The simple formulation “disconnection leads to dysfunction” explained a range of 19th century neurological disorders known as disconnection syndromes. In 1965 the American neurologist Norman Geschwind gave the old theory a brand new look by publishing his studies in a paper entitled “Disconnexion syndromes in animals and man”, which in brief became the manifesto of a new behavioural neurology.

Geschwind outlined a pure disconnectionist framework for the pathogenesis of higher function deficits, regarded as the result from white matter lesions or lesions of the association areas. Geschwind considered association cortices as relay stations between primary motor, sensory and limbic areas.

A disconnectionist paradigm ruled clinical neurology and influenced neuroscience in general for twenty years. Its importance diminished with the discoveries of functional roles for association cortex and the great amount of new insights in neurobiology, but only today, thanks to new techniques to study connections in the living human brain, we can directly test the classical formulation (Catani M. & Ffytche D.H., The rises and falls of disconnection syndromes. Brain 128, (10): 2224-2239, 2005).

Diffusion tensor MRI (DT-MRI) provides information about the structural organization and orientation of white matter fibres and, through the technique of “tractography”, reveals the trajectories of cerebral white matter tracts.

In the classical connectionist model of language the arcuate tract connected Broca’s speech and Wernicke’s comprehension centres: a lesion of the tract resulted in conduction aphasia. However, the heterogeneous clinical presentations of connection aphasia suggest a greater complexity. In fact, using tractography, Catani and his colleagues found a new indirect pathway consisting of two shorter fibre bundles that initially follow the arcuate fasciculus but end in the territory of the inferior parietal lobe, an area thought to play an important role in making language meaningful (Perisylvian language network of the human brain. Ann. Neurol. 57, 8-16, 2005).


BM&L-October 2005