Planum temporale asymmetries correlate with corpus callosum axon fiber density in chimpanzees (Pan troglodytes)

Abstract The corpus callosum (CC) connects homologous cortical structures across hemispheres and is the largest white matter tract in the human brain. Post-mortem studies suggest that CC myelination begins in infancy, reaches a plateau in the middle age, and declines in the later years. The latter is accompanied by myelin disruption and reduction in fiber density and diameter, i.e. changes in intra-/extracellular water space. We used multi-echo T2 imaging to estimate, via multi-exponential T2 relaxation of water, the myelin water fraction (MWF), a direct proxy for myelin content, and geometric mean T2 (geomT2IEW) that reflects water in the intra-/extracellular space, to investigate age differences in five CC regions covering its anterior to posterior span in 395 healthy individuals (7-85 years; 161M+235F). The general linear model analysis of MWF showed main effects of age and age-squared conditioned on interactions by CC region. Univariate polynomial regressions on three age groups (7-29, 30-59, and 60-85 years) revealed the overall quadratic association between age and MWF as mainly driven by the positive linear relationship in the youngest group and minimal differences in the remainder of the lifespan, save for two weak negative linear associations in the anterior/middle CC body. With geomT2, a main linear effect of age, and significant interactions between age and age-squared by region were observed. The positive linear association was especially prominent in the regions with greater fiber density. The results are consistent with CC myelination into adulthood and decreased axonal density and diameter but not prominent myelin degeneration in elderly individuals.

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Fiber-specific white matter reductions in Parkinson hallucinations and visual dysfunction

Neurology ◽

10.1212/wnl.0000000000009014 ◽

2020 ◽

Vol 94 (14) ◽

pp. e1525-e1538 ◽

Cited By ~ 4

Author(s):

Angeliki Zarkali ◽

Peter McColgan ◽

Louise-Ann Leyland ◽

Andrew J. Lees ◽

Geraint Rees ◽

...

Keyword(s):

White Matter ◽

Corpus Callosum ◽

Parkinson Disease ◽

Fiber Bundle ◽

Visual Performance ◽

Visual Hallucinations ◽

Fiber Density ◽

Left Posterior ◽

Parkinson Dementia ◽

Attentional Models

ObjectiveTo investigate the microstructural and macrostructural white matter changes that accompany visual hallucinations and low visual performance in Parkinson disease, a risk factor for Parkinson dementia.MethodsWe performed fixel-based analysis, a novel technique that provides metrics of specific fiber-bundle populations within a voxel (or fixel). Diffusion MRI data were acquired from patients with Parkinson disease (n = 105, of whom 34 were low visual performers and 19 were hallucinators) and age-matched controls (n = 35). We used whole-brain fixel-based analysis to compare microstructural differences in fiber density (FD), macrostructural differences in fiber bundle cross section (FC), and the combined FD and FC (FDC) metric across all white matter fixels. We then performed a tract-of-interest analysis comparing the most sensitive FDC metric across 11 tracts within the visual system.ResultsPatients with Parkinson disease hallucinations exhibited macrostructural changes (reduced FC) within the splenium of the corpus callosum and the left posterior thalamic radiation compared to patients without hallucinations. While there were no significant changes in FD, we found large reductions in the combined FDC metric in Parkinson hallucinators within the splenium (>50% reduction compared to nonhallucinators). Patients with Parkinson disease and low visual performance showed widespread microstructural and macrostructural changes within the genu and splenium of the corpus callosum, bilateral posterior thalamic radiations, and left inferior fronto-occipital fasciculus.ConclusionsWe demonstrate specific white matter tract degeneration affecting posterior thalamic tracts in patients with Parkinson disease with hallucinations and low visual performance, providing direct mechanistic support for attentional models of visual hallucinations.

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