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ORIGINAL ARTICLES

Perisylvian Language Networks of the Human Brain
Marco Catani, MD,1 Derek K. Jones, PhD,1,2 and Dominic H. ffytche, MD1
Early anatomically based models of language consisted of an arcuate tract connecting Broca’s speech and Wernicke’s comprehension centers; a lesion of the tract resulted in conduction aphasia. However, the heterogeneous clinical presentations of conductionaphasia suggest a greater complexity of perisylvian anatomical connections than allowed for in the classical anatomical model. This article re-explores perisylvian language connectivity using in vivo diffusion tensor magnetic resonance imaging tractography. Diffusion tensor magnetic resonance imaging data from 11 right-handed healthy male subjects were averaged, and the arcuate fasciculus of theleft hemisphere reconstructed from this data using an interactive dissection technique. Beyond the classical arcuate pathway connecting Broca’s and Wernicke’s areas directly, we show a previously undescribed, indirect pathway passing through inferior parietal cortex. The indirect pathway runs parallel and lateral to the classical arcuate fasciculus and is composed of an anterior segmentconnecting Broca’s territory with the inferior parietal lobe and a posterior segment connecting the inferior parietal lobe to Wernicke’s territory. This model of two parallel pathways helps explain the diverse clinical presentations of conduction aphasia. The anatomical findings are also relevant to the evolution of language, provide a framework for Lichtheim’s symptom-based neurological model ofaphasia, and constrain, anatomically, contemporary connectionist accounts of language. Ann Neurol 2005;57:8 –16

After Paul Broca’s report1 of a patient with disordered speech production and a lesion of the left posterior inferior frontal gyrus, Carl Wernicke2 described a posterior temporal area devoted to auditory word processing. Wernicke postulated the existence of a direct connection between thetwo areas, and that a lesion of this theoretical pathway would cause an aphasia characterized by normal language comprehension and fluent conversational speech but the inability to repeat what had just been heard. In fact, a prominent pathway connecting posterior frontal and superior temporal lobes had already been described by Burdach and was later confirmed by Dejerine who referred to thepathway as Burdach’s arcuate fasciculus.3 Clinical evidence for Wernicke’s theoretical “conduction” aphasia has accumulated over many years.4 However, such descriptions fall short of supporting Wernicke’s model. The trouble is that many of the cases have lesions involving both the arcuate fasciculus and its overlying cortex. In some patients, the lesion extends directly into Wernicke’s or Broca’sareas, whereas in others it extends to the inferior parietal lobe, a region now recognized as having an important linguistic function in its own right.5 Wernicke’s conduction aphasia thus could be
From the 1Centre for Neuroimaging Sciences, Institute of Psychiatry, King’s College London, London, United Kingdom; and 2Section on Tissue Biophysics and Biomimetics, Laboratory of Integrative Medicine andBiophysics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD. Received Jul 2, 2004, and in revised form Sep 13. Accepted for publication Sep 16, 2004.

equally well explained by cortical deficits as by a true disconnection of Wernicke’s and Broca’s areas. The advent of structural imaging allowed this issue to be addressed in aphasic patientswithout recourse to postmortem dissection. Such studies confirmed that Wernicke’s conduction aphasia could occur with lesions restricted to white matter tracts6,7; however, it also became clear that Wernicke’s original anatomical formulation was incomplete. Wernicke’s model predicted that lesions at any point along the course of the arcuate fasciculus should result in an identical aphasia. Yet,...