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Background: Drug-induced parkinsonism (DIP) is the most common movement disorder induced by antipsychotics. Although DIP is mostly symmetric, asymmetric DIP is reported in a substantial part of the patients. We investigated the frequency of motor asymmetry in DIP and its relationship to the severity of psychopathology in long-stay psychiatric patients. Methods: We obtained data from a cohort study of 207 long-stay psychiatric patients on the frequency and risk factors of tardive dyskinesia, akathisia, tardive dystonia, and DIP. From July 2003 to May 2007 (mean follow-up, 1.1 year) drug-induced movement disorders were assessed at least two times in each patient, with a frequency of persistent DIP of 56.2%. All patients who had at least one time parkinsonism in the upper/lower limb(s) were included for analyses (190 patients, 79 women; mean age, 48.0 +/- 12.9 years). The Unified Parkinson Disease Rating Scale motor scale was used to calculate the frequency of asymmetric parkinsonism. Multilevel mixed models were built to explore the relationship between asymmetry in parkinsonism and the severity of psychopathology, measured on the Clinical Global Impression-Schizophrenia scale severity index (CGI-SCH SI). Results: The frequency of asymmetric parkinsonism was 20.8%. Asymmetry in parkinsonism was associated with symptom severity on all CGI-SCH SI scales (beta range, 0.37-3.74) and significantly associated with the positive symptom scale (beta, 3.74; 95% CI, 0.35-7.31). Conclusion: DIP is asymmetric in a substantial part of patients. Asymmetric presentation of DIP is of clinical relevance as it is related to the severity of psychopathology and may alert the clinician of more severe psychopathology. Future research is recommended to provide insight into the neuropsychopathology and clinical value of asymmetric parkinsonism for psychiatric patients.

Recent studies demonstrate an association between antipsychotic-induced parkinsonism (AIP) and rs4606 SNP of RGS2 gene in Jewish and African-Americans. The current, study investigates the association between rs4606 and AIP or its subsymptoms (rest tremor, rigidity, and bradykinesia) in 112 psychiatric inpatients of African-Caribbean origin. Presence of AIP, rigidity, bradykinesia, and tremor was measured by the UPDRS. We applied chi(2) (or Fisher Exact) and logistic regression analyses in several models including rs4606, age, gender, dose of antipsychotics, and anticholinergics, and two other putatively functional SNPs in DRD2 (-141Clns/Del) and HTR2C (Cys23Ser) genes. In contrast to recent literature, we find no evidence for an association between rs4606 and AIP or any of its subsymptoms. We hypothesize that the observed lack of association is due probably to differences in serotonin 2A-receptor affinities of the antipsychotics utilized (in contrast to the other published studies, the majority of our patients utilized typical antipsychotics). Copyright (C) 2009 John Wiley & Sons, Ltd.

There is increasing evidence for olfactory deficits in patients with extrapyramidal disorders, but little is known about their occurrence in patients with drug-induced extrapyramidal symptoms (EPS). The present study was performed to investigate olfactory function in depressed patients with drug-induced parkinsonism under treatment with D2-blocking neuroleptic drugs compared to depressed controls on similar neuroleptic dose without EPS (no-EPS), and neuroleptic-naive depressed controls (no-NL).A total of 79 depressed patients with (N = 59) and without psychotic features (N = 20) were included in the study. Psychotic patients were treated with D2 blocking neuroleptic drugs. Of the neuroleptic-treated patients, 15 developed EPS. In all patients psychophysical olfactory testing was performed using "Sniffin' Sticks" which included assessment of odor thresholds for phenylethylalcohol (PEA), odor identification, and odor discrimination.Patients in the EPS group had significantly lower olfactory scores than patients in the no-EPS or no-NL groups. Patients in the no-NL and no-EPS groups were not significantly different from each other in terms of olfactory function. Using partial correlations controlling for the patients' age, significant correlations were observed for EPS patients between severity of EPS and odor thresholds and odor identification, but not for odor discrimination. This indicated that olfactory function decreased with increasing severity of EPS symptoms.Our data show that olfactory deficits may be drug-induced in patients with primary affective disorder with a sensitivity toward developing EPS.

Previous studies suggest that many untreated schizophrenia patients exhibit motor disturbances. On the basis of these findings, the authors hypothesized that preexisting extrapyramidal movement disorders may increase the risk of developing neuroleptic-induced parkinsonism (NIP). Thirty-five newly medicated psychotic patients underwent pretreatment clinical and instrumental motor and psychiatric assessments. Posttreatment ratings of parkinsonism were conducted at monthly intervals for the first 3 months and every 3 months thereafter. Thirteen patients (37%) developed NIP. Advanced age and pretreatment extrapyramidal disturbances predicted NIP. Life-table survival curves indicated that patients with pretreatment instrumental rigidity developed clinically significant NIP earlier than those without rigidity. These findings suggest that pretreatment motor dysfunction may be a risk factor for drug-induced parkinsonism, especially among older patients.

The authors prospectively examined elderly patients diagnosed with major depression with psychotic features (MD-P) and patients diagnosed with dementia of the Alzheimer Type (DAT) for neuroleptic-induced parkinsonism (NIP) during perphenazine treatment. Baseline parkinsonian symptoms did not differ between groups. With treatment, mean NIP score doubled in DAT patients but remained unchanged in the MD-P group. The difference between groups was highly significant and remained so after the effects of age, perphenazine dose, and duration of perphenazine treatment were controlled. Although the mechanisms underlying these differences in NIP development remain to be determined, clinical guidelines for neuroleptic dosages in elderly patients need to account for variability in neuroleptic tolerance between diagnostic groups.

Elderly patients are particularly sensitive to the neurologic side effects of psychotropic medications. This increased sensi tivity may be related to brain structural changes associated with aging. In this pilot study, the authors report on the oc currence of caudate hyperintensities, using brain magnetic resonance imaging, in seven elderly depressed subjects who developed neuroleptic-induced parkinsonism. Caudate hyperintensities were not observed in any of the seven healthy elderly controls examined. These results suggest that caudate hyperintensities may render some elderly depressed pa tients susceptible to neuroleptic-induced parkinsonism. (J Geriatr Psychiatry Neurol 1991;4:86-89).

We evaluated 21 right-handed psychiatric patients with tardive dyskinesia (TD) for the presence and laterality of neuroleptic-induced tremor and rigidity. The goals of the study were to assess the frequency and coexistence of TD and neuroleptic-induced parkinsonism (NIP) using instrumental and clinical measurements and to evaluate the hypothesis that when TD and NIP coexisted in the same patient, they were more likely to appear in opposite limbs. Results indicated that a high percentage of TD patients had coexisting rigidity and tremor on the basis of both clinical ratings and instrumental procedures; however, only instrumental procedures were useful in identifying tremor and rigidity asymmetries. We found that TD and tremor or rigidity did not lateralize to opposite limbs, thus weakening the hypothesis that TD and NIP stemmed from reciprocal pathophysiological mechanisms.

We studied the association between polymorphisms of genes coding for dopamine D-2 (DRD2), dopamine D-3 (DRD3), serotonin 2(a) (HTR2A), and serotonin 2(c) (HTR2C) receptors and Antipsychotic-Induced Parkinsonism (AIP), rigidity, bradykinesia, and rest-tremor in African-Caribbeans treated with antipsychotics. Polymorphisms of DRD2 (-141CIns/Del, TaqIA, 957C > T), DRD3 (Ser9Gly), HTR2A (-1438A > G, 102T > C, His452-Tyr), and HTR2C (-759C > T, Cys23Ser) genes were determined according to standard protocols. The Unified Parkinson Disease Rating Scale was used for the measurement of AIP, rigidity, bradykinesia, and rest-tremor. Chi-squared or Fisher's exact tests were applied for the association analyses. The t-test was applied for continuous data. Ninety nine males and 27 females met the inclusion criteria (Schizophr Res 1996, 19:195). In males, but not in females, there were significant associations between -141CDel-allele carriership (DRD2) and rigidity (Fisher's Exact Test: P = 0.021) and between 23Ser-allele carriership (HTR2C) and bradykinesia (P = 0.026, chi(2) = 5.0) or AIP (P = 0.008, chi(2) = 7.1). Rest-tremor was not associated with any of the polymorphisms studied. Analyses of the age, chlorpromazine equivalents, benztropine equivalents, the number of patients using anticholinergic medication, and the utilization patterns of the antipsychotic medication did not show statistically significant differences between patients with and without AIP, rigidity, bradykinesia, rest-tremor. Conducting the analysis without gender stratification did not affect our findings considerably, except for the association between bradykinesia and 23Ser-allele which failed to reach statistical significance in the total sample (P = 0.0646, chi(2) = 3.41). Since AIPs subsymptoms (rigidity, bradykinesia, and rest-tremor) may differ pharmacogenetically, our data strongly support symptom-specific analysis of AIP. However, further research is warranted to confirm our findings. (c) 2008 Wiley-Liss, Inc.

Several studies have reported an apparent protective effect of cigarette smoking for the risk of idiopathic Parkinson's disease (IPD). These observations are supported by neurochemical studies demonstrating enhancement of central dopaminergic neurotransmission by nicotine. We studied the prevalence and severity of neuroleptic-induced parkinsonism (NIP) in relation to cigarette smoking in a homogeneous sample of 130 psychiatric inpatients receiving long-term neuroleptic treatment. Despite the fact that smokers had significantly higher dosage of neuroleptics during the month prior to evaluation and longer exposure to medication, they presented with significantly less prevalence and severity of NIP than nonsmokers. These findings suggest that the inverse association between smoking and IPD may apply to NIP.

"Rubral" tremor is a rare movement disorder that occurs typically with midbrain damage. It is defined by its presence at rest, with sustained posture, and with movement. Whether it is a single-tremor disorder or a combination of two distinct tremors is debated. This report chronicles a severe neuroleptic induced "rubral" tremor in a patient who had had a stable posttraumatic ataxia. The dramatic response to benztropine and bromocriptine is illustrated in the videotape.

Basal ganglia side-effects caused by neuroleptic drugs are frequently ignored, misdiagnosed, or mistreated by the patient or physician. Such side-effects must be anticipated and appropriate management instituted so that patient compliance with the drug regimen is increased and the therapeutic relationship is maintained. Side-effects can be detected in frequent and complete examinations of the head and neck, limbs, and chest and back. The various medications for drug-induced parkinsonism are reviewed, with an emphasis on the indications for selection and the effects of each drug. Common errors in the diagnosis and management of side-effects of neuroleptic drugs are summarized.

The authors studied neuroleptic drug response in 126 inpatients in Japan. They found similar prevalences and risk factors of tardive dyskinesia and neuroleptic-induced parkinsonism in Japan and the West, despite cross-cultural differences in psychiatric practice.

Extrapyramidal disturbances of movement are among the most frequent undesirable concomitant effects of neuroleptic therapy (Ayd 1961; Benkert and Hippius 1980; Haase 1982). It is indisputable that early dyskinesia can be favorably influenced by anticholinergics (e.g.,biperiden or methixene).The neuroleptic-induced parkinsonian syndrome, on the other hand, presents a difficult problem. The discussion is still not concluded as to whether or not the combined administration of neuroleptics and anticholinergics raises the risk of developing late dyskinesia (Haase 1982 and others). This point is particularly important because there is presently no dependable method for treating late dyskinesia (Neumann 1982). The development of drugs with better efficacy than that of anticholinergics or with an alternative approach is thus of substantial clinical importance, especially for chronic schizophrenics under long-term neuroleptic treatment.

The effect of electroconvulsive therapy (ECT) on the severity of neuroleptic-induced parkinsonism was studied in nine schizophrenic inpatients in a longitudinal triphasic design: neuroleptics-neuroleptics plus ECT—neuroleptics. The results suggest that ECT has a true antiparkinsonian potential. The role of ECT in the treatment of Parkinson's disease, especially with therapy-resistant patients complicated with on-off symptoms, is highlighted.

The effect of L-deprenyl on neuroleptic-induced parkinsonism was evaluated in eleven patients. No significant improvement was observed during the treatment with L-deprenyl in the overall assessment. Four patients, however, were considered responders as their total scores on the modified version of Neurological Rating Scale decreased by at least 50%. No somatic or mental complications were observed during the study. The pretreatment platelet monoamine oxidase activity of the responders was slightly but not significantly higher than that of the non-responders. The plasma prolactin (PRL) levels of the patients with high pretreatment levels decreased significantly during the administration of L-deprenyl.

• An increased prevalence of seborrheic dermatitis has previously been noted in idiopathic Parkinson's disease and in postencephalitic parkinsonism. Our study of 42 hospitalized patients with drug-induced parkinsonism and 47 hospitalized psychiatric patients without that disorder showed a statistically significant higher prevalence of clinically diagnosed seborrheic dermatitis in the group with drug-induced parkinsonism (59.5% v 15%). To our knowledge, this is the first report of an increased prevalence of seborrheic dermatitis with drug-induced parkinsonism. ( Arch Dermatol 1983;119:473-475)