Wissam El Hage

Cognitive inhibition and working memory in unipolar depression.

BACKGROUND Over the past decade, evidence has accumulated to suggest that people suffering from Major Depressive Disorder (MDD) present impairment in attention, working memory, executive function, including cognitive inhibition, problem- and task-planning. The aim of the current study was to assess inhibitory mechanisms within working memory with emotionally neutral material in a group of patients suffering from MDD. We hypothesized that impairment in cognitive inhibition is global and not only due to the emotional valence of the stimuli employed for the tasks. METHODS Twenty patients with MDD (DSM-IV) and 20 healthy controls were recruited. To assess cognitive inhibition, we used neutral material, in the form of the Prose Distraction Task (PDT) (Connelly SL, 1991), Trail Making Test (TMT), Modified Card Sorting Test (MCST), Rule Shift Cards (RSC), Stroop test and Hayling Sentence Completion test (HSC). The Modified 6 elements test, the Brixton Spatial Anticipation test, the dual task performance and the verbal fluencies test were also used to assess other executive function such as flexibility, planning tasks and memory. RESULTS Individuals with depression showed impairment in cognitive inhibition. They made more errors on the PDT, alongside slower response times. Slower response times were also observed on the Stroop, TMT and RSC. The MDD group made more errors in HSC and performed worse than controls in the semantic part of verbal fluency and Modified 6 elements tasks. The impairment of access function was significantly associated with the level of depression. CONCLUSION Depressed patients showed inability to inhibit neutral information access to working memory, restrain and delete irrelevant information. This impairment in cognitive inhibition could underlie cognitive slowness and attentional deficits in depression.

Olfaction: A potential cognitive marker of psychiatric disorders

Cognitive deficits are well documented in psychiatric disorders, particularly in schizophrenia and depression. Cognitive activity roots in perceptions. However, research on sensorial alterations in psychiatric conditions has mainly focused on visual or auditory processes and less on olfaction. Here, we examine data on olfactory deficits in psychiatric patients using a systematic review of recent publications. Schizophrenic patients are mainly characterized by no reliable change in odour sensitivity and by a deficit in odour identification, recognition and discrimination. Depressed patients principally exhibit a deficit in the hedonic aspects of this perception, even if, in some case, alterations in sensitivity or identification are also found. Changes in odour perception are also found in dementia and in some neurodegenerative disease, but in this case alterations concern all aspects of the sensorial experience (detection threshold, identification and recognition). Taken together, these data indicate that olfactory abnormalities might be a marker of psychiatric conditions, with a specific pattern for each disease.

Behavioral and neurochemical changes following predatory stress in mice.

This article had several objectives. First it aimed at investigating the anxiogenic-like behaviors elicited by unavoidable cat exposure and/or cat odor across nine strains of mice (BALB/c, C57BL/6, C3H, CBA, DBA/2, NMRI, NZB, SJL, Swiss) in a modified version of the free-exploration test. The second objective was to investigate possible neurochemical changes following cat exposure in Swiss mice by measuring the turnover of dopamine (DA), noradrenaline (NA) and serotonin (5-HT) in several brain regions known to be involved in the modulation of emotional processes (hippocampus, hypothalamus and striatum). Finally, the third objective was to examine the effects of anxiolytic drug treatments on the anxiogenic responses elicited by a cat odor (i.e. a feces) in Swiss mice previously exposed to a cat using the free-exploration test. Results from the strain comparison showed that mice could be divided into three distinct groups: two non-reactive strains (NZB and SJL) which were relatively insensitive to predatory exposure and/or odor; five intermediate-reactive strains (Swiss, NMRI, CBA, C3H and BALB/c) which displayed clear anxiogenic-like responses only when exposed to both cat and, subsequently, to feces; and two high reactive strains (C57BL/6 and DBA/2) which showed anxiogenic-like reactions following cat exposure, regardless of the stimulus (clay or feces) present in the free-exploration cage. Neurochemical data revealed that, while brain levels of NA, DA, 5-HT in cat exposed Swiss mice were not significantly different from those of control animals, turnover rates of these monoamines were increased in the hippocampus (NA and 5-HT), hypothalamus and striatum (DA) after cat exposure. Results from pharmacological experiments indicated that repeated administration of the 5-HT reuptake inhibitor fluoxetine (5-20 mg/kg, twice a day, for 5 days) completely abolished avoidance of the cat feces in Swiss mice previously exposed to the predator. Neither acute nor repeated administration of the classical anxiolytic diazepam was able to reduce avoidance behavior of the anxiogenic stimulus in the free-exploration test. Taken together, these findings indicate that the exposure of mice to unavoidable predatory stimuli is associated with behavioral and neurochemical changes consistent with increased anxiety.

Preserved subcortical volumes and cortical thickness in women with sexual abuse-related PTSD

Posttraumatic stress disorder (PTSD) has been frequently associated with volumetric reductions of grey matter structures (e.g. hippocampus and anterior cingulate), but these results remain controversial, especially in female non-combat-related samples. The present study aimed at exploring whole-brain structures in women with sexual abuse-related PTSD on the basis of cortical and subcortical structure comparisons to a matched pair sample that was well-controlled. Seventeen young women who had experienced sexual abuse and who had a diagnosis of chronic PTSD based on the Clinician Administered PTSD Scale for DSM-IV and 17 healthy controls individually matched for age and years of education were consecutively recruited. Both groups underwent structural magnetic resonance imaging and psychiatric assessment of the main disorders according to Axis I of DSM-IV. The resulting scans were analyzed using automated cortical and subcortical volumetric quantifications. Compared with controls, PTSD subjects displayed normal global and regional brain volumes and cortical thicknesses. Our results indicate preserved subcortical volumes and cortical thickness in a sample of female survivors of sexual abuse with PTSD. The authors discuss potential differences between neural mechanisms of sexual abuse-related PTSD and war-related PTSD.

Long-term impaired memory following predatory stress in mice

Brief exposure of mice to unavoidable predatory stimuli is associated with behavioral and neurochemical changes consistent with increased anxiety and produces short-term impaired learning restored by acute fluoxetine treatment, but not by diazepam. The present study investigated long-lasting changes induced by a unique unavoidable cat exposure in BALB/c mice on learning abilities using learning tests (radial maze, spatial configuration of objects recognition test). Results from the group comparison showed that predatory exposure induced significant learning disabilities in the radial maze (16 to 22 days poststressor) and in the spatial configuration of objects recognition test (26 to 28 days poststressor). These findings indicate that memory impairments may persist for extended periods beyond a predatory stress. This animal model of unique exposure of mice to unavoidable predatory stimuli has proven to be a useful model for the study of reactions to traumatic stress.

Impaired memory following predatory stress in mice is improved by fluoxetine

The first purpose of the present study was to investigate possible effects of predatory stress (i.e., 5-min cat exposure) on short-term learning abilities in Swiss mice using the object recognition test (ORT). The second aim was to evaluate the effects of anxiolytics (i.e., diazepam and fluoxetine) on learning/memory abilities in the ORT following predatory stress. Results showed that predatory exposure impaired learning and produced amnesia of acquired information or impairment to retrieve learned information (48 and 96 h poststressor). The learning impairment in the ORT in stressed mice was restored by acute fluoxetine treatment, but not by diazepam that instead affected learning in nonstressed animals. Taken together, these findings indicate that this animal model of exposure of mice to unavoidable predatory stimuli produces early cognitive changes analogous to those seen in patients with acute stress disorder (ASD).

PTSD psychiatric patients exhibit a deficit in remembering.

This study investigated the effects of PTSD on levels of awareness in a recognition memory task. A group of PTSD psychiatric patients and a control group without any traumatic experience were compared in remembering (R) versus knowing (K) recognition using non-trauma-related words. Results showed that overall recognition did not differ between the two groups, but in the PTSD group a significantly different pattern of Remember and Know responses was produced, indicating a shift from remembering to knowing. However, this shift from remembering to knowing in individuals with PTSD is associated with modifications in the trait anxiety level. These results are interpreted within theoretical frameworks in which R responses could be associated with distinctiveness (Rajaram, 1996) and conceptual processing (Ehlers & Clark, 2000). These collective findings would suggest the possibility that a poor general ability in the formation of source memory may eventually be a common characteristic across different types of PTSD.

Obsessive compulsive disorder in a patient with twiddler's syndrome.

Twiddlers or twist syndrome is the twisting of pulse generators around themselves. It may result from mechanical manipulation that can induce the malfunction of the device. In this case, twiddlers syndrome resulted from compulsive checking of the device. The implantable cardioverter‐defibrillator (ICD) triggered the development of an obsessive compulsive disorder (OCD). Two invasive procedures were required to replace the ICD. Psychiatric intervention prevented the recurrence of twiddlers syndrome in this patient for more than 2 years. We believe that preimplant psychiatric assessment should be the rule.

Olfactory and gustatory functions in bipolar disorders: A systematic review

HIGHLIGHTSPatients with bipolar disorder present with several olfactory and gustatory dysfunctions.Dysfunction in olfactory identification may be potential marker for bipolar disorder.Olfactory acuity is associated with psychosocial and cognitive performances in bipolar disorder.Bipolar patients have more gustatory dysfunction than non‐bipolar depressed patients and controls. ABSTRACT Olfactory and gustatory dysfunctions have been described in different psychiatric disorders. Several studies have found gustatory and olfactory function change in bipolar disorders with various results. The aim of this study is to have a systematic review of studies evaluating gustatory and olfactory function in bipolar disorders. After a systematic search, 15 studies on olfaction and 5 studies on taste were included in this review. The UPSIT (University of Pennsylvania Smell Identification Test) and Sniffin’ Sticks were the most widely used tests to evaluate smell. Some studies on olfaction described dysfunctions in smell identification as potential markers for bipolar disorders. Moreover, olfactory acuity was associated with psychosocial and cognitive performances. For taste, only few studies used standardized tests to evaluate gustation. These studies showed that patients with Bipolar disorders had more gustatory dysfunction compared to controls, and to non‐bipolar depressed patients.

e-PTSD: an overview on how new technologies can improve prediction and assessment of Posttraumatic Stress Disorder (PTSD)

ABSTRACT Background: New technologies may profoundly change our way of understanding psychiatric disorders including posttraumatic stress disorder (PTSD). Imaging and biomarkers, along with technological and medical informatics developments, might provide an answer regarding at-risk patient’s identification. Recent advances in the concept of ‘digital phenotype’, which refers to the capture of characteristics of a psychiatric disorder by computerized measurement tools, is one paradigmatic example. Objective: The impact of the new technologies on health professionals practice in PTSD care remains to be determined. The recent evolutions could disrupt the clinical practices and practitioners in their beliefs, ethics and representations, going as far as questioning their professional culture. In the present paper, we conducted an extensive search to highlight the articles which reflect the potential of these new technologies. Method: We conducted an overview by querying PubMed database with the terms [PTSD] [Posttraumatic stress disorder] AND [Computer] OR [Computerized] OR [Mobile] OR [Automatic] OR [Automated] OR [Machine learning] OR [Sensor] OR [Heart rate variability] OR [HRV] OR [actigraphy] OR [actimetry] OR [digital] OR [motion] OR [temperature] OR [virtual reality]. Results: We summarized the synthesized literature in two categories: prediction and assessment (including diagnostic, screening and monitoring). Two independent reviewers screened, extracted data and quality appraised the sources. Results were synthesized narratively. Conclusions: This overview shows that many studies are underway allowing researchers to start building a PTSD digital phenotype using passive data obtained by biometric sensors. Active data obtained from Ecological Momentary Assessment (EMA) could allow clinicians to assess PTSD patients. The place of connected objects, Artificial Intelligence and remote monitoring of patients with psychiatric pathology remains to be defined. These tools must be explained and adapted to the different profiles of physicians and patients. The involvement of patients, caregivers and health professionals is essential to the design and evaluation of these new tools.