Phillip D Fletcher1, Camilla N Clark1, Jason D Warren2. 1. Dementia Research Centre, UCL Institute of Neurology, University College London, London, UK. 2. Dementia Research Centre, UCL Institute of Neurology, University College London, London, UK jason.warren@ucl.ac.uk.
Sir, The recent study by Perry draws attention to the important issue of abnormally enhanced reward-seeking by patients with frontotemporal dementia (FTD). This issue presents major challenges for the clinical management of these patients and provides a unique window on the neurobiology of brain network disintegration in a diverse group of neurodegenerative pathologies. While Perry and colleagues emphasize seeking of stimuli with clear biological reward potential (sweet foods, drugs of abuse and sex), abnormal reward-seeking in FTD is not restricted to such stimuli. Indeed, one of the most potent inducers of such behaviour in patients with FTD is a stimulus with no clear biological value: music. Abnormal, intense craving for music (musicophilia) is common in FTD and has a cerebral correlate centred on the mesial temporal lobe (Fletcher ).Both in functional imaging studies of the healthy brain and in neurodegenerative disease (Omar ; Salimpoor ; Clark ), music has been shown to engage striatal and basal forebrain regions overlapping or intimately connected with those demonstrated by Perry , in addition to a distributed network of cortical and limbic structures. Why music should behave as a biologically rewarding stimulus remains unresolved although clues may lie with its capacity to encode emotional mental states (Clark ): a cognitive process that is also often catastrophically disrupted in FTD.We therefore suggest music as a promising candidate model system for addressing some of the key questions for future work raised by the study of Perry and colleagues. In particular, as a universal and widely valued, yet abstract stimulus, music is ideally suited to probe interactions between reward, affective and cortical information processing circuitry (Omar ; Salimpoor ). This circuitry is inherently vulnerable in FTD. Moreover, a stimulus that can dissect apart the components of such large-scale brain networks may enable hedonic and physiological phenotyping of a range of other neurodegenerative disorders (including Parkinson’s disease) that also cause profound derangements of reward processing.
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