Autism: a condition of hyperconnectivity?

• decreased minicolumn size

  
  (Casanova 2002)

• early brain overgrowth

  
  (Carper & Courchesne 2000; Sparks et al. 2002; Aylward et al. 2002)

• some similarities to Fra(X)

Recent neuropathological and anatomical results suggest that autism may involve decreased elimination of synapses and/or cells, leading to an overconnected and over-excitable computational structure with consequent reductions in information content, signal-to-noise, and discriminability of competing inputs - in other words, hyper-arousal and impaired selection.

The flood of input generated by over-aroused, under-selective primary processing would from the earliest months of infancy overload nascent higher-order cognitive processes - processes whose development may be independently sabotaged by the same neuropathology that affects primary regions.

Faced with this bottleneck in higher-order cognition, the developing and plastic brain would likely evolve a cognitive style that emphasises low-level features and eschews reliance on global patterns - in other words, weak central coherence.

Weak coherence may in turn impair the use of contextual information in complex perceptual and executive tasks, and perturb or prevent the activity-dependent development of specialised modules for tasks such as theory-of-mind, face processing, and language.

`Functional Anatomy of Compensatory Processing in Autistic Attention: Complementary Roles of Selection and Suppression', Matthew Belmonte, 1 November 2002