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Baudino B. 1, D’agata F. 2, 3, Caroppo P. 2, Castellano G. 1, Cauda S. 1, Manfredi M. 1, Geda E. 3, Castelli L. 3, Mortara P. 2, Orsi L. 2, Cauda F. 3, Sacco K. 3, Ardito R. B. 3, Pinessi L. 2, Geminiani G. 3, Torta R. 4, Bisi G. 1
1 Department of Nuclear Medicine,AOU San Giovanni Battista, Turin, Italy;
2 Department of Neuroscience, AOU San Giovanni Battista, Turin, Italy;
3 Department of Psychology, University of Turin, Turin, Italy;
4 Department of Psychooncology , San Giovanni Battista Hospital, Turin, Italy
AIM: A growing number of neuropsychological studies reported that chemotherapy may impair brain functions, inducing persistent cognitive changes in a subset of cancer survivors. The aim of this paper was to investigate the neural basis of the chemotherapy induced neurobehavioral changes by means of metabolic imaging and neuropsychological testing.
METHODS:We studied the resting brain [18F]FDG-PET/CT images of 50 adult cancer patients with diagnosis of lymphoma: 18 patients were studied prior and 32 after to chemotherapy. All patients underwent to a neuropsychological examination assessing cognitive impairment (tests for shifting attention, verbal memory, phonemic fluency), depression, anxiety and distress.
RESULTS: Compared to no chemotherapy patients, the treated group showed significant bilateral lower rate of glucose metabolism in prefrontal cortices, cerebellum, medial cortices and limbic brain areas. The metabolism of these regions negatively correlated with number of cycles and positively with post-chemotherapy time. The treated group showed a poorer performance in many frontal functions, but similar level of depression, anxiety and distress.
CONCLUSIONS:Chemotherapy induced significant long-term changes in metabolism of multiple regions with a prevailing involvement of the prefrontal cortex. The observed cognitive dysfunctions could be explained by these changes. The recovery from chemotherapy is probably affected by treatment duration and by the time elapsed after its end. We speculated that the mechanism could be an accelerating ageing / oxidative stress that, in some patients at risk, could result in an early and persistent cognitive impairment.