Bradyphrenia in Parkinson's Disease : fact or fiction?

Abstract

Is bradyphrenia in Parkinson's disease fact or fiction? The literature to date both supports and finds no evidence for bradyphrenia or slowed thinking as a specific symptom of Parkinson's disease (PD). When bradyphrenia is identified it can often be partly accounted for by co-existing variables such as age, dementia, depression, visual changes, or visual perceptual deficits. The presence or absence of bradyphrenia seems to vary with disease severity or duration. A number of research studies found that PD participants have visuospatial deficits, and one possibility is that these underlie or exacerbate bradyphrenia; that is visual bradyphrenia might only be demonstrated when a task reaches some level of visuospatial complexity. This question led to the main aim of this thesis; to explore whether visuospatial deficits account for, or exacerbate, bradyphrenia in a PD population when confounding variables (eg; age, dementia, depression) are excluded or controlled for. Twenty-eight non-demented, non-depressed PD participants and 28 Controls matched pair-wise for age, and education, were assessed on a battery of visuospatial and bradyphrenia tests. To assess visuospatial ability, the Visual Object and Space Perception Battery (VOSP), the Rey Complex Figure Test (RCFT) and the Colour Progressive Matrices (CPM) were used. To assess for bradyphrenia, two inspection time tasks were used; The Light Emitting Diode (LED) order of onset task based on research by Phillips et al. (1999), and the Pi symbol task based on research by Johnson et al. (2004). In addition, a rotated alphanumeric mirror-normal decision-making task requiring mental rotation was included. PD symptom severity, laterality of symptom severity, disease duration and the effects of L-dopa medication were assessed. Results demonstrated subtle space perception deficits on the VOSP and no deficits on the RCFT or CPM subtest A (the subtest identified as not relying on executive ability). Results on the bradyphrenia tasks were mixed. Both IT tasks confirmed the presence of bradyphrenia relative to Controls, but the mental rotation task did not. Bradyphrenia on the LED task was significantly reduced in PD participants on Levodopa medication. The other tasks were not affected by medication. Thus, the hypothesis that visuospatial deficits underlie bradyphrenia was not supported by this thesis. Indeed the finding that this group of PD participants did not demonstrate visuospatial deficits on the RCFT and CPM subtest A, when carefully matched to neurologically-normal Controls was an unexpected finding, and raises questions about previous studies that have found visuospatial deficits on the same tasks. As PD participants showed, for example, poor Rey copies, if these had not been compared to the poor copies of their pair-wise matched Controls, one might well conclude that visuospatial deficits are a symptom of PD. One possible explanation for the findings of visuospatial deficits in previous studies could be that in these studies the PD-Control matching was not exact enough. The finding that bradyphrenia is demonstrated on some tasks but not others, and is ameliorated by L-dopa in some tasks but not others, suggests that the three tests used to measure bradyphrenia in this thesis may measure different aspects of information processing. The term "bradyphrenia" is perhaps too generic a term to be of value when examining slowed cognitive processing as a symptom of PD.