Cognitive Deficits and Structural Brain Changes Associated with Dementia and Visual Hallucinations in Parkinson's Disease

Written by: Dulce M. Matamoros Columbie, PhD.

Lecture: University of Barcelona (Spain) 2012

Summary:

Cognitive impairment of different degrees and hallucinations are common complications of chronic Parkinson’s disease (PD). The pathogenesis, pathophysiology, and relationship between cognitive deficits and presence of hallucinations are not fully understood but both impact severely on overall disability and quality of life of PD patients. Cognitive impairment and dementia are the most frequently reported risk factors for visual hallucinations (VH) in PD. Similarly, most studies have found a greater prevalence of psychosis in demented versus non-demented patients with PD. However, although the relationship between VH and cognitive dysfunction is well established, it seems that the emergence of visual hallucinations is not caused directly by the presence of general cognitive impairment because not all PD patients with dementia experienced VH and association studies reported several risk factors for the development of this symptom supporting a multicausal nature of this phenomenon. The data presented in this dissertation intend to give some clues towards a better understanding of the cerebral basis and neuropsychological deficits associated with dementia and visual hallucinations in Parkinson disease patients.

The general aims of this thesis were: 1) To study in vivo structural brain changes associated with dementia and visual hallucinations in Parkinson disease patients.

2) To cognitively characterize a group of non-demented PD patients with VH in a cross-sectional and longitudinal study.

For this purpose, we carried out five studies examining cognitive functions and structural brain characteristics in PD patients using neuropsychological and MRI methods. The first and the second investigations evaluated a sample of PD patients with and without dementia. The three last studies were carried out with non-demented PD patients with and without visual hallucinations.

The results showed that the pattern of cerebral atrophy found in demented PD and PD patients with VH extends well beyond the frontostriatal circuits traditionally described to be responsible for cognitive symptoms in PD. We found grey matter atrophic changes affecting temporal and occipital regions in demented PD patients and in non-demented hallucinating PD patients. These findings stress the importance of the posterior cortical structures in the presence of cognitive impairment and VH in PD patients. We also observed a close relationship between the presence of hallucinations and progressive neuro-psychological impairment. The cognitive impairments in hallucinating PD patients were observed in complex visual functions (visuoperceptive-visuospatial skills and visual memory) as well as semantic processing (such as interpretation of perceptual information). This neuro-psychological pattern is in agreement with the atrophic changes found in our MRI study. The gray matter volume reductions involved not only secondary visual association areas but also tertiary areas implicated in the integration of semantic information.