BackgroundRelapse after treatment for anorexia nervosa (AN) is a significant clinical problem. Given the level of chronicity, morbidity, and mortality experienced by this population, it is imperative to understand the driving forces behind apparently high relapse rates. However, there is a lack of consensus in the field on an operational definition of relapse, which hinders precise and reliable estimates of the severity of this issue. The primary goal of this paper was to review prior studies of AN addressing definitions of relapse, as well as relapse rates.MethodsData sources included PubMed and PsychINFO through March 19th, 2016. A systematic review was performed following the PRISMA guidelines. A total of (N = 27) peer-reviewed English language studies addressing relapse, remission, and recovery in AN were included.ResultsDefinitions of relapse in AN as well as definitions of remission or recovery, on which relapse is predicated, varied substantially in the literature. Reported relapse rates ranged between 9 and 52%, and tended to increase with increasing duration of follow-up. There was consensus that risk for relapse in persons with AN is especially high within the first year following treatment.DiscussionStandardized definitions of relapse, as well as remission and recovery, are needed in AN to accelerate clinical and research progress. This should improve the ability of future longitudinal studies to identify clinical, demographic, and biological characteristics in AN that predict relapse versus resilience, and to comparatively evaluate relapse prevention strategies. We propose standardized criteria for relapse, remission, and recovery, for further consideration.

Recent studies show that higher-order appetitive neural circuitry may contribute to restricted eating in anorexia nervosa (AN) and overeating in bulimia nervosa (BN). The purpose of this study was to determine whether sensitization effects might underlie pathologic eating behavior when a taste stimulus is administered repeatedly. Recovered AN (RAN, n=14) and BN (RBN, n=15) subjects were studied in order to avoid the confounding effects of altered nutritional state. Functional magnetic resonance imaging (fMRI) measured higher-order brain response to repeated tastes of sucrose (caloric) and sucralose (non-caloric). To test sensitization, the neuronal response to the first and second administration was compared. RAN patients demonstrated a decreased sensitization to sucrose in contrast to RBN patients who displayed the opposite pattern, increased sensitization to sucrose. However, the latter was not as pronounced as in healthy control women (n=13). While both eating disorder subgroups showed increased sensitization to sucralose, the healthy controls revealed decreased sensitization. These findings could reflect on a neuronal level the high caloric intake of RBN during binges and the low energy intake for RAN. RAN seem to distinguish between high energy and low energy sweet stimuli while RBN do not.

This chapter covers studies addressing neurobiologic factors that may contribute to body dysmorphic disorder (BDD). There are indications that neurobiologic abnormalities are associated with symptoms in BDD. This includes evidence that the susceptibility for BDD may be partly heritable and that there may be shared genetic factors among the obsessive-compulsive and related disorders (of which BDD is a member) as a group. In addition, studies of brain circuitry in BDD implicate white matter and structural connectivity abnormalities as playing possible roles in the pathophysiology of BDD. Furthermore, studies of visual processing suggest that disturbances in visual perception and visuospatial information processing, characterized by heightened attention to detail and impairment in holistic and global assessment, are also contributory.

This chapter covers the latest studies addressing neurobiological and genetic/heritable factors that may contribute to body dysmorphic disorder (BDD). BDD affects approximately 2% of the population and involves perceived defects of appearance along with obsessive preoccupation and repetitive, compulsive-like behaviors. Studies of visual processing suggest that disturbances in visual perception and visuospatial information processing, characterized by heightened attention to detail and impairment in holistic and global assessment, contribute to the condition. Also reviewed are studies of brain circuitry in BDD, which implicate white matter and structural connectivity abnormalities as playing possible roles in the pathophysiology of BDD. Finally, this chapter reviews the evidence that the susceptibility for BDD may be partly heritable and that there may be shared genetic factors among the obsessive-compulsive and related disorders (of which BDD is a member) as a group.

This chapter addresses the comorbid presentation of body dysmorphic disorder (BDD) and disordered eating. BDD affects approximately 2% of the population and involves perceived defects of appearance along with obsessive preoccupation and repetitive, compulsive-like behaviors. The prevalence of comorbid BDD and eating disorders is high: Approximately one–third of those with BDD will have a comorbid eating disorder, and almost half of those with an eating disorder will have comorbid BDD. There are complicating diagnostic and treatment factors that arise when an individual experiences both. A core feature of these disorders is body image concern, which may be explained by both shared and unique aberrancies in visual and visuospatial processing that have neurobiological underpinnings. Understanding shared and unique pathophysiology may help inform and guide treatment, as well as open up lines of future research into their etiology.