{'fraction_non_alphanumeric': 0.023423423423423424, 'fraction_numerical': 0.0, 'mean_word_length': 6.261437908496732, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Neural Basis of Apathy

This chapter introduces structural neuroimaging methods and presents results from brain imaging studies of the clinical apathy syndrome in neurodegenerative diseases such as Alzheimer’s disease, mild cognitive impairment, Parkinson’s disease, Huntington’s disease, and stroke, and also in schizophrenia, today considered a neurodevelopmental disease. The main method used has been magnetic resonance imaging, which also holds many innovative possibilities for future development. Scientific studies so far have pointed to structural differences in frontal, striatal, anterior cingulate, and parietal brain regions, and of white matter microstructure and connectivity changes as being involved in the apathy syndrome. No single circuit connected to apathy has so far been identified. Brain structure and function, studied at the systems network level, and integrative multimodal imaging approaches, which combine different high-resolution magnetic resonance imaging, magnetic resonance diffusion, and positron emission tomography techniques, can be helpful in resolving future questions.