{'fraction_non_alphanumeric': 0.022289766970618033, 'fraction_numerical': 0.0060790273556231, 'mean_word_length': 5.72108843537415, '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}}
Metabolic impairment of brain metabolism in patients with Lewy body dementia

A reliable assessment of dementia is essential for a differentiated treatment. Recent studies have demonstrated a poor accuracy of clinical criteria for diagnosis of Lewy body dementia. Diffuse Lewy body disease (LBD) is the second most common cause of senile degenerative dementia and is characterized histologically by the occurrence of Lewy bodies in allocortical, neocortical and subcortical structures. Seven male patients (mean age 81 years) with clinically suspected diffuse LBD were investigated with 18F‐fluorodeoxyglucose (FDG)‐PET using a Siemens ECAT‐ART PET‐scanner. The 18F‐FDG‐PET showed a diffuse glucose hypometabolism in the entire cerebral cortex with relative sparing of the primary sensory‐motor cortex in all patients. This diffuse metabolic impairment in the entire cortex with relative sparing of central region seems to be a typical pattern for LBD, distinct from Alzheimer's disease.