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Parkinson Disease: HELP
Articles from Miscellaneous cities in California
Based on 91 articles published since 2010
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These are the 91 published articles about Parkinson Disease that originated from Miscellaneous cities in California during 2010-2020.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4
1 Editorial Editorial and introduction: Behavioral aspects of Parkinson's disease. 2017

Friedman, Joseph H / Bhidayasiri, Roongroj / Truong, Daniel D. ·Butler Hospital, Department of Neurology, Alpert Medical School of Brown University, RI, USA. · Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok 10330, Thailand; Department of Rehabilitation Medicine, Juntendo University, Tokyo, Japan. Electronic address: rbh@chulapd.org. · Truong Neuroscience Institute, Parkinson's and Movement Disorders Institute, Orange Coast Memorial Medical Center, Fountain Valley, CA, USA. ·J Neurol Sci · Pubmed #28087061.

ABSTRACT: -- No abstract --

2 Review Levodopa-induced dyskinesia: clinical features, incidence, and risk factors. 2018

Tran, Tai N / Vo, Trang N N / Frei, Karen / Truong, Daniel D. ·Neurology Department, University Medical Center, Ho Chi Minh City, Vietnam. · Neurology Department, International Neurosurgery Hospital, Ho Chi Minh City, Vietnam. · Loma Linda University, Loma Linda, CA, 92354, USA. · The Truong Neuroscience Institute, Orange Coast Memorial Medical Center, Fountain Valley, CA, 92708, USA. dtruong@pmdi.org. · Department of Psychiatry and Neuroscience, UC Riverside, Riverside, CA, USA. dtruong@pmdi.org. ·J Neural Transm (Vienna) · Pubmed #29971495.

ABSTRACT: Symptoms of Parkinson's disease have been controlled with levodopa for many years; however, motor complications consisting of wearing off of medication effect and dyskinesias tend to occur within a few years of starting levodopa. Motor complications can begin a few months after taking levodopa, with the average time to onset estimated to be 6.5 years. Dyskinesias can be troublesome and require intervention. Levodopa-induced dyskinesia can be composed of a variety of movement disorders including chorea, dystonia, ballism, myoclonus, and akathisia. Based on the clinical pattern, the most common dyskinesia is chorea and choreoathetosis. The clinical manifestations can be divided into three main categories based on their clinical movement patterns and the temporal correlation between the occurrence of dyskinesia and the levodopa dosing: on or peak-dose dyskinesias, biphasic dyskinesias, and Off dyskinesias. Severe cases of dyskinesia have been reported, with the extreme being dyskinesia-hyperpyrexia syndrome. The prevalence of LID has been reported in many studies, but the reported incidence varies. The rate of LID development is from 3 to 94%. The prevalence of LID mainly depends on age at onset, disease duration, and severity, and duration of levodopa therapy. Some of the risk factors for the development of dyskinesia are modifiable. Modifiable risk factors include levodopa dose and body weight. Non-modifiable risk factors include age, gender, duration of disease, clinical subtype, disease progression, disease severity, and genetic factors.

3 Review High-intensity focused ultrasound: past, present, and future in neurosurgery. 2018

Quadri, Syed A / Waqas, Muhammad / Khan, Inamullah / Khan, Muhammad Adnan / Suriya, Sajid S / Farooqui, Mudassir / Fiani, Brian. ·California Institute of Neuroscience, Thousand Oaks, California. · Department of Neurosurgery, Aga Khan University Hospital, Karachi, Pakistan. · University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; and. · Department of Neurosurgery, Institute of Clinical Orthopedic and Neurosciences, Desert Regional Medical Center, Palm Springs, California. ·Neurosurg Focus · Pubmed #29385923.

ABSTRACT: Since Lynn and colleagues first described the use of focused ultrasound (FUS) waves for intracranial ablation in 1942, many strides have been made toward the treatment of several brain pathologies using this novel technology. In the modern era of minimal invasiveness, high-intensity focused ultrasound (HIFU) promises therapeutic utility for multiple neurosurgical applications, including treatment of tumors, stroke, epilepsy, and functional disorders. Although the use of HIFU as a potential therapeutic modality in the brain has been under study for several decades, relatively few neuroscientists, neurologists, or even neurosurgeons are familiar with it. In this extensive review, the authors intend to shed light on the current use of HIFU in different neurosurgical avenues and its mechanism of action, as well as provide an update on the outcome of various trials and advances expected from various preclinical studies in the near future. Although the initial technical challenges have been overcome and the technology has been improved, only very few clinical trials have thus far been carried out. The number of clinical trials related to neurological disorders is expected to increase in the coming years, as this novel therapeutic device appears to have a substantial expansive potential. There is great opportunity to expand the use of HIFU across various medical and surgical disciplines for the treatment of different pathologies. As this technology gains recognition, it will open the door for further research opportunities and innovation.

4 Review Behavioral Phenotyping and Pathological Indicators of Parkinson's Disease in 2017

Maulik, Malabika / Mitra, Swarup / Bult-Ito, Abel / Taylor, Barbara E / Vayndorf, Elena M. ·Department of Chemistry and Biochemistry, University of Alaska FairbanksFairbanks, AK, United States. · Department of Biology and Wildlife, University of Alaska FairbanksFairbanks, AK, United States. · Department of Biological Sciences, California State University, Long BeachLong Beach, CA, United States. · Institute of Arctic Biology, University of Alaska FairbanksFairbanks, AK, United States. ·Front Genet · Pubmed #28659967.

ABSTRACT: Parkinson's disease (PD) is a neurodegenerative disorder with symptoms that progressively worsen with age. Pathologically, PD is characterized by the aggregation of α-synuclein in cells of the substantia nigra in the brain and loss of dopaminergic neurons. This pathology is associated with impaired movement and reduced cognitive function. The etiology of PD can be attributed to a combination of environmental and genetic factors. A popular animal model, the nematode roundworm

5 Review Pharmacokinetics of Rytary 2017

Mittur, Aravind / Gupta, Suneel / Modi, Nishit B. ·Impax Specialty Pharma, a Division of Impax Laboratories Inc., 31047 Genstar Road, Hayward, CA, 94544, USA. · Impax Specialty Pharma, a Division of Impax Laboratories Inc., 31047 Genstar Road, Hayward, CA, 94544, USA. nmodi@impaxlabs.com. ·Clin Pharmacokinet · Pubmed #28236251.

ABSTRACT: Parkinson's disease (PD) is a chronic progressive neurological disorder characterized by resting tremor, rigidity, bradykinesia, gait disturbance, and postural instability. Levodopa, the precursor to dopamine, coadministered with carbidopa or benserazide, aromatic amino acid decarboxylase inhibitors, is the most effective and widely used therapeutic agent in the treatment of PD. With continued levodopa treatment, a majority of patients develop motor complications such as dyskinesia and motor 'on-off' fluctuations, which are, in part, related to the fluctuations in plasma concentrations of levodopa. A new extended-release (ER) carbidopa-levodopa capsule product (also referred to as IPX066) was developed and approved in the US as Rytary

6 Review The sleeping brain in Parkinson's disease: A focus on REM sleep behaviour disorder and related parasomnias for practicing neurologists. 2017

Bhidayasiri, Roongroj / Sringean, Jirada / Rattanachaisit, Watchara / Truong, Daniel D. ·Chulalongkorn Centre of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital and Thai Red Cross Society, Bangkok, Thailand; Department of Rehabilitation Medicine, Juntendo University, Tokyo, Japan. Electronic address: rbh@chulapd.org. · Chulalongkorn Centre of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital and Thai Red Cross Society, Bangkok, Thailand. · Parkinson's and Movement Disorders Institute, Fountain Valley, CA, USA. ·J Neurol Sci · Pubmed #28126342.

ABSTRACT: Sleep disorders are identified as common non-motor symptoms of Parkinson's disease (PD) and recently this recognition has been expanded to include parasomnias, encompassing not only REM sleep behaviour disorder (RBD), but also other non-REM forms. RBD, a prototypical parasomnia in PD, exists even in the prodromal stage of the disease, and is characterized by the presence of dream enactment behaviours occurring alongside a loss of normal skeletal muscle atonia during REM sleep. In contrast, non-REM parasomnias are more frequently observed in the late stage PD. However, the development of these disorders often overlaps and it is not uncommon for PD patients to meet the criteria for more than one type of parasomnias, thus making a clinical distinction challenging for practicing neurologists who are not sleep specialists. Indeed, clinical recognition of the predominant form of parasomnia does not just depend on video-polysomnography, but also on an individual physician's clinical acumen in delineating pertinent clinical history to determine the most likely diagnosis and proceed accordingly. In this review article, we highlight the various forms of parasomnias that have been reported in PD, including, but not limited to, RBD, with a focus on clinical symptomatology and implications for clinical practice. In addition, we review the differences in PD-related parasomnias compared to those seen in general populations. With advances in sleep research and better technology for ambulatory home monitoring, it is likely that many unanswered questions on PD-related parasomnias will soon be resolved resulting in better management of this nocturnal challenge in PD.

7 Review Hallucinations and the spectrum of psychosis in Parkinson's disease. 2017

Frei, Karen / Truong, Daniel D. ·Loma Linda University, Loma Linda, CA, United States. Electronic address: drkpfrei@gmail.com. · The Parkinson's and Movement Disorders Institute, Fountain Valley, CA, United States. ·J Neurol Sci · Pubmed #28108020.

ABSTRACT: Hallucinations and psychosis can be a part of Parkinson's disease and are considered to be a nonmotor symptom or a neuropsychiatric complication of the disease. Hallucinations of different modalities and delusions can occur beyond the common visual hallucinations. The various types of hallucinations and psychotic symptoms comprising the spectrum of Parkinson's disease psychosis is the subject of this review article.

8 Review Oxidative Stress, Pro-Inflammatory Cytokines, and Antioxidants Regulate Expression Levels of MicroRNAs in Parkinson's Disease. 2017

Prasad, Kedar N. ·Engage Global, 245 El-Faisan Drive, San Rafael, CA 94903, United States. ·Curr Aging Sci · Pubmed #28042771.

ABSTRACT: BACKGROUND: Parkinson's disease (PD) is a slow progressive neurodegenerative disease associated with abnormal function of extrapyramidal system. Although several biochemical and genetic defects are identified, increased oxidative stress and chronic inflammation are one of the earliest events that initiate and promote PD. Oxidative stress also participates in impaired nonmotor symptoms. The levels of microRNAs that are evolutionarily conserved single-stranded noncoding RNAs of approximately 22 nucleotide in length may have a role in PD. METHOD: Published studies on changes in the levels of microRNAs in PD were critically reviewed, and the role of Reactive Oxygen Species (ROS), pro-inflammatory cytokines, and antioxidants in regulating the levels of microRNAs was evaluated. RESULTS: MicroRNAs levels were altered in PD. Downregulated microRNAs cause neurodegeneration by decreasing the levels of Nrf2 (nuclear transcriptional factor-2), mTOR (mammalian target of rapamycin), and DJ-1 and Parkin genes; and by increasing the levels of alpha-synuclein, RelA, Bim and Calpain-1, and A2AR (adenosine A2A receptor). Upregulated microRNAs cause degeneration of nerve cells by decreasing the levels of IGF-1 (Insulin Growth Factor-1), GRP78 (glucose regulated protein 78), DJ-1, and Hsc-70 (Heat- Shock Protein-70) that enhanced alpha-synuclein levels. ROS and pro-inflammatory cytokines cause neurodegeneration by altering the levels of microRNAs. Antioxidants that protect neurons by reducing oxidative stress and chronic inflammation altered the levels of microRNAs. CONCLUSION: Increased oxidative stress and chronic inflammation may cause neurodegeneration in PD by altering the levels of microRNAs and their target proteins. Antioxidants may provide neuroprotection by changing the levels of microRNAs and their target proteins.

9 Review The role of β-adrenergic blockers in Parkinson's disease: possible genetic and cell-signaling mechanisms. 2013

Luong, Khanh vinh quoc / Nguyen, Lan Thi Hoàng. ·Vietnamese American Medical Research Foundation, Westminster, CA 92683, USA. lng2687765@aol.com ·Am J Alzheimers Dis Other Demen · Pubmed #23695225.

ABSTRACT: Genetic studies have identified numerous factors linking β-adrenergic blockade to Parkinson's disease (PD), including human leukocyte antigen genes, the renin-angiotensin system, poly(adenosine diphosphate-ribose) polymerase 1, nerve growth factor, vascular endothelial growth factor, and the reduced form of nicotinamide adenine dinucleotide phosphate. β-Adrenergic blockade has also been implicated in PD via its effects on matrix metalloproteinases, mitogen-activated protein kinase pathways, prostaglandins, cyclooxygenase 2, and nitric oxide synthase. β-Adrenergic blockade may have a significant role in PD; therefore, the characterization of β-adrenergic blockade in patients with PD is needed.

10 Review The beneficial role of thiamine in Parkinson disease. 2013

Luong, Khanh V Q / Nguyễn, Lan T H. ·Vietnamese American Medical Research Foundation, Westminster, CA 92683, USA. ·CNS Neurosci Ther · Pubmed #23462281.

ABSTRACT: Parkinson disease (PD) is the second most common form of neurodegeneration among elderly individuals. PD is clinically characterized by tremors, rigidity, slowness of movement, and postural imbalance. In this paper, we review the evidence for an association between PD and thiamine. Interestingly, a significant association has been demonstrated between PD and low levels of serum thiamine, and thiamine supplements appear to have beneficial clinical effects against PD. Multiple studies have evaluated the connection between thiamine and PD pathology, and candidate pathways involve the transcription factor Sp1, p53, Bcl-2, caspase-3, tyrosine hydroxylase, glycogen synthase kinase-3β, vascular endothelial growth factor, advanced glycation end products, nuclear factor kappa B, mitogen-activated protein kinase, and the reduced form of nicotinamide adenine dinucleotide phosphate. Thus, a review of the literature suggests that thiamine plays a role in PD, although further investigation into the effects of thiamine in PD is needed.

11 Review Dysphagia in Parkinson's disease is responsive to levodopa. 2013

Sutton, James P. ·Pacific Neuroscience Medical Group, Oxnard, CA 93030, United States. james.sutton@pacificneuroscience.com ·Parkinsonism Relat Disord · Pubmed #23333537.

ABSTRACT: The role of levodopa in the treatment of dysphagia in Parkinson's disease (PD) has recently been questioned. There are good reasons, however, to "question the question." In this essay, evidence from published literature and clinical experience is presented, as well as a critical review of the first meta-analysis to explore this issue. The evidence presented supports the traditional view that PD dysphagia is responsive to levodopa.

12 Review Vitamin D and Parkinson's disease. 2012

Vinh Quôc Luong, Khanh / Thi Hoàng Nguyên, Lan. ·Vietnamese American Medical Research Foundation, Westminster, California, USA. lng2687765@aol.com ·J Neurosci Res · Pubmed #22930493.

ABSTRACT: Parkinson's disease (PD) is the second most common form of neurodegeneration among the elderly population. PD is clinically characterized by tremors, rigidity, slowness of movement, and postural imbalance. Interestingly, a significant association has been demonstrated between PD and low levels of vitamin D in the serum, and vitamin D supplement appears to have a beneficial clinical effect on PD. Genetic studies have provided the opportunity to determine which proteins link vitamin D to PD pathology, e.g., Nurr1 gene, toll-like receptor, gene related to lipid disorders, vascular endothelial factor, tyrosine hydroxylase, and angiogenin. Vitamin D also exerts its effects on cancer through nongenomic factors, e.g., bacillus Calmette-Guerin vaccination, interleukin-10, Wntβ-catenin signaling pathways, mitogen-activated protein kinase pathways, and the reduced form of the nicotinamide adenine dinucleotide phosphate. In conclusion, vitamin D might have a beneficial role in PD. Calcitriol is best used for PD because it is the active form of the vitamin D(3) metabolite and modulates inflammatory cytokine expression. Further investigation with calcitriol in PD is needed.

13 Review Thiamine and Parkinson's disease. 2012

Lu'o'ng, Khanh vinh quôc / Nguyên, Lan Thi Hoàng. ·Vietnamese American Medical Research Foundation, Westminster, CA, USA. Lng2687765@aol.com ·J Neurol Sci · Pubmed #22385680.

ABSTRACT: Parkinson's disease (PD) is the second most common form of neurodegeneration in the elderly population. PD is clinically characterized by tremors, rigidity, slowness of movement and postural imbalance. A significant association has been demonstrated between PD and low levels of thiamine in the serum, which suggests that elevated thiamine levels might provide protection against PD. Genetic studies have helped identify a number of factors that link thiamine to PD pathology, including the DJ-1 gene, excitatory amino acid transporters (EAATs), the α-ketoglutarate dehydrogenase complex (KGDHC), coenzyme Q10 (CoQ10 or ubiquinone), lipoamide dehydrogenase (LAD), chromosome 7, transcription factor p53, the renin-angiotensin system (RAS), heme oxygenase-1 (HO-1), and poly(ADP-ribose) polymerase-1 gene (PARP-1). Thiamine has also been implicated in PD through its effects on L-type voltage-sensitive calcium channels (L-VSCC), matrix metalloproteinases (MMPs), prostaglandins (PGs), cyclooxygenase-2 (COX-2), reactive oxygen species (ROS), and nitric oxide synthase (NOS). Recent studies highlight a possible relationship between thiamine and PD. Genetic studies provide opportunities to determine which proteins may link thiamine to PD pathology. Thiamine can also act through a number of non-genomic mechanisms that include protein expression, oxidative stress, inflammation, and cellular metabolism. Further studies are needed to determine the benefits of using thiamine as a treatment for PD.

14 Review Stem cell challenges in the treatment of neurodegenerative disease. 2012

Feng, Zhongling / Gao, Feng. ·Bio Group, Nitto Denko Technical Corporation, Oceanside, CA 82058, USA. Zhongling_feng@gg.nitto.co.jp ·CNS Neurosci Ther · Pubmed #22070610.

ABSTRACT: Neurodegenerative diseases result from the gradual and progressive loss of neural cells and lead to nervous system dysfunction. The rapidly advancing stem cell field is providing attractive alternative options for fighting these diseases. Results have provided proof of principle that cell replacement can work in humans with Parkinson's disease (PD). However, three clinical studies of cell transplantation were published that found no net benefit, while patients in two of the studies developed dyskinesias that persisted despite reductions in treatment. Induced pluripotent stem cells (iPSC) have major potential advantages because patient-specific neuroblasts are suitable for transplantation, avoid immune reactions, and can be produced without the use of human ES cells (hESC). Although iPSCs have not been successfully used in clinical trials for PD, patients with amyotrophic lateral sclerosis (ALS) were treated with autologous stem cells and, though they had some degree of decline one year after treatment, they were still improved compared with the preoperative period or without any drug therapy. In addition, neural stem cells (NSCs), via brain-derived neurotrophic factor (BDNF), have been shown to ameliorate complex behavioral deficits associated with widespread Alzheimer's disease (AD) pathology in a transgenic mouse model of AD. So far, the FDA lists 18 clinical trials treating multiple sclerosis (MS), but most are in preliminary stages. This article serves as an overview of recent studies in stem cell and regenerative approaches to the above chronic neurodegenerative disorders. There are still many obstacles to the use of stem cells as a cure for neurodegenerative disease, especially because we still don't fully understand the true mechanisms of these diseases. However, there is hope in the potential of stem cells to help us learn and understand a great deal more about the mechanisms underlying these devastating neurodegenerative diseases.

15 Clinical Trial Pooled Analyses of Phase III Studies of ADS-5102 (Amantadine) Extended-Release Capsules for Dyskinesia in Parkinson's Disease. 2018

Elmer, Lawrence W / Juncos, Jorge L / Singer, Carlos / Truong, Daniel D / Criswell, Susan R / Parashos, Sotirios / Felt, Larissa / Johnson, Reed / Patni, Rajiv. ·Department of Neurology, University of Toledo College of Medicine, 3120 Glendale Avenue, Toledo, OH, 43614, USA. Lawrence.Elmer@utoledo.edu. · Department of Neurology and Movement Disorders, Emory University School of Medicine, Atlanta, GA, USA. · Department of Neurology, University of Miami, Miami, FL, USA. · The Parkinson's and Movement Disorder Institute, Fountain Valley, CA, USA. · Department of Neurology, Washington University, St. Louis, MO, USA. · Struthers Parkinson's Center, Golden Valley, MN, USA. · Adamas Pharmaceuticals, Inc., Emeryville, CA, USA. ·CNS Drugs · Pubmed #29532440.

ABSTRACT: BACKGROUND: Although levodopa is considered the most effective pharmacotherapy for motor symptoms of Parkinson's disease (PD), chronic use is associated with motor complications, including fluctuating response and unpredictable, involuntary movements called dyskinesia. ADS-5102 (amantadine) extended-release (ER) capsules (GOCOVRI OBJECTIVE: In this study, we present pooled results from two randomized, double-blind, placebo-controlled, phase III ADS-5102 trials. PATIENTS AND METHODS: The two studies in PD patients with dyskinesia shared design and eligibility criteria, differing only in treatment duration. Results from common assessment time points were pooled. RESULTS: At 12 weeks, the least squares (LS) mean change in total score on the Unified Dyskinesia Rating Scale among 100 patients randomized to ADS-5102 and 96 patients randomized to placebo was - 17.7 (standard error [SE] 1.3) vs. - 7.6 (1.3) points, respectively (- 10.1 points, 95% confidence interval [CI] - 13.8, - 6.5; p < 0.0001). The relative treatment difference between groups was 27.3% (p < 0.0001). At 12 weeks, the LS mean change in OFF time was - 0.59 (0.21) vs. +0.41 (0.20) h/day, a difference of - 1.00 h/day (95% CI - 1.57, - 0.44; p = 0.0006). For both efficacy measures, a significant difference from placebo was attained by two weeks, the first post-baseline assessment, and was maintained throughout 12 weeks. In the pooled ADS-5102 group, the most common adverse events were hallucination, dizziness, dry mouth, peripheral edema, constipation, falls, and orthostatic hypotension. CONCLUSIONS: These analyses provide further evidence supporting ADS-5102 as an adjunct to levodopa for treating both dyskinesia and OFF time in PD patients with dyskinesia. Clinicaltrials.gov identifier: NCT02136914 and NCT02274766.

16 Clinical Trial ADS-5102 (Amantadine) Extended-Release Capsules for Levodopa-Induced Dyskinesia in Parkinson Disease (EASE LID Study): A Randomized Clinical Trial. 2017

Pahwa, Rajesh / Tanner, Caroline M / Hauser, Robert A / Isaacson, Stuart H / Nausieda, Paul A / Truong, Daniel D / Agarwal, Pinky / Hull, Keith L / Lyons, Kelly E / Johnson, Reed / Stempien, Mary Jean. ·Department of Neurology, University of Kansas Medical Center, Kansas City. · Department of Neurology, University California-San Francisco. · Parkinson's Disease Research, Education and Clinic Center, San Francisco Veterans Affairs Medical Center, San Francisco, California. · Health Byrd Parkinson's Disease and Movement Disorders Center of Excellence, University of South Florida, Tampa. · Parkinson's Disease and Movement Disorders Center of Boca Raton, Boca Raton, Florida. · Wisconsin Institute for Neurologic and Sleep Disorders, Milwaukee. · The Parkinson's and Movement Disorder Institute, Fountain Valley, California. · Booth Gardner Parkinson's Care Center, Evergreen Health, Kirkland, Washington. · Raleigh Neurology Associates, Raleigh, North Carolina. · Adamas Pharmaceuticals Inc, Emeryville, California. ·JAMA Neurol · Pubmed #28604926.

ABSTRACT: Importance: Medical treatment of levodopa-induced dyskinesia (LID) in Parkinson disease (PD) is an unmet need. Objective: To evaluate the efficacy and safety of ADS-5102 (amantadine) extended-release 274-mg capsules for treatment of LID in patients with PD. Design, Setting, and Participants: A randomized, double-blind, placebo-controlled clinical trial was conducted between May 7, 2014, and July 22, 2015, at 44 North American sites among patients with PD treated with levodopa who experienced at least 1 hour of troublesome dyskinesia per day with at least mild functional impact. Interventions: Patients were randomized to receive placebo or 274 mg of ADS-5102 administered orally at bedtime for up to 25 weeks. Main Outcomes and Measures: The primary efficacy analysis was the change from baseline to week 12 in the Unified Dyskinesia Rating Scale total score for ADS-5102 vs placebo in the modified intent-to-treat population. OFF time (amount of time the PD medication is not controlling motor symptoms) was a key secondary end point. Safety analyses included all patients who received the study drug (ADS-5102 or placebo). Results: A total of 189 patients were screened, and 126 were randomized; the modified intent-to-treat population included 121 patients (51 women and 70 men; mean [SD] age, 64.7 [9.1] years). At week 12, the least-squares mean (SE) change in the Unified Dyskinesia Rating Scale score was -15.9 (1.6) for ADS-5102 (n = 63) and -8.0 (1.6) for placebo (n = 58) (treatment difference, -7.9; 95% CI, -12.5 to -3.3; P < .001). OFF time decreased by a mean (SE) of 0.6 (0.3) hours for ADS-5102 and increased by 0.3 (0.3) hours for placebo (treatment difference, -0.9 hours; 95% CI, -1.6 to -0.2; P = .02). Common adverse events for ADS-5102 vs placebo included visual hallucinations (15 [23.8%] vs 1 [1.7%]), peripheral edema (15 [23.8%] vs 0), and dizziness (14 [22.2%] vs 0). Adverse events led to treatment discontinuation for 13 patients receiving ADS-5102 (20.6%) vs 4 patients receiving placebo (6.9%). Conclusions and Relevance: ADS-5102, 274 mg at bedtime, may be an effective treatment for LID. An additional benefit is reduced OFF time. To our knowledge, this is the first demonstration of an oral treatment reducing both LID and OFF time in patients with PD with dyskinesia. Trial Registration: clinicaltrials.gov Identifier: NCT02136914.

17 Clinical Trial Conversion to carbidopa and levodopa extended-release (IPX066) followed by its extended use in patients previously taking controlled-release carbidopa-levodopa for advanced Parkinson's disease. 2017

Tetrud, James / Nausieda, Paul / Kreitzman, David / Liang, Grace S / Nieves, Anette / Duker, Andrew P / Hauser, Robert A / Farbman, Eric S / Ellenbogen, Aaron / Hsu, Ann / Kell, Sherron / Khanna, Sarita / Rubens, Robert / Gupta, Suneel. ·The Parkinson's Institute and Clinical Center, 675 Almanor Ave, Sunnyvale, CA 94085, USA. Electronic address: jtetrud@stanford.edu. · Wisconsin Institute for Neurologic and Sleep Disorders, 945 N 12th St, Milwaukee, WI 53233, USA. Electronic address: nausiedamd@parkcent.com. · The Parkinson's Disease and Movement Disorders Center of Long Island, 283 Commack Rd, Commack, NY 11725, USA. Electronic address: PDMDCLI@aol.com. · The Parkinson's Institute and Clinical Center, 675 Almanor Ave, Sunnyvale, CA 94085, USA. Electronic address: graceliangmd@gmail.com. · Munroe Regional Medical Center, 13940 US-441, Lady Lake, FL 32159, USA. Electronic address: Anette_Nieves@munroeregional.com. · University of Cincinnati, 2600 Clifton Ave, Cincinnati, OH 45220, USA. Electronic address: dukeraa@ucmail.uc.edu. · University of South Florida, 4202 E Fowler Ave, Tampa, FL 33620, USA. Electronic address: rhauser@health.usf.edu. · University of Nevada School of Medicine, 1707 W Charleston Blvd, Las Vegas, NV 89102, USA. Electronic address: efarbman@medicine.nevada.edu. · Quest Research Institute, 28595 Orchard Lake Rd #301, Farmington Hills, MI 48334, USA. Electronic address: aellenbogen@comcast.net. · Impax Laboratories, Inc., 31047 Genstar Road, Hayward, CA 94544, USA. Electronic address: annhsu@aol.com. · Impax Laboratories, Inc., 31047 Genstar Road, Hayward, CA 94544, USA. Electronic address: skell@impaxlabs.com. · Impax Laboratories, Inc., 31047 Genstar Road, Hayward, CA 94544, USA. Electronic address: skhanna@impaxlabs.com. · Impax Laboratories, Inc., 31047 Genstar Road, Hayward, CA 94544, USA. Electronic address: rrubens@impaxlabs.com. · Impax Laboratories, Inc., 31047 Genstar Road, Hayward, CA 94544, USA. Electronic address: sgupta@impaxlabs.com. ·J Neurol Sci · Pubmed #28131167.

ABSTRACT: BACKGROUND: IPX066 (Rytary®; carbidopa and levodopa [CD-LD] extended-release capsules) was designed to achieve therapeutic LD plasma concentrations within 1h of dosing and maintain LD concentrations for a prolonged duration in early or advanced Parkinson's disease (PD). METHODS: In this open-label study, patients underwent 6weeks of conversion to IPX066 from their prior controlled-release (CR)±immediate-release (IR) CD-LD therapy and 6months of maintenance (with an additional 6months of IPX066 at some sites). Clinical utility was assessed at both the end of conversion and maintenance. RESULTS: Among 43 patients initiated on IPX066, 33 completed conversion. The mean LD conversion ratio was 1.8 among 30 patients previously on CR plus IR (and 1.5 among 3 previously taking CR alone). The mean IPX066 dosing frequency was 3.5times/day compared with 2.6times/day for CR plus 4.6times/day for IR previously (and 4.7times/day for CR alone). By patient and clinician global improvement ratings after 6-month maintenance, ≥43.8% of patients were much or very much improved from their previous treatment, and ≥68.8% were at least minimally improved. Adverse events were consistent with those reported in prior IPX066 studies. CONCLUSIONS: These results suggest that advanced PD patients using CR CD-LD±IR can be safely converted to IPX066, with high likelihood of achieving a stable regimen, less frequent LD dosing, and improved overall clinical benefit. TRIAL REGISTRATION: Clinicaltrials.govNCT01411137.

18 Clinical Trial Dose-Response Analysis of the Effect of Carbidopa-Levodopa Extended-Release Capsules (IPX066) in Levodopa-Naive Patients With Parkinson Disease. 2016

Mao, Zhongping Lily / Modi, Nishit B. ·Impax Specialty Pharma, a division of Impax Laboratories, Inc, Hayward, CA, USA. ·J Clin Pharmacol · Pubmed #26632091.

ABSTRACT: Parkinson disease is an age-related disorder of the central nervous system principally due to loss of dopamine-producing cells in the midbrain. Levodopa, in combination with carbidopa, is widely regarded as an effective treatment for the symptoms of Parkinson disease. A dose-response relationship is established for carbidopa-levodopa extended-release capsules (IPX066) in levodopa-naive Parkinson disease patients using a disease progression model. Unified Parkinson Disease Rating Scale (UPDRS) part II plus part III scores from 171 North American patients treated with placebo or IPX066 for approximately 30 weeks from a double-blind, parallel-group, dose-ranging study were used to develop the pharmacodynamic model. The model comprised 3 components: a linear function describing disease progression, a component describing placebo (or nonlevodopa) effects, and a component to describe the effect of levodopa. Natural disease progression in early Parkinson disease as measured by UPDRS was 11.6 units/year and faster in patients with more severe disease (Hoehn-Yahr stage 3). Maximum placebo/nonlevodopa response was 23.0% of baseline UPDRS. Maximum levodopa effect from IPX066 was 76.7% of baseline UPDRS, and the ED50 was 450 mg levodopa. Equilibration half-life for the effect compartment was 62.8 days. Increasing age increased and being female decreased equilibration half-life. The quantitative model allowed description of the entire time course of response to clinical trial intervention.

19 Clinical Trial Gastroretentive carbidopa/levodopa, DM-1992, for the treatment of advanced Parkinson's disease. 2015

Verhagen Metman, Leo / Stover, Natividad / Chen, Cuiping / Cowles, Verne E / Sweeney, Michael. ·Rush University Medical Center, Chicago, IL, USA. · University of Alabama at Birmingham, AL, USA. · Depomed Inc., Newark, CA, USA. ·Mov Disord · Pubmed #25847690.

ABSTRACT: OBJECTIVES: This study was undertaken to compare efficacy, tolerability, and pharmacokinetics of DM-1992, an extended-release formulation of carbidopa/levodopa (CD/L-dopa) with immediate-release (IR) CD/L-dopa in patients with advanced Parkinson's disease. METHODS: This randomized, open-label, crossover study included a 3-d baseline and two 10-d treatment periods. Patients with daily OFF time of 2.5 h or more taking 400 mg or more L-dopa/d in four or more divided doses were titrated to stable regimens of DM-1992 2 times per day or CD/L-dopa IR 3 times to 8 times per day. Patients were allowed to take rescue CD/L-dopa as needed. Using home diaries, patients recorded OFF time and ON time with or without troublesome dyskinesia during baseline and treatment days 7 through 9. During 12-h clinic visits on day 10, plasma samples were collected for pharmacokinetics, and motor performance was assessed hourly. RESULTS: Thirty-four patients were enrolled; mean baseline L-dopa dosage was 968 mg/d. After titration, CD/L-dopa IR was dosed 4.8 times per day and DM-1992, 2 times per day. Rescue CD/L-dopa IR was given 1.3 times during the DM-1992 arm and 0.2 times during the CD/L-dopa IR arm. The reduction from baseline in % OFF time was greater for DM-1992 compared with CD/L-dopa IR (-5.52% vs. +1.33%; P = 0.0471). At steady-state, compared with CD/L-dopa IR, DM-1992 exhibited a smoother plasma L-dopa concentration profile mostly because of a significantly higher (day 10) predose L-dopa concentration, associated with enhanced motor performance. Although more patients taking DM-1992 had one or more adverse events (AEs) than CD/L-dopa IR patients (35% vs. 15%), no pattern to the AEs was seen, nor any resulting discontinuations. CONCLUSIONS: DM-1992 was associated with a reduction in %OFF time compared with CD/L-dopa IR despite a reduced dosing frequency. Although the open-label study design and the greater number of rescue doses during the DM-1992 arm call for caution in interpreting the results, the elevated predose plasma L-dopa concentration (12 h after DM-1992 administration) lends objective support to our findings, suggesting that phase 3 studies are warranted.

20 Clinical Trial Comparison of IPX066 with carbidopa-levodopa plus entacapone in advanced PD patients. 2014

Stocchi, Fabrizio / Hsu, Ann / Khanna, Sarita / Ellenbogen, Aaron / Mahler, Andreas / Liang, Grace / Dillmann, Ulrich / Rubens, Robert / Kell, Sherron / Gupta, Suneel. ·Institute for Research and Medical Care (IRCCS) San Raffaele, Rome, Italy. Electronic address: fabrizio.stocchi@fastwebnet.it. · Impax Laboratories, Hayward, CA, USA. · Quest Research Institute, Farmington Hills, MI, USA. · Neurozentrum Achim, Niedersachsen, Germany. · The Parkinson's Institute and Clinical Center, Sunnyvale, CA, USA. · Saarland University, Homburg/Saar, Germany. ·Parkinsonism Relat Disord · Pubmed #25306200.

ABSTRACT: BACKGROUND: IPX066, an investigational extended-release carbidopa-levodopa (CD-LD) preparation, has demonstrated a rapid attainment and prolonged maintenance of therapeutic LD plasma concentrations in advanced Parkinson's disease (PD). This phase-3 crossover study assessed its efficacy and safety vs. CD-LD plus entacapone (CL + E). METHODS: At baseline, all patients had motor fluctuations despite a stable regimen of CL + E or CD-LD-entacapone combination tablets (CLE). The study included a 6-week conversion from CL + E or CLE to IPX066, followed by two 2-week, double-blind crossover treatment periods in randomized order, one on IPX066 (and placebo CL + E), the other on CL + E (and placebo IPX066), separated by 1-week open-label IPX066 treatment. The primary efficacy measure was mean percent daily "off" time during waking hours (from patient diaries). RESULTS: Of 91 randomized patients, 84 completed the study. Their median daily LD dosage was 1495 mg from IPX066 and 600 mg from CL + E, corresponding, after correction for bioavailability, to an approximately 22% higher LD exposure on IPX066. Compared with CL + E, IPX066 demonstrated a lower percent "off" time (24.0% vs. 32.5%; p < 0.0001), lower "off" time (3.8 vs. 5.2 h/day; p < 0.0001), and higher "on" time without troublesome dyskinesia (11.4 vs. 10.0 h/day; p < 0.0001). Other endpoints, including patient-reported treatment preference, also favored IPX066 (p < 0.05). During double-blind treatment, 20.2% and 13.6% of patients reported adverse events on IPX066 and CL + E, respectively. The most common were dyskinesia (4 patients), insomnia (3), and confusional state (3) for IPX066, and fall (2) for CL + E. CONCLUSIONS: In advanced PD, IPX066 showed improved efficacy, compared with CL + E, and appeared to be well tolerated.

21 Clinical Trial A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. 2014

Anonymous1120789 / Beal, M Flint / Oakes, David / Shoulson, Ira / Henchcliffe, Claire / Galpern, Wendy R / Haas, Richard / Juncos, Jorge L / Nutt, John G / Voss, Tiffini Smith / Ravina, Bernard / Shults, Clifford M / Helles, Karen / Snively, Victoria / Lew, Mark F / Griebner, Brian / Watts, Arthur / Gao, Shan / Pourcher, Emmanuelle / Bond, Louisette / Kompoliti, Katie / Agarwal, Pinky / Sia, Cherissa / Jog, Mandar / Cole, Linda / Sultana, Munira / Kurlan, Roger / Richard, Irene / Deeley, Cheryl / Waters, Cheryl H / Figueroa, Angel / Arkun, Ani / Brodsky, Matthew / Ondo, William G / Hunter, Christine B / Jimenez-Shahed, Joohi / Palao, Alicia / Miyasaki, Janis M / So, Julie / Tetrud, James / Reys, Liza / Smith, Katharine / Singer, Carlos / Blenke, Anita / Russell, David S / Cotto, Candace / Friedman, Joseph H / Lannon, Margaret / Zhang, Lin / Drasby, Edward / Kumar, Rajeev / Subramanian, Thyagarajan / Ford, Donna Stuppy / Grimes, David A / Cote, Diane / Conway, Jennifer / Siderowf, Andrew D / Evatt, Marian Leslie / Sommerfeld, Barbara / Lieberman, Abraham N / Okun, Michael S / Rodriguez, Ramon L / Merritt, Stacy / Swartz, Camille Louise / Martin, W R Wayne / King, Pamela / Stover, Natividad / Guthrie, Stephanie / Watts, Ray L / Ahmed, Anwar / Fernandez, Hubert H / Winters, Adrienna / Mari, Zoltan / Dawson, Ted M / Dunlop, Becky / Feigin, Andrew S / Shannon, Barbara / Nirenberg, Melissa Jill / Ogg, Mattson / Ellias, Samuel A / Thomas, Cathi-Ann / Frei, Karen / Bodis-Wollner, Ivan / Glazman, Sofya / Mayer, Thomas / Hauser, Robert A / Pahwa, Rajesh / Langhammer, April / Ranawaya, Ranjit / Derwent, Lorelei / Sethi, Kapil D / Farrow, Buff / Prakash, Rajan / Litvan, Irene / Robinson, Annette / Sahay, Alok / Gartner, Maureen / Hinson, Vanessa K / Markind, Samuel / Pelikan, Melisa / Perlmutter, Joel S / Hartlein, Johanna / Molho, Eric / Evans, Sharon / Adler, Charles H / Duffy, Amy / Lind, Marlene / Elmer, Lawrence / Davis, Kathy / Spears, Julia / Wilson, Stephanie / Leehey, Maureen A / Hermanowicz, Neal / Niswonger, Shari / Shill, Holly A / Obradov, Sanja / Rajput, Alex / Cowper, Marilyn / Lessig, Stephanie / Song, David / Fontaine, Deborah / Zadikoff, Cindy / Williams, Karen / Blindauer, Karen A / Bergholte, Jo / Propsom, Clara Schindler / Stacy, Mark A / Field, Joanne / Mihaila, Dragos / Chilton, Mark / Uc, Ergun Y / Sieren, Jeri / Simon, David K / Kraics, Lauren / Silver, Althea / Boyd, James T / Hamill, Robert W / Ingvoldstad, Christopher / Young, Jennifer / Thomas, Karen / Kostyk, Sandra K / Wojcieszek, Joanne / Pfeiffer, Ronald F / Panisset, Michel / Beland, Monica / Reich, Stephen G / Cines, Michelle / Zappala, Nancy / Rivest, Jean / Zweig, Richard / Lumina, L Pepper / Hilliard, Colette Lynn / Grill, Stephen / Kellermann, Marye / Tuite, Paul / Rolandelli, Susan / Kang, Un Jung / Young, Joan / Rao, Jayaraman / Cook, Maureen M / Severt, Lawrence / Boyar, Karyn. ·Department of Neurology, Weill Cornell Medical College, New York Hospital, New York. · Department of Biostatistics, University of Rochester Medical Center, Rochester, New York. · Department of Neurology, Georgetown University, Washington, DC. · National Institutes of Health, Bethesda, Maryland. · Department of Neurosciences, University of California, San Diego, La Jolla. · Department of Neurology, Emory University School of Medicine, Wesley Woods Center, Atlanta, Georgia. · Department of Neurology, Oregon Health and Science University, Portland. · Merck, New Jersey. · Biogen Idec, Cambridge, Massachusetts. · Department of Neurosciences, University of California, San Diego, La Jolla10VA Medical Center, San Diego, California. · Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles. · Department of Biostatistics, University of Rochester Medical Center, Rochester, New York12Department of Neurology, University of Rochester, Rochester, New York. · Québec Memory and Motor Skills Disorders Research Center, Clinique Sainte-Anne, Québec, Canada. · Rush University Medical Center, Chicago, Illinois. · Booth Gardner Parkinson's Care Center, EvergreenHealth, Kirkland, Washington. · London Health Sciences Centre, London, Ontario, Canada. · Overlook Medical Center, Atlantic Neuroscience Institute, Summit, New Jersey. · Department of Neurology, University of Rochester, Rochester, New York. · Columbia University Medical Center, Neurological Institute, New York, New York. · Department of Neurology, University of Texas Health Science Center at Houston. · Department of Neurology, Baylor College of Medicine, Houston, Texas. · Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada. · The Parkinson's Institute and Clinical Center, Sunnyvale, California. · Department of Neurology, University of Miami School of Medicine, Miami, Florida. · Institute for Neurodegenerative Disorders, New Haven, Connecticut. · Department of Neurology, Butler Hospital, Providence, Rhode Island26Alpert Medical School, Brown University, Providence, Rhode Island. · Department of Neurology, Butler Hospital, Providence, Rhode Island27Port City Neurology, Inc, Scarborough, Maine. · Department of Neurology, University of California, Davis, School of Medicine and Sacramento VA Medical Center, Sacramento. · Port City Neurology, Inc, Scarborough, Maine. · Colorado Neurological Institute, Englewood. · Milton S. Hershey Medical Center, Department of Neurology, Pennsylvania State Hershey College of Medicine, Hershey. · Ottawa Hospital Civic Site, Ottawa, Ontario, Canada. · Avid Radiopharmaceuticals, Philadelphia, Pennsylvania. · Department of Neurology, Emory University School of Medicine, Wesley Woods Center, Atlanta, Georgia33Atlanta VA Medical Center, Atlanta, Georgia. · Muhammad Ali Parkinson Center, Barrow Neurological Institute, St Joseph's Hospital and Medical Center, Phoenix, Arizona. · Department of Neurology, University of Florida Center for Movement Disorders and Neurorestoration, Gainesville. · Glenrose Rehabilitation Hospital, University of Alberta, Edmonton, Alberta, Canada. · Department of Neurology, University of Alabama at Birmingham. · Center for Neurological Restoration, Department of Neurology, Cleveland Clinic, Cleveland, Ohio. · Department of Neurology, Johns Hopkins University, Baltimore, Maryland. · Feinstein Institute for Medical Research, Center for Neurosciences, Manhasset, New York. · Department of Neurology, New York University Langone Medical Center, New York. · Department of Neurology, Boston University School of Medicine, Boston, Massachusetts. · The Parkinson's and Movement Disorder Institute, Fountain Valley, California. · State University of New York, Downstate Medical Center, Brooklyn, New York. · Department of Neurology, University of South Florida, Tampa. · Department of Neurology, University of Kansas Medical Center, Kansas City. · Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. · Department of Neurology, Georgia Health Science University, Augusta. · Department of Neurology, University of Louisville, Kentucky. · University of Cincinnati College of Medicine, Cincinnati, Ohio. · Department of Neurology, Medical University of South Carolina, Charleston. · Associated Neurologists, PC, Danbury, Connecticut. · Department of Neurology, Washington University in St Louis, Missouri. · Movement Disorders Center, Albany Medical Center, Albany, New York. · Parkinson's Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic, Scottsdale, Arizona. · Center for Neurological Health, University of Toledo, Toledo, Ohio. · Department of Neurology, Medical University of Ohio at Toledo. · Department of Neurology, University of Colorado Health Science Center, Denver. · Department of Neurology, University of California, Irvine Medical Center, Irvine. · Banner Sun Health Research Institute, Sun City, Arizona. · Department of Neurology, University of Saskatchewan, Royal University Hospital, Saskatchewan, Canada. · Department of Neurology, University of California, San Diego, La Jolla. · Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois. · Department of Neurology, Medical College of Wisconsin, Milwaukee. · Department of Neurology, Duke University, Durham, North Carolina. · State University of New York Upstate Medical Center and Syracuse VA Medical Center, Syracuse. · Department of Neurology, University of Iowa, Iowa City. · Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts. · Department of Neurology, University of Vermont College of Medicine, Burlington. · Department of Neurology, Ohio State University, Columbus. · Department of Neurology, Indiana University School of Medicine, Indianapolis. · Department of Neurology, University of Tennessee Health Science Center, Memphis. · Department of Neurology, CHUM-Hôpital Notre-Dame, Montréal, Québec, Canada. · Department of Neurology, University of Maryland School of Science, Baltimore. · Department of Neurology, University of Sherbrooke, Québec, Canada. · Department of Neurology, Louisiana State University Health Science Center, Shreveport. · Lewis Hall Singletary Oncology Center, Thomasville, Georgia. · Parkinson and Movement Disorders Center of Maryland, Elkridge. · Department of Neurology, University of Minnesota, Minneapolis. · Department of Neurology, University of Chicago, Chicago, Illinois. · Department of Neurology, Ochsner Clinic Foundation, New Orleans, Louisiana. · Department of Neurology, Beth Israel Medical Center, New York, New York. ·JAMA Neurol · Pubmed #24664227.

ABSTRACT: IMPORTANCE: Coenzyme Q10 (CoQ10), an antioxidant that supports mitochondrial function, has been shown in preclinical Parkinson disease (PD) models to reduce the loss of dopamine neurons, and was safe and well tolerated in early-phase human studies. A previous phase II study suggested possible clinical benefit. OBJECTIVE: To examine whether CoQ10 could slow disease progression in early PD. DESIGN, SETTING, AND PARTICIPANTS: A phase III randomized, placebo-controlled, double-blind clinical trial at 67 North American sites consisting of participants 30 years of age or older who received a diagnosis of PD within 5 years and who had the following inclusion criteria: the presence of a rest tremor, bradykinesia, and rigidity; a modified Hoehn and Yahr stage of 2.5 or less; and no anticipated need for dopaminergic therapy within 3 months. Exclusion criteria included the use of any PD medication within 60 days, the use of any symptomatic PD medication for more than 90 days, atypical or drug-induced parkinsonism, a Unified Parkinson's Disease Rating Scale (UPDRS) rest tremor score of 3 or greater for any limb, a Mini-Mental State Examination score of 25 or less, a history of stroke, the use of certain supplements, and substantial recent exposure to CoQ10. Of 696 participants screened, 78 were found to be ineligible, and 18 declined participation. INTERVENTIONS: The remaining 600 participants were randomly assigned to receive placebo, 1200 mg/d of CoQ10, or 2400 mg/d of CoQ10; all participants received 1200 IU/d of vitamin E. MAIN OUTCOMES AND MEASURES: Participants were observed for 16 months or until a disability requiring dopaminergic treatment. The prospectively defined primary outcome measure was the change in total UPDRS score (Parts I-III) from baseline to final visit. The study was powered to detect a 3-point difference between an active treatment and placebo. RESULTS: The baseline characteristics of the participants were well balanced, the mean age was 62.5 years, 66% of participants were male, and the mean baseline total UPDRS score was 22.7. A total of 267 participants required treatment (94 received placebo, 87 received 1200 mg/d of CoQ10, and 86 received 2400 mg/d of CoQ10), and 65 participants (29 who received placebo, 19 who received 1200 mg/d of CoQ10, and 17 who received 2400 mg/d of CoQ10) withdrew prematurely. Treatments were well tolerated with no safety concerns. The study was terminated after a prespecified futility criterion was reached. At study termination, both active treatment groups showed slight adverse trends relative to placebo. Adjusted mean changes (worsening) in total UPDRS scores from baseline to final visit were 6.9 points (placebo), 7.5 points (1200 mg/d of CoQ10; P = .49 relative to placebo), and 8.0 points (2400 mg/d of CoQ10; P = .21 relative to placebo). CONCLUSIONS AND RELEVANCE: Coenzyme Q10 was safe and well tolerated in this population, but showed no evidence of clinical benefit. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00740714.

22 Article Increases in institutionalization, healthcare resource utilization, and mortality risk associated with Parkinson disease psychosis: Retrospective cohort study. 2019

Wetmore, James B / Li, Suying / Yan, Heng / Irfan, Muna / Rashid, Nazia / Peng, Yi / Gilbertson, David T / Shim, Andrew. ·Chronic Disease Research Group, Hennepin Healthcare Research Institute, 701 Park Ave., Suite S4.100, Minneapolis, MN, 55415, USA; Division of Nephrology, Department of Medicine, Hennepin Healthcare, 701 Park Ave., Minneapolis, MN, 55415, USA. Electronic address: James.Wetmore@hcmed.org. · Chronic Disease Research Group, Hennepin Healthcare Research Institute, 701 Park Ave., Suite S4.100, Minneapolis, MN, 55415, USA. Electronic address: sli@cdrg.org. · Chronic Disease Research Group, Hennepin Healthcare Research Institute, 701 Park Ave., Suite S4.100, Minneapolis, MN, 55415, USA. Electronic address: hyan@cdrg.org. · Department of Neurology, Hennepin Healthcare, 701 Park Ave., Minneapolis, MN, 55415, USA. Electronic address: Irfan007@umn.edu. · Department of Pharmacy, Keck Graduate Institute, 535 Watson Dr, Claremont, CA, 91711, USA. Electronic address: nazrashidpharmd@gmail.com. · Chronic Disease Research Group, Hennepin Healthcare Research Institute, 701 Park Ave., Suite S4.100, Minneapolis, MN, 55415, USA. Electronic address: ypeng@cdrg.org. · Chronic Disease Research Group, Hennepin Healthcare Research Institute, 701 Park Ave., Suite S4.100, Minneapolis, MN, 55415, USA. Electronic address: dgilbertson@cdrg.org. · ACADIA Pharmaceuticals Inc., 3611 Valley Centre Dr., San Diego, CA, 92130, USA. Electronic address: ashim@ACADIA-Pharm.com. ·Parkinsonism Relat Disord · Pubmed #31679990.

ABSTRACT: INTRODUCTION: Patients with Parkinson disease (PD) often develop psychosis (P). The association of PDP with death and long-term custodial care (CC) has not been well studied. METHODS: Medicare Parts A, B, and D data, 2007-2015, were used to define cohorts of PD and PDP patients. PD was defined by ≥ 2 ICD-9-CM codes (332.0x) at least 30, but no more than 365, days apart, and PDP by ≥ 2 codes for psychotic symptoms. Outcomes were CC use, defined as nursing home stays of >100 consecutive days, and death. To compare the association of PDP with outcomes, PDP patients were matched to PD patients without psychosis. RESULTS: Within 1 year of PDP diagnosis, 12.1% of PDP patients used CC, versus 3.5% of non-PDP patients 1 year after the matching date; corresponding percentages at 5 years were 25.8% and 10.0%. Cumulative incidence curves for CC and for death differed significantly (P < 0.0001). PDP was associated with RRs of 3.38 (95% CI, 2.93-3.90) for CC and 1.34 (1.23-1.45) for death. Other factors associated with CC were age (3.57, 2.08-6.14, age ≥90 versus ≤70 years) and female sex (1.37, 1.18-1.58). Female sex was associated with a lower RR for death (0.76, 0.70-0.82). Health care utilization and costs were substantially higher for PDP than for non-PDP patients. CONCLUSION: In PD patients, psychosis was associated with a more than 3-fold increased risk of CC and a nearly one-third increased risk of death. Women entered CC more often than men, likely because they lived longer in the setting of PD.

23 Article Reader response: Early predictors of mortality in parkinsonism and Parkinson disease: A population-based study. 2019

Keller, David L. ·(Lomita, CA). ·Neurology · Pubmed #31383807.

ABSTRACT: -- No abstract --

24 Article Nicotine Bitartrate Reduces Falls and Freezing of Gait in Parkinson Disease: A Reanalysis. 2019

Lieberman, Abraham / Lockhart, Thurmon E / Olson, Markey C / Smith Hussain, Victoria A / Frames, Christopher W / Sadreddin, Arshia / McCauley, Margaret / Ludington, Elizabeth. ·Muhammad Ali Parkinson Center, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, United States. · Ira A. Fulton Schools of Engineering, Arizona State University, Phoenix, AZ, United States. · California Pacific Neuroscience Institute, California Pacific Medical Center, San Francisco, CA, United States. · Neuraltus Pharmaceuticals, Inc., San Bruno, CA, United States. ·Front Neurol · Pubmed #31133957.

ABSTRACT:

25 Article Patient Views on Telemedicine for Parkinson Disease. 2019

Spear, Kelsey L / Auinger, Peggy / Simone, Richard / Dorsey, E Ray / Francis, Jessica. ·Chicago Medical School, Rosalind Franklin University of Medicine & Science, North Chicago, IL, USA. · Center for Health + Technology, University of Rochester Medical Center, Rochester, NY, USA. · Simone Consulting Services, Silicon Valley, CA, USA. ·J Parkinsons Dis · Pubmed #31127732.

ABSTRACT: BACKGROUND: Telemedicine is increasingly used for Parkinson disease, but the perspectives of persons with Parkinson disease have not been systematically assessed. METHODS: We therefore conducted a national online survey, and 781 individuals with Parkinson disease responded. RESULTS: Of these, 76% indicated high interest, and 29% reported prior telemedicine experience. The top advantages included access to specialists (62%), convenience (60%), and time savings (59%). The most common disadvantages were the lack of hands-on care (69%), lack of intimacy (43%), and technical difficulties (37%). CONCLUSIONS: In this non-representative sample, interest in telemedicine was high but tempered by the concern for loss of high touch care.

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