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ABSTRACT: A range of impulse control disorders (ICDs) are reported to occur in Parkinson's disease (PD). However, alterations in brain activity at rest and during risk taking occurring with ICDs in PD are not well understood. We used both arterial spin labeling perfusion functional magnetic resonance imaging (fMRI) to directly quantify resting cerebral blood flow (CBF) and blood oxygenation level dependent (BOLD) fMRI to measure neural responses to risk taking during performance on the Balloon Analogue Risk Task (BART). Eighteen PD patients, either with a diagnosis of one or more ICDs (N = 9) or no lifetime ICD history (N = 9), participated. BOLD fMRI data demonstrated that PD patients without an ICD activate the mesocorticolimbic pathway during risk taking. Compared with non-ICD patients, ICD patients demonstrated significantly diminished BOLD activity in the right ventral striatum during risk taking and significantly reduced resting CBF in the right ventral striatum. ICDs in PD are associated with reduced right ventral striatal activity at rest and diminished striatal activation during risk taking, suggesting that a common neural mechanism may underlie ICDs in individuals with PD and those without PD. Thus, treatments for ICDs in non-PD patients warrant consideration in PD patients with ICDs. © 2010 Movement Disorder Society
Movement Disorders 08/2010; 25(11):1660 - 1669. · 4.51 Impact Factor
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Sarra Nazem BA,
Andrew D. Siderowf MD,
John E. Duda MD,
Gregory K. Brown PhD,
Tom Ten Have PhD, Matthew B. Stern MD,
Daniel Weintraub MD,
Sarra Nazem,
Andrew D. Siderowf,
John E. Duda,
Gregory K. Brown,
Tom Ten Have,
Matthew B. Stern,
Daniel Weintraub
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ABSTRACT: Parkinson's disease (PD) is a chronic, disabling illness affecting primarily the elderly and is associated with a high prevalence of depression. Although these are known risk factors for suicidal and death ideation, little is known about the prevalence and correlates of such ideation in PD. A convenience sample of 116 outpatients with idiopathic PD at two movement disorders centers were administered a modified Paykel Scale for suicidal and death ideation, as well as an extensive psychiatric, neuropsychological, and neurological battery. Univariate and multivariate logistic regression models were used to determine the correlates of suicidal or death ideation. Current death ideation (28%) or suicide ideation (11%) were present in 30% of the sample, and 4% had a lifetime suicide attempt. On univariate logistic regression analysis, increasing severity of depression (odds ratio = 2.92, 95% CI 2.01–4.24, P < 0.001), impulse control disorder (ICD) behaviors sometime during PD (odds ratio = 6.08, 95% CI 1.90–19.49, P = 0.002), and psychosis (odds ratio = 2.45, 95% CI 1.05–5.69, P = 0.04) were associated with either ideation. On multivariate logistic regression analysis, only increasing severity of depressive symptoms (odds ratio = 2.76, 95% CI 1.88–4.07, P < 0.001) predicted suicidal or death ideation. In conclusion, active suicidal or death ideation occurs in up to one-third of PD patients. Comorbid psychiatric disorders, more than PD-related disease variables, are associated with this ideation, highlighting the need for a comprehensive approach to the clinical care of PD patients. © 2008 Movement Disorder Society
Movement Disorders 08/2008; 23(11):1573 - 1579. · 4.51 Impact Factor
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ABSTRACT: Recent studies have linked dopamine agonist (DA) usage with the development of impulse control disorders (ICDs) in Parkinson's disease (PD). Little is known about optimal management strategies or the long-term outcomes of affected patients. To report on the clinical interventions and long-term outcomes of PD patients who developed an ICD after DA initiation. Subjects contacted by telephone for a follow-up interview after a mean time period of 29.2 months. They were administered a modified Minnesota Impulse Disorder Interview for compulsive buying, gambling, and sexuality, and also self-rated changes in their ICD symptomatology. Baseline and follow-up dopamine replacement therapy use was recorded and verified by chart review. Of 18 subjects, 15 (83.3%) participated in the follow-up interview. At follow-up, patients were receiving a significantly lower DA levodopa equivalent daily dosage (LEDD) (Z = −3.1, P = 0.002) and a higher daily levodopa dosage (Z = −1.9, P = 0.05), but a similar total LEDD dosage (Z = −0.47, P = 0.64) with no changes in Unified Parkinson's Disease Rating Scale motor score (Z = −1.3, P = 0.19). As part of ICD management, 12 (80.0%) patients discontinued or significantly decreased DA treatment, all of whom experienced full or partial remission of ICD symptoms by self-report, and 10 (83.3%) of whom no longer met diagnostic criteria for an ICD. For PD patients who develop an ICD in the context of DA treatment, discontinuing or significantly decreasing DA exposure, even when offset by an increase in levodopa treatment, is associated with remission of or significant reduction in ICD behaviors without worsening in motor symptoms. © 2007 Movement Disorder Society
Movement Disorders 12/2007; 23(1):75 - 80. · 4.51 Impact Factor
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Laurie J. Ozelius PhD,
Tatiana Foroud PhD,
Susanne May PhD,
Geetha Senthil PhD,
PhD Paola Sandroni MD,
Phillip A. Low MD,
Stephen Reich MD,
Amy Colcher MD, Matthew B. Stern MD,
William G. Ondo MD, [......],
William G. Ondo,
Joseph Jankovic,
Neng Huang,
Caroline M. Tanner,
Peter Novak,
Sid Gilman,
Frederick J. Marshall,
G. Frederick Wooten,
Thomas C. Chelimsky,
Clifford W. Shults
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ABSTRACT: Multiple system atrophy (MSA) is characterized clinically by Parkinsonism, cerebellar dysfunction, and autonomic impairment. Multiple mutations in the LRRK2 gene are associated with parkinsonian disorders, and the most common one, the G2019S mutation, has been found in ∼1% of sporadic cases of Parkinsonism. In a well-characterized cohort of 136 subjects with probable MSA and 110 neurologically evaluated control subjects, none carried the G2019S mutation. We conclude that the G2019S mutation in the LRRK2 gene is unlikely to be associated with MSA. © 2007 Movement Disorder Society
Movement Disorders 03/2007; 22(4):546 - 549. · 4.51 Impact Factor
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ABSTRACT: The objective of this study was to determine effect sizes for both antidepressant treatment and placebo for depression in Parkinson's disease (PD), and to compare the findings with those reported in elderly depressed patients without PD. Recent reviews have concluded that there is little empiric evidence to support the use of antidepressants in PD; however, available data has not been analyzed to determine the effect size for antidepressant treatment in PD depression. A literature review identified antidepressant studies in PD. Suitable studies were analyzed using meta-analytic techniques, and effect sizes were compared with those from antidepressant studies in elderly patients without PD. Large effect sizes were found for both active treatment and placebo in PD, but there was no difference between the two groups. In contrast, active treatment was superior to placebo in depressed elderly patients without PD. In PD, increasing age and a diagnosis of major depression were associated with better treatment response. Results also suggest that newer antidepressants are well tolerated in PD. Despite the high prevalence of depression and antidepressant use in PD, controlled treatment research has been almost nonexistent. Meta-analysis results suggest a large but nonspecific effect for depression treatment in PD. In addition, PD patients may benefit less from antidepressant treatment, particularly selective serotonin reuptake inhibitors, than do elderly patients without PD. © 2005 Movement Disorder Society
Movement Disorders 06/2005; 20(9):1161 - 1169. · 4.51 Impact Factor
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Sofia A. Oliveira PhD,
William K. Scott PhD,
Eden R. Martin PhD,
Martha A. Nance MD,
Ray L. Watts MD,
Jean P. Hubble MD,
William C. Koller MD,
Rajesh Pahwa MD, Matthew B. Stern MD,
Bradley C. Hiner MD, [......],
Gary W. Small MD,
Frank Mastaglia MD,
Jeffrey M. Stajich PA-C,
Fengyu Zhang PhD,
Michael W. Booze BS,
Michelle P. Winn MD,
Lefkos T. Middleton MD,
Jonathan L. Haines PhD,
Margaret A. Pericak-Vance PhD,
PhD Jeffery M. Vance MD
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ABSTRACT: Parkin, an E2-dependent ubiquitin protein ligase, carries pathogenic mutations in patients with autosomal recessive juvenile parkinsonism, but its role in the late-onset form of Parkinson's disease (PD) is not firmly established. Previously, we detected linkage of idiopathic PD to the region on chromosome 6 containing the Parkin gene (D6S305, logarithm of odds score, 5.47) in families with at least one subject with age at onset (AAO) younger than 40 years. Mutation analysis of the Parkin gene in the 174 multiplex families from the genomic screen and 133 additional PD families identified mutations in 18% of early-onset and 2% of late-onset families (5% of total families screened). The AAO of patients with Parkin mutations ranged from 12 to 71 years. Excluding exon 7 mutations, the mean AAO of patients with Parkin mutations was 31.5 years. However, mutations in exon 7, the first RING finger (Cys253Trp, Arg256Cys, Arg275Trp, and Asp280Asn) were observed primarily in heterozygous PD patients with a much later AAO (mean AAO, 49.2 years) but were not found in controls in this study or several previous reports (920 chromosomes). These findings suggest that mutations in Parkin contribute to the common form of PD and that heterozygous mutations, especially those lying in exon 7, act as susceptibility alleles for late-onset form of Parkinson disease. Ann Neurol 2003
Annals of Neurology 04/2003; 53(5):624 - 629. · 11.09 Impact Factor
