Midsagittal corpus callosal thickness and cognitive impairment in Parkinson's disease

Abstract

People diagnosed with Parkinson's disease (PD) can experience significant neuropsychiatric symptoms, including cognitive impairment and dementia, the neuroanatomical substrates of which are not fully characterised. Symptoms associated with cognitive impairment and dementia in PD may relate to direct structural changes to the corpus callosum via primary white matter pathology or as a secondary outcome due to the degeneration of cortical regions. Using magnetic resonance imaging, the corpus callosum can be investigated at the midsagittal plane, where it converges to a contiguous mass and is not intertwined with other tracts. The objective of this project was thus twofold: First, we investigated possible changes in the thickness of the midsagittal callosum and cortex in patients with PD with varying levels of cognitive impairment; and secondly, we investigated the relationship between the thickness of the midsagittal corpus callosum and the thickness of the cortex. Study participants included cognitively unimpaired PD participants (n = 35), PD participants with mild cognitive impairment (n = 22), PD participants with dementia (n = 17) and healthy controls (n = 27). We found thinning of the callosum in PD-related dementia compared with PD-related mild cognitive impairment and cognitively unimpaired PD participants. Regression analyses found thickness of the left medial orbitofrontal cortex to be positively correlated with thickness of the anterior callosum in PD-related mild cognitive impairment. This study suggests that a midsagittal thickness model can uncover changes to the corpus callosum in PD-related dementia, which occur in line with changes to the cortex in this advanced disease stage.

Keywords: Parkinson's disease; corpus callosum; dementia; mild cognitive impairment.

FIGURE 1

Generation of mid‐sagittal thickness streamlines. (a) Mid‐sagittal callosal segmentation in an example subject; (b) non‐overlapping cross‐sectional contour lengths (streamlines) numbered from 0 at the intersection of the inferior and superior contours of the corpus callosum, moving anteriorly to node 100 at the most rostral end of the corpus callosum; (c) thickness of each streamline at the 100 nodes

FIGURE 2

Summary corpus callosum thickness profiles for all experimental groups. Streamline data represent the estimated averages for each group after controlling for head size and age, with error bars representing standard error of the mean

FIGURE 3

Group differences in midsagittal plane corpus callosum thickness. Areas of the corpus callosum where the thickness is reduced in one group compared with the other. Significant p values (<0.05) appear in light blue, becoming warmer in colour with lower values. Raw p values are presented in the left column, with Bonferroni corrected p values presented on the right. Positioning of streamlines is guided by the image at the top. The genu of the corpus callosum points to the right of the image, whereas the splenium faces left

FIGURE 4

Group differences in cortical thickness, Controls and Parkinson's disease (PD) groups. Areas of the cortex where the thickness is reduced in one group compared with the other. Raw p values are presented in the left column, with Bonferroni corrected p values presented on the right. Abbreviations: ENT, entorhinal cortex; FUS, fusiform cortex; INFP, inferior parietal cortex; IT, inferior temporal cortex; LOCC, lateral occipital cortex; LORB, lateral orbitofrontal cortex; MORB, medial orbitofrontal cortex; MT, middle temporal cortex; PARA, parahippocampal cortex; PREC, precentral cortex; PCUN, precuneus; POPE, pars opercularis; PROB, pars orbitalis; PTRI, pars triangularis; RMF, rostral middle frontal; ST, superior temporal cortex; SMARG, supramarginal gyrus; INS, insula cortex

FIGURE 5

Group differences in cortical thickness, Parkinson's disease (PD) groups. Areas of the cortex where the thickness is reduced in one group compared with the other. Raw p values are presented in the left column, with Bonferroni corrected p values presented on the right. Abbreviations: ENT, entorhinal cortex; FUS, fusiform gyrus; IT, inferior temporal cortex; INFP, inferior parietal cortex; INS, insula cortex; LORB, lateral orbitofrontal cortex; MT, middle temporal cortex; PARA; parahippocampal gyrus; PTRI, pars triangularis; RMF, rostral middle frontal cortex; SF, superior frontal; SMARG, supramarginal cortex; ST, superior temporal cortex; TT, transverse temporal cortex

FIGURE 6

Correlation between callosal thickness and cortical thickness. Beta correlation coefficients show the directionality of the relationship between callosal and cortical thicknesses. Associated corrected p values are presented in Figure S1. Abbreviations: PO, pars orbitalis; MO, medial orbitofrontal cortex; LOR, lateral orbitofrontal cortex; PT, pars triangularis; POP, pars opercularis; RMF, rostral middle frontal cortex; CMF, caudal middle frontal cortex; SF, superior frontal cortex; PRE, precentral cortex; PARA, paracentral cortex; ENT, entorhinal cortex; FUS, fusiform gyrus; PH, parahippocampal gyrus; ST, superior temporal cortex; TT, transverse temporal cortex; MT, medial temporal cortex; IT, inferior temporal cortex; IN, insula; POS, postcentral cortex; SP, superior parietal cortex; SM, supramarginal cortex; IP, inferior parietal cortex; PC, precuneus; CUN, cuneus; PER, pericalcarine cortex; LIN, lingual cortex; LOC, lateral occipital cortex; RAN, rostral anterior cingulate; CAN, caudal anterior cingulate cortex; PCC, posterior cingulate cortex; IST, isthmus cingulate cortex