Theory of Stuttering – Blog
Theory of Stuttering – Blog
In the main text (Footnote in Section 2.1), I have reported a case in which life-long stuttering disappeared after tumor surgery that resulted in a cerebellar lesion. This happened in 2012. A scientific case report has not yet been published, but Martin Sommer, who is investigating this case at the Göttingen University, reported about it in a lecture given at a meeting of German speech therapists. In the video below (in German language), the case is topic from 35.23 to 39.50. Beneath the video, you find an English translation. It was not quite easy to make, and I did not translate all the little repetitions, mistakes, and corrections common in spontaneous speech. Click on the video to watch from the start; click here to watch (on YouTube) from 35.23, where the part about the cerebellum begins.
The loop that processes external signals does not run via the basal ganglia, but via the cerebellum […]. Thus, there is an additional preparation of voluntary movements sent via the cerebellum, which also finely adjusts movement. And here, this is quite interesting – originally, we did not think that this has influence, but in the self-help scene, we found a case report: A 52-year-old woman who had stuttered since childhood […]. Only because of a meningioma – an acoustic neuroma, sorry – and this was operated, and the lady had bad luck. She got a cerebellar lesion left as a concupiscence of the neuroma surgery, that is, it had worked badly.
Now, it is so that she has no longer stuttered since then. We thought we should investigate this, and therefore […], after she had recovered from surgery, after rehab and so on, we had her again in MRI. You can see well here, compared with a speech task (there are umpteen results to this); here shown in Broca’s area BA44, how controls activate in speaking (stuttering controls were also included), and the patient before and after the operation, and we see: Due to the cerebellar lesion, the damage in the left part of the cerebellum, a significantly normalized blood flow in the Broca’s area. There are further data; we are just in a discussion about this. […] Investigating the fiber tracts, we find weakening in fiber tracts not only in the cerebellum (where one would expect it), but also in the corpus callosum and various other areas.
Exciting question: How to explain this? One could argue that the left cerebellum influences right premotor areas. If this input right drops out, then there is a disruption right-frontal, or less right premotor activity which, in turn, cannot influence as much as before the left speech center. That is, the cerebellar damage has a long-distance effect on the right premotor areas, which, in turn, has an effect on the left side. This is consistent with the finding that the corpus callosum showed weakened fiber tracts. Our interpretation, at the moment, is, therefore, that there is less right-prefrontal activity; interhemispheric inhibition is weaker, and speech becomes more fluent.
It is somewhat difficult; we are not yet at the end with the discussion. I cannot recommend inflicting yourself a cerebellar injury, since the patient, of course, walked away with a number of other impairments. It is really a hard case, but we can learn a lot from it about stuttering. It brings us to the point, that there seem to be not only supporting inputs, but obviously also inhibiting ones. And, possibly, the activity of the right prefrontal areas not advantageous, at least for speech fluency. Due to this input being no longer effective, she speaks more fluently. This is astonishing at first view, that there are inputs which impair speech flow, but you all know the scene in “The King’s Speech”: The acoustic input is masked, and suddenly, he is fluent. That is, the experiences with masked or delayed acoustic input show us that inhibiting inputs must exist.
So far my translation of Martin Sommer’s report. I think the results and Martin Sommer’s cautious interpretation do not contradict my theory. Poor processing of the sensory (mainly auditory) feedback of speech results in invalid error signals. An error signal may even be elicited when the person trues to initiate a word without the attention system being adjusted in a way that auditory feedback is properly processed.
The cerebellum is involved in error correction based on sensory feedback (Seidler et al., 2013); it is part of a network that generates an error signal in response to distorted auditory feedback during articulation (Zheng, Munhall, & Johnsrude, 2010). The cerebellum influences motor control by projections via the medial thalamus to the striatum, preferentially affecting the indirect pathway of the basal ganglia (Bostan & Strick, 2018). The indirect pathway has an overall inhibitory effect on the cortex (Chang & Guenther, 2019).
An further possibility could be that invalid error signals from the cerebellum, via the subthalamic nucleus (STN), influence the so-called hyperdirect pathway of the basal ganglia. The hyperdirect pathway is involved in a global response suppression mechanism (Frank, 2006). It generates stop signals inhibiting unwanted movements in conflict situations and perhaps also movements that are evaluated as erroneous by a monitoring entity in the brain. This response suppression mechanism has been assumed to immediately cause the interruption of speech flow in stuttering (Neef et al., 2016, 2017).
(I removed a paragraph because it was half-baked and, as I meanwhile have realized, not quite correct. I will address this issue in a further blog post.)
Some days ago, I put a paper with the above title online (see here). Previously I submitted it for publication in JSLHR and JFD; in both cases, it was rejected by the editors without regular anonymous peer review. By JSLHR, the paper was rejected without rationale; JFD told me that it “is very speculative, not supported by direct evidence.”
I think it is important to understand the purpose of the paper: to explain why a fact that has been regarded as evidence against feedback theories of stuttering is no evidence against such theories. To this end, it is sufficient to propose a valid explanation, and ‘valid’ means that this explanation is (a) coherent and consistent in itself and (b) consistent with the available data.
I do neither claim that my explanation is true, nor that it is the only possible one. However, as far as I know, it is the only explanation of this problem that has been proposed until now. Therefore, and as long as no better one is proposed, my explanation should be accepted as a candidate for the true explanation. Previously, there was no explanation for some facts that seemed to be paradoxical and enigmatic. Now, there is a plausible explanation that allows us to understand those facts such that they no longer appear paradoxical and enigmatic. I think that makes a difference.
In the table below, I have listed all arguments my explanation consists of and the corresponding empirical evidence or logical relation. All references in the table are also included in the paper. I think that’s a good way to review a theory paper. If you still find something that is speculative, i.e., neither empirically nor logically reasoned, please let me know.
Tablee: Structure of the arguments contained in the theory paper “Why does stuttering disappear when one’s own voiec is not heard? External and internal auditory feedback and their impact on stuttering.”
| Assumptions and assertions contained in the paper |
Empirical evidence, logical derivation, or reference |
| (1) Auditory feedback, i.e., feedback of one’s own speech in the auditory modality is necessary for the control of fluent speech. |
This is evident by the Lee effect: Delayed auditory feedback causes prolonged and disfluent speech in normally fluent individuals. (e.g., Lee, 1950)* |
| (2) Hypothesis: Developmental stuttering is caused by insufficient inte- gration of auditory feedback in the control of speech, or, in other words, by a dissocia- tion of speech production from speech perception. |
Suggested by weaker or de- layed responses to manipula- tions of auditory feedback, (e.g., Cai et al., 2012, 2014; Daliri et al., 2018; Loucks et al., 2012; Tourville et al., 2013) and by deactivation of secondary auditory cortex areas during speech, (e.g., Brown et al., 2005; Budde et al., 2014; Fox et al., 1996; Ingham et a., 2003; Stager et al., 2003; Toyomura et al., 2011) |
| (3) Auditory feedback can be provided in two ways: via an external and via an internal feedback loop. The external loop is what is usually called auditory feedback. |
Perceptual Loop Model (Levelt, 1989) which is part of the standard model of speech production. |
| (4) During silent mouthing and during speaking under com- plete auditory masking, one’s own voice is heard via the internal feedback loop just as during inner speech (silent reading, verbal thinking). |
This has been assumed and was presupposed in experi- ments by several experts (e.g., Brocklehurst & Corley, 2011; Lackner & Tuller, 1979; Oppenheim & Dell, 2010, 2008; Postma & Kolk, 1993) |
| (5) The internal feedback loop closely connects speech production with speech perception in the brain. |
e.g., Smith, Wilson, & Reisberg (1995), Smith, Reisberg, & Wilson (1992), Tian & Poeppel (2010, 2012) |
| (6) PWS are fluent during mouthing and under auditory masking not because they do not hear themselves speak. |
According to (2), they hear themselves speak internally via the internal feedback loop. |
| (7) PWS are fluent during mouth- ing and under complete audi- tory masking because of the close connection between speech production and speech perception when they use the internal feedback loop. |
This is only the inversion of the hypothesis (2): Sufficient inte- gration of auditory feedback in spech control saves from stuttering. |
| (8) The internal feedback loop (in humans generally) works only if external auditory feed- back is not provided, i.e., when one’s own voice is not heard externally. |
Direct evidence: Smith, Reisberg, & Wilson (1992) Indirect evidence: We would hear ourselves doubly because internal and external feedback take different time (Lackner & Tuller, 1979; Vigliocco & Hartsuiker, 2002). |
| (9) Detection of speech errors prior to articulation is no evidence that both feedback loops work concurrently. |
No monitoring takes place via the internal loop during overt speech(Huettig & Hartsuiker, 2010). Pre-articuiatory error- detection seems to be part of a general (not speech-specific) production-based conflict monitoring mechanism (Nozari, Dell, & Schwartz, 2011;Ganushchak & Schiller, 2008; Ries et al., 2011; Trewartha & Philips, 2013) |
| (10) The State Feedback Control model (Hickok, Houde, & Rong, 2011; Hickok, 2012) which implies pre-articulatory monitoring of internal auditory feedback during overt speech is incorrect. |
The model is inconsistent with the Lee effect: Delayed external auditory feedback would not affect speech fluency if external auditory feedback was irrelevant for speech control (as the model assumes). |
| (11) The internal feedback loop cannot compensate for a possible deficit in the external feedback loop in normal condi- tions, i.e., when one’s own voice is externally heard. |
This follows from (8): Both the feedback loops do not work concurrently, thus, one cannot compensate for a deficit in the other one. |
| (12) The fact that stuttering dis- appears when no external auditory feedback is available does not contradict the hypo- thesis that poor involvement of external auditory feedback in speech control causes stuttering. |
This follows from (3) and (8). |
*) Further evidence comes from audio-phonatory coupling, i.e., the fact that the duration of long syllables is controlled by the auditory feedback of the syllable start (Kalveram & Jäncke, 1989). I have not mentioned this in the paper because the Lee effect (which is more famous) is a manifestation of audio-phonatory coupling.