Dewi Guardia

Imagining One's Own and Someone Else's Body Actions: Dissociation in Anorexia Nervosa

Background Patients with anorexia nervosa (AN) usually report feeling larger than they really are. This body overestimation appears to be related not only to the patient’s body image but also to an abnormal representation of the body in action. In previous work on a body-scaled anticipation task, anorexic patients judged that they could not pass through a door-like aperture even when it was easily wide enough - suggesting the involvement of the body schema. In the present study, we sought to establish whether this erroneous judgment about action is specifically observed when it concerns one’s own body or whether it is symptomatic of a general impairment in perceptual discrimination. Methods Twenty-five anorexic participants and 25 control participants were presented with a door-like aperture. They had to judge whether or not the aperture was wide enough for them to pass through (i.e. first-person perspective, 1PP) and for another person present in the testing room to pass through (i.e. third-person perspective, 3PP). Results We observed a higher passability ratio (i.e. the critical aperture size to shoulder width ratio) in AN patients for 1PP but not for 3PP. Moreover, the magnitude of the passability ratio was positively correlated not only with the extent of the patient’s body and eating concerns but also with the body weight prior to disease onset. Our results suggest that body overestimation can affect judgments about the capacity for action but only when they concern the patient’s own body. This could be related to impairments of the overall network involved in the emergence of the body schema and in one’s own perspective judgments. Conclusion Overestimation of the body schema might occur because the central nervous system has not updated the new, emaciated body, with maintenance of an incorrect representation based on the patient’s pre-AN body dimensions.

Pharmacological Treatments for Cocaine Dependence: Is There Something New?

INTRODUCTION There is no specific and approved treatment, by regulatory authorities, for cocaine dependence. Therefore, developing new medications for the treatment of this disease continues to be a research priority. Recent advances in neurobiology and brain imaging studies have suggested several promising pharmacological approaches. MATERIALS AND METHODS Literature searches were conducted for the period from January 1990 to February 2011 using PubMed, EMBASE, PsycInfo, the NIDA research monograph index and the reference list of clinicaltrials.gov, which are the main electronic sources of ongoing trials. RESULTS Recent controlled clinical studies have highlighted some very promising medications, especially glutamatergic (N-Acetylcysteine, modafinil, topiramate) and GABAergic (vigabatrin) agents, agonist replacement therapy (sustained-release methylphenidate, d-amphetamine) and dopamine agents (disulfiram). Additionally, immunotherapy is a new and promising pharmacological approach. CONCLUSION Promising pharmacological approaches have emerged for the treatment of cocaine dependence, but larger, randomized, placebo-controlled studies are needed for some medications. Preclinical studies suggest new targets of interest in cocaine dependence. The optimal therapeutic platform is the combination of pharmacotherapies with behavioral therapies.

Increased prevalence of psychotic disorders among third-generation migrants: Results from the French Mental Health in General Population survey

There is very strong evidence that the prevalence of psychosis is elevated in migrant populations and that this risk persists into the second generation. However, these results have not been replicated in France, and the prevalence of psychotic disorders in the third generation of migrants remains unknown. Based on the Mental Health in General Population survey (n=37063), we report for the first time the increased prevalence of psychotic disorders in migrants in France, which persists into the second generation for a single psychotic episode (SPE) (OR=1.43, 95% CI [1.02-2.03], p<0.03) and into the third generation for recurrent psychotic disorder (RPD) (OR=1.78, 95% CI [1.45-2.18], p<0.0001) after adjustment for age, sex, level of education and cannabis use. Complementary statistical analyses of our sample showed a significantly higher risk of SPE in migrants from the French West Indies and Africa (χ(2)=17.70, p<0.01). These results are consistent with the socio-developmental model and the psychosis continuum hypothesis.

Spatial orientation constancy is impaired in anorexia nervosa

In anorexia nervosa (AN), body distortions have been associated with parietal cortex (PC) dysfunction. The PC is also the anatomical substrate of a supramodal reference framework involved in spatial orientation constancy. Given the impaired spatial orientation constancy found in hemineglect, we sought to determine whether similar disturbances could be observed in anorexic patients. We investigated the effect of passive lateral body inclination on the tactile subjective vertical (SV). Fifty participants (25 AN patients and 25 healthy controls) were asked to manually set a rod into the vertical position under three postural conditions. For tilted conditions, we observed a significant deviation of the tactile SV towards the body. This effect was abnormally accentuated in AN patients and might be caused by higher weighting with respect to the egocentric frame of reference. Our findings reinforce the role of the PC in AN and suggest that this dysfunction affects spatial orientation constancy as well as body boundaries.

GABAergic and Glutamatergic Modulation in Binge Eating: Therapeutic Approach

Lifetime prevalence estimates for binge eating disorder (BED) and bulimia nervosa (BN) are 3.5% and 1.5% among women and 2.0% and 0.5% among men, respectively. Night eating syndromes (NES) affect 1.1%-1.5% of the general population. All of these disorders induce an impaired quality of life and significant disability. Symptom overlaps are reported between substance use disorders and eating disorders such as BED, BN and NES. A growing body of evidence suggests that γ-amino-butyric acid (GABA) and glutamate modulation pathways might be useful targets in the treatment of alcohol and substance use disorders. Their involvement in the reward process and in the regulation of food intake could be the source of new pharmacological strategies for the treatment of eating disorders. We review published data on the efficacy and safety of drugs targeting the GABA and glutamate modulation pathways for the treatment of BED, BN and NES. Preliminary results indicate that baclofen and topiramate are effective in reducing binge eating, craving and weight gain. However, the potential clinical drug-placebo difference is not detected for acamprosate and lamotrigine. Limitations of these studies are discussed. In view of these data, first- and second-line pharmacological interventions are proposed.

Body distortions after massive weight loss: lack of updating of the body schema hypothesis

Behavioural therapy and bariatric surgery often produce rapid, massive body weight loss that may impact a patient’s ability to gauge his/her new body shape. Although the patient is aware of the weight loss, he/she continues to feel obese, as if there was a conflict between the previous body schema and the new one. Here, we report the case of a 40-year-old woman who developed major body distortions after massive weight loss. Psychometric and behavioural assessments revealed strong disturbances in several tasks involving body representation. In particular, we observed abnormal behaviour in a body-scaled action task. Our findings suggest that the rapidity of our patient’s weight loss prevented her central nervous system from correctly updating the body schema.

Painfully thin but locked inside a fatter body: abnormalities in both anticipation and execution of action in anorexia nervosa

BackgroundPeople with anorexia nervosa (AN) usually report feeling broader than they really are. The objective of the present study was to better understand the body schemas involvement in this false self-representation in AN. We tested the potential for correction of the body schema impairment via the sensorimotor feedback provided by a real, executed action and relative to an imagined action. We also took account of the impact of the AN patients’ weight variations on the task outcomes.MethodsFourteen inpatient participants with AN and fourteen control participants were presented with a doorway-like aperture. The participants had to (i) judge whether or not various apertures were wide enough for them to pass through in a motor imagery task and then (ii) actually perform the action by passing through various apertures.ResultsWe observed a higher passability ratio (i.e. the ratio between the critical aperture size and shoulder width) in participants with AN (relative to controls) for both motor imagery and real action. Moreover, the magnitude of the passability ratio was positively correlated with weight recovery.ConclusionThe body schema alteration in AN appears to be strong enough to affect the patients actions. Furthermore, the alteration resists correction by the sensorimotor feedback generated during action. This bias is linked to weight variations. The central nervous system might be locked to a false representation of the body that cannot be updated. Moreover, these results prompt us to suggest that emotional burden during weight recovery could also alter sensorimotor aspects of body representation. New therapeutic methods should take account of body schema alterations in AN as adjuncts to psychotherapy.

Disruption of spatial task performance in anorexia nervosa.

In anorexia nervosa (AN), body distortions have been associated with parietal cortex (PC) dysfunction. The PC is the anatomical substrate for a supramodal reference framework involved in spatial orientation constancy. Here, we sought to evaluate spatial orientation constancy and the perception of body orientation in AN patients. In the present study, we investigated the effect of passive lateral body inclination on the visual and tactile subjective vertical (SV) and body Z-axis in 25 AN patients and 25 healthy controls. Subjects performed visual- and tactile-spatial judgments of axis orientations in an upright position and tilted 90° clockwise or counterclockwise. We observed a significant deviation of the tactile and visual SV towards the body (an A-effect) under tilted conditions, suggesting a multisensory impairment in spatial orientation. Deviation of the Z-axis in the direction of the tilt was also observed in the AN group. The greater A-effect in AN patients may reflect reduced interoceptive awareness and thus inadequate consideration of gravitational inflow. Furthermore, marked body weight loss could decrease the somatosensory inputs required for spatial orientation. Our study results suggest that spatial references are impaired in AN. This may be due to particular integration of visual, tactile and gravitational information (e.g. vestibular and proprioceptive cues) in the PC.

Pharmacological Approaches of Binge Drinking

Binge Drinking (BD) is often considered to be recurrent alcohol abuse amongst adolescents and young adults. However, the close link between adolescence and impulsivity has led many authors to define BD as intoxication-seeking behaviour. Medications may sometimes be justified because of the major short-term and long-term risks that underlie the most severe BD-related behaviours. The most common consequences in the long run are the occurrence of alcohol dependence, psycho- and neurodevelopmental disruptions and alcohol liver disease. To understand the specificities of BD among other forms of alcohol addiction, this article is based on a two-headed conception of alcohol dependence: on one hand, psychological dependence, which refers to the behavioural habituation of alcohol intake, clinically results in craving and is neurobiologically supported by the reward system, particularly the dopaminergic mesolimbic pathway (MLP); on the other hand, physical dependence, which refers to the pharmacological tolerance induced by chronic alcohol intake, results in Alcohol Withdrawal Syndrome (AWS) and is neurobiologically supported by the imbalance between GABA and Glutamate-NMDA neurotransmission. Medications for psychological dependence include anticraving drugs, which all act by regulating MLP. Medications for physical dependence on alcohol include GABA-A and perhaps GABA-B agonists and some NMDA antagonists. In practice, many alcohol-dependence treatments seem to have a dual action. This article proposes an attempt to classify current and forthcoming medications for alcohol addiction based on this two-headed approach to treating alcohol dependence. Drawing from this classification, specific therapeutic schemes for treating BD are proposed, with currently approved alcohol medications and possible future treatments. These schemes are justified by recent literature on the subject and propose to prioritize pure anticraving medications, taking into account the clinical specificities of BD. Furthermore, these schemes also mention harm-reductive neuroprotective and hepatoprotective strategies, which could be included in the arsenal of possible medications for BD in the near future.

Prediction of trauma-related disorders: a proposed cutoff score for the peritraumatic distress inventory.

In the month following a motor vehicle accident, the rate of posttraumatic stress disorder (PTSD) and other trauma-related disorders (ie, mood, other anxiety disorders, and substance use disorders) may reach 30%.1 From a clinical perspective, there is an unmet need to develop screening tools that can help identify individuals at risk of developing such disorders. The Peritraumatic Distress Inventory (PDI) is a 13-item self-report measure—validated in several languages—that has been shown in several studies to predict the development of posttraumatic stress symptoms or disorder.2–4 In a prospective study of 79 motor vehicle accident victims, Nishi et al5 proposed an optimum cutoff point of 23 for the PDI to predict acute PTSD 1 month after the accident. However, to this day, the measure has not been used to predict the full spectrum of trauma-related disorders. The aim of this study was to fill that gap. Method. The study, approved by an independent ethics committee, included 211 subjects consecutively hospitalized in a Trauma Center following a motor vehicle accident from January 2003 to July 2006. The PDI was administered within 5 days of admission after written informed consent was obtained. Six weeks after the accident, the patients underwent a semistructured PTSD diagnostic interview6 as well as the Mood, Anxiety, and Substance Use Disorders sections of a structured psychiatric interview7 by trained psychiatrists. Partial PTSD as described by Blanchard et al8 was also screened for. Subjects with a history of posttraumatic amnesia were excluded. Nineteen subjects were lost at the 6-week follow-up and therefore dropped from the analyses. Results. The final cohort consisted of 192 subjects, 137 adult men and 55 women. The mean age of subjects was 35.14 years (SD = 15.39). Injury severity was classified as mild (10%), moderate (49%), or severe (41%). In the final cohort, 154 subjects fulfilled DSM-IV-TR criteria A1 and A2 for trauma exposure. The mean PDI total score was 15.68 (SD = 8.71). At the follow-up, 66 patients fulfilled criteria for partial (n = 31) or full (n = 35) PTSD, 19 for major depressive disorder, 10 for at least 1 anxiety disorder, and 3 for a psychoactive substance disorder. No association was found between injury severity and PTSD (χ2 = 0.96, df = 1, NS). The PDI score was, however, significantly associated with an increased risk of acute PTSD (χ2 = 5.15, df = 1, P = .02). According to the occurrence of traumatic events, receiver operating characteristic curve analysis showed an area under the curve (AUC) of 0.7 (Figure 1). The optimum predictive cutoff point of the PDI was a score of 14 (sensitivity 68%, specificity 61%). On the one hand, 90% of the victims with a PDI score > 28 developed PTSD or partial PTSD at follow-up. On the other hand, 90% of those with a score < 7 did not develop PTSD. In order to detect PTSD or partial PTSD 6 weeks later, we propose a cutoff score of 14 (PTSD: sensitivity 84% and specificity 47%, AUC 0.6; partial PTSD: sensitivity 73% and specificity 60%, AUC 0.7). Figure 1 Receiver Operating Characteristic (ROC) Curve for Occurrence of PTSD and PDI Scorea The PDI could be a useful tool for screening individuals at risk of developing trauma-related disorders. We recommend that trauma survivors with a PDI score 28 would need immediate care and follow-up. Finally, for those with a score of 7 through 28, we propose a checkup after a few weeks.