Objective: We sought to establish whether patients with Parkinson's disease (PD) exhibit change in religiosity as a function of disease progression and asymmetry, medication regimens, mood dysfunction, sex, and age. Method: We assessed both controlled (conscious reflection) and automatic (semantic priming) modes of religiosity. In the main study, self-reported religiosity, cognitive, and clinical measures were assessed in 71 patients with midstage PD and 75 age-matched controls with non-neurological chronic health conditions. To understand a potential mechanism associated with change in religiosity in PD patients, we supplemented the findings with pilot investigations. The pilot included 21 PD patients and utilized a different self-report measure than that of the main study and assessed automatic activation of religious concepts both on and off levodopa. Results: The main study results demonstrated that PD patients consistently scored lower in five of six dimensions of religiosity. Multivariate linear regression demonstrated that self-reported religiosity was related to disease stage, asymmetry, and male gender. Results are discussed in the context of other neurologic correlates of religiosity. The pilot study on religious concept activation suggested that the mechanism is organic and hemisphere dependent. On/off drug testing confirmed these findings to be independent of medication effects. Gain/decay semantic modeling suggested that right and left forebrain pathways selectively mediated the time constant of gain and decay, respectively, for religious concepts. Conclusion: PD patients exhibit significant differences in both controlled and automatic access to religious concepts with mid/late-stage, male, left-onset patients most impaired in access to religious cognition. The findings indicate that aspects of religious/spiritual cognition appear related to specific cerebral structures.
|Original language||English (US)|
|Number of pages||12|
|Journal||Journal of Clinical and Experimental Neuropsychology|
|State||Published - Oct 2011|
Bibliographical noteFunding Information:
The authors thank Ariel Brown and Erica Harris for assistance in participant recruiting, testing, and data management. The authors report no conflicts of interest. This is based on work supported by the Office of Research Development, Medical Research Service, Department of Veterans Affairs and the National Institute of Deafness and other Communication Disorders (NIDCD) Grant 5RO1DC007956–03.
- Frontal lobes
- Gain/decay hypothesis
- Neurodegenerative disorders
- Semantic memory