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.

Corpus callosum and cerebellum participate in semantic dysfunction of Parkinson’s disease: a diffusion tensor imaging-based cross-sectional study

“…Importantly, impairment in anterior corpus callosum area strongly affected verbal fluency in patients with multiple sclerosis [30]. In PD patients, it has been reported that volume reduction of corpus callosum was associated with language impairment, however, the posterior corpus callosum was found to be associated with language ability more [31,32], which is in contrary to our study. The F-mi is a part of genu of corpus callosum that connect the medial and lateral surfaces of bilateral frontal cortices [33].…”

Altered Callosal Morphology and Connectivity in Asymptomatic Carotid Stenosis

“…The corpus callosum (CC) is the largest white matter fiber tract connecting the two hemispheres, facilitating interhemispheric integration and intrahemispheric specialization, and playing a role in language dominance, handedness, gender difference, and intelligence. 6,7 Callosal atrophy has been documented in Parkinson's disease 8 and Alzheimer's disease, 9 and is a hallmark of neurodegenerative diseases, but studies in ACS patients are lacking.…”

Pathobiology of Cognitive Impairment in Parkinson Disease: Challenges and Outlooks

“…Compared to a control group, PD-NC individuals suffered from gray matter (GM) atrophy mainly in prefrontal and limbic lobes and left temporal gyrus [ 156 ]. Voxel-based morphometry (VBM) in PD patients with SCD or subjective memory complaints revealed reduced GM intensities in anterior cingulate and right parietal lobe [ 55 , 217 ] and mild thinning of the midsagittal corpus callosum [ 218 ]. Mild atrophy affected the orbitofrontal regions, left superior parietal lobule, and more widespread limbic and fronto-parietal cortices [ 158 ].…”

“…The involvement of the corpus callosum, cingulum and major association tracts in PD-MCI but not in PD-NC [ 157 , 178 , 179 ] as well as increased hyperintensity in frontal and interhemispheric WM (genu and body of corpus callosum) were seen [ 178 , 180 , 239 ]. Thinning of the corpus callosum was correlated with the thickness of the left orbitofrontal cortex in PD-MCI [ 218 ]. The corpus callosum and cingulum bundle showed the same trend to decline with cognitive dysfunction [ 240 ].…”

“…WM abnormalities were widespread [ 42 ], involving multiple brain regions with a heterogenous pattern of abnormal diffusivity adjacent to cortical and limbic areas [ 238 ]. Thinning of the corpus callosum and microstructural WM abnormalities were associated with changes in the orbitofrontal cortex and contributed to CI by disrupting information transfer across interhemispheric and callosal-cortical projections [ 218 , 265 ]. The strongest of DTI changes occurred in the most anterior and posterior callosal segments, reflecting fronto-striatal and posterior cortical type cognitive deficits [ 265 ].…”