Search

Introduction: This research aimed to investigate the pathophysiological mechanism of how drug-induced parkinsonism (DIP) affects the integrity of the white matter (WM) fiber microstructure as measured by magnetic resonance diffusion tensor image (DTI) fractional anisotropy (FA) and mean diffusivity (MD). Methods: We recruited 17 participants diagnosed with DIP, 20 Parkinson's disease (PD) patients, and 16 normal controls (NCs) with a similar age, gender, and years of education. Subsequently, all participants underwent DTI magnetic resonance imaging scanning. To analyze the data, we utilized the software packages Functional MRI of the Brain Centre (FMRIB) Diffusion Toolbox (FDT), developed by the FMRIB laboratory at Oxford University, and tract-based spatial statistics (TBSS). Results: The Argentina Hyposmia Rating Scale (AHRS) scores of patients in DIP group were markedly higher than those in PD patients group. Compared with the NC group, the FA values in the genu and body of the corpus callosum (CC), anterior limb of the right internal capsule, bilateral anterior corona radiata, bilateral superior corona radiata, right external capsule, and right superior fronto-occipital fasciculus (could be a part of the anterior internal capsule) were significantly decreased in the DIP group; however, no significant cluster was found in MD. Conclusions: The present study provides novel insights into the alterations in WM microstructure among DIP patients, suggesting that these methodologies have the potential to aid in the early diagnosis and treatment of DIP. [ABSTRACT FROM AUTHOR]

• We used resting-state EEG to investigate neural markers characterizing drug-induced parkinsonism and Parkinson's disease. • Drug-induced parkinsonism patients exhibited higher theta band power than Parkinson's disease patients and controls. • Drug-induced parkinsonism patients showed increased theta and delta band coherence compared with Parkinson's disease. Drug-induced parkinsonism (DIP) ranks second to Parkinson's disease (PD) in causing parkinsonism. Despite sharing similar symptoms, DIP results from exposure to specific medications or substances, underscoring the need for accurate diagnosis. Here, we used resting-state electroencephalography (rsEEG) to investigate neural markers characterizing DIP and PD. We conducted a retrospective analysis of rsEEG recordings from 18 DIP patients, 43 de novo PD patients, and 12 healthy controls (HC). After exclusions, data from 15 DIP, 41 PD, and 12 HC participants were analyzed. EEG spectral power and inter-channel coherence were compared across the groups. Our results demonstrated significant differences in rsEEG patterns among DIP, PD, and HC groups. DIP patients exhibited increased theta band power compared with PD patients and HC. Moreover, DIP patients showed higher delta band coherence compared with PD patients. The current study highlights the differences in EEG spectral power and inter-channel coherence between DIP and PD patients. Our results suggest that rsEEG holds promise as a valuable tool for capturing differential characteristics between DIP and PD patients. [ABSTRACT FROM AUTHOR]

Introduction and purpose: The parkinsonian syndrome is a component of Parkinson's disease. A thorough neurological examination can detect symptoms belonging to the parkinsonian syndrome. Diagnosis using the Queen Square Brain Bank criteria is based on the presence of bradykinesia along with one additional symptom in the patient. These include muscle rigidity or resting tremors at a frequency of 4-6 Hz, or postural disturbances that cannot be explained by visual, vestibular, cerebellar, or deep sensory disorders. The parkinsonian syndrome can occur in idiopathic Parkinson's disease, hereditary disorders, secondary parkinsonism, or be part of an atypical parkinsonian syndrome. The aim of the study was to discuss the diagnostic features and differences in the occurrence of the parkinsonian syndrome as a component of Parkinson's disease, both within the context of other neurological disorders. Materials and method: The foundation of the research was medical articles gathered from the Google Scholar database. The studies were conducted by analyzing keywords such as "parkinsonism," "druginduced parkinsonism," and "vascular parkinsonism". Results: Secondary parkinsonism, or secondary parkinsonism syndrome, can be indicated by clinical features such as: disease onset below the age of 40, abrupt onset, rapid disease progression, symptoms related to medication use, and symptoms associated with the underlying condition. In addition to clinical evaluation, imaging studies are also employed. Conclusions: Various conditions can lead to the development of secondary parkinsonism, including hydrocephalus, brain tumors, encephalitis, cerebral atherosclerosis, traumatic brain injuries, medications, and poisoning. The aforementioned conditions exert different mechanisms of influence on the central nervous system. [ABSTRACT FROM AUTHOR]

In the first half of the 20th century, well before the antipsychotic era, paratonia, Gegenhalten and psychomotor hypertonia were described as new forms of hypertonia intrinsic to particular psychoses and catatonic disorders. A series of astute clinical observations and experiments supported their independence from rigidity seen in Parkinson's disease. After World War II, motor disorders went out of fashion in psychiatry, with drug-induced parkinsonism becoming the prevailing explanation for all involuntary resistance to passive motion. With the 'forgetting' of paratonia and Gegenhalten , parkinsonism became the prevailing reading grid, such that the rediscovery of hypertonia in antipsychotic-naive patients at the turn of the 21st century is currently referred to as "spontaneous parkinsonism", implicitly suggesting intrinsic and drug-induced forms to be the same. Classical descriptive psychopathology gives a more nuanced view in suggesting two non-parkinsonian hypertonias: (i) locomotor hypertonia corresponds to Ernest Dupré's paratonia and Karl Kleist's reactive Gegenhalten ; it is a dys-relaxation phenomenon that often needs to be activated. (ii) Psychomotor hypertonia is experienced as an admixture of assistance and resistance that partially overlaps with Kleist's spontaneous Gegenhalten , but was convincingly isolated by Henri Claude and Henri Baruk thanks to electromyogram recordings; psychomotor hypertonia is underpinned by "anticipatory contractions" of cortical origin, occurrence of which in phase or antiphase with the movement accounted for facilitation or opposition to passive motions. This century-old knowledge is not only of historical interest. Some results have recently been replicated in dementia and as now known to involve specific premotor systems. [ABSTRACT FROM AUTHOR]

Introduction and aim of work: The parkinsonian syndrome is a component of Parkinson's disease. A thorough neurological examination can detect symptoms belonging to the parkinsonian syndrome. Diagnosis using the Queen Square Brain Bank criteria is based on the presence of bradykinesia along with one additional symptom in the patient. These include muscle rigidity or resting tremors at a frequency of 4-6 Hz, or postural disturbances that cannot be explained by visual, vestibular, cerebellar, or deep sensory disorders. The parkinsonian syndrome can occur in idiopathic Parkinson's disease, hereditary disorders, secondary parkinsonism, or be part of an atypical parkinsonian syndrome. The aim of the study was to discuss the diagnostic features and differences in the occurrence of the parkinsonian syndrome as a component of Parkinson's disease, both within the context of other neurological disorders. Materials and methods: The foundation of the research was medical articles gathered from the Google Scholar database. The studies were conducted by analyzing keywords such as "parkinsonism," "drug-induced parkinsonism," and "vascular parkinsonism." Results: Secondary parkinsonism, or secondary parkinsonism syndrome, can be indicated by clinical features such as: disease onset below the age of 40, abrupt onset, rapid disease progression, symptoms related to medication use, and symptoms associated with the underlying condition. In addition to clinical evaluation, imaging studies are also employed. Various conditions can lead to the development of secondary parkinsonism, including hydrocephalus, brain tumors, encephalitis, cerebral atherosclerosis, traumatic brain injuries, medications, and poisoning. The aforementioned conditions exert different mechanisms of influence on the central nervous system.

Background Vietnam-era veterans were exposed to Agent Orange (AO), which is associated with a high prevalence of Parkinson's disease (PD). However, little is known about the development of PD-like symptoms caused by drug-induced parkinsonism (DIP) in such populations. This study aimed to investigate PD incidence and PD risk following exposure to AO or DIP-risk drugs in veterans. Methods A retrospective cohort study was conducted using 12 years (2009–2020) of electronic medical records of the Veterans Health Service Medical Center, the largest Veterans Affairs hospital in South Korea (n  = 37,246; 100% male; age, 65.57 ± 8.12 years). Exposure to AO or DIP-risk drugs, including antipsychotic, prokinetic, anti-epileptic, dopamine-depleting and anti-anginal agents, was assessed in veterans with PD, operationally defined as having a PD diagnosis and one or more prescriptions for PD treatment. The PD risk was calculated using multiple logistic regression analysis adjusted for age and comorbidities. Results The rates of DIP-risk drug use and AO exposure were 37.92% and 62.62%, respectively. The PD incidence from 2010 to 2020 was 3.08%; 1.30% with neither exposure, 1.63% with AO exposure, 4.38% with DIP-risk drug use, and 6.33% with both. Combined exposure to AO and DIP-risk drugs increased the PD risk (adjusted odds ratio = 1.68, 95% confidence interval, 1.36–2.08, P  < 0.001). Conclusions The PD incidence was 1.31 times higher with AO exposure alone and 1.68 times higher with AO exposure and DIP-risk drug use. The results suggest the necessity for careful monitoring and DIP-risk drug prescription in patients with AO exposure. [ABSTRACT FROM AUTHOR]

Matthew Feldman,&ast; Sarah Marmol,&ast; Jason Margolesky Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA&ast;These authors contributed equally to this workCorrespondence: Jason Margolesky, Department of Neurology, University of Miami Miller School of Medicine, 1150 NW 14th St, Miami, FL, 33136, USA, Email jhmargolesky@med.miami.eduAbstract: Parkinsonism refers to the clinical combination of bradykinesia, rigidity, tremor, and postural instability. Parkinsonism is often neurodegenerative, but it can be secondary or iatrogenic, as in drug-induced parkinsonism (DIP), which is the topic of this review. We review the pathophysiology of DIP, differentiate DIP and idiopathic Parkinson’s disease (PD), list culprit medications in the development of DIP, discuss the diagnosis of DIP as well as the motor and nonmotor signs and symptoms that can help with differentiation of DIP and PD, and detail the management of DIP.Keywords: drug-induced parkinsonism, neuroleptic-induced parkinsonism, Parkinson’s disease

Antipsychotic-induced parkinsonism (AIP) is one of the prognostically unfavorable complications of psychopharmacotherapy in patients with schizophrenia. Many studies have investigated various drugs that are used to treat this neurological side effect. This review analyzes drugs that are used and may be perspective for the treatment of AIP. We searched for full-text publications in Russian and English in the following databases: E-Library, PubMed, Web of Science, Springer, using keywords and combined word searches over the past decade (2011—2020). The review covers drugs that are promising for the correction of AIP, including anticholinergic drugs; NMDA receptor antagonists; dopamine receptor agonists; selective inhibitors of monoamine oxidase B; catecholamine transferase inhibitors; melatonin preparations; melatonin receptor agonists; benzodiazepines; herbal preparations traditionally used for the prevention and correction of extrapyramidal syndrome of various etiologies. Currently, a small number of medications are used in clinical practice for the treatment of AIP. However, not all of them are registered in the Russian Federation. Along with the differences in the mechanisms of AIP pathogenesis in specific patients, the limited choice of AIP treatments makes it difficult to solve the problem of adverse neurological complications of psychopharmacotherapy in schizophrenia.

Introduction: Few epidemiological studies have assessed the risk of parkinsonisms after prolonged use of neuroleptics. We aimed to examine the long-term risk of degenerative parkinsonisms (DP) associated with previous use of neuroleptics.Methods: All residents in Piedmont, Northern-west Italy, older than 39 years (2,526,319 subjects), were retrospectively followed up from 2013 to 2017. Exposure to neuroleptics was assessed through the regional archive of drug prescriptions. The development of DP was assessed using the regional archives of both drug prescriptions and hospital admissions. We excluded prevalent DP cases at baseline as well as those occurred in the first 18 months (short-term risk). The risk of DP associated with previous use of neuroleptics was examined through Cox regression, using a matched cohort design.Results: The risk of DP was compared between 63,356 exposed and 316,779 unexposed subjects. A more than threefold higher risk of DP was observed among subjects exposed to antipsychotics, compared to those unexposed (HR = 3.27, 95% CI 3.00-3.57), and was higher for exposure to atypical than typical antipsychotics. The risk decreased after 2 years from therapy cessation but remained significantly elevated (HR = 2.38, 95% CI 1.76-3.21).Conclusions: These results indicate a high risk of developing DP long time from the start of use and from the cessation for both typical and atypical neuroleptics, suggesting the need of monitoring treated patients even after long-term use and cessation. [ABSTRACT FROM AUTHOR]

The article presents a clinical case of neuroleptic malignant syndrome (NMS) and DIP after a single dose of thiorizadine, and discusses the issues of differential diagnosis and treatment methods. A 57-year-old patient with long-term remission of schizophrenia due to insomnia was prescribed thiorizadine. After a single dose, symptoms of parkinsonism in the form of hypokinesia, muscle rigidity and bradyphrenia developed and began to progress. Three weeks later NMS developed, and treatment was carried out in the intensive care unit. When signs of parkinsonism persisted, she was hospitalized in the neurological department. Regression of symptoms occurred by her taking amantadine sulfate.

Introduction: Considering the difficulties of differentiating Parkinson’s disease (PD) from drug-induced Parkinsonism (DIP) in patients receiving antipsychotics, developing robust diagnostic tools is essential. Herein, we used the metaiodobenzylguanidine (MIBG) scan to assess its diagnostic accuracy for this purpose. Methods: 44 DIP patients and 32 patients with PD as controls were enrolled. All the participants underwent a cardiac 131I-MIBG scan. Statistical analysis was conducted to determine the significance of the results, and accuracy analyses were conducted to calculate the related sensitivity and specificity of the MIBG scan. Results: The mean age of PD and DIP groups were 62.6 ± 5.9 and 51.5 ± 10.8 years, respectively. The mean duration of drug consumption in the DIP group was 52.2 ± 29.4 days (the mean interval between drug initiation and DIP onset was 28.5 ± 20.5). Symptoms relief occurred 40 ± 24.2 days after drug discontinuation. In the PD group, 15.6% showed negative and 84.4% positive results on the MIBG scan. In the DIP group, 86.4% were negative, and the remaining were positive. The difference in MIBG uptake between the two groups was statistically significant (P-value

Brainstem auditory evoked response (BAER) is a non-invasive modality that can be used to investigate brainstem neuronal function in movement disorders. The differentiation between drug-induced parkinsonism (DIP) and Parkinson's disease (PD) can be very challenging. Although PD and DIP to some extent display similar clinical symptoms, the underlying pathophysiologic mechanisms are entirely different. Given these differences in pathogenesis, and the diagnostic utility of BAER for detecting brainstem function, BAER may help to distinguish between PD and DIP. This study aimed to assess the accuracy and predictive values of BAER parameters in differentiating DIP from PD. We prospectively studied143 participants classified within three groups, including 50 controls, 57 PD, and 36 DIP. BAER was performed on all patients in the study. Patients in the DIP group were followed up for at least one year after discontinuation of the causative drug and examined for final diagnosis. We compared BAER latencies of the three groups and measured sensitivity, specificity, predictive values, likelihood ratios, and accuracy of BAER in diagnosing DIP. Waves V, I-V, and III-V latencies were significantly prolonged among the PD patients compared to the DIP and the control group; however, there were no significant differences in BAER latencies between the DIP and the control group. Waves V and I-V latencies revealed the highest accuracy (86% and 79%, respectively) in distinguishing DIP from PD with high negative predictive value(89% and 83%, respectively) as well as a high negative likelihood ratio (0.2and 0.3, respectively). This study showed that waves V and I-V latencies are significantly prolonged in PD patients compared to those with DIP, consistent with the proposed mechanisms of neurodegeneration in PD, particularly in the midbrain and pons. Consequently, BAER could be used as a useful diagnostic tool for differentiating DIP from PD. [ABSTRACT FROM AUTHOR]

Abstract Background Parkinson’s disease (PD) and drug-induced parkinsonism (DIP) are the major diseases of parkinsonism. To better understand parkinsonism, we aimed to assess the prevalence and incidence of PD and DIP in Korea from 2012 to 2015. Methods We used the Health Insurance Review and Assessment Service database, which covers the entire population in Korea. We used claims during 2011–2015 to assess epidemiology of PD and DIP during 2012–2015. Retrospective cross-sectional study design was employed to assess prevalence, whereas retrospective cohort study design was used to determine incidence. Patients with at least one claim with ICD-10 G20 and who received antiparkinsonian drugs for at least 60 days were classified as having PD. We excluded patients with antiparkinsonian drugs that can be used for indications other than PD. Patients with at least one claim with ICD-10 G211 or G251 during the prescription period of drugs that are frequently related with DIP were classified as having DIP. Incident cases had a disease-free period of 1 year before diagnosis. To evaluate the significance of changes in the prevalence or incidence over time, Poisson regression was used to determine p for trend. Results The prevalence of PD increased from 156.9 per 100,000 persons in 2012 to 181.3 per 100,000 persons in 2015 (p for trend

Objective: The objective of this study is to examine the effectiveness of an accelerometer-based compact system in detecting and quantifying drug-induced parkinsonism (DIP) in patients with schizophrenia.Method: A pilot study controlled clinical trial comprising 6 people with schizophrenia and 11 control subjects was conducted at Alfred Health, Melbourne. Participants had their movements assessed using Barnes Akathisia Rating Scale (BARS), Simpson Angus Scale (SAS) and Movement Disorder Society Unified Parkinson's Disease Rating Scale Part III (MDS-UPDRS III) followed by an assessment of gait using three triaxial accelerometers.Results: Median BARS, SAS, MDS-UPDRS III and accelerometer scores were significantly higher for patients with schizophrenia than controls. Accelerometers detected three times more rest tremor than clinical rating scales. Patients with schizophrenia had 70% of their dynamic acceleration at frequencies between 4 and 10 Hz, which is almost twice that observed in the control population (38%). Accelerometer scores were significantly correlated with BARS scores.Conclusion: Accelerometers were able to accurately detect patients with DIP better than some clinical rating scale including the SAS. Further larger-scale studies must be conducted to further demonstrate the accuracy of accelerometers in detecting DIP. [ABSTRACT FROM AUTHOR]

Objective: In a substantial portion of patients with drug-induced parkinsonism (DIP), parkinsonism may persist for long periods after discontinuation of offending drugs, suggesting subtle underlying neurodegeneration. We hypothesized that patients with DIP have impaired functional connectivity (FC) of brain networks, which may determine the reversibility of parkinsonism.Methods: In this case-control study, we consecutively recruited 60 patients with DIP and 32 healthy controls. We used independent component analysis and dual regression of functional magnetic resonance imaging data to identify seven resting-state networks and compared FC of the networks between the DIP and control groups. Among regions where the two groups showed a significant difference in the FC with sensorimotor network, we compared the FC between patients who had completely recovered (n = 21) and those who had partially recovered (n = 39) within 3 months of cessation of the offending drugs.Results: Patients with DIP had decreased FC between the sensorimotor network and widespread brain regions, when compared to healthy controls. FC in the prefrontal regions was negatively correlated with parkinsonian motor score. Patients who partially recovered had a significantly lower FC in the prefrontal and cerebellar regions than those who recovered completely, providing a useful predictor of recovery status.Conclusions: Patients with DIP had decreased FC of the sensorimotor network, which correlated with the severity of parkinsonism and predicted the recovery status after cessation of offending drugs. Impaired FC of the sensorimotor network can be used as a biomarker to evaluate the severity and prognosis of DIP. [ABSTRACT FROM AUTHOR]

Background: Sulpiride is a highly selective dopamine D2 receptor antagonist and is commonly used in psychiatric disorders, Tourette syndrome, peptic ulcer disease (PUD), and gastroesophageal reflux disease (GERD). However, sulpiride has been recognized as a potential cause of drug-induced parkinsonism (DIP) for a long time. In this study, we aimed to focus on analysis of sulpiride-induced parkinsonism (SIP) in PUD and GERD patients based on a nationwide population. Methods: Data were obtained from the Taiwan's National Health Insurance Research Database. The study enrolled 5,275 PUD or GERD patients, of whom were divided into two groups, based on their exposure (1,055 cases) or non-exposure (4,220 cases) to sulpiride. Results: During the study period (2000–2012), the incidence rate of parkinsonism was 261.5 and 762.2 per 100,000 person-years in the control and sulpiride-treated groups, respectively. For patients with at least 14 days of prescription for sulpiride, the adjusted hazard ratio (aHR) was 2.89, 95% confidence interval (CI): 2.04-4.11. Patients with age more than 65 years (aHR = 4.99, 95% CI = 2.58-9.65), hypertension (aHR = 2.39, 95% CI = 1.49-3.82), depression (aHR = 2.00, 95% CI = 1.38-2.91), and anxiety (aHR = 1.45, 95% CI = 1.01-2.09) had significant higher risk of developing parkinsonism. An average annual cumulative sulpiride dose > 1,103 mg was accompanied by the greatest risk of SIP; sulpiride use for ≥ 9 days is a cut-off point for predicting future SIP. Conclusion: At the population level, sulpiride may be frequently prescribed and apparently effective for PUD and GERD. SIP is associated with older age, hypertension, depression or anxiety comorbidities. Physicians should be aware of the neurogenic adverse effects, even when the drug is only used in low-dose or a short duration. [ABSTRACT FROM AUTHOR]

Introduction: Drug-Induced Parkinsonism (DIP) is the second most common cause of parkinsonism after idiopathic Parkinson's disease. Little is known about DIP epidemiology. Using VigiBase®, the objective of this study was to assess the main characteristics of DIP reporting around the world.Methods: We described reports recorded in the WHO pharmacovigilance database, Vigibase® and classified as "Parkinsonism" between 2000 and 2017. Differences of reporting between geographical locations and characteristics of reports were investigated using disproportionality analysis with calculation of Reporting Odds Ratios (ROR) and its 95% confidence interval.Results: Among the 9,009,107 reports recorded in VigiBase®, 4565 (0.05%) were DIP. Co reported terms were mainly "tremor" (n = 408, 8.9%), "gait disturbance" (n = 209, 4.6%) and "extrapyramidal disorders" (n = 180, 3.9%). DIP reports were significantly more frequent in men (ROR = 1.4; 95% CI 1.3-1.5) and in patients aged 75 and over (ROR = 2.12; 95% CI 1.98-2.26). Compared to all other continents, risk of reporting drug-induced parkinsonism was higher in Europe (ROR = 2.89; 95% CI 2.73-3.07), Africa (ROR = 1.81; 95% CI 1.46-2.25) and Oceania (ROR = 1.50; 95% CI 1.27-1.77). The risk was lower in Asia (ROR = 0.55; 95% CI 0.51-0.59) and America (ROR = 0.55 95% CI 0.51-0.59). The highest risk of DIP reporting was found with sulpiride and haloperidol followed by risperidone, aripiprazole, paliperidone, metoclopramide, olanzapine, quetiapine and clozapine.Conclusion: Risk of DIP reports was higher in men, in people aged 75 and over and in Europe. Main drugs involved are antipsychotics not only drugs from the first generation but also those from the second one. [ABSTRACT FROM AUTHOR]

Drug-induced Parkinsonism is often reversible after withdrawal of the causative drug. Its clinical course, however, is not well understood, as the majority of cases are caused by drugs prescribed by departments outside of neurology. We reviewed 21 cases of drug-induced parkinsonism for several factors, including age, sex, causative drug and reason for prescription, department by which it was prescribed, and outcome. The age at onset ranged from 40 to 87 years, with an average Hoehn and Yahr Scale score of 4, indicating severe disability. Sulpiride was the most commonly observed causative drug (71.4%). All causative drugs were prescribed in non-neurological departments and over one half were prescribed in non-psychiatric departments; most were prescribed to treat depression or abdominal discomfort. Ten patients (48%) were previously diagnosed with a neuromuscular disease, including cerebrovascular diseases and Parkinson’s disease. Recovery was observed in 15 cases (71%) after withdrawal of the causative drug, but lingering symptoms were observed in the remaining cases. It is suggested that physicians should be more cautious of Parkinsonian side effects when prescribing such drugs.

Drug-induced parkinsonism is the second common movement disorder after Parkinson's disease. It occurs due to the use of not only neuroleptics but also some other medications as pregabalin. Pregabalin is an antiepileptic drug and a structural analog of gamma-aminobutyric acid (GABA), and its use decreases the release of several neurotransmitters. In this case report, we present a 53-year-old female patient with the signs of parkinsonism following pregabalin treatment. Drug-induced parkinsonism was diagnosed based on the clinical features, investigations, and resolution of the complaints. The symptoms relieved after the treatment stopped at a follow-up of 10 days. Due to the rare report of pregabalin-induced parkinsonism, we aim to enhance clinicians' awareness of pregabalin's probable side effects. [ABSTRACT FROM AUTHOR]

Objective: Compare clinical characteristics and outcomes in cases where DAT-SPECT imaging is used to distinguish Parkinson's disease from Drug-Induced Parkinsonsim.Background: Clinical uncertainty in diagnosing Parkinson's disease is common when patients are on dopamine-blocking medications. DAT-SPECT imaging can improve diagnostic certainty but little data are available on clinical characteristics and outcomes associated with normal and abnormal scan results.Methods: Retrospective chart review of patients seen at a movement disorders center between 2011 and 2017 where DAT-SPECT was ordered to distinguish Parkinson's disease from Drug-induced Parkinsonism. Descriptive statistics were calculated for variables of interest and compared by scan result. Chi-squared analyses was carried out for categorical variables and students' t-tests for continuous values.Results: 51 patients met inclusion criteria with 36 normal scans and 15 abnormal scans. Those with greater than 2 cardinal manifestations (tremor, rigidity, akinesia, postural instability) were more likely to have an abnormal scan (63.89% vs 93.33%, p = 0.04). No other clinical characteristics assessed were associated with scan results. Atypical antipsychotics (aripiprazole 39.21%, olanzapine 31.37%) and mood stabilizers (valproic acid 33.33%, lithium 17.65%) were most commonly associated with suspected Drug-induced Parkinsonism cases. A post-scan change in management occurred in 41.18% of patients. 55.56% of patients with normal scans responded to changes in the offending medication, with 16.66% taking over 3 months to show improvement.Conclusions: Many DAT-SPECT scans at our institution are ordered to distinguish Parkinson's disease from Drug-induced Parkinsonism because clinical characteristics alone are unreliable. DAT-SPECT results lead to changes in management and the outcomes of these changes are consistent with scan results. [ABSTRACT FROM AUTHOR]

Objectives: To determine the prevalence of vascular parkinsonism (VasP) in a stroke prevention clinic (SPC).Background: VasP can be defined by an onset of parkinsonism with prominent gait problems occurring within 1 year of stroke.Methods: We created a screening strategy based on the Tanner Questionnaire (TQ), a validated scale for parkinsonism, and the creation of a 4-point Five-Minute Assessment Scale (FMAS) operationalizing Zijlmans' criteria for the diagnosis of VasP. Consecutive stroke patients were screened over a 12-month period using the TQ and the FMAS. SAS statistical software was used.Results: Two hundred forty patients (52.5% females) were screened (mean age of 65 years, standard deviation, 14.5). Twenty-five percent of patients had a TQ score ≥ 4 with a median FMAS of 2. In this group, 32.6% (15/46) were found to have parkinsonism. Seventeen percent (8/46) were diagnosed with VasP having an FMAS of 4. Seventy-five of the participants obtained a TQ ≤ 3, with a median FMAS of 1. Only 1 patient in this group had parkinsonism (1.9%; 1/194). Using a cutoff of 4 points in the TQ resulted in a sensitivity of 93.8%, a specificity of 86.2% for parkinsonism, and a sensitivity of 100% with a specificity of 83% for VasP. Patients with FMAS = 4 (VasP) attained higher scores in the TQ with a median of 5 (Spearman rank correlation coefficient for the TQ and the FMAS (rs) = .447, P < .0005).Conclusions: We documented a prevalence of 3% (8/240) for VasP in an SPC. We propose a new, easier, and unified 2-step TQ-FMAS screening strategy for this condition. [ABSTRACT FROM AUTHOR]

Introduction: We have recently demonstrated evidence of nigro-striatal denervation, disease progression and response to levodopa in a subgroup of patients with schizophrenia who developed parkinsonism.Objective: In the present study, we investigated whether axial parkinsonian signs might be an early manifestation of parkinsonism in schizophrenia not necessarily related to chronic administration of antipsychotic drugs (AP) drugs.Methods: From a baseline cohort of 299 schizophrenic patients who did not satisfy the diagnostic criteria for parkinsonism (presence of at least two of the following appendicular signs: bradykinesia, tremor, rigidity), we identified a group of patients who manifested two out of three axial parkinsonian signs (abnormality of trunk posture, hypomimia and short-step gait). Accordingly, we obtained two sub-groups of patients with schizophrenia, with (Schiz-Axial, N = 26), and without parkinsonian axial signs (Schiz-NO-Axial, N = 273). Clinical and demographical variables were compared between groups. The motor section of the Unified Parkinson's disease rating scale (UPDRS) was employed to measure motor disability.Results: Schiz-Axial patients were significantly older (p = 0.007) and had longer disease duration (p = 0.04) compared to Schiz-NO-Axial. The two groups did not differ for variables related to AP treatment. Total UPDRS motor score (p < 0.0001) as well as limb (p < 0.0001) and axial (p < 0.0001) UPDRS sub-scores were increased in Schiz-Axial patients compared to Schiz-NO-Axial.Conclusions: Our findings provide evidence that axial parkinsonian signs might be an early manifestation of parkinsonism in schizophrenia associated to older age and longer disease duration. [ABSTRACT FROM AUTHOR]

Background: Epidemiological studies of drug-induced parkinsonism remain limited.Objectives: To investigate the incidence and time trends of drug-induced parkinsonism over 30 years in a geographically defined American population.Methods: We used the medical records-linkage system of the Rochester Epidemiology Project to identify all persons in Olmsted County, Minnesota, who received a screening diagnostic code for parkinsonism from 1976 through 2005. A movement disorders specialist reviewed the complete medical records of each person to confirm the presence of drug-induced parkinsonism associated with dopamine-blocking or dopamine-depleting medications.Results: Among 906 incident cases of parkinsonism from 1976 to 2005, 108 persons had drug-induced parkinsonism (11.9%). The average annual incidence rate of drug-induced parkinsonism was 3.3 per 100,000 person-years, was higher in women, and increased with older age. Drug-induced parkinsonism was the fifth-most common type of parkinsonism overall; however, it was the most common type among persons younger than age 40 years. Typical antipsychotic drugs were the most common class of drugs associated with parkinsonism, whereas atypical antipsychotic drugs were rarely involved. The incidence rate of drug-induced parkinsonism decreased 32.0% per decade (relative risk = 0.68; 95% confidence interval: 0.49-0.94) and 68.6% over the 30 years of the study. The decrease was similar in men (65.2%) and women (69.4%); however, the trend was significant only in women.Conclusions: The incidence of drug-induced parkinsonism increased with older age and was higher in women at all ages. Typical antipsychotic drugs were the most common cause. The incidence of drug-induced parkinsonism decreased over the 30 years of the study because of changes in drug use. © 2016 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Drug-induced parkinsonism (DIP) is classically described as acute/subacute, bilateral symmetric syndrome in which tremor is infrequent compared to Parkinson's disease. Most DIP cases are caused by classic (CN) and second-generation neuroleptics (SN), and calcium channel blockers (CCB). We evaluated potentially distinctive demographic and clinical features in DIP among different drug classes. This was a prospective study of reversible DIP related to single selected drugs on each class. Baseline assessment included demographic, clinical data, and scales for staging, severity of motor signs of parkinsonism, tremor, and other involuntary movements. Six months after medication withdrawal, patients were reassessed. Those with no parkinsonian signs were included in the final sample. 157 cases were included after strict criteria were applied. Most common agents were haloperidol, levomepromazine, and chlorpromazine for the CN-DIP group, flunarizine and cinnarizine for the CCB-DIP group, and risperidone and olanzapine for the SN-DIP group. Drug exposure was shorter for CN-DIP cases; duration of parkinsonism was longer in the CCB-DIP group. CN-DIP had worse bradykinesia, rigidity, axial, total motor, and disease stage scores, with higher frequency of rigid-akinetic parkinsonism. Tremor scores were worse for CCB-DIP cases. SN-DIP presented as a less severe but similar form of CN-DIP. Tardive-type involuntary movements were less common in the SN-DIP group. DIP profile differs significantly depending on drug class involved, not only in terms of severity, but also regarding the differential combination of signs. These findings may help guiding clinicians in screening and diagnosing DIP in patients exposed to these drugs. [ABSTRACT FROM AUTHOR]

Lithium is a mood stabilizer rarely associated with drug-induced parkinsonism (DIP). We present a case of an elderly woman with bipolar disorder who developed parkinsonian symptoms after chronic lithium administration despite therapeutic serum levels. Upon evaluation, classic parkinsonian signs of muscle rigidity, tremor, bradykinesia, freezing of gait, and cognitive decline were observed. Initially, she was diagnosed with Parkinson's disease (PD); however, DaTscan SPECT imaging clarified the diagnosis as DIP. As the daily lithium dosage was reduced, the patient's motor symptoms improved. This report emphasizes close monitoring of lithium levels in geriatric populations and the need to consider lithium-induced parkinsonism when PD symptoms appear in chronic lithium users. [ABSTRACT FROM AUTHOR]

This report attempts to highlight that use of an antipsychotic and concurrent chronic use of methamphetamine can cause drug-induced parkinsonism. Methamphetamine is usually not encountered in the list of agents that induce drug-induced parkinsonism and so its consideration particularly during chronic use by a patient who is also on an antipsychotic is worthwhile because of its popularity as an illegal narcotic. This case report describes just such a case of drug-induced parkinsonism which is a subacute syndrome that mimics Parkinson’s disease. Although less alarming than dystonia, it is more common, more difficult to treat and can be the cause of significant disability during maintenance treatment especially in the elderly. In most cases, symptoms are reversible in days or weeks, but occasionally, especially in the elderly, or if long-acting injectable antipsychotics are used—as in this case—symptoms may last for weeks or months. The report also illustrates the neuronal workings due to chronic methamphetamine-use and the additive effects of dopamine blockade by antipsychotics such as haloperidol. [ABSTRACT FROM AUTHOR]

Drug-induced parkinsonism is caused by an offending drug and should resolve after the causative agent has been withdrawn. However, in a number of patients, symptoms persist or may even worsen over time, suggesting the development of concomitant Parkinson's disease. The prevalence estimates of Parkinson's disease after neuroleptic exposure are unexpectedly high, suggesting a causal relationship. We critically review available literature in this regard, and some pathophysiological hypotheses that might explain such a relationship are suggested. Some patients may have an undetermined genetic susceptibility to parkinsonism. We speculate that the possible neurotoxic effect of neuroleptics exerted on a susceptible dopaminergic system would lead over the long-term to a self-fostering, progressive process. Knowledge gaps and future perspectives are discussed. © 2015 International Parkinson and Movement Disorder Society [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of the present study is to investigate whether there are geographic differences in the etiology of parkinsonism (PA). BACKGROUND: 72% of patients with PA evaluated at movement disorders clinics in the Northern Hemisphere are diagnosed with Parkinson's disease (PD). Data regarding other regions are not available. METHODS: We reviewed the charts of all patients with PA seen at the Federal University of Minas Gerais Movement Disorders Clinic from July 1993 through October 1995. PA was diagnosed by the presence of at least two of the following: rest tremor, bradykinesia, rigidity, and postural instability. The different etiologies were diagnosed based on standard clinical criteria RESULTS: During the period of the study, PA was recognized in 338 subjects. The following clinical diagnoses were made: PD (68.9%), drug-induced PA (DIP) (13.3%), vascular PA (4.7%), Progressive supranuclear palsy (PSP) (2%), multiple system atrophy (MSA) (1.8%), others (9.7%). Cinnarizine, haloperidol and flunarizine were the commonest drugs related to DIP. CONCLUSIONS: Similarly to other studies, PD accounts for about 70% of PA patients. However, there are differences between our results and previous series. DIP is much more common in the present series. This may be accounted for a more liberal use of antidopaminergic drugs in our environment, especially Calcium channel blockers. The lower frequency of MSA and PSP in our study may reflect a short follow-up, since many patients initially diagnosed with PD later are found to have Parkinson-plus syndromes.

We performed a clinical report based, descriptive and retrospective study, aimed at comparing Flunarizine/Cinnarizine-induced parkinsonism (FCIP) patients and Parkinson's disease (PD) patients. The FCIP group (n = 30) presented a lower frequency of rigidity and unilateral tremor than the PD group (n = 70). All FCIP patients improved, 13 after dopaminergic treatment. FCIP patients who improved spontaneously presented lower frequency of rigidity, compared with the other FCIP subgroup and PD group. FCIP patients who did not improve spontaneously showed a clinical pattern similar to PD patients. [ABSTRACT FROM AUTHOR]

Background and purpose Differentiating idiopathic Parkinson's disease from secondary parkinsonian syndromes is crucial since their management and prognosis differ considerably. Functional imaging of the dopaminergic pathway by means of [¹²³I] FP- CIT SPECT (Da TSCAN) might be useful in this regard, but its role is still controversial. The accuracy of Da TSCAN in the differential diagnosis between Parkinson's disease and vascular or drug-induced parkinsonism was therefore systematically reviewed. Methods MEDLINE and CENTRAL were searched for studies aiming to determine accuracy measures (sensitivity, specificity, diagnostic odds ratio, positive and negative likelihood ratios) of Da TSCAN in differentiating between Parkinson's disease and vascular or drug-induced parkinsonism. Results Five studies were included. Pooled accuracy measures in differentiating between Parkinson's disease and vascular or drug-induced parkinsonism were relatively high, with sensitivity and specificity values above 85% and 80%, respectively. Conclusions Da TSCAN might accurately differentiate between early Parkinson's disease and secondary parkinsonian conditions, namely vascular or drug-induced, in patients with clinically unclear parkinsonism. However, all the studies reviewed here show several methodological limits, which prevent definitive conclusions on the role of Da TSCAN being drawn in this context. Further studies are needed to confirm our results and definitely evaluate the utility of Da TSCAN in differentiating between Parkinson's disease and vascular or drug-induced parkinsonism. [ABSTRACT FROM AUTHOR]

Drug-induced parkinsonism is the second most common cause of parkinsonism after Parkinson's disease and their distinction has crucial implications in terms of management and prognosis. However, differentiating between these conditions can be challenging on a clinical ground, especially in the early stages. We therefore performed a review to ascertain whether assessment of non-motor symptoms, or use of ancillary investigations, namely dopamine transporter imaging, transcranial sonography of the substantia nigra, and scintigraphy for myocardial sympathetic innervation, can be recommended to distinguish between these conditions. Among non-motor symptoms, there is evidence that hyposmia can differentiate between patients with "pure" drug-induced parkinsonism and those with degenerative parkinsonism unmasked by an anti-dopaminergic drug. However, several issues, including smoking history and cognitive functions, can influence smell function assessment. Higher diagnostic accuracy has been demonstrated for dopamine transporter imaging. Finally, preliminary evidence exists for sympathetic cardiac scintigraphy to predict dopaminergic pathway abnormalities and to differentiate between drug-induced parkinsonism and Parkinson's disease. Imaging of the dopaminergic pathway seems to be the only, reasonably available, technique to aid the differential diagnosis between drug-induced parkinsonism and Parkinson's disease. [ABSTRACT FROM AUTHOR]

Abstract: Background: Drug-induced Parkinsonism is common, causes significant morbidity, and can be clinically indistinguishable from idiopathic Parkinson's disease. Additionally, drug-induced Parkinsonism may, in some cases, represent “unmasking” of incipient Parkinson's disease. Clinical features or tests that distinguish degenerative from pharmacologic Parkinsonism are needed. Methods: We performed a retrospective case-control study of 97 drug-induced Parkinsonism subjects and 97 age-matched patients with Parkinson's disease. We compared the frequency of subjective motor and non-motor complaints, objective motor findings (Unified Parkinson's Disease Rating Scale Part III) and, where available, objective olfactory tests. We also performed a nested case-control study wherein we compared these same features between drug-induced Parkinsonism patients based on whether or not they recovered after changing the offending agent. Results: Non-motor symptoms including constipation and sexual dysfunction were more common in Parkinson's disease than in drug-induced Parkinsonism. While total motor scores were similar between groups, Postural Instability-Gait Difficulty scores were also higher in Parkinson's disease. Features that were significantly different or showed a trend towards significance in both comparisons included subjective loss of facial expression, dream-enactment behavior, autonomic complaints and Postural Instability-Gait Difficulty scores. Hyposmia was more common in Parkinson's disease and was strongly predictive of persistent drug-induced Parkinsonism after therapy change (odds ratio 30.3, 95% confidence interval: 1.5–500, p = 0.03). Conclusions: A constellation of motor and non-motor features may differentiate unmasked Parkinson's disease from drug-induced Parkinsonism. In particular, olfactory testing may offer a simple and inexpensive method to help predict outcomes in drug-induced Parkinsonism and, potentially, identify a cohort of pre-motor Parkinson's disease. [Copyright &y& Elsevier]

Abstract: DIP is a heterogeneous clinical syndrome; some patients develop persistent and worsening of parkinsonian symptoms after discontinuation of the offending drug, or Parkinson''s disease (PD) reappears later after a full remission from DIP. However, it is difficult to predict the prognosis in patients with DIP. Herein, we evaluated whether the combined use of 18F-N-(3-fluoropropyl)-2beta-carbon ethoxy-3beta-(4-iodophenyl) nortropane (FP-CIT) PET and cardiac MIBG scintigraphy can be used to help distinguish the prognosis in patients with DIP. Among 20 patients enrolled, 16 showed normal DAT uptake and normal myocardial sympathetic innervation. After withdrawal of the suspected drugs, the patients experienced a clinical remission of parkinsonian motor symptoms within 3 months and did not experience any new movement symptoms after at least 2 years of follow-up. Two patients with a moderate decrease in DAT uptake and impaired sympathetic denervation showed worsening of motor manifestations 3 months after discontinuation of the drugs. Another two patients with normal DAT uptake and decreased MIBG uptake, presented full remission of motor symptoms within 2 months after discontinuation of the drugs. However, these two patients eventually developed parkinsonism within 2 years of the follow-up period. The follow-up scans revealed severe decreased DAT uptake in the putamen and similar ranges of cardiac sympathetic denervation. The results suggest that the combined use of these techniques can predict the prognosis of DIP and suggest a proper therapeutic plan for DIP. [Copyright &y& Elsevier]

Abstract: Adenosine A2A and dopamine D2 receptors interact to regulate diverse aspects of ventral and dorsal striatal functions related to motivational and motor processes, and it has been suggested that adenosine A2A antagonists could be useful for the treatment of depression, parkinsonism and other disorders. The present experiments were performed to characterize the effects of MSX-4, which is an amino acid ester prodrug of the potent and selective adenosine A2A receptor antagonist MSX-2, by assessing its ability to reverse pharmacologically induced motivational and motor impairments. In the first group of studies, MSX-4 reversed the effects of the D2 antagonist eticlopride on a concurrent lever pressing/chow feeding task that is used as a measure of effort-related choice behavior. MSX-4 was less potent after intraperitoneal administration than the comparison compound, MSX-3, though both were equally efficacious. With this task, MSX-4 was orally active in the same dose range as MSX-3. MSX-4 also reversed the locomotor suppression induced by eticlopride in the open field, but did not induce anxiogenic effects as measured by the relative amount of interior activity. Behaviorally active doses of MSX-4 also attenuated the increase in c-Fos and pDARPP-32(Thr34) expression in nucleus accumbens core that was induced by injections of eticlopride. In addition, MSX-4 suppressed the oral tremor induced by the anticholinesterase galantamine, which is consistent with an antiparkinsonian profile. These actions of MSX-4 indicate that this compound could have potential utility as a treatment for parkinsonism, as well as some of the motivational symptoms of depression and other disorders. [Copyright &y& Elsevier]

Abstract: Background: Drug-induced parkinsonism (DIP) is seen in one third of patients exposed to antipsychotic drugs and may lead to complications related to dysphagia and falls. Aside from skilled neurological examination, no tool has been validated to facilitate detection and follow-up. Objective: In this pilot study, three validated screening instruments were tested in an age-biased cohort of schizophrenia patients, including four items of the Liverpool University Neuroleptic Side-Effects Rating Scale (LUNSERS) and two brief questionnaires designed for community survey of parkinsonism. Method: Fifty-six subjects living with chronic schizophrenia between 50 and 75years of age underwent a motor evaluation along the original Unified Parkinson''s Disease Rating Scale-section III and answered questions along the selected screening instruments, and results compared to those of 16 patients with Parkinson''s disease (PD) and 15 neurologically unimpaired volunteers. Odds ratios, sensitivity, specificity, and their 95% confidence intervals, were calculated. Results: All three screening instruments correctly identified the PD state and distinguished PD from healthy participants. Eighteen (32%) schizophrenic patients displayed objective motor signs of parkinsonism. A single item of the LUNSERS (shakiness) significantly distinguished DIP from DIP-free patients, with a sensitivity of 61.1% and a specificity of 83.3%. The positive predictive value was 63.5% and the negative predictive value was 81.9%. The two other screening methods showed insufficient predictive value. Conclusion: Apart from a single query on shakiness, none of the tools examined were adequate to screen for DIP in patients treated for schizophrenia. A different instrument is necessary to monitor this important adverse effect in schizophrenia. [Copyright &y& Elsevier]

Abstract: Dopamine D2 and adenosine A2A receptors interact to regulate aspects of motor and motivational function, and it has been suggested that adenosine A2A antagonists could be useful for the treatment of parkinsonism and depression. The present experiments were performed to characterize the effects of Lu AA47070, which is a phosphonooxymethylene prodrug of a potent and selective adenosine A2A receptor antagonist, for its ability to reverse the motor and motivational effects of D2 antagonism. In the first group of studies, Lu AA47070 (3.75–30mg/kg IP) was assessed for its ability to reverse the effects of the D2 receptor antagonist pimozide (1.0mg/kg IP) using several measures of motor impairment, including catalepsy, locomotion, and tremulous jaw movements, which is a rodent model of parkinsonian tremor. Lu AA47070 produced a significant reversal of the effects of pimozide on all three measures of parkinsonian motor impairment. In addition, Lu AA47070 was able to reverse the effects of a low dose of the D2 antagonist haloperidol on a concurrent lever pressing/chow feeding task that is used as a measure of effort-related choice behavior. The ability of Lu AA47070 to reverse the effects of D2 receptor blockade suggests that this compound could have potential utility as a treatment for parkinsonism, and for some of the motivational symptoms of depression. [Copyright &y& Elsevier]

Abstract: Objective: To investigate the etiologic diagnoses of parkinsonism, underlining aspects of each form and comparing our findings with those published in a similar setting, 10 years before. Methods: A large cohort of 1528 patients with parkinsonism was analyzed, gathering data on demography, motor and non-motor characteristics, as well as the final etiologic diagnoses based on established criteria. Results: Parkinson''s disease (PD) was the most common diagnosis representing 74.7%, followed by drug-induced parkinsonism (DIP) in 7.9%, vascular parkinsonism (VP) in 3.9%, other neurodegenerative disorders in 10%, and rare sporadic causes, divided as genetic, infectious and others, that summed 3.5%. Comparative analysis of these groups showed that each has particularities that extend beyond their diagnostic criteria. Conclusions: The main conclusions are that the most important causes of parkinsonism in this setting are typical, with PD been the most common diagnosis, although other causes were frequent, encompassing one fourth of all cases. Although DIP was identified in a particularly large part of this cohort, this proportion is smaller than demonstrated previously in a Brazilian study conducted in the 90s. This decrease probably reflects higher awareness regarding the risk of this motor complication and the more widely used newer antipsychotics. [Copyright &y& Elsevier]

To determine clinical predictors and accuracy of 123I-FP-CIT SPECT imaging in the differentiation of drug-induced parkinsonism (DIP) and Parkinson’s disease (PD). Several clinical features and 123I-FP-CIT SPECT images in 32 patients with DIP, 25 patients with PD unmasked by antidopaminergic drugs (PDu) and 22 patients with PD without a previous history of antidopaminergic treatment (PDc) were retrospectively evaluated. DIP and PD shared all clinical features except symmetry of parkinsonian signs which was more frequently observed in patients with DIP (46.9%) than in patients with PDu (16.0%, p<0.05) or PDc (4.5%, p<0.01). Qualitatively 123I-FP-CIT SPECT images were normal in 29 patients with DIP (90.6%) and abnormal in all patients with PD, and this imaging technique showed high levels of accuracy. DIP and PD are difficult to differentiate based on clinical signs. The precision of clinical diagnosis could be reliably enhanced by 123I-FP-CIT SPECT imaging. [ABSTRACT FROM AUTHOR]

This report describes a case of likely drug-induced Parkinsonism (DIP) identified by the pharmacist. A 54-year-old female patient was referred by a physician to the pharmacist in a rural, integrated care team for a comprehensive medication review (CMR) to address the patient's concerns of possible Parkinson's disease (PD). While PD may occur over the progression of age, medications that affect dopamine transport can also cause DIP, a secondary form of Parkinson's disease. Although PD and DIP may be clinically indistinguishable, differentiation may be possible by reviewing a patient's medication history for any potential causative drugs correlating to the timeline of the onset of symptoms. In this case, the pharmacist reviewed the medication profile and identified medications that could be responsible for causing DIP, specifically bupropion. The pharmacist suggested discontinuing bupropion and identifying another option for treating depression. The patient appreciated the suggestion and education, but ultimately preferred continuing her bupropion therapy instead of discontinuing therapy or changing to an alternative agent. At a follow-up meeting with the pharmacist, not only was the patient still experiencing tremors despite taking carbidopa/levodopa, but additional medications known to be potential inducers of tremors were added to her regimen. Although the pharmacist repeatedly discussed DIP with the patient and believed stopping bupropion would determine whether her Parkinsonism was PD or DIP, ultimately the patient continued taking bupropion because of concerns related to depression severity and the impact on her well-being. The patient's wishes were respected. [ABSTRACT FROM AUTHOR]

Objective The purpose of the present study was to examine the relationship between drug-induced parkinsonism (DIP) and subjective non-motor cognitive impairments in schizophrenia by performing comprehensive assessments of extrapyramidal side effects (EPS) and the subjective cognitive-perceptual functioning. Methods Ninety-one outpatients with schizophrenia were evaluated for DIP and other EPS. Subjective cognitive-perceptual dysfunction was comprehensively assessed using the Frankfurt Complaint Questionnaire (FCQ). To examine the association between DIP and non-motor cognitive-perceptual dysfunction, Pearson's partial correlation analysis was performed between the FCQ scores and the severity of DIP, controlling for relevant variables. Results The analysis revealed that the severity of DIP had a significant correlation with the total FCQ score (p < 0.05). In phenomenological subscales, the severity of DIP showed significant correlations with “deterioration of discrimination,” “psychomotor disorder,” “perceptual disorder,” “cognitive floating,” and “automatic behavior disorder” (p < 0.05). Conclusions The results of our study suggest that DIP is significantly associated with a wide range of subjective non-motor cognitive impairments. Clinicians should be careful of the appearance of DIP and the associated non-motor cognitive-perceptual symptoms, which may cause considerable distress and reduce the quality of life in an already vulnerable group of patients. Copyright © 2009 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Abstract: The authors investigated the subjective cognitive dysfunction associated with drug-induced parkinsonism (DIP) among 58 stabilized schizophrenic outpatients. Subjective cognitive dysfunction was comprehensively assessed using the Frankfurt Complaint Questionnaire (FCQ). Multivariate analysis revealed that the DIP group scored significantly higher on the total FCQ score than the non-DIP group. In phenomenological subscale scores, the DIP group had significantly higher scores on “deterioration of discrimination”, “psychomotor disorder”, and “perceptual disorder” than the non-DIP group. These results suggest that DIP is significantly associated with subjective cognitive-perceptual dysfunction, reflecting the complex nature of DIP that includes motor and cognitive aspects. [Copyright &y& Elsevier]