Introductory Chapter: Neuropsychology of Eating Disorders

1. Introduction

Since the 1990s, the body of knowledge in the field of neuropsychology applied to eating disorder (ED) has been growing steadily, making it possible to operationalise and quantify cognitive processes involved in them and allowing new ways of prevention and treatment [1].

In order to frame the role of neuropsychology in the assessment and treatment of EDs, it is necessary to mention the endophenotypes. Currently, the diagnosis of EDs is made on the basis of the clinically observable phenotype. Behaviours, cognitions and emotions are altered around a pathological core: In anorexia nervosa, it is underweight and overcontrol in the restrictive subtype; in bulimia nervosa and other ED, it is impulsivity or loss of control.

Diagnostic categories help in assessment, treatment and prognosis. However, it is also a fact that there is a wide intra-categorical diagnostic heterogeneity, comorbidity and symptomatic fluctuation between disorders.

Neuropsychology is bringing to light endophenotypes of different groups of disorders, making the DSM classification more dimensional. Endophenotypes bring quantitative measures of disorders to the exclusive use of scales and questionnaires. They also serve as a measure to evaluate the efficacy of new treatments. Another important contribution would be the explanation of comorbidity [2].

In spite of the findings described below, neuropsychology has not yet been able to establish a firm explanatory model for ED. Neuropsychological traits could be new targets for treatment of ED with a dimensional and transdiagnostic approach. The various studies involving neuroimaging measures reveal changes in both large brain areas (frontal and parietal cortex) and specific areas (caudate nucleus, thalamus and inferolateral frontal cortex) in patients with an acute-phase of ED, comparing with healthy people and patients suffering from other psychological disturbances, as well as with anorexia nervosa patients in recovery or remission phase. Among the actual neuropsychological findings, studies to date have not found a very different neuropsychological profile between AN and BN [2, 3].

Despite these limitations, studies have yielded very consistent findings on three main types of neurocognitive impairments: weak central coherence, difficulties in set-shifting tasks (a component of executive function) and impulsivity. In these, the frontal lobe is generally involved.

According to the literature, impairments in central coherence and set-shifting tasks in AN and BN are postulated to be potential endophenotypes or specific traits because they are not related to nutritional status; they occur, to some degree, in relatives without the disorder, and they persist after treatment (e.g. in the disorder and persist after treatment). In other words, they would be risk or predisposing factors rather than the consequence of the eating disorder itself.

On the other hand, impulsivity and compulsivity could also be endophenotypes that shared between EDs, obsessive-compulsive disorder (OCD), substance abuse, mania, attention deficit hyperactivity disorder (ADHD), schizophrenia, autism spectrum and personality disorders [4].

In a recent article, a similar performance has been found in the ED group with respect to the control group, by means of neuropsychological tests. It can be explained by a detail-based information processing style without a change of judgement in the set-shifting tasks. In addition, depressive symptoms seem to be a vulnerability factor correlating with the development of the disorder. Authors state that a neuropsychological intervention of ED would provide new treatment techniques in a complementary way to those already applied. It would favour a more dimensional approach by bringing to light new therapeutic targets and it would also treat the comorbidity of these disorders by acting on the common factors. Consequently, new lines of research in applied neuropsychology are suggested.

In other studies, a relationship has been found between cognitive flexibility and depressive emotional state regardless of ED pathology, which reinforces the idea that this performance is more related to depression than to the characteristics of the disorder, and its effect may be confounded by the usual comorbidity between the two. Specifically, this comorbidity can be seen in the significant differences observed between groups, with higher rates of depression in ED patients, with a particular incidence of suicidal ideation and change in eating habits, than in the general sample.

Similarly, the significant results that point to the relationship between cognitive interference and obsession with thinness outline the relationship between cognitive inflexibility and obsession, a common binomial in AN. The presence of this cognitive rigidity with one of the indices characteristics of ED has led to an assessment of its possible endophenotypic value, which could, with further research, help in early detection and intervention. The same suspicion and interest are aroused by the relationship between basic psychological processes of motor speed and bulimia. The hypothesis of automaticity in the visual search process could be indicative of greater impulsivity, which is reflected in a shorter execution time. Impulsivity, which is considered to result in a lack of control in the face of immediate reinforcement, is a characteristic of BN and could therefore also be suspected as an endophenotypic and early indicator of the disorder [5].

With respect to general emotional results, it has been observed that the commission of errors in some tasks is associated with higher rates of depression and higher speed in automatic reading is associated with anxiety as a trait. These data, which may respond to the characteristics of cognitive inflexibility and slowing of the former and impulsivity of the latter, have not been found to be related to eating disorder indicators, supporting studies in this line. The need for further research in this regard, trying to separate the effects of comorbidity from those linked to the Eating Disorders, may give results very interesting and provide significant working information for the reinforcement of therapy with these patients [5, 6].

There are some points related to the neuropsychology of eating disorders that should be clarified in future analysis: a) In the case of anorexia nervosa, different studies comparing patients and control groups have not yield conclusive results; b) considering different Eating Disorders (e.g. anorexia, bulimia, binge eating disorder) the comparison among them with respect to neuropsychological functions does not give clear results; c) the role of variables such as depression, anxiety and obsessionality needs to be clarified: which is their role as mediator and/or moderator variables?; d) the neuropsychological commonalities between the so-called extreme weight conditions (anorexia, obesity) need to be clarified; e) what is the link between neuropsychological dysfunctions in and biomarkers in eating disorders? This remains unclear; f) is a neuropsychological disturbance in anorexia nervosa an initial factors or simply a mere consequence?; g) apart from the relevance of neuropsychological alterations in eating behaviour, the association between body image dissatisfaction/distortion and neuropsychological dysfunctions needs to be defined; h) the similarities found in anorexia nervosa and other mental disorders respecting neuropsychological dysfunction are not well established; i) the same applies to the relationship between neuropsychological performance in patients with anorexia nervosa and other variables such as personality or gender [7].