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Structural brain changes associated with starvation and clinical measurements were explored in four females with anorexia nervosa with different clinical course, at baseline and 1-year follow-up, after receiving intensive inpatient treatment at a specialized eating disorder unit. Global volume alterations were associated with weight changes. Regional volume alterations were also associated with weight changes, with the largest changes occurring in the nucleus accumbens, amygdala, pallidum, and putamen. Largest changes in cortical thickness occurred in the frontal and temporal lobes. The results are preliminary; however, they show that fluctuations in weight are associated with brain volume alterations, especially gray matter. We suggest that these parts of the brain are vulnerable to starvation and malnutrition, and could be a part of the pathophysiology of AN.

Background Anorexia nervosa (AN) is a severe mental illness, with an unknown etiology. Magnetic resonance imaging studies show reduced brain volumes and cortical thickness in patients compared to healthy controls. However, findings are inconsistent, especially concerning the anatomical location and extent of the differences. The purpose of this study was to estimate and compare brain volumes and regional cortical thickness in young females with AN and healthy controls. Methods Magnetic resonance imaging data was acquired from young females with anorexia nervosa (n = 23) and healthy controls (n = 28). Two different scanner sites were used. BMI varied from 13.5 to 20.7 within the patient group, and 11 patients had a BMI > 17.5. FreeSurfer was used to estimate brain volumes and regional cortical thickness. Results There were no differences between groups in total cerebral cortex volume, white matter volume, or lateral ventricle volume. There were also no volume differences in subcortical grey matter structures. However the results showed reduced cortical thickness bilaterally in the superior parietal gyrus, and in the right inferior parietal and superior frontal gyri. Conclusions The functional significance of the findings is undetermined as the majority of the included patients was already partially weight-restored. We discuss whether these regions could be related to predisposing factors of the illness, or whether they are regions that are more vulnerable to starvation, malnutrition or associated processes in AN.

Background Neuroimaging allows for the identification of brain abnormalities and alterations that are associated with anorexia nervosa (AN). We performed a scoping review to map out the extent and nature of recent research activity on functional magnetic resonance imaging (fMRI) in individuals diagnosed with, or recovered from, AN (AN-REC). Main text A literature search of PubMed, Psychinfo and Embase was conducted using the search terms “anorexia nervosa” AND “functional magnetic resonance imaging.” We included fMRI studies that involved a comparison between individuals with AN or AN-REC and healthy controls published in English language between 2010 and 2015. A total of 49 papers were included, regardless of the experimental stimuli or paradigm. Conclusions Findings varied considerably across studies, reflecting methodological differences in study design, such as sample differences and experimental paradigms. Collectively, studies published during the past five years suggest altered activation in regions related to the fronto-striato and the limbic circuits, which are theorized to have an important role in the pathophysiology of AN.

Anorexia nervosa is a serious illness with major physical and psychological morbidity. It has largely been understood in terms of cultural and environmental explanations. However these are insufficient to explain the diverse clinical features of the illness, nor its rarity given the universality of sociocultural factors. Over the last 20 years, there has been a steady accumulation of neurobiological evidence requiring a re-formulation of current causal models. We now offer a new empirically-derived hypothesis implicating underlying rate-limiting dysfunction of insula cortex as a crucial risk factor for the development of anorexia nervosa. Supporting evidence for this hypothesis is drawn from anatomical and clinical research of insula cortex damage in humans and neuroscientific studies of relevant clinical features including taste, pain perception and reward processing. This hypothesis, if sustainable, would be the first fully to explain the disorder and predicts promising novel treatment possibilities including Cognitive Remediation and Motivation Enhancement Therapies. The knowledge that the challenging behaviours, so characteristic of AN, are the result of underlying cerebral dysfunction, rather than being purely volitional, could help to reduce the stigma patients experience and improve the therapeutic alliance in this poorly understood and difficult to treat disorder.