Abstract
IntroductionThe Behavioral Inhibition System (BIS) and the Behavioral Activation System (BAS) have been theorized as neural systems that regulate approach/withdrawal behaviors. Behavioral activation/inhibition balance may change in neurodegenerative disease based on underlying alterations in systems supporting motivation and approach/withdrawal behaviors, which may in turn be reflected in neuropsychiatric symptoms.MethodA total of 187 participants (31 patients diagnosed with behavioral variant of FTD [bvFTD], 13 semantic variant of primary progressive aphasia [svPPA], 14 right temporal variant FTD [rtFTD], 54 Alzheimer’s disease [AD], and 75 older healthy controls [NCs]) were included in this study. Changes in behavioral inhibition/activation were measured using the BIS/BAS scale. We analyzed the correlation between regional atrophy pattern and BIS/BAS score, using voxel-based morphometry (VBM).ResultsADs had significantly higher BIS scores than bvFTDs and NCs. bvFTDs activation-reward response (BAS-RR) was significantly lower than ADs and NCs, though their activation-drive (BAS-D) was significantly higher than in ADs. Both AD and rtFTD patients had abnormally low activation fun-seeking (BAS-FS) scores. BIS score correlated positively with right anterior cingulate and middle frontal gyrus volume, as well as volume in the right precentral gyrus and left insula/operculum.ConclusionsAD, bvFTD, and rtFTD patients show divergent patterns of change in approach/withdrawal reactivity. High BIS scores correlated with preservation of right-predominant structures involved in task control and self-protective avoidance of potentially negative reinforcers. Damage to these regions in bvFTD may create a punishment insensitivity that underlies patients’ lack of self-consciousness in social contexts.
Highlights
The Behavioral Inhibition System (BIS) and the Behavioral Activation System (BAS) have been theorized as neural systems that regulate approach/withdrawal behaviors
This study revealed that the BIS/BAS questionnaire was able to depict different patterns of motivational set among patients with behavioral variant frontotemporal dementia (bvFTD), right temporal variant of FTD (rtFTD), semantic variant of primary progressive aphasia (svPPA), and Alzheimer’s disease (AD), and suggests that the behavioral inhibition system-related behaviors may have correlates in the brain structure of
Apathy in bvFTD is known to have a distinct clinical profile characterized by loss of interest in personal affairs and responsibilities, social withdrawal and loss of awareness of personal hygiene. (Quaranta et al 2012), related with prominent atrophy in the ventral striatum (Eslinger et al 2012). This phenomenologic difference in apathetic behavior between AD and bvFTD may arise from differences in the BAS motivation regulation system; our results suggest that the apathy in bvFTD patients may be partly characterized as reduced function in the reward responsiveness aspect of behavioral activation system
Summary
The Behavioral Inhibition System (BIS) and the Behavioral Activation System (BAS) have been theorized as neural systems that regulate approach/withdrawal behaviors. High BIS scores correlated with preservation of right-predominant structures involved in task control and self-protective avoidance of potentially negative reinforcers Damage to these regions in bvFTD may create a punishment insensitivity that underlies patients’ lack of self-consciousness in social contexts. One dominant theory proposed by Gray (1987), suggests that two general neural systems coordinate adaptive behavior, the behavioral inhibition system (BIS), and the behavioral activation system (BAS) They suggest that the BIS is involved in processing signals related to punishment, novelty, and fear. The complementary BAS system is theorized to control approach behavior in response to reward cues and positive affect This theory is one of the most dominant biologically based personality theories, and has motivated investigations of the neurophysiological (Coan and Allen 2003) (Hawk and Kowmas 2003; Reuter et al 2006), and molecular genetic basis of behavioral inhibi-
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