Aim: Correlations between motor function and frontal-executive function in Parkinson's disease (PD) have been examined previously, but correlations with other cognitive domains remain unknown. We examined the correlation between motor dysfunction and cognitive impairment with regard to their precise domains. Methods: Motor and cognitive functions were assessed in 61 patients. To assess motor function, the Unified Parkinson's Disease Rating Scale (UPDRS) was administered. The UPDRS score was assessed as general motor function with a sum of Parts II and III, and as subscores of individual motor symptoms (rigidity, tremor, akinesia and postural instability). To assess cognitive function, the Montreal Cognitive Assessment (MoCA) and the Frontal Assessment Battery (FAB) were administered. MoCA was assessed by a total score and subscores of six cognitive subdomains: visuospatial, executive, attention/concentration/working memory, language, memory and orientation. The correlation coefficients of both MoCA and FAB with patient background and motor symptoms were compared using Spearman's correlation coefficient. Results: General motor function and the subscore of postural instability showed significant negative correlations with MoCA, FAB, and the subdomains of visuospatial, executive and orientation skills. Tremor and rigidity showed no significant correlation with any cognitive assessment. Akinesia showed significant negative correlation with MoCA, and the subdomains of visuospatial and orientation skills. Conclusions: In patients with PD, specific motor and cognitive functions correlate, with particular regard to postural instability and visuospatial skills. The correlations suggest functional links between a number of cerebral cortices and subcortical structures, and a common pathophysiology for motor and cognitive impairments in PD.

Background and aim Toxic oligomeric α-synuclein (αS; O-αS) has been suggested to play a central role in the pathogenesis of Lewy body diseases such as Parkinson’s disease (PD). Cerebrospinal fluid (CSF) levels of αS, O-αS, total and phosphorylated tau, and amyloid β 1–42 (Aβ1–42) are thought to reflect the pathophysiology or clinical symptoms in PD. In this study, we examined correlations of the CSF levels of these proteins with the clinical symptoms, and with each other in drug-naïve patients with PD. Methods Twenty-seven drug-naïve patients with PD were included. Motor and cognitive functions were assessed using the Unified Parkinson’s Disease Rating Scale (UPDRS), Montreal Cognitive Assessment (MoCA), and Neurobehavioral Cognitive Status Examination (COGNISTAT). CSF levels of total αS, O-αS, Aβ1–42, total tau and tau phosphorylated at threonine 181 (P-tau181p) were measured. CSF levels of these proteins were compared with clinical assessments from the UPDRS, MoCA and COGNISTAT using Spearman correlation analysis. Spearman correlation coefficients among CSF protein levels were also evaluated. Results CSF levels of αS were negatively correlated with UPDRS part III (motor score) ( p < 0.05) and bradykinesia ( p < 0.01), and positively correlated with COGNISTAT subtest of judgement ( p < 0.01) and CSF levels of Aβ1–42 ( p < 0.001), total tau ( p < 0.001) and P-tau181p ( p < 0.01). Lower CSF levels of Aβ1–42, total tau and P-tau181p were significantly related to worsening of some motor and/or cognitive functions. The CSF level of O-αS showed no correlation with any motor and cognitive assessments or with CSF levels of the other proteins. Conclusion CSF levels of αS are correlated with some clinical symptoms and CSF levels of other pathogenic proteins in drug-naïve PD patients. These correlations suggest a central role for interaction and aggregation of αS with Aβ1–42, tau, and phosphorylated tau in the pathogenesis of PD. Although O-αS has been shown to have neurotoxic effects, CSF levels do not reflect clinical symptoms or levels of other proteins in cross-sectional assessment. Electronic supplementary material The online version of this article (10.1186/s12883-019-1346-y) contains supplementary material, which is available to authorized users.

BackgroundEffects of dopaminergic medication on executive function in patients with Parkinson’s disease (PD) are inconsistent.ObjectiveWe examined the effect of dopaminergic medication on executive function in 24 drug-naïve PD patients (de novo group) and in 21 PD patients on chronic dopaminergic medication (chronic medication group).MethodsPD patients without dementia were included in this study. For the de novo group patients, dopaminergic medication was initiated, and the dose was increased to improve motor symptoms. For the chronic medication group patients, dopaminergic medication was adjusted to relieve clinical problems. All participants were tested prior to and at 4–7 months after the drug initiation/adjustment. Executive function was assessed by using the Behavioral Assessment of the Dysexecutive Syndrome (BADS). Motor function was assessed by using the Unified Parkinson’s Disease Rating Scale (UPDRS; part III). Improvement in executive function was compared with a simultaneous change in levodopa equivalent doses (LED) of dopaminergic medication and with improvement in motor functions.ResultsThe mean standardized BADS scores showed no significant improvement in both the groups. In the de novo group, percent improvement in the standardized BADS scores showed a significant positive correlation with the LED, but not with percent improvement in UPDRS part III. In the chronic medication group, percent improvement in the standardized BADS scores was negatively correlated with change in the LED, but not with percent improvement in UPDRS part III. Multiple regression analysis using improvement in the standardized BADS score as a dependent variable and patient’s background factors (ie, age, education, disease duration, and motor and executive assessments at baseline) as independent variable showed that improvement in the executive assessment is significantly correlated with the LED only in the de novo group.ConclusionEffects of dopaminergic drug adjustment on executive function differ according to the patient’s clinical stage and depend on LED in de novo stage.

Marchiafava-Bignami disease (MBD) is a rare alcohol-associated disorder. Clinical features include not only disturbed consciousness, dysarthria, tetraparesis, astasia-abasia, and symptoms of interhemispheric disconnection as initial symptoms but also cognitive deficits as clinical outcomes. The clinical significance of cerebral microhemorrhage (CMH) has been recognized in patients with cognitive deficits; however, the presence of CMH in patients with MBD has not been emphasized. The aim of the present study was to clarify the relationship between CMH and MBD. For this purpose, we report four patients with MBD, who showed asymmetrical hypointense areas in multiple cortico-subcortical regions on susceptibility-weighted imaging (SWI). All cases had a history of chronic alcohol abuse and symmetrical lesions in the entire corpus callosum. These patients' clinical symptoms included not only coma, dysarthria, and astasia-abasia as initial symptoms but also dementia as a clinical outcome. SWI showed asymmetrical hypointense areas in the multiple cortico-subcortical regions, indicating the presence of CMH. Compared with patients with normal cognitive function, demented patients showed higher severity of CMH. Our report would indicate that CMH is an important factor indicating the severity of dementia in patients with MBD.

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