Prosopagnosia: The Inability to Recognize Faces

Most people recognize familiar faces rapidly, accurately and effortlessly. However, this is not true for individuals with prosopagnosia, who show a deficit in recognizing familiar people by their faces.

Prosopagnosia is defined as an acquired deficit in face recognition caused by brain damage. It usually results from damage to the FFA areas in the temporal lobe, typically as the result of a stroke or other event that prevents oxygen from reaching these areas of the brain.

The word prosopagnosia, from the Greek prosopon (face) and a-gnois (without knowledge), was coined for the first time by the German neurologist Bodamer (1947) who described three cases, including a 24 year old man who lost his ability to recognize faces after suffering a bullet wound to his head.

In contrast, he was able to identify familiar people through other sensory modalities such as hearing and touch, or even through extra-facial visual cues such as gait and physical mannerisms. This case reflects an acquired condition, that is, a condition that was not present from birth but that followed some traumatic events, thus it is known as acquired prosopagnosia.

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Acquired Prosopagnosia: History of the Condition

Michael is a 62 years old man who suffered a stroke while he was fishing at a lake in a small village not too far from Sydney. Peter, his son, who luckily was with him in that moment, promptly transferred his father to the closest hospital.

A few hours later the doctor gave the bad news to the family: Michael had had stroke in the right hemisphere of his brain. Two months later Michael underwent a neuropsychological examination to evaluate his cognitive functions. His language, memory, attention and the capacity to recognize objects were largely intact, however, Michael was no longer able to memorize new faces nor to recognize familiar faces.

He could only recognize his wife and his son by using extra-facial tools, such as the hair-style or a particular outfit. It has been also reported that on some occasions Michael could not recognize himself in the mirror or even in pictures taken a few months before the injury. By using his own words:

Michael suffers from acquired prosopagnosia. Public awareness of this particular condition rose in the 80s by the beautiful descriptions provided by Dr Oliver Sacks, who described in his book the case of a “man who mistook his wife for a hat”, due to a severe impairment in visual recognition.

The first observation that face recognition can be impaired in brain injured individuals can be traced back to the ancient Greeks (Thucidydes II, 49-50), with reports of soldiers injured in the Peloponnesian War who exhibited “strange behaviors” including severe memory problems and an inability to recognize friends (Schmalzl, 2007).

Jumping back to the nineteenth century, similar difficulties were reported in patients who suffered neurological diseases. The first scientific observation of a patient’s inability to recognize familiar faces comes from Wigan who, in 1844, described a man with a complete impairment in remembering faces.

Other descriptions came from Quaglino (1867), Jackson (1872), Charcot and Bernard (1883), and Wilbrand (1892) who described patients with serious impairments in perceiving, remembering and recognize faces; even very familiar faces and sometimes their own face in the mirror.

Prosopagnosia describes a condition of face blindness. Patients can recognize other objects, but they can no longer recognize faces. Most people can recognize a face regardless of context.

One can recognize his or her father’s face, regardless of where one sees it. If the father’s face is in the newspaper, on the “fan-cam” at a sporting event, or in a family album, it can be recognized. A patient with prosopagnosia cannot do this. However, characteristics that are not facial in nature can help the patient recognize a familiar face. For example, if the patient’s spouse always wears a trademark hat, recognition can occur by noting the hat.

The face recognition system is mediated by different anatomical sources spanning from posterior to most anterior brain regions.

According to the Haxby model, the first area involved in the face processing is the OFAA that, in turn, will send information to FFA and other areas. From this view it follows that a selective lesion involving the OFA will cause abnormal functioning of all other face areas.

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