Neuropsychological profiles and their correlation to motor symptoms in newly diagnosed Parkinson disease patients with mild cognitive impairment

Background & Objectives: Frontal executive dysfunction, which is hypothesized to reflect dorsolateral prefrontal function, predominates in Parkinson’s disease (PD). Visuospatial dysfunction and episodic memory deficit, which are associated with the posterior cortical area, are critical symptoms of mild cognitive impairment in PD (PD-MCI). The first aim of this study is to investigate whether dominant cognitive deficits are caused by posterior cortical dysfunction in drug naïve, de novo PD-MCI patients. The second aim is to analyze the relationship between parkinsonian motor symptoms and the cognitive domain in these patients. Methods: Newly diagnosed PD patients who had not received treatment were divided into two subgroups as follows: PD-MCI (n=39) and PD patients with normal cognition (PD-NC) (n=39). Various neuropsychological tests were performed in all of the patients. The parkinsonian motor subscores were divided into tremor, rigidity, axial impairment, bulbar dysfunction and bradykinesia by the UPDRS motor scores. Results: Verbal episodic memory (immediate recall; p = 0.0001, delayed recall; p = 0.0001, recognition; p = 0.003), visual episodic memory (immediate recall; p = 0.0001, delayed recall; p = 0.002) and visuospatial function (p = 0.046) were lower in the PD-MCI group than in the PD-NC group. In the analysis of the correlation of the motor components to the cognitive tests, impairment in visual episodic memory correlated with axial symptoms (immediate recall; r = -0.441, p = 0.021, delayed recall; r = -0.393, p = 0.042). The contrast program test correlated with bradykinesia (r = -0.479, p = 0.013) Conclusion: Episodic memory and visuospatial dysfunction, which reflect impairment of the posterior cortical area, are critical cognitive deficits, and memory impairment is correlated with the axial symptoms that are associated with non-dopaminergic pathways in newly diagnosed PD-MCI patients. Neurology Asia 2014; 19(1) : 19 – 25 Address correspondence to: Sang Jin Kim, Department of Neurology, Busan Paik Hospital, Inje University College of Medicine, Gaegeum-2 dong, Jin-gu, Busan, 614-735, South Korea. Tel: +82 51 890 6425; Fax: +82 51 895 6367; E-mail: [email protected] INTRODUCTION Although Parkinson’s disease is classically defined as a motor disorder, non-motor symptoms (NMS) are an important part of the clinical features of PD. Cognitive dysfunction is one of the NMS that could occur even in the early stages of PD, and PD patients present with a wide spectrum of cognitive dysfunction ranging from mild cognitive impairment (PD-MCI) to PD dementia (PDD). Despite the heterogeneous characteristics of cognitive deficit in PD, deficits of memory, visuospatial ability and executive functions are consistent findings, regardless of the presence or absence of dementia. Initially, some reports of cognitive impairment in PD have been focused on frontal-type dysfunction, which is associated with disconnection of the fronto-striatal circuits, particularly in newly diagnosed and nonmedicated PD patients. The frontal executive dysfunction in PD, which involves manipulation of information within the working memory, has been related to specific under activation in regions of the basal ganglia (BG) and/or frontal cortex. The executive and working memory deficits in the early stage of PD is similar to those observed in frontal lobe-damaged patients. A process leading to dementia such as PDD is associated with more posterior cortical deficits resulting in aphasia, apraxia and agnosia, which resemble deficits observed in patients with temporal lobe damage and cortical dementia. Different patterns of cognitive impairments that are associated with the various PD motor types have been reported. Bradykinesia and rigidity, which are controlled by the dopaminergic Neurology Asia March 2014 20 networks, were associated with frontal executive dysfunction. Whereas axial impairment such as postural instability, gait disturbances and/or bulbar dysfunction are associated with visuospatial function and episodic memory, which indicate dysfunction of the posterior region. Posterior cortical deficits are associated with the axial motor symptoms of PD, such as postural and gait dysfunction, that reflect a non-dopaminergic pathology. Prominent axial impairment in PD patients could be related to the faster conversion of cognitive decline in PDD. The first aim of this study is to investigate whether the cognitive deficits in newly diagnosed, drug naive PD patients with MCI are associated with temporoparietal dysfunction or frontal dysfunction. The second aim is to analyze the correlation between motor signs and cognition domains.