A multidimensional examination of affective and cognitive empathy in anorexia nervosa.

Socio-emotional features are crucial in the development and maintenance of anorexia nervosa (AN). The present study investigates the patterns of altered and preserved empathic abilities in AN. Empathy is an umbrella term that comprises the ability to recognise another's emotional state, take another's perspective, and fantasise (cognitive empathy), as well as the ability to experience vicarious emotions and signal them (affective empathy). These empathic abilities were measured in 43 AN patients and 33 healthy women through a multi-method approach comprising self-report measures, behavioural tasks and bodily correlates. Further, we assessed self-reported approach-avoidance attitudes towards suffering others. Results showed that, within the domain of cognitive empathy, AN patients reported impairment in recognising emotional expressions of anger and fantasising. Concerning affective empathy, they manifested lower sharing of others' positive emotions, higher self-reported distress, and higher facial expressiveness during a video depicting a suffering person. Finally, AN patients reported lower motivation to approach suffering others. Our results draw a complex picture of preserved and altered empathic abilities in AN and capture which are the deficits mediated by the higher levels of anxiety and depression reported by the AN population and those that seem to persist independently from these co-morbid conditions.

Microbiome and substances of abuse.

There is a growing amount of evidence showing a reciprocal relation between the gut microbiota and the brain. Substance use disorders (SUD), which are a major cause of preventable morbidity and mortality worldwide, have an influence on the gut microbiota and on the gut-brain axis. The communication between the microbiota and the brain exists through different pathways: (1) the immune response elicited by bacterial products, coupled with alterations of the intestinal barrier allowing these products to enter the bloodstream, (2) the direct and indirect effects of bacterial metabolites such as short chain fatty acids (SCFAs) or tryptophan on the brain, (3) and the hypothalamic-pituitary-adrenal (HPA) axis, whose peripheral afferents can be influenced by the microbiota, and can in turn activate microglia. Among substances of abuse, alcohol has been the subject of the greatest number of studies in this field. In some but not all patients suffering from alcohol-use-disorder (AUD), alcohol alters the composition of the gut microbiota and the permeability of the intestinal barrier, directly and through dysbiosis. It has also been well demonstrated that alcohol induces a peripheral inflammation; it is still unclear whether it induces a central inflammation, as there are contradictory results in human studies. In animal studies, it has been shown that neuroinflammation increases during alcohol withdrawal. Literature on opioids and stimulants is less numerous. Chronic morphine intake induces dysbiosis, increased intestinal permeability and a probable neuroinflammation, which could explain symptoms such as tolerance, hyperalgesia and deficit in reward behavior. Cocaine induces a dysbiosis and conversely the microbiome can modulate the behavioral response to stimulant drugs. Tobacco cessation is associated with an increase in microbiota diversity. Taken together, the findings of our narrative literature review suggest a bidirectional influence in the pathogenesis of substance use disorders.

Targeting the gut microbiota to treat alcoholic liver diseases: evidence and promises.

The human intestine is colonized by a variety of microbes that influence the metabolic responses, the immune system and the nervous system. Dietary patterns are important factors that shape the composition of the gut microbiota. Many animal models of alcohol exposure have highlighted the key role of the alcohol-induced gut microbiota alterations, leaky gut and translocation of microbial products in the development of alcoholic liver disease (ALD). However, in humans, there is no clear picture defining an "alcoholic microbiome", and the link between intestinal dysbiosis and ALD development is far from being understood. Although we do not comprehend all the mechanistic insights, clinical studies aiming at modulating the gut microbiota of alcoholic patients have shown some beneficial effects. Here we review the potential therapeutic effects of probiotics in ALD and give some clinical perspectives on the role of prebiotics and the use of fecal microbiota transplantation.

Link Between Anhedonia and Depression During Early Alcohol Abstinence: Gender Matters.

AIMS: The aim of the present study was to evaluate the relation between anhedonia and depression in alcohol use disorders (AUD) during detoxification: Is trait anhedonia measured at the beginning of detoxification predictive of depressive symptoms observed at the end? Does state anhedonia recover during detoxification as depression does? Gender differences that have been previously observed for depression in AUD were also explored. METHODS: 81 AUD inpatients were tested at T1 (day 1) and T2 (day 14-18) of withdrawal with the trait Physical Anhedonia Scale, the state anhedonia Snaith-Hamilton Pleasure Scale, the Beck depression inventory and the Spielberger State Anxiety Inventory and compared to 34 control participants, matched for age and gender. RESULTS: AUD patients scored significantly higher than controls on depression, anxiety and state and trait anhedonia when they just entered the detoxification unit. Depression, anxiety and state anhedonia decreased between T1 and T2 in AUD patients. In women, state anhedonia at T1 was predictive of depressive symptoms at T2 over and above anxiety and depression at T1. CONCLUSION: In AUD, state anhedonia recovers during detoxification, concurrently to other affective-related symptoms. However, in women, trait anhedonia predicts the level of depression at the end of detoxification, above and beyond anxiety. This finding stresses the importance of addressing anhedonia in the treatment of AUD and emphasizes the need for targeted interventions within clinical settings in this gender. Clinical consequences are discussed.

[What is the role of the gut microbiota in the development of alcohol use disorders?] / Troubles liés à l'usage d'alcool : et si l'addiction trouvait son origine dans l'intestin ?

Alcohol addiction is a complex and multifactorial disease influenced by social, psychological and biological aspects. The current pharmacological drugs used in the management of alcohol dependence have shown only a modest efficacy and the relapse rate remains high in this disease. Recently, the gut microbiota, a huge and dynamic ecosystem made up of billions of microorganisms living in our intestine, has been shown to regulate many important functions for human health. Indeed, the gut microbiota is known to influence our metabolism, our immune system as well as our nervous system with consequences for brain functions, mood and behaviour. We have shown that heavy and chronic alcohol consumption induced important changes in the composition of the gut microbiota. Furthermore, the microbial changes are associated with the severity of depression, anxiety and alcohol craving that are important factors predicting the risk of relapse. This suggests the existence of a gut-brain axis in alcohol dependence and supports the development of new therapeutic alternatives, targeting the gut microbiota, in the management of alcohol dependence.

L'addiction à l'alcool est une maladie complexe, impliquant à la fois des facteurs sociaux, psychologiques et biologiques. La prise en charge des patients alcoolo-dépendants est difficile car les médicaments actuels ont une efficacité limitée dans le maintien de l'abstinence, et le taux de rechute reste très élevé. Récemment, le microbiote intestinal, un écosystème constitué de milliards de micro-organismes vivant dans notre intestin, est devenu un acteur clé de la santé humaine. Il est connu pour réguler notre métabolisme, notre système immunitaire, mais également notre système nerveux, et donc notre comportement et notre humeur. Nos études récentes ont montré que la consommation abusive d'alcool entraîne des modifications importantes de la composition du microbiote intestinal. Nous avons également montré que ces altérations microbiennes étaient associées à la sévérité des symptômes de dépression, d'anxiété et d'appétence à l'alcool, suggérant ainsi l'existence d'un dialogue entre l'intestin et le cerveau. Ces résultats encouragent la recherche de nouvelles pistes thérapeutiques, ciblant le microbiote intestinal, dans le traitement de la dépendance à l'alcool.

The link between inflammation, bugs, the intestine and the brain in alcohol dependence.

In recent years, some new processes have been proposed to explain how alcohol may influence behavior, psychological symptoms and alcohol seeking in alcohol-dependent subjects. In addition to its important effect on brain and neurotransmitters equilibrium, alcohol abuse also affects peripheral organs including the gut. By yet incompletely understood mechanisms, chronic alcohol abuse increases intestinal permeability and alters the composition of the gut microbiota, allowing bacterial components from the gut lumen to reach the systemic circulation. These gut-derived bacterial products are recognized by immune cells circulating in the blood or residing in target organs, which consequently synthesize and release pro-inflammatory cytokines. Circulating cytokines are considered important mediators of the gut-brain communication, as they can reach the central nervous system and induce neuroinflammation that is associated with change in mood, cognition and drinking behavior. These observations support the possibility that targeting the gut microbiota, by the use of probiotics or prebiotics, could restore the gut barrier function, reduce systemic inflammation and may have beneficial effect in treating alcohol dependence and in reducing alcohol relapse.

Alcohol-induced hypertension: an important healthcare target in Belgium.

Excessive alcohol intake is one of the leading causes of premature death in Europe and particularly in Belgium. Belgian people are consuming more alcohol per year than the European average. It is well established that excessive alcohol consumption is a significant predictor of the development of hypertension (HTN). Two million adults in Belgium suffer from HTN and this number will increase to three million by 2025. Less than 50% of Belgian people treated for HTN are well-controlled. Alcohol reduction in patients with HTN can significantly lower systolic and diastolic blood pressure. After reviewing the epidemiology of HTN and alcohol disorders in Belgium, this paper will focus on the rationale for alcohol screening and brief intervention in primary care. It will also describe the barriers to alcohol screening, and what could be the benefits of alcohol screening for our healthcare system. The authors believe that early identification through alcohol screening and brief intervention in general practice can help to improve the management of patients with HTN, to reach the targets of the WHO Global Action Plan, i.e., a 25% relative reduction in the risk of premature mortality from cardiovascular diseases, cancer, diabetes or chronic respiratory diseases. They are also convinced that this would allow achieving major healthcare savings.

[Long-term psychiatric consequences of carbon monoxide poisoning: a case report and literature review]. / Intoxication au monoxyde de carbone: quelles séquelles neuropsychiatriques? A propos d'un cas clinique et revue de la littérature.

Carbon monoxide intoxication (COI) can result in severe neuropsychiatric lesions that are however granted little attention in literature. Following the description of affective and neurological symptoms in a 37-year-old female patient five years following COI, we will review, across the literature (Medline 1974--2006), the long-term neuropsychiatric consequences, etiopathogenic hypotheses, prognoses and treatments to apply. Subjective symptoms are reported by the quasi-totality of patients for over more than 30 years following COI. More than half of patients are diagnosed as suffering from cognitive impairments and other neurological symptoms after years following COI. Affective disorders are observed in almost three-fourths of patients and personality disorders in more than half. Numerous cerebral lesions and perfusion disorders can be observed through IRM, PET scan and SPECT and related to the clinical symptomatology of the patient. COI may constitute a risk factor in the waking of long-term neuropsychiatric disorders in a context of environmental and neurobiological complex factor interaction. A close follow-up must be envisaged with neuropsychiatric assessments and regular neuroimagery in order to adapt at best therapeutic interventions to the patient's clinical status. First and foremost prevention and education remain the key solution to the reduction of morbidity and mortality of COI.

Alcohol dependence is associated with reduced plasma and fundic ghrelin levels.

BACKGROUND: Conflicting data concerning the involvement of ghrelin in the pathophysiology of alcohol dependence have been reported. The aim of this study is to investigate how chronic alcohol ingestion influences plasma ghrelin levels and whether potential changes observed in plasma relate to modifications in ghrelin production in the stomach where this peptide is primarily synthesized. MATERIALS AND METHODS: Fifty-one consecutive alcoholics admitted for alcohol withdrawal were prospectively enrolled and compared to a control group of 32 healthy volunteers matched for age, sex, height and weight. All subjects underwent fasting plasma ghrelin determination. Twenty-seven randomly selected alcoholics and 17 controls underwent gastroscopy for fundic and duodenal biopsies. Tissues were fixed for histology or frozen in liquid nitrogen for ghrelin protein and mRNA determinations by a radioimmunoassay and quantitative polymerase chain reaction, respectively. Alcohol consumption was normalized to body weight (BW) or body mass index (BMI) given the influence of BW and volume distribution on alcohol levels. RESULTS: Plasma and fundic ghrelin protein levels were significantly decreased in alcoholics. Fundic but not plasma ghrelin protein levels inversely correlated with alcohol consumption normalized to BW or BMI. Ghrelin mRNA levels in fundic biopsies were similar in alcoholics and controls. No significant differences in duodenal ghrelin protein and mRNA levels were found between both groups. CONCLUSIONS: Alcoholism was associated with decreased plasma ghrelin levels partly due to reduced ghrelin production in the stomach. Alcohol affected ghrelin production on the post-transcriptional level in the fundus, whereas duodenal ghrelin secretion did not respond in a similar manner to alcohol intake.

Alcoholism leads to early perceptive alterations, independently of comorbid depressed state: an ERP study.

INTRODUCTION: Alcoholism is associated with a deficit in the processing of emotional facial expressions (EFE) and with a delayed P3b component, partially mediated by earlier perceptive deficits (P100, N170). Since alcohol dependence often occurs with depression, we aim at investigating whether classical event-related potentials (ERP) alterations observed in alcoholism are modulated or not by depression. METHODS: Four groups (controls; alcoholics; depressed; alcoholics-depressed) of 12 participants performed two different discrimination tasks, a gender and an emotional one. They had to decide as quickly as possible about the gender or the emotion displayed by facial stimuli during an ERP recording session (32 channels). Reaction times (RTs), P100, N100, N170 and P3b were recorded. RESULTS: At the behavioural level, control participants discriminated EFE (but not gender) more rapidly than the three other groups. At the ERP level, the differences observed on RTs for emotional task were neurophysiologically indexed by a delayed P3b component. This delay was associated with earlier ERP alterations (P100, N100, N170), but only in participants suffering from alcohol dependence, in association or not with depression. DISCUSSION: On the one hand, individuals with alcoholism, associated or not with a comorbid depression, were impaired in the processing of EFE. This deficit was neurophysiologically indexed by early perceptive (P100, N100, N170) and decisional (P3b) alterations. On the other hand, non-alcoholic patients with depression only exhibited P3b impairment. These results lead to potential implications concerning the usefulness of the ERP for the differential diagnosis in psychiatry, notably concerning the comorbidities in alcoholism.

Face processing in chronic alcoholism: a specific deficit for emotional features.

BACKGROUND: It is well established that chronic alcoholism is associated with a deficit in the decoding of emotional facial expression (EFE). Nevertheless, it is still unclear whether this deficit is specifically for emotions or due to a more general impairment in visual or facial processing. This study was designed to clarify this issue using multiple control tasks and the subtraction method. METHODS: Eighteen patients suffering from chronic alcoholism and 18 matched healthy control subjects were asked to perform several tasks evaluating (1) Basic visuo-spatial and facial identity processing; (2) Simple reaction times; (3) Complex facial features identification (namely age, emotion, gender, and race). Accuracy and reaction times were recorded. RESULTS: Alcoholic patients had a preserved performance for visuo-spatial and facial identity processing, but their performance was impaired for visuo-motor abilities and for the detection of complex facial aspects. More importantly, the subtraction method showed that alcoholism is associated with a specific EFE decoding deficit, still present when visuo-motor slowing down is controlled for. CONCLUSION: These results offer a post hoc confirmation of earlier data showing an EFE decoding deficit in alcoholism by strongly suggesting a specificity of this deficit for emotions. This may have implications for clinical situations, where emotional impairments are frequently observed among alcoholic subjects.

Successful treatment of alcohol withdrawal with trazodone.

Trazodone, a second generation antidepressant, is helpful in the treatment of lasting alcohol withdrawal symptoms, such as sleep disturbances and craving. We report a case suggesting that trazodone is also efficient for the treatment of the acute phase of alcohol withdrawal treatment. A 30-year-old male patient with severe alcohol withdrawal symptoms was successfully treated with an adjuvant administration of 600 mg trazodone per day, while he had remained symptomatic for several days under high doses of diazepam and clomethiazolum. Controlled trials with trazodone for this indication could be useful.

Non-epileptic seizures: delayed diagnosis in patients presenting with electroencephalographic (EEG) or clinical signs of epileptic seizures.

The clinical differentiation between epileptic seizures (ES) and non-epileptic seizures (NES) is often difficult and mostly based on the presence or absence of widely recognized features of ES such as tongue biting, falling, incontinence or concomitant epileptic abnormalities in the electroencephalogram (EEG). We retrospectively analysed the records of all patients referred to our Epilepsy Centre for refractory epilepsy and finally diagnosed with NES between 1980 and 1999 ( n= 103), half of them also exhibiting ES. The mean time-lapse between first attack and NES diagnosis was 8.7 +/- 1.3 years and 16.5 +/- 1.4 years for the NES and NES + ES groups respectively. At least one of the usual signs associated with generalized tonic-clonic seizures (tongue biting, falling or incontinence) was reported by 66% and 60% of patients with NES or NES + ES respectively. Interictal EEG abnormalities were recorded in 16% of NES patients vs. 80% of NES + ES patients. In the NES group, delay before establishing the correct diagnosis was significantly longer when the patients exhibited > or =1 symptom(s) of generalized seizures, or when patients exhibited interictal EEG abnormalities. Upon admission, 72% of NES patients and all NES + ES patients were being treated with antiepileptic drugs (AEDs).We conclude that EEG or clinical abnormalities suggestive of epileptic seizures are common in undiagnosed NES patients. Such diagnostic pitfalls, besides considerably delaying NES diagnosis, also considerably delay appropriate treatment implementation.