The 170ms Response to Faces as Measured by MEG (M170) Is Consistently Altered in Congenital Prosopagnosia.

Modularity of face processing is still a controversial issue. Congenital prosopagnosia (cPA), a selective and lifelong impairment in familiar face recognition without evidence of an acquired cerebral lesion, offers a unique opportunity to support this fundamental hypothesis. However, in spite of the pronounced behavioural impairment, identification of a functionally relevant neural alteration in congenital prosopagnosia by electrophysiogical methods has not been achieved so far. Here we show that persons with congenital prosopagnosia can be distinguished as a group from unimpaired persons using magnetoencephalography. Early face-selective MEG-responses in the range of 140 to 200ms (the M170) showed prolonged latency and decreased amplitude whereas responses to another category (houses) were indistinguishable between subjects with congenital prosopagnosia and unimpaired controls. Latency and amplitude of face-selective EEG responses (the N170) which were simultaneously recorded were statistically indistinguishable between subjects with cPA and healthy controls which resolves heterogeneous and partly conflicting results from existing studies. The complementary analysis of categorical differences (evoked activity to faces minus evoked activity to houses) revealed that the early part of the 170ms response to faces is altered in subjects with cPA. This finding can be adequately explained in a common framework of holistic and part-based face processing. Whereas a significant brain-behaviour correlation of face recognition performance and the size of the M170 amplitude is found in controls a corresponding correlation is not seen in subjects with cPA. This indicates functional relevance of the alteration found for the 170ms response to faces in cPA and pinpoints the impairment of face processing to early perceptual stages.

Age-dependent face detection and face categorization performance.

Empirical studies on the development of face processing skills with age show inconsistent patterns concerning qualitative vs. quantitative changes over time or the age range for peak cognitive performance. In the present study, we tested the proficiency in face detection and face categorization with a large sample of participants (N = 312; age range: 2-88 yrs). As test objects, we used so-called Mooney faces, two-tone (black and white) images of faces lacking critical information of a local, featural and relational nature, reflecting difficult real world face processing conditions. We found that performance in the assessment of gender and age from Mooney faces increases up to about age 15, and decreases from 65 years on. The implications of these findings are discussed in the light of classic and recent findings from face development literature.

Visual mental imagery in congenital prosopagnosia.

Congenital prosopagnosia (cPA) is a selective impairment in the visual learning and recognition of faces without detectable brain damage or malformation. There is evidence that it can be inherited in an autosomal dominant mode of inheritance. We assessed the capacity for visual mental imagery in 53 people with cPA using an adapted Marks' VVIQ (Vividness of Visual Imaging Questionnaire). The mean score of the prosopagnosic group showed the lowest mental imagery scores ever published for a non-brain damaged group. In a subsample of 12 people with cPA, we demonstrated that the cPA is a deficit of configural face processing. We suggest that the 'VVIQ-PA' (VVIQ-Prosopagnosia) questionnaire can help to confirm the diagnosis of cPA. Poor mental imagery, a configural face processing impairment and clinical prosopagnosia should be considered as symptoms of a yet poorly understood hereditary cerebral dysfunction.

Simulation of talking faces in the human brain improves auditory speech recognition.

Human face-to-face communication is essentially audiovisual. Typically, people talk to us face-to-face, providing concurrent auditory and visual input. Understanding someone is easier when there is visual input, because visual cues like mouth and tongue movements provide complementary information about speech content. Here, we hypothesized that, even in the absence of visual input, the brain optimizes both auditory-only speech and speaker recognition by harvesting speaker-specific predictions and constraints from distinct visual face-processing areas. To test this hypothesis, we performed behavioral and neuroimaging experiments in two groups: subjects with a face recognition deficit (prosopagnosia) and matched controls. The results show that observing a specific person talking for 2 min improves subsequent auditory-only speech and speaker recognition for this person. In both prosopagnosics and controls, behavioral improvement in auditory-only speech recognition was based on an area typically involved in face-movement processing. Improvement in speaker recognition was only present in controls and was based on an area involved in face-identity processing. These findings challenge current unisensory models of speech processing, because they show that, in auditory-only speech, the brain exploits previously encoded audiovisual correlations to optimize communication. We suggest that this optimization is based on speaker-specific audiovisual internal models, which are used to simulate a talking face.

Neural and genetic foundations of face recognition and prosopagnosia.

Faces are of essential importance for human social life. They provide valuable information about the identity, expression, gaze, health, and age of a person. Recent face-processing models assume highly interconnected neural structures between different temporal, occipital, and frontal brain areas with several feedback loops. A selective deficit in the visual learning and recognition of faces is known as prosopagnosia, which can be found both in acquired and congenital form. Recently, a hereditary sub-type of congenital prosopagnosia with a very high prevalence rate of 2.5% has been identified. Recent research results show that hereditary prosopagnosia is a clearly circumscribed face-processing deficit with a characteristic set of clinical symptoms. Comparing face processing of people of prosopagnosia with that of controls can help to develop a more conclusive and integrated model of face processing. Here, we provide a summary of the current state of face processing research. We also describe the different types of prosopagnosia and present the set of typical symptoms found in the hereditary type. Finally, we will discuss the implications for future face recognition research.

Prosopagnosia in biographies and autobiographies.

Prosopagnosia is a selective impairment of the visual learning and recognition of faces. The congenital type, which is not accompanied by detectable brain damage or malformation, was recently found to be far more common than previously known. Therefore, one should expect that at least a few biographies or autobiographies would reveal a prosopagnosia. In this paper we present an autobiography and a biography describing five cases of congenital prosopagnosia. These biographic descriptions of prosopagnosia add further evidence to the assumption that the congenital type of prosopagnosia is not a rare condition, and not as socially crippling as one might expect.

Gaze behaviour in hereditary prosopagnosia.

Prosopagnosia is the inability to recognize someone by the face alone in the absence of sensory or intellectual impairment. In contrast to the acquired form of prosopagnosia we studied the congenital form. Since we could recently show that this form is inherited as a simple monogenic trait we called it hereditary form. To determine whether not only face recognition and neuronal processing but also the perceptual acquisition of facial information is specific to prosopagnosia, we studied the gaze behaviour of four hereditary prosopagnosics in comparison to matched control subjects. This rarely studied form of prosopagnosia ensures that deficits are limited to face recognition. Whereas the control participants focused their gaze on the central facial features, the hereditary prosopagnosics showed a significantly different gaze behaviour. They had a more dispersed gaze and also fixated external facial features. Thus, the face recognition impairment of the hereditary prosopagnosics is reflected in their gaze behaviour.