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Best of AofA: In Plain Sight: Freud, Face Blindness and Autism

Posted Jun 01 2011 12:00am

Freud This post ran in January. We'll be bringing back "best of posts" throughout the summer.

By Dan Olmsted

Consider this description: “She complained that she could not recognize people; that she used to be able to recognize faces without having to think about it and work at it. Now she was obliged to do laborious ‘recognizing work’ and had to say to herself ‘this person’s nose is such-and-such, his hair is such-and-such, so he must be so and so.’ All the people she saw seemed like wax figures without any connection with her.”

Now this one: “Although I myself may be unable to recognize a particular face, I can recognize various things about a face: that there is a large nose, a pointed chin, tufted eyebrows, or protruding ears. Such features become the identifying markers by which I recognize people. … I think that a significant part of what is variously called my ‘shyness,’ my ‘reclusiveness,’ my ‘social ineptitude,’ my ‘eccentricity,’ even my ‘Asperger’s syndrome,’ is a consequence and a misinterpretation of my difficulty recognizing faces.”

And, finally, this: A child with an autism diagnosis displayed very little functional language in his young life, but soon after undergoing a new treatment he told his mother, “I want to see you.” Taken aback – both because he rarely spoke meaningfully and because she knew there was nothing wrong with his eyesight -- she replied, “Don’t you see me?” Her son’s response: “In pieces.”

These three descriptions come from very different times and places: The first is Sigmund Freud and Josef Breuer’s account of Anna O., the initial case study in their 1895 book “Studies on Hysteria,” which launched the psychoanalytic movement and the modern age of psychiatry. The second is from a recent New Yorker article by Oliver Sacks, the esteemed neurologist and writer, describing his own condition. And the third is a mother telling me about her son at the National Autism Association conference in Tampa in November.

Differences aside, I believe they are all describing an underlying phenomenon that goes by the intimidating name of prosopagnosia – more familiarly, face-blindness. It is a fascinating disorder and one that may be much more common than we recognize – 2.5 percent of the population, or almost 8 million people, affected to some extent, Sacks believes.

As so often happens with such conditions, the focus of interest on face-blindness remains mostly on the exotic features themselves, with little interest in why such a strange deficit, one so central to functioning as a social human being, would occur, why it has come to prominence relatively recently, and why it may now affect so many people. When etiology is considered at all, it is usually passed off, without much evidence, as a genetic or organic condition to which some people, and indeed some families, are heir, or as the obvious result of head trauma or illness.

There may indeed be genetic vulnerability, and brain damage can certainly bring on any Freud sign   number of strange conditions, as Sacks has amply documented in works such as “The Man Who Mistook His Wife for a Hat.” But when taken together and examined in depth, these three cases, and more, point to similar and surprising roots – to the prospect of toxic injury to a particular part of the brain, an injury that strikes at the core of how we connect with others. Cutting to the chase, it looks to me like metals might be implicated; one strong candidate in at least some of those cases is mercury, a known neurotoxin.

That bald statement, of course, needs to be supported by evidence. In this, the first in an AOA series called “In Plain Sight” that examines potential environmental contributions to modern illness and disability, let’s look at prosopagnosia and its implications with fresh eyes. (A tip of the hat to Contributing Editor Teresa Conrick, whose series on visual issues in autism is both original and important, and who provided references for the mercury section.)

(Photo: Olmsted and Blaxill in Vienna.)


Twenty years ago, when I was an editor at a magazine in Washington, I worked with Oliver Sacks on a cover story. Brief though the association was, it left me with an indelible impression of a brilliant, humanistic and wide-ranging scientist whose passions were hardly confined by his job description. We met in New York – as I recall, his apartment/office was perched a few floors above one or the other of the Villages. In person, Sacks had a digressive style that matched his writing, associations and tangents jostling to overtake the main thrust of conversation just as footnotes threaten to hijack his texts. But he always wound up precisely at his destination, seemingly oblivious to distractions that included the awful din of New York street noise. (He did retreat to a home on City Island, in the Long Island Sound, on weekends.)

After the story appeared, tied to the movie version of his splendid book “Awakenings,” he wrote me a kind note and our paths diverged.

Now, though, I find myself drawn back int0 Oliver Sacks’ orbit because of an article he wrote in The New Yorker of August 30, 2010, “A Neurologist’s Notebook – Face-Blind: Why are some of us terrible at recognizing faces?”  (The piece was picked up and popularized by Sanjay Gupta on the CBS Evening News.) Sacks cannot remember faces. And I mean he really cannot remember faces – sometimes even his own. “On several occasions,” he writes, “I have apologized for almost bumping into a large bearded man, only to realize the large bearded man was myself in a mirror.” His misadventures extend to geography and directions; he has walked right past his own building, not recognizing it.

So while all of us have varying degrees of facial recall and situational awareness – I happen to have a keen memory for faces and patterns but am clueless with respect to driving and road directions (fortunately, there’s an app for that)  – this extreme is obviously pathological and problematic. Sacks says it keeps him away from social gatherings, and requires hard work to even begin to compensate. A classic instance is when Sacks, a few minutes after a session with his psychoanalyst, encountered “a soberly dressed man who greeted me in the lobby of the building.” Yes, it was the psychoanalyst he had just seen, and Sacks notes: “This failure to recognize him came up as a topic in our next session; I think that he did not entirely believe me when I maintained that it had a neurological basis rather than a psychiatric one.”

As I read Sacks’ piece and especially this passage, my amazement grew, for I had encountered these symptoms, and this setting, before -- as Mark Blaxill and I researched our recent book, “The Age of Autism – Mercury, Medicine, and a Man-made Epidemic.”


It is necessary to state briefly the premise of our book’s Chapter 2, “The Age of Hysteria.” We propose – apparently for the first time -- that several of the foundational cases of “hysteria” treated by Sigmund Freud as psychiatric disorders were actually mercury poisoning. The keys that led to this observation were Freud’s own comments that more than half of the severe cases he saw had fathers with syphilis infections acquired before marriage, and, separately, that a high proportion of hysteria patients were involved in nursing. This, we suggest, is because both situations brought his subjects into direct contact with mercury in the form of rubs and antiseptics. The children of syphilitics were often young women who were the primary caregivers for their father, and the standard syphilis treatment of the day involved mercury rubs, potions and injections. Similarly, nurses used mercury both in medicine and as the new state-of-the-art antiseptic, mercuric chloride.

This may sound like a loose association, but we were amazed how closely the facts fit our hypothesis in case after case; to date, there has been no serious effort to rebut it. We argue that this pattern was evident beginning with the very first case in “Studies on Hysteria,” Anna O., whose symptoms I described above. She was actually Breuer’s patient; Freud never met her. Here is how we describe the case in the book:


In July 1880 a young woman named Bertha Pappenheim (Breuer called her Anna O., using initial letters that preceded those of her real name) fell sick while tending her father during a sudden illness. Her symptoms were both bizarre and diverse, from severe visual-field constriction, tremors, contractures, and hallucinations — including “hallucinations of absence” in which only Breuer would be visible to her in a room full of people—to inexplicable speech disruptions.

… During the summer of 1880, the family vacation turned into a nightmare when Anna’s father, a grain merchant, fell ill with what was described as a peripleuritic abscess—probably a pulmonary complication of the tuberculosis then sweeping Vienna. A surgeon was called from the capital, and as Anna waited for him, sitting at her father’s bedside, she had the first of her symptoms—her right arm became paralyzed and she hallucinated snakes coming out of her fingernails.

Her father’s health never recovered, and she faithfully attended him upon the family’s return to Vienna. But her symptoms worsened and were joined by a relentless cough. During the last few months of his illness, she herself was barred from the sickroom and sometimes confined to bed. Breuer was called in to treat the cough (he may also have been the family physician), and, given her florid mental symptoms, he diagnosed the cough as hysterical—a tussis nervosa

After that, “a series of severe disorders that were apparently [emphasis in original] quite new developed in quick succession: pains at the back of her head . . . a complaint that the walls are falling in . . . paresis of the front neck muscles. . . . contracture and anaesthesia of the right upper, and, after some time, of the right lower extremity.”

There were also problems with speech. “For as the contractures developed, a deep functional disorganization of speech set in. The first thing that became noticeable was that she could not find words and gradually this became worse. Then her speech lost all grammatical structure, the syntax was missing, as was the conjugation of verbs, so that in the end she was using only infinitives that were incorrectly formed from a weak past participle, and no articles. As the disorder developed she could find almost no words at all.”

Most remarkable perhaps were the ways in which her sight was affected. “There was high-degree restriction of the field of vision. Looking— with delight—at a bunch of flowers she could only ever see one flower at a time. She complained that she could not recognize people; that she used to be able to recognize faces without having to think about it and work at it. Now she was obliged to do laborious ‘recognizing work’ and had to say to herself ‘this person’s nose is such-and-such, his hair is such-and-such, so he must be so and so.’ All the people she saw seemed like wax figures without any connection with her.”


The paralysis and the restriction of the visual field are dead giveaways for mercury poisoning, a clue we believe Breuer and Freud missed as they tried to jam her symptoms into their new theory of psychogenic causality (in this case, despair over her father’s illness). What is inarguable based on Breuer’s own description is that Anna O. – the very first psychoanalytic patient – suffered from one of the earliest descriptions of sudden-onset face-blindness.

It is ironic that more than a century later, Oliver Sacks’ half-jokingly suggests his own psychoanalyst might view his face-blindness as a psychiatric symptom. But it is more than ironic, because there is overwhelming evidence from Sacks’ writing that he also had the kind of toxic exposures we believe made Anna O. face-blind. Sacks’ 2001 book “Uncle Tungsten” is an autobiography of his own youth; his Uncle Dave – dubbed Uncle Tungsten -- ran a factory that used the metal tungsten to make lights; this helped spark Sacks’ budding intellectual interests. The book’s first sentence:

“Many of my childhood memories are of metals: these seemed to exert a power over me from the start. They stood out, conspicuous against the heterogeneousness of the world, by their shining, gleaming quality, their silverness, their smoothness and weight. They seemed cool to the touch, and they rang when they were struck.”

Sacks the schoolboy was an amateur chemist of considerable ability before he ever set foot in the world of neurology:  There is the child staring agog at the Periodic Table of Elements in a London museum; visiting Uncle Dave at his factory and watching him perform experiments with tungsten and other metals; setting up his own chemistry lab at home and creating just about every amalgam, meltdown and explosion his inventive mind could conjure. (His parents, both doctors, were remarkably permissive on this score.)

“Every month or so, I stocked my lab with visits to a chemical supply house … Beneath the serried urns and bottles on the shelves were great carboys of acid – sulfuric, nitric, aqua regia; globular china bottles of mercury (seven pounds of this would fit into a bottle the size of a fist), and slabs and ingots of the commoner metals.” Sacks took home whatever he wanted and experimented with abandon, his curiosity overcoming caution:

 “When one of my mercury fillings came out, I was able to distill off the mercury, unchanged.” “Reading of Lavoisier and the ‘pneumatic’ chemists who preceded him stimulated me to experiment more with heating metals and making oxygen, too. I wanted to heat it by making mercuric oxide – the way Priestly had first made it in 1774 – but I was afraid, until the fume cupboard was installed, of toxic mercury fumes” – suggesting that after the cupboard was in place, such concerns evaporated along with the mercury.

These descriptions go on at length – they are the heart of the book -- and involve just about every conceivable toxic exposure, up to and including radium and ultra-violet rays.


So Anna O., we proposed in “The Age of Autism,” was face-blind as a result of exposure to a neurotoxic metal, mercury.  Oliver Sacks, I believe, fits the same pattern. And, because face-blindness is a frequent feature of autism, it brings us back to the fundamental contention of our book – that autism is a man-made illness first induced by a new kind of mercury exposure, an exposure evident in the 11 children described by Leo Kanner in his 1943 paper, “Autistic Disturbances of Affective Contact.”

We outline the commercialization of ethyl mercury in three new compounds in the 1930s – a seed disinfectant, a lumber fungicide and a vaccine preservative called thimerosal. In several cases, we believe, the links are quite startling: Case 2’s father was a plant pathologist experimenting on seeds with an ethyl mercury dust called Ceresan at the time his son was born; Case 7’s mother was a public health pioneer developing the well-baby visit at Harvard – and promoting the first use of the mercury-preserved diphtheria vaccine – when that child was born. Background exposures to toxins were manifest in most of the other cases as well – one father was a chemist, another a forestry professor, another a mining engineer in England who likely had exposure to metals. Four fathers were psychiatrists, putting them all in close proximity to mercury that was still used to treat neurosyphilis in the 1930s. This, we believe, is too much to be coincidence and needs to be seriously considered by those who have absolved mercury of any role in autism and continue its use in flu shots for pregnant women and for infants.


But is there any direct evidence for mercury in face-blindness? Oh yes. “In 1969 employees of a mercury thermometer manufacturing company in Florida developed symptoms of mercury intoxication,” according to a study published in 1972. (Fred Q. Vroom and Melvin Greer, Mercury Vapour  Intoxication, Brain, 1972:95, 305-318.) “The nine patients most severely affected were examined, and they described the working conditions … the oven doors were cracked … There was inadequate ventilation; work clothes were not changed, and employees ate and smoked in contaminated areas.”

The two authors – from the Division of Neurology of the University of Florida Department of Medicine – described typical symptoms of mercury poisoning including insomnia, irritability, tremors and a cough for three months first thought to be “nervousness” (remember Freud’s description of Anna O.’s chronic cough as a tussis nervosa?). They also tested for memory problems, another sign of mercury poisoning, by showing each worker 12 faces they should easily have recognized. Here’s how they did:

-- Case 1 got 9 right.

-- Case 2 was “borderline with 8 of 12 faces correctly identified.”

-- Case 3, “only 6 of 12 faces were recognized,” which was clearly abnormal.

-- Case 4, 11 of 12, “normal.”

-- Case 5, “Non-verbal memory tested by facial recognition was no better than chance (5 of 12 faces correctly identified).”

-- Case 6, “no better than chance (4 of 12 faces were correctly identified)”

-- Case 7, “very slowly over 3 to 4 minutes,” 8 faces were recognized.

-- Case 8, tested after 11 months, normal with 9 of 12 recognized.

-- Case 9, tested after 15 months, normal with 11 of 12 recognized.

“Facial recognition, a test of right temporal lobe function, was persistently abnormal in 4 patients and was borderline in 2,” they concluded. And they noted that the “classical signs and symptoms of mercury intoxication were evident in all 9 patients” including – alert the media – “acute and chronic gastro-intestinal symptoms such as diarrhoea…”


It is not a stretch to see how face-blindness, along with other sensory processing difficulties including hearing and touch, could explain much of the behavior that defines autism. What if your own parents were literally unrecognizable? What if you yourself remained a stranger in the mirror? What if humans seemed like Anna O.’s “wax figures” – lacking the characteristics that make the rest of us recognize them as animate objects, different from a toaster or a chair? What if you saw people in pieces?

It wouldn’t be surprising if a study of such children were headlined, “Mother Is Just Another Face In The Crowd to Autistic Children.” That was indeed the title of a 2001 article in Science Daily that begins, “Unlike normally developing and mentally retarded children, autistic 3- and 4-year-olds do not react to a picture of their mother but do react when they see a picture of a familiar toy, a University of Washington psychologist has found.”

The psychologist is Geraldine Dawson, now the science director at Autism Speaks, who reported: "We know that even newborn babies are drawn to face-like stimuli. This inborn interest in faces is the start of social development. This new study tells us something very fundamental about abnormalities in autism.”

The mechanics of face-blindness have been at least partly identified over the past few years, and the key cog appears to be a part of the brain called the fusiform gyrus. The connection was first made less than two decades ago by a team led by Nancy Kanwisher at the Massachusetts Institute of Technology, but it has now become a focus of attention in autism research, for obvious reasons. One recent study found, according to its title, that “Face processing occurs outside the fusiform ‘face area’ in autism.” That would certainly be consistent with an inability to distinguish people from objects. Another study, in the Oxford Journals, found “Neurons in the fusiform gyrus are fewer and smaller in autism.” And research now under way and supported by Autism Speaks is titled How Does the Brain Develop Differently in Autism? “When autistic individuals interact, they spend less time looking at the faces of others with whom they are communicating, and when they do, they tend to focus on one particular facial feature,” according to the study leader, Gene Blatt of the
School of Medicine at
Boston University.

“Previous studies suggest that a cause of this disability may lie in the part of the brain known as the fusiform gyrus, or fusiform face area. Neuroimaging techniques such as magnetic resonance imaging (MRI) show that this part of the brain is less active during face processing. This hyperactivity may ‘short circuit’ the brain's ability to interpret facial cues during social interactions.”


As my co-author Mark Blaxill likes to say, facts cluster around a good hypothesis. Besides Oliver Sacks’ own heavy metal exposures, he points us inadvertently to more clues. A 1955 paper about face-blindness by an English neurologist “brought the issue to the fore,” Sacks writes. In June 1953, the subject, called “A.H.,” suffered an apparent stroke and from then on was blind to both faces and many objects. “I can see the eyes, nose, and mouth quite clearly but they don’t add up. They all seem chalked in, like on a blackboard.”

Sacks notes in passing that A.H. was “a mining engineer in a Welsh colliery.” (A colliery is a coal mine.) Hold on -- a mining engineer? Where have we seen that before? That was also the profession of the father of Leo Kanner’s Case 4, also in England. So both the case that brought face-blindness to the fore, as well as one of the initial autism families, had heightened risk of exposure to metals (mercury, arsenic and lead are constituents of coal; mercury is used in silver and gold mining, and mercury fulminate was employed to blast open new mining areas).

Facts cluster: I quickly came across a book titled, “Face Blind,” by Bill Choisser, which he calls “the world’s first book about face blindness.”  (HERE) And what does this first author tell us?

“I arrived on the scene in a coal mining town in the foothills of the Illinois Ozarks in 1946. For my first three years, all I did was scream and rock. I never spoke a word. … Sometime between age 3 and 4 my brain matured to the point I could make sense out of the distorted garbage that is called ‘speech’, and I began to talk.”

While these symptoms – which obviously match some of the criteria for autism – resolved, his face-blindness remained.

Another clue provided by Sacks comes from “Uncle Tungsten.” Sacks devotes a footnote stretching over three pages (told you!) to Henry Cavendish, the British scientist who discovered hydrogen. Cavendish was the subject of a 19th century biography by George Wilson that painted him as a very unusual man, who “felt himself separated” from others. “A sense of isolation from his brethren,” Wilson wrote, made him shrink from their society and avoid their presence, but he did as one conscious of an infirmity, not boasting of an excellence.”

From this and other descriptions by Wilson, Sacks deduces that “Cavendish’s remoteness and ingenuousness” suggest Asperger’s syndrome, and “I now think Wilson’s biography may be the fullest account we are ever likely to have of the life and mind of a unique artistic genius.”

Well, then, to Wilson’s biography we go.  (HERE) By now, the curious reader may suspect what we do indeed find. Cavendish’s first published work was called “Experiments in Arsenic” – a substance so often equated with its poisonous effect on humans that it’s worth pointing out arsenic is a metal. Cavendish, like the youthful Oliver Sacks in his own lab, was literally playing with fire. Cavendish's arsenic paper, writes Wilson, “is otherwise remarkable for its speculations on the nature of ‘red fumes” ... which attended the action of nitric acid on arsenious acid, and for its discussion of the solution of metals in acids, and the reduction of the former by heat and inflammable matter.”

At the same time, Cavandish began a series of “Experiments on Heat,” and the results  were quoted in a 1783 paper titled “On the Congelation of Quicksilver.” Cavendish was also the first to publish a paper on the freezing of mercury, and the word appears 45 times in Wilson’s biography (quicksilver, 19).

I don’t accept Sacks’ view that Cavendish probably had Asperger’s – we’d need to know more than is available about his early years – but I agree that he was atypical and unsociable to the point of having some sort of deficit that he experienced as disabling. And chemicals, especially metals, were very much in evidence.


You wouldn’t suspect it from the current direction of mainstream research, but chemical exposure and autism have been joined from the beginning. The father of the first autistic child to appear at Johns Hopkins, in 1935, was a chemist with the U.S. Patent Office. In the 1970s, respected autism researcher Mary Coleman, working with Bernard Rimland, found that a “quite startling” one-quarter of children with autism she studied had parents with occupational exposure to chemicals, compared with only one percent of U.S. parents overall; several of the parents of affected children were in fact chemists – sometimes chemists married to chemists. This finding was corroborated a few years later by one of her students, Thomas Felicetti, but the “chemical connection” – one of the strongest clues ever developed to the nature of the disorder -- has been lost in the rush for genetic explanations. 

So finding an unusual chemical history – specifically, metals and mercury -- in the background of people with a disorder like face-blindness is not really that startling to anyone pursuing an environmental theory of autism causation. Putting aside for the moment labels like autism and Asperger’s and prosopagnosia, it’s pretty obvious such toxins can damage the ability of humans to engage with others as social beings -- to fully enter the world we are so finely made to inhabit. That’s a nightmare, but it also means such risks could be identified, prevented, perhaps even reversed.

This hopeful idea, though, is getting almost no attention from the medical industry. Going back to Sigmund Freud, the pattern looks awfully familiar.


Dan Olmsted is Editor of Age of Autism.

Posted by Age of Autism at June 07, 2011 at 5:43 AM Permalink

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