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As a paper just published in Frontiers in Psychology points out, congenital and early blindness appears to protect against schizophrenia. As the authors note, “across all past papers, there has not been even one reported case of a congenitally blind person who developed schizophrenia.” However, this is not so with blindness developed later in life. The authors conclude that it must be brain changes that occur secondarily to congenital and early blindness—not blindness itself—that protect against schizophrenia. They then go on to give an account of what those changes may be.
But the authors also point out that autism is very common in blind children by contrast to both congenital deafness and deaf-blindness, which are associated with increased risk of psychosis. Indeed, an earlier study confirmed previous ones in finding that “there are blind children who do not satisfy the diagnostic criteria for autism, but who nevertheless have marked impairments in interpersonal engagement," adding that "These are the very same children who also manifest several additional ‘autistic features.’”
Another additional autistic feature—albeit a comparatively rare one—is savantism, and here it may be worth pointing out that the combination of blindness, autism, and musical genius is unusually frequent. (The classic case is Blind Tom and his living equivalent is Leslie Lemke, as I explain in The Imprinted Brain).
Furthermore, the cognitive, sensory, and neurological factors that are cited as contributing protection against schizophrenia in the Frontiers in Psychology paper are frequently found in people with autism. The very first one the authors mention—pitch discrimination—is a case in point. Some estimate that up to a third of all people with autism have perfect pitch, and enhanced sensitivity to sound is widely reported in autism. Sense of smell is also superior in autism: In one study by Tavassoli and others due to appear in Autism, an autistic group proved able to detect a test odor at a mean distance of almost twice that of normal controls. The study also found a quantitative relationship between levels of enhanced sensory processing and the number of autistic traits, with greater severity of autistic behaviour related to higher sensory perception.
Although mentalistic deficits combined with mechanistic and sensory compensations seem to be a primary developmental factor in autism, they are probably a secondary consequence of the loss of sight in blind individuals. For example, gaze-monitoring is one of the key factors in mentalism (or mind-reading skills) because it conveys so much information about what a person is thinking, feeling, or intending. Indeed, deficits here are one of the earliest and most reliable indicators of autism. Obviously, this skill is totally lacking in the blind, whose mind-reading abilities must be correspondingly compromised by their incapacity to monitor gaze. But such mentalistic deficits might be compensated for through greater sensitivity in other senses, such as touch, which certainly substitutes for vision in reading Brail, and is generally enhanced in the congenitally blind. But studies also show a lower threshold of sensitivity to touch in people with autism as compared to non-autistic controls. Indeed, there is evidence that enhanced sensitivity to touch and to sound are correlated in autism.
Vision has also been found to be strikingly enhanced in some people with high-functioning autism, whose acuity is on a level with that of birds of prey (almost three times better than average). And although there is obviously no direct parallel with congenital blindness here, the authors of the Frontiers of Psychology study point out that the congenitally blind are protected from the abnormal visual inputs which have been implicated in schizophrenia. Furthermore, the visual cortex in congenitally blind people is thicker than in the sighted, but as the authors point out this thickening “is thought to be characterized by a less than normal amount of pruning, due to deprivation of visual experience.” Schizophrenics, by contrast, have a thinner cortex.
In previous posts, I have drawn attention to both proliferation of neurons in the frontal brain and of dendrites in those with autism, who typically are born with bigger brains and thicker cortices than normal. And as I also pointed out, brain development is more like sculpture than building: neurons are pruned to produce the end result, not incrementally added. So the lack of such pruning may be another feature common to both autism and congenital blindness.
Finally, the authors point out that “it has already been demonstrated in schizophrenia that improving auditory precision by repeated practicing of tone discrimination leads to improvements in auditory and (more interestingly) higher-level cognitive functions.” Indeed, they even mention “fostering cognitive reserve” as a corrective to what I would call the hyper-mentalism of schizophrenia.
The imprinted brain theory’s diametric model of mental illness proposes that autism is the mentalistic opposite of psychoses such as schizophrenia. Put very crudely, the diametric model suggests that the best way to cure psychotics is to make them somewhat autistic, and pitch-discrimination training in particular and fostering cognitive reserve, in general, are examples of how this can be done, as I pointed out in an earlier post. Indeed, anything that can push the balance in the autistic direction will suffice to counter psychotic tendencies, and early-onset blindness certainly appears to do so where providing protection from schizophrenia is concerned—just as the diametric model predicts.
For a later post on this subject, click here.
With thanks and acknowledgment to my colleague, Bernard Crespi, for kindly bringing this material to my attention, and to Teresa Tavassoli for advice on the study in press.
