Reported rates of bipolar syndromes are highly variable between studies because of age differences, differences in diagnostic criteria, or restriction of sampling to clinical contacts.

In 1395 adolescents aged 14–17 years, DSM-IV (hypo)manic episodes (manic and hypomanic episodes combined), use of mental health care, and five ordinal subcategories representing the underlying continuous score of (hypo)manic symptoms (‘mania symptom scale’) were measured at baseline and approximately 1.5, 4 and 10 years later using the Munich-Composite International Diagnostic Interview (DIA-X/M-CIDI).

Incidence rates (IRs) of both (hypo)manic episodes and (hypo)manic symptoms (at least one DSM-IV core symptom) were far higher (714/105 person-years and 1720/105 person-years respectively) than traditional estimates. In addition, the risk of developing (hypo)manic episodes was very low after the age of 21 years [hazard ratio (HR) 0.031, 95% confidence interval (CI) 0.0050–0.19], independent of childhood disorders such as attention deficit hyperactivity disorder (ADHD). Most individuals with hypomanic and manic episodes were never in care (87% and 62% respectively) and not presenting co-morbid depressive episodes (69% and 60% respectively). The probability of mental health care increased linearly with the number of symptoms on the mania symptom scale. The incidence of the bipolar categories, in particular at the level of clinical morbidity, was strongly associated with previous childhood disorders and male sex.

This study showed, for the first time, that experiencing (hypo)manic symptoms is a common adolescent phenomenon that infrequently predicts mental health care use. The findings suggest that the onset of bipolar disorder can be elucidated by studying the pathway from non-pathological behavioural expression to dysfunction and need for care.

Animal models of anxiety disorders emphasize the crucial role of locus ceruleus–noradrenergic (norepinephrine, NE) signaling, the basolateral amygdala (BLA) and their interactions in the expression of anxiety-like behavioral responses to stress. Despite clinical evidence for the efficacy of a β-noradrenergic receptor blockade with propranolol in the alleviation of anxiety symptoms and the secondary prevention of post traumatic stress disorder, preclinical evidence for a β-noradrenergic modulation of BLA activity in humans is missing.

We combined functional magnetic resonance imaging in healthy volunteers with probabilistic mapping of intra-amygdalar responses to fearful, neutral and happy facial expressions to test the hypothesis that a β-noradrenergic receptor blockade with propranolol would inactivate the BLA.

Consistent with our a priori hypothesis, propranolol diminished BLA responses to facial expressions, independent of their emotional valence. The absence of activity changes in probabilistically defined visual control regions underscores the specific action of propranolol in the BLA.

Our findings provide the missing link between the anxiolytic potential of propranolol and the biological basis of β-noradrenergic activation in the human BLA as a key target for the pharmacological inhibition of anxiety neurocircuitry. Moreover, our findings add to emerging evidence that NE modulates both the reactivity (sensitivity) and the operating characteristics (specificity) of the BLA via β-noradrenergic receptors.

Childhood traumatic events and functional abnormalities of the hypothalamus–pituitary–adrenal (HPA) axis have been widely reported in psychiatric patients, although neither is specific for any diagnosis. Among the limited number of studies that have evaluated these topics, none has adopted a trans-diagnostic approach. The aim of the present research is to explore the relationship between childhood stressors, HPA axis function and psychiatric symptoms, independent of the diagnosis.

A total of 93 moderate to severely ill psychiatric out-patients of Florence and Pisa University Psychiatric Units and 33 healthy control subjects were recruited. The assessment consisted of salivary cortisol pre- and post-low dose (0.5 mg) Dexamethasone, early and recent life events, 121 psychiatric symptoms independent of diagnosis, SCID, BPRS.

In total, 33.5% of patients were Dexamethasone Suppression Test (DST) non-suppressors, compared with 6.1% of controls (p=0.001). Among patients, non-suppression was associated with particular symptoms (i.e. depressive and psychotic), but not to any specific diagnosis. Early stressful life events were significantly associated with higher salivary cortisol levels, with DST non-suppression and with approximately the same subset of symptoms. A recent stressful event seemed to be associated to the HPA response only in those subjects who were exposed to early traumata.

Our report suggests a relationship between life stress, HPA axis and psychopathology. A cluster of specific psychiatric symptoms seems to be stress related. Moreover, it seems that an abnormal HPA response is possibly triggered by an excessive pressure in vulnerable individuals.

In this study we compared subjects with obsessive and/or compulsive symptoms who did not meet all criteria for obsessive–compulsive disorder (OCD) (subthreshold subjects) to subjects with full-blown OCD and also to subjects without obsessions or compulsions.

The data were derived from the Netherlands Mental Health Survey and Incidence Study (NEMESIS), a large representative sample of the general Dutch population (n=7076). Using the Composite International Diagnostic Interview, Version 1.1 (CIDI 1.1), three groups were distinguished: subjects without lifetime obsessions or compulsions (94.2%), subthreshold subjects (4.9%) and subjects with full-blown OCD according to DSM-III-R (0.9%). These three groups were compared on various items, including psychological vulnerability, health and functional status, psychiatric co-morbidity and seeking treatment.

Subthreshold and OCD subjects had similar scores on the majority of the items measured. Thus, there was little difference between subthreshold and OCD subjects in health, functional status, psychological vulnerability and psychiatric co-morbidity. However, OCD and subthreshold subjects scored worse on most of these items when compared to the controls without obsessions or compulsions.

Having obsessions and compulsions is associated with substantial suffering and disability. Most subjects with obsessions and/or compulsions are not diagnosed with OCD according to the DSM-III-R criteria although these subjects generally display similar consequences to full-blown OCD subjects. We recommend that these subthreshold cases receive special attention in the development of DSM-V.

Response to antidepressant medication is higher in comparator versus placebo-controlled randomized controlled trials (RCTs). Patient expectancy is an important influence on clinical outcome in the treatment of depression and may explain this finding. The results are reported from a pilot RCT studying expectancy and depression outcome in placebo-controlled versus comparator treatment conditions.

Out-patients aged 18–65 years with major depressive disorder (MDD) were enrolled in this 8-week RCT. Subjects were randomized to placebo-controlled (escitalopram or placebo) or comparator (escitalopram or citalopram) administration of antidepressant medication. Subjects reported their expected likelihood and magnitude of depression improvement before and after randomization using questions from the Credibility and Expectancy Scale (CES). A regressed change model of post-randomization expectancy of improvement was fit to the data to determine whether subjects in the comparator group reported greater expectancies of improvement than subjects in the placebo-controlled group.

Twenty subjects with mean age 56.5±11.7 years, a baseline Hamilton Depression Rating Scale (HAMD) score of 24.2±5.3, baseline Beck Depression Inventory (BDI) score of 24.9±6.4 and baseline Clinical Global Impressions (CGI) – Severity score of 4.0±0.3 were enrolled in the study. Adjusting for other factors, the effect of group assignment on expected magnitude of improvement was significant and large (effect size 1.5). No group differences in expected likelihood of improvement were found.

Randomization to comparator versus placebo-controlled administration of antidepressant medication produced greater expectancies of how much patients would improve during the trial. This expectancy difference may explain the higher response and remission rates that are observed in comparator versus placebo-controlled trials.

The DSM-IV symptom criteria for major depressive disorder (MDD) are somewhat lengthy, with many studies showing that treatment providers have difficulty recalling all nine symptoms. Moreover, the criteria include somatic symptoms that are difficult to apply in patients with medical illnesses. In a previous report, we developed a briefer definition of MDD that was composed of the mood and cognitive symptoms of the DSM-IV criteria, and found high levels of agreement between the simplified and full DSM-IV definitions. The goal of the present study was to replicate these findings in another large sample of psychiatric out-patients and to extend the findings to other patient samples.

We interviewed 1100 psychiatric out-patients and 210 pathological gamblers presenting for treatment and 1200 candidates for bariatric surgery. All patients were interviewed by a diagnostic rater who administered a semi-structured interview. We inquired about all symptoms of depression for all patients.

In all three samples high levels of agreement were found between the DSM-IV and the simpler definition of MDD. Summing across all 2510 patients, the level of agreement between the two definitions was 95.5% and the κ coefficient was 0.87.

After eliminating the four somatic criteria from the DSM-IV definition of MDD, a high level of concordance was found between this simpler definition and the original DSM-IV classification. This new definition offers two advantages over the current DSM-IV definition – it is briefer and it is easier to apply with medically ill patients because it is free of somatic symptoms.

Severity is an important characteristic of major depression (MD) and an ‘episode specifier’ in DSM-IV classifying depressive episodes as ‘mild’, ‘moderate’ or ‘severe’. These severity subtypes rely on three different measures of severity: number of criteria symptoms, severity of the symptoms and degree of functional disability. No prior empirical study has evaluated the coherence and validity of the DSM-IV definition of severity of MD.

In a sample of 1015 (518 males, 497 females) Caucasian twins from a population-based registry who met criteria for MD in the year prior to interview, factor analysis and logistic regression were conducted to examine the inter-relationships of the three severity measures and their associations with a wide range of potential validators including demographic factors, risk for future episodes, risk of MD in the co-twin, characteristics of the depressive episode, the pattern of co-morbidity, and personality traits.

Correlations between the three severity measures were significant but moderate. Factor analysis indicated the existence of a general severity factor, but the factor was not highly coherent. The three severity measures showed differential predictive ability for most of the validators.

Severity of MD as defined by the DSM-IV is a multifaceted and heterogeneous construct. The three proposed severity measures reflect partly overlapping but partly independent domains with differential validity as assessed by a wide range of clinical characteristics. Clinicians should probably use a combination of severity measures as proposed in DSM-IV rather than privileging one.

The relationship between metabolic control and cognitive function in adolescents with type 1 diabetes (DM type 1) is not clear. We compared the quality of glycemic control (GC) and cognitive measures in adolescents with DM type 1 to find out if the quality of diabetes management is related to cognitive impairment.

We assessed executive functions (EFs) and other neuropsychological and psychosocial variables in 70 adolescent patients with DM type 1 and 20 age-matched controls. Patients were divided into two groups according to their last hemoglobin A1c (HbA1c): acceptable (HbA1c 5.9–8.0%, mean 6.9%, 36 patients, mean age 14 years) and non-optimal (HbA1c 8.2–11.6%, mean 9.3%, 34 patients, mean age 15.6 years).

We found impaired EFs, mainly problems of concept formation (p=0.038), cognitive flexibility (p=0.011) and anticipation (p=0.000), in the patients with DM type 1. Both groups did not differ in intelligence, most assessed EFs and adjustment to chronic illness (Youth Self-Report; YSR). Younger patients (<15 years) were cognitively less flexible. GC was worse in older patients and in patients with longer duration of the disease. We also found significant differences between patients with diabetes and controls concerning somatic complaints, internalizing problems (Child Behavior Checklist; CBCL) and social activity (CBCL and YSR).

DM type 1 is associated with cognitive deficits in adolescents independent of the quality of metabolic control and the duration of the disease. These deficits are probably related to the disease, especially in patients with early-onset diabetes.

Autistic spectrum disorder (ASD) is characterized by stereotyped/obsessional behaviours and social and communicative deficits. However, there is significant variability in the clinical phenotype; for example, people with autism exhibit language delay whereas those with Asperger syndrome do not. It remains unclear whether localized differences in brain anatomy are associated with variation in the clinical phenotype.

We used voxel-based morphometry (VBM) to investigate brain anatomy in adults with ASD. We included 65 adults diagnosed with ASD (39 with Asperger syndrome and 26 with autism) and 33 controls who did not differ significantly in age or gender.

VBM revealed that subjects with ASD had a significant reduction in grey-matter volume of medial temporal, fusiform and cerebellar regions, and in white matter of the brainstem and cerebellar regions. Furthermore, within the subjects with ASD, brain anatomy varied with clinical phenotype. Those with autism demonstrated an increase in grey matter in frontal and temporal lobe regions that was not present in those with Asperger syndrome.

Adults with ASD have significant differences from controls in the anatomy of brain regions implicated in behaviours characterizing the disorder, and this differs according to clinical subtype.

Cannabis use is associated with altered neurocognitive functioning in severe mental disorders, but data are still inconclusive and there are no studies of bipolar disorder. The aim of this study was to investigate the association between cannabis use and neurocognition in bipolar disorder compared with schizophrenia in a naturalistic setting.

A total of 133 patients with bipolar disorder and 140 patients with schizophrenia underwent neuropsychological assessments and clinical characterization including measures of substance use. Relationships between cannabis users and neurocognitive function were explored in the two diagnostic groups. Possible interactions between diagnosis and cannabis use were investigated, and findings were controlled for possible confounders.

In bipolar disorder subjects, cannabis use was associated with better neurocognitive function, but the opposite was the case for the schizophrenia subjects. There was a statistically significant interaction effect of diagnosis and cannabis use on focused attention (p=0.019), executive functioning (verbal fluency – set shifting) (p=0.009), logical memory-learning (p=0.007) and on logical memory-recall (p=0.004). These differences in neurocognitive function could not be explained by putative confounders.

The findings suggest that cannabis use may be related to improved neurocognition in bipolar disorder and compromised neurocognition in schizophrenia. The results need to be replicated in independent samples, and may suggest different underlying disease mechanisms in the two disorders.

Previous research suggests, though not consistently, that maternal psychological distress during pregnancy leads to adverse birth outcomes. We investigated whether maternal psychological distress affects fetal growth during the period of mid-pregnancy until birth.

Pregnant women (n=6313) reported levels of psychological distress using the Brief Symptom Inventory (anxious and depressive symptoms) and the Family Assessment Device (family stress) at 20.6 weeks pregnancy and had fetal ultrasound measurements in mid- and late pregnancy. Estimated fetal weight was calculated using head circumference, abdominal circumference and femur length.

In mid-pregnancy, maternal distress was not linked to fetal size. In late pregnancy, however, anxious symptoms were related to fetal size after controlling for potential confounders. Anxious symptoms were also associated with a 37.73 g [95% confidence interval (CI) −69.22 to −6.25, p=0.019] lower birth weight. When we related maternal distress to fetal growth curves using multilevel models, more consistent results emerged. Maternal symptoms of anxiety or depression were associated with impaired fetal weight gain and impaired fetal head and abdominal growth. For example, depressive symptoms reduced fetal weight gain by 2.86 g (95% CI −4.48 to −1.23, p<0.001) per week.

The study suggests that, starting in mid-pregnancy, fetal growth can be affected by different aspects of maternal distress. In particular, children of prenatally anxious mothers seem to display impaired fetal growth patterns during pregnancy. Future work should address the biological mechanisms underlying the association of maternal distress with fetal development and focus on the effects of reducing psychological distress in pregnancy.

Body image distortion is a key symptom of anorexia nervosa. In behavioral research two components of body image have been defined: attitudes towards the body and body size experience. Neuroimaging studies concerning own body image distortions in anorexia nervosa have revealed an inconsistent pattern of results and are constrained by the fact that no direct distinction between the different parts of body image has been made.

The present study therefore set out to investigate the neural correlates of two parts of the own body image using functional magnetic resonance imaging (fMRI): satisfaction rating and size estimation for distorted own body photographs in patients with anorexia nervosa and controls.

Anorectic patients were less satisfied with their current body shape than controls. Patients further demonstrated stronger activation of the insula and lateral prefrontal cortex during the satisfaction rating of thin self-images. This indicates a stronger emotional involvement when patients are presented with distorted images close to their own ideal body size. Patients also overestimated their own body size. We were able to show complex differential modulations in activation of the precuneus during body size estimation in control and anorectic subjects. It could be speculated that a deficit in the retrieval of a multimodal coded body schema in precuneus/posterior parietal cortex is related to body size overestimation.

We were able to find specific behavioral responses and neural activation patterns for two parts of body image in anorexia nervosa and healthy controls. Thus, the present results underline the importance of developing research and therapeutic strategies that target the two different aspects of body image separately.

Depressed patients show impaired performance following negative feedback; the probability of committing an error is increased immediately after an error. This deficit is assumed to be highly specific and to represent a trait marker of major depressive disorder (MDD). Inconsistencies in currently available data could reflect inter-individually different strategies to regulate negative affect. The present study examined modulation of performance following negative feedback by cognitive reappraisal to regulate aversive affect in depressed patients.

Thirty-three depressed patients and 33 control subjects performed tasks of varying difficulty over a prolonged time. Emotional feedback was given immediately after each trial. Performance was further analysed within subgroups using cognitive reappraisal of aversive events with high and low frequency.

A significant group by task difficulty interaction for absolute number of subsequent errors revealed that depressed patients were especially impaired when receiving negative feedback more frequently. An increased probability of subsequent errors was shown in patients irrespective of task difficulty. Analysis of subgroups revealed higher absolute number and probability of subsequent errors only in depressed patients habitually not using cognitive reappraisal to regulate aversive emotions. Depressed patients using this strategy did not differ from controls.

The present results replicate the observation of impaired performance in depressed patients following failure feedback. Most importantly, a subgroup of patients who habitually rely on cognitive reappraisal of aversion-eliciting events, such as negative performance feedback, was not impaired. This modulatory influence of emotion regulation strategies on performance subsequent to negative feedback suggests that training emotion regulation in achievement situations should be incorporated in current concepts to prevent relapse.

Preparing for potentially threatening events in the future is essential for survival. Anticipating the future to be unpleasant is also a cognitive key feature of depression. We hypothesized that ‘pessimism’-related emotion processing would characterize brain activity in major depression.

During functional magnetic resonance imaging, depressed patients and a healthy control group were cued to expect and then perceive pictures of known emotional valences – pleasant, unpleasant and neutral – and stimuli of unknown valence that could have been either pleasant or unpleasant. Brain activation associated with the ‘unknown’ expectation was compared with the ‘known’ expectation conditions.

While anticipating pictures of unknown valence, activation patterns in depressed patients within the medial and dorsolateral prefrontal areas, inferior frontal gyrus, insula and medial thalamus were similar to activations associated with expecting unpleasant pictures, but not with expecting positive pictures. The activity within a majority of these areas correlated with the depression scores. Differences between healthy and depressed persons were found particularly for medial and dorsolateral prefrontal and insular activations.

Brain activation in depression during expecting events of unknown emotional valence was comparable with activation while expecting certainly negative, but not positive events. This neurobiological finding is consistent with cognitive models supposing that depressed patients develop a ‘pessimistic’ attitude towards events with an unknown emotional meaning. Thereby, particularly the role of brain areas associated with the processing of cognitive and executive control and of the internal state is emphasized in contributing to major depression.

Little is known about the association of eating disorder subtypes across multiple categories of substance use in population-based samples. We examined the association between eating disorders and substance use in a large population-based sample.

Female participants (n=13 297) were from the Swedish Twin Registry [Lichtenstein et al., Twin Research and Human Genetics (2006) 9, 875–882]. Substance use was examined in four defined groups – (1) anorexia nervosa (AN); (2) bulimia nervosa (BN); (3) AN and BN (ANBN); and (4) binge eating disorder (BED) as well as a referent group without eating disorder (no ED). Secondary analyses examined differences between restricting AN (RAN) and binge and/or purge AN (ANBP).

In general, eating disorders were associated with greater substance use relative to the referent. The AN group had significantly increased odds for all illicit drugs. Significant differences emerged across the RAN and ANBP groups for alcohol abuse/dependence, diet pills, stimulants, and polysubstance use with greater use in the ANBP group. Across eating disorder groups, (1) the BN and ANBN groups were more likely to report alcohol abuse/dependence relative to the AN group, (2) the ANBN group was more likely to report diet pill use relative to the AN, BN and BED groups, and (3) the BN group was more likely to report diet pill use relative to the no ED, AN and BED groups.

Eating disorders are associated with a range of substance use behaviors. Improved understanding of how they mutually influence risk could enhance understanding of etiology and prevention.

Bulimia nervosa (BN) is a serious psychiatric disorder characterized by frequent episodes of binge eating and inappropriate compensatory behavior. Numerous trials have found that antidepressant medications are efficacious for the treatment of BN. Early response to antidepressant treatment, in the first few weeks after medication is initiated, may provide clinically useful information about an individual's likelihood of ultimately benefitting or not responding to such treatment. The purpose of this study was to examine the relationship between initial and later response to fluoxetine, the only antidepressant medication approved by the US Food and Drug Administration (FDA) for the treatment of BN, with the goal of developing guidelines to aid clinicians in deciding when to alter the course of treatment.

Data from the two largest medication trials conducted in BN (n=785) were used. Receiver operating characteristic (ROC) curves were constructed to assess whether symptom change during the first several weeks of treatment was associated with eventual non-response to fluoxetine at the end of the trial.

Eventual non-responders to fluoxetine could be reliably identified by the third week of treatment.

Patients with BN who fail to report a ⩾60% decrease in the frequency of binge eating or vomiting at week 3 are unlikely to respond to fluoxetine. As no reliable relationships between pretreatment characteristics and eventual response to pharmacotherapy have been identified for BN, early response is one of the only available indicators to guide clinical management.

Biases in emotional processing and cognitions about the self are thought to play a role in the maintenance of eating disorders (EDs). However, little is known about whether these difficulties exist pre-morbidly and how they might contribute to risk.

Female dieters (n=82) completed a battery of tasks designed to assess the processing of social cues (facial emotion recognition), cognitions about the self [Self-Schema Processing Task (SSPT)] and ED-specific cognitions about eating, weight and shape (emotional Stroop). The 26-item Eating Attitudes Test (EAT-26; Garner et al.1982) was used to assess subclinical ED symptoms; this was used as an index of vulnerability within this at-risk group.

Regression analyses showed that biases in the processing of both neutral and angry faces were predictive of our measure of vulnerability (EAT-26). In the self-schema task, biases in the processing of negative self descriptors previously found to be common in EDs predicted vulnerability. Biases in the processing of shape-related words on the Stroop task were also predictive; however, these biases were more important in dieters who also displayed biases in the self-schema task. We were also able to demonstrate that these biases are specific and separable from more general negative biases that could be attributed to depressive symptoms.

These results suggest that specific biases in the processing of social cues, cognitions about the self, and also about eating, weight and shape information, may be important in understanding risk and preventing relapse in EDs.

Previous research indicates that individuals with seasonal depression (SD) do not exhibit the memory biases for negative self-referent information that characterize non-seasonal depression (NSD). The current study extended this work by examining processing of self-referent emotional information concerning potential future events in SD.

SD and NSD patients, along with never-depressed controls, completed a scenario-based measure of likelihood estimation for future positive and negative events happening either to the self or to another person.

SD patients estimated future negative events as more likely to happen to both the self and others, relative to controls. In contrast, in the NSD sample this bias was specific to self-referred material. There were no group differences for positive events.

These data provide further evidence that the self-referent bias for processing negative information that characterizes NSD can be absent in SD, this time in the domain of future event processing.

A wide range of neuropsychiatric conditions, including schizophrenia and autistic spectrum disorder (ASD), are associated with impairments in social function. Previous studies have shown that individuals with schizophrenia and ASD have deficits in making a wide range of social judgements from faces, including decisions related to threat (such as judgements of approachability) and decisions not related to physical threat (such as judgements of intelligence). We have investigated healthy control participants to see whether there is a common neural system activated during such social decisions, on the basis that deficits in this system may contribute to the impairments seen in these disorders.

We investigated the neural basis of social decision making during judgements of approachability and intelligence from faces in 24 healthy participants using functional magnetic resonance imaging (fMRI). We used conjunction analysis to identify common brain regions activated during both tasks.

Activation of the amygdala, medial prefrontal cortex, inferior prefrontal cortex and cerebellum was seen during performance of both social tasks, compared to simple gender judgements from the same stimuli. Task-specific activations were present in the dorsolateral prefrontal cortex in the intelligence task and in the inferior and middle temporal cortex in the approachability task.

The present study identified a common network of brain regions activated during the performance of two different forms of social judgement from faces. Dysfunction of this network is likely to contribute to the broad-ranging deficits in social function seen in psychiatric disorders such as schizophrenia and ASD.

Patients with anorexia nervosa (AN) overestimate their size despite being severely underweight. Whether this misperception echoes an underlying emotional disturbance or also reflects a genuine body-representation deficit is debatable. Current measures inquire directly about subjective perception of body image, thus distinguishing poorly between top-down effects of emotions/attitudes towards the body and disturbances due to proprioceptive disorders/distorted body schema. Disorders of body representation also emerge following damage to the right parietal lobe. The possibility that parietal dysfunction might contribute to AN is suspected, based on the demonstrated association of spatial impairments, comparable to those found after parietal lesion, with this syndrome.

We used a behavioral task to compare body knowledge in severe anorexics (n=8), healthy volunteers (n=11) and stroke patients with focal damage to the left/right parietal lobe (n=4). We applied a psychophysical procedure based on the perception, in the dark, of an approaching visual stimulus that was turned off before reaching the observer. Participants had to predict whether the stimulus would have hit/missed their body, had it continued its linear motion.

Healthy volunteers and left parietal patients estimated body boundaries very close to the real ones. Conversely, anorexics and right parietal patients underestimated eccentricity of their left body boundary.

These findings are in line with the role the parietal cortex plays in developing and maintaining body representation, and support the possibility for a neuropsychological component in the pathogenesis of anorexia, offering alternative approaches to treatment of the disorder.