Time Elasticity, Stuttering, and Pagoclone Trials

Researchers at UCLA conducted an experiment regarding the estimation of time intervals.  Subjects, some of whom were on stimulants, were asked to give their subjective estimates of the time elapsed between a start signal and an end signal.  The actual length of the interval was 53 seconds.  The average time estimates of the non-stimulant group was 67 seconds, while that of the stimulant group was 91 seconds.

Stimulants increase the dopaminergic activity in the brain.  The perception of time-intervals is thought to be mediated by spiny neurons in the striatum of the basal ganglia, whereby timing initiates with a burst of dopamine and ends with a recognized signal.

Naturally occurring variations of dopamine levels in the striatum may affect fluency levels for a subgroup of stutterers.  So the relevance of this study is that these individuals may find that they have an expanded subjective experience of time much like the stimulant group in the experiment.  And this time elasticity may vary during periods of lesser or greater fluency as dopaminergic activity is at different levels.

On the other hand, the subgroup of stutterers whose fluency may be governed by a deficiency of dopamine may find that their subjective experience of time is contracted.  In the experiment above they might underestimate the time interval.

An interesting experiment for individuals would be the following: Upon awaking in the morning, look at the clock.  Remain in bed for a few minutes, estimate how much time you think has elapsed, and then compare it with the clock time.  Calculate the ratio of estimated time to clock time and record it.  During the day, observe your level of fluency (in particular, as close to waking time as possible).  For example rate it on a 1 to 10 scale.  After several months, compare the time interval ratios to your fluency levels (i.e., by eyeballing or more rigorously by a correlational analysis) in order to determine if there is an association between the two measures. 

IF the time interval ratio is a plausible proxy for dopamine levels and IF stuttering is affected by dopamine levels, then you should get a reasonable correlation between the two measures.  We would expect the correlation to be positive for the subgroup disfluent for high levels of dopamine and negative for the subgroup disfluent as a result of low levels.

In previous posts, we suggested that stutterers involved in clinical drug trials be screened on the basis of their subgroup membership.  There is no reason to dilute the clinical trials group, for example in pagoclone studies, with individuals whose fluency is not affected by high dopamine levels.  In particular, we suggested that the response of their fluencies to a benzodiapine might be a criterion for identifying subgroups.  

But governmental drug administration agencies (such as the FDA) may disapprove of the selection of individuals for drug trials based on their responses to another drug.  So the use of time elasticity measures as discussed above might qualify as an alternative selection mechanism.

Limbic Stuttering

We have previously discussed the possibility that stuttering may have two components: one generated by brain disfunctions and the other generated by the “mind.”  The mind is a manifestation of the brain and involves, in particular, emotions.  Hence, we now refer to stuttering generated by the mind as limbic stuttering, since the limbic system is instrumental in determining emotions. 
  

Limbic stuttering may be engendered, for example, by a specific social context (e.g., speaking before an audience) or by an anticipatory emotional reaction when coming upon a word having a sound over which one has previously blocked (e.g., any words starting with “f” such as “favorite”).

As discussed previously, some theories of stuttering posit that the disruption of timing signals between the basal ganglia and speech motor areas in the left cortical hemisphere contributes to or causes stuttering.  The dorsal striatum in the basal ganglia is involved in the timing of speech and excessive dopaminergic activity in the dorsal striatum disrupts timing signals for a subgroup of stutterers. 

The ventral striatum, in physical proximity to the dorsal striatum, is part of the limbic circuitry governing emotions.  Emotional activation of the ventral striatum (e.g., coming upon a feared word) further contributes to the dopaminergic activity that disrupts timing. 

Is there any way that we could empirically determine if a blocking incident is limbic stuttering?  To answer this question, consider a technique for preempting a block.  Namely, when you come to a block, don’t try to plow through it.  Rather, stop, go back several words and continue with your sentence.  So you might be trying to say, “Let me tell you about my favorite restaurant in New York,” and you perceive a block on the word “favorite.” 

Then the approach might be to say, “Let me tell you about my (block) tell you about my favorite restaurant in New York.”  Chances are that if the block was not limbic-based, you will be able to complete your sentence without a block.  I say “chances are,” since there is a probability that a brain-based block (as opposed to mind) may again repeat itself on the word “favorite.”

Note that this approach of repeating several words is related to voluntary stuttering on a syllable such as “f-f-f-favorite,” and might be characterized as voluntary phrase stuttering.  If block occurrences in one’s speech are not excessively frequent, then this approach may not be viewed as disfluency from the listener’s point of view.  

However, it is unlikely that the technique will be effective for limbic stuttering since anticipatory fear will repeatedly activate the dopaminergic system.  Thus, the technique’s lack of efficacy might be regarded as an indicator of limbic stuttering.