Stuttering as an emotional/psychological problem. PWS and “experts” alike have fallen for this myth. The nature of stuttering makes it damned perplexing.
Many researchers and speech-language pathologists (SLPs), including those who are PWS themselves, continue to let themselves be misled by the Primary Paradox–and keep trying to explain stuttering by building elaborate paradigms based on learned behavior or psychological aspects such as anticipatory/avoidance reactions or conflict and assertiveness issues.
All that may be irrelevant. It’s my view that if the neurologic flaw could somehow be instantly corrected, the stutter would disappear just as quickly. What would that say about the importance of psychological theories or learned behavior? (Later in this section, I’ll detail a couple of anecdotal cases in which stuttering did disappear instantly.)
For years I rationalized that stuttering was an emotional or psychological disorder myself. I believed that idea because it was the only information I had ever been exposed to. Everything I read or heard offered up that theory. The vagueness and lack of logic of it all was puzzling, but I believed the “experts.” Then my view changed as I learned about other neurologic disorders and about how the brain works. I also learned to have a healthy skepticism for what “experts” say. Other disorders once thought psychological in origin began yielding their neurologic and genetic roots: dyslexia, Tourette’s syndrome, clinical depression, attention deficit hyperactive disorder (ADHD), obsessive-compulsive disorder (OCD), and so forth. Now it seems just common sense to look at stuttering as a neurologic flaw.
A spokesperson for the Speech Foundation of America once said that the Hollins precision fluency shaping program “totally ignores the psychological side of stuttering, and that just isn’t healthy.” On the one hand, I think it’s healthy to de-emphasize the psychological side of stuttering, because stuttering has been over-saturated in psychobabble and needs to be viewed as the biologic disorder it is. On the other hand, many PWS may very well need to deal with psychological issues caused by their stutters.
The originator of the Hollins program said his peers were “outraged” when he started out. He said they warned him that he was going to ruin people by treating their stuttering as a physically-based problem, that the underlying emotional cause would manifest itself somewhere else, perhaps something worse. He said that just hasn’t happened. Stuttering may cause emotional and psychological problems, not the other way around.
There seem to be many “experts” who do not wish to see yet another so-called psychological disorder unveiled as a biologic disorder.
Even a professor emeritus of psychiatry and pediatrics at a major university is not above falling prey to the Primary Paradox. He once asked: If stuttering is a physical problem, why do people hardly stutter at all in non-threatening situations, such as talking to their dog, yet stutter badly in tense situations, such as when making a speech?
Nonstutterers (and PWS themselves) who blindly believe such authorities may think that PWS should be able to overcome stuttering by “relaxing” or “slowing down” or rooting out its origin in some childhood trauma or aberrant relationship with a parent or sibling.
Simple logic can fail us when we don’t have enough accurate information to fill in the blanks. Logic seems to say that if you can talk with little or no stuttering when you’re alone or speaking to a pet, then you should be able to do the same thing in front of other people. But you can’t, and that’s damn perplexing and frustrating.
A recent brain imaging study (detailed later) found inherent differences in speech areas of PWS as compared to non-PWS. These differences persisted even when PWS were not stuttering (in choral reading). Thus, greater fluency in certain situations–when speaking alone or doing choral reading–may indicate only that the neurologic block is somehow temporarily bypassed in those situations.
This may be due to a lessening in the excitation feedback component of stuttering. If you take excitation feedback away, a PWS could speak as fluently around other people as he does when alone. Though he’d still have the neurologic speech block–the block would just remain dormant.
It’s interesting to note that a neurogenic (acquired) stutter caused by an actual brain injury (a lesion in a particular area) is not variable–it manifests the same way all the time. Though PWS are stutterers all the time (and have the most problems consistently with the same particular sounds depending on the individual), the manifestation of the problem is somewhat variable due to some dynamic interplay of neurologic factors which have not yet been uncovered. This “biorhythmic-like” waxing and waning of stuttering severity many PWS relate is common also to other neurologic disorders.
Movie-makers have fallen for the myths. The character who stutters miraculously overcomes his stutter immediately after taking an action that has an emotionally “profound” effect on him. In One Flew Over the Cuckoo’s Nest, the stutterer is cured after having sex with a nurse. In A Fish Called Wanda, the stutterer is fluent after running over a nemesis with a highway roller tractor. This stuff may make good drama but it just helps reinforce the myths and stigmas about stuttering. Many people form their opinions based on such inaccurate drivel.
The psychobabble stuff continues to hurt the cause of the stuttering community. People who believe the psychological ideas don’t take stuttering as seriously as they might a true “medical” disorder. And PWS continue to be saddled with the stigma that they’re somehow weaker emotionally than their nonstuttering counterparts. All this translates directly to lack of support and funding for research on stuttering.
Case in point: Here’s a quote from a researcher that appeared in the American Journal of Medical Genetics: “Among the factors contributing to the absence of ongoing studies to map the susceptibility loci (the genes) for stuttering is…the suspicion that the more benign nature of the stuttering phenotype makes it a less attractive candidate for funding the expensive and time-consuming typing necessary for linkage studies.”
As with most things, it’s a matter of money and lobbying power. Most PWS, I’d think, don’t consider stuttering to be “benign” (harmless). Neither does the American Psychiatric Association. According to their Diagnostic and Statistical Manual of Mental Disorders, stuttering is a disabling disorder, affecting one’s academic or occupational achievement or social communication.
We go backwards and continue to shoot ourselves in the foot when we lay stuttering at the doorstep of “unresolved emotional issues.” Psychological issues may aggravate stuttering, just as they may aggravate diabetes or high blood pressure, but it’s very unlikely they are causal.
In a book called The Death of Psychiatry, maverick psychiatrist E. Fuller Torrey calls psychiatrists “witch doctors” and Sigmund Freud a “fraud.” His premise is that many psychiatric patients with so-called mental illnesses or emotional disorders have true brain diseases or disorders, and these conditions are not brought on by bad parenting or some other childhood experience. These patients belong within the field of neurobiology rather than psychiatry or psychotherapy. The remaining patients, he says, have inter- or intra-personal problems and they belong in counseling, but that’s a matter of education.” There’s really no need for psychiatry,” he holds.23 Needless to say, he’s taken a lot of flack for daring to tread on sacred turf. (I trust he means much of traditional psychiatry. Many psychiatrists are coming to recognize, and work in accordance with, the neurobiologic basis of such conditions. And I firmly believe that stuttering’s rightful home lies within the folds of neurobiology.)
Tension in the larynx. Another misguided, simplistic notion is that tension in the larynx or external articulators is the cause of stuttering and correcting that will alleviate the problem. Many people (lay and expert alike) see the external contortions and struggles and make the inaccurate assumption that the problem must lie in those external struggling body parts. The block seems to be in the external parts. But it’s the brain that controls those external parts, and the block is in the brain. The observable struggles are the result of the neurologic block of speech output–they occur because the PWS tries to force his articulators through the block. These outward manifestations are symptoms, not causes. If the brain block were not present, there would be no external symptoms.
Stress. Then there’s that old bugaboo “stress.” Stress may aggravate stuttering just as it may aggravate diabetes and high blood pressure–but stress doesn’t cause any of these conditions. For decades, the medical community swallowed the myth that stress caused stomach ulcers. Then a physician discovered it wasn’t stress after all, but a type of bacteria. That got him the cold shoulder from his peers at first. Old ideas, even if inaccurate, are hard to break loose from. But the facts proved him right and doctors have had to make an attitude adjustment. Now they prescribe antibiotics which cure the ulcer.
Stuttering as learned behavior. Some say that the observable struggles accompanying stuttering are learned behaviors. Conditioning may play some role here, but, again, if somehow the neurologic flaw causing stuttering were instantly corrected, these struggles would immediately disappear along with the stutter. As a disease or disorder goes, so do its symptoms. It’s important to treat the cause, not the symptoms.
And many experts believe that stuttering itself is learned behavior. I think it’s unlikely that a child with normal neurologic speech function can “learn” a chronic, life-long stutter–short of some kind of extreme “brainwashing” procedure or fluke. There would have to be a predisposition to develop stuttering.
Many experts may fall into this trap because they believe that normal speech function is learned, and if speech function is learned, then why can’t stuttering be learned?
But speech function is not learned in the classic sense of skills such as tennis, golf, typing, and so forth. Humans have an inborn speech function “template”–special brain areas devoted to language–that gives us a special facility for acquiring speech (and the same for overall language function). This template expresses itself at a certain developmental stage. Similar “templates” allow us to acquire vision and hearing “skills” without trying, with only passive exposure to the environment. The acquisition of speech is almost a birthright.
Your vocabulary of words may be learned in a more classic sense. But your speaking accent even appears to be passively acquired. And, surprisingly, many language researchers believe that even the rules of grammar are inborn and universal. The thousands of languages the world over appear to share common basic grammatical rules that don’t have to be learned.
There are several other ways the acquisition of speech differs from learned skills such as golf and tennis.
People of very low intellect often acquire fluent, glib speech. Speech acquisition is universal. It’s passively acquired–all you need is exposure to other people who talk. If you aren’t exposed to speech during the early critical developmental period, the ability to acquire speech properly may be lost forever. Skills such as golf or tennis require formal practice, and can be learned quite proficiently in adulthood.
There’s certainly no classic reward element in “learning” to stutter as there is for golf or tennis–only punishment and humiliation.
There are a variety of skill levels in learned behaviors, but a basic “sameness” in the ability to speak “skillfully.”
If speech function is not a core (inborn) trait (like, for example, shyness, aggressiveness, sexual orientation), then it’s about as close as you can get. If speech function is learned, it’s more “instinctive learning.” Nonstutterers can’t stutter–their fluent brain circuitry won’t allow it (people, including actors, can pretend to stutter, but they have difficulty understanding how to fake it). So the idea that you can start out with normal speech function and somehow “learn” stuttering doesn’t make much sense to me.
Anecdotal case 1. At the 1996 National Stuttering Project (NSP) in Denver, a 72-year-old gentleman came to my brain neuropatterning workshop. He had been a stutterer up until the time he had a stroke. He said that when he awoke in the hospital, he had some paralysis due to the stroke, but everything else appeared normal except for one thing–he no longer stuttered! He was amazed that he now talked fluently to the nurses. And his “cure” has persisted to this day. Apparently the stroke, in this rare instance, just happened to damage some brain area that played a key role in causing his stutter. Doesn’t this case, at least anecdotally, strongly suggest the same point that I’ve made before: that stuttering is based physically in the brain and if we could somehow correct the flaw, the stutter would disappear instantly? That’s just what happened to this gentleman. His memory and other cognitive facilities remained intact. If emotional issues or learned behavior cause stuttering, where did these things suddenly evaporate to? Now the fellow can’t stutter even if he tries, because the neurologic flaw that caused his stutter is no longer a factor.
Anecdotal case 2. An NSP member who has a severe stutter suffered a head injury and temporarily stopped stuttering. She posted a message about her experience on one of the Internet Listservs for stuttering. She said she was perfectly fluent for a couple of months, then her stutter returned. Apparently, the head injury temporarily altered or put out of commission the area of her brain which caused the stutter. One of the psychological theorists who believes that stuttering is a learned “habit” suggested that memory loss from the head injury may have caused her to “forget” her stutter and when her memory returned, so did her stutter. She posted back that she had remembered her stutter as soon as she regained consciousness from the head injury, but still did not stutter for two months. She said she couldn’t understand how anyone could possibly think that stuttering was a habit. The psychological theorist had no reply to this.
It’s important to note, too, that strokes and head injuries are more likely to cause stuttering than “cure” it. So I would wait for a safer method to alleviate stuttering. (In the interim, you can use the non-invasive techniques of the neuropatterning Home Course.)
Another point: If you had amnesia (memory loss), it’s highly likely you’d still stutter. Memory has no more to do with causing or perpetuating stuttering than it has to do with causing or perpetuating dyslexia or Tourette’s syndrome.
Time to re-think the learning model? Since the 1960s, the learning/conditioning models of stuttering have been advanced by Wendell Johnson and others. Such a model may seem reasonable, because learning and conditioning play a role in most of what we do. It’s my belief, though, that whatever role learning and conditioning play in stuttering, it’s not a primary role.
Some learning theory proponents rationalize that stuttering may be initially caused by a neurologic flaw, but the initial flaw quickly goes away, and learning/conditioning take over to maintain the stutter.
The basis of such thinking may be the observation that some kids go through a temporary period of stuttered speech during the normal developmental stage of consolidating neurologic organization (lateralization, hemispheric dominance, etc.). This process appears to be intimately related to the proper development of speech and other language functions. In due course, the temporary flaw rights itself and the stutter falls away.
Those who push the learning theories seem to think that this developmental neurologic flaw spontaneously rights itself in all kids, and those who develop a chronic stutter do so because they “learn” to stutter during the time they have the temporary stutter. Thus, learning and conditioning are responsible for maintaining the stutter after the neurologic flaw has gone away. I think that’s quite a stretch.
A far more likely explanation is simply that the original neurologic flaw fails to right itself and persists, producing a chronic stutter. There’s likely a genetic basis for this.
Attempts have been made to explain the Primary Paradox as a learning/conditioning phenomenon. That is, the reason you stutter when aware of a human listener (but not when speaking alone or to a pet) is because of “cues” (conditioning). But some PWS also stutter when speaking alone or to a pet. And, a PWS may stutter or be fluent at different times in similar situations when talking to the same person(s). (Did Pavlov’s dog salivate to the bell just some of the time?) Again, learning/conditioning may play a role, but probably not a primary role.
There’s no need to inject learning/conditioning into the equation as a primary player. The “learning” argument apparently isn’t made for other neurologic disorders such as Tourette’s syndrome, dyslexia, autism, OCD, and ADHD. The neurologic flaw that initially causes these disorders apparently maintains them. Why should stuttering be any different? It’s a mistake to look at stuttering in a vacuum.
If you take away the neurologic flaw, you take away the stutter, regardless of the effects of learning and conditioning. And the converse: If you take away learning and conditioning, the stutter would remain (because the neurologic flaw would still be there). And the same would hold true for the other disorders mentioned above. As research on the brain and stuttering continues, perhaps we’ll get a definitive answer.
The learning/conditioning idea has been bought by much of the establishment (including many SLPs who themselves stutter), and has solidified into dogma that is taught in academic speech pathology courses.
In light of our current understanding of genetics, the brain, and other neurologic disorders, I think it’s time to re-think the learning/conditioning theory of stuttering and demote it to a lesser role. It isn’t needed and isn’t capable of explaining many of the manifestations of stuttering (e.g., the inheritance factor, the waxing/waning aspect of stuttering that shows its kinship to other neurologic disorders).
As I’ve mentioned before, we haven’t yet nailed down exactly what causes stuttered speech, but since it’s obviously a flaw in speech function, and since we know that speech function is controlled by the brain, it seems much more likely that the cause of stuttering would be due to some kind of dysfunction where speech originates, rather than something else.
There’s much inaccurate thinking and misinformation to counter.
Changing the confusing terminology. I’m also lobbying to change the confusing terminology. Instead of using terms such as “mental illness” or “mental disorder” (and “psychological” or “emotional” disorder), let’s use a term more descriptive of a condition’s biologic origin–for example, “neurobiologic disorder.” That term more readily indicates that the origin of the disorder is in the brain. This removes much of the stigma associated with these conditions. These disorders could then be recognized as the “medical” conditions they are. Which would also translate into more research funding and medical insurance coverage. The specific name of the disorder could be attached, for example: neurobiologic disorder/depression, neurobiologic disorder/OCD, neurobiologic disorder/ADHD, neurobiologic disorder/stuttering, and so forth.