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The effective management of OFF episodes remains an important unmet need for patients with Parkinson's disease (PD) who develop motor complications with long-term levodopa therapy. Istradefylline is a selective adenosine A

Dementia due to Parkinson's disease and Alzheimer's disease are associated with behavioural and psychological symptoms, including psychosis. Long-term management presents a challenge for health care providers and caregivers. Symptoms of psychosis include hallucinations and delusions; if untreated, these can lead to institutionalisation, decreased quality of life, and significant patient and caregiver distress. A critical step in the effective management of dementia-related psychosis (DRP) is the identification and diagnosis of affected patients. The lack of a standardised diagnostic approach presents a barrier to treatment and there are no consensus guidelines for DRP. Furthermore, there are no approved therapies for the treatment of DRP. Antipsychotic medications are often prescribed off-label, even though some are associated with an increased risk of adverse events or mortality. We present currently available screening tools and guidelines for the diagnosis and treatment of Parkinson's disease psychosis and DRP in the context of what is needed for effective management of psychosis.KEY POINTSWe present currently available screening tools and guidelines for Parkinson's disease psychosis and dementia-related psychosis, and discuss the unmet need for simple clinical diagnostic tools and treatment guidelines.The identification of psychosis is variable across different settings and specialties, without a unified approach to screening, definition, or diagnosis.Currently used tools for defining and assessing psychosis in a research setting are usually too cumbersome for everyday clinical practice.The development of a standardised set of diagnostic criteria would provide clinicians the opportunity to improve the detection, treatment, and quality of life of patients and their caregivers.

A clinical trial in advanced Parkinson's disease (APD) has established the superiority of carbidopa/levodopa enteral suspension (CLES) in reducing total patient "off" time (OFF) and increasing total "on" time without troublesome dyskinesia (ON-woTD) over orally administered immediate-release carbidopa/levodopa tablets (IR-CL). However, temporal patterns of these improvements throughout the waking day have not been examined. In this analysis, time to ON-woTD after waking and patterns of motor-symptom control throughout the waking day were compared between CLES and IR-CL.Post hoc analyses of APD patient-diary data from the phase 3 randomized controlled trial were used to compare changes in time to ON-woTD after waking, motor-symptom control throughout the waking day, occurrence of extreme fluctuations between OFF and "on" with troublesome dyskinesia, and motor-state transitions with CLES versus IR-CL from baseline to week 12.The sample included 33 CLES-treated and 30 IR-CL-treated patients. Among the CLES group, the percentage of patient days achieving ON-woTD within 30 min of waking was three times higher at week 12 versus baseline (33% vs. 11%, p = 0.0043); no significant change occurred with IR-CL. When the waking day was divided into four 4-h periods, CLES versus IR-CL treatment produced significantly greater reductions in OFF during three periods, and two periods had increased ON-woTD. Fewer CLES-treated patients had extreme fluctuations at week 12 (3% vs. 23%, p = 0.0224) compared to IR-CL-treated patients. From baseline to week 12, CLES-treated patients had greater reductions in the average number of motor-state transitions compared to IR-CL-treated patients (- 1.6, p = 0.0295).CLES-treated patients experienced a more rapid onset of ON-woTD after waking and greater consistency of ON-woTD throughout their waking day than IR-CL-treated patients.In advanced Parkinson’s disease, patients’ motor-symptom states (such as “on” time without troublesome dyskinesia [good “on” time] and “off” time), and the timing at which they occur, can impact patients’ quality of life and ability to complete activities of daily living. Carbidopa/levodopa enteral suspension is administered continuously into the jejunum, potentially reducing some of the motor-state variation that is common with orally administered carbidopa/levodopa, including delayed “on” time after waking and transitions between “off” and “on” throughout the day. In post hoc analyses of clinical trial data, patterns of motor-states across the waking day were compared between carbidopa/levodopa enteral suspension and orally administered immediate-release carbidopa/levodopa at week 12. Outcomes included time to good “on” after waking; occurrence of extreme fluctuations between “off” time and “on” time with troublesome dyskinesia; time in each motor-state during 4-h intervals across the day; and frequency of motor-state transitions. Three times as many carbidopa/levodopa enteral suspension-treated patients achieved good “on” within 30 min of waking after 12 weeks versus baseline, whereas no significant change was observed for the orally administered immediate-release carbidopa/levodopa group. Compared to orally administered immediate-release carbidopa/levodopa-treated patients, fewer carbidopa/levodopa enteral suspension-treated patients experienced extreme fluctuations, had greater reductions in motor-state transitions, and greater reductions in duration of “off” during three of the four intervals in the day. These findings provide a first look at the impact of carbidopa/levodopa enteral suspension on motor-state patterns throughout the day, and suggest that carbidopa/levodopa enteral suspension provides more consistent motor-symptom control and predictable benefit throughout the day than orally administered carbidopa/levodopa.

Over half of Parkinson's disease (PD) patients develop psychotic symptoms, and PD psychosis (PDP) is associated with significant distress to patients, caregiver burden, and impairs quality of life. Pharmacological therapy is limited to atypical antipsychotics.This review will summarize efficacy but will focus on the safety of antipsychotics for treating PDP, and in particular the off-target safety issues including cognitive impairment, sleep disturbance, cardiovascular effects, and motor function.Pimavanserin is the only medication approved in the US for treating PDP, however clozapine is also considered efficacious. Despite lack of substantial evidence for efficacy, quetiapine is commonly used to treat PDP. Despite the effectiveness of pimavanserin and clozapine for treating PDP, a need exists for additional pharmacological agents that are effective for PDP while providing an acceptable safety and tolerability profile. Medications to treat PDP should avoid worsening motor function, and also minimize sleep disturbances, cognitive impairment, cardiovascular effects, and other non-motor safety concerns. A neutral effect or reduction in mortality risk associated with PD and PDP would be ideal, and low rate of discontinuation due to AEs is desirable. Lastly, medications that can be used safely in combination with other pharmacological agents is essential.

Immediate-release (IR) amantadine has been used for treatment of levodopa induced dyskinesia (LID). The immediate-release/extended-release (IR/ER) amantadine formulation OS320 (OSMOLEX ER®) contains an IR outer layer and ER core for once-daily dosing.Report individual and pooled results for the similarly designed double-blind, placebo-controlled ALLAY-LID I and II trials, assessing IR/ER-amantadine for LID.PD patients with LID were randomized to IR/ER-amantadine 193 mg, 258 mg, or placebo. Primary endpoint was Unified Dyskinesia Rating Scale (UDysRS) score change from baseline to Day 98. Secondary outcome was ON time without troublesome dyskinesia based on diaries. Exploratory outcomes were other diary states (including OFF), MDS-UPDRS Parts II + III and Fatigue Severity Scale.Overall, 222 individuals enrolled (N = 87 ALLAY-LID I, N = 135 ALLAY-LID II); both trials terminated early for sponsor's decision. While ALLAY-LID I did not meet its primary endpoint, a significant reduction in UDysRS scores versus placebo was observed in ALLAY-LID II for both 193 mg and 258 mg doses. In the pooled analysis, placebo-adjusted UDysRS score differences were -5.5 [-9.8, -1.2], p = 0.012 and -5.2 [-9.5, -0.9], p = 0.017, respectively. IR/ER-amantadine 258 mg significantly increased time spent ON without troublesome dyskinesia in ALLAY-LID II and pooled analysis. Reductions in ON time with dyskinesia supported the primary outcome. There was no effect on OFF time or other outcomes. Overall, 13.3% (193 mg), 18.7% (258 mg) and 11.1% (placebo) discontinued for adverse events, most commonly hallucinations (4.0%, 10.7%, and 1.4%, respectively).IR/ER-amantadine significantly reduced LID in ALLAY-LID II but not in ALLAY-LID I; post-hoc pooled data also indicated a positive treatment effect on LID.

Standardized and validated criteria to define advanced Parkinson's disease (PD) or identify patient eligibility for device-aided therapy are needed. This study assessed the psychometric properties of clinical indicators of advanced PD and eligibility for device-aided therapy in a large population.This retrospective analysis of the Adelphi Parkinson's Disease Specific Programme collected data from device-aided therapy-naïve people with PD in G7 countries. We assessed the presence of 15 clinical indicators of advancing PD and seven indicators of eligibility for device-aided therapy in patients classified with advanced PD or as eligible for device-aided therapy by the treating physician. Accuracy was assessed using area under the curve (AUC) and multivariable logistic regression models. Construct validity was examined via known-group comparisons of disease severity and burden among patients with and without each clinical indicator.Of 4714 PD patients, 14.9% were classified with advanced PD and 17.5% as eligible for device-aided therapy by physician judgment. The presence of each clinical indicator was 1.9- to 7.3-fold more likely in patients classified with advanced PD. Similarly, the presence of device-aided therapy eligibility indicators was 1.8- to 5.5-fold more likely in patients considered eligible for device-aided therapy. All indicators demonstrated high clinical screening accuracy for identifying advanced PD (AUC range 0.84-0.89) and patients eligible for device-aided therapy (AUC range 0.73-0.80). The Unified Parkinson's Disease Rating Scale (UPDRS) score, cognitive function, quality of life, and caregiver burden were significantly worse in indicator-positive patients.Specific clinical indicators of advanced PD and eligibility for device-aided therapy demonstrated excellent psychometric properties in a large sample, and thus may provide an objective and reliable approach for patient identification and treatment optimization.Advanced Parkinson’s disease (PD) refers to the stage of disease when motor complications are difficult to manage with standard therapy. Patients reaching this stage of the disease may benefit from a treatment change from pills to the so-called device-aided therapies. However, there is currently no unanimous definition of advanced PD, which makes it challenging to identify suitable candidates for device-aided therapies. There is urgent need to define specific features (or ‘clinical indicators’) to support healthcare professionals and patients in the identification of advanced PD as well as to define suitability for device-aided therapy. This study aimed to assess the accuracy of 15 clinical indicators and seven device-aided therapy eligibility criteria using information from a large database of 4714 patients in G7 countries. Physicians classified 14.9% of patients as having advanced PD and 17.5% were judged to be eligible for device-aided therapy. Each clinical indicator or device-aided therapy eligibility indicator was detected more frequently in patients classified as having advanced PD and in patients considered eligible for device-aided therapy, respectively. All indicators had high accuracy for identifying advanced PD and device-aided therapy-eligibility. These previously identified clinical indicators of advanced PD and device-aided therapy eligibility may provide an objective and reliable approach for patient screening and treatment optimization.

Droxidopa is approved to treat neurogenic orthostatic hypotension (nOH) symptoms in patients with autonomic failure based on short-term clinical trial data. Additional data on the long-term efficacy of droxidopa are needed. We have evaluated the 12-week efficacy and tolerability of droxidopa in patients with nOH in an open-label period of an ongoing phase 4 study .Patients received 12 weeks of open-label treatment with an individually optimized droxidopa dose (100-600 mg, 3 times daily) as identified during a preceding titration period. Patient-reported outcomes included the Orthostatic Hypotension Symptom Assessment (OHSA), Orthostatic Hypotension Daily Activity Scale (OHDAS), and clinician- and patient-rated Clinical Global Impression-Severity (CGI-S) scales. Supine blood pressure (BP) and adverse events (AEs) were recorded.Data from 114 patients enrolled into the 12-week open-label period were available for analyses. After 12 weeks of droxidopa treatment, patients reported significant (P 0.0001) improvements from baseline in OHSA and OHDAS composite and individual item scores and on clinician and patient CGI-S scores. Mean ± SD supine systolic and diastolic BP at week 12 increased by 15.5 ± 22.9 and 7.8 ± 11.7 mmHg from baseline, respectively (P 0.0001 for both). The most frequently reported AEs were falls (17%), headache (13%), and dizziness (9%); one (0.9%) patient reported an AE of supine hypertension.During 12 weeks of open-label treatment, droxidopa was associated with significant improvement from baseline in nOH symptoms and activities of daily living. No clinically important changes in supine hypertension or AEs of concern were observed. These results support the efficacy of droxidopa beyond 2 weeks of treatment.NCT02586623.

Background: Glucocerebrosidase gene (GBA) mutations influence the risk and prognosis of Parkinson’s disease (PD), possibly through accumulation of glycosphingolipids, including glucosylceramide (GL-1). Venglustat, a glucosylceramide synthase inhibitor, is investigated in patients with PD and GBA mutations. Methods: Part 1 of the phase 2 MOVES-PD trial (NCT02906020) is a randomised, double-blinded, placebo-controlled, dose-escalation study performed at 13 sites in six countries. Eligible participants were 18–80 years old and had PD diagnosis and heterozygous GBA mutation. Per regulatory agency request, Japanese participants were evaluated separately from those outside Japan. Participants were randomised to three doses of once-daily orally administered venglustat or placebo by an interactive voice-response system, in a sequential cohort design, and were followed up to 36 weeks (52 weeks for Japanese participants). The primary endpoint was safety and tolerability of venglustat versus placebo. Secondary and exploratory endpoints included venglustat pharmacokinetics and pharmacodynamics. Findings: Between Jan 26, 2017, and Oct 17, 2018, 29 participants were randomised to venglustat (Japanese, n=9; non-Japanese, n=13) or placebo (n=3; n=4). Eight (89%) Japanese and 12 (92%) non-Japanese venglustat-treated participants experienced at least one adverse event (AE) versus two (67%) and four (100%) participants from the respective placebo groups. Most AEs were mild or moderate, and no serious AEs or deaths occurred. Two venglustat-treated non-Japanese participants discontinued due to AEs (confusional state and panic attack). Over 4 weeks, venglustat exposure in plasma and cerebrospinal fluid (CSF) increased, and GL-1 levels in plasma and CSF decreased, both in a dose-dependent manner. At the highest dose, CSF GL-1 decreased by 72·0% in Japanese and 74·3% in non-Japanese participants. Interpretation: Venglustat showed favourable safety and tolerability in MOVES-PD Part 1 and its target engagement was achieved in the CSF. Part 2 will assess the efficacy of venglustat at the dose selected in Part 1. Trial Registration: This trial is registered with ClinicalTrials.gov, number NCT02906020. Funding Statement: Supported by Sanofi. Declaration of Interests: MJP, SJMG, PM, SS, JS, SW, and SPS report receiving personal compensation as employees of Sanofi. HS reports receiving grant support from Boehringer Japan, Dainippon Sumitomo, Kyowa Hakko-Kirin, and Otsuka, and honoraria from Dainippon Sumitomo, Kyowa Hakko-Kirin, Medtronic, Novartis Pharma KK, Otsuka FP, and Takeda. TH reports receiving speaker’s honoraria and research funding from Dainippon Sumitomo, Eisai Co, Ltd, Kyowa Hakko-Kirin, Novartis Pharma KK, Otsuka, Sanofi, and Takeda, and grant support from Dainippon Sumitomo, Eisai Co, Ltd, the Setsuro Fujii Memorial, the Osaka Foundation for Promotion of Fundamental Medical Research, and the Japan Agency for Medical Research and Development under grant number 19dm0107156, the Setsuro Fujii Memorial. TG reports receiving speaker’s honoraria from MedUpdate, Novartis, Teva, and UCB Pharma, and grant support from the German Research Foundation, the German Federal Ministry of Education and Research, the European Commission, the Helmholtz Association, and the Michael J Fox Foundation; he also serves as chairman of the Scientific Advisory Board of the “Joint Programming for Neurodegenerative Diseases” program, funded by the European Commission. SHI has received honoraria for CME services, consulting, research grants, and/or promotional speaking on behalf of AbbVie, Acadia, Acorda, Adamas, Addex, Affiris, Alexva, Allergan, Amarantus, Amneal, Aptinyx, Axial, Axovant, Benevolent, Biogen, Britannia, Cadent, Cala, Cerecor, Cerevel, Cipla, Eli Lilly, Enterin, GE Healthcare, Global Kinetics, Impax, Impel, Intec Pharma, Ipsen, Jazz, Kyowa, Lundbeck, Merz, the Michael J Fox Foundation, Mitsubishi Tanabe, Neuralys, Neurocrine, Neuroderm, Parkinson Study Group, Pharma2B Prilenia, Promentis, Revance, Roche, Sanofi, Sunovion, Sun Pharma, Teva, Theravance, UCB, US WorldMeds and Zambon. RNA reports research support from the NIH, the Department of Defense, the Parkinson’s Foundation, and the Michael J Fox Foundation, and receives consultation fees from Janssen, Restorbio, Roche, and Sanofi. GC reports participating on Data and Safety Monitoring Boards for Avexis Pharmaceuticals, Biolinerx, Brainstorm Cell Therapeutics, CSL Behring, Galmed Pharmaceuticals, Horizon Pharmaceuticals, Hisun Pharmaceuticals, Mapi Pharmaceuticals, Merck, Merck/Pfizer, Neurim, Novartis, Ophazyme, Opko Biologics, Reata Pharmaceuticals, Receptos/Celgene, Sanofi-Aventis, Teva Pharmaceuticals, Vivus, NHLBI(Protocol Review Committee), and NICHD (OPRU oversight committee); reports receiving consulting fees or participating on advisory boards from Biogen, Click Therapeutics, Genentech, Genzyme, Gilgamesh Pharmaceuticals, GW Pharmaceuticals, Klein-Buendel Incorporated, Medimmune, MedDay, Novartis, Osmotica Pharmaceuticals, Perception Neurosciences, Recursion Pharmaceuticals, Roche, Somahlution, and TG Therapeutics; is employed by the University of Alabama at Birmingham; and is President of Pythagoras, Inc, a private consulting company located in Birmingham, AL, USA. NH reports receiving consulting fees for participating in advisory boards from Dainippon Sumitomo, Eisai, FP, Kyowa Hakko-Kirin, Ono, Otsuka, Tanabe-Mitsubishi, and; grant support from Biogen, Boehringer Japan, Boston Scientific, Eisai, Medtronic, Meiji, Otsuka, and Takeda; and honoraria from Dainippon, FP, Novartis, Otsuka, and Takeda. GUH reports receiving consulting fees or participating on advisory boards from AbbVie, Alzprotect, Asceneuron, Biogen, Biohaven, Lundbeck, Novartis, Retrotope, Roche, Sanofi, UCB, and the Weston Brain Institute, and has received honoraria for scientific presentations from AbbVie, Biogen, Roche, Teva, UCB, and Zambon. KM reports receiving consulting fees from Ceraspir, GE Healthcare, Invicro, LTI, Lundbeck, the Michael J Fox Foundation, Neuroderm, Neuron23, Proclara, Roche, Takeda, and UBC. AHVS reports receiving consulting fees from Inflammazome, Kyowa, Prevail, and Sanofi. CRS is named as co-inventor on a US patent application on sphingolipids biomarkers that is jointly held by Brigham & Women’s Hospital and Sanofi; has consulted for Sanofi; has collaborated with Genzyme, Lysosomal Therapies, Opko, Pfizer, and Proteome Sciences; is on the Scientific Advisory Board of the American Parkinson Disease Association; has served as Advisor to the Michael J Fox Foundation, NIH, Department of Defense, and Google; and has received funding from the NIH, the US Department of Defense, the Michael J Fox Foundation, and the American Parkinson Disease Association. TS reports receiving consulting fees and honoraria from Acadia, Adamas, Teva, and UCB Pharma; consulting fees from AbbVie, Acorda, Anavex, Allergan, NeuroDerm, PhotoPharmics, Revance, Sanofi, Sunovion, Voyager, US WorldMeds, and the Michael J Fox Foundation; and research funding from Biogen, NeuroDerm, Roche, Sanofi, NINDS, the Michael J Fox Foundation, and the Parkinson Foundation. NG reports owning stock from BOL, Lysosomal Therapeutic Ltd and Vibrant; has served as a consultant for AbbVie, Biogen, BOL, Denali, NeuroDerm, Pharma2B, Sanofi Genzyme and Vibrant; has participated in advisory boards for Biogen, Denali, NeuroDerm, Sanofi Genzyme and Sionara; has received honoraria from AbbVie, Sanofi Genzyme and the Movement Disorder Society; and has received grants from Biogen, Ionis, the European Union, the Israel Science Foundation, the Michael J Fox Foundation and the National Parkinson Foundation. TZF received compensation as an employee of Sanofi at the time the study was conducted, and is currently employed by Alnylam Pharmaceuticals (Cambridge, MA, USA). Ethics Approval Statement: This study was conducted in accordance with international ethics guidelines, including the Declaration of Helsinki and the International Council for Harmonisation guidelines for good clinical practice, and all applicable laws, rules, and regulations. All study procedures were approved by local institutional ethics review boards of participating sites, and participants provided written informed consent.

Neurogenic orthostatic hypotension (NOH) is an orphan disease that primarily affects patients with neurodegenerative disorders such as Parkinson's disease and multiple system atrophy. The first step in the management of NOH is to discontinue or minimize the use of drugs that lower blood pressure. Nonpharmacologic therapy for NOH includes physical countermaneuvers, compression abdominal binders and lower extremity stockings, recognition and avoidance of orthostatic stressors, hydration, and salt supplementation. The management of NOH should also include interventions to prevent falls. Pharmacotherapy for NOH includes the mineralocorticoid drug fludrocortisone to expand plasma volume and the sympathomimetic drugs midodrine and droxidopa. Clinical efficacy, tolerability, and the role of each drug in the treatment paradigm are reviewed here.

Neurogenic orthostatic hypotension (nOH) is due to failure of the autonomic nervous system to regulate blood pressure in response to postural changes due to an inadequate release of norepinephrine, leading to orthostatic hypotension and supine hypertension. nOH is common in Parkinson’s disease (PD). Prevalence varies throughout the course of PD, ranging from 40% to 60%, and resulting in symptomatic nOH in approximately half. Symptomatic nOH, including lightheadedness, can limit daily activities and lead to falls. Symptomatic nOH can also limit therapeutic options for treating PD motor symptoms. Clinical evaluation should routinely include symptom assessment and blood pressure measurement of supine, sitting, and 3-minute standing; 24-hour ambulatory blood pressure monitoring can also be helpful. Non-pharmacological management of symptomatic nOH involves education, physical maneuvers, and adequate hydration. Current pharmacological treatment of symptomatic nOH includes salt supplement, fludrocortisone, midodrine, pyridostigmine, and other empiric medications. Despite these options, treatment of symptomatic nOH remains suboptimal, often limited by severe increases in supine blood pressure. Droxidopa, an oral prodrug converted by decarboxylation to norepinephrine, is a promising therapeutic option for symptomatic nOH in PD, improving symptoms of nOH, daily activities, falls, and standing systolic blood pressure in several recent trials. These trials demonstrated short-term efficacy and tolerability, with comparable increases in standing and supine blood pressures. Longer-term studies are ongoing to confirm durability of treatment effect.

Parkinson’s disease psychosis (PDP) occurs frequently in patients with Parkinson’s disease (PD) and involves a spectrum of symptoms, from mild hallucinations to those that are more disruptive, as well as delusions, particularly around spousal infidelity and theft of money or possessions. Risk factors for PDP include dopaminergic (and other) medications, cognitive disorders, sleep disorders, and duration of PD. Emerging evidence suggests that PDP also reflects underlying PD pathology. Routine querying of major PDP symptoms can hasten recognition and allow earlier diagnosis of PDP. Mild hallucinations with retained insight are frequent and may be tolerable by patients and caregivers, but symptoms that can be considered as psychosis will typically increase in frequency and severity. Increasing PDP results in patient distress, increased caregiver burden, and is a leading cause of long-term nursing home placement. PDP has also been associated with an increased risk for morbidity and mortality. Ongoing research into the prevalence, risk factors, phenomenology, pathophysiology, and emerging pharmacotherapy for PDP provides hope for improved diagnosis and management of PDP.

Objective To evaluate the possible association of Parkinson disease (PD) and melanoma in North America. Design, Setting, and Patients Thirty-one centers enrolled patients with idiopathic PD. At visit 1, a neurologist obtained a medical history. At visit 2, a dermatologist recorded melanoma risk factors, performed a whole-body examination, and performed a biopsy of lesions suggestive of melanoma for evaluation by a central dermatopathology laboratory. We compared overall prevalence of melanoma with prevalence calculated from the US Surveillance Epidemiology and End Results (SEER) cancer database and the American Academy of Dermatology skin cancer screening programs. Results A total of 2106 patients (mean [SD] age, 68.6 [10.6] years; duration of PD, 7.1 [5.7] years) completed the study. Most (84.8%) had received levodopa. Dermatology examinations revealed 346 pigmented lesions; dermatopathological findings confirmed 20 in situ melanomas (0.9%) and 4 invasive melanomas (0.2%). In addition, histories revealed 68 prior melanomas (3.2%). Prevalence (5-year limited duration) of invasive malignant melanoma in the US cohort of patients with PD (n = 1692) was 2.24-fold higher (95% confidence interval, 1.21-4.17) than expected in age- and sex-matched populations in the US SEER database. Age- or sex-adjusted relative risk of any melanoma for US patients was more than 7 times that expected from confirmed cases in American Academy of Dermatology skin cancer screening programs. Conclusions Melanoma prevalence appears to be higher in patients with PD than in the general population. Despite difficulties in comparing other databases with this study population, the study supports increased melanoma screening in patients with PD.