Per Alm has posted a long comment on my last post on whether the basal ganglia is involved in PDS. Click on "Comments" at the bottom of my previous post, or go directly using this
link. Let me summarise what (I think) he said.
1) The basal ganglia could well NOT be dysfunctional and still be involved in PDS as part of a wider system often called the basal ganglia-thalamocortical circuit, which would show dysfunction.
2) The fluency-inducing effects provide the strongest argument in favour.
3) Brain anomaly studies by Foundas et al, Sommer et al, and Jaencke et al. are interesting but too preliminary for final judgment.
4) But their findings could fit: "the basal ganglia generates go-signals based on the input from widespread cortical regions, but the input from the sensorimotor cortex can be assumed to be especially important. If the signals from the sensorimotor cortex to the basal ganglia are disrupted, distorted, or weak, the basal ganglia will not be able to do their part of the job. The result will be distorted output from the basal ganglia to the SMA, which will make it difficult for SMA to generate the final go-signals for the speech segments."
5) "Stuttering with adult onset has been reported after lesions in various parts of this circuit, like the basal ganglia, the thalamus, and the SMA. However, the characteristics of the disorder can be expected to be somewhat different depending on location and nature of the dysfunction. "
6) There is a lack of CLEAR experimental evidence as experiments have not been specifically set up to study basal ganglia effects and brain imaging studies have weaknesses.
7) But, "In fact, the meta-analysis by Brown, Ingham et al. did find differences in basal ganglia activation between stuttering persons and controls. The controls showed a weak left globus pallidus activation, which was not shown by the stuttering persons."
8) Per goes and gives an possible explanation for 7). [please refer to his comments for the details]
9) Factors within the basal ganglia might well increase or decrease the risk for stuttering in the proposed model like the number of dopamine receptors.
I still have to digest all his comments. Especially on brain anatomy, where I need to learn more about. I am also a bit reluctant to go into too detailed discussion as I don't want to loose every reader of my blog. But please feel free to post detailed comments.
But here are some challenges to Per, which might be hard to overcome
1) Devise experiments that can unambiguously test aspects of the theory. For example, which experiments could be made that can FALSIFY the basal ganglia theory?
2) Show that the possible dysfunctions, that you state, of the basal ganglia circuit (which not only caters for aspects of speech that PDS affects) does not have any effects on other brain functions. This circuit seems to be rather distributed and entertaining many regions, and I find it hard to imagine a dysfunction not having more widespread effects. And I also find it hard to see why so many different factors result in basically the same symptoms.
3) Avoid arguments that are prone to logical fallacies. For example, I am a bit uncomfortable with Per referring to arguments like "different types of stuttering", "also other factors can influence", "the wider circuit", "several potential problems when studying stuttering by means of functional brain imaging". It might be true that many factors influence PDS or that there are different types, but then how can your theory be (or how can you make your theory) testable / falsifiable? It might be true that, as you state, there are several potential problems with brain imaging, but then how can you use brain imaging results to defend/falsify your theory?
Tom
Let me summarise what (I think) he said.
1) The basal ganglia could well NOT be dysfunctional and still be involved in PDS as part of a wider system often called the basal ganglia-thalamocortical circuit, which would show dysfunction.
2) The fluency-inducing effects provide the strongest argument in favour.
3) Brain anomaly studies by Foundas et al, Sommer et al, and Jaencke et al. are interesting but too preliminary for final judgment.
4) But their findings could fit: "the basal ganglia generates go-signals based on the input from widespread cortical regions, but the input from the sensorimotor cortex can be assumed to be especially important. If the signals from the sensorimotor cortex to the basal ganglia are disrupted, distorted, or weak, the basal ganglia will not be able to do their part of the job. The result will be distorted output from the basal ganglia to the SMA, which will make it difficult for SMA to generate the final go-signals for the speech segments."
5) "Stuttering with adult onset has been reported after lesions in various parts of this circuit, like the basal ganglia, the thalamus, and the SMA. However, the characteristics of the disorder can be expected to be somewhat different depending on location and nature of the dysfunction. "
6) There is a lack of CLEAR experimental evidence as experiments have not been specifically set up to study basal ganglia effects and brain imaging studies have weaknesses.
7) But, "In fact, the meta-analysis by Brown, Ingham et al. did find differences in basal ganglia activation between stuttering persons and controls. The controls showed a weak left globus pallidus activation, which was not shown by the stuttering persons."
8) Per goes and gives an possible explanation for 7). [please refer to his comments for the details]
9) Factors within the basal ganglia might well increase or decrease the risk for stuttering in the proposed model like the number of dopamine receptors.
I still have to digest all his comments. Especially on brain anatomy, where I need to learn more about. I am also a bit reluctant to go into too detailed discussion as I don't want to loose every reader of my blog. But please feel free to post detailed comments.
But here are some challenges to Per, which might be hard to overcome
1) Devise experiments that can unambiguously test aspects of the theory. For example, which experiments could be made that can FALSIFY the basal ganglia theory?
2) Show that the possible dysfunctions, that you state, of the basal ganglia circuit (which not only caters for aspects of speech that PDS affects) does not have any effects on other brain functions. This circuit seems to be rather distributed and entertaining many regions, and I find it hard to imagine a dysfunction not having more widespread effects. And I also find it hard to see why so many different factors result in basically the same symptoms.
3) Avoid arguments that are prone to logical fallacies. For example, I am a bit uncomfortable with Per referring to arguments like "different types of stuttering", "also other factors can influence", "the wider circuit", "several potential problems when studying stuttering by means of functional brain imaging". It might be true that many factors influence PDS or that there are different types, but then how can your theory be (or how can you make your theory) testable / falsifiable? It might be true that, as you state, there are several potential problems with brain imaging, but then how can you use brain imaging results to defend/falsify your theory?
Tom