Corpus callosum area has been examined in neurodegenerative diseases as a marker for cortical pathology and for differential diagnosis; however, it has not been examined in Parkinson’s disease (PD). We compared callosal area in patients with PD and PD with dementia (PDD) to healthy controls and patients with Alzheimer’s disease (AD). We subsequently compared our results to a meta-analysis of studies examining callosal area in AD, frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). For the imaging study, midsagittal T1-weighted MRIs were analyzed and the callosal area was determined in patients with PD (n = 24), PDD (n = 25), AD (n = 16) and controls (n = 27). The meta-analysis combined results from all publications (Medline or PubMed) representing unique samples and measuring callosal area in AD, FTD, PSP, and CBD. We found that PD and PDD patients did not show statistically significant callosal atrophy compared to controls (effect size d, 95% CI, d = 0.13, –0.26 to 0.52, and d = 0.05, –0.44 to 0.33, respectively) or AD. The AD patients had a significant loss of callosal area compared to controls (d = –0.58, –1.01 to –0.15). Dementia severity was correlated with total callosal atrophy in AD (R = 0.66, p < 0.01) but not in PDD patients (R = 0.18, p > 0.1). The meta-analysis revealed significant combined effect sizes for callosal atrophy of: AD (d = –1.03, –1.13 to –0.93), FTD (d = –1.21, –1.56 to – 0.86), PSP (d = –1.09, –1.38 to –0.81), and CBD (d = –1.80, –2.18 to –1.43). We conclude that PD and PDD patients do not have callosal atrophy in contrast to other neurodegenerative diseases, including AD. Callosal atrophy was correlated with dementia severity in patients with AD but not PDD.
