Disconnection of cortical face network in prosopagnosia revealed by diffusion tensor imaging

Abstract

Current anatomic models of face processing propose a ‘core’ system (occipital face area - OFA, the fusiform face area - FFA, and superior temporal sulcus - STS) and a multi-modal ‘extended’ system, which includes anterior temporal cortex. Classic models of prosopagnosia suggest that disruption of face processing may occur from disconnection within such a network, though most current studies have focused on damage to the modules themselves. In this report we describe the white matter changes in a prosopagnosic patient with only modest cortical damage.

Patient R-AT1 acquired prosopagnosia following a right amygdalohippocampectomy for epilepsy, which resulted in lesion of the anterior part of the inferior longitudinal fasciculus (ILF). We used functional MRI (face-objects comparison) to localise regions in the core system, all of which were still present in R-AT1, and then performed diffusion tensor imaging (DTI) tractography to visualise tracts extending from these regions in R-AT1and 8 healthy controls. Tracts from the OFA of R-AT1's intact left hemisphere extended along the ILF, towards the anterior temporal lobe. In the lesioned right hemisphere of R-AT1, tracts from posterior occipitotemporal regions did not extend far anteriorally. Compared to controls, a region of reduced fractional anisotropy (FA: DTI index associated with white matter structural integrity) was found in the patient's right hemisphere ILF, adjacent and superior to the patient's FFA.

These inter-subject and inter-hemispheric differences may reflect a retrograde degeneration of ILF tracts in the patient's lesioned right hemisphere. Hence, disruption of connections in the face-processing network between posterior occipitotemporal face-selective areas and anterior temporal cortex may contribute to R-AT1's prosopagnosia, particularly since the amount of cortical damage in R-AT1 is modest and in a location unusual for prosopagnosia.

Footnotes

 LL was supported by a Michael Smith Foundation for Health Research Post-doctoral Fellowship. MS was supported by a Canadian Institutes of Health Research Fellowship Award through the UBC Strategic Program in Neurobiology and Behaviour. CF was supported by a Canadian Institutes of Health Research Canada Graduate Scholarship Doctoral Research Award and a Michael Smith Foundation for Health Research Senior Graduate Studentship. GI was supported by a Michael Smith Foundation for Health Research Post-doctoral Fellowship and the Alzheimer Society of Canada. JB was supported by a Michael Smith Foundation for Health Research Senior Scholar Award and a Canada Research Chair.