Progressive worsening of spatial and chromatic processing deficits in Parkinson disease

CONTEXT: Impairments of color discrimination (CD) and contrast sensitivity are established signs of Parkinson disease (PD), but their temporal evolution has not been studied. OBJECTIVE: To determine whether there is progressive, longitudinal deterioration of color discrimination (CD) and contrast sensitivity (CS) in PD. DESIGN: A prospective study. SETTING: Tertiary care center-based sample of PD patients without dementia with normal visual acuity (Snellen fraction >0.6 in the best eye). MAIN OUTCOME MEASURES: With a mean +/- SD interval of 19.8 +/- 2.8 months, the following tests were applied twice in 28 patients: the Lanthony D15 test and the Farnsworth Munsell 100 Hue test as tests of CD and the monocular and binocular Pelli-Robson test and the binocular Vistech tables as tests of CS. RESULTS: There was deterioration of both CD (Farnsworth Munsell 100 hue test: P =.002) and CS (binocular Vistech test at a spatial frequency of 6 cycles per degree, P<.001). Both deficits correlated with age, and the chromatic deficit additionally correlated with higher impairment of motor function (Unified Parkinson's Disease Rating Scale motor section, P =.04) and activities of daily life (Unified Parkinson's Disease Rating Scale activities of daily living section, P =.006). Patients with the highest pathologic psychiatric rating score (Brief Psychiatric Rating Scale) performed worse on both CS (P =.02) and CD (P =.01) at the second examination. CONCLUSIONS: Impairments of CD and CS in PD are progressive over time. Visual deficits may influence overall motor function and lead to enhanced motor impairment.     

Photoreceptor layer thinning in idiopathic Parkinson's disease

This study was undertaken to quantify retinal and intra‐retinal layer thicknesses in Parkinson's disease (PD), and to evaluate whether retinal structural changes may be related to altered discrimination of color vision and to severity and duration of PD disease. We examined 97 PD patients and 32 healthy controls (HC) with spectral‐domain optical coherence tomography (OCT), including intra‐retinal layer segmentation. In total, we compared 111 retinal nerve fiber layer (RNFL)‐scans and 114 macula scans from 68 PD patients with 62 RNFL and 63 macula scans from 32 HC. For clinical evaluation of disease severity, we used the Unified Parkinson's Disease Rating Scale (UPDRS) motor examination. To determine color discrimination, we performed the Farnsworth Munsell 100 Hue Test (FMT) in a subgroup of PD patients. We found significant combined outer nuclear and photoreceptor layer thinning in PD versus HC (118.6 vs. 123.5 µm, P = 0.001). Differences in RNFL, total macular volume, or the other retinal layer thicknesses were not detected. The OCT measures were not associated with disease severity, duration, or color vision. By showing photoreceptor cell layer thinning, our findings support previous in vivo and autopsy studies demonstrating retinal alterations in PD. Optical coherence tomography may help to assess morphological retinal changes in PD patients; however, the utility of OCT in routine clinical practice may be limited because many PD patients have difficulties complying with OCT investigation because of disease‐related symptoms such as tremor, axial rigidity, or cognitive impairment. © 2014 International Parkinson and Movement Disorder Society     

Color vision in Parkinson’s disease and essential tremor

Background and purpose: Decreased visual function is one of the non‐motor dysfunctions of Parkinson’s disease (PD). Recent evidences suggest that essential tremor (ET) is not ‘pure’ motor disorder and there is growing evidence that this disease is a multiple‐system disorder. In some cases, it is difficult to differentiate ET from PD. In addition, there is considerable controversy regarding the relationship between PD and ET. The objective of this study was to compare color discrimination dysfunction amongst patients with PD and ET and to investigate the clinical relevance. Methods: Case–control comparisons of 54 patients with PD, 36 patients with ET, and 34 age‐matched controls were performed. All cases underwent Farnsworth–Munsell 100 Hue test (FMT) and clinical assessments on medication. In addition, the association between color vision abnormalities and motor handicaps was investigated. Results: There were significant differences in the total error scores (TES) of the FMT amongst the three groups; patients with the PD had higher TES than the patients with ET and the controls after adjustments for age. In addition, the motor symptom severity in PD correlated with the FMT abnormalities, especially with regard to the axial symptoms. Conclusion: The results of this study suggest that color vision abnormalities may be one of the non‐motor clinical characteristics of PD‐related dysfunction in contrast to ET. In addition, the severity of axial motor symptoms was closely related to visual dysfunction. Confirmation of these findings as well as the mechanisms underlying these results requires further study.     

Cortical thinning associated with mild cognitive impairment in Parkinson's disease

The aim of this study was to investigate patterns of cortical atrophy associated with mild cognitive impairment in a large sample of nondemented Parkinson's disease (PD) patients, and its relation with specific neuropsychological deficits. Magnetic resonance imaging (MRI) and neuropsychological assessment were performed in a sample of 90 nondemented PD patients and 32 healthy controls. All underwent a neuropsychological battery including tests that assess different cognitive domains: attention and working memory, executive functions, memory, language, and visuoperceptual‐visuospatial functions. Patients were classified according to their cognitive status as PD patients without mild cognitive impairment (MCI; n = 43) and PD patients with MCI (n = 47). Freesurfer software was used to obtain maps of cortical thickness for group comparisons and correlation with neuropsychological performance. Patients with MCI showed regional cortical thinning in parietotemporal regions, increased global atrophy (global cortical thinning, total gray matter volume reduction, and ventricular enlargement), as well as significant cognitive impairment in memory, executive, and visuospatial and visuoperceptual domains. Correlation analyses showed that all neuropsychological tests were associated with cortical thinning in parietotemporal regions and to a lesser extent in frontal regions. These results provide neuroanatomic support to the concept of MCI classified according to Movement Disorders Society criteria. The posterior pattern of atrophy in temporoparietal regions could be a structural neuroimaging marker of cognitive impairment in nondemented PD patients. All of the neuropsychological tests reflected regional brain atrophy, but no specific patterns were seen corresponding to impairment in distinct cognitive domains. © 2014 International Parkinson and Movement Disorder Society     

Longitudinal brain atrophy distribution in advanced Parkinson's disease: What makes the difference in “cognitive status” converters?

We investigated the brain atrophy distribution pattern and rate of regional atrophy change in Parkinson's disease (PD) in association with the cognitive status to identify the morphological characteristics of conversion to mild cognitive impairment (MCI) and dementia (PDD). T1‐weighted longitudinal 3T MRI data (up to four follow‐up assessments) from neuropsychologically well‐characterized advanced PD patients (n = 172, 8.9 years disease duration) and healthy elderly controls (n = 85) enrolled in the LANDSCAPE study were longitudinally analyzed using a linear mixed effect model and atlas‐based volumetry and cortical thickness measures. At baseline, PD patients presented with cerebral atrophy and cortical thinning including striatum, temporoparietal regions, and primary/premotor cortex. The atrophy was already observed in “cognitively normal” PD patients (PD‐N) and was considerably more pronounced in cognitively impaired PD patients. Linear mixed effect modeling revealed almost similar rates of atrophy change in PD and controls. The group comparison at baseline between those PD‐N whose cognitive performance remained stable (n = 42) and those PD‐N patients who converted to MCI/PDD (“converter” cPD‐N, n = 26) indicated suggested cortical thinning in the anterior cingulate cortex in cPD‐N patients which was correlated with cognitive performance. Our results suggest that cortical brain atrophy has been already expanded in advanced PD patients without overt cognitive deficits while atrophy progression in late disease did not differ from “normal” aging regardless of the cognitive status. It appears that cortical atrophy begins early and progresses already in the initial disease stages emphasizing the need for therapeutic interventions already at disease onset.     

Parkinson's disease‐cognitive rating scale: A new cognitive scale specific for Parkinson's disease

Cognitive defects associated with cortical pathology may be a marker of dementia in Parkinson's disease (PD). There is a need to improve the diagnostic criteria of PD dementia (PDD) and to clarify the cognitive impairment patterns associated with PD. Current neuropsychological batteries designed for PD are focused on fronto‐subcortical deficits but are not sensitive for cortical dysfunction. We developed a new scale, the Parkinson's Disease‐Cognitive Rating Scale (PD‐CRS), that was designed to cover the full spectrum of cognitive defects associated with PD. We prospectively studied 92 PD patients [30 cognitively intact (CogInt), 30 mild cognitive impairment (MCI), 32 PDD] and 61 matched controls who completed the PD‐CRS and neuropsychological tests assessing the cognitive domains included in the PD‐CRS. Acceptability, construct validity, reliability, and the discriminative properties of the PD‐CRS were examined. The PD‐CRS included items assessing fronto‐subcortical defects and items assessing cortical dysfunction. Construct validity, test‐retest and inter‐rater reliability of PD‐CRS total scores showed an intraclass correlation coefficient >0.70. The PD‐CRS showed an excellent test accuracy to diagnose PDD (sensitivity 94%, specificity 94%). The PD‐CRS total scores and confrontation naming item scores‐assessing “cortical” dysfunction—independently differentiated PDD from non‐demented PD. Alternating verbal fluency and delayed verbal memory independently differentiated the MCI group from both controls and CogInt. The PD‐CRS appeared to be a reliable and valid PD‐specific battery that accurately diagnosed PDD and detected subtle fronto‐subcortical deficits. Performance on the PD‐CRS showed that PDD is characterized by the addition of cortical dysfunction upon a predominant and progressive fronto‐subcortical impairment. © 2008 Movement Disorder Society     

Color vision and macular recovery time in epileptic adolescents treated with valproate and carbamazepine

Visual dysfunction has been reported in patients diagnosed with epilepsy. Some of these visual disturbances may be attributable to either the disease process, or the anticonvulsant therapy prescribed to control the seizures. The aims of our study were to evaluate whether color vision and macular function are impaired in epileptic adolescents, to study if the monotherapy with valproic acid (VPA) and carbamazepine (CBZ) can affect color vision and macular function and to determine the possible relationship between color vision, retinal function and antiepileptic drugs (AEDs) dosage and their serum concentrations. We examined 45 (16 male and 29 female, mean age ± SD, 15.71 ± 2.01 years) Caucasian epileptic patients suffering from various types of cryptogenic epilepsy before the beginning of therapy and after 1 year of VPA or CBZ monotherapy and 40 sex‐ and age‐matched healthy controls. Color vision was assessed by Farnsworth Munsell (FM) 100‐hue test and total error score (TES) was evaluated. This test consists of colored caps: the testee has to arrange the caps according to their colors macular function was assessed by nyctometry evaluating initial recovery time (IRT) and summation method (SM). This test evaluates visual acuity after a period of intense illumination of macula. Analysis of variance was used to evaluate the difference between controls and patients; moreover, Pearson's correlation test have been performed. Before the beginning of therapy, there were no differences in color vision and macular function between controls and epileptic patients. After 1 year, the patients, treated with VPA or CBZ, showed a deficit in FM 100‐hue test. At nyctometry, all patients showed no significant variation of macular function between baseline evaluation and second evaluation at end of the follow‐up. Our study demonstrates that, in our group of epileptic patients, epilepsy per se does not affect color vision and retinal function. In contrast, after 1 years of therapy with VPA and CBZ these patients showed a deficit in FM 100‐hue test although nyctometry evaluation continued to be normal allowing to exclude an impairment in macular function. Further investigations are required to determine the pathophysiological alteration(s) that are at the basis of color perception defects.     

Striato‐cortical connections in Parkinson's and Alzheimer's diseases: Relation to cognition

Background : Functional connectivity is abnormal in PD and in early Alzheimer's disease. Objectives : The objective of this study was to evaluate resting‐state striato‐cortical connectivity in PD and Alzheimer's disease and assess their relation to cognitive outcomes. Groups with mild cognitive impairment as a result of different pathologies (PD vs. Alzheimer's disease) were also compared. Methods : Seed‐based connectivity of the dorsal, middle, and ventral striatum was analyzed in 111 patients using functional MRI. The correlation between connectivity at regions of between‐group differences and clinical outcomes was assessed. Results : Patients showed lower striatal connectivity than controls. Connectivity between the middle (associative) striatum and precuneus negatively correlated with executive functions in PD and with memory performance in Alzheimer's disease. PD with cognitive impairment showed decreased connectivity of the dorsal (motor) striatum when compared with early Alzheimer's disease. Conclusions : Striatal connectivity was reduced in patients when compared with controls. Similar compensatory mechanisms were employed to overcome various cognitive deficits in PD and Alzheimer's disease. © 2017 International Parkinson and Movement Disorder Society     

Decreased color discrimination and contrast sensitivity in Parkinson's disease

Patients with Parkinson's disease (PD) often complain of blurred vision or even of distinctive visual disturbances like hallucinations and illusions. Recent studies have emphasized the potential influence of primary visual deficits of color and contrast discrimination. To study primary visual function, we studied color discrimination (CD) and contrast sensitivity (CS) during 'on' medication in PD patients and compared them to non-PD subjects. Twenty one PD patients were compared to 30 age-matched controls using CD tested by the D-15 Lanthony test (D15) and the Farnsworth-Munsell 100 Hue test (FM) and CS tested by the Pelli-Robson (PL) and the Vis-Tech tables (VT). We excluded subjects with a visual acuity 相似文献   

Distinct patterns of regional cerebral glucose metabolism in Parkinson's disease with and without mild cognitive impairment

There is no consensus with regard to the clinical and neuroimaging characteristics of prodromal dementia in Parkinson's disease (PD). To delineate functional neuroimaging features of PD with mild cognitive impairment (PDMCI) and with no cognitive impairment (PDNC), we compared regional cerebral glucose metabolism (CMRglc) amongst 13 patients with PDMCI, 27 with PDNC, and 13 healthy controls. The PDNC patients had limited areas of hypometabolism in the frontal and occipital cortices. In the PDMCI patients, there were extensive areas of hypometabolism in the posterior cortical regions, including the temporo‐parieto‐occipital junction, medial parietal, and inferior temporal cortices. The present results suggest that posterior cortical dysfunction is the primary neuroimaging feature of PD patients at risk for dementia. © 2009 Movement Disorder Society     

Impaired sense of smell and color discrimination in monogenic and idiopathic Parkinson's disease

Olfaction is typically impaired in idiopathic Parkinson's disease (IPD), but its role is uncertain in monogenic PD. Diminished color discrimination has been suggested as another early sign of dopaminergic dysfunction but not been systematically studied. Furthermore, it is unknown whether both deficits are linked. We examined 100 patients with IPD, 27 manifesting mutation carriers (MC), 20 nonmanifesting mutation carriers (NMC), and 110 controls. Participants underwent a standardized neurological examination, the University of Pennsylvania Smell Identification Test (UPSIT), the Farnsworth‐Munsell (FM) color discrimination test, and mutation testing in known PD genes. The monogenic group consisted of 15 Parkin (6MC/9NMC), 17 PINK1 (10MC/7NMC), 8 LRRK2 (4MC/4NMC), 3 SNCA (MC), and 4 ATP13A2 (MC) carriers. Olfaction was most impaired in IPD (UPSIT percentiles 10.1 ± 13.5) compared with all other groups (MC 13.8 ± 11.9, NMC 19.6 ± 13.0, controls 33.8 ± 22.4). Within MC, carriers of two mutations in Parkin and PINK1 showed higher UPSIT percentiles than LRRK2 and SNCA carriers. Color discrimination was reduced in IPD (FM total error score 134.8 ± 92.7). In MC (122.4 ± 142.4), the reduction was most pronounced in LRRK2, NMC (80.0 ± 38.8) were comparable with controls (97.2 ± 61.1). UPSIT and FM scores were correlated in the control (r = ?0.305; P = 0.002) and the IPD group (r = ?0.303; P = 0.006) but not among mutation carriers. First, we confirmed olfaction and color discrimination to be impaired in IPD and suggest olfaction to be a premotor sign. Second, olfaction differed between carriers with one and two mutations in Parkin/PINK1‐associated PD. Third, olfaction and color discrimination impairment do not necessarily evolve in parallel. © 2010 Movement Disorder Society     

Olfactory performance and resting state functional connectivity in non‐demented drug naïve patients with Parkinson's disease

Olfactory performance in Parkinson's disease (PD) is closely associated with subsequent cognitive decline. In the present study, we analyzed the olfaction‐dependent functional connectivity with a hypothesis that olfactory performance would influence functional connectivity within key brain areas of PD. A total of 110 nondemented drug‐naïve patients with PD were subdivided into three groups of high score (PD‐H, n = 23), middle score (PD‐M, n = 64), and low score (PD‐L, n = 23) based on olfactory performance. We performed the resting‐state functional connectivity with seed region of interest in the posterior cingulate cortex (PCC) and caudate. An analysis of functional connectivity revealed that PD‐L patients exhibited a significant attenuation of cortical functional connectivity with the PCC in the bilateral primary sensory areas, right frontal areas, and right parietal areas compared to PD‐H or PD‐M patients. Meanwhile, PD‐L patients exhibited a significant enhancement of striatocortical functional connectivity in the bilateral occipital areas and right frontal areas compared to PD‐H or PD‐M patients. In the voxel‐wise correlation analysis, olfactory performance was positively associated with cortical functional connectivity with the PCC in similar areas of attenuated cortical connectivity in PD‐L patients relative to PD‐H patients. On the other hand, the cortical functional connectivity with the caudate was negatively correlated with olfactory performance in similar areas of increased connectivity in PD‐L patients relative to PD‐H patients. The present study demonstrated that resting state functional connectivity exhibits a distinctive pattern depending on olfactory performance, which might shed light on a meaningful relationship between olfactory impairment and cognitive dysfunction in PD. Hum Brain Mapp 36:1716–1727, 2015. © 2014 Wiley Periodicals, Inc.     

Functional brain networks and cognitive deficits in Parkinson's disease

Graph‐theoretical analyses of functional networks obtained with resting‐state functional magnetic resonance imaging (fMRI) have recently proven to be a useful approach for the study of the substrates underlying cognitive deficits in different diseases. We used this technique to investigate whether cognitive deficits in Parkinson's disease (PD) are associated with changes in global and local network measures. Thirty‐six healthy controls (HC) and 66 PD patients matched for age, sex, and education were classified as having mild cognitive impairment (MCI) or not based on performance in the three mainly affected cognitive domains in PD: attention/executive, visuospatial/visuoperceptual (VS/VP), and declarative memory. Resting‐state fMRI and graph theory analyses were used to evaluate network measures. We have found that patients with MCI had connectivity reductions predominantly affecting long‐range connections as well as increased local interconnectedness manifested as higher measures of clustering, small‐worldness, and modularity. The latter measures also tended to correlate negatively with cognitive performance in VS/VP and memory functions. Hub structure was also reorganized: normal hubs displayed reduced centrality and degree in MCI PD patients. Our study indicates that the topological properties of brain networks are changed in PD patients with cognitive deficits. Our findings provide novel data regarding the functional substrate of cognitive impairment in PD, which may prove to have value as a prognostic marker. Hum Brain Mapp 35:4620–4634, 2014. © 2014 Wiley Periodicals, Inc .     

Mild Cognitive Impairment in Parkinson’s Disease

Prospective studies conducted during the last decade have shown that the majority of patients with Parkinson’s disease (PD) develop dementia. In addition, using a variety of definitions and methods, more recent research suggests that approximately a quarter of PD patients without dementia have mild cognitive impairment (PD-MCI). Furthermore, several studies have shown that approximately 20% have MCI even at time of diagnosis of PD. The typical cognitive deficits include visuospatial, attentional, and executive deficits, but memory deficits have also been shown. The etiology of PD-MCI is not known, but it is likely that mechanisms known to contribute to dementia in PD (ie, limbic and cortical Lewy bodies, amyloid plaques, and cholinergic deficits) play a role, in addition to dysfunction of dopaminergic frontostriatal circuits. PD-MCI predicts a shorter time to dementia, and preliminary evidence suggests that this is particularly true for posterior cognitive deficits. There are currently no systematic clinical trials in PD-MCI.     

Mild cognitive impairment in old-age depression is associated with increased EEG slow-wave power

Reversible dementia in geriatric depression is known to be a risk factor for irreversible dementia. Whether just mild cognitive deficits in elderly depressed patients hold a similar risk is not known yet. It may be suggested that elderly depressed patients with mild cognitive deficits, who are prone to develop dementia, show EEG alterations similar to those observed in demented patients. We studied the relationships between cognitive performance, severity of depressive symptoms and quantitative EEG parameters in 31 unmedicated, nondemented, depressed patients aged 60 years or more. Twenty-one of the patients showed a cognitive performance characteristic of mild cognitive impairment. In these patients, the mean delta and theta power was significantly higher than in the patients without cognitive impairment. Total delta power was negatively correlated with cognitive performance. There was no relationship between cognitive performance or EEG parameters and the severity of depression.     

Cognitive impairment and resting‐state network connectivity in Parkinson's disease

The purpose of this work was to evaluate changes in the connectivity patterns of a set of cognitively relevant, dynamically interrelated brain networks in association with cognitive deficits in Parkinson's disease (PD) using resting‐state functional MRI. Sixty‐five nondemented PD patients and 36 matched healthy controls were included. Thirty‐four percent of PD patients were classified as having mild cognitive impairment (MCI) based on performance in attention/executive, visuospatial/visuoperceptual (VS/VP) and memory functions. A data‐driven approach using independent component analysis (ICA) was used to identify the default‐mode network (DMN), the dorsal attention network (DAN) and the bilateral frontoparietal networks (FPN), which were compared between groups using a dual‐regression approach controlling for gray matter atrophy. Additional seed‐based analyses using a priori defined regions of interest were used to characterize local changes in intranetwork and internetwork connectivity. Structural group comparisons through voxel‐based morphometry and cortical thickness were additionally performed to assess associated gray matter atrophy. ICA results revealed reduced connectivity between the DAN and right frontoinsular regions in MCI patients, associated with worse performance in attention/executive functions. The DMN displayed increased connectivity with medial and lateral occipito‐parietal regions in MCI patients, associated with worse VS/VP performance, and with occipital reductions in cortical thickness. In line with data‐driven results, seed‐based analyses mainly revealed reduced within‐DAN, within‐DMN and DAN‐FPN connectivity, as well as loss of normal DAN‐DMN anticorrelation in MCI patients. Our findings demonstrate differential connectivity changes affecting the networks evaluated, which we hypothesize to be related to the pathophysiological bases of different types of cognitive impairment in PD. Hum Brain Mapp, 36:199–212, 2015. © 2014 Wiley Periodicals, Inc.     

Color discrimination in schizophrenia

Neuropsychiatric conditions that involve dopaminergic depletion have been associated with color discrimination deficits along the blue-hue (tritan, or short-wavelength-sensitive) axis. Because dopamine dysregulation may be a major factor in schizophrenia, we investigated color vision in this disorder. The performance of males with schizophrenia (SZ, n = 16) and normal male control subjects (CS, n = 14) was evaluated on five measures of color discrimination. SZ made more hue discrimination errors than CS, but no pattern emerged regarding a hue-specific axis of deficit. Dosage of anti-psychotic medication was not correlated with performance on hue discrimination. These results suggest that in medicated patients with schizophrenia, the dopaminergic disturbance, which may involve system hyperactivity, does not produce tritan-specific color deficits that have been observed in disorders involving dopaminergic hypoactivity.     

Morphological cerebral correlates of CERAD test performance in mild cognitive impairment and Alzheimer's disease

The objective of this study was to investigate the association between structural cerebral changes and neuropsychological deficits in mild cognitive impairment (MCI) and Alzheimer's disease (AD). Sixty patients with MCI, 34 patients with mild to moderate AD, and 32 healthy controls underwent both extensive neuropsychological assessment (CERAD test battery) and high-resolution structural magnetic resonance imaging. We used optimized voxel based morphometry to investigate (i) differences in gray matter density between the three aforementioned groups and (ii) the putative relations of CERAD test performance with atrophic brain changes. When compared to the healthy controls, the AD patients and, to a lesser extent, patients with MCI showed significant density losses predominantly in the medial temporal lobe. Deficits in verbal fluency and word finding were significantly correlated with left fronto-temporal and left temporal (including hippocampal) changes, respectively. Decreased scores in immediate and delayed recall and in delayed recognition were associated with several cortical and subcortical sites including the parahippocampal and posterior cinguli gyri, the right thalamus, and the right hippocampus, whereas deficits in constructional praxis and constructional praxis recall referred to sites in the left thalamus and cerebellum, and the temporal cortices (bilaterally), respectively. Our findings lend further support for medial temporal lobe degeneration in MCI and AD and demonstrate that cognitive deficits as assessed on the CERAD do not simply refer to specific changes in discrete cerebral sites but rather reflect morphological alterations in widespread networks.     

Motion integration deficits are independent of magnocellular impairment in Parkinson's disease

Motion processing involves multiple hierarchical steps, from the magnocellular pathway, sensitive to high temporal frequency modulations, to subsequent motion integration within the visual cortical dorsal stream. We have tested whether motion integration deficits in mild Parkinson disease (PD) can be explained by visual deficits in earlier processing nodes. Contrast sensitivity deficits in the magnocellular pathway, were compared with speed discrimination of local dots moving in random directions, speed and direction discrimination of moving surfaces and motion integration as measured by 2D coherence thresholds (n = 27). We have found that low-level magnocellular impairment in PD does not explain deficits in subsequent steps in motion processing. High-level performance was abnormal in particular for tasks requiring perception of coherently moving surfaces. Motion coherence deficits were predictive of visuomotor impairment, corroborating a previous magnetic stimulation study in normal subjects. We conclude that dorsal stream deficits in PD have a high-level visual cortical basis independent of low-level magnocellular damage.     

Aberrant cerebral network topology and mild cognitive impairment in early Parkinson's disease

The aim of this study was to assess whether mild cognitive impairment (MCI) is associated with disruption in large‐scale structural networks in newly diagnosed, drug‐naïve patients with Parkinson's disease (PD). Graph theoretical analyses were applied to 3T MRI data from 123 PD patients and 56 controls from the Parkinson's progression markers initiative (PPMI). Thirty‐three patients were classified as having Parkinson's disease with mild cognitive impairment (PD‐MCI) using the Movement Disorders Society Task Force criteria, while the remaining 90 PD patients were classified as cognitively normal (PD‐CN). Global measures (clustering coefficient, characteristic path length, global efficiency, small‐worldness) and regional measures (regional clustering coefficient, regional efficiency, hubs) were assessed in the structural networks that were constructed based on cortical thickness and subcortical volume data. PD‐MCI patients showed a marked reduction in the average correlation strength between cortical and subcortical regions compared with controls. These patients had a larger characteristic path length and reduced global efficiency in addition to a lower regional efficiency in frontal and parietal regions compared with PD‐CN patients and controls. A reorganization of the highly connected regions in the network was observed in both groups of patients. This study shows that the earliest stages of cognitive decline in PD are associated with a disruption in the large‐scale coordination of the brain network and with a decrease of the efficiency of parallel information processing. These changes are likely to signal further cognitive decline and provide support to the role of aberrant network topology in cognitive impairment in patients with early PD. Hum Brain Mapp 36:2980–2995, 2015. © 2015 Wiley Periodicals, Inc.