My brother had a cleft palate when he was born. During foetal development, when the two sides of his face came together, there was a fault in the process and the two sides of the roof of his mouth did not meet. This had to be corrected with surgery. He had great difficulty with language as a child. When he started school no one could understand him except his family. In many ways he was a normal child but there was always something different about him. I am quite sure he was never examined by a doctor for the odd aspects of his behavior. Later, a number of people thought he had mild Asperger’s syndrome. But when he was young that sort of thing was not known on the rural prairies.
But in the back of my mind is a conversation I had with a neuroscience tutor many years ago. Drinking in a pub with other students and tutors, I was asked to explain my dyslexia (also never looked at by a doctor) – how it felt from the inside. I started and at some point said that it might be that I was left-handed but right-eyed, and one of the tutors interrupted and said that theory was wrong. He asked me a lot of questions that had nothing to do with reading or writing. But they did seem at the time to be hitting a bunch of odd things where my answers were surprising to the group. I remember two in particular: do you hear something but not clearly and then about the time you ask ‘what?’ you know what was said?; and, which do you identify most with your conscious mind or your unconscious mind? Some in the group thought I was not being truthful and said things like, “if you really were like that then we would be able to tell and you seem perfectly normal.” Then came the weird question: does anyone closely related to you have a harelip or a cleft palate? And when I said my brother did, the question was – is he ‘normal’? I had to say that he was not as normal as all that and maybe somewhat handicapped with language. Well, says the tutor, “you probably have part of the connection between the two hemispheres missing, and probably your brother has more missing than you.” It was an eye-opener for me about how others viewed themselves just as it was for them to hear my answers.
That conversation stayed there in the back of my mind, without proof or disproof, for close to 40 years. Recently there has been work on dyslexics showing that a very particular part of the nerve connections between the two hemisphere is missing (the corpus callosum is partially missing in the auditory/language region). The fault is graphically shown in the paper: Plessen et al; Less developed corpus callosum in dyslexic subjects – a structural MRI study; Neuropsychologia (2002) (pdf).
Very recently it has been shown that some corpus callosum faults may be partially made up for by the creation of unusual communication nerve connections between the hemispheres. Tovar-Moll et al; Structural and functional brain rewiring clarifies preserved interhemispheric transfer in humans born without the corpus callosum; PNAS (2014) (PNAS). Here is the abstract:
Significance: Individuals subjected to surgical transection of the corpus callosum (“split-brains”) fail to transfer information between the cerebral hemispheres, a condition known as “disconnection syndrome.” On the other hand, subjects born without the callosum (callosal dysgenesis, CD) typically show preserved interhemispheric communication. To clarify this paradox, which has defied neuroscientists for decades, we investigated CD subjects using functional and structural neuroimaging and neuropsychological tests. Results demonstrated the existence of anomalous interhemispheric tracts that cross through the midbrain and ventral forebrain, linking the parietal cortices bilaterally. These findings provide an explanation for the preserved cross-transfer of tactile information between hemispheres in CD. We suggest that this condition is associated with extensive brain rewiring, generating a new circuitry that provides functional compensatory interhemispheric integration.
Abstract: Why do humans born without the corpus callosum, the major interhemispheric commissure, lack the disconnection syndrome classically described in callosotomized patients? This paradox was discovered by Nobel laureate Roger Sperry in 1968, and has remained unsolved since then. To tackle the hypothesis that alternative neural pathways could explain this puzzle, we investigated patients with callosal dysgenesis using structural and functional neuroimaging, as well as neuropsychological assessments. We identified two anomalous white-matter tracts by deterministic and probabilistic tractography, and provide supporting resting-state functional neuroimaging and neuropsychological evidence for their functional role in preserved interhemispheric transfer of complex tactile information, such as object recognition. These compensatory pathways connect the homotopic posterior parietal cortical areas (Brodmann areas 39 and surroundings) via the posterior and anterior commissures. We propose that anomalous brain circuitry of callosal dysgenesis is determined by long-distance plasticity, a set of hardware changes occurring in the developing brain after pathological interference. So far unknown, these pathological changes somehow divert growing axons away from the dorsal midline, creating alternative tracts through the ventral forebrain and the dorsal midbrain midline, with partial compensatory effects to the interhemispheric transfer of cortical function.