Abstract
Whole-brain voxel-based morphometry (VBM) studies of progressive supranuclear palsy (PSP) have demonstrated heterogeneous findings regarding gray matter (GM) abnormalities. Here, we used Seed-based d Mapping, a coordinate-based meta-analytic approach to identify consistent regions of GM anomalies across studies of PSP. Totally, 18 original VBM studies, comprising 284 patients with PSP and 367 healthy controls were included. As compared to healthy controls, patients with PSP demonstrated significant GM reductions in both cortical and subcortical regions, including the frontal motor cortices, medial (including anterior cingulate cortex) and lateral frontal cortices, insula, superior temporal gyrus, striatum (putamen and caudate nucleus), thalamus, midbrain, and anterior cerebellum. Our study further suggests that many confounding factors, such as age, male ratio, motor severity, cognitive impairment severity, and illness duration of PSP patients, and scanner field-strength, could contribute to the heterogeneity of GM alterations in PSP across studies. Our comprehensive meta-analysis demonstrates a specific neuroanatomical pattern of GM atrophy in PSP with the involvement of the cortical-subcortical circuitries that mediate vertical supranuclear gaze palsy, motor disabilities (postural instability with falls and parkinsonism), and cognitive-behavioral disturbances. Confounding factors merit attention in future studies.
Highlights
Progressive supranuclear palsy (PSP) is a clinical syndrome characterized mainly by early postural instability with falls, vertical supranuclear gaze palsy, parkinsonism, and cognitive-behavioral disturbances that lead to significant disabilities with a mean survival of 6.38 years [1,2,3,4,5]
18 original studies reporting gray matter (GM) differences between 284 patients with progressive supranuclear palsy (PSP) and 367 healthy controls were included in this meta-analysis [14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31]
Three of the 17 studies explicitly indicated that the samples included two subtypes of PSP, PSP-RS and PSP-parkinsonism variant (PSP-P) [18, 27, 29]
Summary
Progressive supranuclear palsy (PSP) is a clinical syndrome characterized mainly by early postural instability with falls, vertical supranuclear gaze palsy, parkinsonism, and cognitive-behavioral disturbances that lead to significant disabilities with a mean survival of 6.38 years [1,2,3,4,5]. PSP is a rapidly progressive neurodegenerative disorder, pathologically confirmed by the accumulation of tau protein and neuropil threads in cortical and subcortical structures [3, 6]. Its differential diagnosis from other parkinsonian disorders is critical but presents challenges in clinical practice, especially in the early disease stages [3, 8]. Despite impressive advances in understanding its pathophysiology, the reliably validated www.impactjournals.com/oncotarget biomarkers for the ante-mortem diagnosis and the prognosis of PSP have not yet been established [3, 4, 9, 10]
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