FFA

Fusiform face area (FFA)

Fusiform face area (FFA) is a part of the brain in the inferior-temporal cortex, which appears to specialize in face recognition.

In a nutshell, people suffering from acquired prosopagnosia have lost the ability to properly recognize faces, which was absolutely normal before a neurological event, whereas people with congenial prosopagnosia have never developed typical face recognition abilities despite the absence of any evident neurological problem.

In the remainder of this entry, we will learn about both forms of prosopagnosia and about their similarities and differences. Both conditions represent unique opportunities for cognitive science to understand the normal cognitive and neural aspects of face processing.

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:

My life changed completely; I feel so uncomfortable and ashamed of my condition that I rather stay at home avoiding meeting friends that, certainly, I cannot recognize.Michael, acquired prosopagnosia patient

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.

At the time it was not possible to conduct non-invasive examinations of the brain anatomy after the injury (e.g., structural MRI); however the clinical features of the patients who typically reported left hemiplegia led some investigators, such as Quaglino, to argue for right-sided brain lesions.

A few decades later, Hoff and Poetzl (1937) explicitly suggested that face recognition might be a separate function that can be impaired following brain injury. However, it was not until 1947 that Bodamer described the inability to recognize familiar faces to be a selective form of visual agnosia, referring to it as prosopagnosia. Since Bodamer’s seminal paper, more than a hundred case reports of prosopagnosia have been published (De Haan, 2001).

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. One way to test this hypothesis is by investigating in detail single case studies of prosopagnosics using human neuroimaging.

Over the last 10 years Rossion and collaborators provided extensive reports of PS, a woman born in 1950 that sustained a severe close-head injury in 1992 after being hit by a bus. This accident mainly caused a brain lesion in the lateral part of the occipito and temporal lobes bilaterally. Even many years after the accident and after neuropsychological rehabilitation PS still presents a massive prosopagnosia that prevents her from recognizing famous and familiar people by their faces.

This impairment contrasts with her excellent person recognition from people’s voice, hairstyle, gait, size and posture (Rossion et al., 2003). For example, she could feel a sense of familiarity only for 14 aces of 60 that she knows really well by their names, and she could recognize only four of them. Despite this difficulty with face recognition, PS did not report any complaints about object recognition that, as demonstrated neuropsychological tests, is well within the normal range. The interesting aspect about PS’s case is that she has a brain lesion that affects the normal activity of the right OFA, sparing the more anterior FFA.

In other words, by using fMRI it is possible to see the FFA, but not the OFA. This suggests that visual information can reach the FFA, where neural activity categorizes the perceived stimulus as a face, without receiving any information from the OFA, areas where featural processing is taking place. This and further experimental evidence (Ewbank et al., 2012) posits against a hierarchical proposal of visual areas, and suggests that the OFA plays a crucial role for normal face processing.

PS’s case represents an example of how a single-case detailed analysis conducted at a behavioral and neural level can provide precious information about normal and abnormal aspects of face recognition. Studies in acquired prosopagnosia have demonstrated:

1. Left side (posterior) lesions are often characterized by a general visual agnosia that can involve faces (in this case prosopagnosia is just a symptom of a more general agnostic problem).
2. Right sided (posterior) lesions cause prosopagnosia as a distinct syndrome characterized by the impairment in familiarity feelings (i.e., telling whether the seen face is familiar or not) and holistic processing (i.e., processing the spacing between features).

With this, we bring this entry to a close. Congenital prosopagnosia is discussed next Opens in new window.