Abstract
PurposeThe aim of the present study was to investigate the executive function of inhibitory control in anorexia nervosa (AN), which is considered as an underlying pathophysiology of restricting eating.MethodsIn this work, we examined the function of response inhibition in 27 unmedicated AN patients and 30 healthy controls (HC) using stop-signal tasks with different demand loads. Two event-related potentials (ERP) during the stop-signal tasks, N2 and P300, were compared between the AN and HC groups.ResultsWe found attenuated P300 amplitudes and delayed N2 latencies in AN patients across all three demand loads compared to HCs. We also found significant interaction between group and level of demand load. N2 latencies were prolonged when the inhibitory demand was lower in the AN group, whereas no differences in N2 latencies were found across different demand loads in HCs.ConclusionsTaken together, altered P300 amplitudes and N2 latencies may be associated with impaired response inhibition in AN patients. In particular, alterations of fronto-central N2 activations were demand-related, which might contribute to an aberrant inhibitory control process in AN.Level of evidenceLevel II, controlled trial without randomization.
Highlights
Anorexia nervosa (AN) is an eating disorder characterized by restrained eating, being significantly underweight, disturbance in self-perception of weight/shape, and intense fear of gaining weight or becoming fat (American Psychiatric Association, DSM-V, 2013) [1, 2]
Behavioural accuracy and reaction time were measured in 25 AN subjects and 30 healthy controls (HC)
Post hoc t tests with Bonferroni correction showed that the accuracy for stop-signal delay (SSD) of 100 ms was the highest (94.9%), followed by the 250 ms (83.1%) and the 300 ms (74.3%)
Summary
Anorexia nervosa (AN) is an eating disorder characterized by restrained eating, being significantly underweight, disturbance in self-perception of weight/shape, and intense fear of gaining weight or becoming fat (American Psychiatric Association, DSM-V, 2013) [1, 2]. The disease commonly begins during adolescence in young females, its lifetime prevalence is 3.6% [3] and it has a high mortality rate of 20% [4]. AN in young men is common; the lifetime prevalence is 0.24%, higher than expected, which has not been sufficiently noted [5]. Though the aetiology of AN remains unknown [1, 6, 7], deficits in executive function (i.e., inhibitory control in particular) are considered to play a key role in the pathophysiology of the disease [8,9,10,11,12,13]. Neuropsychological studies have reported lower rates of motor impulsivity [9] and greater subjective self-control in AN patients compared with healthy controls [10].
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