Electroencephalography in eating disorders

Abstract

Clinical applications of electroencephalography (EEG) are used with different objectives, EEG being a noninvasive and painless procedure. In respect of eating disorders, in the 1950s a new line of study about the neurological bases of anorexia nervosa was started and has since been developed. The purpose of this review is to update the existing literature data on the main findings in respect of EEG in eating disorders by means of a search conducted in PubMed. Despite the fact that weight gain tends to normalize some brain dysfunctions assessed by means of EEG, the specific effect of gaining weight remains controversial. Different studies have reported that cortical dysfunctions can be found in patients with anorexia nervosa even after weight gain, whereas others have reported a normalization of EEG in respect of the initial reduced alpha/ increased beta power in those patients with refeeding. Findings of studies that have analyzed the possible relationship between eating disorders and depression, based on sleep EEG disturbances, do not support the idea of eating disorders as a variant of depression or affective disorders. Some EEG findings are very consistent with previous neuroimaging results on patients with anorexia nervosa, reporting neural disturbances in response to stimuli that are relevant to the pathology (eg, stimuli like food exposure, different emotional situations, or body images).

Anorexia: Anormal Phobia of Normal Weight

“…Our findings are different for other studies for EEG in anorectic girls which mainly confirmed the dominance of beta brain waves and hyperarousal due to anxiety [28][29][30][31].…”

Neuropsychology of eating disorders: 1995–2012

“…The neuropsychological functions in ED have been accompanied by studies based on neuroimaging and neurophysiology in order to correlate structural and functional brain changes with neuropsychological findings 83,84. Due to the enormous amount of variables (weight, duration of illness, medications, etc), it is difficult to demonstrate the correlation between brain changes and functional changes.…”

Modulation of food consumption and sleep–wake cycle in mice by the neutral CB1 antagonist ABD459

“…In addition, diurnal vigilance patterns are modulated by food availability, such that starvation coincides with heightened wakefulness and overall sleep reduction, increasing energy expenditure (Yamanaka et al , 2003; Koban et al , 2008), and obesity increases sleep (Laposky et al , 2006). However, this relationship is controversial and it remains unclear whether the nutritional stage determines global brain activity and sleep abnormalities, or vice versa (Jauregui-Lobera, 2012). Ideally, treatment to normalize (increase/reduce) food intake should mimic mental states of hunger/satiety, but not otherwise interfere with vigilance.…”