Neuroleptic-induced Movement Disorders Research Articles

Tardive Dystonia Related with Aripiprazole

Tardive dystonia is characterized by sustained, generally slow involuntary twisting movements. It is estimated to occur at a frequency of 1% to 4% among patients who are taking an antipsychotic agent. Unlike the first generation antipsychotics, the second generation antipsychotics are less likely to cause neuroleptic-induced movement disorder. For aripiprazole, only a few cases have been reported for tardive dystonia. We present a young male, who developed a severe tardive dystonia after taking aripiprazole for 5 years. The patient was admitted to for the treatment of both hisdystonic and psychotic symptoms. Olanzapine was administered instead of aripiprazole and while his psychotic symptoms improved, the dystonic symptoms were continued. Therefore, olanzapine was switched to clozapine while augmenting with benzodiazepine, anti-cholinergic, and ginko biloba to control his tardive dystonia. After 2 weeks of treatment, the dystonic movement decreased remarkably.

Prevalence of neuroleptic-induced movement disorders: an 8-year follow-up study in chronic schizophrenia inpatients

Background: Atypical antipsychotic drug use by schizophrenia patients in Estonia increased from 32% in 2004 to 61% in 2009.Aims: To assess the prevalence of neuroleptic-induced movement disorders in the Estonian institutionalized population of schizophrenia patients twice over a period of eight years, before and after introduction of atypical antipsychotic drugs using DSM-IV criteria.Methods: DSM-IV criteria and specific rating scales were used to evaluate the prevalence of neuroleptic-induced movement disorders among 72 patients who participated in the study in 2009 compared to 99 patients who participated in 2001.Results: Despite increased use of atypical antipsychotics in the study population (up to 30% from 20%), the proportion of movement disorder-free population remained the same over 8 years – 38.9% in 2001 versus 38.4% in 2009. There were significant intra-individual fluctuations. Use of a typical antipsychotic resulted in an almost seven times higher risk of tardive dyskinesia after 8 years. Doses of antipsychotic drugs had no effect on the severity of neuroleptic-induced movement disorders.Conclusions: Unfortunately, in 18% of patients the switch of medication from typical to atypical did not change the overall prevalence of neuroleptic-induced movement disorders in the group. The long-term benefit of atypical antipsychotics requires further research in patients who are treated with antipsychotics for years.

Antipsychotic Medication Induced Movement Disorders: The Case of Amanuel Specialized Mental Hospital, Addis Ababa, Ethiopia

Background: Neuroleptic-induced movement disorders constitute a worldwide problem in the treatment of schizophrenia because of the limited affordability of atypical antipsychotic drugs. The observable features of acute Parkinsonism; such as limb stiffness and slowness of movement are a social and functional handicap. The same is true for the restless movements and agitation associated with acute akathisia. Tardive dyskinesia, on the other hand is a permanent condition that affects quality of life. However, very few studies have been conducted to estimate the prevalence of Neuroleptic-induced movement disorders and their associated factors among psychotic patients in Ethiopia. Thus the aim of this study was to determine the prevalence of conventional antipsychotic induced movement disorders and associated factors among psychotic patients treated at Amanuel mental specialized Hospital. Method: Hospital based cross-sectional study was conducted by using established clinical rating scales to identify cases of conventional antipsychotic-induced movement disorders in Amanuel mental specialized Hospital on a sample of 377 psychotic outpatients. Systematic random sampling method was employed to select subjects. Logistic regression was used for comparison of the subjects with and without Neuroleptic-induced movement disorders. Results: the prevalence of Neuroleptic-induced movement disorders, namely; neuroleptic-induced Parkinsonism, neuroleptic-induced Akathisia and neuroleptic-induced tardive dyskinesia were found to be 46.4%, 28.6% and 11.9% respectively. Khat (Catha Edulis) use, AOR=1.93, 95%CI: 1.01-3.66, was factors remained to be associated with the presence of NIA. Alcohol use, AOR = 3.25, 95%CI: 1.04-10.16, was associated with TD. Being on chlorpromazine equivalent dose range of >=400mg/day, AOR =4.32, 95%CI: 2.25-8.30, AOR = 3.677, 95%CI: 1.807-7.482, AOR=4.157, 95%CI: 1.165-14.834 were associated with Parkinsonism, Akathisia and TD respectively. Conclusions and Recommendation: Considerable number of patients with psychotic disorders suffered from a conventional antipsychotic -induced movement disorder. Khat, alcohol and high dose of drugs were found to be associated with conventional antipsychotic Induced movement disorders. Designing treatment guideline, increasing availability of drugs with minimal side effects and psycho-education for patients and their family is essential to reduce these devastating side effects.

P-1115 - Prevalence of conventional antipsychotic induced movement disorders and factors associated with them among psychotic patients treated at amanuel mental specialized hospital; aa, ethiopia

Background Neuroleptic-induced movement disorders constitute a worldwide problem in the treatment of schizophrenia because of the limited affordability of atypical antipsychotic drugs. However, the prevalence of Neuroleptic-induced movement disorders and their associated factors have not been studied in psychotic patients in Ethiopia. Objective To determine the prevalence of conventional antipsychotic induced movement disorders and associated factors among psychotic patients at Amanuel mental specialized Hospital. Method Hospital based cross-sectional study was conducted by using established clinical rating scales to identify cases of conventional antipsychotic-induced movement disorders in Amanuel mental specialized Hospital samples of 377 psychotic outpatients. Systematic random sampling method was employed to select subjects. Logistic regression was used for comparison of the subjects with and without Neuroleptic-induced movement disorders. Findings and conclusions Neuroleptic-induced movement disorders according to the clinical rating scales were found in: 175(46.4%) had neuroleptic-induced Parkinsonism, 108(28.6%) had neuroleptic-induced Akathisia and 45(11.9%) had neuroleptic-induced tardive dyskinesia. Khat use AOR = 1.93, 95%CI: 1.01–3.66 was factors remained to be associated with the presence of NIA. Alcohol use AOR = 3.25, 95%CI: 1.04–10.16 was associated with TD. Being on chlorpromazine equivalent dose range of > = 400 mg/day AOR = 4.32, 95%CI: 2.25–8.30, AOR = 3.68, 95%CI: 1.81–7.48, AOR = 4.16, 95%CI: 1.17–14.83 were associated with Parkinsonism, Akathisia and TD respectively. In conclusion, many patients with psychotic disorders suffered from a conventional antipsychotic -induced movement disorder. Khat, alcohol and high dose of drugs were found to be associated with conventional antipsychotic Induced movement disorders.

Recognizing movement disorders: Reviving old practices

Movement disorders have many different presentations and are defined as a group of syndromes that affect the ability for one to control movement in a given muscle or muscle group. Many of the medications we use to treat psychiatric illness (antipsychotics, lithium, and valproic acid) have the potential to cause movement disorders, often referred to as extrapyramidal side effects, though predictability is lacking. Antipsychotic-induced dopamine blockade can lead to acute dystonia, akathisia, and Parkinsonism, all of which are generally reversible if treatment is discontinued. A neuroleptic-induced movement disorder that may be irreversible is tardive dyskinesia. Both lithium and valproic acid may cause tremor, the presentation of which will be explored in this issue of the Mental Health Clinician. Less often, our antidepressants may induce movement disorders similar to those caused by antipsychotics. In 2009, the U.S. Food and Drug Association placed a black box warning on the medication metoclopramide, a gastrointestinal motility agent that has some dopamine blockade effects, warning of its risk of causing tardive dyskinesia. This prompted a slew of lawsuits against manufacturers of this medication and the doctors who prescribed it without informing their patients or monitoring for this known side effect.

Tardive Tourette-Like Syndrome in a Patient Treated With Paliperidone

Tardive Tourette-Like Syndrome in a Patient Treated With Paliperidone

Pharmacogenomic Implications of Variants of Monoaminergic-Related Genes in Geriatric Psychiatry

Response to psychiatric medications in later life is highly heterogeneous and complex. Monoaminergic-related polymorphisms may influence medication response and susceptibility to side effects in elderly individuals. Individuals with the lower function short (S) allele of the serotonin transporter gene (SLC6A4) insertion/deletion (indel) promoter polymorphism (5-HTTLPR) have both increased the likelihood of adverse drug events and increased the need for higher antidepressant concentrations to obtain maximum antidepressant response. By contrast, carriers of the higher expression homozygous long allele (L/L) genotype may respond at lower concentrations. The differential role of these polymorphisms appears at early stages of treatment rather than in the final antidepressant outcome. Research findings suggest that the rs25531 SNP may influence functional expression of the L allele. Similarly, a variable number of tandem repeats in the second intron of the serotonin transporter gene may influence the expression of SLC6A4 and the implications of these variants may be influenced by aging. Two polymorphisms, rs2242466 (-182T/C) and rs5569 (1287G/A), in the norepinephrine transporter gene (SLC6A2 or NET) have been associated with antidepressant response. Studies in dopamine-related polymorphisms have focused on associations with neuroleptic-induced movement disorders. The rs1800497 variant (Taq1A) of the dopamine receptor D2 (DRD2) gene located in a noncoding 3´ region may regulate expression of D2 receptors. The rs6280 variant (Ser9Gly) of the dopamine receptor 3 (DRD3) gene may influence the binding affinity of D3 receptors as a result of serine to glycine substitution of the receptor protein. A multicenter collaborative research effort would be an effective strategy to increase sample sizes to further investigate how gene variants impact the pharmacodynamics and pharmacokinetics of psychotropic drugs in elderly persons.

Cross-cultural psychopharmacology: a review

Cross-cultural psychopharmacology seeks to determine whether there are differences in responses to psychopharmacologic agents among various ethnic groups and the reason for such variations. During the past four decades numerous clinical reports have addressed potential differences in therapeutic dosages and side effects of psychotropic medications between various ethnic groups. In addition, several rigorously designed studies have focused on ethnic differences in pharmacokinetics (including absorption, metabolism, distribution and excretion) and pharmacodynamics (including receptor-coupling activity). These ethnic variations are mainly influenced by genetic predisposition but are also influenced by other factors such as culture, environment, psychosocial supports, and attitudes towards pharmacology. This presentation will provide a critical review of the existing information in regard to psychotropic medications including neuroleptics, antidepressants, lithium, and benzodiazepines among various ethnic groups. Also included will be data on neuroleptic-induced movement disorders, the clinical implications of genetic polymorphism of cytochrome P-450 isoenzymes, recommendations on how to better design a pharmacological approach in the treatment of psychiatric disorders among different ethnic groups, as well as recent advances and future directions regarding cross-cultural issues of psychopharmacology.

Atypical Antipsychotic Adjustments and Side-Effects over Time in Adults with Intellectual Disability, Tardive Dyskinesia, and Akathisia

Atypical antipsychotic use is prevalent in ID, and can result in serious side effects, particularly long-term. The purpose of this paper was to examine side effects over time and adjustments in atypicals in ID, tardive dyskinesia (TD), and akathisia. Side effects of 84 ID adults were assessed across four administrations of the Matson Evaluation of Drug Side-Effects (MEDS). Persons with TD or akathisia who experienced changes in atypicals were more likely to evince side effects. These trends were evident across total MEDS scores and subscales for cardiovascular and hematology, CNS for parkinsonism/dyskinesia and behavioral/akathisia. Atypical antipsychotic use poses a risk for side effects in individuals with ID, particularly in relation to medication adjustments over time and the presence of neuroleptic-induced movement disorders.

Improvement in Pisa Syndrome and Tardive Dyskinesia Following Aripiprazole Treatment

Back to table of contents Previous article Next article LETTERFull AccessImprovement in Pisa Syndrome and Tardive Dyskinesia Following Aripiprazole TreatmentJia-Chi Shan M.D.,Mei-Chih Meg Tseng M.D., M.Sc.,Jia-Chi Shan M.D.Search for more papers by this author,Mei-Chih Meg Tseng M.D., M.Sc.Search for more papers by this author,Published Online:1 Jul 2009AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Tardive dystonia and tardive dyskinesia, parts of a group of delayed-onset neuroleptic-induced movement disorders, may coexist but are postulated to be different in prevalence, demographic profiles, clinical presentations, and to have different neurochemical mechanisms. 1 Drug-induced Pisa syndrome, manifesting as a tonic lateral flexion of trunk after exposure to neuroleptics, consists of both acute and persistent types. Thus, Pisa syndrome can also be viewed as an atypical subtype of tardive dystonia. 1 , 2 Aripiprazole exerts a therapeutic effect by partial D2 agonism rather than D2 receptor blockage, 3 implying its possibly beneficial effect to delayed-onset extrapyramidal symptoms. Previous reports often focused on the issue relevant to either one of the tardive syndromes. We report on a patient whose Pisa syndrome and tardive dyskinesia were improved following aripiprazole treatment. Case Report Ms. Y, a 31-year-old schizophrenia patient (DSM-IV criteria), had psychotic symptoms onset at the age of 20. Her symptoms were rapidly alleviated after 6 months of sulpiride therapy with trihexyphenidyl. She had received treatment with trifluoperazine, haloperidol, clotiapine, and zotepine in the following years for intermittent relapsing symptoms. Oral-buccal-lingual dyskinesia was first noticed after she had been treated with risperidone for 2 years. Her antipsychotic was then switched to olanzapine. Moreover, she developed left-tilting of her trunk and right-sided rotation of her neck with subjective stiffness in her chin and shoulders during olanzapine treatment. A diagnosis of tardive dystonia was made according to Burke and colleagues’ criteria. 4 Her dystonic reaction showed no improvement after high-dose anticholinergic medication (biperiden, 8 mg) was added on and olanzapine was withdrawn. Lingual dyskinesia was partially ameliorated after replacement of olanzapine by amisulpride for 2 months, but Pisa syndrome did not improve. Eventually, aripiprazole and amantadine were substituted for amisulpride and biperiden, respectively. Tardive dyskinesia disappeared in one month, and Pisa syndrome was improved significantly after 2 months’ administration of aripiprazole, 30 mg/day, and amantadine, 200 mg/day. Discussion Despite the sharing dopamine blockade in the pathogenesis of Pisa syndrome and tardive dyskinesia, cholinergic-dopaminergic imbalance may better account for the former whereas dopamine receptor hypersensitivity may account for the latter. 2 Our patient developed persistent motor symptoms insidiously after long-term conventional and atypical antipsychotics, which excluded an acute tonic reaction. 2 This patient’s tardive syndromes were neither resolved by withdrawal of olanzapine (a multi-acting receptor-targeted antipsychotic with high 5HT2/D2 ratio), nor treatment of amisulpride (a D2/D3 receptor antagonist with high D3/D2 ratio). 3 Unlike other atypical antipsychotics, aripiprazole shows higher affinity at D2 receptors than at 5-HT2 receptors, and its weak partial 5HT 1A agonism is demonstrated in a recent study. 5 Thus, aripiprazole successfully improved both tardive dyskinesia and Pisa syndromes, possibly because it can reverse D2 receptor hypersensitivity and restore cholinergic-dopaminergic balance via D2 partial agonism. As for amantadine, there has been no substantial evidence regarding its effect on treating tardive dystonia. The role played by amantadine in this patient was unclear. In summary, we suggest that aripiprazole is a potential drug for the management of Pisa syndrome coexistent with tardive dyskinesia. Aripiprazole is also a drug candidate to study the differential neurochemical mechanism of various subtypes of tardive syndromes.Department of Psychiatry, National Taiwan University Hospital, Taipei, TaiwanDepartment of Psychiatry, National Taiwan University Hospital, Yun-Lin Branch, Douliou; Department of Psychiatry, College of Medicine, National Taiwan University, Taipei, Taiwan

Targeting therapy for movement disorders

It remains a common misconception that neurologists are physicians who are skilled only in making a diagnosis but who are disinterested in therapy of patients. However, there have been major advances on several neurological fronts in the past 50 years. Therapeutics of Parkinson's Disease and Other Movement Disorders, edited by Mark Hallett and Werner Poewe, is a well organised summary of the state-of–the-art treatments in movement disorders. The book is divided into nine sections covering the major areas in movement disorders: Parkinson's disease (PD) and atypical parkinsonism, tremor, dystonia, and muscle spasms, other hyperkinetic movement disorders, cerebellar, gait, and balance disorders, and psychogenic movement disorders. The editors have assembled a panel of leading international experts as chapter authors within each section, who ably provide the balance between scientific rigour and “personal clinical acumen and therapeutic wisdom”. Each chapter and section is led by a concise summary of disease pathophysiology, followed by a detailed review of treatment. This approach enables understanding of the therapies within a broader mechanistic framework. Rather than simply putting together a list of randomised controlled trials or declaring therapy an evidence-free zone, most of the contributors synthesise the body of current knowledge and present a practical approach to help deal with the immediate needs of the individual patient. Their work is both cause for optimism and sober reflection. James Parkinson recommended “at whatever period of the disease it might be proposed to attempt the cure, blood should be first taken from the upper part of the neck…” as therapy for shaking palsy. The Nobel-prize winning discovery by Arvid Carlsson that dopamine is a neurotransmitter led to dopamine-replacement therapy for PD more than 40 years ago—one of the greatest success stories in neurological therapeutics. Yet this effective symptomatic therapy remains an exception rather than the rule for neurodegenerative diseases, and, almost 200 years on from Parkinson's recommendations, we are still searching for a cure. Most of the chapters cite up-to-date references, but, as inevitably happens with the prolonged process of publishing a book, some findings have been omitted. For example, some of the more recent gene discoveries in familial PD and the link between glucose transporter gene defects and paroxysmal exercise-induced dystonia are not included. Recent randomised, double-blind, controlled studies supporting the use of domperidone as treatment for orthostatic hypotension and macrogol as treatment for constipation in PD, two common non-motor symptoms, escape mention. The chapter on Wilson's disease is written by a recognised authority who strongly advocates avoiding D-penicillamine; however, this treatment remains favoured by other experts and is the only affordable option in many countries. Some practical guidance for those who have need of its use would have been beneficial. The chapter on myoclonus could have been enhanced by more detailed discussion of the importance of neurophysiological characterisation of myoclonus for therapy, and the section on neuroleptic-induced movement disorders could have been improved by a broader discussion of the nosological, diagnostic, and management challenges of neuroleptic malignant syndrome. Overall, this book can be strongly recommended and is an asset to libraries of both movement disorder specialists and general neurologists. Its logical structure, linking therapy with underlying pathophysiology, means that it will remain a useful reference even as new therapies inevitably emerge.

Genetic study of BDNF, DRD3, and their interaction in tardive dyskinesia

Tardive dyskinesia (TD) is a neuroleptic-induced movement disorder. Its pathophysiology is unclear. The most consistent genetic findings have shown an association with the Ser9Gly polymorphism of the DRD3 gene. However, only few polymorphisms within DRD3 has been tested, and a comprehensive examination of DRD3 in TD is still lacking. Further, brain-derived neurotrophic factor (BDNF), a neuronal growth and survival peptide, regulates DRD3 expression and may be involved in the neuronal degeneration observed in TD. In the present study, we investigated 15 tag DRD3 polymorphisms and four tag BDNF polymorphisms for association with TD in our sample of Caucasian schizophrenia patients ( N = 171). While BDNF markers showed no association, a haplotype containing rs3732782, rs905568, and rs7620754 in the 5′ region of DRD3 was associated with TD diagnosis (p[10,000 permutations] = 0.007). We also found evidence of interaction between BDNF and DRD3 polymorphisms. Further studies are needed to confirm these findings.

Neuroleptic-induced movement disorders in a naturalistic schizophrenia population: diagnostic value of actometric movement patterns

BackgroundNeuroleptic-induced movement disorders (NIMDs) have overlapping co-morbidity. Earlier studies have described typical clinical movement patterns for individual NIMDs. This study aimed to identify specific movement patterns for each individual NIMD using actometry.MethodsA naturalistic population of 99 schizophrenia inpatients using conventional antipsychotics and clozapine was evaluated. Subjects with NIMDs were categorized using the criteria for NIMD found in the Diagnostic and Statistical Manual for Mental Disorders – Fourth Edition (DSM-IV).Two blinded raters evaluated the actometric-controlled rest activity data for activity periods, rhythmical activity, frequencies, and highest acceleration peaks. A simple subjective question was formulated to test patient-based evaluation of NIMD.ResultsThe patterns of neuroleptic-induced akathisia (NIA) and pseudoakathisia (PsA) were identifiable in actometry with excellent inter-rater reliability. The answers to the subjective question about troubles with movements distinguished NIA patients from other patients rather well. Also actometry had rather good screening performances in distinguishing akathisia from other NIMD. Actometry was not able to reliably detect patterns of neuroleptic-induced parkinsonism and tardive dyskinesia.ConclusionThe present study showed that pooled NIA and PsA patients had a different pattern in lower limb descriptive actometry than other patients in a non-selected sample. Careful questioning of patients is a useful method of diagnosing NIA in a clinical setting.

Prevalence of neuroleptic-induced movement disorders in psychotic patients within peripheral New Zealand mental health services: Ethnic variation

Prevalence of neuroleptic-induced movement disorders in psychotic patients within peripheral New Zealand mental health services: Ethnic variation

Reduction in Neuroleptic-Induced Movement Disorders After a Switch to Quetiapine in Patients With Schizophrenia

Persistent neuroleptic-induced movement disorders limit effective pharmacological management of psychotic disorders. Although antipsychotic switching is a common strategy for managing extrapyramidal side effects (EPSs), there is insufficient empirical support to guide the clinician. We designed the present study to examine whether patients with preexisting EPS switched to quetiapine would show greater reduction in EPS compared with control patients. Twenty-two patients with schizophrenia meeting clinical criteria for tardive dyskinesia or coexisting parkinsonism were randomized either to switch from their current antipsychotic to quetiapine (n = 13) or to remain on their current treatment (n = 9). A battery of standard clinical assessments for EPS along with electromechanical instrumental measures was administered before randomization and again 1 and 3 months postrandomization. We observed significant reduction in parkinsonism (P < 0.001) and akathisia (P = 0.02) based on clinical assessments and dyskinesia (P < 0.05) based on instrumental assessment for the quetiapine group. Subjects remaining on current treatment exhibited an increase in rigidity (P < 0.05) based on instrumental measures. These findings support the switching to quetiapine in the management of preexisting neuroleptic-induced extrapyramidal side effects.

Vitamin B6 Treatment in Acute Neuroleptic-Induced Akathisia

Treatment strategies for acute neuroleptic-induced akathisia (NIA) contain anticholinergic (antimuscarinic) agents, dopamine agonists, gamma-aminobutyric acid (GABA)-ergic agents, beta-blockers, benzodiazepines, and serotonin antagonists. Nevertheless, many patients who suffer from acute akathisia fail to respond to treatment. In earlier studies, vitamin B6 was found to be effective in the treatment of neuroleptic-induced movement disorders. The purpose of this study was to evaluate the efficacy of vitamin B6 in the treatment of acute NIA. This is the first report of B6 as a treatment for NIA. This study was conducted in 2 mental health centers from February 2003 to November 2003. Twenty schizophrenia and schizoaffective inpatients with a DSM-IV diagnosis of NIA were randomly divided to receive vitamin B6 600 mg/day b.i.d. (N = 10) or placebo (N = 10) twice a day for 5 days in a double-blind design. The Barnes Akathisia Scale (BAS), the Brief Psychiatric Rating Scale (BPRS), and the Clinical Global Impressions scale (CGI) were used to assess the severity of NIA and psychotic symptoms. The BAS assessment was made at baseline and every day during the study. The BPRS and CGI were completed at baseline and at the end of the study. The vitamin B6-treated patients in comparison with the placebo group showed a significant improvement on the subjective-awareness of restlessness (p = .0004), subjective-distress (p = .01), and global (p = .004) subscales of the BAS. The objective subscale did not demonstrate significant positive results (p = .079), but there was a trend of symptom amelioration in the vitamin B6 group. A reduction of at least 2 points on the BAS global subscale was noted in 8 patients in the vitamin B6 group (80%), and in only 3 patients in the placebo group (30%) (p = .037). Our preliminary results indicate that high doses of vitamin B6 may be useful additions to the available treatments for NIA, perhaps due to its combined effects on various neurotransmitter systems.

Prevalence of neuroleptic-induced movement disorders in chronic schizophrenia inpatients.

Since most of the world's schizophrenia patients are treated with conventional antipsychotics, the authors evaluated various methods for establishing the prevalence of neuroleptic-induced movement disorders in these patients. DSM-IV criteria and established score thresholds on a movement disorder rating scale were used to identify cases of neuroleptic-induced movement disorder in a representative Estonian patient sample of 99 chronic institutionalized schizophrenia patients, 18-65 years old, treated with conventional neuroleptics (79.8%) or clozapine (20.2%). Neuroleptic-induced movement disorders according to DSM-IV criteria were found in 61.6% of the group: 31.3% had neuroleptic-induced akathisia, 23.2% had neuroleptic-induced parkinsonism, and 32.3% had neuroleptic-induced tardive dyskinesia. Prevalence rates for akathisia and tardive dyskinesia were similar when either DSM-IV criteria or rating scale scores were used, but the prevalence rate for parkinsonism was much lower per DSM-IV criteria than according to rating scale score. Nearly two-thirds of chronic schizophrenia patients suffered from a neuroleptic-induced movement disorder. Globally, extrapyramidal adverse effects still impose a huge burden on the majority of neuroleptic-treated individuals with schizophrenia. The discrepancy between the standard identification methods for neuroleptic-induced movement disorder indicate the need for further research.

Atypical antipsychotic use in treating adolescents and young adults with developmental disabilities.

To study the usage, efficacy, and side effects patterns of atypical neuroleptics (atypicals) in adolescents and young adults with developmental disabilities (DDs) (mental retardation). We undertook a chart review of adolescents and young adults (under age 25 years) seen by our specialized mental health team. Risperidone and olanzapine were by far the most frequently prescribed atypicals. Robust clinical effects were noted for both psychotic and nonpsychotic disorders. Most patients tolerated atypicals well, although a significant minority did experience neuroleptic induced movement disorders (NIMDs), particularly dystonias and dyskinesias. Female patients with DDs appear to be at particular risk of NIMDs. Atypicals are useful in treating various conditions associated with DDs. This population, however, seems particularly sensitive to NIMDs, hence caution and close monitoring are required.

Hormone replacement therapy in postmenopausal women with schizophrenia: positive effect on negative symptoms?

Background: Some studies of premenopausal women suggest that the severity of psychopathology associated with schizophrenia may be related to levels of estrogen. Methods: We examined psychopathology in community-dwelling postmenopausal women with schizophrenia who had received ( n = 24) versus had never received ( n = 28) hormone replacement therapy. Results: Users of hormone replacement therapy and nonusers did not differ significantly with respect to age, ethnicity, education, age of onset, duration of schizophrenia, global cognitive functioning, or neuroleptic-induced movement disorders. The hormone replacement therapy users received lower average daily doses of antipsychotic medication; they had similar levels of positive symptoms but significantly less severe negative symptoms compared with hormone replacement therapy nonusers, independent of differences in antipsychotic dosage. Conclusions: Our results suggest that the use of hormone replacement therapy in conjunction with antipsychotic medication in postmenopausal women with schizophrenia may help reduce negative, but not positive, symptoms.

The preventative role of antioxidants (selegiline and vitamin E) in a rat model of tardive dyskinesia

Background: We examined the potential protective effects of two potent antioxidants, selegiline and vitamin E, in a rodent model of tardive dyskinesia (TD), viz. neuroleptic-induced spontaneous orofacial movements. Methods: Rats were treated with fortnightly injections of fluphenazine decanoate for 12 weeks, and examined at baseline and at fortnightly intervals for vacuous chewing movements, mouth tremors and tongue protrusions. Results: The administration of fluphenazine led to a progressive increase of all three types of orofacial movements. In the first study, the impact of the concomitant administration of selegiline on orofacial movements was examined. Selegiline led to a reduction in orofacial movements in neuroleptic-treated rats to the level of control rats not being administered a neuroleptic drug. In the second study, rats were fed diets either high or low in their vitamin E content. High and low vitamin E diets did not significantly affect neuroleptic-induced orofacial movements. Conclusions: Our studies provide some support for the hypothesis that oxidative injury may play a role in the genesis of neuroleptic-induced movement disorder, and prompt further examination of this hypothesis in both animals and humans.