The rises and falls of disconnection syndromes

Abstract

In a brain composed of localized but connected specialized areas, disconnection leads to dysfunction. This simple formulation underlay a range of 19th century neurological disorders, referred to collectively as disconnection syndromes. Although disconnectionism fell out of favour with the move against localized brain theories in the early 20th century, in 1965, an American neurologist brought disconnection to the fore once more in a paper entitled, 'Disconnexion syndromes in animals and man'. In what was to become the manifesto of behavioural neurology, Norman Geschwind outlined a pure disconnectionist framework which revolutionized both clinical neurology and the neurosciences in general. For him, disconnection syndromes were higher function deficits that resulted from white matter lesions or lesions of the association cortices, the latter acting as relay stations between primary motor, sensory and limbic areas. From a clinical perspective, the work reawakened interest in single case studies by providing a useful framework for correlating lesion locations with clinical deficits. In the neurosciences, it helped develop contemporary distributed network and connectionist theories of brain function. Geschwind's general disconnectionist paradigm ruled clinical neurology for 20 years but in the late 1980s, with the re-emergence of specialized functional roles for association cortex, the orbit of its remit began to diminish and it became incorporated into more general models of higher dysfunction. By the 1990s, textbooks of neurology were devoting only a few pages to classical disconnection theory. Today, new techniques to study connections in the living human brain allow us, for the first time, to test the classical formulation directly and broaden it beyond disconnections to include disorders of hyperconnectivity. In this review, on the 40th anniversary of Geschwind's publication, we describe the changing fortunes of disconnection theory and adapt the general framework that evolved from it to encompass the entire spectrum of higher function disorders in neurology and psychiatry.

Symmetries in human brain language pathways correlate with verbal recall

“…In addition, there is an indirect pathway (21) consisting of two segments, an anterior segment linking Broca's territory with the inferior parietal lobe (Geschwind's territory) (21), and a posterior segment linking Geschwind's territory with Wernicke's territory (13,20,21). Not only does this arrangement support the more flexible architecture of parallel processing (23), but it is also in keeping with recent functional neuroimaging findings (8,16,24) and contemporary models of language disorders (5,23,25). The current study focused on the lateralization of these pathways and possible behavioral advantages related to the degree of lateralization.…”

White Matter Integrity Reductions in Intermittent Explosive Disorder

“…Given the importance of the inferior parietal and posterior temporal cortex in social cognition (Decety and Lamm, 2007;Young et al, 2010), and evidence for disturbed social cognition in IED , findings of disrupted white matter connectivity in these tracts in IED could be of considerable importance. First described by Theodore Meynert (Wernicke, 1874), lesioning of the SLF was proposed by Norman Geschwind to cause a set of disconnection syndromes, characterized by impairments in language and praxis (Geschwind, 1965a, b;Catani and Ffytche, 2005). The SLF can be divided into four subcomponents (Makris et al, 2005).…”

The anatomy of cerebral achromatopsia: A reappraisal and comparison of two case reports

“…In the present comparison between the cases of Madame R and Madame D, however, simple consideration of cortical lesion location did not permit to reach a satisfactory account of the dramatic differences between the consequences of their brain lesions. On the other hand, by taking into account white matter pathways, an approach sometimes defined as hodotopic (see Catani and ffytche, 2005), it was possible to articulate a more plausible, if speculative, explanation of an otherwise mysterious pattern of lesion-symptom mapping.…”