Thursday, January 27, 2011

Placebos, Suggestibility, and Hypnosis

In a twist on the use of placebos, a study was conducted with patients experiencing irritable bowel syndrome (IBS). They were explicitly ingormed that they would be receiving a placebo and it was suggested that the placebo had been shown in the past to relieve IBS symptoms through the mind-body healing process. The bottles containing the sugar pills were labeled "Placebo."

IBS is a disorder of the lower intestinal tract involving abdominal pain and abnormal bowel movements, and emotional stress or mood disorders, such as anxiety or depression, often make the symptoms worse.

Based on a self-reported questionnaire, the placebo group indicated significantly better pain relief and reduction in the severity of other symptoms compared to those who received routine treatment. The conclusion was that communication of a positive outcome was a factor in the effectiveness of the placebo and the suggestibility of the trial participants played a role.

Reports on the study can be found at the following URLs:

Ailments that involve subjective judgments by the patient such as "how do you feel" for depressive patients or "rank the intensity of your pain" for IBS sufferers tend to be particularly amenable to placebo treatments. In the case of stuttering, evaluations of treatment efficacy for relieving symptoms may be a bit more objective. A third party (neither treater nor treated) can, for example, count the number of disfluencies normalized on some word count or speaking time scale.

Nevertheless, since we have previously argued that stuttering is basically a mind-body problem, with a substantial mind contribution, we might very well expect that results of an "open knowledge" placebo trial for stutterers might have similar results as that for the IBS study.

On the other hand, some participants in the pagoclone trials have reported that their fluencies had deteriorated during periods when they (thought they) were switched to the placebo treatments. While these periods of disfluency might be attributed to fluency variations while they were on pagoclone, I would prefer to give the benefit of the doubt to the pagoclone trial participants at this point in time until the results of the trials are published. If, for example, previous periods of greater disfluency lasted typically for days or weeks, while the placebo was administered for months (during which disfluency persisted), then this would be evidence that the disfluency was attributable to the cessation of pagoclone treatment.

The world can be divided into two types: Those who are suggestible and those who are not. More accurately, the characteristic of suggestibility may lie on a spectrum--individuals are suggestible to varying degrees. The placebo response is thought, at least in part, to be based on individual differences in suggestibility. Those who are suggestible may be more responsive to medical treatments (real or placebo) on the basis of patient belief in addition to a possible physiological mechanism. If this is the case, then controlled double blind trials of medical treatments could be improved by either controlling for suggestibility or, in the extreme case, eliminating highly suggestible individuals from the trials through prescreening.

The personality characteristic of suggestibility may be difficult to measure objectively. However, the ease with which an individual can be hypnotized as well as the depth of the hypnosis might be taken as a proxy for suggestibility, although evaluating "hypnotizability" might be a relatively subjective endeavor.

The Mental Measurements Yearbook does not indicate the existence of any psychological tests for the personality characteristic of suggestibility. However, the Multidimensional Iowa Suggestibility Scale (MISS), recently developed by Kotov, R.I. et al, is a self-reporting questionnaire that attempts to get at various dimensions of suggestibility. The questionnaire can be found at the following URL:

The results from this questionnaire might be biased for individuals who have read this post and who would prefer to convince themselves or a clinician that they are not suggestible.

Monday, January 24, 2011

Communication Impacts of Stuttering

We have previously discussed stuttering in terms of its impact on fluency-- namely the smoothness and flow with which sounds, syllables, words and phrases are joined together when speaking. Fluency relates to the mechanics of speech and the ease/rapidity of oral verbal expression. Fluency enables an individual to deliver informational content quickly and with the appearance of expertise. Stuttering, on the other hand, is characterized by breaks in the fluidity of speech in addition to the repetition of parts of speech and, as such, represents a breakdown in the ability to communicate.

We can view interpersonal oral communication as consisting of two parts--namely content (what you say) and style (how you say it). Content involves purely the non-emotional information contained in the words being uttered while style involves the emotional information that is conveyed while speaking.

Consider a fluent person trying to give an oral presentation while juggling three balls in the air. Assuming that the individual does not have a high degree of proficiency with the mechanics of juggling, he may experience difficulty in concentrating on the presentation. This is exactly what happens to a stutterer who has to struggle with the mechanics of talking and is less able to focus on content as well as style.

Stuttering affects the ability, while speaking, to be articulate. Being articulate relates to the mental fluidity in the formulation and expression of thoughts, concepts, and ideas with clarity, eloquence, and effectiveness. Disfluency may hinder the train of thought, impinging negatively on formulation. One's brain in organizing thoughts generally runs faster than one's mouth. However, when one's mouth runs appreciably slower than one's brain, as with stutterers, then the ability to formulate thoughts with clarity during oral communication may be adversely affected.

Communication involves certain nonverbal elements such as voice quality, emotion and speaking style (i.e., paralanguage) as well as rhythm, cadences, intonation, emphases, and stress (prosodic features). These elements, which contribute to style (i.e, emotional content), may be affected by stuttering. The energy devoted to the mechanics of speaking substantially diminishes focus on these non-verbal elements. In addition, halting speech will certainly affect the prosodic features, namely the rhythm, cadence, and intonation of speech, which may distort or effectively eliminate expression of the communication's emotional content.

The social development of a disfluent individual may be adversely affected in the formative years during adolescence and young adulthood. In this time period, social interaction is very important for the formation of personality as the young person experiments with various identities and behaviors. Communication with his or her peer group is very important at this stage. Unfortunately, a person who stutterers may not get much out of this development stage, since his attention may be focused on the mechanics of speech, he may be ostracized somewhat by his peer group, and the disfluency may severely limit his communication capabilities in terms of both content and style. The normal give and take of conversation during which ideas and concepts are bandied about and the ability to think on the fly in the course of a conversation may not be cultivated in a person who stutters.

Given all of these impacts of stuttering, an individual experiencing this ailment in addition to being less fluent, might also be expected to be less articulate and socially skilled.

Sunday, January 16, 2011

Endogenously Reducing Dopamine

An interesting article in Time magazine (January 12, 2011) regarding the enhancement of cognitive performance discussed the use of Adderall (a stimulant) to improve cognitive performance by increasing levels of dopamine. However, it was found that there was no statistically significant difference in cognitive performance of Adderall relative to a placebo, suggesting that you can get the same dopamine boosting benefits of the drug by believing you will do well which itself releases dopamine. This is an example of the mind coming into play to influence bodily functions (in this case, cognition which is a function of the brain).

In a previous post (Parkinsons Disease, Dopamine, and Stuttering), we pointed out that patients suffering from Parkinsons disease who received a placebo showed a substantial increase of dopamine activity according to brain imaging results. So we speculated that a nocebo-like effect of context on stuttering might also increase the level of dopamine activity in the brains of stutterers, thus negatively affecting their fluency.

We can turn this argument around and ask whether or not a placebo, which could be an endogenously influenced state of mind, might reduce dopaminergic activity and hence improve fluency. This endogenous mind state might be produced solely by the individual himself through some sort of mental manipulation.

Consider the case of King George VI as depicted in the film, The Kings Speech.  We should not automatically assume that the success of King George VI in giving his wartime speech with relative fluency was due solely from fluency shaping techniques and modifications in the mechanics of his speech suggested by his therapist. We should also consider the possibility that he harnessed his mind in such a way as to generate a placebo-like effect whereby the dopaminergic activity in the relevant parts of his brain actually decreased. Granted, the king had a cheerleader in the form of his therapist (who may be regarded as an exogenous influence), but nevertheless we must consider the possibility of purely endogenous influences as well.

There are anecdotal reports of individuals achieving similar effects--namely the attorney who was fluent in a professional setting but would stutter with friends and family, and the college professor who claimed to be able to "psyche himself up" prior to teaching a class through some sort of mental preparation so as to lecture fluently. The mechanisms by which this happens are obscure and resistant to simple codification such as "pop this pill one hour before..." The "buttons" that are pressed and the "switches" that are flipped in the mind to activate the "internal cheer leader" and to achieve these feats are unknown. Yet, consider the possibility that it could be done by some individuals.

The manipulation of dopaminergic activity through endogenous brain states might be comparable to the modification of the neurotransmitter endorphin levels claimed by practitioners of meditation techniques. But with meditation, there exists a well codified regimen, if practiced leads to the desired results.

It is not clear whether all stutterers can control their fluency by manipulating their endogenous mind states or if this approach is limited to a subset based perhaps on the intensity of the underlying physical cause of stuttering (rated on a scale of 1 to 10). It may be that only those individuals with relatively mild physical causes of stuttering (and presumably lower dopaminergic disfunction) can achieve fluency by endogenously manipulating their mind states.

Tuesday, January 11, 2011

Serotonin, Dopamine, and Stuttering

As in the previous post, which raised the possibility that viruses cause stuttering, this post again addresses the question as to what might be the root cause of excessive dopaminergic activity.

Reiterating the discussion in the post entitled "Antidepressants May Affect Stuttering," SSRIs inhibit the reuptake of serotonin by presynaptic neurons permitting greater concentrations of serotonin in the synapses. Excessive serotonin concentrations may highjack dopamine active transporters (DATs) prohibiting them from doing their job of dopamine reuptake. Consequently, synaptical concentrations of dopamine may be higher, leading to disfluency.

Now consider the possibility that some stutterers might have excessive levels of naturally occurring synaptical serotonin (i.e., independent of whether or not they take antidepressants). This may be the result of a low density of SERTs to reuptake serotonin or of the brain's overactive production of serotonin. At any rate, such a situation might lead to the highjacking of DATs resulting in less reuptake of dopamine, greater concentrations of dopamine, and greater disfluency. If this were the case, we might consider selective serotonin reuptake enhancers (SSREs) to reduce the levels of serotonin.

Independent of whether or not they take antidepressants, some individuals may have lower densities of DATs in the brain impairing its ability to reuptake dopamine, again leading to higher concentrations of dopamine and, hence, adversely affecting fluency. So we might consider the possibility of a class of drugs which we could call dopamine reuptake enhancers (DREs) that would reduce the levels of dopamine in the synapses by making the DATs more efficient with respect to dopamine reuptake.

Are there drugs that are reuptake enhancers?  With respect to the reuptake of dopamine, I am unaware of the existence of any such drugs. The only known drug that enhances the reuptake of serotonin is tianeptine. Tiapentine has low affinity for SERTs, so its effect on serotonin reuptake appears to be indirect. Newer research seems to indicate that tiapentine acts through some downstream mechanism that is not yet fully understood.

What the discussion above illustrates is that the relationships among neurotransmitters and their effects on the brain are very complex. There are interrelationships among the various neurotransmitters and these connections are currently not fully understood by the research community. Given the relationships among the dopaminergic, GABAergic, and serotonergic systems we have thus far seen, the obvious explanation of excessive dopamine as the root cause of disfluency may be overly simplistic.

Moreover, stutterers may fall into various subgroups, for example, characterized by excessive serotonin production, low SERT densities, insufficient DAT activity, other inadequacies of the dopaminergic or GABAergic systems, etc. And the appropriate therapeutic drug treatments to get at the root source for these different subgroups may not be the same.

In future posts, we will further discuss relationships between the serotonergenic and dopaminergic systems