previous antiparkinsonian drug. However, benztropine treated patients had a significant increase in tardive dyskinesia compared to their condition during procyclindine treatment, and significantly more anxiety and depression than ethopropazine treated patients. This suggests that benztropine is not the anticholinergic drug of choice in the treatment of neuroleptic-induced parkinsonian symptoms, because of its more toxic central and peripheral atropinic effect.

Topics: Adult; Benztropine; Clinical Trials as Topic; Double-Blind Method; Dyskinesia, Drug-Induced; Female; Fluphenazine; Humans; Male; Middle Aged; Parkinson Disease, Secondary; Phenothiazines; Procyclidine; Schizophrenia; Tropanes

Deanol acetamidobenzoate was administered in double-blind, crossover fashion with placebo to five patients with tardive dyskinesia, three patients with Huntington's chorea, and one patient with posthemiplegic chorea. No significant effect on dyskinesia was observed. Preliminary administration of physostigmine salicylate to patients with tardive dyskinesia had a variable effect, while benztropine mesylate produced no change. Since the status of deanol as an effective precursor of acetylcholine is uncertain, further trials with putative cholinergic agents remain warranted in choreiform syndromes.

Topics: Benztropine; Clinical Trials as Topic; Deanol; Double-Blind Method; Drug Evaluation; Dyskinesia, Drug-Induced; Ethanolamines; Humans; Huntington Disease; Male; Middle Aged; Physostigmine

Tardive dyskinesia (TD) may be a clinical manifestation of a relative imbalance between the inversely related dopaminergic (DA) and acetylcholinergic (ACh) influences in the central nervous system (CNS). Six patients were evaluated with single challenge doses of a DA agonist, levodopa, and antagonist, droperidol, as well as with an ACh agonist, physostigmine, an antagonist, benztropine, and a placebo. A single blind trial with deanol and placebo followed. Responses, measured by an electrophysiological technique, formed two subgroups. The patients who improved with a DA antagonist or an ACh agonist improved while taking deanol. Another group of patients were made worse with a DA antagonist or ACh agonist and were worsened or had no response while taking deanol. While the results add support to the concept of counterbalancing DA-ACh influences in TD, further investigation of TD subtypes and predictors of drug response is warranted.

Topics: Adult; Benztropine; Clinical Trials as Topic; Deanol; Dopamine; Droperidol; Dyskinesia, Drug-Induced; Humans; Levodopa; Male; Middle Aged; Parasympatholytics; Physostigmine; Placebos; Time Factors

Benztropine is an anticholinergic drug used as a therapy for Parkinson's disease and treatment for extrapyramidal side effects. While tardive dyskinesia is an involuntary movement disorder that often occurs gradually after long-term use of medications, it does not commonly present acutely.. A 31-year-old White woman experiencing psychosis presented with spontaneous, acute-onset dyskinesia induced with the withdrawal of benztropine. She had been followed in our academic outpatient clinic for medication management and intermittent psychotherapy.. The pathophysiology of tardive dyskinesia is not fully understood, but several hypotheses exist, including the involvement of changes in basal ganglia neuronal systems. To our knowledge, this is the first case report to document acute-onset dyskinesia associated with the withdrawal of benztropine.. his case report, which describes an atypical response to discontinuing benztropine, might offer the scientific community potential clues to better understand the pathophysiology of tardive dyskinesia.

Topics: Adult; Antipsychotic Agents; Benztropine; Dyskinesia, Drug-Induced; Female; Humans; Tardive Dyskinesia

Topics: Antipsychotic Agents; Benztropine; Candidiasis, Oral; Child; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Humans; Male; Muscarinic Antagonists; Risperidone; Stress Disorders, Post-Traumatic; Xerostomia

Extrapyramidal symptoms (EPSs) (dystonic reaction, rigidity, and akathisia) occur as a result of D2 receptor blockade. Selective serotonin-reuptake inhibitors (SSRIs) have been reported to induce extrapyramidal signs and symptoms but tricyclic antidepressants have been rarely reported. Among the side effects attributed to valproic acid administration, the production of EPS is very rare, particularly in children. In this paper we present a case (10-year-old girl) under multiple pharmacologic treatment who developed EPSs (oculogyric crisis) shortly after the adjunct of imipramine to a combination of methylphenidate and valproic acid. Oculogyric crisis occurred on the third day of this combination treatment and these symptoms included ocular pain and sustained upward gaze. Benztropine 2 mg i.m. resulted in rapid relief of oculogyric crisis symptoms.

Topics: Attention Deficit Disorder with Hyperactivity; Benztropine; Bipolar Disorder; Child; Comorbidity; Dose-Response Relationship, Drug; Drug Interactions; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Female; Humans; Imipramine; Injections, Intramuscular; Methylphenidate; Neurologic Examination; Ocular Motility Disorders; Psychotropic Drugs; Valproic Acid

We studied whether movements associated with tardive dyskinesia (TD) served operant functions in 2 men with developmental disabilities. We found that TD-related movements occurred more frequently in the alone and attention conditions and less frequently in control and demand conditions. Our findings suggest that TD-related movements may not be maintained by social reinforcers and that decreases in TD movements are possibly a result of engagement in activities that are incompatible with TD movements.

Topics: Antipsychotic Agents; Benztropine; Clozapine; Dyskinesia, Drug-Induced; Humans; Male; Middle Aged; Observer Variation; Psychotic Disorders; Severity of Illness Index; Videotape Recording

Topics: Benztropine; Clozapine; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Female; Humans; Middle Aged; Schizophrenia, Paranoid; Substance Withdrawal Syndrome

Anticholinergic syndrome can develop in multiple clinical situations. The disturbance of the central nervous system muscarinic transmission by acetylcholine antagonists or lack of acetylcholine can result in this unpredictable behavioral syndrome. Health care professionals should do the following: Be familiar with common drugs or drug combinations that may induce this condition; Be aware of patients who may be at greatest risk; Be able to identify the cluster of signs and symptoms of anticholinergic toxicity; and Implement appropriate nursing treatment interventions for patients with anticholinergic syndrome. Because this condition is constantly changing, it often is misdiagnosed. Much remains to be studied and understood about the neurophysiology of this condition. Central cholinergic transmission is blocked with the use of many anticholinergic drugs in numerous patient settings. Because acetylcholine plays a significant role in modulating the interactions among most other central transmitters, excessive blockage of this neurotransmitter may result in the unpredictable behavioral condition known as anticholinergic syndrome.

Topics: Adolescent; Benztropine; Cholinergic Antagonists; Dose-Response Relationship, Drug; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Haloperidol; Humans; Male; Nursing Diagnosis; Psychoses, Substance-Induced; Risk Factors; Syndrome

Depression is commonly associated with the longitudinal course of schizophrenia. Several etiologies for this problem have been proposed but, to our knowledge, noncompliance with antiparkinsonian medications has not been considered.. Case histories of two patients who were noncompliant and one who threatened noncompliance with antiparkinsonian medications are presented. All three patients were diagnosed with schizophrenia by DSM-III-R criteria and had been clinically stable for long periods.. All three patients became depressed when their adjunctive benztropine was stopped, and their depressions remitted when their benztropine was reinstated.. Noncompliance with antiparkinsonian medications may be associated with a reversible depression in patients receiving maintenance neuroleptics for schizophrenia. Since this is a newly described phenomenon, the scope of the problem is not known; however, it may contribute to the wide prevalence of depressive symptoms in schizophrenia. Clinical measures to facilitate detection of such noncompliance are discussed.

Topics: Adult; Antiparkinson Agents; Antipsychotic Agents; Basal Ganglia Diseases; Benztropine; Depressive Disorder; Dyskinesia, Drug-Induced; Female; Humans; Male; Parkinson Disease, Secondary; Schizophrenia; Treatment Refusal

Topics: Adult; Basal Ganglia Diseases; Benztropine; Clozapine; Dyskinesia, Drug-Induced; Female; Humans; Ocular Motility Disorders; Schizophrenia, Paranoid

This report describes a patient with schizophrenia who developed episodes of ocular dystonia as a delayed side effect of neuroleptic medication. Each episode was preceded and accompanied by marked agitation, stereotypic behaviour and exacerbation of hallucinations. Both the psychotic and dystonic symptoms responded to anticholinergic medication. The theoretical and practical implications of this observation are discussed.

Topics: Adult; Antipsychotic Agents; Benztropine; Chlorpromazine; Dose-Response Relationship, Drug; Dyskinesia, Drug-Induced; Fluphenazine; Haloperidol; Humans; Infusions, Intravenous; Male; Neurologic Examination; Ocular Motility Disorders; Psychoses, Substance-Induced; Schizophrenia; Schizophrenic Psychology

Marching-in-place (MIP) was observed in 12 out of 133 (9%) chronically hospitalized psychiatric patients and in none of 60 hospital staff controls. The prevalence was similar in both sexes. MIP was associated with tardive dyskinesia or parkinsonism or both but did not occur alone. Counting the number of steps per minute provides a reliable method to quantify MIP and may permit a simple objective method for investigating the neuropharmacology of this phenomenon. Preliminary observations suggest that anticholinergic agents may improve MIP in some patients but worsen it in others.

Topics: Adult; Antipsychotic Agents; Benztropine; Chronic Disease; Dyskinesia, Drug-Induced; Female; Humans; Male; Middle Aged; Motor Activity; Propranolol; Schizophrenia; Stereotyped Behavior

Topics: Antiemetics; Benztropine; Dyskinesia, Drug-Induced; Humans; Tropanes

We describe a group of psychotic patients who became worse early in the course of neuroleptic treatment. Characteristics of this group were: predominantly female sex, relatively brief onset, family history of affective disorder, hypomotoric presentation, and severe neuroleptic side effects. We propose that some patients with affective psychoses are uniquely susceptible to profound blockade of the nigrostriatal dopaminergic system by neuroleptics.

Topics: Adolescent; Adult; Antipsychotic Agents; Benztropine; Chlorpromazine; Dyskinesia, Drug-Induced; Female; Haloperidol; Humans; Male; Psychoses, Substance-Induced; Psychotic Disorders; Thiothixene

Topics: Adult; Benztropine; Dyskinesia, Drug-Induced; Female; Fluphenazine; Humans; Patient Compliance; Schizophrenia

Cancer patients commonly receive neuroleptics as antiemetics to relieve nausea and vomiting induced by chemotherapeutic agents. Respiratory dyskinesia, an infrequent, acute, neuroleptic-induced, dystonic reaction, is a potentially life-threatening entity that responds promptly to anticholinergic medication.

Topics: Adult; Antiemetics; Antineoplastic Combined Chemotherapy Protocols; Benztropine; Droperidol; Dyskinesia, Drug-Induced; Humans; Male; Respiration

We report an unusual case of benztropine-induced acute dystonia and dyskinesia without findings of acute anticholinergic toxicity in a 20-month-old child. Laboratory analysis of blood, urine, and gastric contents demonstrated the presence of an atropinic compound and diphenhydramine only, suggesting the association of benztropine and acute dystonia. Effects of benztropine on neuronal uptake of dopamine may represent a possible mechanism for this unusual adverse effect.

Topics: Accidents; Acute Disease; Benztropine; Dyskinesia, Drug-Induced; Dystonia; Emergencies; Humans; Infant; Male; Therapeutic Irrigation; Tropanes

Two different studies were performed in subhuman primates in an attempt to induce symptoms of tardive dyskinesia. The first study lasted for over 5 years. This involved elderly Macaca speciosa. The animals were given first 25 mg of fluphenazine decanoate and later the enanthate IM (3.2 mg/kg) every 2 weeks and on 5 days a week, haloperidol, first IM and later PO. Haloperidol was given first in doses of 1.0 mg/kg and ultimately after years of therapy, in doses of 6.4 mg/kg per day. Those animals who survived gained weight to over 10 kg. After neuroleptic withdrawal, tardive dyskinesia became evident in 1 month. The symptoms of tardive dyskinesia following cessation of medication lasted a maximum of 1 year. This animal model produced very impressive symptoms in one of the three animals treated who survived. This is not a very practical animal model from the aspects of economics (costly), time (5 years), and animal availability (rare and endangered species). However, the symptoms of tardive dyskinesia are very striking and identical with human tardive dyskinesia in a susceptible animal. A more practical experimental animal model involved Cebus apella. Depot fluphenazine (0.1 to 3.2 mg/kg) was given continuously every 2 weeks for 1 year. In this species the symptoms of tardive dyskinesia became progressively prolonged and intense with each course of fluphenazine therapy and withdrawal, suggesting that reversible tardive dyskinesia may turn into irreversible tardive dyskinesia. With each succeeding course of fluphenazine therapy (1 month) and withdrawal (1-3 months), the animals appeared to be sensitized to both the acute extrapyramidal and the tardive dyskinesia symptoms. These animals were also given various experimental drug treatments including biperiden lactate, benztropine mesylate, and d-amphetamine after they developed signs of tardive dyskinesia.

Topics: Animals; Antipsychotic Agents; Benztropine; Cebus; Death, Sudden; Disease Models, Animal; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Female; Fluphenazine; Haloperidol; Humans; Macaca; Male; Motor Activity; Stereotyped Behavior; Substance Withdrawal Syndrome

Three patients are presented in whom TD either disappeared (2 cases) or improved (one case) after discontinuing antiparkinsonian medication without changing the concurrent neuroleptic treatment. In addition, two of the patients presented some "complications" secondary to the TD in the form of frequent falling, psychosocial impairment and suicidal ruminations. The implications of these findings are discussed in the light of the current literature.

Topics: Antiparkinson Agents; Benztropine; Dyskinesia, Drug-Induced; Female; Humans; Middle Aged; Tropanes

Tardive dyskinesia appeared in a 17-year-old boy following withdrawal of pimozide (Orap) and thioridazine (Melleril). The choreodyskinetic movements, which were limited to the limbs and the trunk, cleared with anticholinergic drugs but were dramatically worsened by dopaminergic receptor blockers. Therefore, therapy with an initial high dose of benztropine mesylate (Cogentin) associated with bromazepam (Lexotan) was instituted and was well tolerated.

Topics: Adolescent; Benztropine; Bromazepam; Dyskinesia, Drug-Induced; Humans; Lightning; Male; Parasympatholytics; Pimozide; Thioridazine

Rabbit syndrome is an uncommon, tongue-sparing, orofacial movement disturbance, rapid and regular in nature and associated with prolonged use of neuroleptics. Two cases reports illustrate how anticholinergic agents successfully treat the disorder. The syndrome is distinguished from tardive dyskinesia, which tends to be exacerbated by anticholinergic agents.

Topics: Aged; Antipsychotic Agents; Basal Ganglia Diseases; Benztropine; Diagnosis, Differential; Dyskinesia, Drug-Induced; Female; Humans; Male; Middle Aged

Topics: Animals; Benztropine; Biperiden; Cebus; Disease Models, Animal; Dyskinesia, Drug-Induced; Female; Fluphenazine; Macaca; Male; Parasympatholytics; Species Specificity; Syndrome

Topics: Adult; Akathisia, Drug-Induced; Amoxapine; Benztropine; Depressive Disorder; Dibenzoxazepines; Dyskinesia, Drug-Induced; Humans; Male; Psychomotor Agitation

1. This report describes two cases of psychotic syndrome from benztropine (Cogentin), which was used to treat haloperidol-induced extrapyramidal side effects. The patients' symptomatology meets DSM III criteria for delirium. Both patients displayed repetitive motor automatisms (stereotypy). 2. Symptomatology appeared one-to-two days after the start of benztropine 2 mg b.i.d. and subsided one-to-several days after benztropine was stopped. Treatment consisted of administration of sedative hypnotic drugs. 3. The literature on anticholinergic-induced psychotic syndromes is surveyed. Particular attention is drawn to the occurrence of stereotypy. 4. It is proposed, on the basis of a review of animal and clinical data, that stereotypies in delirious patients are related to muscarinic blockade in the central nervous system. This model is used to explain repetitive motor automatisms which are seen in Alzheimer's disease. 5. The paper concludes with brief guidelines for the management of anticholinergic delirium.

Topics: Adult; Aged; Benztropine; Delirium; Diazepam; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Ethchlorvynol; Female; Haloperidol; Humans; Imipramine; Phenobarbital; Psychoses, Substance-Induced; Stereotyped Behavior; Substance-Related Disorders; Tropanes

Topics: Adolescent; Akathisia, Drug-Induced; Benztropine; Diagnosis, Differential; Dyskinesia, Drug-Induced; Humans; Intellectual Disability; Male; Psychomotor Agitation; Tropanes

10 long-term schizophrenic patients with tardive dyskinesia were studied over 14 weeks and maintained on their usual neuroleptic medications while anticholinergic antiparkinson drugs were employed and then discontinued, and the cycle then repeated. Discontinuation of anticholinergic medications resulted in improvement in dyskinetic movements and vice versa. Estimation of haloperidol equivalents in serum at four times suggested that changes in severity of tardive dyskinesia were not caused by changes in blood levels of neuroleptics. Levels of pituitary hormones were also estimated at four times. Prolactin levels tended to diminish in men over the course of the experiment. Growth hormone and thyrotropin values were mainly stable. However, the growth hormone levels peaked during the final 'off anticholinergic' condition and thyrotropin levels were consistently elevated.

Topics: Adult; Aged; Antiparkinson Agents; Antipsychotic Agents; Benztropine; Dopamine; Dyskinesia, Drug-Induced; Female; Growth Hormone; Humans; Male; Middle Aged; Orphenadrine; Parasympatholytics; Prolactin; Sex Factors; Thyrotropin; Trihexyphenidyl

Topics: Amantadine; Animals; Antipsychotic Agents; Benztropine; Dextroamphetamine; Drug Synergism; Dyskinesia, Drug-Induced; Haloperidol; Humans; Male; Motor Activity; Parasympatholytics; Rats; Stereotyped Behavior

Some patients with tardive dyskinesia fit the cholinergic-dopaminergic imbalance theory, but some do not. In an attempt to study his heterogeneity further, the authors measured the responses of 10 patients with tardive dyskinesia to intravenous challenge doses of drugs that facilitate or inhibit acetylcholine transmission (physostigmine or benztropine, respectively). They then measured the response of these patients to an open outpatient deanol trial. They found that the responses of half of the patients followed the classic theory, 2 responded paradoxically, and 3 responsed inconsistently. They suggest that there is a subgroup of tardive dyskinesia patients who fit the theory but that more research is needed to identify the subgroups who do not.

Topics: Acetylcholine; Antipsychotic Agents; Benztropine; Drug Administration Schedule; Dyskinesia, Drug-Induced; Female; Humans; Male; Physostigmine; Receptors, Dopamine

Topics: Benztropine; Dyskinesia, Drug-Induced; Haloperidol; Humans; Parkinson Disease, Secondary; Tourette Syndrome

Three patients with low grade tardive dyskinesia developed an acute episode of abnormal involuntary movements after a single injection of fluphenazine decanoate. All three patients had their symptoms relieved after treatment with antiparkinsonian medication. The differential diagnosis of these movements is discussed, and a possible animal model for this phenomenon is described.

Topics: Benztropine; Dyskinesia, Drug-Induced; Female; Fluphenazine; Humans; Male; Middle Aged; Schizophrenia

Topics: Aged; Benztropine; Dyskinesia, Drug-Induced; Female; Haloperidol; Humans; Paranoid Disorders; Physostigmine

Topics: Aged; Antiparkinson Agents; Antipsychotic Agents; Benztropine; Dyskinesia, Drug-Induced; Humans; Middle Aged; Trihexyphenidyl

Topics: Benztropine; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Humans; Imipramine; Middle Aged; Substance Withdrawal Syndrome; Thioridazine

Topics: Adolescent; Benztropine; Dyskinesia, Drug-Induced; Haloperidol; Humans; Male; Parasympatholytics; Substance Withdrawal Syndrome

This report describes a male college student who experienced akinesia lasting almost 3 weeks following withdrawal from relatively brief, low-dose neuroleptic treatment. The literature is reviewed and the case is discussed with special focus upon the duration of extrapyramidal side effects. These syndromes are often undiagnosed or misdiagnosed and lead to unnecessary morbidity and noncompliance with recommended pharmacotherapy.

Topics: Adult; Antipsychotic Agents; Benztropine; Dyskinesia, Drug-Induced; Humans; Male; Psychotic Disorders; Substance Withdrawal Syndrome

The authors conducted an extensive pharmacological analysis of a patient severely affected by tardive dyskinesia. No drug treatment gave lasting clinical improvement. Several agents recently recommended for this condition, dimethyl aminoethanol, clozapine, and thioridazine, failed to modify the dyskinesia. Reserpine caused a worsening of the symptoms. A paradoxical and unexpected improvement was observed with apomorphine injections and with low-dosage oral L-dopa. These two drugs may have acted by stimulating presynaptic inhibitory dopamine receptors.

Topics: Adrenergic alpha-Agonists; Adult; Amantadine; Apomorphine; Benztropine; Clozapine; Deanol; Dextroamphetamine; Dose-Response Relationship, Drug; Drug Antagonism; Drug Tolerance; Dyskinesia, Drug-Induced; Female; Haloperidol; Humans; Levodopa; Physostigmine; Receptors, Dopamine; Reserpine; Stimulation, Chemical; Thioridazine

A case report is presented of a patient with remitting tardive dyskinesia coexistent with neuroleptic-induced parkinsonism. The patient received benztropine and physostigmine challenges on successive days and the effects on both syndromes are described. The clinical course of both diseases is discussed in terms of a balance hypothesis between dopaminergic and cholinergic neurotransmission.

Topics: Acetylcholine; Adult; Benztropine; Corpus Striatum; Dopamine; Dyskinesia, Drug-Induced; Fluphenazine; Haloperidol; Humans; Male; Parkinson Disease, Secondary; Physostigmine; Schizophrenia, Paranoid; Thioridazine; Tranquilizing Agents

Topics: Acute Disease; Basal Ganglia Diseases; Benztropine; Dyskinesia, Drug-Induced; Female; Humans; Middle Aged; Remission, Spontaneous; Tranquilizing Agents; Tropanes