Comment: Frontal lobes, executive dysfunction, gait, and the fallacy of pseudo-transitivityAuthor Response:
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WriteClick contributors this week address the issues of certainty and error in scientific publications. In reference to “Pattern of brain tissue loss associated with freezing of gait in PD” by Filippi et al., Dr. Montgomery reiterates the importance of setting forth alternatives when discussing a hypothesis in order to avoid inadvertently providing a false sense of validity. Dr. Walker calls attention to a genetic sequencing error made in a report published by Saiki et al. in 2003 which significantly alters the emphasis of the original publication. The authors acknowledge the error in a letter that will be linked to their original article. Megan Alcauskas, MD, and Robert C. Griggs, MD
We thank Dr. Montgomery1 for his stimulating comments on our article. Our study showed that a specific pattern of brain network damage involving frontal and parietal cortices occurs in patients with Parkinson disease (PD) and freezing of gait (FOG).2 Although voxel-based morphometry may not be sensitive enough to depict damage to subcortical and brainstem nuclei, this finding suggests that impairment of the frontoparietal network may play a role in the development of FOG in PD. Furthermore, we suggested that the occurrence of FOG in patients with PD may be related to cognitive frontal dysfunction. This is based not only on the commonality of frontal lobe pathology between the 2 clinical manifestations but also on the evidence that patients with PD with FOG have frontal executive deficits compared with patients with PD without FOG. In addition, FOG severity correlated with the degree of frontal executive dysfunction. Gait is a complex movement with multiple contributions from many brain regions. Although the mechanisms responsible for FOG are unclear,3 our findings suggest a role for frontoparietal damage and executive dysfunction, yet still unobserved pathologies may be directly responsible for FOG.
Author Response:
The response of Filippi et al. to my Comment accompanying their article2 reiterates the original arguments. Their inferences are appropriate as a hypothesis and may be proven correct, as I previously stated.1 However, their hypothesis has no greater epistemic standing than any number of alternatives which they fail to consider. Failure to genuinely discuss alternatives may further a false sense of validity which is not offset by use of qualifiers such as “may” or “suggests” in their own inferences. They fail to differentiate correlation from cause and effect. Their reasoning is insufficient validation as it relies on the logical fallacy of pseudotransitivity which is of the form: if a implies c and b implies c, then a implies b. This fallacy is repeated throughout their attempted causal explanation from executive dysfunction (a) implying attention or perceptual problems (c) and PD (b) being associated with attention or perceptual problems (c). The fallacy is very seductive because it is such a powerful—and some would argue—necessary route to hypothesis generation but it is not a method of validation. Great confusions are created when the fallacy is taken as validation, as they seemed to have done.
Footnotes
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Author disclosures are available upon request (journal{at}neurology.org).
References
- 1.↵
- Montgomery EB Jr.
- 2.↵
- Kostić VS,
- Agosta F,
- Pievani M,
- et al
- 3.↵
- Nutt JG,
- Bloem BR,
- Giladi N,
- Hallett M,
- Horak FB,
- Nieuwboer A
- Copyright © 2012 by AAN Enterprises, Inc.
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