Comment: Frontal lobes, executive dysfunction, gait, and the fallacy of pseudo-transitivity.

COMMENT: FRONTAL LOBES, EXECUTIVE DYSFUNCTION, GAIT, AND THE FALLACY OF PSEUDO-TRANSITIVITY Massimo Filippi, Federica Agosta, Milan, Italy; Vladimir Kostić, Belgrade, Serbia; on behalf of all authors of “Pattern of brain tissue loss associated with freezing of gait in Parkinson disease”: 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.