The face is a vital part of humans, as from it, it is possible to tell people apart. Using the face alone, people are able to distinguish between males and females, familiar and unfamiliar faces, in addition to recognizing an individual’s own face. While the lack of recognition of one’s own face may seem farfetched, people suffering from prosopagnosia indeed have a problem recognizing faces. This paper will look at prosopagnosia; a condition in which individuals have difficulties recognizing faces, and in extreme cases, their own faces. The paper will look at the process of facial recognition in the brain; the development of the condition; signs and symptoms of the disorder; its prevalence; and treatment.
The face is the most commonly used distinguishing factor that helps to tell people apart. Using the face alone, people are able to distinguish between males and females, familiar and unfamiliar faces, in addition to recognizing an individual’s own face. While the lack of recognition of one’s own face may seem farfetched, people suffering from prosopagnosia indeed have a problem recognizing faces. The disorder, also known as face blindness or facial agnosia impairs an individual’s ability to recognize faces, whether familiar or not, and in extreme cases, such individuals have a problem recognizing their own faces. Astonishing is that the progression of the disorder may cause people with the disorder to be unable to distinguish between a face and an object. While not related to any form of memory dysfunction, loss, impaired vision or learning disability, research into the disorder points to abnormalities especially to the right fusiform gyrus; a part of the neural system controlling facial perception and memory (NINDS, 2007).
The process of facial recognition is complex, and in order to appreciate the impact of the disorder, it is only prudent first to understand the facial recognition process. According to Meadows (1974), most prosopagnosia patients have posteriorly placed cerebral lesions, most of which have resulted in visual defects. However, to understand the effect of these lesions and visual defects, it is important to understand the visualization process. The complexity of facial recognition begins with the fact that visual achievement is a gestalt-like process, given the resistance of most faces to verbal interpretation (Meadows, 1974). While humans can recognize more than 1,000 faces, it may be impossible to describe the faces verbally, given that some recognition involves the discernment of the fine details of the faces being recognized (Meadows, 1974). Visualization thus, is highly dependent on the brains ability to learn visual pattern discriminations that are extremely intricate.
The complexity involved in facial recognition makes it stand apart from other visual experiences. The complexity of facial recognition demands that the brain be able to distinguish minor and intimate details of the face (Meadows, 1974). Most of these details are largely indescribable by verbal means, making the recognition processes complex yet very important in telling apart different people as well as referring to their look-alikes among other facial descriptions.
Studies involving brain imaging have helped identify parts of the brain stimulated with the viewing of faces. The cortical regions activated at the sight of faces have helped identify the regions affected in patients with prosopagnosia (Hadjikhani & Gelder, 2002). From the studies, the cortical regions have shown response in a highly discriminative manner to face stimuli. Specifically “A region in the mid-fusiform gyrus known as the fusiform face area (FFA) produces at least twice the response in fMRI to face stimuli (including cartoon faces, cat faces, and inverted faces) as to a wide variety of control stimuli such as houses, hands, the backs of human heads, scrambled faces, and flowers” (Hadjikhani & Gelder, 2002, p. 176). Additionally, the inferior occipital, although lacking in-depth research, has shown strong response to faces than other objects (Hadjikhani & Gelder, 2002). The studies on different parts of the human brain show that there are specific areas within the human brain that are responsible for face recognition, as shown by the reaction to faces.
Lee et al.’s (2009) research into developmental prosopagnosia informs that face processing includes a number of hierarchical stages and concurrent processes within the distributed cortical network. Face processing, therefore, begins with the retinal image captured by the eye’s retina. Through the low-level vision, the mind records local details that include lines and edges. The intermediate-level form vision then takes in contours. View-dependent representation of the face on the other hand is processed by the high-level form vision posterior parts of the brain that include the fusiform face area (FFA), occipito-temporal cortex (OTC), and the occipital face area (OFA), all of which help in structural encoding (Lee et al., 2009). The anterior OTC on the other hand is responsible for view-invariant representation, which then builds face recognition units. Finally, the hippocampus (HPC) and prefrontal cortex (PFC) are involved in abstract identity representation: in this case memory of the face and knowledge of the person (Lee et al., 2009). The two (HPC and PFC) are consequently responsible for building cognitive units, semantic information nodes as well as name nodes, ensuring that individuals can attach names to faces, as well as other metadata such as place of meeting among other personal information.
Apart from its complexity, face processing is unique and specific, a fact that distinguishes it from processing other objects. Individuals with normal face recognition abilities are inclined to process faces as wholes. Specifically, as the Brain Injury Association (2013) informs, people process faces by accounting for the relationship between the features of the face instead of a focus on the features themselves. This processing is perhaps the reason for difficulties in recognizing faces when upside down as opposed to the easy recognition of other objects. Further, the fact that face recognition takes into account the relationship between features is the reason for the ease in remembering faces within the context of the whole face rather than as separate viewing of the features (Brain Injury Association, 2013)
In its basic sense, prosopagnosia is a derivative of the Greek words “prosopon” and “agnosia.” The two mean “face” and “not knowing” respectively, thus jointly the inability to recognize faces. The disorder is a neurological dysfunction whose features include the impairment in face recognition (Lee et al., 2009). Before in-depth research into the disorder, there was a general assumption that the disorder was a result of brain damage—for instance, a stroke that affected a specific region of the brain region. Regarding the cause of the disorder, the Brain Injury Association (2013) states that regardless of its happening by itself or along other related and unrelated difficulties, the disorder results from damage to particular brain areas. Research on the process of face recognition puts the fusiform gyrus at the center of recognition. Naturally, therefore, the occipital lobes and the temporal lobes, both of which are instrumental in memory and perception are affected to cause prosopagnosia (Brain Injury Association, 2013). Specifically, the fusiform gyrus, a region in the temporal lobe is usually affected for the development of the disorder. It is especially the instrumental role that the region (fusiform gyrus) plays in face recognition, which has led to its labeling as the fusiform face area (FFA). Although there are two fusiform gyrus in the brain (each on the left and right hemispheres), the gyrus on the right plays an important role in face processing and recognition.
Russel, Chatterjee and Nakayama’s research on developmental prosopagnosia suggests that damage to the fusiform gyrus traditionally relates to difficulties in the mind’s recognition and perception of faces. This is different from the difficulties related to access of memories of faces experienced with damage to other areas of the temporal lobes (Brain Injury Association, 2013; Russel, Chatterjee and Nakayama, 2012). It is therefore possible that there are two subtypes of prosopagnosia: one affecting the way we perceive faces (apperceptive prosopagnosia), and the other affecting our memory for faces (associative prosopagnosia) (Brain Injury Association, 2013, p. 3). As a disorder, injury to the brain is the main cause of prosopagnosia; however, it is a rarity for the confinement of a brain injury to only a specific part of the brain. Besides, given its accompaniment with other cognitive and visual difficulties, it may be difficult to specifically point out the nature of an individual’s face processing challenges in relation to the two subtypes (apperceptive and associative).
Reference to brain injury and the development of prosopagnosia largely points at external injury to the brain that causes the disorder. There are, however, other individuals, who have the developmental form of the disorder, which happens without the individual having any brain injury. This is referred to as developmental prosopagnosia, wherein the people with the disorder are unable to develop the visual means required for face recognition (Brain Injury Association, 2013). Research into developmental prosopagnosia suggests that there is a genetic link to the development of the disorder, given reports of multiple members of the same family having the disorder (Brain Injury Association, 2013). Further research on developmental prosopagnosia on identical and non-identical twins has rightly pointed to the genetic basis of the disorder, wherein there was a strong correlation of face recognition tests between identical tests than there was between non-identical twins (Brain Injury Association, 2013). Research, nonetheless, has not been able to mark out a specific gene responsible for the development of the condition.
The Brain Injury Association (2013) suggests that there is a possibility that developmental prosopagnosia has correlations with other conditions. The Association cites case reports documenting the experiencing of uncorrected visual problems for a long time during childhood, among people with developmental prosopagnosia. Such experiences may have caused proper development of the parts of the brain responsible for vision. Even more is the knowledge of difficulty in recognition of faces among autistic spectrum disorder patients; given the patients’ impaired social functioning, failing memory and the inability among the patients in interpreting the emotional and mental states of others (Brain Injury Association, 2013).
In looking at the causes of developmental prosopagnosia, there is a debate on whether the inability to recognize faces is in relation to the organization of the brain. One side of the debate contends that the brain’s organization follows a domain specific line, while the other contends on domain general line (Russell, Chatterjee & Nkayama, 2012). Therefore, “According to the domain-specific account, the mind is divided according to the content of the information processed while in the domain-general account, the mind is divided according to the kinds of processes it carries out” (Russell, Chatterjee & Nkayama, 2012, p. 335). The debate is in reference to the two types of prosopagnosia, on whether the condition affects the recognition of faces, or the process involved in the recognition of faces. Yet the debate invokes a third opinion on the cause of the disorder in relation to developmental prosopagnosia. According to the third opinion, “Rather than being a deficit in face specific processes or expert specific processes, developmental prosopagnosia could be due to a deficit in a visual competency that is more relevant for recognizing faces than for recognizing other kinds of objects” ( Russell, Chatterjee & Nkayama, 2012, p. 335). The third opinion, hence, argues that the condition is not a result of abnormal development of face-specific neural circuits or expertise-specific neural circuits; rather the uncharacteristic development of a perceptual ability vital in the recognition of faces that causes the disorder.
Even with the debate on the causes of the disorder, it is important to note that the condition affects only a small portion of the population. The Brain Injury Association approximates that the condition affects only about 2 percent of the population. The percentage is similar to what Kennerknecht et al. (2006) found in their study on the prevalence of the disorder, where of the 689 candidates involved in the study, 2.47 percent had prosopagnosia. From the study, it is apparent that prosopagnosia’s prevalence is among the highest for a monogenic disorder (Kennerknecht et al., 2006).
Prosopagnosia additionally, affects both male and female in equal measure, and for developmental prosopagnosia, it is most commonly hereditary. In a study of the prevalence of the condition, Kennerknecht et al. (2006) discovered that a familial history of the condition showed a father, two daughters and a son as having the disorder. The study, which involved the family, with one of the daughters as the subject, discovered that the girl had problems recognizing familiar people reliably (Kennerknecht et al., 2006). Further probing of the family discovered that her father, brother, and middle sister also had complains regarding the face recognition mistakes they made in their daily lives. The disorder’s genetic link is perhaps cemented by a study that found familial recurrence of the disorder in more than our generations, inclusive of a father-to-son transmission (Kennerknecht et al., 2006).
The risk of developing the condition is highly heightened with a family history of the disorder. As aforementioned, prosopagnosia emanates from brain injury, and on specific areas of the brain (Hadjikhani & Gelder, 2002). Such injuries are secondary causes of the disorder. The risk is therefore real for anyone with a family history of the disorder. The genetic link makes anyone with a family member who has the disorder vulnerable to developing the disorder or passing it down to the next generation (Kennerknecht et al., 2006).
In the study by Kennerknecht et al., the discovery of the girl’s condition became evident through the difficulty she had in recognizing familiar people reliably. While this is a mild case of the disorder, in extreme cases of the disorder, patients exhibit the inability to recognize faces, including family members and their own. Additionally, the inability to recognize an individual because they have a different haircut, walking style or change in clothes points to prosopagnosia.
The inability to recognize faces for prosopagnosia patients results from their inability to make a relation between face features. Thus, although they are able to make out all the features of the face, they have difficulty in using the information to recognize familiar faces. Simply put, they have a difficulty in the holistic processing of faces (Hadjikhani & Gelder, 2002). Instead of processing faces in their completeness, prosopagnostics regard each feature of the face separately, processing the face in a fragmentary manner, looking at each feature of the face in turn. The result of the fragmented manner is that face recognition takes longer in addition being difficult to process. Moreover, this distorts the spatial relationship between the different features of the face, which are some of the most important information for accurate face recognition (Brain Injury Association, 2013).
Mild prosopagnosia means that the individual is capable of recognizing close friends and relatives. This is, however, only under normal circumstances. For patients with a severe case of the disorder, they may not recognize the relatives, friends and even themselves, especially with changes in gait, hairstyle or clothing. Additionally, it is easy to spot patients with the disorder since they (prosopagnostics) rely on other cues other than facial recognition to identify others. These cues include hairstyles, voice, body shape, gait and sometime characteristic facial expressions (Duchaine, 2011).
Another symptom for the disorder is the inability to identify people out of their normal context. Duchaine (2011) enthuses that context is an important element for prosopagnostics, in that it helps them recognize people within a particular context. Thus, it is possible for individuals with the disorder to identify colleagues at their place of work. However, prosopagnostics may be at loss in identifying their colleagues at a different place, say at the shopping mall (Duchaine, 2011). Interestingly, such individuals use more than facial cues for recognition, in addition to storing other facial cues as a means of facial recognition (Duchaine, 2011).
Although the above symptoms flag the possibility of the individual to have prosopagnosia, the diagnosis of the disorder requires a cognitive assessment session to determine the possibility of the disorder. Diagnosis for the disorder involves referral of the individuals to a clinical neuropsychologist or a professional with a private practice. Referrals may also be directed to a researcher specializing in the field, in addition to self-referrals (Brain Injury Association, 2013). The diagnostic test for prosopagnosia involves tests aimed at assessing an individual’s face recognition ability, in addition to the individual’s cognitive and visual skills. The assessment in this case aims at finding out the patient’s ability to memorize and later recognize a range of face the patient has never seen before. The test also assesses the ability of the patient to identify famous faces, pick out similarities and differences between face set side by side as well as pass judgment on age, gender or emotional expression from a set of faces (Brain Injury Association, 2013).
The aim of the tests is to assess the difficulties in memory, attention or vision and their contribution to the recognition difficulty. Sad, however, there is no known treatment for the condition as it is permanent, especially for developmental prosopagnosia. This means that the condition does not improve, although some researchers are working on programs to help improve face recognition skills. Such programs are not capable of offering any actual or permanent cure; however, research extrapolates that regular training involving faces has a chance of improving face recognition abilities.
Duchaine, B. (2011). Handbook of Face Perception. Oxford: Oxford University Press
Hadjikhani, N. & Gelder, B. (2002). Neural Basis of Propagnosia: An fMRI Study. Human Brain Mapping, 16, 176-182
Kennerknecht, I. et al. (2006). First Report of Prevalence of Non-Syndromic Hereditary Prosopagnosia (HPA). American Journal of Medical Genetics Part A, 140A, 1617-1622
Lee, Y. et al. (2009). Three cases of developmental prosopagnosia from one family: Detailed neuropsychological and psychophysical investigation of face processing. Cortex, 1-16
Meadows, J., C. (1974). The anatomical basis of prosopagnosia. Journal of Neurology, Neurosurgery, and Psychiatry, 37, 489-501
NINDS (2007). NINDS Prosopagnosia Information Page. NINDS. Retrieved from http://www.ninds.nih.gov/disorders/prosopagnosia/Prosopagnosia.htm
Russel, R., Chatterjee, G. & Nakayama, K. (2012). Developmental prosopagnosia and super-recognition: No special role for surface reflectance processing. Neuropsychologia, 50, 334-340
The Brain Injury Association (2013). Prosopagnosia: Face Blindness after Brain Injury. Nottingham, NIA.