He noted that the underlying disconnection mechanism is improved by the facilitating effect of unblocking methods (in the tactile, somesthetic, auditory, and visual systems), so that pathways other than the one impaired by the brain lesion are used.
In 1998, Fritson[9] presented a mechanistic account of how dysfunctional integration among neuronal systems arises, based on the central role played by synaptic plasticity in shaping the connections.
This modulation is mediated by ascending neurotransmitter systems that: (i) have been implicated in schizophrenia; and (ii) are known to be involved in consolidating synaptic connections during learning.
The autism group at Cambridge University[12] provided evidence that the functional connectivity of medial temporal lobe structures specifically is abnormal in people with Asperger’s syndrome, at least during fearful face processing.
Melillo and Leisman have similarly concluded that a functional disconnection syndrome is a basis for explaining the symptoms of autistic spectrum disorder.