Prosopagnosia: Whose face is that?

Prosopagnosia: Whose face is that?
Published on April 15, 2012 by Jenni Ogden, Ph.D. Psychology Today.
How many of you find movies and TV shows confusing because the same blonde woman appears to be both the murderer and the murdered? And then she appears again as the detective! If this is a common problem for you, and your partner is constantly having to explain who is who, you may have a mild form of prosopagnosia

Until quite recently, it was thought that this was a rare neurological disorder that occurred only after brain damage or disease, usually to the occipital (visual) lobes at the back of the brain, or to the adjacent temporal lobes. But it is now a matter of scientific record that mild forms of developmental or congenital prosopagnosia occur in the normal, healthy population. Oliver Sacks, the neurologist and author of so many amazing books about brain damaged patients, has quite a severe case of congenital prosopagnosia. He describes his symptoms in his book, “The Minds Eye,” in the chapter called “Face-Blind.” For example, on one occasion he was to meet his personal assistant of six years in his publisher’s office. He sat in the waiting room without realizing that the young woman also sitting there and smiling at him was his assistant! After about five minutes she told him who she was; she’d been testing him to see how long he took to recognize her. Like many people with prosopagnosia, Sacks also has a problem with recognizing places: he can go for a walk around the block his house is in, and then be unable to find it: he walks past it time and again. 

Sacks’s difficulties are at the severe end of the spectrum of congenital face and place recognition problems. Most non brain-damaged people with prosopagnosia will be much less affected. Probably people very well known to them will be readily recognized, and it is only when they meet people they don’t see very often that they have difficulty. If your only problem is keeping track of who is who in movies, then your prosopagnosia is at the very mild end of the spectrum, and would likely not even be significant enough to earn the prosopagnosia label .
Congenital face-blindness appears to be inherited, and affects around 1 in every 50 people. So if this is you, you are not alone: in the USA you join a group of more than 6 million. It behoves film makers to make their characters as different as possible, especially in those complex murder mysteries! If you think you might have this problem you can test yourself by signing on at www.faceblind.org/facetests/

My association with prosopagnosia has been with the rare, acquired form of the disorder, following brain damage. These cases are fascinating—at least to the researcher! Most patients with acquired prosopagnosia have damage to both occipital lobes, often extending to the pathways to the temporal “memory” lobes as well. I have a patient, Michael, who crashed his motorcycle and was in a coma for many months. On regaining consciousness, he was found to be totally blind, a consequence of damage to the visual cortex of both his occipital lobes. But, to everyone’s amazement, many years later Michael began to see dim lights, and an intensive rehabiitation programme was begun to try and bring back his sight. He slowly began to improve and soon could see quite well, but in his central vision only; his peripheral sight was lost. However, although he could describe the shapes of what he was seeing, and even copy pictures reasonably accurately (although painstakingly slowly), he had no idea what he was seeing or drawing. He had visual object agnosia; an inability to know what an object was on sight. He also had no idea whose face he was looking at. Show him a picture of a cat’s face and his mother’s face and he couldn’t tell them apart.


In stark contrast, he could read letters and words. In these rare cases of acquired prosopagnosia it has been found that some prosopagnosics also have dyslexia; that is they cannot recognize words (but can recognize objects), and other prosopagnosics have visual object agnosia (but can recognize words). One theory is that this depends on which occipital lobe is most severely damaged: if it is the right one, in the “‘visuospatial” hemisphere, then the patient will have visual object agnosia, and if it is the left one, in the language hemisphere, the patient will have dyslexia.


Prospagnosia and visual object agnosia are purely visual disorders. If Michael’s mother spoke, he immediately recognized her. If I showed him a bunch of keys, he didn’t know what they were, but if I jangled them or put them in his hand, he immediately recognized them.


Michael had other even rarer visual disorders; he couldn’t recognize colors or even imagine them from his past memories of what color an object or animal was. He said a sparrow—a common, nondescript brown bird— was blue. He had also lost his ability to form or "see" visual images: he had lost his mind’s eye. Related to this, he insisted he never dreamed, at least in visual images. But his most disabling problem was his loss of his entire past life: he could not remember any personal event that had ever happened to him, including his 21^st birthday, a large gathering with all his friends, with a live band, dancing, a feast, and an enormous birthday cake, just three years before his accident. After many experiments I finally concluded this dramatic autobiographical memory loss was a consequence of how he had stored his pre-accident memories; predominantly as visual images. Thus when he tried to recall them, because he had no visual imagery, it was as if he had no memory of the event. This theory was supported by the fact that he could remember sounds from his past; for example when he woke up from his coma, he was able to identify boats in the harbor nearby the hospital from the sounds of their individual fog horns (he had worked previously as a seaman).  He also remembered songs from his past, found the smell of motorcycles intoxicating and nostalgic, and told me he could remember what making love felt like (but had no recall of with whom he had made it)!


So what about his ability to form new memories? His brain damage did result in some separate problems with learning new information, but these were mild. For example, if I phone him out of the blue, perhaps years after we last talked, he immediately recognizes my voice and recalls many of our past experiments. He is able to store and recall new events, but they are non-visual memories, similar, I imagine, to the memories of a blind person. This is the way he described a barbeque he shared with friends four days earlier. “I had a ball. It was a beautiful, sunny day after all that rain we’ve been having. They had some really good spicy sausages and of course I got drunk later in the evening.” No amount of coaxing could bring forth any visual descriptions.


Michael had physical problems as well; he had lost an arm in the accident, and because of multiple fractures in his legs he walked with a severe limp. He had every excuse to lead an isolated, miserable existence, but there was never any chance of that. He proved a wonderful research participant; he loved participating in experiments and testing himself. He lived in his own small house, with a helper coming in daily, and his faithful friends took him places he couldn’t have managed by himself. A highlight was an overseas trip from New Zealand to the USA. With Michael in the sidecar, his friend Lou drove his Harley-Davidson the length of Route 66, including a few side trips. On their return, Lou gave him a photograph album to remind Michael of their trip, but then realized that was no use; Michael couldn’t recognize the pictures. So he put together a series of musical CDs beginning with “Leaving on a Jet Plane,” and including many songs like “New Orleans,” “Needles and Pins” (a reference to Michael’s numb backside when they’d been travelling for a long time), and “Grand Canyon.” The CD finished, of course with “Harley-Davidson Blues.”