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• The Corpus Callosum: evolving duties throughout life
  Jonathan T. Kleinman
  Published on: 13 April 2016

• Published on: 13 April 2016

  The Corpus Callosum: evolving duties throughout life

  • Jonathan T. Kleinman
  • Other Contributors:
    • Ola A. Selnes

  Those who do not stop asking silly questions become scientists.

  Dear Editor,

  To date, most studies investigating functional correlates of corpus callosum morphometry have been based on small samples. Jokinen and colleagues link mental slowing on specific tasks to atrophy in distinct subdivisions of the corpus callosum (CC) in a large sample of older adults with white matter lesions(1). The authors hypoth...

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  Those who do not stop asking silly questions become scientists.

  Dear Editor,

  To date, most studies investigating functional correlates of corpus callosum morphometry have been based on small samples. Jokinen and colleagues link mental slowing on specific tasks to atrophy in distinct subdivisions of the corpus callosum (CC) in a large sample of older adults with white matter lesions(1). The authors hypothesize that corpus callosum atrophy contributes to cognitive decline in the elderly perhaps as a result of reduced "connnectivity" between cortical regions. Aside from the usual perils of attributing functional significance to variations in volume of anatomical structures, this brings up broader questions about the functional role of this magnificent interhemispheric commissure.

  In order to integrate this information into what is known about the function/s of the CC, it may be helpful to step back and review proposed 'functions'� of the CC throughout the life-span. Beyond non-speficic descriptors such as "functional connectivity", it is difficult to find substantial information on more specific functions of the 200 million fibers that make up the CC, and readily observable deficits that arise from disconnection. Many investigators have examined the morphology of the CC and linked development, abilities, and deficits to structure. While these investigations have advanced our understanding of the normal variability of this structure in normal controls and patient populations, they have not shown us clearly what the CC is for, or why it is an essential part of the human brain. Another method that has recently been used to evaluate the integrity of the fiber tracts of the CC is diffusion tensor imaging (DTI). Will these increasingly detailed pictures of connections bring us closer to understanding the actual 'function'� of the corpus callosum? We think not.

  Neuroscientists, at heart, have always attempted to tie functions to anatomical structures. We favor simplicity and clarity. We enjoy being able to put a pin next to a structure and say, 'this is what X does'. This approach has worked well for many structures within the brain, midbrain, pons, and medulla. The function/s of the CC have not been so easy to 'pin down'.

  Initial observations and studies of patients who had undergone callosotomy or commissurotomy (cutting of the anterior and posterior commsures as well) for the treatment of intractable epilepsy surprised everyone because of the relative lack of obvious postoperative functional deficits associated with this major neurosurgical intervention. The patients lived with complete informational segregation, but without major behavioral, emotional, or personality changes. Their minimal deficits only become noticeable through specific questions and intricate task design(2). These observations truly begged (and still beg) what does the CC 'do'�? But, could we be asking the wrong question entirely? Is a more appropriate question, 'What does the CC enable?'

  Throughout different periods of our lives the CC may enable multiple distinct tasks and functions. The corpus callosum likely plays one of its major roles during early development, both in utero and post birth in early childhood during critical periods. This has recently been demonstrated for the visual cortex(3), but may likely extend to other sensory and cortical area maturation by interhemispheric communication via corpus callosum (although much more research is needed). Inhibition of this function seems to severely inhibit cortical maturation, normal development, and leads to long lasting visual problems.

  In children with agenesis of the CC, they only perform well on cognitive tasks when they possess a normal or slightly enlarged anterior commissure(4). These data indicate just how crucial interhemispheric communication is for normal cortical development. During childhood and into early adulthood cortical activity (e.g. playing the piano) significantly changes the myelination patterns within the CC. These changes are beginning to be recognized as a complex form of synaptic plasticity(5). Therefore even into adulthood a significant form of plasticity seems to be possible through modification/efficiency changes of interhemispheric informational transfer via the CC.

  In old age it appears that the CC may enable inter-hemispheric processing and recruitment of increased cortical areas for processing demands(1). Without the ability to recruit contralateral areas because of damage or hypertrophy we observe mental slowing. Recruitment of the contralateral hemisphere enabled by the corpus callosum may be an important compensatory mechanism for sustained high-level cognitive functioning in older adults(3).

  At all ages, callosal disconnection causes informational segregation although observation of these disturbances often involves contrived questions. The expected deficits are often 'masked'� in young individuals as they have an increased cognitive reserve. What happens to these patients 20, 30, or 40 years after surgical sectioning? Do they develop cognitive slowing and executive deficits as described by Jokinen and colleges earlier than expected(1)?

  Therefore, we may try thinking about this structure similar to a researcher in the field or cortical plasticity. At different times throughout development (or in the life of a specific cell) and life, the CC has multiple main functions. The enabled functions may not be the 'reason' that the CC exists, they may simply be a manifestation of the brain's ability to use and reuse the same structures for highly different roles. The CC may be the brain's 'optimizer of function'� through enabling an array of interhemispheric transfer and inhibition.

  Physicist Leon Lederman

  References

  1. Jokinen H, Ryberg C, Kalska H, et al. Corpus callosum atrophy is associated with mental slowing and executive deficits in subjects with age-related white matter hyperintensities: the LADIS Study. J Neurol Neurosurg Psychiatry 2007;78:491-6.

  2. Gazzaniga MS. Forty-Five years of split-brain research and still going strong. Nat Rev Neurosci 2005;6:653-9.

  3. Caleo M, Restani L, Gianfranceschi L, et al. Transient synaptic silencing of developing striate cortex has persistent effects on visual function and plasticity. J Neurosci 2007;27:4530-40.

  4. Paul LK, Brown WS, Adolphs R, et al. Agenesis of the corpus callosum: genetic, developmental and functional aspects of connectivity. Nat Rev Neurosci 2007;8:287-299.

  5. Fields RD. Myelination: and overlooked mechanism of synaptic plasticity? Neuroscientist 2005;6:528-531.

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  Conflict of Interest:
  None declared.

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