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1. A randomized clinical trial of coenzyme Q10 and GPI-1485 in early Parkinson disease

Author

Margaret Marie Cox, Stephanie Sendek, Margaret F. Turk, Julie H. Carter, Susan C. Fagan, Lorelei Derwent, Oksana Suchowersky, Jay S. Schneider, Linda Paul, Gwyn Vernon, Stephen Gollomp, Karl Kieburtz, Debbie Baker, I. Van Bodis-Wollner, Germaine McInnes, Marian A. Perez, G. Webster Ross, Katharine Pabst, Jorge L. Juncos, Chad W. Christine, Jessie Roth, Joseph M. Savitt, Peter A LeWitt, Hubert H. Fernandez, Matthew Brodsky, Mark F. Lew, Jay M. Gorell, Natividad R. Stover, Paulo Guimaraes, Andrew Feigin, Anita Blenke, Martha Nance, Elizabeth Hayes, Andrew Siderowf, W.R. Wayne Martin, Tammie Kelsey, Susan Bennett, Sharon McCarthy, Charles H. Adler, Beverly Olsen, Pauline LeBlanc, Richard B. Dewey, Rodger J. Elble, Richard S. Burns, Carlos Singer, Amy Parsons, John W. Taylor, Tracy Stewart, Maryan DeAngelis, Barbara C. Tilley, William J. Weiner, Brad A. Racette, Wendy R. Galpern, Michael J. Aminoff, Kapil D. Sethi, Jayaraman Rao, Robert A. Hauser, Debbie Fraser, Connie Kawai, David Coffey, Kelly E. Lyons, Kristine Wernette, Becky Dunlop, Holly Delgado, Marlene Lind, Rajesh Pahwa, Chris Weaver, Ray L. Watts, Patricia Deppen, Ryan J. Uitti, Marwan N. Sabbagh, Lynn Marlor, Joann Belden, Burton L. Scott, Theresa McClain, Roger L. Albin, John Y. Fang, Zoran Obradov, Yuko Y. Palesch, Maureen Cook, Pamela Andrews, Jeana Jaglin, Joanne Wojcieszek, Mary Louise Musante Weeks, Susan Peterson, James H. Bower, Maureen A. Leehey, Joanne Field, Lisa M. Shulman, Caroline M. Tanner, Jacob I. Sage, Jordan J. Elm, Joseph Jankovic, Patrick D. Mauldin, Aileen Shinaman, Peng Huang, G. Frederick Wooten, Alicia Brocht, Gordon H. Brown, Peggy Roberge, Dorothy Shearon, Buff Dill, Margaret F. Keller, Charlene Young, Christine Hunter, Janis M. Miyasaki, Susan Torgrimson, Cornelia Kamp, Brigid Hayward, Christopher G. Goetz, Emily Kosa, Marilyn Flewellen, David Simon, Rebecca McMurray, Sue Reichwein, Jacci Bainbridge, Robert W. Hamill, Stephanie Terashita, Kathleen M. Shannon, Frederick Wooten, Danna Jennings, Shana Krstevska, and Bernard Ravina

Subjects
Male, medicine.medical_specialty, Future studies, Neurology, Ubiquinone, Coenzymes, Disease, Placebo, Tacrolimus, law.invention, chemistry.chemical_compound, Double-Blind Method, Randomized controlled trial, law, Rating scale, Internal medicine, Humans, Medicine, Aged, Coenzyme Q10, business.industry, Headache, Nausea, Parkinson Disease, Middle Aged, Clinical trial, chemistry, Physical therapy, Female, Neurology (clinical), business
Abstract

Objective: To determine if future studies of coenzyme Q10 and GPI-1485 in Parkinson disease (PD) may be warranted. Methods: We conducted a randomized, double-blind, calibrated futility clinical trial of coenzyme Q10 and GPI-1485 in early untreated PD using placebo data from the DATATOP study to establish the futility threshold. Results: The primary outcome measure (change in total Unified Parkinson's Disease Rating Scale scores over 1 year) did not meet the prespecified criteria for futility for either agent. Secondary analyses using calibration controls and other more recent placebo data question the appropriateness of the predetermined definition of futility, and suggest that a more restrictive threshold may be needed. Conclusions: Coenzyme Q10 and GPI-1485 may warrant further study in Parkinson disease, although the data are inconsistent. Additional factors (cost, availability of other agents, more recent data on placebo outcomes, other ongoing trials) should also be considered in the selection of agents for Phase III studies. NEUROLOGY 2007;68:20-28

Published
2007

2. Mutations in LRRK2 other than G2019S are rare in a north american–based sample of familial Parkinson's disease

Author

S. Chouinard, A. Kaczmarek, Susan Mendick, Sharon Evans, P. M. Conneally, Roberta Winnick, Andrew Feigin, L. Elmer, Nathan Pankratz, Barbara Shannon, E. Aiken, T. Ajax, C. Horn, Christine Hunter, J. Mannetter, Margaret F. Turk, Donald S. Higgins, Miodrag Velickovic, C. Dingmann, Maryan DeAngelis, Kapil D. Sethi, M. Marotta-Kollarus, L. Woodward, M. Stacy, Cheyl A. Halter, Karen Williams, Carolyn Peterson, Nestor Galvez-Jimenez, Margaret C. Lannon, C. Schell, Kelvin L. Chou, Tatyana Simuni, H. Poiffaut, Stewart A. Factor, H. Shill, Joseph Jankovic, Michel Panisset, Tatiana Foroud, Juliette Harris, Deborah Judd, A. Podichetty, S. Phipps, Kathy Davis, Joann Belden, V. E. Elsaesser, S. Narayan, J. Fraser, Clifford W. Shults, K. Williamson, Aileen Shinaman, S. Wilson, William C. Nichols, L. Marlor, John M. Bertoni, Joanne Wojcieszek, Cheryl Halter, Kenneth Marek, P. Ryan, Alice Rudolph, Christopher F. O'Brien, Karen Blindauer, Karyn Boyar, Jayaraman Rao, Kelly E. Lyons, Becky Dunlop, C. Costan-Toth, Lauren Seeberger, Ryan J. Uitti, Karen Marder, Stephen G. Reich, David Oakes, Lisa Scollins, Jean Hall, Joanna Hamann, Mandar Jog, Eric Siemers, E. Ohmann, E. Licari, Frederick J. Marshall, Mark Forrest Gordon, Maureen Cook, Peter A. LeWitt, Vincent Calabrese, Jeannine Petit, Diane K. Marek, Rachel Saunders-Pullman, Peggy Roberge, C. Joubert, Hubert H. Fernandez, K. Ligon, J. Carpenter, Lewis Sudarsky, J. Danielson, William C. Koller, David Simon, Michael W. Pauciulo, Danna Jennings, Joseph H. Friedman, and Cliff Shults

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Parkinson's disease, Adolescent, Glycine, Pedigree chart, Disease, Protein Serine-Threonine Kinases, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, medicine.disease_cause, Central nervous system disease, Degenerative disease, Serine, medicine, Humans, Genetic Testing, Aged, Aged, 80 and over, Family Health, Genetics, Mutation, business.industry, Parkinson Disease, Middle Aged, medicine.disease, LRRK2, nervous system diseases, Neurology, North America, Cohort, Female, Neurology (clinical), business
Abstract

A total of 956 individuals with Parkinson's disease (PD) from 430 multiplex PD pedigrees were screened for 12 previously reported, pathogenic LRRK2 mutations: R793M, L1114L, I1371V, R1441C, R1441G, R1441H, Y1699C, M1869T, I2012T, I2020T, G2385R, and IVS31 +3G > A. Previous screening identified the LRRK2 G2019S mutation in 5% of our families. Only 1 of the 12 newly screened mutations, R1441C, was detected in a single family in our patient cohort. These results indicate that, although the G2019S mutation remains the most common mutation identified in familial PD patients, other mutations in LRRK2 are infrequent.

Published
2006

3. Genome-wide linkage analysis and evidence of gene-by-gene interactions in a sample of 362 multiplex Parkinson disease families

Author

Cheryl Horn, Tatiana Foroud, Ryan J. Uitti, Maureen A. Leehey, Rachel Saunders Pullman, Lisa Scollins, Sabrina Phipps, Alice Rudolph, Tanya Simuni, Lisa M. Shulman, Julie So, Barbara Shannon, Paul J. Tuite, Joan Young, Judith Dobson, Paul Atchison, John M. Bertoni, Karen Blindauer, William C. Nichols, Janet Mannetter, Anette Nieves, William J. Weiner, Jayaraman Rao, Kelly E. Lyons, Nathan Pankratz, Paul Gordon, P. Michael Conneally, Joanna Hamman, Andrew Feigin, Susan Rolli, Brian Wulbrecht, Robyn Schacherer, Todd Ajax, Laura Good, Francis O. Walker, James Sutton, Karyn Boyar, Brad A. Racette, Juliette Harris, Melinda Meacham, Annette Kaczmarek, Mandar Jog, Lisa Giffin, Roger Kurlan, Kelli Williamson, Jeannine Petit, An Tran, Joan Werner, Anthony E. Lang, Maureen Cook, Robert L. Rodnitzky, Mayank Pathak, William C. Koller, Sharon Evans, Bala V. Manyam, Donna Schwieterman, Carolyn Peterson, Cheryl Halter, Clifford W. Shults, Marguerite Wieler, Joseph Jankovic, Vincent Calabrese, Mark Forrest Gordon, Jill R. Murrell, Neal Hermanowicz, Stewart A. Factor, Miodrag Velickovic, Theresa Derian, W.R. Wayne Martin, Galit Kleimer-Fisman, Richard B. Dewey, Shari Niswonger, Hunter Homes, J. Carpenter, Victoria Hunt, Lewis Sudarsky, Mark Stacy, Debra Berry, Claire Corwin, Sean K. Uniacke, G. David Podskalny, David Simon, Christine Hunter, Daniel D. Truong, Peggy Roberge, Kelly Dustin, Kapil D. Sethi, Brad Hutchinson, Un Jang Kang, Karen Marder, and Margaret F. Turk

Subjects
Male, Genotype, Genetic Linkage, Biology, Genome, Gene mapping, Gene interaction, Genetic linkage, Genetics, Humans, Family, Genetic Predisposition to Disease, Allele, Molecular Biology, Alleles, Genetics (clinical), X chromosome, Family Health, Chromosomes, Human, X, Chromosomes, Human, Pair 10, Genome, Human, Chromosome Mapping, Chromosome, Parkinson Disease, General Medicine, Chromosomes, Human, Pair 2, Mutation, Female, Human genome, Lod Score
Abstract

Parkinson disease (PD) is the second most common neurodegenerative disorder. We studied 754 affected individuals, comprising 425 sibling pairs, to identify PD susceptibility genes. Screening of the parkin gene was performed in a subset of the sample having earlier age of PD onset or a positive LOD score with a marker in the parkin gene. All subjects were evaluated using a rigorous neurological assessment. Two diagnostic models were considered for genome-wide, non-parametric linkage analyses. Model I included only those individuals with a more stringent diagnosis of verified PD (216 sibling pairs) and resulted in a maximum LOD score of 3.4 on chromosome 2. Model II included all affected individuals (425 sibling pairs) and yielded a LOD score of 3.1 on the X chromosome. Our large sample was then employed to test for gene-by-gene (epistatic) interactions. A genome screen using the 23 families with PD patients having a mutation in only one allele of the parkin gene detected evidence of linkage to chromosome 10 (LOD=2.3). The 85 families with a very strong family history of PD were employed in a genome screen and, in addition to strong evidence of linkage to chromosome 2 (LOD = 4.9), also produced a LOD of 2.4 on chromosome 14. A genome screen performed in the 277 families without a strong family history of PD detected linkage to chromosomes 10 (LOD = 2.4) and X (LOD = 3.2). These findings demonstrate consistent evidence of linkage to chromosomes 2 and X and also support the hypothesis that gene-by-gene interactions are important in PD susceptibility.

Published
2003

4. R1514Q substitution in Lrrk2 is not a pathogenic Parkinson's disease mutation

Author

Karen Williams, Carolyn Peterson, S. Narayan, Margaret F. Turk, Julie H. Carter, C. Schell, Carlos Singer, Chad W. Christine, Paul J. Tuite, Robyn Schacherer, J. Whetteckey, S. Phipps, Diane K. Marek, William C. Nichols, John M. Bertoni, A. H. Rajput, Kenneth Marek, An Tran, P. Ryan, J. Hevezi, Joan Werner, Kelvin L. Chou, S. Chouinard, James Sutton, Margaret C. Lannon, T. Ajax, Joan Young, Deborah Judd, L. Zelaya, David Grimes, Magali Fernandez, Theresa A. Zesiewicz, Mark Stacy, Peggy Gray, Debra Berry, Michael J. Aminoff, C. Horn, C. Costan-Toth, J. Mannetter, Patricia Simpson, Susan Rolandelli, Tatiana Foroud, T. Tra, S. Wilson, Judith Dobson, Nestor Galvez-Jimenez, Donna Schwieterman, Shirley Uy, K. Price, J. Wojcieszek, Anette Nieves, Paul Atchison, Susan Bennett, L. Klassen, A. Podichetty, Vincent Calabrese, Becky Dunlop, D. Kamp, Holly Delgado, Sandra Roque, Maureen A. Leehey, Richard Camicioli, Julie So, Jayaraman Rao, Kelly E. Lyons, Kapil D. Sethi, A. Wang, Lynn Marlor, David Oakes, S. Culver, Juan Sanchez-Ramos, L. Woodward, J. Danielson, Jeannine Petit, Joann Belden, E. Licari, M. Meacham, Deborah Fontaine, Sharon Evans, C. Stone, S. Morehouse, Christopher F. O'Brien, G. Podskalny, J. Fraser, Anthony E. Lang, W.R. Wayne Martin, Carmen Serrano, H. Poiffaut, Stewart A. Factor, Joanne Wojcieszek, S. Belber, L. Davis, C. Allen, J. Hall, Judy Richman, Joseph Jankovic, Carson Reider, Stephen G. Reich, Stephanie Thomas, Kathy Davis, Richard B. Dewey, Karen Marder, T. Demarcaida, A. Kaczmarek, Lauren Seeberger, C. Halter, Mary Lou Klimek, Donald S. Higgins, Miodrag Velickovic, Joanna Hamann, Eric Siemers, E. Ohmann, C. Dingmann, Galit Kleiner-Fisman, Shari Niswonger, Theresa Derian, Maryan DeAngelis, Aileen Shinaman, Tilak Mendis, M. Rundle, Susan Mendick, L. Giffin, Karen Blindauer, Paul Gordon, Andrew Feigin, L. Shulman, Maureen Cook, Brian Wulbrecht, Rajesh Pahwa, T. Foroud, Un Jung Kang, Arthur Watts, Oksana Suchowersky, C. Joubert, J. Vo, Mandar Jog, M. Panisset, Roberta Winnick, Ronald F. Pfeiffer, Barbara Shannon, Jean P. Hubble, Clifford W. Shults, T. Gales, Tanya Simuni, M. Wolff, Hubert H. Fernandez, Pam Andrews, Karyn Boyar, Brad A. Racette, Vicki Hunt, Christine Hunter, Daniel D. Truong, L. Good, Robert L. Rodnitzky, P. Rodriguez, Sandra K. Kostyk, T. Shirley, Cheryl Halter, Peter A LeWitt, W. Weiner, Ryan J. Uitti, Lisa Scollins, Marc L. Gordon, J. Carpenter, Alice Rudolph, Lewis Sudarsky, Robert A. Hauser, Cliff Shults, Bala V. Manyam, Francis O. Walker, Juliette Harris, Marguerite Wieler, K. Dustin, Kelli Williamson, Brenda Pfeiffer, William C. Koller, Frederick J. Marshall, V. Hagen, A. Campbell, B. Hutchinson, L. Elmer, Anja Rudolph, K. Haas, Tori Ross, Rachel Saunders-Pullman, Nathan Pankratz, E. Aiken, Mariann DiMinno, Peggy Roberge, Arif Dalvi, B. Hayward, Mayank Pathak, David Simon, Michael W. Pauciulo, Holly A. Shill, M. Marotta-Kollarus, K. Ligon, Alok Sahay, Joseph H. Friedman, Neal Hermanowicz, E. Julian-Baros, Irenita Gardiner, N. Luong, Danna Jennings, R. Kurlan, and P. M. Conneally

Subjects
Adult, Male, Parkinson's disease, Adolescent, Genotype, Arginine, Guanine, Protein Serine-Threonine Kinases, Biology, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, medicine.disease_cause, Diagnosis, Differential, chemistry.chemical_compound, Degenerative disease, medicine, Humans, Point Mutation, Aged, Aged, 80 and over, Genetics, Mutation, Substitution (logic), Adenine Nucleotide Translocator 1, Genetic Variation, Parkinson Disease, Middle Aged, medicine.disease, LRRK2, nervous system diseases, Amino Acid Substitution, Neurology, chemistry, Female, Neurology (clinical), Carrier Proteins
Abstract

Mutations in LRRK2 were first reported as causing Parkinson's disease (PD) in late 2004. Since then, approximately a dozen LRRK2 substitutions have been identified that are believed to be pathogenic mutations. The substitution of adenine for guanine at nucleotide 4541 (4541G>A) in LRRK2 was recently reported. This substitution resulted in the replacement of an arginine at position 1514 with a glutamine (R1514Q). Although this substitution was not found in a large cohort of controls, its pathogenicity could not be verified. We have now genotyped the R1514Q substitution in a sample of 954 PD patients from 429 multiplex PD families. This substitution was identified in 1.8% of the PD patients; however, the majority of the PD sibships segregating this substitution were discordant for this putative mutation. In addition, the R1514Q substitution was detected in 1.4% of neurologically evaluated, control individuals. These data suggest that the R1514Q variant is not a pathogenic LRRK2 mutation. We believe it is imperative that the causative nature of any newly identified genetic variant be determined before it is included in any panel for diagnostic testing.

Published
2007

5. Long-term outcome of early versus delayed rasagiline treatment in early Parkinson's disease

Author

Micki McCollister, Julie Hevezi, Naomi Santoni, Tracey Tam, Rajesh Pahwa, Cynthia Alcorn-Costa, Barbara Fussell, Xiaoming Lu, Cheryl Armstrong, Peggy Gray, Patricia Dyches, Jovianna N. Wellinghoff, Shaunna Caouette, James B. Osborne, William C. Koller, Tilak Mendis, Shantelle Coe, Jacqueline Nash, Shirley Uy, Howard I. Hurtig, Susan Rolli, Tracy Stewart, Judy Richman, Susan Rolandelli, William G. Ondo, Cathi A. Thomas, Melodie Moterson, Maryan DeAngelis, Sheila Everett, Mary Mathews, Linda L. Mann, Eric Molho, Lorette J. Jenkins, Jessie Roth, Sandra K. Kostyk, Deborah L. Caputo, Ali H. Rajput, Jean Ayan, Un Jung Kang, Paul Atchison, Jo Belden, Julie So, Andew Feigin, Lisa Johnston, Lawrence I. Golb, Howard H. Hurtig, Larisa I. Skrypnik, Michael J. Aminoff, J. Carpenter, Patricia Seuffert, Carlos Singer, Amy Parsons, Kapil D. Sethi, Mark Forrest Gordon, Pam King, Mary Lloyd, Katherine B. Hawthorne, Linda Klassen, Shoba Narayan, Cathy R. Anderson, Patricia Kaminski, Karen Caplan, Robert A. Hauser, Dinorah Bateman, Erica Barnabei, Cheryl Fitzer-Attas, Kellie Gelles, Tamara Gales, Joanne Wojcieszek, Robert Hauser, Teri Radam, Karen Stavris, Carolyn C. Weeks, Marlene Gerow, Connie Kawai, Tracey Borst, Caroline M. Tanner, Charles H. Adler, Mickie Welsh, Nancy Pearson, Anita Lopez, Georgia Germain, Cathy W. Allen, Marianne Ewasnishin, Lisa Tagg, Brenda Ebbitt, Myrna Schear, Jean A. Jaglin, Roberta Winnick, Dawn Miller, Nancy Saton, Suzanne W. Schuman, Davoud Mohtat, Barbara Shannon, Vincent Calabrese, Mark F. Lew, Janis M. Miyasaki, William J. Weiner, Jody Lowery, Christine Hunter, Diane Brown, Keely Haas, Paul J. Tuite, Peter A. LeWitt, Mirann DiMinno, Cheryl Cooper, Peter Novak, Robert G. Feldman, Joanne Hamann, Sharon Evans, W.R. Wayne Martin, Mark Stacy, Debra Berry, Sharon Wortzel, John M. Bertoni, Kenneth Marek, Kelli Williamson, Lisa Gauger, Cheryl Newcomb, Carolyn Peterson, K. Ligon, Stephanie Newman, Vanessa Patterson, Peggy Roberge, Arif Dalvi, Laura Sutherland, Frederick J. Marshall, Scott Cradr, Karen Betcher, Carolyn Deloa, Jean P. Hubble, Kathleen M. Shannon, Sharyn Parness, Neila Mendis, Germanine McInnes, Adrienne Baranauskas, and Irenita Gardiner

Subjects
Adult, Male, medicine.medical_specialty, Parkinson's disease, Monoamine Oxidase Inhibitors, Time Factors, Placebo, Severity of Illness Index, Drug Administration Schedule, law.invention, Central nervous system disease, Antiparkinson Agents, Levodopa, chemistry.chemical_compound, Randomized controlled trial, Double-Blind Method, law, Internal medicine, Severity of illness, medicine, Humans, Longitudinal Studies, Aged, Retrospective Studies, Rasagiline, Dose-Response Relationship, Drug, Reproducibility of Results, Retrospective cohort study, Parkinson Disease, Middle Aged, medicine.disease, Surgery, Clinical trial, Treatment Outcome, Neurology, chemistry, Indans, Quality of Life, Female, Neurology (clinical), Psychology
Abstract

The purpose of this study to compare the long-term clinical outcome of early versus delayed rasagiline treatment in early Parkinson's disease (PD). Subjects (N = 404) were randomly assigned to initial treatment with rasagiline (early-start group) or placebo for 6 months followed by rasagiline (delayed-start group) in the TEMPO study. Subjects who chose to participate in an open-label extension (N = 306) continued to receive rasagiline as well as other PD medications as needed. Average (+/-SD) duration in the study was 3.6 +/- 2.1 years; 177 subjects received rasagiline for > or =5.0 years. Over the entire 6.5-year follow-up period, the adjusted mean difference in change from baseline in total UPDRS scores was 2.5 units (SE 1.1; P = 0.021) or 16% (SE 5.7; P = 0.006) in favor of the early-start versus delayed-start rasagiline group. Although the interaction between treatment and time was significant, values for the early-start group were better than the delayed-start group across all time points. Significantly less worsening (percent change) in total UPDRS scores was observed in the early-start group at the time points 0.5, 1.5, 2.0, 3.0, 4.5, 5.0, and 5.5 years (P < 0.05). Compared to delayed start, early initiation of rasagiline provided long-term clinical benefit, even in the face of treatment with other dopaminergic agents. This might reflect enduring benefits due to neuroprotection or effects on compensatory mechanisms in early PD.

Published
2008

6. Reliability of reported age at onset for Parkinson's disease

Author

Richard B. Dewey, Andrew Feigin, Melinda Jones, Lisa Giffin, Ryan J. Uitti, Margaret F. Turk, Neal Hermanowicz, Brad Hutchinson, Tatiana Foroud, G. David Podakalny, A. Wolff, Janet Mannetter, William C. Nichols, Oksana Suchowersky, Carson Reider, David Oakes, Todd Ajax, Peter F. Castelluccio, Cheryl A. Halter, Lisa M. Shulman, Kelly Dustin, Barbara Shannon, Peggy Roberge, James Sutton, Mary Lou Klimek, and Vincent Calabresse

Subjects
Gerontology, Adult, Male, Pediatrics, medicine.medical_specialty, Parkinson's disease, Disease, Sampling Studies, Central nervous system disease, Degenerative disease, Surveys and Questionnaires, medicine, Humans, Family history, Age of Onset, Reliability (statistics), Aged, Aged, 80 and over, business.industry, Medical record, Data Collection, Siblings, Reproducibility of Results, Parkinson Disease, Middle Aged, medicine.disease, Neurology, Female, Neurology (clinical), Age of onset, business
Abstract

An individual's age at onset of Parkinson disease (PD) can be collected through a variety of sources, including medical records, family report, and clinical observation. The most common source of PD age at onset information in the research setting is family-report, which is then typically used to classify a subject as juvenile, young, or late age at onset. The reliability of the family-reported age at onset of PD has not been rigorously examined. The present study used data from individuals diagnosed with PD to evaluate the reliability of age at onset information by comparing data obtained from three sources: 1) the subject's medical records, 2) a Family History Questionnaire, and 3) a Subject History Questionnaire. Among the 149 subjects with data for all three age at onset sources, the estimated reliability was R = 0.94. Similar reliability was observed when the sample was stratified based on gender, age at examination, disease duration, first symptom of PD, and years of education. The three measures of age at onset of PD show excellent agreement, strengthening confidence in the reliability of the reported age of clinical onset for PD.

Published
2003

7. Poster 222: Vitamin D Supplementation Practices and Efficacy in Medical Center Employees

Author

Lynn A. Klanchar, David X. Cifu, Barry M. Skoblar, Peggy Roberge, Robert A. Adler, Gopi Kasturi, and Abu Qutubuddin

Subjects
medicine.medical_specialty, Rehabilitation, Vitamin d supplementation, business.industry, medicine.medical_treatment, Physical Therapy, Sports Therapy and Rehabilitation, medicine.disease, vitamin D deficiency, medicine, Physical therapy, Center (algebra and category theory), Dietary supplementation, business
Published
2008

8. Efficacy of multidisciplinary treatment program on long-term outcomes of individuals with Parkinsons disease

Author

William Carne, Peggy Roberge, Abu Qutubuddin, David X. Cifu, Mark S. Baron, Paul Marcinko, Vincent P. Calabrese, Treven C. Pickett, Kathryn L. Holloway, and Brian Mutchler

Subjects
Male, medicine.medical_specialty, Time Factors, Neurology, Parkinson's disease, medicine.medical_treatment, Psychological intervention, Neuropsychological Tests, Risk Assessment, Severity of Illness Index, Support group, Levodopa, Rating scale, Severity of illness, medicine, Humans, Physical Therapy Modalities, Aged, Probability, Retrospective Studies, Aged, 80 and over, Patient Care Team, Rehabilitation, business.industry, Parkinson Disease, Retrospective cohort study, Middle Aged, medicine.disease, Combined Modality Therapy, Treatment Outcome, Dopamine Agonists, Disease Progression, Physical therapy, Female, business, Follow-Up Studies, Program Evaluation
Abstract

We examined the impact of multidisciplinary clinical management of the Parkinson's Disease Research, Education, and Clinical Center program on Parkinson's disease progression. Initial and follow-up scores on the Part III Motor Examination subscale of the Unified Parkinson's Disease Rating Scale (UPDRS) were examined. Overall, 37 (75.5%) of the 49 patients demonstrated stable or improved UPDRS motor scores at 1- to 3-year follow-up; in the 1-year group (n = 28), 22 patients (78.6%) improved, while 6 (21.4%) worsened. In the 2-year group (n = 15), 10 (66.7%) improved, while 5 (33.3%) worsened. In the 3-year group (n = 6), 5 (83.3%) improved, while 1 (16.7%) worsened. Multidisciplinary interventions included neurology (95.9% of patients), physiatry (93.9%), nursing (87.8%), psychology (42.9%), medication changes (59.2% increases, 18.4% decreases), rehabilitation therapies (physical, occupational, speech-language, 67.3%), functional diagnostic testing (18.4%), support group (16.3%), home exercise instruction (85.7%), and disease and wellness education (81.6%). Improved and worsened patients did not significantly differ on the individual program components. Clinical implications and study limitations are discussed.

Published
2005

9. Efficacy of a multidisciplinary treatment program on one-year outcomes of individuals with Parkinson's disease

Author

Mark S. Baron, Kathryn L. Holloway, Vincent Calabrese, Paul Marcinko, Treven C. Pickett, David X. Cifu, Peggy Roberge, Brian Mutchler, Abu Qutubbudin, and William Carne

Subjects
Male, Patient Care Team, medicine.medical_specialty, Parkinson's disease, Rehabilitation, Neurology, business.industry, medicine.medical_treatment, Psychological intervention, Physical Therapy, Sports Therapy and Rehabilitation, Parkinson Disease, Disease, medicine.disease, Support group, Treatment Outcome, Rating scale, Cohort, medicine, Physical therapy, Disease Progression, Humans, Neurology (clinical), business, Aged
Abstract

The efficacy of the multidisciplinary treatment approach to the management of Parkinson's disease (PD) was examined at a regional Veteran's Administration Parkinson's Disease Research, Education and Clinical Center (PADRECC). The records of 43 consecutive individuals with PD were examined. The Unified Parkinson's Disease Rating Scale (UPDRS) was employed to assess disease progression. Changes between initial and one-year follow-up UPDRS motor functioning (Part III) scores were compared to expected disease progression from prior research. In this cohort, thirty patients (69.8%) had improved, 2 were unchanged (4.7%) and 11 patients (25.6%) had worsened at the mean 12.2-month follow-up period. The range of multidisciplinary interventions included neurology (100%), physiatrist (93%), and psychology (41.9%) visits, medication changes (60.5%), rehabilitation therapy (62.8%), functional diagnostic testing (16.3%), support group (9.3%), home exercise programs (86%), and disease and wellness education (83.7%). Statistical analyses of the individual components of the program did not demonstrate significant differences between improvers and non-improvers. Clinical implications and study limitations are discussed.

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