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a disconnection strongaccountstrong of gerstmann syndrome functional
A Disconnection Account of Gerstmann
Syndrome: Functional Neuroanatomy
Evidence
Elena Rusconi, PhD,1,2 Philippe Pinel, PhD,1,3,4 Evelyn Eger, MD,1,3,4 Denis LeBihan, MD, PhD,3,4
Bertrand Thirion, PhD,3 Stanislas Dehaene, PhD,1,3,4 and Andreas Kleinschmidt, MD, PhD1,3,4
Objective: To examine the functional neuroanatomy that could account for pure Gerstmann syndrome, which is the selective
association of acalculia, finger agnosia, left-right disorientation, and agraphia.
Methods: We used structural and functional neuroimaging at high spatial resolution in healthy subjects to seek a shared cortical
substrate of the Grundsto¨rung posited by Gerstmann, ie, a common functional denominator accounting for this clinical tetrad.
We construed a functional activation paradigm that mirrors each of the four clinical deficits in Gerstmann syndrome and
determined cortical activation patterns. We then applied fiber tracking to diffusion tensor images and used cortical activation
foci in the four functional domains as seed regions.
Results: None of the subjects showed parietal overlap of cortical activation patterns from the four cognitive domains. In every
subject, however, the parietal activation patterns across all four domains consistently connected to a small region of subcortical
parietal white matter at a location that is congruent with the lesion in a well-documented case of pure Gerstmann syndrome.
Interpretation: Our functional neuroimaging findings are not in agreement with Gerstmann’s postulate of damage to a com-
mon cognitive function underpinning clinical semiology. Our evidence from intact functional neuroanatomy suggests that pure
forms of Gerstmann’s tetrad do not arise from lesion to a shared cortical substrate but from intraparietal disconnection after
damage to a focal
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