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Background Few studies assess the relationships between nonmotor aspects of experiences of daily living and cognitive functioning in Parkinson's disease (PD). Objective To evaluate the relationships among the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) part I items and neuropsychological tests in PD.Methods: We assessed 151 PD patients with the MDS-UPDRS part I and a battery of cognitive tests focused on the following 5 cognitive domains: attention/working memory, executive functioning, recent memory, language, visuoperception. Raw scores for individual cognitive tests were transformed to z scores, and cognitive domain scores were calculated by averaging z scores within each domain. Individual items from the MDS-UPDRS part I were entered in a stepwise linear regression analysis assessing item contribution to cognitive domain scores. Results The MDS-UPDRS part I item scores for hallucinations and psychosis and light headedness on standing predicted attention/working memory domain scores (P = 0.004). These same item scores, along with apathy, depressed mood, and dopamine dysregulation syndrome, predicted executive functioning (P = 0.044). The apathy and dopamine dysregulation syndrome items predicted language (P = 0.006). In addition, the cognitive impairment and sleep items were predictors of recent memory (P = 0.031). None of the items were predictors of visuoperception (P = 0.006). Other part I items were not significantly related to cognitive domain scores. Conclusions Specific nonmotor MDS-UPDRS part I items, particularly mood, behavior, and autonomic-related items, exhibited significant relationships with cognitive domains. The highest number of items were predictive of the executive functioning domain, which is the hallmark cognitive dysfunction in PD.

Huntington's disease (HD) is characterized by motor, cognitive, and psychiatric dysfunction. HD progression causes loss of automaticity, such that previously automatic tasks require greater attentional resources. Dual-task (DT) paradigms and fast-paced gait may stress the locomotor system, revealing deficits not seen under single-task (ST). However, the impact of gait "stress tests" on HD individuals needs further investigation. Therefore, the aims of this study were to investigate whether: 1) fast-paced and dual-task walking uncover deficits in gait and turning not seen under single-task, 2) cognitive and gait outcomes relate to fall incidence, and 3) gait deficits measured with wearable inertial sensors correlate with motor symptom severity in HD as measured by the Unified Huntington's disease Rating Scale-total motor score (UHDRS-TMS). Seventeen HD (55 ± 9.7 years) and 17 age-matched controls (56.5 ± 9.3 years) underwent quantitative gait testing via a 25m, two-minute walk test with APDMTM inertial sensors. Gait was assessed under a 1) ST, self-selected pace, 2) fast-as-possible (FAP) pace, and 3) verbal fluency DT. The UHDRS-TMS and a cognitive test battery were administered, and a retrospective fall history was obtained. During ST, DT, and FAP conditions, HD participants demonstrated slower gait, shorter stride length, and greater lateral step and stride length variability compared to controls (p

Background Loss-of-function mutations in the GBA gene are associated with more severe cognitive impairment in PD, but the nature of these deficits is not well understood and whether common GBA polymorphisms influence cognitive performance in PD is not yet known. Methods We screened the GBA coding region for mutations and the E326K polymorphism in 1,369 PD patients enrolled at eight sites from the PD Cognitive Genetics Consortium. Participants underwent assessments of learning and memory (Hopkins Verbal Learning Test–Revised), working memory/executive function (Letter-Number Sequencing Test and Trail Making Test A and B), language processing (semantic and phonemic verbal fluency), visuospatial abilities (Benton Judgment of Line Orientation), and global cognitive function (MoCA). We used linear regression to test for association between genotype and cognitive performance with adjustment for important covariates and accounted for multiple testing using Bonferroni's corrections. Results Mutation carriers (n = 60; 4.4%) and E326K carriers (n = 65; 4.7%) had a higher prevalence of dementia (mutations, odds ratio = 5.1; P = 9.7 × 10−6; E326K, odds ratio = 6.4; P = 5.7 × 10−7) and lower performance on Letter-Number Sequencing (mutations, corrected P[Pc] = 9.0 × 10−4; E326K, Pc = 0.036), Trail Making B-A (mutations, Pc = 0.018; E326K, Pc = 0.018), and Benton Judgment of Line Orientation (mutations, Pc = 0.0045; E326K, Pc = 0.0013). Conclusions Both GBA mutations and E326K are associated with a distinct cognitive profile characterized by greater impairment in working memory/executive function and visuospatial abilities in PD patients. The discovery that E326K negatively impacts cognitive performance approximately doubles the proportion of PD patients we now recognize are at risk for more severe GBA-related cognitive deficits. © 2015 International Parkinson and Movement Disorder Society

Objective We examined tolerability of preoperative neuropsychological testing (the Core Assessment Program for Surgical Interventional Therapies in Parkinson's Disease [CAPSIT-PD] protocol) for DBS. We also examined factors that may influence tolerability, including fatigue, global cognitive function, depression, and patient-based characteristics. Methods In this retrospective study, we reviewed preoperative neuropsychological testing results from 35 patients who were scheduled to undergo DBS. We examined the overall tolerability of the full battery and the tolerability of each test. We placed attention on a test's placement in the fixed order of the battery to measure whether there was a clustering of poorly tolerated tests toward the end of the battery as an indication of fatigue. Spearman's rank correlation was used to determine the relationship between tolerability and (1) global cognitive function, (2) depression, and (3) patient-based characteristics. Results Fourteen subjects (40%) were able to tolerate the full battery and completed all 10 tests. The domains that were least tolerated pertained to executive function and procedural memory. There was a consistent time-based tolerability pattern that was observed. There was a significant correlation between tolerability and global cognitive function (ρ = 0.344; P = 0.043), but not depression (P = 0.197). There was a significant correlation between tolerability and age (ρ = −0.491; P = 0.003) and disease duration (ρ = −0.442; P = 0.008), but not UPDRS-III scores (P = 0.284). Conclusion Our results have shown limited tolerability of the full neuropsychological battery as outlined by the CAPSIT-PD protocol. We suggest the consideration of updating the neuropsychological assessment used in the CAPSIT-PD protocol.

Author(s): Srivatsal, S; Cholerton, B; Leverenz, JB; Wszolek, ZK; Uitti, RJ; Dickson, DW; Weintraub, D; Trojanowski, JQ; Van Deerlin, VM; Quinn, JF; Chung, KA; Peterson, AL; Factor, SA; Wood-Siverio, C; Goldman, JG; Stebbins, GT; Bernard, B; Ritz, B; Rausch, R; Espay, AJ; Revilla, FJ; Devoto, J; Rosenthal, LS; Dawson, TM; Albert, MS; Mata, IF; Hu, SC; Montine, KS; Johnson, C; Montine, TJ; Edwards, KL; Zhang, J; Zabetian, CP | Abstract: Background: Increasing evidence suggests that genetic factors play a role in the variability associated with cognitive performance in Parkinson's disease (PD). Mutations in the LRRK2 gene are the most common cause of monogenic PD; however, the cognitive profile of LRRK2-related PD is not well-characterized. Methods: A cohort of 1,447 PD patients enrolled in the PD Cognitive Genetics Consortium was screened for LRRK2 mutations and completed detailed cognitive testing. Associations between mutation carrier status and cognitive test scores were assessed using linear regression models. Results: LRRK2 mutation carriers (n=29) demonstrated better performance on the Mini Mental State Examination (P=0.03) and the Letter-Number Sequencing Test (P=0.005). A smaller proportion of LRRK2 carriers were demented (P=0.03). Conclusions: Our cross-sectional study demonstrates better performance on certain cognitive tests, as well as lower rates of dementia in LRRK2-related PD. Future longitudinal studies are needed to determine whether LRRK2 mutation carriers exhibit slower cognitive decline.

Two methods for estimating premorbid IQ were employed in a sample of 199 dementia patients and 26 control subjects: (1) the National Adult Reading Test (NART), a present ability measure, and (2) an age, sex, race, education and occupation regression formula-a demographically based estimate. The dementia sample consisted of probable Alzheimer's disease, multi-inf arct dementia and a mixture of the two. Controls consisted of the spouses of the patient sample. The patient sample was divided into three levels of dementia severity equated for age and level of education. The NART estimates in the mild and moderate/severe dementia groups differed significantly from those for the very mildly demented patients and controls. The results suggest that the applicability of the NART in estimating premorbid IQ in dementia may be limited.

Two methods were used to estimate premorbid IQ in a sample of 68 patients with mild dementia: (1) the National Adult Reading Test (NART), a present ability measure, and (2) an age, sex, race, education and occupation regression formula, a demographically based estimate (DIQ). The dementia sample consisted of probable Alzheimer's disease, multi-infarct dementia and a mixture of the two. The sample was divided into three levels of language disturbances (no language disturbance, naming or fluency disturbance, or both naming and fluency disturbance) based upon performance on the Visual Naming test and the Controlled Oral Word Association test. The NART IQ estimates in patients with one or more language disturbances were significantly lower than those in patients without language disturbances despite equivalent DIQ and Mini-Mental Status exam performance. The results suggest that the applicability of the NART to dementia patients with prominent language disturbances is limited.

Objective:To investigate atrophy of the corpus callosum on MRI in Parkinson disease (PD) and its relationship to cognitive impairment.Methods:One hundred patients with PD and 24 healthy control participants underwent clinical and neuropsychological evaluations and structural MRI brain scans. Participants with PD were classified as cognitively normal (PD-NC; n = 28), having mild cognitive impairment (PD-MCI; n = 47), or having dementia (PDD; n = 25) by Movement Disorder Society criteria. Cognitive domain (attention/working memory, executive function, memory, language, visuospatial function) z scores were calculated. With the use of FreeSurfer image processing, volumes for total corpus callosum and its subsections (anterior, midanterior, central, midposterior, posterior) were computed and normalized by total intracranial volume. Callosal volumes were compared between participants with PD and controls and among PD cognitive groups, covarying for age, sex, and PD duration and with multiple comparison corrections. Regression analyses were performed to evaluate relationships between callosal volumes and performance in cognitive domains.Results:Participants with PD had reduced corpus callosum volumes in midanterior and central regions compared to healthy controls. Participants with PDD demonstrated decreased callosal volumes involving multiple subsections spanning anterior to posterior compared to participants with PD-MCI and PD-NC. Regional callosal atrophy predicted cognitive domain performance such that central volumes were associated with the attention/working memory domain; midposterior volumes with executive function, language, and memory domains; and posterior volumes with memory and visuospatial domains.Conclusions:Notable volume loss occurs in the corpus callosum in PD, with specific neuroanatomic distributions in PDD and relationships of regional atrophy to different cognitive domains. Callosal volume loss may contribute to clinical manifestations of PD cognitive impairment.

The objective of our study was to compare Movement Disorder Society Task Force criteria for diagnosis of Parkinson's disease dementia (PDD) with the gold standard of traditional neuropsychological testing. A short checklist (Level I) and a protocol of neuropsychological tests (Level II) have been proposed by a Movement Disorder Society Task Force but not fully validated in clinical practice. Ninety-one Parkinson's disease (PD) subjects were categorized as having dementia or no dementia based on a battery of neuropsychological test results and clinical judgment. The isolated components needed for Level I and Level II diagnoses were then culled from the neuropsychological evaluations and independently used to designate PDD. Compared with traditional neuropsychological testing, the sensitivity and specificity of Level I criteria for PDD was 66.7% and 98.8%, and for Level II criteria 100% and 92.7%, respectively. Using Level II criteria, 6 additional subjects were diagnosed with PDD that were classified as having no dementia when full neuropsychological data were used for the diagnosis. These 6 subjects had more education years and were less impaired on cognitive tests. The Movement Disorder Society's Level II criteria more frequently classify subjects with PDD than does traditional neuropsychological testing. Whereas Level II criteria may overclassify subjects as having PDD, they are very accurate in ruling out dementia. Movement Disorder Society's criteria are practical and timesaving, although full neuropsychological testing may still be needed. © 2014 International Parkinson and Movement Disorder Society

Visual hallucinations are frequent, disabling complications of advanced Parkinson's disease, but their neuroanatomical basis is incompletely understood. Previous structural brain magnetic resonance imaging studies suggest volume loss in the mesial temporal lobe and limbic regions in subjects with Parkinson's disease with visual hallucinations, relative to those without visual hallucinations. However, these studies have not always controlled for the presence of cognitive impairment or dementia, which are common co-morbidities of hallucinations in Parkinson's disease and whose neuroanatomical substrates may involve mesial temporal lobe and limbic regions. Therefore, we used structural magnetic resonance imaging to examine grey matter atrophy patterns associated with visual hallucinations, comparing Parkinson's disease hallucinators to Parkinson's disease non-hallucinators of comparable cognitive function. We studied 50 subjects with Parkinson's disease: 25 classified as current and chronic visual hallucinators and 25 as non-hallucinators, who were matched for cognitive status (demented or non-demented) and age (± 3 years). Subjects underwent (i) clinical evaluations; and (ii) brain MRI scans analysed using whole-brain voxel-based morphometry techniques. Clinically, the Parkinson's disease hallucinators did not differ in their cognitive classification or performance in any of the five assessed cognitive domains, compared with the non-hallucinators. The Parkinson's disease groups also did not differ significantly in age, motor severity, medication use or duration of disease. On imaging analyses, the hallucinators, all of whom experienced visual hallucinations, exhibited grey matter atrophy with significant voxel-wise differences in the cuneus, lingual and fusiform gyri, middle occipital lobe, inferior parietal lobule, and also cingulate, paracentral, and precentral gyri, compared with the non-hallucinators. Grey matter atrophy in the hallucinators occurred predominantly in brain regions responsible for processing visuoperceptual information including the ventral 'what' and dorsal 'where' pathways, which are important in object and facial recognition and identification of spatial locations of objects, respectively. Furthermore, the structural brain changes seen on magnetic resonance imaging occurred independently of cognitive function and age. Our findings suggest that when hallucinators and non-hallucinators are similar in their cognitive performance, the neural networks involving visuoperceptual pathways, rather than the mesial temporal lobe regions, distinctively contribute to the pathophysiology of visual hallucinations and may explain their predominantly visual nature in Parkinson's disease. Identification of distinct structural MRI differences associated with hallucinations in Parkinson's disease may permit earlier detection of at-risk patients and ultimately, development of therapies specifically targeting hallucinations and visuoperceptive functions.

The recently proposed Movement Disorder Society (MDS) Task Force diagnostic criteria for mild cognitive impairment in Parkinson's disease (PD-MCI) represent a first step toward a uniform definition of PD-MCI across multiple clinical and research settings. However, several questions regarding specific criteria remain unanswered, including optimal cutoff scores by which to define impairment on neuropsychological tests. Seventy-six non-demented PD patients underwent comprehensive neuropsychological assessment and were classified as PD-MCI or PD with normal cognition (PD-NC). The concordance of PD-MCI diagnosis by MDS Task Force Level II criteria (comprehensive assessment), using a range of standard deviation (SD) cutoff scores, was compared with our consensus diagnosis of PD-MCI or PD-NC. Sensitivity, specificity, and positive and negative predictive values were examined for each cutoff score. PD-MCI subtype classification and distribution of cognitive domains impaired were evaluated. Concordance for PD-MCI diagnosis was greatest for defining impairment on neuropsychological tests using a 2 SD cutoff score below appropriate norms. This cutoff also provided the best discriminatory properties for separating PD-MCI from PD-NC compared with other cutoff scores. With the MDS PD-MCI criteria, multiple domain impairment was more frequent than single domain impairment, with predominant executive function, memory, and visuospatial function deficits. Application of the MDS Task Force PD-MCI Level II diagnostic criteria demonstrates good sensitivity and specificity at a 2 SD cutoff score. The predominance of multiple domain impairment in PD-MCI with the Level II criteria suggests not only influences of testing abnormality requirements, but also the widespread nature of cognitive deficits within PD-MCI.

Importance Parkinson disease (PD) is heterogeneous in symptom manifestation and rate of progression. Identifying factors that influence disease progression could provide mechanistic insight, improve prognostic accuracy, and elucidate novel therapeutic targets. Objective To determine whether GBA mutations and the E326K polymorphism modify PD symptom progression. Design, Setting, and Participants The entire GBA coding region was screened for mutations and E326K in 740 patients with PD enrolled at 7 sites from the PD Cognitive Genetics Consortium. Detailed longitudinal motor and cognitive assessments were performed with patients in the on state. Main Outcomes and Measures Linear regression was used to test for an association between GBA genotype and motor progression, with the Movement Disorder Society–sponsored version of the Unified Parkinson’s Disease Rating Scale Part III (MDS-UPDRS III) score at the last assessment as the outcome and GBA genotype as the independent variable, with adjustment for levodopa equivalent dose, sex, age, disease duration, MDS-UPDRS III score at the first assessment, duration of follow-up, and site. Similar methods were used to examine the association between genotype and tremor and postural instability and gait difficulty (PIGD) scores. To examine the effect of GBA genotype on cognitive progression, patients were classified into those with conversion to mild cognitive impairment or dementia during the study (progression) and those without progression. The association between GBA genotype and progression status was then tested using logistic regression, adjusting for sex, age, disease duration, duration of follow-up, years of education, and site. Results Of the total sample of 733 patients who underwent successful genotyping, 226 (30.8%) were women and 507 (69.2%) were men (mean [SD] age, 68.1 [8.8] years). The mean (SD) duration of follow-up was 3.0 (1.7) years. GBA mutations (β = 4.65; 95% CI, 1.72-7.58; P = .002), E326K (β = 3.42; 95% CI, 0.66-6.17; P = .02), and GBA variants combined as a single group (β = 4.01; 95% CI, 1.95-6.07; P = 1.5 × 10 −4 ) were associated with a more rapid decline in MDS-UPDRS III score. Combined GBA variants (β = 0.38; 95% CI, 0.23-0.53; P = .01) and E326K (β = 0.64; 95% CI, 0.43-0.86; P = .002) were associated with faster progression in PIGD scores, but not in tremor scores. A significantly higher proportion of E326K carriers (10 of 21 [47.6%]; P = .01) and GBA variant carriers (15 of 39 [38.5%]; P = .04) progressed to mild cognitive impairment or dementia. Conclusions and Relevance GBA variants predict a more rapid progression of cognitive dysfunction and motor symptoms in patients with PD, with a greater effect on PIGD than tremor. Thus, GBA variants influence the heterogeneity in symptom progression observed in PD.

Mild cognitive impairment is increasingly recognized as a construct in Parkinson's disease (PD) and occurs in about 25% of nondemented PD patients. Although executive dysfunction is the most frequent type of cognitive deficit in PD, the cognitive phenotype of PD mild cognitive impairment (PD-MCI) is broad. PD-MCI subtypes are represented by amnestic and nonamnestic domain impairment as well as single- and multiple-domain impairment. However, it is unclear whether patients with different PD-MCI subtypes also differ in other clinical characteristics in addition to cognitive profile. We studied 128 PD-MCI subjects at our Movement Disorders center, comparing clinical, motor, and behavioral characteristics across the PD-MCI subtypes. We found varying proportions of impairment subtypes: nonamnestic single domain, 47.7%; amnestic multiple domain, 24.2%; amnestic single domain, 18.8%; and nonamnestic multiple domain, 9.5%. Attentional/executive functioning and visuospatial abilities were the most frequently impaired domains. PD-MCI subtypes differed in their motor features, with nonamnestic multiple-domain PD-MCI subjects showing particularly pronounced problems with postural instability and gait. Differences among PD-MCI subtypes in age, PD duration, medication use, mood or behavioral disturbances, and vascular disease were not significant. Thus, in addition to differing cognitive profiles, PD-MCI subtypes differed in motor phenotype and severity but not in mood, behavioral, or vascular comorbidities. Greater postural instability and gait disturbances in the nonamnestic multiple-domain subtype emphasize shared nondopaminergic neural substrates of gait and cognition in PD. Furthermore, increased burden of cognitive dysfunction, rather than type of cognitive deficit, may be associated with greater motor impairment in PD-MCI.

Volumetric measures of mesial temporal lobe structures on MRI scans recently have been explored as potential biomarkers of dementia in patients with PD, with investigations primarily focused on hippocampal volume. Both in vivo MRI and postmortem tissue studies in Alzheimer's disease, however, demonstrate that the entorhinal cortex (ERC) is involved earlier in disease-related pathology than the hippocampus. The ERC, a region integral in declarative memory function, projects multimodal sensory information to the hippocampus through the perforant path. In PD, ERC atrophy, as measured on MRI, however, has received less attention, compared to hippocampal atrophy. We compared ERC and hippocampal atrophy in 12 subjects with PD dementia including memory impairment, 14 PD subjects with normal cognition, and 14 healthy controls with normal cognition using manual segmentation methods on MRI scans. Though hippocampal volumes were similar in the two PD cognitive groups, ERC volumes were substantially smaller in the demented PD subjects, compared to cognitively normal PD subjects (P < 0.05). In addition, normalized ERC and hippocampal volumes for right and left hemispheres were significantly lower in the demented PD group, compared to healthy controls. Our findings suggest that ERC atrophy differentiates demented and cognitively normal PD subjects, in contrast to hippocampal atrophy. Thus, ERC atrophy on MRI may be a potential biomarker for dementia in PD, particularly in the setting of memory impairment.

The objective of this work was to evaluate the Movement Disorders Society (MDS) Task Force-proposed screening checklist for detecting Parkinson's disease dementia (PD-D) in relation to full neuropsychological testing. An MDS Task Force has proposed diagnostic procedures for PD-D, which have not been fully validated against more extensive neuropsychological testing. PD subjects were recruited from 2 specialty centers. A neuropsychologist evaluated them for dementia as part of routine clinical care. Independent clinical neurologists administered the MDS PD-D screening checklist. Diagnosis of PD-D by the 2 methods was compared. Ninety-one PD subjects had a mean age of 66.3 (SD = 9.7) years and a mean PD duration of 8.8 (SD = 6.1) years. Seven subjects (7.7%) met all 8 screening checklist criteria from the MDS PD-D screening tool and were classified as probable PD-D. Fifteen (16.5%) subjects were classified as PD-D by full neuropsychological assessment. The screening checklist showed 100% specificity, but only 46.7% sensitivity, for diagnosing PD-D compared to the full neuropsychological assessment. PD-D cases missed by the PD-D screening tool were largely due to 2 checklist items that were not endorsed (absence of depression and Mini-Mental State Examination [MMSE] scores

The objective of this study is to assess the association between tic severity, attention deficit disorder, obsessive-compulsive behavior, and quality of life (QOL) in children with Gilles de la Tourette syndrome (GTS). GTS is a multidimensional disorder with disturbances in motor function and behavior. However, little is known about what variables are associated with QOL in these patients. We evaluated 56 outpatients with a diagnosis of GTS. The mean age was 10 (range 5-17 years). Tics were assessed with the Yale Global Tic Severity Scale (YGTSS). Behavioral scales included the Leyton Obsessional Inventory-Child Version, Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS), and Attention-Deficit/Hyperactivity Disorder (ADHD) rating scale. The patient's parent also completed the TNO-AZL Children's Quality of Life scale (TACQOL). YGTSS scores ranged from 4 to 30, indicating mild to moderate tic severity. Motor and phonic tic ratings were not correlated with QOL. However, both ADHD and OCD were significantly related to QOL. Subanalysis of ADHD subtypes demonstrated that inattentiveness but not hyperactivity predicted lower QOL. When ADHD, Leyton OCD, and tic severity were considered simultaneously, tic severity remained non-significant, while both ADHD and OCD remained significant contributors to QOL. In summary, in patients with mild to moderate GTS, QOL relates primarily to co-morbidities of ADHD and obsessive-compulsive behavior. ADHD with predominantly inattentive symptoms, rather than hyperactivity symptoms, was associated with lower QOL. To improve QOL, clinicians must consider treatments of co-morbidities among tic patients.

The optimal properties of a comprehensive (level II) neuropsychological battery for determining Parkinson's disease mild cognitive impairment (PD-MCI) by Movement Disorder Society (MDS) Task Force criteria remain unresolved.Seventy-six nondemented PD patients underwent PD-MCI classification using a consensus diagnosis and level II criteria. We examined the optimal number of tests in each of the five designated cognitive domains, identified the best tests within each domain, and determined the best overall battery for PD-MCI level II diagnosis.A battery with two tests per domain provided a highly practical, robust diagnostic assessment. Level II testing with the two best tests and impairment defined as 2 standard deviations below norms was highly sensitive and specific for PD-MCI diagnosis.Our findings strongly support the MDS Task Force Level II testing recommendations, provide a framework for creating an optimal, efficient neuropsychological test battery for PD-MCI diagnosis, and offer specific test recommendations.

Objective In subjects with psychogenic movement disorders (PMDs), we conducted a 6 month randomized, cross-over design study to assess the effect of 3 months of psychodynamic psychotherapy followed by observation by the neurologist vs. observation by the neurologist, then 3 months of psychiatric intervention. Background PMDs are often disabling but no uniformly successful treatment strategies have been identified. Short term, open label psychodynamic psychotherapy has been successful in improving PMDs but whether PMDs improve equally well with neurological observation and support has not been tested. Design Fifteen patients with PMDs were randomized to immediate vs. delayed (after 3 months) weekly psychodynamic psychotherapy for 12 weeks. During the phase without psychiatric intervention, they were monitored by the treating neurologist. Patients were assessed at baseline, 3 and 6 months. Change in their movement disorder was assessed using a clinical global impression scale change (CGI-c), depression and anxiety using the Hamilton Depression Scale (HAM-D) and Beck Anxiety Inventory (Beck-A). Results Fourteen women and one man, age 42.3 ± 11, disease duration 63.2 ± 73 months, were randomized to immediate (7 patients) or delayed (8 patients) treatment. Over the six month study, PMDs, depression and anxiety were significantly improved but time was the determinant factor without an independent effect of treatment assignment. Conclusion In this group of PMD patients, where patients were kept within the medical system and involved in a research program, PMDs as well as depression and anxiety improved, but without specific benefit time-linked to psychotherapy as opposed to neurological observation and support.

Cognitive dysfunction is one of the hallmarks of Huntington's disease (HD) and may precede the onset of motor symptoms. The Montreal Cognitive Assessment (MoCA), a brief cognitive screening instrument with high specificity and sensitivity for detecting early cognitive impairments, has not been studied in the HD population. In this study, we compare the MoCA with the mini-mental state examination (MMSE) as a screening tool for cognitive dysfunction among 53 patients with HD. The mean MMSE score was 26 +/- 2.4, and mean MoCA score was 21 +/- 4.4. Twenty-one patients (81%) of those who scoredor=26 on the MMSE had the MoCA score26. Thirty-two patients (78%) of those who scoredor=24 on the MMSE had the MoCA score24. The MoCA may be a more sensitive screening tool for cognitive impairments in HD relative to the MMSE.

The Mini-Mental State Examination (MMSE) is a commonly used test for screening cognitive impairment and dementia. The questions assess different cognitive areas such as orientation, attention, memory, language, and visuoconstruction. The MMSE is helpful in scaling cognitive impairment, documenting cognitive changes over time, and assessing the effects of therapeutic agents on cognition.

Besides the motor dysfunction, which is a well-known feature of Parkinson's disease (PD), nonmotor features affecting cognition, behavior, and mood are commonly present in PD and troublesome for both patients and caregivers. The neuropsychological assessment forms an important component of the evaluation of these nonmotor features, thereby providing screening or diagnostic tests for clinical care or research, and subsequently, longitudinal assessments of cognitive and behavioral change.

The heterogeneity within vascular dementia has made neuropsychological research in this area difficult to interpret. We studied a subtype of vascular dementia, Binswanger's disease (BD), diagnosed according to recently specified clinical and radiological criteria. Measures of episodic and semantic memory were administered to BD patients, patients with Alzheimer's disease (AD) comparable to the BD sample in dementia severity, age, and education, and normal controls. Episodic memory was more defective in AD than in BD; these patient groups were equally impaired on measures of semantic memory. The findings suggest that assessment of episodic memory may be useful in differentiating AD from BD.

Background PMD are disabling, but lack any generally accepted treatment strategies. Design/methods Ten patients with PMD received treatment with Psychodynamic Psychotherapy. Patients were assessed with psychiatric rating scales and the movement disorder was rated by a blinded rater with the Psychogenic Movement Disorder Rating Scale (PMDRS). Results Total mean PMDRS ( p =0.0195), total PMDRS function scores ( p =0.0142), Hamilton depression scores ( p =0.009), Beck anxiety scores ( p =0.002), and GAF ( p =0.0083) all improved with psychotherapeutic intervention. Conclusions Psychotherapy and appropriate use of adjunct psychiatric medication can be a successful intervention for PMD.

This paper reports findings on the respiratory/phonatory subsystems from an on-going study investigating the effect of unilateral electrostimulation of the subthalamic nucleus (STN) on different speech subsystems in people with Parkinson's disease (PD). Speech recordings were made in the medication-off state at baseline, three months post surgery with stimulation-on, and with stimulation-off, in six right-handed PD patients. Subjects completed several speech tasks. Acoustic analyses of the maximally sustained vowel phonation were reported. The results were compared to the scores of the motor section of the Unified Parkinson's Disease Rating Scale (UPDRS-III) obtained under the same conditions. Results showed that stimulation-on improved UPDRS-III scores in all six subjects. While mild improvement was observed for all subjects in the Stimulation-on condition, three subjects received left-STN stimulation showed a significant decline in vocal intensity and vowel duration from their baseline indicating the speech function was very susceptible to micro lesions due to the surgical procedure itself when the surgical site was in the dominant hemisphere.

Objective: To compare diagnostic classification differences for Parkinson9s disease dementia (PDD) patients between the new Movement Disorder Society (MDS) criteria for detecting PDD and routine neuropsychological testing. Background Diagnostic criteria for PDD have been proposed by a MDS Task Force. MDS PDD diagnosis includes criteria based on a checklist (Level 1) and additional specific criteria based on more complete neuropsychological tests (Level II). Few studies have compared outcomes of these MDS criteria to the diagnosis of PDD based on routine neuropsychological testing that does not utilize the MDS criteria. Design/Methods: Parkinson9s disease (PD) subjects were recruited from those scheduled for neuropsychological testing at two specialty PD centers. All subjects were categorized as having PDD or no PDD based on routine neuropsychological test results and clinical judgment of the neuropsychologist. In addition, Level 1 and Level II MDS diagnostic criteria for PDD were applied to each subject based on the same test results by a blinded neurologist. Results: We tested 91 PD subjects, with mean age 66.3 (SD=9.7). All subjects classified as PDD by the neuropsychologists (n = 9) were also classified as having PDD using the MDS checklist criteria (Level 1). However, there were an additional 6 subjects diagnosed with PDD using the MDS Level II criteria who were classified as having no dementia by the neuropsychologists. These 6 cases had more significantly more education (15.5 vs 10.6 years), better MMSE scores (26.33 vs 20.4), and less impairment on several cognitive tests compared to the group concordant for PDD by both MDS criteria and the neuropsychologist designation. Conclusions: MDS Level II criteria diagnoses PDD more frequently compared to routine neuropsychological testing and may be more sensitive to impairment in cases with higher education levels and where the cognitive function is not as severely impaired. Supported by: Salary support for the Rush University Medical Center study participants was provided by the Parkinson9s Disease Foundation. Disclosure: Dr. Barton has received personal compensation for activities with Teva Neurosciences, Allergan, Inc., Merz Pharma, Lundbeck Research USA, Inc., Merck-Serono, IMPAX, Allergan and Parkinson Disease Foundation. Dr. Bernard has nothing to disclose. Dr. Stebbins has received personal compensation for activities with Impax Laboratories, Inc., Ceregene, Inc., Biovail Technologies, Ltd., Santhera Pharmaceuticals, and Ingenix Pharmaceutical Services. Dr. Stebbins has received research support from the National Institutes of Health, American Cancer Society, the Michael J. Fox Foundation, and Fragile-X Foundation. Dr. Goldman has received personal compensation for activities with Movement Disorder Society, American Geriatric Society, Johns Hopkins Dystonia and Spasticity Practicum as a speaker. Dr. Goldman has received research support from the Parkinson9s Disease Foundation and the National Institute of Health. Dr. Dubois has received personal compensation for activities with Bristol-Myers Squibb, Roche, Elan, Eli Lilly, Eisai, and Janssen as a consultantDr. Dubois has received personal compensation for serving on the advisory board of Bristol-Myers Squibb, Roche, Elan, Eli Lilly, Eisai, and Janssen.Dr. Dubois has received research support from Novartis and Sanofi-Aventis. Dr. Goetz has received personal compensation for activities with Asubio Pharmaceuticals Inc., Campbell Alliance, CNS Therapeutics, Curry Rockerfeller Group, Health Advances, Impax Pharmaceuticals, Ingenix, Juvantia Pharma LTD as a consultant and participant on an advisory board. Dr. Goetz has received personal compensation in an editorial capacity for Movement Disorders and Oxford University Press. Dr. Goetz has received research support from Michael J. Fox Foundation, National Institute of Health and Parkinson9s Disease Foundation.

Background Daytime and nighttime sleep disturbances and cognitive impairment occur frequently in Parkinson's disease (PD), but little is known about the interdependence of these non-motor complications. Thus, we examined the relationships among excessive daytime sleepiness, nighttime sleep quality and cognitive impairment in PD, including severity and specific cognitive deficits. Methods Ninety-three PD patients underwent clinical and neuropsychological evaluations including the Epworth Sleepiness Scale (ESS) and Pittsburgh Sleep Quality Index (PSQI). Patients were classified as having normal cognition (PD-NC), mild cognitive impairment (PD-MCI), or dementia (PDD) using recently proposed Movement Disorder Society PD-MCI and PDD criteria. Relationships between the sleep and cognitive measures and PD cognitive groups were examined. Results The PD cohort included PD-NC ( n = 28), PD-MCI ( n = 40), and PDD ( n = 25) patients. ESS scores, as a measure of daytime sleepiness, were significantly worse ( p = 0.005) in cognitively impaired PD patients, particularly PDD patients. ESS scores correlated significantly with Mini-Mental State Examination scores and also with cognitive domain scores for attention/working memory, executive function, memory, and visuospatial function. In contrast, PSQI scores, as a measure of nighttime sleep quality, neither differed among cognitive groups nor correlated with any cognitive measures. Conclusions Daytime sleepiness in PD, but not nighttime sleep problems, is associated with cognitive impairment in PD, especially in the setting of dementia, and attention/working memory, executive function, memory, and visuospatial deficits. The presence of nighttime sleep problems is pervasive across the PD cognitive spectrum, from normal cognition to dementia, and is not independently associated with cognitive impairment or deficits in cognitive domains.

An experiment was conducted to test the validity of the ANSRI by determining whether self-report of physiological response to emotion-provoking imagery could predict individuals' patterns of physiological response to the same imagery. Fifty two undergraduate volunteers completed the ANSRI and, 2 weeks later, reconstructed their original imagery (fear, anger, sadness, joy, activity situations) while seven physiological response systems were recorded polygraphically. The ANSRI scales for a condition (e.g. fear) were entered as predictors of each electrophysiological measure recorded under that condition in Stepwise Multiple Regression Analyses. Forty-nine percent of the analyses were statistically significant (mean R = 0.52; 27% of the variance). Every electrophysiological variable was significantly predicted by the ANSRI's scales under at least one imagery condition, or by using the mean response to items across the five conditions. Cardiovascular, respiration and electrodermal measures were predicted best. Every ANSRI P scale corresponding to an electrophysiological measure was a major variable in the significant prediction of that measure in at least condition.

Background Our primary objective was to determine the relationship between global cognitive function and specific domains of gait and balance in a cohort of Parkinson’s disease (PD) subjects. In a secondary analysis, we determined whether specific cognitive domains correlated with gait and balance performance. Methods Fourteen PD subjects (mean age 61.1 ± 7.8 years) were recruited from the Rush University Medical Center Movement Disorders clinic. Subjects underwent clinical assessment using the motor subsection of the Unified Parkinson’s Disease Rating Scale (UPDRS) followed by quantitative gait and balance assessments using the APDM Mobility Lab™ system (Mobility Lab, APDM Inc., Portland, OR). Subjects completed global cognitive testing using the Mattis Dementia Rating Scale (MDRS) as well as domain specific cognitive measures. Spearman’s rho was used to assess correlations between cognitive measures and gait and balance function, with False Discovery Rate (FDR) correction for multiple comparisons. Results Global cognitive function had the strongest correlation with stride velocity (r = 0.816, p = 0.001), turn duration (r = −0.806, p = 0.001), number of steps to turn (r = −0.830, p = 0.001), and mean velocity of postural sway in the medio-lateral direction (r = −0.726, p = 0.005). A significant correlation was found between processing speed and two turning measures (turn duration, r = −0.884, p = 0.001; number of steps to turn, r = −0.954, p