Face forgetting is a Greek word composed of two parts "προσωπον" meaning face and "αμνησια" meaning to forget. Face forgetting is a selective neural impairment in the ability to learn new faces. There is a special neural network for processing faces as opposed to other non-face objects. It is also a deficit in the part of this neural network responsible for encoding perceptions as memories. Prosopagnosia manifests itself in patients as an inability to recognize people they have previously encountered based on their faces. In this way, prosopagnosia is easily mistaken for prosopagnosia. Prosopagnosia is defined as the inability to perceive or recognize faces and is also a deficit that occurs early in the neural network during the processing of facial stimuli. Prosopagnosia occurs when the brain attempts to encode processed facial stimuli into memory. A person with prosopagnosia cannot even recognize the faces of family members over a lifetime. People with prosopagnosia have a memory for facial stimuli they learned before the onset of their condition or for facial stimuli they have encountered repeatedly over long periods of time. Currently, there are only two cases of prosopagnosia that have been diagnosed, and this is likely due to the fact that prosopagnosia can be misdiagnosed as prosopagnosia based on symptoms. Some clinicians have even recognized the differences between deficits in face perception and facial memory encoding and have classified the deficits as subcategories of prosopagnosia. This lack of consistency within the scientific community in classifying patients with facial memory encoding deficits is one reason why the diagnosis of this condition is rare. Most of the current information about how face forgetting occurs in the brain is speculative and has not been proven due to the lack of studies on the condition. A correct diagnosis of face forgetting may occur when doctors are able to tell the difference between prosopagnosia and face forgetting. Face forgetting can be genetic or acquired as a result of accidental brain damage. The exact cause of face forgetting has not been investigated because there are only two known cases. Each group of doctors who have studied currently diagnosed face forgetting has proposed slightly different explanations for why. Dr. Tippett's group described face forgetting as a "dissociation between learning mechanisms and domain-specific representations"—in other words, a general dysfunction in the brain's ability to encode a representative face stimulus into memory. Dr. Williams's group hypothesized that face forgetting is caused by the inability of the fusiform face area to maintain a stable representation of new faces long enough to be encoded into memory. This conclusion is based in part on the patient's different responses to familiar and unfamiliar faces within the fusiform face area as seen in blood oxygenation responses recorded during functional magnetic resonance imaging tests. Visual stimuli are processed within the brain by several biological neural networks. Given the importance of the ability to recognize faces and associate information with others, humans have developed a distinct neural network for processing facial stimuli. Since the discovery of this distinct network, the anatomical structures involved have been studied in depth. Initial processing of visual stimuli occurs in the prefrontal cortex, the posterior parietal cortex, and the precuneus. The stimuli are then identified as facial processing and more precisely. The stimuli occur within the fusiform face area, the occipital lobe, and the face-selective area of the superior temporal sulcus. The fusiform face area serves low-level tasks such as distinguishing between details and similar known objects. The occipital lobe and the superior temporal sulcus serve higher-level processing tasks such as associating a person’s identity with their face and processing emotions based on the arrangement of facial features, respectively. Once facial stimuli are processed, they are encoded into memory. This involves several brain structures including the temporal lobe and the hippocampus. The storage and retrieval of these memories involves the same regions as the fusiform face area and the occipital cortex. The frontal and posterior parietal cortex performed the primary processing tasks. The following criteria are used to diagnose patients with acquired face amnesia: In acquired face amnesia, face recognition must match the timing of the lesion; that is, faces encountered before the lesion are recognized as familiar, while faces encountered after the lesion are considered unfamiliar. Face memory and recognition tests are essential to ensure an accurate diagnosis of prosopagnosia and prosopagnosia. Several face memory and recognition tests have been developed and used by researchers in the past, including the Warrington Face Recognition Memory Test, the Benton Face Recognition Test, and the Cambridge Face Recognition and Face Memory Test, which were developed to address the shortcomings of the first two tests. The Warrington Face Recognition Memory Tests contain a wealth of information about non-internal facial features. The Benton Face Recognition Test allows the test taker to rely on features that match the strategies used, such as the hairline and eyebrows, rather than recognizing the facial configuration. The Cambridge Face Recognition Test allows participants to look at a target face and then rank 6 other faces according to their similarity to the target face. People with prosopagnosia will fail this test, while people with prosopagnosia will pass it, making this test a hallmark for differentiating between the two disorders. The Cambridge Face Memory Test gives participants 20 seconds to look at a set of target faces. Participants are then shown one of the test cases from the first set of target faces, and are given a score based on how many target faces they can correctly recognize from the test cases. The test is repeated using different target faces with different levels of Gaussian noise. A person with normal face processing abilities on this test will score an average of 80%, while a person with poor face processing or face memory will score less than 50%. Face forgetting was first proposed as a distinct neurological disorder in 1996. Doctors observed a patient who appeared to have prosopagnosia after a temporal lobe injury. This initial patient was unable to recognize faces of people he encountered after the injury but had no problem recognizing faces of people he had previously known. This discrepancy led doctors to view the deficit as involving encoding facial memories rather than just perception. This was the first case of acquired face forgetting. More than a decade later, another group of scientists came across a similar patient. The group initially thought the patient had prosopagnosia based on her symptoms. However, after further investigation, they discovered that the problem was not with face recognition, because the patient had been able to pass the Cambridge Face Recognition Test but had shown an inability to remember facial stimuli based on poor scores on the Cambridge Face Memory Test. Upon this discovery, the doctors found research that had been done on the initial case of prosopagnosia and reached the same diagnosis. After this case, the criteria for diagnosing prosopagnosia were refined from a list of specific symptoms to a more formal scale that required a normal score on the Face Recognition Test and a significantly low score on the Face Memory Test. In the second case of prosopagnosia, the patient reported a lifelong deficit in the ability to remember faces. This suggests that damage to the neural network vital to face processing could be genetic or accidental brain damage. There are many implications for the field of neuroscience that the discovery of face forgetting supports. Within the biological neural network involved in processing visual stimuli is a special network for face processing. This neural network is present from birth, as evidenced by newborns who show a predisposition to follow face-like patterns. Normal infants are able to recognize familiar faces, as evidenced by the fact that infants react differently when people approach them depending on whether they are familiar or not. Based on evolutionary theory, for a unique biological neural network to arise and be inherited, some survival or fitness advantage must be present. It has been suggested that the ability to recognize faces is important for seeing another person as friend or foe. This network specializes over time to become more adept at distinguishing facial features between familiar people, ethnic groups, and age groups. This has led to a phenomenon known as the interracial effect, where people are much better at distinguishing between faces of people from the same group. Other implications of face forgetting include a division of labor within the brain. People with acquired face forgetting are able to recognize familiar faces before brain damage occurs. This implies a division of labor between primary memory encoding and information storage and also suggests that these tasks are performed in different regions within the brain. Face forgetting is characterized as a deficit in encoding facial memories, while prosopagnosia is a deficit in recognizing facial information. The fact that there are multiple divisions of labor within the neural network vital for face processing and other neural networks in general makes it difficult to distinguish between disorders such as face forgetting and face forgetting.