Brain plasticity following corpus callosum agenesis or loss: a review of the Probst bundles

Front Neuroanat. 2023 Nov 6:17:1296779. doi: 10.3389/fnana.2023.1296779. eCollection 2023.

Abstract

The corpus callosum is the largest axonal tract in the human brain, connecting the left and right cortical hemipheres. This structure is affected in myriad human neurodevelopmental disorders, and can be entirely absent as a result of congenital or surgical causes. The age when callosal loss occurs, for example via surgical section in cases of refractory epilepsy, correlates with resulting brain morphology and neuropsychological outcomes, whereby an earlier loss generally produces relatively improved interhemispheric connectivity compared to a loss in adulthood (known as the "Sperry's paradox"). However, the mechanisms behind these age-dependent differences remain unclear. Perhaps the best documented and most striking of the plastic changes that occur due to developmental, but not adult, callosal loss is the formation of large, bilateral, longitudinal ectopic tracts termed Probst bundles. Despite over 100 years of research into these ectopic tracts, which are the largest and best described stereotypical ectopic brain tracts in humans, much remains unclear about them. Here, we review the anatomy of the Probst bundles, along with evidence for their faciliatory or detrimental function, the required conditions for their formation, patterns of etiology, and mechanisms of development. We provide hypotheses for many of the remaining mysteries of the Probst bundles, including their possible relationship to preserved interhemispheric communication following corpus callosum absence. Future research into naturally occurring plastic tracts such as Probst bundles will help to inform the general rules governing axon plasticity and disorders of brain miswiring.

Keywords: brain development; callosotomy; commissurotomy; ectopic tracts; interhemispheric communication; longitudinal callosal bundle; neurodevelopmental plasticity; split brain.

Publication types

  • Review

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work received support from the Australian Research Council (DP160103958, DE1610101394, DP200103093), the National Health and Medical Research Council (1175825 and 2013349), the Brain and Behavior Research Foundation (30819), and The University of Queensland Research Training Scholarship.