Brown, Ingham, Ingham, Laird and Fox have commented on Alm's work: "[He] proposed a model in which the core dysfunction of stuttering was suggested to be an “impaired ability of the basal ganglia to produce timing cues for the initiation” of speech motor activity (p. 325). Unfortunately, this proposal provided no predictions about whether particular nuclei/circuits of the basal ganglia would be over- or underactivated during stuttering. [Our] meta-analysis data did not provide strong indications either favoring or opposing this model." They then go over various activitation signals in various experiments, and discuss its possible relevance to a dysfunction in the basal ganglia. But conclude that "Although the basal ganglia may certainly be playing a contributing role in stuttering, this role is in need of elucidation in future studies."
Doesn't look promising for PDS as they don't agree?? ON THE CONTRARY, I think this is GREAT progress in PDS research. At least to me! :-) Their (constructive) discussion shows that PDS research has moved closer to the core of PDS and research issues can FINALLY be decided by inconsistency or experimental findings, and not on authority or intuition. They are able to ask concrete and by-experiment answerable questions. They are able to do this, because brain imaging is delivering them DIFFERENCES between PDS and control subjects. So you can actually construct a theory and decide whether it is correct or incorrect. I find this very exciting.
So what's my view on the basal ganglia theory? Is it right or not? I have to admit, that I haven't YET read word-by-word Alm's theory and their article. So I might say something factually wrong. But, what I find very striking is that both works by Alm and Brown & InghamS et al. seems complementary. Brown & InghamS might have a theory (using partially efference copies) to understand brain activation patterns, but they remain silent of why and what it is that causes "failure to properly initiate the motor plan". And that's exactly the end product of Alm's work: "Stuttering is suggested to be caused by a disturbance of the medial system, in most cases in the basal ganglia. The core dysfunction is proposed to be impaired "go-signals" from the medial system, supposed to trigger the next motor segment in speech". BUT I am not sure he can explain why there should be brain anomalies as found by Sommer et al. , Foundas et al. , and Jancke et al. . And experimentally it seems to be on weak grounds, as Brown & InghamS say, "[Our] meta-analysis data did not provide strong indications either favoring or opposing this model." So it seems strong conceptually but no clear experimental signal, which should have been found by now??
So my pinch-of-salt is: The basal ganglia is involved but there is no dysfunction. To understand this, we need to talk about postmen! :-) Imagine two postmen are responsible for delivering your mail. But you only see one of them delivering mail to you. So you blame the other one for not delivering mail. But he might be a hardworking postman, but unfortunately he is the postman that your dog doesn't like! So both postmen are "functional", but it's your dog who makes the selection. The same might happen for the basal ganglia. It might work perfectly well and projects time signals into speech areas perfectly well, but that the area is not integrating them well. And this might be the anomaly area found. Paradoxically, most components of the basal ganglia theory would survive neatly like explaining fluency inducing effects i.e. the different system projects to a properly working area that integrates the signals well. Interestingly, factors that impact the functioning of the basal ganglia would still play a role, because a strong performance by the basal ganglia could well give PDS people enough timing signal to speak fluently, but a bad day or stress or emotions makes it worse. This would actually explain why the basal ganglia has not been singled out by experiments.
I am just making guesses, so please comment if you disagree. But I like this way of explaining things, and my brain has not YET found anything that rules it out.
Doesn't look promising for PDS as they don't agree?? ON THE CONTRARY, I think this is GREAT progress in PDS research. At least to me! :-) Their (constructive) discussion shows that PDS research has moved closer to the core of PDS and research issues can FINALLY be decided by inconsistency or experimental findings, and not on authority or intuition. They are able to ask concrete and by-experiment answerable questions. They are able to do this, because brain imaging is delivering them DIFFERENCES between PDS and control subjects. So you can actually construct a theory and decide whether it is correct or incorrect. I find this very exciting.
So what's my view on the basal ganglia theory? Is it right or not? I have to admit, that I haven't YET read word-by-word Alm's theory and their article. So I might say something factually wrong. But, what I find very striking is that both works by Alm and Brown & InghamS et al. seems complementary. Brown & InghamS might have a theory (using partially efference copies) to understand brain activation patterns, but they remain silent of why and what it is that causes "failure to properly initiate the motor plan". And that's exactly the end product of Alm's work: "Stuttering is suggested to be caused by a disturbance of the medial system, in most cases in the basal ganglia. The core dysfunction is proposed to be impaired "go-signals" from the medial system, supposed to trigger the next motor segment in speech". BUT I am not sure he can explain why there should be brain anomalies as found by Sommer et al. , Foundas et al. , and Jancke et al. . And experimentally it seems to be on weak grounds, as Brown & InghamS say, "[Our] meta-analysis data did not provide strong indications either favoring or opposing this model." So it seems strong conceptually but no clear experimental signal, which should have been found by now??
So my pinch-of-salt is: The basal ganglia is involved but there is no dysfunction. To understand this, we need to talk about postmen! :-) Imagine two postmen are responsible for delivering your mail. But you only see one of them delivering mail to you. So you blame the other one for not delivering mail. But he might be a hardworking postman, but unfortunately he is the postman that your dog doesn't like! So both postmen are "functional", but it's your dog who makes the selection. The same might happen for the basal ganglia. It might work perfectly well and projects time signals into speech areas perfectly well, but that the area is not integrating them well. And this might be the anomaly area found. Paradoxically, most components of the basal ganglia theory would survive neatly like explaining fluency inducing effects i.e. the different system projects to a properly working area that integrates the signals well. Interestingly, factors that impact the functioning of the basal ganglia would still play a role, because a strong performance by the basal ganglia could well give PDS people enough timing signal to speak fluently, but a bad day or stress or emotions makes it worse. This would actually explain why the basal ganglia has not been singled out by experiments.
I am just making guesses, so please comment if you disagree. But I like this way of explaining things, and my brain has not YET found anything that rules it out.
Tom