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1.  A randomized, double-blind, placebo-controlled trial of antidepressants in Parkinson disease 
Richard, I.H. | McDermott, M.P. | Kurlan, R. | Lyness, J.M. | Como, P.G. | Pearson, N. | Factor, S.A. | Juncos, J. | Serrano Ramos, C. | Brodsky, M. | Manning, C. | Marsh, L. | Shulman, L. | Fernandez, H.H. | Black, K.J. | Panisset, M. | Christine, C.W. | Jiang, W. | Singer, C. | Horn, S. | Pfeiffer, R. | Rottenberg, D. | Slevin, J. | Elmer, L. | Press, D. | Hyson, H.C. | McDonald, W. | Richard, Irene | McDonald, William | McDermott, Michael | Como, Peter G. | Kurlan, Roger | Lyness, Jeffrey M. | Pearson, Nancy | Sommerfeld, Barbara | Deeley, Cheryl | de la Torre, Tania | Barnard, Michele | Wilson, April | Lincoln, Maryann | Damgaard, Paula | Gerstenhaber, Melissa | Dustin, Kelly | Zappala, Nancy | Swartz, Camille | Creech, Mary | Shipley, Elda | Blankenship, Samantha | Beland, Monica | Roth, Jessie | Burnette, Heather | Foxworth, Tamara | Quesada, Monica | Lloyd, Mary | Pfeiffer, Brenda | Hansen, Joy | Folie, Joy | Wagner, Renee | Spears, Julia | Taylor, Colleen | Brown, Rachel | Iguchi, Lisa | Lim, Chen | LaDonna, Kori | Megens, Julie | Menza, Matthew | Cummings, Jeffrey | Hamer, Robert | Shannon, Kathleen | Odenkirchen, Joanne | Conwit, Robin | Beck, Christopher | LaDonna, Donna | Bausch, Jan | Kim, Scott | Chismar, Ron | Quinn, Sinead | Bean, Steve | Daigneault, Susan | Lindsay, Patricia | Ross, Tori | Kompoliti, Katie
Neurology  2012;78(16):1229-1236.
Objective:
To evaluate the efficacy and safety of a selective serotonin reuptake inhibitor (SSRI) and a serotonin and norepinephrine reuptake inhibitor (SNRI) in the treatment of depression in Parkinson disease (PD).
Methods:
A total of 115 subjects with PD were enrolled at 20 sites. Subjects were randomized to receive an SSRI (paroxetine; n = 42), an SNRI (venlafaxine extended release [XR]; n = 34), or placebo (n = 39). Subjects met DSM-IV criteria for a depressive disorder, or operationally defined subsyndromal depression, and scored >12 on the first 17 items of the Hamilton Rating Scale for Depression (HAM-D). Subjects were followed for 12 weeks (6-week dosage adjustment, 6-week maintenance). Maximum daily dosages were 40 mg for paroxetine and 225 mg for venlafaxine XR. The primary outcome measure was change in the HAM-D score from baseline to week 12.
Results:
Treatment effects (relative to placebo), expressed as mean 12-week reductions in HAM-D score, were 6.2 points (97.5% confidence interval [CI] 2.2 to 10.3, p = 0.0007) in the paroxetine group and 4.2 points (97.5% CI 0.1 to 8.4, p = 0.02) in the venlafaxine XR group. No treatment effects were seen on motor function.
Conclusions:
Both paroxetine and venlafaxine XR significantly improved depression in subjects with PD. Both medications were generally safe and well tolerated and did not worsen motor function.
Classification of Evidence:
This study provides Class I evidence that paroxetine and venlafaxine XR are effective in treating depression in patients with PD.
doi:10.1212/WNL.0b013e3182516244
PMCID: PMC3324323  PMID: 22496199
2.  Ocular Motor and Sensory Function in Parkinson Disease 
Ophthalmology  2011;119(1):178-182.
Purpose
To evaluate the effect of dopaminergic medication and deep brain stimulation on ocular function in Parkinson disease (PD) and to measure vision-related quality of life in subjects with PD.
Design
Prospective comparative case series.
Participants and Controls
Twenty-seven PD and 16 control subjects were recruited.
Methods
We measured visual acuity, ocular motor function, convergence, and vision-related quality of life using the Visual Function Questionnaire–25 (VFQ-25). Visual sensory and motor measurements were made during the “on” and “off” states of PD dopaminergic treatment.
Main Outcome Measures
Convergence ability and vision related quality of life.
Results
The PD subjects had a mean age of 58.8 years; 30% were female. Their mean duration of PD was 10.9 ± 6.8 years. The control subjects had a mean age of 61.6 years; 56% were female. There was no difference in visual acuity, contrast sensitivity or color vision of the PD subjects in their “on” state compared with controls. Convergence amplitudes measured with base-out prism were significantly poorer in PD subjects compared with controls (24.1 ± 8 Δ vs 14.8 ±10.3 Δ; P=0.003). The mean composite VFQ-25 score was significantly worse in the PD subjects compared with the controls (87.1 ± 8.69 vs 96.6 ± 3.05; P=0.0001).
Comparing the PD subjects in their “on” with their “off” states, there was no difference in distance exodeviation, near exodeviation or ocular ductions. Mean convergence amplitudes and near point of convergence were better in the “on” state compared with the “off” state, 14.8±10.3 Δ vs 10.7±9.0 Δ, (P=0.0006), and 13.1±9.1 cm vs 18.1±12.2, (P=0.002), respectively.
Conclusions
Convergence ability is significantly poorer in PD subjects in both their “on” and “off” states compared with controls, but significantly improves with systemic dopaminergic treatment. Ocular motor function in PD subjects fluctuates in response to treatment, which complicates ophthalmic management. PD subjects have a significant reduction in vision-related quality of life, especially near activities, that is not associated with visual acuity.
doi:10.1016/j.ophtha.2011.06.040
PMCID: PMC3251710  PMID: 21959370
3.  Creation of an Open-Access, Mutation-Defined Fibroblast Resource for Neurological Disease Research 
PLoS ONE  2012;7(8):e43099.
Our understanding of the molecular mechanisms of many neurological disorders has been greatly enhanced by the discovery of mutations in genes linked to familial forms of these diseases. These have facilitated the generation of cell and animal models that can be used to understand the underlying molecular pathology. Recently, there has been a surge of interest in the use of patient-derived cells, due to the development of induced pluripotent stem cells and their subsequent differentiation into neurons and glia. Access to patient cell lines carrying the relevant mutations is a limiting factor for many centres wishing to pursue this research. We have therefore generated an open-access collection of fibroblast lines from patients carrying mutations linked to neurological disease. These cell lines have been deposited in the National Institute for Neurological Disorders and Stroke (NINDS) Repository at the Coriell Institute for Medical Research and can be requested by any research group for use in in vitro disease modelling. There are currently 71 mutation-defined cell lines available for request from a wide range of neurological disorders and this collection will be continually expanded. This represents a significant resource that will advance the use of patient cells as disease models by the scientific community.
doi:10.1371/journal.pone.0043099
PMCID: PMC3428297  PMID: 22952635
4.  Atomoxetine for the treatment of executive dysfunction in Parkinson’s disease 
Introduction
Executive dysfunction (ED) is a prominent and often disabling feature of cognitive impairment in Parkinson’s disease (PD). Few studies have examined treatments. Given the role of noradrenergic pathology in ED, atomoxetine, a norepinephrine reuptake inhibitor indicated for attention deficit hyperactivity disorder (ADHD), may be a potential treatment for PD-related ED.
Methods
12 patients with PD and disabling ED completed an 8-week pilot open-label, flexible dose (25 to 100 mg/day) trial of atomoxetine.
Results
On primary outcome measures, atomoxetine was associated with improved ED based on the Clinical Global Impression-Change Scale (75% positive response rate; 95% CI: 43%-95%, p<.05) and behavioral measures of ED [Frontal Systems Behavior Scale (FrSBE) Executive Dysfunction and Connors Adult ADHD Rating Scale (CAARS) inattention/memory subscales]. Adverse effects included sleep and gastrointestinal disturbances and hypomania.
Conclusion
Atomoxetine is tolerable in PD and may benefit clinical manifestations of ED, warranting further study in controlled trials.
doi:10.1002/mds.22307
PMCID: PMC2683743  PMID: 19025777
Executive Dysfunction; Parkinson’s disease; Cognition; Norepinephrine Reuptake inhibition; Atomoxetine

Results 1-4 (4)