Clinical Impressions Example Speech Therapy: Fill & Download for Free

I know what I hear with a cochlear implant (CI) is a far cry from natural hearing. In an abstract way, I know the sound I hear is highly digitized and pixelated, but I have no other frame of reference for understanding sound.Learning how to hear with a CI, particularly for someone born profoundly deaf, isn't an easy or simple journey. I don't regret going on the journey, but there were no roses or rainbows along the way.Before the Cochlear ImplantI was born profoundly deaf. My deafness was so severe that no hearing aid on the market was any help. I thought they were toys and would feed them to my dog, to my mother's horror. The only sound I could sense was some vibrations from very loud noises. I was off the charts in terms of dB loss, which is relatively rare.Once my mother understood the profundity of my deafness, she decided to abandon speech training in favor of sign language. The extent of my speech training was teaching me not to make sounds during inappropriate times, like church services. (This is called the "voice off" mode.)Through sign language (initially Signed Exact English, then American Sign Language) and reading, I had access to visual languages. By six years old, I was perfectly on par with my hearing peers in terms of language development, albeit visually, not auditory. My brain was functioning quite well; my ears weren't.I knew there was a thing called "sound" in an abstract way. It was kind of like how you know there are atoms and electrons, even though you can't directly see or touch them. Seeing others move their lips and understand each other seemed almost magical. I considered it close to a form of mind-reading that I wasn't privy to.In 1991, I became one of the first few hundred children to receive a CI after the FDA approved it for pediatric use. I was six.Neurologically speaking, I was past my prime.[1] Considering the profundity of my deafness and my advanced age, doctors didn't quite know how well I would ever hear. Most of the children who received a CI during the clinical trials once had hearing. I was uncharted territory at that time, so the doctors warned my parents not to expect too much. In 2014, the field of auditory training for children with CIs has developed by leaps and bounds, so my case wouldn't be as much of a conundrum today.The Beginning of the Cochlear Implant ExperienceAbout a month after the surgery, I returned to New York City to get my CI turned on.It was in a windowless room in a cramped hospital on the Upper East Side. The audiologist and my mother watched me as they turned on the external processor.[2] After the audiologist placed the magnet on my head and turned it on with her computer, it was game time.And ... nothing.I didn't hear or feel a thing. My brain wasn't capable of processing the new stimuli, so it simply didn't. This seemed very wrong to me, so I ran down the hall, screaming. With my six-year-old logic, I thought I just needed a louder noise. Still nothing.Disappointed, my mother and I left the hospital wondering if the surgery had been worth it at all. As we waited to cross the street, someone started a motorcycle behind me, and I felt something. I couldn't even quantify it. It wasn't tactile. It wasn't visual. It was painful, like sharp prickling somewhere in the depths of my brain.That was the first sound I "heard." I was not impressed. It was so painful and bewildering that I wanted to cry. Suddenly, I had this foreign sensation in my mind that I couldn't make sense of. It almost felt like an invasion. Sound - the furthest thing from magic I could imagine.With time (and my parents' insistence that I keep my CI on), the sensation became less frightening, and more familiar. Sound, however, never became natural or completely comfortable. It was (and still is) a chore to hear, more akin to taking out the trash than playing.I proceeded to spend hours every day in intensive speech therapy simply learning what sound was and how to interpret what the differences in sound meant.As part of my training, my speech therapist vocalized common syllables like aaa, ahhhh, ssss, ssshhh. To test my comprehension, she laid out three cups that represented three different syllables. After she vocalized one (with her mouth covered), I would have to choose the right cup. She made training as fun as possible, but it was still work.Slowly, I began to understand that different sounds could be translated into words and sentences. It was a long and arduous process. It took me nearly three years before I could understand the most rudimentary spoken sentences. My listening skills were at the level of a two-year-old as my writing and reading skills were a decade ahead.Frankly, I hated learning how to hear and listen. It took hours out of every single day ... and mind you, I was still a child. The last thing I wanted to do was spend even more time cooped up with adults in windowless rooms when my friends were out playing. (Always windowless. Always.)By nine, I was starting to speak, laboriously and unintelligibly. Instead of simply identifying my speech therapist's vocalizations, I would repeat them back to her. Once I (somewhat) mastered the syllables, my speech therapists would read children's books aloud and I would repeat the words back at her. It wasn't until I was 13 that I felt confident enough to speak in public. Now, I speak nearly every day.This artificial way of learning how to listen and speak has affected how I think about speaking. I wouldn't say that I listen to my own voice as hearing people do. Rather, I focus on the physical act of speaking (tongue positions, air flow, etc.) as I'm speaking. So, it's a different cognitive process. I still need instruction on how to pronounce new words, particularly words with foreign origins.That is how I learned to speak and listen.What I Hear TodayI know what I hear with a CI is different than natural hearing. I miss things that others don't, but I don't know exactly what I'm missing.Not only is the range of frequencies much more limited with CIs, but subtle differences in intonation and pitch are flattened. It's like looking at a very pixelated painting; you grasp the gist, but the nuance is completely lost.Here's a CI simulator:As you can probably hear, what I hear is quite different from natural hearing. One of my hearing friends described the simulator as Darth Vader. Well, that's my auditory world ... Darth Vader wheezing. Good thing I think he's a cool character.The low resolution form of hearing affects a lot of things: my speech comprehension, my speech, and sound interpretation.The sound pixelation makes it hard for me to differentiate sounds of similar frequencies. Low frequency sounds are particularly problematic for me since CIs are more attuned to higher frequencies. For example, if there is low-frequency background noises, it'll be very difficult for me to understand male voices.Functionally, I'm hard-of-hearing.The digitized sound that the CI provides also affects my speech. A kind way of describing my speech would be somewhat halting, robotic monotone. I do not have the "deaf accent," but I have a completely unidentifiable accent. People constantly ask me what country I'm from, and become very confused when I tell them that I was born and raised in the United States.Even now, more than 20 years after implantation, listening and speaking involve cognitive work. I don't hear every syllable, so there's guesswork involved. If you say, "Hello, Cristina. How are you?" I'll probably hear something like, He-lo, Cr-tina. Ow --- U? It takes me a few moments to fill in the spaces, and sometimes I make mistakes.Another aspect of hearing with a CI is the ability to turn off sound. Since I don't sleep with my processor on, every morning I must brace myself for the deluge of noises. Even in quiet environments, there are hundreds of small noises, the refrigerator humming, the breeze blowing outside, even your own breathing. They're white noise, inconsequential to most people, except me. It takes time for my brain to filter out the white noise, and until that time, it's almost a painful experience of overstimulation.That is, more or less, how I hear with a CI._______[1]: This phenomenon is called Neuroplasticity. It has to do with the ability to create or change neural pathways and synapses. The older we get, our ability to create and change our neural pathway becomes diminished.[2]: CIs have both internal and external components. Cochlear implantN.B. For everyone who reads this, please do not take my experience as a predictor for other children with CIs. There are a lot of individual variables involved: age, cognitive capacity, language acquisition, among others. Considering my age, I perform fairly decently with my CI, but others outperform and underperform me.Author's Note: this article focuses on the process and sensation of hearing with a CI. There is, however, a cultural component to receiving a CI. See here for more details: Cristina Hartmann's answer to What is life like after a cochlear implant (bionic ear) for a person born deaf?

Wendell Johnson was a tall, knobby 20-year-old farm boy when he arrived at the University of Iowa in Iowa City to study English in 1926. The class president and valedictorian of his tiny high school in Roxbury, Kan., Johnson was engaging, ''quite a clown'' in the estimation of the folks back home. He also stuttered grotesquely, often rendered speechless by the impediment. His inability to express himself nudged him toward writing and literature, and he developed a penchant for antic humor, which kept him popular despite his silence. It also propelled him to U. Iowa, the most famous center for stuttering research in the world. Around the country, speech pathology was fighting to be recognized as a science, and Iowa was the new discipline's polestar. Dozens of experiments were under way when Johnson arrived, and he enthusiastically threw himself into the invigorating work, switching to psychology for his master's study. ''I became a speech pathologist because I needed one,'' he'd later say.Many of his fellow graduate students stuttered almost as painfully as he did, and they'd use one another as guinea pigs. They'd draw blood, hook themselves to electrodes, strike their knees to test reflexes, whip out notebooks in midstride and transcribe their own and others' faltering speech. They'd administer electroshock and shoot guns off near each other's ears to see if being startled affected stuttering. (It didn't, although the same experiment performed on normal speakers did affect their speech.) They'd also put casts on one another's arms, since it was hoped that immobilizing a person's dominant hand somehow would untangle confused brain signals. At one point, about 30 stutterers, including Johnson, wandered the Iowa campus with their arms wrapped in plaster, sometimes playing wrong-handed badminton. ''We knew that we were working on something central in the life of a human being,'' one of Johnson's contemporaries told an Iowa historian. ''We weren't just puttering around on the fringes.''At the time, physiology had become the favored explanation at Iowa for stuttering. The department's lead professors were certain that the disorder originated in misdirected brain signals. They had used a new device called an electromyograph to study neuromus-cular activity in stutterers, nonstutterers and, in one experiment, people who were drunk (students who, solely in the interests of science, had become soused; the researchers skirted Prohibition by requisitioning alcohol from the university hospital.) The readouts from the booze-tinged subjects showed, to no one's surprise, impair-ment. Intriguingly, more comprehensive experiments showed that stutterers had subtle neuromuscular responses different from those of their nonstuttering peers.But Johnson, by 1937 an ambitious assistant professor, wasn't convinced. His life story suggested otherwise. He'd spoken fine until he was 5 or 6, when a teacher mentioned to his parents that he was starting to stutter. Gradually an obsession with his speech took hold. His voice grew hesitant. He self-consciously repeated sounds. Those, of course, are among the hallmarks of stammering. By worrying about the problem, he decided, he'd produced it. His disorder lay not in his brain, in biology, but in his learned behavior. Stuttering, he later concluded, ''begins not in the child's mouth but in the parent's ear.''This idea was provocative and powerful, with enormous implications for speech therapy. If stuttering is learned behavior, it can be unlearned. Biography, however, isn't proof. Johnson, to validate his thesis, needed to design an experiment that induced stuttering. If, he reasoned, any and every child could be made to stutter, then obviously no underlying physiological defect was required. If stuttering could be called forth in normal youngsters, it would be proved as a learned, conditioned response In the fall of 1938, Wendell Johnson recruited one of his clinical psychology graduate students, 22-year-old Mary Tudor, who was avid but timorous, to undertake exactly that experiment. She was to study whether telling nonstuttering children that they stuttered would make it so. Could she talk children into a speech defect? The university had an ongoing research relationship with an orphanage in Davenport, Iowa, so Johnson suggested she base her study there. And thus, on Jan. 17, 1939, Mary Tudor drove along the high, swooping bluffs overlooking the Mississippi River to the Soldiers and Sailors Orphans' Home. She toted notepads, chalkboards, a Smedley dynamometer (to measure hand strength) and a cumbersome Dictaphone.The study she began that morning is now the subject of a multimillion-dollar lawsuit against the State of Iowa and the University of Iowa. Despite its 64-year-old provenance, it has occasioned a spate of recent articles in newspapers and speech-sciences journals and a full-day symposium at the Graduate Center of the City University of New York in December. Something happened at the orphanage in Davenport that seems to have been unintended by Johnson and unmeasurable by his science. Only now, at a remove of decades, can we begin to digest and appreciate what the Tudor study tells us about the origins of speech defects, as well as the ethics of science, the brittleness of children and the egos of driven men.The Iowa soldiers and Sailors Orphans' Home was founded as a refuge for the offspring of men killed in the Civil War. By 1939, at the height of the Great Depression, it housed more than 600 orphans and demi-orphans (those whose destitute parents, although alive, couldn't care for them) in clusters of small cottages. Not as harsh as the nearby Industrial School for Boys in Eldora, Iowa, or as forlorn as the Institute for Feeble-Minded Children at Glenwood, it was nevertheless spare, joyless and regimented. Children rose at 5:30 a.m., had breakfast and cleaned until school began. They marched in long, careful lines, to facilitate order.Mary Tudor's research at the Iowa Home began with the selection of 22 subjects. None were told the intent of her research. They believed that they were to receive speech therapy. Her experimental design was complicated. She was not only trying to induce stammering in healthy children; she was also trying to see whether telling stutterers that their speech was fine would produce a change. Included among the 22 subjects were 10 orphans whom teachers and matrons had marked as stutterers before the study began. Tudor and five other graduate students who agreed to serve as judges listened to each of the children speak, graded them on a scale from 1 (poor) to 5 (fluent) and concurred with the school's assessment. ''Unwilling to talk but certain definite 'stuttering' phenomena,'' a researcher wrote of one boy, ''tension, prolongations, explosiveness, repetitions. A stutterer.'' The 10 stuttering children were divided into two groups. Five were assigned to Group IA, the experimental set. They would be told: ''You do not stutter. Your speech is fine.'' The five in Group IB would serve as controls and be told, ''Yes, your speech is as bad as people say.''The remaining 12 children were chosen at random from the population of normally fluent orphans. Six of these were assigned to IIA, the group that eventually would lead to the lawsuit and contention. These children, ranging in age from 5 to 15, were to be told that their speech was not normal at all, that they were beginning to stutter and that they must correct this immediately. The final six children in Group IIB, similar in age to those in IIA, were normal speakers who were to be treated as such and given compliments on their nice enunciation.On that first January visit, Tudor tested each child's I.Q. and handedness. A voguish theory then held that stuttering was caused by a cerebral imbalance. If, for example, you were born left-handed but were using your right hand, your nerve impulses would misfire, affecting your speech. Johnson felt the notion was nonsense, but he was thorough and suggested Tudor discern each child's handedness. She had them draw on chalkboards and squeeze the bulb of the dynamometer. Most were right-handed, but a sprinkling of lefties ran through all the groups. There was no correlation between handedness and speech in this subject crop. That was an auspicious start.The experimental period lasted from January until late May 1939, and the actual intervention consisted of Tudor driving to Davenport from Iowa City every few weeks and talking with each child for about 45 minutes. She followed an agreed-upon script. In her dissertation, she reported that she talked to the stuttering youngsters who were going to be told that they did not stutter. She said to them, in part, ''You'll outgrow [the stuttering], and you will be able to speak even much better than you are speaking now. . . . Pay no attention to what others say about your speaking ability for undoubtedly they do not realize that this is only a phase.''To the nonstuttering youngsters in IIA, who were to be branded stutterers, she said: ''The staff has come to the conclusion that you have a great deal of trouble with your speech. . . . You have many of the symptoms of a child who is beginning to stutter. You must try to stop yourself immediately. Use your will power. . . . Do anything to keep from stuttering. . . . Don't ever speak unless you can do it right. You see how [the name of a child in the institution who stuttered severely] stutters, don't you? Well, he undoubtedly started this very same way.''From the first, the children in IIA responded. After her second session with 5-year-old Norma Jean Pugh, Tudor wrote, ''It was very difficult to get her to speak, although she spoke very freely the month before.'' Another in the group, 9-year-old Betty Romp, ''practically refuses to talk,'' a researcher wrote in his final evaluation. ''Held hand or arm over eyes most of the time.'' Hazel Potter, 15, the oldest in her group, became ''much more conscious of herself, and she talked less,'' Tudor noted. Potter also began to interject and to snap her fingers in frustration. She was asked why she said 'a' so much. '''Because I'm afraid I can't say the next word.' Why did you snap your fingers? 'Because I was afraid I was going to say ''a.'''''All of the children's schoolwork fell off. One of the boys began refusing to recite in class. The other, 11-year-old Clarence Fifer, a chubby, diffident child, started anxiously correcting himself. ''He stopped and told me he was going to have trouble on words before he said them,'' Tudor reported. She asked him how he knew. He said that the sound '''wouldn't come out. Feels like it's stuck in there.'''The sixth orphan, Mary Korlaske, a 12-year-old, grew withdrawn and fractious. During their sessions, Tudor asked whether her best friend knew about her ''stuttering,'' Korlaske muttered, ''No.'' ''Why not?'' Korlaske shuffled her feet. ''I hardly ever talk to her.'' Two years later, she ran away from the orphanage and eventually ended up at the rougher Industrial School for Girls. ''I couldn't never tell my husband about it,'' Korlaske, now Mary Nixon, said in a brief telephone conversation in January. ''It just ruined my life.'' Her voice broke. ''I can't talk no more,'' she said, and with an audible oath, she hung up.Mary Tudor herself wasn't untouched. Three times after her experiment had officially ended she returned to the orphanage to voluntarily provide follow-up care. She told the IIA children that they didn't stutter after all. The impact, however well meaning, was questionable. she wrote to Johnson about the orphans in a slightly defensive letter dated April 22, 1940, ''I believe that in time they . . . will recover, but we certainly made a definite impression on them.'' The emphasis is hers.SIGN UP FOR THE NEW YORK TIMES MAGAZINE NEWSLETTER: The best of The New York Times Magazine delivered to your inbox every week, including exclusive feature stories, photography, columns and more.Sign UpWhen Wendell Johnson was a boy, he ran the rounds of contemporary stuttering therapies. His family doctor gave him sugar pills. A faith healer, thundering from a high stage, frightened and disappointed him. He went to a chiropractor. At 16, with his speech almost unintelligible, he begged to be allowed to attend a far-off stuttering ''school.'' There, for three months, he recited aloud in a deliberately flat monotone and swung dumbbells while metronomically chanting, ''Have more backbone and less wishbone.'' None of this cured him, and abruptly, he quit. ''I went to the station, stuttered to the ticket agent and to the conductor and . . . closed my eyes in despair,'' he wrote in ''Because I Stutter,'' his first book. ''I was terribly ashamed. . . . I hated stuttering.''His affliction shaped and spurred the remainder of his life and career. ''Like most stutterers, he was baffled by his stuttering,'' wrote Oliver Bloodstein, Ph.D., a professor emeritus of speech at Brooklyn College and Johnson's most distinguished pupil. ''He spent hours trying to figure out what he was doing that made him stutter.''This lacerating curiosity drove him to undertake a series of ingenious experiments, before and after the Tudor study, into the essential nature of stammering itself. What is it? How does it work? To answer these questions, he began by giving stutterers a page bordered in red and having them read aloud in front of an audience, where their stuttering would become worse. Afterward, the subjects tended to stutter painfully anytime they read a page marked with red, even when reading to a single person. Next, he blacked out words over which a particular stuttering reader had stumbled. When the person reached the word next to the one crossed out, he'd stutter. He'd become accustomed to stumbling there and, even without the troublesome word, he still did. These results said to Johnson that stuttering was indisputably a conditioned, learned response.He also proved that individual stutterers were consistent. They tended to stumble over the same sounds (although the sounds themselves varied from person to person) and grew to dread them, often substituting entire words. (''My f-f-fa . . . dad.'') They'd also whisper. When they were about to reach troublesome fricatives, their eyes would bulge. They'd thump their knees, click their fingers, rasp desperately or shake their heads in a spasmodic attempt to force out the sound. Johnson defined those actions as the associated behaviors of stuttering and claimed that in adults they would diminish if the stutterer relaxed and didn't anticipate a speech block. He liked to point out that in certain situations even the most afflicted don't stutter, during, for instance, singing or in unpressured speech with infants or dogs. ''One severe stutterer virtually lived the life of a nomad because he was able to communicate vocally only whenever he established himself in a new town,'' wrote Oliver Bloodstein, who did Johnson's fieldwork.Johnson's findings about the nature of stuttering, once it has begun, remains the accepted wisdom to this day. The disorder does respond to conditioning, and once established, stuttering can have a ruinous momentum. Often, the worse someone stutters, the more he fears speaking, and the worse his speech becomes.What Johnson's thinking did not explain is why severe stuttering starts. Episodes of speech disfluency are common among adults and children, especially the very young. But about 5 percent of all youngsters exhibit clinical stammering, according to Ehud Yairi, a professor of speech and hearing science at the University of Illinois. Of these, about 75 percent recover without treatment, but about 1 percent of all people (about three million Americans) continue to stutter noticeably into adulthood. It is those whom Johnson studied in his work on the progression of the disorder. Why, though, were those few stricken in the first place?Johnson had no family history of stuttering and dismissed the possibility that the condition could be heritable. ''Stuttering is learned behavior, Johnson said, and he repeated it again and again,'' Bloodstein wrote in an e-mail message. ''It virtually became his mantra.'' He had indirect, anecdotal data, too, that backed his contention. Beginning in 1934, he and his assistants questioned the mothers of dozens of young stutterers, asking when the disorder had begun and how the family had responded. He also tested age-matched ''normal'' speakers and found that they had many speech defects as well. Unfortunately for the ''stutterers,'' Johnson said, their parents overreacted, made the children panic and produced full-blown stuttering. The diagnosis caused the condition. Johnson termed this the diagnosogenic theory, and it became the cornerstone for his writing and teaching, his growing fame and eventually the basis for his ideas about the treatment of stuttering children. It also, by its dictates, should have ensured that all the orphans in Mary Tudor's Group IIA would stutter soon after Tudor began telling them that they did.But they did not. In fact, the most telling aspect of Mary Tudor's experiment is that it failed completely. Of the six normal children who were falsely labeled stutterers, two actually improved their speech fluency, according to the researchers' ratings, over the course of the five-month study -- one by almost a full point, from 3 to 3.8. Another's fluency rose from 3 to 3.6. For two others, their fluency ratings didn't budge. Of the two children whose fluency fell, one, Clarence Fifer, dropped from 2.6 to 2, the second, Hazel Potter, from 3.1 to 2.8.The other primary study group fared little better. Of the actual stutterers who were told they now spoke fine, two showed slight improvements in fluency, two decreased in fluency and one was unchanged. The results for each of the groups were ''not only insignificant, but also in the wrong (unexpected) direction,'' concluded Yairi and a colleague in an article in the May 2002 issue of The American Journal of Speech-Language Pathology.The experiment did, however, have an impact. In each case, the nonstuttering children of Group IIA began to act like stutterers. ''All of the children in this group showed overt behavioral changes,'' Mary Tudor wrote in her thesis, ''that were in the direction of the types of inhibitive, sensitive, embarrassed reactions shown by many adult stutterers in reaction to their speech. There was a tendency for them to become less talkative.'' They also, during their sessions with her and in front of the researchers, shuffled their feet, whispered, snapped their fingers, gulped, gasped and clamped their mouths shut. They looked like stutterers. They spoke fine.It seems highly unlikely that you can make a stutterer. You can induce the accompanying tics -- the shuffling and the self-consciousness. Those can be taught and reinforced. But clinical stuttering cannot. It exists or it doesn't. Johnson's theory was not upheld. After Mary Tudor submitted her completed master's thesis in August 1939 with a dedication to Johnson, it sank straightaway into obscurity. Johnson did not oversee its publication, as he often did with his students' theses. He did not include it in his otherwise comprehensive indexes of University of Iowa stuttering research. Not until 2001 did it receive national press attention, in a series of articles in The San Jose Mercury News. However, the thesis, which was available at the university library, did have a ghost life among Iowa speech pathology students. ''Those who had heard about it nicknamed it the 'Monster Study,''' remembers Franklin Silverman, a professor of speech pathology at Marquette University and a former student of Johnson's. ''It reminded people of the Nazi experiments on human subjects. The other professors at the time told him that it would ruin his reputation to publish the data. It was chilling and disturbing, especially to think that Wendell Johnson, of all people, had sanctioned it. He knew the pain of being told that you stutter.''It is an ugly thing, after all, to experiment on orphans. And Johnson's admirers, who still are legion, struggle to understand why he proposed and designed the project. ''I have to assume it was because he firmly believed that it would serve a greater good, that it would help thousands of other children who stuttered and that any damage would be temporary and reversible,'' says D.C. Spriestersbach, vice president and dean emeritus of the University of Iowa and another of Johnson's students. ''He was a wonderful, empathetic man, and he understood the torment of a speech defect. He wouldn't have been able to bear it if he thought he'd actually forced someone to stutter.''He pauses. ''But he never talked about the Tudor study to me or anyone else that I'm aware of. So all I can do really is guess.''During the 1940's, when Johnson, despite his speech impairment, was one of the most popular lecturers on the Iowa campus, he used to exhort his students to question ''the voice of authority.'' He'd say, ''Whenever you hear a dogmatic, absolutist statement from any kind of 'expert,' ask, 'What do you mean and how do you know?''' t h e Tudor study was not only morally troubling; its results must have been, for Johnson, confounding. The data threatened to undercut his belief, which was unswerving, that stuttering is purely behavioral. ''It ran counter to what he stood for,'' says Gerald Zimmermann, a former speech professor at Iowa and now a literacy specialist. ''I wouldn't want to publicize a blow like that either. But, hey, that's science.''Johnson sometimes referred to the study in lectures, claiming that it had caused an orphan, presumably Hazel Potter, to stutter and therefore validated his diagnosogenic ideas. But the researchers, in their final evaluation, graded her a nonstutterer.Johnson did not mention the study again. In 1959, he published his famous ''Onset of Stuttering,'' which laid out the diagnosogenic theory in detail. However, nowhere in its pages does he mention the orphan experiment. The Tudor study ''should have been discussed,'' Zimmermann says. ''It should have been part of the record and the canon. Maybe everyone would have supported the diagnosogenic theory anyway. Johnson was persuasive. But at least a question would have been raised.''From the 1950's until the early 1980's, Johnson's theory, unsullied by doubts, was the underpinning of most childhood speech intervention in America. Therapists, swayed by diagnosogenic theory, declined to work directly with young stutterers, fearing that the therapy could worsen the affliction. They'd instead counsel a child's parents, telling them to stop worrying so much. Sometimes this helped the child. Other times it didnt Today, one of the most widely accepted models for explaining persistent stuttering is that a genetic component provides a biological predisposition to stutter. Not everyone with ''stuttering genes'' progresses, of course, to a full-blown disorder. There are environmental cues that are necessary. One of these may be a panic-stricken parent. In a child with a sensitive temperament, a father or mother's reaction may push the child over the edge. In this way, Wendell Johnson's thesis partly survives. But as the sole predictor of stuttering, diagnosogenic theory has been thoroughly overthrown. ''No one believes anymore that only your parents make you stutter,'' says Robert Goldfarb, head of the Ph.D. program in speech and hearing sciences at the CUNY Graduate Center and the organizer of the symposium there. ''It's probably a shame for speech therapy and for parents that anyone ever did.''Nowadays, researchers think that the most helpful form of speech therapy is working directly with children. In face-to-face sessions with their therapists, children are encouraged to practice breath control, easing words out instead of forcing them and stretch out sounds to make them longer. One can't help wondering what would have happened had Johnson published the Tudor findings. Would the results have raised issues that might have led to an earlier shift in treatment for stuttering children? And would those young stutterers have been better served by this more direct intervention? We can't know. Though researchers now have more success reducing disfluency in children, the discipline of speech therapy remains inexact and, for some stutterers, eternally ineffective. ''We don't have any way of measuring the impact of having lost the Tudor study for all those years,'' Zimmermann says.Perhaps Johnson felt the need to protect a doctrine that explained not only a crippling affliction but also the very arc of his life. Wendell Johnson ''was outgoing,'' Oliver Bloodstein wrote. ''He was comradely. But he was also hard at work for recognition in his field . . . like so many gifted people, he was burdened with an unshakable conviction that he was right.''The reverberations of the 64-year-old Tudor study will sound for years. The three surviving orphans from Group IIA, Norma Jean Pugh (now Kathryn Meacham), Mary Korlaske (now Mary Nixon) and Hazel Potter (now Hazel Dornbush), are each suing the State and University of Iowa for millions of dollars, citing among other things the infliction of emotional distress and fraudulent misrepresentation. The estates of the three deceased orphans will be part of the suit. ''I think that a jury will agree that even if these people's speech wasn't exactly ruined, their lives were,'' says Evan Douthit, a Kansas City, Mo., attorney who is representing five of the claimants. ''Kathryn Meacham has thought of herself as a freak all her life. She still hates to talk, except to her family and a few people in her church. She's a sad, sad lady.''Hazel Potter Dornbush is scrappy and decisive at 79. ''Imagine trying to wreck a little child's voice,'' she says. ''But I've moved on. I married a good man. I talk O.K. Even the orphanage wasn't that bad. There were always other children around, so it wasn't lonely.'' She pauses. ''I don't really remember being that close to any,'' she adds, suddenly puzzled. ''But back then, you know, I was quiet.''In 1965, at 59, Wendell Johnson sat at his desk still defending diagnosogenic theory. He was preparing an entry for the Encyclopaedia Britannica on ''Speech Disorders'' when he suffered a massive heart attack. The 4,000-word essay, completed and published posthumously, brooks no dissent. ''The child learns speech-disruptive behavior as he tries to keep from stuttering and so to gain approval,'' he writes. Johnson's didacticism lessens near the end, however, and he grows almost gentle. ''Persons with speech disorders . . . have traditionally known the scorn, ridicule and even revulsion of their society,'' he writes in the voice of a man driven all his life to make sense of the ability to speak.

Keto diets have become incredibly popular. Early research suggests this high-fat, very low-carb diet may benefit several health conditions. Although some of the evidence is from case studies and animal research, results from human-controlled studies are also promising.Here are 15 health conditions that may benefit from a ketogenic diet.1. EpilepsyEpilepsy is a disease that causes seizures due to excessive brain activity. Anti-seizure medications are effective for some people with epilepsy. However, others don’t respond to the drugs or can’t tolerate their side effects.Of all the conditions that may benefit from a ketogenic diet, epilepsy has by far the most evidence supporting it. In fact, there are several dozen studies on the topic.Research shows that seizures typically improve in about 50% of epilepsy patients who follow the classic ketogenic diet. This is also known as a 4:1 ketogenic diet because it provides 4 times as much fat as protein and carbs combined.The modified Atkins diet (MAD) is based on a considerably less restrictive 1:1 ratio of fat to protein and carbs. It has been shown to be equally effective for seizure control in most adults and children older than two years of age.The ketogenic diet may also have benefits on the brain beyond seizure control. For example, when researchers examined the brain activity of children with epilepsy, they found improvements in various brain patterns in 65% of those following a ketogenic diet — regardless of whether they had fewer seizures.2. Metabolic SyndromeMetabolic syndrome sometimes referred to as prediabetes, is characterized by insulin resistance. You can be diagnosed with metabolic syndrome if you meet any 3 of these criteria:Large waistline: 35 inches (89 cm) or higher in women and 40 inches (102 cm) or higher in men.Elevated triglycerides: 150 mg/dl (1.7 mmol/L) or higher.Low HDL cholesterol: Less than 40 mg/dL (1.04 mmol/L) in men and less than 50 mg/dL (1.3 mmol/L) in women.High blood pressure: 130/85 mm Hg or higher.Elevated fasting blood sugar: 100 mg/dL (5.6 mmol/L) or higher.People with metabolic syndrome are at increased risk of diabetes, heart disease and other serious disorders related to insulin resistance. Fortunately, following a ketogenic diet may improve many features of metabolic syndrome.Improvements may include better cholesterol values, as well as reduced blood sugar and blood pressure. In a controlled 12-week study, people with metabolic syndrome on a calorie-restricted ketogenic diet lost 14% of their body fat. They decreased triglycerides by more than 50% and experienced several other improvements in health markers.3. Glycogen Storage DiseasePeople with glycogen storage disease (GSD) lack one of the enzymes involved in storing glucose (blood sugar) as glycogen or breaking glycogen down into glucose. There are several types of GSD, each based on the enzyme that is missing.Typically, this disease is diagnosed in childhood. Symptoms vary depending on the type of GSD and may include poor growth, fatigue, low blood sugar, muscle cramps, and an enlarged liver. GSD patients are often advised to consume high-carb foods at frequent intervals so glucose is always available to the body.However, early research suggests that a ketogenic diet may benefit people with some forms of GSD. For example, GSD III, also known as Forbes-Cori disease, affects the liver and muscles.Ketogenic diets may help relieve symptoms by providing ketones that can be used as an alternative fuel source. GSD V, also known as McArdle disease, affects the muscles and is characterized by a limited ability to exercise.In one case, a man with GSD V followed a ketogenic diet for one year. Depending on the level of exertion required, he experienced a dramatic 3- to 10-fold increase in exercise tolerance. However, controlled studies are needed to confirm the potential benefits of ketogenic diet therapy in people with glycogen storage disease.4. Polycystic Ovary Syndrome (PCOS)Polycystic ovary syndrome (PCOS) is a disease marked by hormonal dysfunction that often results in irregular periods and infertility. One of its hallmarks is insulin resistance, and many women with PCOS are obese and have a hard time losing weight.Women with PCOS are also at an increased risk for type 2 diabetes. Those who meet the criteria for metabolic syndrome tend to have symptoms that affect their appearance. Effects may include increased facial hair, acne and other signs of masculinity related to higher testosterone levels.A lot of anecdotal evidence can be found online. However, only a few published studies confirm the benefits of low-carb and ketogenic diets for PCOS. In a 6-month study of eleven women with PCOS following a ketogenic diet, weight loss averaged 12%.Fasting insulin also declined by 54% and reproductive hormone levels improved. Two women suffering from infertility became pregnant.5. DiabetesPeople with diabetes often experience impressive reductions in blood sugar levels on a ketogenic diet. This is true of both type 1 and type 2 diabetes. Indeed, dozens of controlled studies show that a very low-carb diet helps control blood sugar and may also provide other health benefits.In a 16-week study, 17 of 21 people on a ketogenic diet were able to discontinue or decrease diabetes medication dosage. Study participants also lost an average of 19 pounds (8.7 kg) and reduced their waist size, triglycerides, and blood pressure. In a 3-month study comparing a ketogenic diet to a moderate-carb diet, people in the ketogenic group averaged a 0.6% decrease in HbA1c. 12% of participants achieved an HbA1c below 5.7%, which is considered normal.6. Some CancersCancer is one of the leading causes of death worldwide. In recent years, scientific research has suggested that a ketogenic diet may help some types of cancer when used along with traditional treatments such as chemotherapy, radiation, and surgery. Many researchers note that elevated blood sugar, obesity, and type 2 diabetes are linked to breast and other cancers. They suggest that restricting carbs in order to lower blood sugar and insulin levels may help prevent tumor growth.Mice studies show ketogenic diets may reduce the progression of several types of cancer, including cancers that have spread to other parts of the body. However, some experts believe the ketogenic diet may be particularly beneficial for brain cancer. Case studies and patient data analyses have found improvements in various types of brain cancer, including glioblastoma multiforme (GBM) — the most common and aggressive form of brain cancer.One study found 6 out of 7 GBM patients had a modest response to an unrestricted-calorie ketogenic diet combined with an anti-cancer drug. Researchers noted that the diet is safe but probably of limited use alone.Some researchers report the preservation of muscle mass and slowed tumor growth in cancer patients who follow a ketogenic diet in conjunction with radiation or other anti-cancer therapies. Although it may not have a significant impact on disease progression in advanced and terminal cancers, the ketogenic diet has been shown to be safe in these patients and potentially improve quality of life.Randomized clinical studies need to examine how ketogenic diets affect cancer patients. Several are currently underway or in the recruiting process.7. AutismAutism spectrum disorder (ASD) refers to a condition characterized by problems with communication, social interaction and, in some cases, repetitive behaviors. Usually diagnosed in childhood, it is treated with speech therapy and other therapies. Early research in young mice and rats suggests ketogenic diets may be helpful for improving ASD behavior patterns. Autism shares some features with epilepsy, and many people with autism experience seizures related to the over-excitement of brain cells.Studies show that ketogenic diets reduce brain cell over-stimulation in mouse models of autism. What’s more, they appear to benefit behavior regardless of changes in seizure activity.A pilot study of 30 children with autism found that 18 showed some improvement in symptoms after following a cyclical ketogenic diet for 6 months. In one case study, a young girl with autism who followed a gluten-free, dairy-free ketogenic diet for several years experienced dramatic improvements.These included resolution of morbid obesity and a 70-point increase in IQ. Randomized controlled studies exploring the effects of a ketogenic diet in ASD patients are now underway or in the recruiting process.8. Parkinson’s DiseaseParkinson’s Disease (PD) is a nervous system disorder characterized by low levels of the signaling molecule dopamine. The lack of dopamine causes several symptoms, including tremor, impaired posture, stiffness, and difficulty walking and writing. Because of the ketogenic diet’s protective effects on the brain and nervous system, it’s being explored as a potential complementary therapy for PD.Feeding ketogenic diets to rats and mice with PD led to increased energy production, protection against nerve damage and improved motor function. In an uncontrolled study, seven people with PD followed a classic 4:1 ketogenic diet. After 4 weeks, five of them averaged a 43% improvement in symptoms. The effects of a ketogenic diet on PD is another area that needs controlled studies.9. ObesityMany studies show that very low-carb, ketogenic diets are often more effective for weight loss than calorie-restricted or low-fat diets . What’s more, they typically provide other health improvements as well. In a 24-week study, men who followed a ketogenic diet lost twice as much fat as men who ate a low-fat diet.In addition, the ketogenic group’s triglycerides dropped significantly, and their HDL (“good”) cholesterol increased. The low-fat group had a smaller drop in triglycerides and a decrease in HDL cholesterol.Ketogenic diets’ ability to reduce hunger is one of the reasons why they work so well for weight loss. A large analysis found that very low-carb, calorie-restricted ketogenic diets help people feel less hungry than standard calorie-restricted diets.Even when people on a ketogenic diet are allowed to eat all they want, they generally end up eating fewer calories due to the appetite-suppressing effects of ketosis.In a study of obese men who consumed either a calorie-unrestricted ketogenic or moderate-carb diet, those in the ketogenic group had significantly less hunger, took in fewer calories and lost 31% more weight than the moderate-carb group.10. GLUT1 Deficiency SyndromeGlucose transporter 1 (GLUT1) deficiency syndrome, a rare genetic disorder, involves deficiency of a special protein that helps move blood sugar into the brain. Symptoms usually begin shortly after birth and include developmental delay, difficulty with movement and sometimes seizures. Unlike glucose, ketones don’t require this protein to cross from the blood to the brain. Therefore, the ketogenic diet can provide an alternative fuel source that these children’s brains can use effectively.Indeed, ketogenic diet therapy seems to improve several symptoms of the disorder. Researchers report decreased seizure frequency and improvement in muscle coordination, alertness, and concentration in children on ketogenic diets.As with epilepsy, the modified Atkins diet (MAD) has been shown to provide the same benefits as the classic ketogenic diet. However, the MAD offers greater flexibility, which may result in better compliance and fewer side effects. In a study of 10 children with GLUT1 deficiency syndrome, those who followed the MAD experienced improvements in seizures. At six months, 3 out of 6 became seizure-free..11. Traumatic Brain InjuryTraumatic brain injury (TBI) most commonly results from a blow to the head, a car accident or a fall in which the head strikes the ground. It can have devastating effects on physical function, memory and personality.Unlike cells in most other organs, injured brain cells often recover very little, if at all. Because the body’s ability to use sugar following head trauma is impaired, some researchers believe the ketogenic diet may benefit people with TBI .Rat studies suggest that starting a ketogenic diet immediately after brain injury can help reduce brain swelling, increase motor function and improve recovery. However, these effects appear to occur mainly in younger rather than older rats. That said, controlled studies in humans are needed before any conclusions can be reached.12. Multiple SclerosisMultiple sclerosis (MS) damages the protective covering of nerves, which leads to communication problems between the brain and body. Symptoms include numbness and problems with balance, movement, vision and memory.One study of MS in a mouse model found that a ketogenic diet suppressed inflammatory markers. The reduced inflammation led to improvements in memory, learning and physical function.As with other nervous system disorders, MS appears to reduce the cells’ ability to use sugar as a fuel source. A 2015 review discussed ketogenic diets’ potential to assist with energy production and cell repair in MS patients.Additionally, a recent controlled study of 48 people with MS found significant improvements in quality of life scores, cholesterol and triglycerides in the groups who followed a ketogenic diet or fasted for several days. More studies are currently underway.13. Nonalcoholic Fatty Liver DiseaseNonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the Western world. It is strongly linked to type 2 diabetes, metabolic syndrome and obesity, and there’s evidence that NAFLD also improves on a very low-carb, ketogenic diet.In a small study, 14 obese men with metabolic syndrome and NAFLD who followed a ketogenic diet for 12 weeks had significant decreases in weight, blood pressure and liver enzymes. What’s more, an impressive 93% of the men had a reduction in liver fat, and 21% achieved complete resolution of NAFLD.14. Alzheimer’s DiseaseAlzheimer’s disease is a progressive form of dementia characterized by plaques and tangles in the brain that impair memory. Interestingly, Alzheimer’s disease appears to share features of both epilepsy and type 2 diabetes: seizures, the inability of the brain to properly use glucose and inflammation linked to insulin resistance.Animal studies show that a ketogenic diet improves balance and coordination but doesn’t affect the amyloid plaque that is a hallmark of the disease. However, supplementing with ketone esters appears to reduce amyloid plaque. In addition, supplementing people’s diets with ketone esters or MCT oil to increase ketone levels has been shown to improve several Alzheimer’s disease symptoms.For example, one controlled study followed 152 people with Alzheimer’s disease who took an MCT compound. After 45 and 90 days, this group showed improvements in mental function, while the placebo group’s function declined. Controlled studies testing the modified Atkins diet and MCT oil in people with Alzheimer’s disease are currently in progress or in the recruiting stage.15. Migraine HeadachesMigraine headaches typically involve severe pain, sensitivity to light and nausea. Some studies suggest migraine headache symptoms often improve in people who follow ketogenic diets. One observational study reported a reduction in migraine frequency and pain medication use in people following a ketogenic diet for one month.An interesting case study of two sisters following a cyclical ketogenic diet for weight loss reported that their migraine headaches disappeared during the 4-week ketogenic cycles but returned during the 8-week transition diet cycles. However, high-quality studies are needed to confirm the results of these reports.Take-Home MessageKetogenic diets are being considered for use in several disorders due to their beneficial effects on metabolic health and the nervous system. However, many of these impressive results come from case studies and need validation through higher-quality research, including randomized controlled trials.With respect to cancer and several other serious diseases on this list, a ketogenic diet should be undertaken only in addition to standard therapies under the supervision of a doctor or qualified healthcare provider.Also, no one should consider the ketogenic diet a cure for any disease or disorder on its own. Nonetheless, ketogenic diets’ potential to improve health is very promising.