ABSTRACT
Given mounting evidence that auditory, visual and/or motor dysfunction may not cause developmental dyslexia, but are often associated with it, the present paper proposes a new neurological model of dyslexia that explains how a specific phonological deficit might arise, and sometimes occur together with a more general sensorimotor syndrome. Based on a review of the neurology of dyslexia, the model specifies that: (1) genetically determined focal cortical anomalies in specific left perisylvian language areas are the underlying cause of the phonological deficit; (2) 76this phonological deficit is the primary cause of reading impairment; (3) under certain hormonal conditions during gestation, these cortical anomalies induce secondary disruption in sensory pathways, notably in the thalamus. The disruption may even extend to further areas, like the posterior parietal cortex and even the cerebellum; and (4) when this happens, the individual affected displays one or several components of a sensorimotor syndrome, which may in some cases aggravate the reading impairment. The model generalizes to specific language impairment and possibly to other domain-specific developmental disorders, each particular disorder characterized by the specific location of the brain anomalies.
