Dataset Information

Functional MRI reveals compromised neural integrity of the face processing network in congenital prosopagnosia.

ABSTRACT: The summed activity of multiple nodes of a distributed cortical network supports face recognition in humans, including "core" ventral occipitotemporal cortex (VOTC) regions, and "extended" regions outside VOTC. Many individuals with congenital prosopagnosia-an impairment in face processing-exhibit normal blood oxygenation level-dependent (BOLD) activation in the core VOTC regions. These individuals evince a reduction in the structural integrity of the white matter tracts connecting VOTC to anterior temporal and frontal cortices, part of the "extended" face network. The impairment in congenital prosopagnosia may arise, therefore, not from a dysfunction of the core VOTC areas but from a failure to propagate signals between the intact VOTC and the extended nodes of the network. Using the fMR adaptation paradigm with famous and unknown faces, we show that individuals with congenital prosopagnosia evince normal adaptation effects in VOTC, indicating sensitivity to facial identity, but show no differential activation for familiar versus unknown faces outside VOTC, particularly in the precuneus/posterior cingulate cortex and the anterior paracingulate cortex. Normal BOLD activation in VOTC is thus insufficient to subserve intact face recognition, and disrupted information propagation between VOTC and the extended face processing network may explain the functional impairment in congenital prosopagnosia.

SUBMITTER: Avidan G

PROVIDER: S-EPMC2711224 | biostudies-literature | 2009 Jul

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Functional MRI reveals compromised neural integrity of the face processing network in congenital prosopagnosia.

Avidan Galia G Behrmann Marlene M

Current biology : CB 20090528 13

The summed activity of multiple nodes of a distributed cortical network supports face recognition in humans, including "core" ventral occipitotemporal cortex (VOTC) regions, and "extended" regions outside VOTC. Many individuals with congenital prosopagnosia-an impairment in face processing-exhibit normal blood oxygenation level-dependent (BOLD) activation in the core VOTC regions. These individuals evince a reduction in the structural integrity of the white matter tracts connecting VOTC to anter ...[more]

PMID: 19481456

Similar Datasets

Project description:BACKGROUND: Prosopagnosia is a selective deficit in facial identification which can be either acquired, (e.g., after brain damage), or present from birth (congenital). The face recognition deficit in prosopagnosia is characterized by worse accuracy, longer reaction times, more dispersed gaze behavior and a strong reliance on featural processing. METHODS/PRINCIPAL FINDINGS: We introduce a conceptual model of an apperceptive/associative type of congenital prosopagnosia where a deficit in holistic processing is compensated by a serial inspection of isolated, informative features. Based on the model proposed we investigated performance differences in different face and shoe identification tasks between a group of 16 participants with congenital prosopagnosia and a group of 36 age-matched controls. Given enough training and unlimited stimulus presentation prosopagnosics achieved normal face identification accuracy evincing longer reaction times. The latter increase was paralleled by an equally-sized increase in stimulus presentation times needed achieve an accuracy of 80%. When the inspection time of stimuli was limited (50 ms to 750 ms), prosopagnosics only showed worse accuracy but no difference in reaction time. Tested for the ability to generalize from frontal to rotated views, prosopagnosics performed worse than controls across all rotation angles but the magnitude of the deficit didn't change with increasing rotation. All group differences in accuracy, reaction or presentation times were selective to face stimuli and didn't extend to shoes. CONCLUSIONS/SIGNIFICANCE: Our study provides a characterization of congenital prosopagnosia in terms of early processing differences. More specifically, compensatory processing in congenital prosopagnosia requires an inspection of faces that is sufficiently long to allow for sequential focusing on informative features. This characterization of dysfunctional processing in prosopagnosia further emphasizes fast and holistic information encoding as two defining characteristics of normal face processing.

Project description:Rationale: Face expertise is a pivotal social skill. Developmental prosopagnosia (DP), i.e., the inability to recognize faces without a history of brain damage, affects about 2% of the general population, and is a renowned model system of the face-processing network. Within this network, the right Fusiform Face Area (FFA), is particularly involved in face identity processing and may therefore be a key element in DP. Neural representations within the FFA have been examined with Representational Similarity Analysis (RSA), a data-analytical framework in which multi-unit measures of brain activity are assessed with correlation analysis. Objectives: Our study intended to scrutinize modifications of FFA-activation during face encoding and maintenance based on RSA. Methods: Thirteen participants with DP (23-70 years) and 12 healthy control subjects (19-62 years) participated in a functional MRI study, including morphological MRI, a functional FFA-localizer and a modified Sternberg paradigm probing face memory encoding and maintenance. Memory maintenance of one, two, or four faces represented low, medium, and high memory load. We examined conventional activation differences in response to working memory load and applied RSA to compute individual correlation-matrices on the voxel level. Group correlation-matrices were compared via Donsker's random walk analysis. Results: On the functional level, increased memory load entailed both a higher absolute FFA-activation level and a higher degree of correlation between activated voxels. Both aspects were deficient in DP. Interestingly, control participants showed a homogeneous degree of correlation for successful trials during the experiment. In DP-participants, correlation levels between FFA-voxels were significantly lower and were less sustained during the experiment. In behavioral terms, DP-participants performed poorer and had longer reaction times in relation to DP-severity. Furthermore, correlation levels were negatively correlated with reaction times for the most demanding high load condition. Conclusion: We suggest that participants with DP fail to generate robust and maintained neural representations in the FFA during face encoding and maintenance, in line with poorer task performance and prolonged reaction times. In DP, alterations of neural coding in the FFA might therefore explain curtailing in working memory and contribute to impaired long-term memory and mental imagery.

Project description:Damage to the right fusiform face area can disrupt the ability to recognize faces, a classic example of how damage to a specialized brain region can disrupt a specialized brain function. However, similar symptoms can arise from damage to other brain regions, and face recognition is now thought to depend on a distributed brain network. The extent of this network and which regions are critical for facial recognition remains unclear. Here, we derive this network empirically based on lesion locations causing clinically significant impairments in facial recognition. Cases of acquired prosopagnosia were identified through a systematic literature search and lesion locations were mapped to a common brain atlas. The network of brain regions connected to each lesion location was identified using resting state functional connectivity from healthy participants (n = 1000), a technique termed lesion network mapping. Lesion networks were overlapped to identify connections common to lesions causing prosopagnosia. Reproducibility was assessed using split-half replication. Specificity was assessed through comparison with non-specific control lesions (n = 135) and with control lesions associated with symptoms other than prosopagnosia (n = 155). Finally, we tested whether our facial recognition network derived from clinically evident cases of prosopagnosia could predict subclinical facial agnosia in an independent lesion cohort (n = 31). Our systematic literature search identified 44 lesions causing prosopagnosia, only 29 of which intersected the right fusiform face area. However, all 44 lesion locations fell within a single brain network defined by connectivity to the right fusiform face area. Less consistent connectivity was found to other face-selective regions. Surprisingly, all 44 lesion locations were also functionally connected, through negative correlation, with regions in the left frontal cortex. This connectivity pattern was highly reproducible and specific to lesions causing prosopagnosia. Positive connectivity to the right fusiform face area and negative connectivity to left frontal regions were independent predictors of prosopagnosia and predicted subclinical facial agnosia in an independent lesion cohort. We conclude that lesions causing prosopagnosia localize to a single functionally connected brain network defined by connectivity to the right fusiform face area and to left frontal regions. Implications of these findings for models of facial recognition deficits are discussed.

Dataset Information

Functional MRI reveals compromised neural integrity of the face processing network in congenital prosopagnosia.

Publications

Functional MRI reveals compromised neural integrity of the face processing network in congenital prosopagnosia.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets