PT  - JOURNAL ARTICLE
AU  - Audrey E De Paepe
AU  - Joanna Sierpowska
AU  - Clara García-Gorro
AU  - Saül Martinez-Horta
AU  - Jesus Perez-Perez
AU  - Jaime Kulisevsky
AU  - Nadia Rodriguez-Dechicha
AU  - Irene Vaquer
AU  - Susana Subira
AU  - Matilde Calopa
AU  - Esteban Muñoz
AU  - Pilar Santacruz
AU  - Jesus Ruiz-Idiago
AU  - Celia Mareca
AU  - Ruth de Diego-Balaguer
AU  - Estela Camara
TI  - F44 Disentangling apathy subtypes in huntington’s disease: a white matter biomarker of disease profile and progression
AID  - 10.1136/jnnp-2018-EHDN.148
DP  - 2018 Sep 01
TA  - Journal of Neurology, Neurosurgery & Psychiatry
PG  - A55--A56
VI  - 89
IP  - Suppl 1
4099  - http://jnnp.bmj.com/content/89/Suppl_1/A55.3.short
4100  - http://jnnp.bmj.com/content/89/Suppl_1/A55.3.full
SO  - J Neurol Neurosurg Psychiatry2018 Sep 01; 89
AB  - Along with motor and cognitive deterioration, neuropsychiatric symptoms form a common feature of Huntington’s disease. Of these, apathy has been shown to most highly correlate with disease progression, often emerging prior to clinical diagnosis. However, due to the multidimensional nature of apathy, its elusive etiology, and the lack of operative diagnostic criteria, treatment options are limited. The present study combine diffusion tensor imaging (DTI) with precise apathy scales to investigate the relationship between white matter microstructural change and apathy in premanifest (n=22) and early manifest Huntington’s disease (n=24) compared with controls (n=35).Global apathy was measured using both the short Problem Behavior Assessment and the Lille Apathy Rating Scale, short-form. Principle component analysis of the LARS-s produced three apathy subtypes: emotional, cognitive, and auto-activation deficit. We found that premanifest participant’s portrayed significantly higher auto-activation deficit apathy, with early manifest patients additionally showing significantly increased apathy in cognitive apathy as well as global apathy. Analysis by DTI showed a significant rightward disturbance in the uncinate fasciculus (UF), the frontostriatal tract (FST), and the dorsolateral prefrontal cortex to caudate nucleus tract (dlPFC-cn). Importantly, specific apathy subtypes were found to be associated with discrete tracts. Specifically, higher levels of subtype-specific apathy correlated with a lateralized decrease in structural connectivity in the dlPFC-cn and FST for the cognitive domain of apathy and in the UF for auto-activation deficit, predominantly on the right side. That apathy subtypes are associated with distinct white matter substrates supports the importance of an individualized approach to its diagnosis and treatment.