Equal is Fair



Finding an deficit that links the disparate impairments associated with dyslexia would be major breakthrough. In a recent article in TiCS, offers a viable candidate for such a deficit – and has done a remarkable job of finding links that are plausible if still mostly circumstantial. Her stimulating article raises numerous directions for future research.

The epidemiology of dyslexia is poorly documented. Although many deficits have been reported, how often they occur and co-occur at different ages in different languages is still unknown.

There are few points which prove the causes of Dyslexia:

(i)               Prominent candidate genes for dyslexia are implicated in cell migration.

(ii)             Disorders of brain development often involve disturbances of interneuron migration and integration.

(iii)            Anomalies in the migration of GABAergic interneurons may underlie a variety of developmental disorders. Such anomalies can be regional rather than global.

(iv)            GABAergic interneuron pathology impairs lateral inhibition, affecting discrimination of competing types of sensory information.

(v)              Auditory processing at multiple time and frequency scales in parallel requires resolution of such competing information, and similarly for vision.

(vi)            For some unknown reason, the processing of lower temporal frequency auditory information is particularly vulnerable.