Objective: To investigate apathy-associated metabolic changes in Parkinson’s disease.

Background: Apathy is a behavioral syndrome manifested as a decrease in goal-directed behaviors. It has been associated with overlapping depression and cognitive impairment. It has been reported that patients with apathy have lower metabolic activity in frontal, temporal and cerebellar areas, involved in reward, emotion and cognition¹.

Method: We prospectively examined a series of patients from a longitudinal study for the study of cognitive and behavioral impairment in PD. They underwent neurological, cognitive, psychiatric examination and 18F-FDG-PET. They were divided into apathetic and non-apathetic as per Starkstein apathy scale (cutoff 14). Multiple regression analysis was performed adjusting results for MOCA, age, disease duration and UPDRS III; followed by Akaike information criterion to determine the best fitting model to explain 18F-FDG-PET quantification differences.

Results: Apathy was detected in half of the cohort (14/28). The apathetic group resulted to be older (68 vs 75yo, p0.01) and differences in MOCA and Beck scales were not statistically significant.  Disease duration was longer in apathetic patients although it was not statistically significant (58 vs 88 months, p0.07). UPDRS III, LED and agonist intake differences were not statistically significant.

Several areas resulted to be hypometabolic in the apathetic group compared to the non-apathetic. However, several of those areas were also seen as hypometabolic in relation to age, disease duration and cognitive status (depression did not seem to affect FDG values in our population). The areas in which hypometabolism was proved to be explained by apathy were the bilateral rolandic operculum (p0.03 left/0.01 right), bilateral supplementary motor area (p0.02/0.02), bilateral superior frontal gyri (p0.03/0.01), right middle frontal gyri (p0.03), left inferior frontal gyri (p0.03), left insula (p0.03), and left cerebellum (p0.03). Hypometabolism in left middle frontal gyri, bilateral rectus gyri, right cuneate gyrus, bilateral fusiform gyrus, left supramarginal,  left angular gyrus, left precuneus and bilateral temporal lobes was explained by both apathy and cognition.

Conclusion: Our findings support previous reports^2,3 findings. Interestingly, we were able to observe here that it could also be related to hypofunction of the rolandic operculum and cerebellum, supporting their influence on apathy.

References: 1. Starkstein SE, Preziosi TJ, Bolduc PL, Robinson RG. Depression in Parkinson’s disease. J Nerv Ment Dis. 1990 Jan;178(1):27-31
2. Robert G, Le Jeune F, Lozachmeur C, Drapier S, Dondaine T, Péron J, Travers D, Sauleau P, Millet B, Vérin M, Drapier D. Apathy in patients with Parkinson disease without dementia or depression: a PET study. Neurology. 2012 Sep 11;79(11):1155-60.
3. Pagonabarraga J, Kulisevsky J, Strafella AP, Krack P. Apathy in Parkinson’s disease: clinical features, neural substrates, diagnosis, and treatment. Lancet Neurol. 2015 May;14(5):518-31.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/metabolic-imaging-correlates-of-apathy-in-parkinsons-disease/