Abstract
Objective:To determine if behavioral symptoms in patients with primary progressive aphasia (PPA) were associated with degeneration of a ventral frontotemporal network.Methods:We used diffusion tensor imaging tractography to quantify abnormalities of the uncinate fasciculus that connects the anterior temporal lobe and the ventrolateral frontal cortex. Two additional ventral tracts were studied: the inferior fronto-occipital fasciculus and the inferior longitudinal fasciculus. We also measured cortical thickness of anterior temporal and orbitofrontal regions interconnected by these tracts. Thirty-three patients with PPA and 26 healthy controls were recruited.Results:In keeping with the PPA diagnosis, behavioral symptoms were distinctly less prominent than the language deficits. Although all 3 tracts had structural pathology as determined by tractography, significant correlations with scores on the Frontal Behavioral Inventory were found only for the uncinate fasciculus. Cortical atrophy of the orbitofrontal and anterior temporal lobe cortex was also correlated with these scores.Conclusions:Our findings indicate that damage to a frontotemporal network mediated by the uncinate fasciculus may underlie the emergence of behavioral symptoms in patients with PPA.
Highlights
Our findings indicate that damage to a frontotemporal network mediated by the uncinate fasciculus may underlie the emergence of behavioral symptoms in patients with progressive aphasia (PPA)
Thirtythree patients with PPA and 26 healthy controls matched for age, sex, and handedness were enrolled through the Primary Progressive Aphasia Program at the Cognitive Neurology and Alzheimer’s Disease Centre, Northwestern University Feinberg School of Medicine
The PPA-S group were younger compared to the other variants and had higher prevalence of behavioral symptoms as reported in the Frontal Behavioral Inventory (FBI) total scores and FBI positive symptoms scores
Summary
We used diffusion tensor imaging tractography to quantify abnormalities of the uncinate fasciculus that connects the anterior temporal lobe and the ventrolateral frontal cortex. We measured cortical thickness of anterior temporal and orbitofrontal regions interconnected by these tracts. Thirtythree patients with PPA and 26 healthy controls matched for age, sex, and handedness were enrolled through the Primary Progressive Aphasia Program at the Cognitive Neurology and Alzheimer’s Disease Centre, Northwestern University Feinberg School of Medicine. The diagnosis of PPA was based on at least a 2-year history of progressive, isolated deterioration of speech or language functions. All patients were classified into 1 of the 5 PPA variants based on several recent diagnostic classification guidelines.. Patients with PPA who presented a severe (e.g., Boston Naming Test ,50%) single isolated language symptom (anomia or dyslexia) without fulfilling the criteria for the other variants were classified as unclassified variant.. All patients were classified into 1 of the 5 PPA variants based on several recent diagnostic classification guidelines. Patients with PPA who presented a severe (e.g., Boston Naming Test ,50%) single isolated language symptom (anomia or dyslexia) without fulfilling the criteria for the other variants were classified as unclassified variant. Patients with PPA with a combination of agrammatism and semantic impairments were classified as mixed PPA.
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