Prosopagnosia, or face blindness, is a neuropsychological disorder that impairs the recognition of faces. This condition can also affect the recognition of places and cars, as well as the interpretation of facial expressions. However, it is important to highlight that prosopagnosia does not impact intellectual, sensory, or cognitive abilities. Therefore, individuals with this disorder can still identify people using non-facial cues.
Prosopagnosia, a condition characterized by the inability to recognize familiar people solely by their faces, often requires alternative methods to compensate for this impairment. These methods include relying on traits like voice, gait, clothing, hairstyle, and other non-facial information. The social consequences of prosopagnosia can be significant as individuals with this condition struggle to identify familiar faces even if they are famous individuals, close friends, family members or when looking at themselves in a mirror. The term “prosopagnosia” was coined in 1947 by Bodamer, a German neurologist (Ellis & Florence, 1990).
The term prosopagnosia, which refers to a difficulty in identifying faces, comes from the Greek word for face (prosopon) and the medical condition known as agnosia. As stated by Bodamer, acquired prosopagnosia can be attributed to brain damage caused by head trauma, stroke, or degenerative disease. Individuals with acquired prosopagnosia initially possess normal abilities in recognizing faces but eventually experience impairments. On the other hand, congenital prosopagnosia can manifest at birth without any documented brain injury.
Prosopagnosia, which is also referred to as face blindness, is a condition that specifically hinders the ability to identify faces. This impairment is distinct from other conditions that may also impact face recognition (Young, 1992). Individuals with prosopagnosia can still recognize people using non-facial cues. However, Young (1992) conducted a case study on patient K.S., who struggled with identifying individuals based on their faces and names. The difficulty was attributed to difficulties in retrieving semantic information about people’s identities. It should be noted that prosopagnosia encompasses various types of recognition impairments and can differ among patients.
In their 1986 study, Bruce & Young proposed that breakdowns at various stages or levels of recognition are associated with different types of recognition impairments. Prosopagnosia, a condition typically acquired in adulthood or during childhood development due to brain injury, is believed to be linked to lesions in the ventral occipitotemporal regions (Damasio et al., 1982). Research suggests that prosopagnosia is more commonly associated with unilateral lesions in the right cerebral hemisphere compared to the left side (Damasio et al., 1982; Farah, 1990).
Initially, autopsy reports suggested only a small number of individuals with prosopagnosia had bilateral lesions (Damasio et al., 1982), but later perspectives argue that the extent of lesions may have been underestimated and more cases could have bilateral lesions due to limited resolution in brain imaging techniques (Farah, 1990). Despite differing views on this matter, there have been instances where individuals diagnosed with prosopagnosia had bilateral lesions. For example, patient FE (Bobes et al., 2004) suffered a head trauma resulting in bilateral lesions.
Following their recuperation, the person experienced difficulty in recognizing familiar individuals solely through facial appearance. Magnetic resonance imaging (MRI) exhibited detailed brain lesion images and disclosed that the harm to the ventral occipitotemporal area was more extensive on the right side. This suggests that the right hemisphere may play a significant role in prosopagnosia. Lately, there has been growing attention towards developmental prosopagnosia.
The functional deficits in brain imaging studies of individuals with developmental prosopagnosia, a condition characterized by impaired face recognition, are similar to those with acquired prosopagnosia. There is little evidence of a structural brain deficit in individuals with developmental prosopagnosia (Bentin et al. 1999). In a study conducted by Hadjikhani and de Gelder (2002), they identified the fusiform face area (FFA) located in the midfusiform gyrus and the inferior occipital gyrus (IOG) as two crucial regions for normal face recognition in humans. They examined three patients in their study – one with pure developmental prosopagnosia and two who had experienced a head injury in childhood – all of whom displayed severe impairments in face recognition.
The patients in this study did not have any structural abnormalities in their brain scans. However, they exhibited functional deficiencies in the fusiform face area (FFA) and the inferior occipital gyrus (IOG). Unlike normal subjects, these regions did not show stronger responses to faces than objects. Despite this, the patients had no trouble distinguishing between faces and objects and showed a partially normal pattern of activation when viewing objects. Therefore, it is concluded that their difficulty in recognizing faces stems from the lack of functionality in the FFA and IOG rather than an inability to detect them. This suggests a functional model for prosopagnosia.
Prosopagnosia, a type of agnosia, extends beyond slight impairment. People with prosopagnosia cannot recognize faces but can still identify objects. McCarthy and Warrington (as cited in Farah & Ratcliff, 1994) found a patient who had difficulty recognizing pictures of everyday objects but had no trouble with familiar face images. This dual dissociation supports the idea that facial recognition and object identification rely on separate mechanisms that function autonomously.
The location of brain cells responsible for face recognition is still unknown, but functional models have been developed to aid in our understanding of face recognition and prosopagnosia. Bruce and Young (1986) proposed a highly influential model which breaks down face recognition into various steps, with three steps particularly relevant to prosopagnosia. The first step is structural encoding, which encompasses view-centred descriptions and expression-independent descriptions. View-centred descriptions are derived from visual input and provide information for analyzing expressions, facial speech, and directing visual processing.
To identify a person by their face, it is essential to transform descriptions that focus on specific facial features into unbiased descriptions. These transformed descriptions then stimulate the activation of units responsible for recognizing faces. People with prosopagnosia may have trouble recognizing faces due to difficulties in accurately encoding facial structure, resulting in challenges in tasks related to perceiving faces. They are unable to perceive attributes like age or gender and struggle with determining if two faces belong to the same individual. Moreover, these face recognition units store descriptions of familiar faces and when encountering a familiar face, they send signals to the cognitive system and activate nodes associated with personal identity.
Person identity nodes provide access to semantic information about individuals. The inability to recognize familiar individuals may not be solely attributed to impaired face recognition units, as person identity nodes can gather information from non-facial cues as well. Some individuals with prosopagnosia may experience issues with the connection between their face recognition units and person identity nodes. In the case of Patient P. H. (Young, 1992), they exhibit impairment in tasks that require a connection between face perception processes and the semantic information associated with faces. Notably, P. H. is unable to recognize familiar individuals based solely on their faces, but is able to recognize them relatively well when presented with their names.
In summary, face identity nodes can generate contact names independently of semantic information about the person. The link between face recognition units and name generation is exemplified by the case study of patient P. H. (Humphreys & Bruce, 1989). This patient demonstrated implicit recognition of faces and was able to quickly associate correct names with appropriate faces, but struggled to learn the association between names and a person’s occupation.
It seems that the access to face recognition units is intact, but there is impaired access to person identity nodes. According to Bruce & Young (1986), they provided a functional framework for face recognition, identifying several stages. The breakdown of one stage or disconnection of two stages causes prosopagnosia. Moreover, this impairment primarily affects overt recognition but has less impact on covert recognition. Prosopagnosia is linked to a deficit in configural processing, which refers to the inability to perceive relationships among facial features.
Individuals with prosopagnosia have difficulty perceiving the spatial relationships between facial features and often rely on a feature-based strategy for recognizing faces. Humphreys & Bruce (1989) conducted a study involving a prosopagnosic patient named R.B., testing their ability to detect spatial relationships by presenting patterns of faces with configurable features or non-face patterns with jumbled and symmetrical features. R.B. had to determine whether each pattern was a face or “nonface”. Compared to people without prosopagnosia, R.B. responded faster to non-faces rather than faces, indicating that they did not consider the spatial relationships between facial features but instead evaluated each feature individually for face recognition. Hence, this research suggests that prosopagnosia is linked to impaired configural processing capacity.
Farah et al. (1995) conducted another study comparing the processing of upright and inverted faces in a prosopagnosic patient called LH and normal subjects using a face-matching task. LH demonstrated better accuracy and speed when matching inverted faces compared to upright ones.
Contrary to expectations, individuals without any visual impairments performed significantly better at recognizing upright faces compared to inverted ones. Furthermore, these normal subjects exhibited the “face inversion effect,” meaning they struggled to perceive an inverted face as a whole and instead relied on a feature-based approach. This resulted in longer reaction times and lower accuracy for inverted faces compared to upright ones. In contrast, patient LH displayed an “inversion superiority effect,” meaning he was actually better at recognizing inverted faces than upright ones. This suggests that LH’s superior performance with inverted faces may be attributed to the absence of valid configural processing or the implementation of an effective feature-based strategy.
Configural processing is the perception of a visual item as a whole, and it may explain why some individuals with prosopagnosia can still recognize faces. Prosopagnosia, or difficulty in recognizing faces, has two functional explanations for this impairment. Both explanations suggest that normal face recognition processes are not functioning correctly, but they have different perspectives. It seems that prosopagnosia can manifest in different impairments, so neither explanation can explain all cases of the condition.
There is a correlation between prosopagnosia and brain dysfunctions as suggested by neuropsychological explanations.
References
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- Bobes, M. A. , Lopera, F. , Coma, L. D. , Galan, L. , Carbonell, F. , Bringas, M. L. , & Valdes-Sosa, M. (2004). Brain potentials reflect residual face processing in a case of prosopagnosia. Cognitive Neuropsychology, 21(7), 691-718.
- Bruce, V. & Young, A. (1986).
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- Farah, M. J. , Wilson, K. D. , Drain, H. M. & Tanaka, J. R. (1995). The inverted face inversion effect in prosopagnosia: Evidence for Mandatory, face-specific perceptual mechanisms.
- Vision Research, 35(14), 2089-2093. Hadjikhani, N. & Gelder, B. (2002). Neural basis of prosopagnosia: An fMRI Study. Human Brain Mapping, 16, 176-182. Humphreys, G. W. & Bruce, V. (1989). Visual Cognition: Computational, experimental, and neuropsychological perspectives. (pp. 89-101).
- East Sussex: Lawrence Erlbaum Associates. Young, A. W. (1992). Face recognition impairments. Philosophical Transaction of the Royal Society, London, Series B 335, 47-54.
