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Published on: February 1, 2016
by Kay Jackson for MedPage Today:
While strong sucrose preference is a marker of frontotemporal dementia syndromes, hyperphagia is present in all patients with behavioral variant frontotemporal dementia and semantic dementia is characterized by rigid eating behavior, a study showed.
What’s more, dissociated neural networks appear to control this behavior, said researchers. An increased caloric intake correlated with atrophy in the cingulate cortices, thalami, and cerebellum was observed on MRI in patients with behavioral variant frontotemporal dementia, and also involved the orbitofrontal cortices and nucleus accumbens in patients with semantic dementia, according to Rebekah M. Ahmed, MBBS, of Neuroscience Research Australia, Randwick, New South Wales, and colleagues. Marked hyperphagia was present exclusively in all patients with behavioral variant frontotemporal dementia, making it a valuable diagnostic marker, they reported in JAMA Neurology.
“An understanding of the networks that control this eating behavior offers opportunities for targeted treatments that can modify eating behavior, metabolic abnormalities, and disease progression and provides insights into structures that control eating behavior in healthy individuals,” wrote the investigators.
The study, conducted from Nov. 1, 2013, through May 31, 2015, recruited a total of 49 patients with dementia (19 with behavioral variant frontotemporal dementia, 15 with semantic dementia, and 15 with Alzheimer disease [AD]) and compared their eating behaviors with 25 healthy controls. The mean age of patients in all four groups ranged from 62 to 66 years. Groups were matched for BMI and data analysis took place from June 1 to Aug. 31, 2015.
The behavioral variant frontotemporal dementia group was more functionally impaired relative to the groups of patients with AD (FRS; P=0.009) or semantic dementia (P<0 .001), said the investigators. Based on caregiver surveys, the behavioral variant frontotemporal dementia group also had more severe eating disturbance (P<0.005 for all).
All study participants were given an ad libitum breakfast test meal and their total caloric intake and food preferences measured. The Appetite and Eating Habits Questionnaire (APEHQ) and the Cambridge Behavioral Inventory (CBI) were used to measure changes in eating behavior.
Participants were asked to rate how much they liked three different desserts with sucrose contents of 26%, 39% and 60%. Voxel-based morphometry analysis of whole-brain 3-T high-resolution brain magnetic resonance imaging was used to measure gray matter density changes in the different groups and determine the relationship to eating behaviors, said the investigators.
The study showed that patients with behavioral variant frontotemporal dementia had the highest mean total caloric intake of 1,344 calories while patients with Alzheimer disease had a mean total of 710 calories and patients with semantic dementia had a mean total of 573 calories. By comparison, control group participants had a mean total caloric intake of 603 calories (P<0.001). Patients with behavioral variant frontotemporal dementia and semantic dementia had the strongest sucrose preference of the four groups.
With all patient groups combined, total caloric intake on the ad libitum breakfast test meal was associated with total scores on caregiver ratings of eating changes on the APEHQ (rs = 0.496, P<0.001), CBI eating (rs = 0.502, P<0.001), overall ratings of behavioral changes (CBI total: rs = 0.598, P<0.001), and level of functional impairment (FRS: rs = −0.599, P<0.001).
Until now, assessment of eating changes in behavioral variant frontotemporal dementia has been carried out using caregiver questionnaires, they noted. These survey-based studies have suggested that eating changes in behavioral variant frontotemporal dementia are associated with a breakdown in reward pathways caused by atrophy of right-sided anterior and subcortical structures. “We did not find involvement of the orbitofrontal cortex in the behavioral variant frontotemporal dementia group,” said the investigators, “suggesting that eating behavior in this group is not simply related to a faitlure of inhibitory control.”
Although the semantic dementia group did not exhibit increased total caloric intake, a number of the patients had rigid eating behavior, refusing food altogether or eating only small amounts. These behaviours may be related to neurological changes that result in a loss of knowledge about food, noted Ahmed and colleagues.
MRI studies showed that patients with behavioral variant frontotemporal dementia and semantic dementia who indicated a preference for the sweetest dessert was correlated with volume loss in bilateral orbitofrontal cortices and insula-striatal structures, including the nucleus accumbens, amygdala extending into the temporal occipital cortex, lingual gyrus, and cerebellum, said the researchers.
Results from this study provide the most rigorous assessment to date of the concept that behavioral abnormalities in frontotemporal dementia result from a network of brain regions, noted Jennifer L. Whitwell, PhD, of the Mayo Clinic, Rochester, Minn., in an accompanying editorial. Still, she emphasized, these results will need to be validated, possibly using task-free functional MRI to determine functional connections and how network disruptions are linked to behavior.
“This study should be applauded for performing such detailed and prospective assessments of eating behaviors in frontotemporal dementia,” wrote Whitwell. Not only does this study provide quantitative data ideal for use in neuroimaging correlations, she pointed out, but it is the first study to assess MRI correlates of eating behavior separately within patients with behavioral variant frontotemporal dementia and semantic dementia.
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