Full Syndrome Research Articles

No Reliable Evidence That Emotional Disorders Are Proximal Antecedents, Concomitants, or Short-Term Consequences of First Episode Alcohol Use Disorders in a Representative Community Sample.

Emotional disorders and alcohol use disorders (AUDs) frequently demonstrate significant 12-month and lifetime comorbid associations. This comorbidity has been incorporated into influential theories of addiction processes that posit direct or indirect causal associations between these disorder categories. There is currently no consensus, however, about the sequencing of these disorders. In this research, longitudinal data from a regionally representative community sample were used to evaluate whether emotional disorders constitute a proximal antecedent, concomitant, or short-term consequence of first episode (or index) AUDs. Participants were 131 persons with index AUD episodes lasting 12 months or more and 131 matched controls. For each participant with an AUD, the presence or absence of an emotional disorder was coded for three time intervals: (a) the 12 months preceding full syndrome AUD episode onset; (b) the last 12 months of the AUD episode; and (c) the 12 months following complete symptom AUD episode offset. These intervals, referenced to participant age, were matched to those of control participants, and emotional disorder rate comparisons subsequently performed both within and between groups. Findings indicated an absence of significant within- or between-subject differences in emotional disorder rates, suggesting that the association between AUDs and emotional disorders is neither directional nor systematic. There was also no indication that the length of the AUD episode increased risk for an emotional disorder in the year following AUD offset. Overall, this research suggests that emotional disorders are generally independent events in relation to the index AUD episode.

Differential Recruitment of Brain Regions During Response Inhibition in Children Prenatally Exposed to Alcohol.

Response inhibition is a distinct aspect of executive function that is frequently impaired in children with fetal alcohol spectrum disorders (FASD). We used a Go/NoGo (GNG) task in a functional MRI protocol to investigate differential activation of brain regions in the response inhibition network in children diagnosed with full or partial fetal alcohol syndrome (FAS/PFAS), compared with healthy controls. A rapid, event-related task with 120 Go and 60 NoGo trials was used to study children aged 8 to 12years-8 with FAS/PFAS, 17 controls. Letters were projected sequentially, with Go and NoGo trials randomly interspersed across the task. BOLD signal in the whole brain was contrasted for the correct NoGo minus correct Go trials between the FAS/PFAS and control groups. Compared to the FAS/PFAS group, controls showed greater activation of the inferior frontal and anterior cingulate network linked to response inhibition in typically developing children. By contrast, the FAS/PFAS group showed greater BOLD response in dorsolateral prefrontal cortex and other middle prefrontal regions, suggesting compensation for inefficient function of pathways that normally mediate inhibitory processing. All group differences were significant after control for potential confounding variables. None of the effects of prenatal alcohol exposure on activation of the regions associated with response inhibition were attributable to the effects of this exposure on IQ. This is the first FASD GNG study in which all participants in the exposed group met criteria for a diagnosis of full FAS or PFAS. Although FASD is frequently comorbid with attention deficit hyperactivity disorder, the pattern of brain activation seen in these disorders differs, suggesting that different neural pathways mediate response inhibition in FASD and that different interventions for FASD are, therefore, warranted.

The Role of Antipsychotic Medications in Metabolic Syndrome Amongst a Predisposed Population: Review of The Saudi Case

Kingdom of Saudi Arabia (KSA) is the largest (in terms of area) Arab state of Western Asia with population of a nearly 20 million. 22.4% of Saudi patients reporting to services for mental disorders are suffering from schizophrenia. Globally, claims have been raised over the role of atypical antipsychotics. They have been suggested to be related with noteworthy cardiometabolic risk, and with pharmacological events that may intercede that threat. Weight gain, increased risk for dyslipidemia, diabetes, obesity, accelerated cardiovascular ailment, and premature fatality have been associated to drugs in this category as well. Amisulpride, olanzapine, risperidone, clozapine, quetiapine are the most commonly used anti-schizophrenic medications in KSA with no previous studies reported to assess their unwanted side effects. Whereby, a recent study noticed that patients on antipsychotic medications in Saudi Arabia possess several risk factors. The need for detailed research on this matter is compounded by a metabolically undesirable postnatal and gestational environment, which is widespread in the KSA, adjoins to the receptiveness of the already genetically liable person to a lifetime of insulin resistance and associated morbidities. Moreover, the prevalence of conventional risk factors for diabetes mellitus type 2, such as the full metabolic syndrome (MetSy) and its individual symptoms and criteria, have been reported in adult Saudis, 37% of whom have the full MetSy. The published literature survey is suggestive of an urgent demographical analysis and epidemiological survey to ascertain number of individuals affected with schizophrenia, this will also paw the ways to formulate strategy to address various issues pertaining to structural adjustments in health care services provided to the mentally ill patients in KSA.

Eye movement as a biomarker of schizophrenia: Using an integrated eye movement score.

Studies have shown that eye movement abnormalities are possible neurophysiological biomarkers for schizophrenia. The aim of this study was to investigate the utility of eye movement abnormalities in identifying patients with schizophrenia from healthy controls. Eighty-five patients with schizophrenia and 252 healthy controls participated in this study. Eye movement measures were collected from free viewing, fixation stability, and smooth pursuit tests. In an objective and stepwise method, eye movement measures were extracted to create an integrated eye movement score. The discriminant analysis resulted in three eye movement measures; the scanpath length during the free viewing test, the horizontal position gain during the fast Lissajous paradigm of the smooth pursuit test, and the duration of fixations during the far distractor paradigm of the fixation stability test. An integrated score using these variables can distinguish patients with schizophrenia from healthy controls with 82% accuracy. The integrated score was correlated with Wechsler Adult Intelligence Scale-Third Edition full scale IQ, Positive and Negative Syndrome Scale scores, and chlorpromazine equivalents, with different correlation patterns in the three eye movement measures used. The discriminant analysis in subgroups matched for age, sex, years of education, and premorbid IQ revealed a sustained classification rate. We established an integrated eye movement score with high classification accuracy between patients with schizophrenia and healthy controls, although there was a significant effect of medication. This study provides further evidence of the utility of eye movement abnormalities in schizophrenia pathology and treatment.

Acute and chronic gregarisation are associated with distinct DNA methylation fingerprints in desert locusts.

Desert locusts (Schistocerca gregaria) show a dramatic form of socially induced phenotypic plasticity known as phase polyphenism. In the absence of conspecifics, locusts occur in a shy and cryptic solitarious phase. Crowding with conspecifics drives a behavioural transformation towards gregariousness that occurs within hours and is followed by changes in physiology, colouration and morphology, resulting in the full gregarious phase syndrome. We analysed methylation-sensitive amplified fragment length polymorphisms (MS-AFLP) to compare the effect of acute and chronic crowding on DNA methylation in the central nervous system. We find that crowd-reared and solitary-reared locusts show markedly different neural MS-AFLP fingerprints. However, crowding for a day resulted in neural MS-AFLP fingerprints that were clearly distinct from both crowd-reared and uncrowded solitary-reared locusts. Our results indicate that changes in DNA methylation associated with behavioural gregarisation proceed through intermediate states that are not simply partial realisations of the endpoint states.

Pulmonary surfactant protein adenosine triphosphate-binding-cassette-A3 gene composite mutations in infant congenital interstitial lung disease: report of a case and review of literature

6 cases died, and 6 cases survived, including 4 cases with pulmonary function disturbance to different degrees; 12 cases had ABCA3 gene mutations, 9 cases had composite ABCA3 gene mutations, in 11 cases the mutation occured in the exon of coding region, in 1 case in the intron, 9 cases had heterozygous mutations, 3 cases had homozygous mutations. Conclusion: The main phenotypes of ABCA3 mutation associated with ILD were full term neonatal respiratory distress syndrome or progressive tachypnea or dyspnea unexplained in infants. The chest HRCT showed two diffuse pulmonary interstitial changes. ABCA3 mutation mainly was multi-site composite mutations and heterozygous mutations in the exon of coding region.

The Impact of Blood Pressure and Visceral Adiposity on the Association of Serum Uric Acid With Albuminuria in Adults Without Full Metabolic Syndrome

The impact of metabolic phenotypes on the association of uricemia with urinary albumin/creatinine ratio (uACR) remains unresolved. We evaluated the association between serum uric acid and uACR in persons with 0, and 1-2 metabolic syndrome (MetS) components and determined the modification effects of visceral adiposity index (VAI), mean arterial pressure (MAP), and fasting glucose on this association. Using data from a cross-sectional survey of a representative Czech population aged 25-64 years (n = 3612), we analyzed 1,832 persons without decreased glomerular filtration rate <60ml/min/1.73 m2, diabetes, and MetS. MetS components were defined using the joint statement of the leading societies. Of the 1,832 selected participants, 64.1% (n = 1174) presented with 1-2 MetS components (age 46.3±11.2; men 51.7%), whereas 35.9% (n = 658) were free of any component (age 39.4±10.0; men 34.2 %). In fully adjusted multiple linear regression models for uricemia, uACR was an independent factor for increase in uric acid levels only in persons with 1-2 MetS components (standardized beta (Sβ) 0.048; P = 0.024); however, not in those without any component (Sβ 0.030; P = 0.264). Uric acid levels increased by the interaction of uACR with VAI (Sβ 0.06; P = 0.012), and of uACR with MAP (Sβ 0.05; P = 0.009). Finally, the association of uACR with uricemia was confined to persons whose VAI together with MAP were ≥the median of 1.35 and 98mm Hg, respectively (Sβ 0.190; P < 0.001). We demonstrated a strong modification effect of VAI and MAP on the association between uACR and uricemia, which suggests obesity-related hypertension as the underlying mechanism.

Steroid Metabolomic Disease Signature of Nonsyndromic Childhood Obesity.

The profile of urinary steroids as measured by gas chromatography-mass spectrometry defines a subject's "steroidal fingerprint." Here, we clustered steroidal fingerprints to characterize patients with nonsyndromic childhood obesity by "steroid metabolomic signatures." Nonsyndromic obesity is a symptom of different diseases and conditions, some of them will have their own signature. A total of 31 steroid metabolites were quantified by gas chromatography-mass spectrometry, and their excretion rates were z-transformed. Using MetaboAnalyst 3.0, we divided the subjects into 5 distinctive groups by k-means clustering. Steroidal fingerprints and clinical/biochemical data of patients in each cluster were analyzed. A total of 87 obese children (44 females), aged 8.5-17.9 years, were clinically characterized, and their 24-hour urine was collected. Cluster 1 (n = 39, 21 females) had normal steroid profile. Cluster 2 (n = 20, 11 females) showed mild, nonspecific elevation of C19 and C21 steroids, females' resistance to polycystic ovary morphology, and hirsutism. Cluster 3 (n = 7 female), with relative 21-hydroxylase insufficiency, was characterized by partial or full polycystic ovary syndrome. Cluster 4 (n = 4 males), showed markedly elevated C21 steroids and imbalance in the 11β-hydroxysteroid dehydrogenase system, higher insulin, increased frequency of glucose/insulin index more than 0.3, γ-glutamyl transpeptidase activity, systolic blood pressure, and tendency to liver steatosis. Cluster 5 (n = 17, 5 females) had elevated dehydroepiandrosterone and 17-OH-pregnenolone metabolites, suggesting 3β-hydroxysteroid dehydrogenase insufficiency but no clinically unique phenotype. Z-score body mass index values were not significantly different between the clusters. We defined a novel concept of disease-specific steroid metabolomic signature based on urinary steroidal gas chromatography-mass spectrometry. Clustering by software designed for metabolic data analysis reclassified childhood obesity into 5 groups with distinctive signatures; groups require further definition and may require cluster-specific therapeutic strategies.

Association of attention-deficit/hyperactivity disorder with gambling disorder.

Attention-deficit/hyperactivity disorder (ADHD) is a frequent mental disorder with childhood onset and high persistence into adulthood. There is much evidence that ADHD increases the risk for the development of other psychiatric disorders and functional problems in several domains of everyday life. In this study, the association of ADHD with gambling disorder (GD) was investigated. 163 adult subjects suffering from GD were examined for childhood and current ADHD according to DSM-5 as well as co-morbid psychiatric disorders. Moreover, characteristics of gambling behavior have been evaluated. The prevalence of lifetime ADHD was 28.8%, with 25.2% of the study population presenting ADHD as a full syndrome according to DSM-5. The prevalence of co-morbid substance use disorders and adjustment disorders and cluster B personality disorders was higher in GD patients with current ADHD than in the group without. Also, an increased rate of suicide attempts was detected in gamblers with ADHD. In contrast with gamblers without ADHD, those with ADHD were reported to spend more time with gambling, a sedative effect of gambling and a faster development of GD. The high prevalence of ADHD in patients with GD indicates that childhood ADHD is a risk factor for the development of GD in later life. Moreover, treatment of patients with GD and ADHD is complicated by a high rate of co-morbid disorders. Regarding therapeutic approaches, it should be considered that functional aspects of gambling differ in GD patients with and without ADHD.

White matter deficits mediate effects of prenatal alcohol exposure on cognitive development in childhood.

Fetal alcohol spectrum disorders comprise the spectrum of cognitive, behavioral, and neurological impairments caused by prenatal alcohol exposure (PAE). Diffusion tensor imaging (DTI) was performed on 54 children (age 10.1 ± 1.0 years) from the Cape Town Longitudinal Cohort, for whom detailed drinking histories obtained during pregnancy are available: 26 with full fetal alcohol syndrome (FAS) or partial FAS (PFAS), 15 nonsyndromal heavily exposed (HE), and 13 controls. Using voxelwise analyses, children with FAS/PFAS showed significantly lower fractional anisotropy (FA) in four white matter (WM) regions and higher mean diffusivity (MD) in seven; three regions of FA and MD differences (left inferior longitudinal fasciculus (ILF), splenium, and isthmus) overlapped, and the fourth FA cluster was located in the same WM bundle (right ILF) as an MD cluster. HE children showed lower FA and higher MD in a subset of these regions. Significant correlations were observed between three continuous alcohol measures and DTI values at cluster peaks, indicating that WM damage in several regions is dose dependent. Lower FA in the regions of interest was attributable primarily to increased radial diffusivity rather than decreased axonal diffusivity, suggesting poorer axon packing density and/or myelination. Multiple regression models indicated that this cortical WM impairment partially mediated adverse effects of PAE on information processing speed and eyeblink conditioning. Hum Brain Mapp 37:2943-2958, 2016. © 2016 Wiley Periodicals, Inc.

The Intersession Process in Psychotherapy for Anorexia Nervosa: Characteristics and Relation to Outcome.

The "inter session process" (ISP) is defined as therapy-related conscious thoughts, memories, and emotions that patients and therapists experience between psychotherapy sessions. It indicates how the participants process and use treatment. The main aim of this study is to describe the ISP characteristics of patients in outpatient treatment for anorexia nervosa (AN). An additional aim is to explore the relation between patients' ISP and treatment outcome. Patients taking part in a randomized controlled trial on outpatient psychotherapy for AN (ANTOP) filled in the Intersession Experience Questionnaire before each of the 40 psychotherapy sessions. Trajectories of different aspects of the ISP were analyzed with growth curve models based on orthogonal polynomials and tested for differences between 3 outcome categories (recovery, partially recovered, full syndrome AN). Data from 108 cases were available for analysis. ISP facets showed diverse, mostly nonlinear, trajectories over the course of treatment. Less favorable outcomes were associated with higher levels of patients' experiencing negative emotions when recalling therapeutic dialogue, thinking about therapy during dreaming/drowsy states, and applying therapeutic learning (in the second half of treatment). Findings confirm an overall relation between ISP and treatment outcome. In outpatient treatment in AN, patients with a less successful course seem to be more preoccupied with therapy and therapist between sessions. For the ISP facet "applying therapeutic learning," findings point to an optimal range dependent on treatment phase. Growth curve modeling is required to describe the nonlinear trajectories of ISP facets.

Thinking dimensional: prevalence of DSM-5 early adolescent full syndrome, partial and subthreshold eating disorders in a cross-sectional survey in German schools

ObjectivesInvestigating for the first time in Germany Diagnostic and Statistical Manual Fifth Edition (DSM-5) prevalences of adolescent full syndrome, Other Specified Feeding or Eating Disorder (OSFED), partial and subthreshold anorexia...

Early symptoms of nicotine dependence among adolescent waterpipe smokers

BackgroundAlthough waterpipe smoking is increasingly popular among youth and can lead to nicotine dependence (ND), no studies have documented how ND develops in waterpipe smokers. We examined the emerging symptoms...

Epileptogenesis in neurocutaneous disorders with focus in Sturge Weber syndrome.

Epilepsy is a major morbidity in Sturge Weber syndrome, a segmental vascular neurocutaneous disorder classically associated with facial angiomas, glaucoma, and leptomeningeal capillary-venous type vascular malformations. The extent of the latter correlates with neurological outcome. Post-zygotic mosaicism for the activating mutation p.R183Q of the GNAQ gene has been identified as the major cause. GNAQ encodes for an alpha subunit of a heterotrimeric G protein critical to blood vessel development. The earlier the timing of the mutation in development, the more severe the involvement, e.g. from isolated port-wine stains to the full syndrome. The strongest predictors of adverse outcomes are MRI and the presence of angiomas involving any part of the forehead, delineated inferiorly from the outer canthus of the eye to the top of the ear, and including the upper eyelid. The neurological course may be progressive and the typical constellation of symptoms is focal onset seizures, hemiparesis, headache, stroke-like episodes, behavior problems, intellectual disability, and visual field deficits. Antiseizure medications are effective in about half of patients. The presence of localized seizures, focal neurological deficits, and drug resistant epilepsy indicate epilepsy surgical evaluation. Earlier seizure onset, i.e. before six months of age, is associated with a more severe course with significant residual deficits. Factors contributing to epileptogenesis include decreased brain tissue perfusion due to abnormal venous drainage, anoxic injury contributing to cerebral calcification, breakdown of the blood-brain barrier, and the presence of developmental cortical malformations. Pre-symptomatic prophylactic treatment may be a future option to modify the course of the disease including the associated epileptogenesis.

Relation Between Obesity, Metabolic Syndrome, Successful Long-Term Weight Reduction, and Right Ventricular Function.

This study sought to examine the relationships between right ventricular (RV) function and geometry, morbid obesity with and without the metabolic syndrome, and the effect of long-term weight loss. Obese (n = 153, BMI 41.2 ± 8.7 kg/m(2)) and healthy non-obese control subjects (n = 38, BMI 25.5 ± 3.3 kg/m(2)) of similar age and gender distribution were prospectively studied during the course of a 1-year weight reduction program with echocardiography at baseline and after one year of follow up. Function and geometry of the right heart were evaluated by tricuspid annular plane systolic excursion (TAPSE), tricuspid annular systolic velocity (TDI S'), RV myocardial performance index (TEI), RV end-diastolic (RVEDD) and end-systolic diameter (RVESD), area of the right atrium (RAA), and systolic pulmonary artery pressure (PAP). Whereas parameters of systolic and diastolic LV function were significantly worse in the obese subjects than those in the non-obese subjects (EF 66 ± 6 versus 69 ± 6%, P = 0.004; E/E' 7.4 ± 2.5 versus 6.3 ± 2.6, P = 0.010), parameters of RV function (TAPSE 25.6 ± 4.5 versus 25.1 ± 3.5 mm, P = 0.528; TDI S' 13.5 ± 2.9 versus 13.8 ± 2.9 mm/second, P = 0.553; TEI 0.25 ± 0.13 versus 0.28 ± 0.09, P = 0.283) as well as geometry measurements were comparable between the obese and non-obese participants and also in obese subjects with full blown metabolic syndrome. Additionally, successful weight reduction did not alter the RV parameters. Nevertheless, in the few obese subjects with RV dysfunction (n = 7), metabolic syndrome parameters were more pronounced than in obese with normal RV function.Morbid obesity with and without the metabolic syndrome is accompanied by an impaired LV systolic and diastolic function. In contrast, RV function appears to be less affected by obesity independent of the presence of the metabolic syndrome.

Families are Under No Obligation to Put Their Children at Risk by Participating in the Corrupt Current US National Immunization Program

Families are Under No Obligation to Put Their Children at Risk by Participating in the Corrupt Current US National Immunization Program Ginger Taylor My name is Ginger Taylor, and I hold an MS in Clinical Counseling from Johns Hopkins University. I am the mother of a 14–year–old vaccine injured child with an autism diagnosis, and our family no longer participates in the vastly corrupt and broken US National Immunization Program. Because of my experiences, I have become a state and national leader on vaccine safety and vaccine choice issues, co–founding The Canary Party, and The Maine Coalition for Vaccine Choice. I have two sons, born in 2000 and 2002, and vaccinated them roughly according the the recommended schedule. My second son suffered what we now recognize as an adverse vaccine reaction to his first dose of the Hep B vaccine, but it was not recognized as such by either myself or his pediatricians at the time, so he continued to be vaccinated according to the CDC recommended schedule. Following his 18 month appointment, he suffered a severe neurological regression, displayed symptoms of GI distress, showed signs of an autoimmune condition, and was diagnosed with autism six months later. His was a text book case of vaccine induced encephalopathy, per the Health and Human Services (HHS), Human Resources and Services Administration (HRSA), Vaccine Injury Table established by the Vaccine Injury Compensation Program (VICP), displaying symptoms including: 1. A significant change in mental status that is not medication related; specifically a confusional state, or a delirium, or a psychosis; 2. A significantly decreased level of consciousness, which is independent of a seizure and cannot be attributed to the effects of medication; including: A. Decreased or absent response to environment (responds, if at all, only to loud voice or painful stimuli); [End Page 181] B. Decreased or absent eye contact (does not fix gaze upon family members or other individuals); or C. Inconsistent or absent responses to external stimuli (does not recognize familiar people or things). Please see http://www.hrsa.gov/vaccinecompensation/vaccineinjurytable.pdf for more info. Despite this, and despite my repeated attempts to have my son’s pediatrician investigate his condition as a vaccine reaction, no such inquiry was undertaken, and these symptoms were used instead to give him a diagnosis of autism. I would not read the VICP Vaccine Injury Table to learn that his were the symptoms of a well established vaccine injury for several years, and until after the three year statute of limitations had expired for me to file for compensation for his disability. After being abandoned by the mainstream medical system, we sought expensive, out of pocket, alternative medical care, which proved very fruitful for our son. Although we lost our home over the choice, we still would make the same decision, as it dramatically increased his health and functioning. We are pleased to report that, while he still has full syndrome autism, he has gone from severe to a much higher functioning level. Most importantly, he is a very happy child. Despite our earnest attempts, 12 years and four pediatricians later, we still cannot simply get him evaluated for this HHS established vaccine injury. Last year I filed a complaint against my own pediatrician with the state medical board, reporting that after multiple requests to evaluate my son for the condition, he had simply ignored my appeals as my previous pediatricians had. I asked the board to rule on whether or not my son had the right to an evaluation per an established standard of care, noting that if I had taken him to the doctor and reported that I believed he had a broken leg, their failure to assess him would constitute medical neglect. The board investigated the matter, but their ruling did not address the question of what the duty of the doctor is to a patient reporting vaccine adverse reactions, and simply gave a non sequitur response to close the case. Their action was a de facto ruling that no doctor has an obligation to investigate suspected vaccine injuries, and evidence that the medical establishment’s response to vaccine adverse reactions is systematized medical negligence. Our experience is...

Medication Use and Metabolic Syndrome Among Overweight/Obese Patients With and Without Binge-Eating Disorder in a Primary Care Sample.

To examine metabolic factors among overweight/obese individuals with binge-eating disorder (BED) and non-binge-eating overweight/obese (NBO) patients recruited from primary care and to examine and compare medication use by these groups. Participants were 102 adults recruited for a weight loss study within primary care centers who were assessed for BED (28 [38%] met DSM-5 BED criteria). Participants completed a medication log, had physiologic measurements taken, and were evaluated for the presence of metabolic syndrome using 2 methods. Data were collected between February 2012 and October 2012. The BED group had a higher mean body mass index (BMI), a higher pulse, and a larger waist circumference than the NBO group. Of the sample, 65% reported current medication use (prescription and/or over-the-counter medications): 19.6% took 3 to 4 medications and 15.7% took ≥ 5 medications. Aside from vitamin and over-the-counter allergy pill use, there were no differences in medication use between BED and NBO patients. Full metabolic syndrome (≥ 3 criteria met) was present in 31.5% of the sample when using objective measurement alone, and 39.1% of the sample when defined by objective measurement and pharmacologic management. No significant differences were observed regardless of definition. Despite higher BMI, pulse, and waist circumference, the current sample of BED patients in primary care did not present with poorer metabolic health than NBO patients.

Somatostatin-Immunoreactive Pancreaticoduodenal Neuroendocrine Neoplasms: Twenty-Three Cases Evaluated according to the WHO 2010 Classification

Background/Objective: Neuroendocrine neoplasms of the pancreas and duodenum with predominant or exclusive immunoreactivity for somatostatin (pdSOMs) are rare, and knowledge about tumour biology, treatment, survival and prognostic factors is limited. This study aims to describe clinical, pathological and biochemical features as well as treatment and prognosis of pdSOMs. Design: Twenty-three patients with pdSOM (9 duodenal, 12 pancreatic and 2 unknown primary tumours) were identified from our prospective neuroendocrine tumour database, and data according to the study aims were recorded. Results: Among the 9 patients with duodenal SOM, the male/female ratio was 4/5. All males and 1 female had neurofibromatosis type 1. Seven patients had stage 1A/B and 2 had stage 2B disease. The Ki-67 index was 1-5% (median 2%). Plasma somatostatin was elevated in the patients with 2B disease. Of the 14 patients with pancreatic SOM or an unknown primary tumour, the male/female ratio was 2/12. One male had multiple endocrine neoplasia type 1. Five had stage 1A/2B and 9 had stage 4. The Ki-67 index was 1-40% (median 7%). Plasma somatostatin was elevated in 7 patients. Patients reported symptoms related to the somatostatinoma syndrome, but none fulfilled the criteria for a full syndrome. Primary tumour in the pancreas, metastatic disease at diagnosis and higher tumour grade were all associated with significantly poorer survival. Conclusion: None of the patients with pdSOM presented with the full somatostatinoma syndrome. Prognostic factors are localisation of the primary tumour, dissemination and tumour grade. A Ki-67 index of 5% may discriminate the course of the disease.

Dépression mixte et DSM-5 : mise au point critique

Mixed depression is a depressive syndrome characterized by the presence, along with the typical depressive symptoms of depression, of those of over activation and excitation. If sometimes this activation is expressed by classical hypomanic symptoms, it is often observed by means of more subtle expression: inner tension, crowded thoughts, dramatic expression suffering, and unproductive agitation. It is important to identify mixed depression because such patients are particularly at risk of suicidal behaviors, substance abuse and therapeutic resistance. Even if therapeutic strategies continue to be discussed, treatments should rely on mood stabilizers and antipsychotics instead of antidepressants as in pure depression. Even though the concept of mixed depression has been described for more than twenty years, first by Koukopoulos and then by other authors, it had been little studied, especially because it did not appear in international psychiatric classifications. The DSM-IV supported a very narrow conception of the mixed states because the criteria required simultaneous full manic and full depressive syndromes, corresponding only to some dysphoric manias. The recently published DSM-5proposes modifications in mood and bipolar disorder classifications, and especially introduces the possibility to specify depressive and manic episodes with "mixed features". To diagnose depression with mixed features, a full depressive syndrome has to be present together most of time with three hypomanic symptoms, except symptoms that are considered as overlapping (that can be observed either in mania or in depression), i.e. agitation, irritability and distractibility. Critical analysis of DSM criteria and review of literature. We first analyzed the clinical relevance of the definition of depression with mixed features which could correspond to mixed depression. The problem is that the hypomanic symptoms allowed by the manual lead to symptom associations that are rather illogical (as euphoria with depression) or improbable (as increased or excessive involvement in activities that have a high potential for painful consequences). Also, some more specific symptoms that can be observed in mixed depression are not mentioned (such as hypersensitivity to light or noise, absence of motor retardation, dramatic expressivity of suffering). The DSM-5, as did DSM-IV, refers to an understanding of mixed depression as a simple addition of depressive and manic symptoms. The classification does not take into account that the symptoms could be rather different from hypomania, as the expression of an overactive thought in a depressed mind. Secondly, we reviewed cohort studies using the DSM-5criteria (or similar criteria with the exclusion of overlapping symptoms), and as a consequence of the poorly defined symptoms, we found that the diagnosis of mixed depression according to DSM-5is almost impossible, either in unipolar or in bipolar depression. We think, with others, that the definition of the mixed depression by the DSM-5is not clinically relevant and misses important information about the concept. Clinicians can be attentive to the identification of mixed character in depression, even if DSM-5criteria are not fully met. Unfortunately, the DSM-5definition could undermine research efforts for a better understanding of epidemiology, phenomenology and therapeutics of mixed depression. We propose and discuss alternative solutions for defining mixed depression, such as the absence of exclusion of "overlapping" symptoms, a more insighted phenomenology, or a dimensional approach.

High prevalence of posttraumatic stress in patients with primary hypertension.

Posttraumatic stress disorder (PTSD) is associated with a higher rate of arterial hypertension. However, data about prevalence rates of PTSD in patients suffering from arterial hypertension as well as the relation to blood pressure (BP) control are lacking. We recruited 145 patients with primary hypertension from March to November 2012 at the cardiologic outpatient clinic at Ulm University Medical Center. Symptoms of PTSD (assessed with the Posttraumatic Diagnostic Scale), perceived stress (Perceived Stress Scale; Trier Inventory for Chronic Stress), depression and anxiety (Hospital Anxiety and Depression Scale) were assessed by self-report. Office BP was measured and medical data were collected. Criteria for a full PTSD syndrome were met by 13 patients (9%). Posttraumatic stress was higher in the group of patients with controlled (M=10.9, S.D.=9.8) than in those with uncontrolled hypertension (M=3.9, S.D.=5.4; P<.001). In linear regression, only status of hypertension control (beta=.39, P<.001) predicted posttraumatic stress significantly, even after controlling for important cofactors. PTSD is highly prevalent in hypertensive patients, especially in those with controlled hypertension. An explaining mechanism could be the higher use of health care by patients suffering from PTSD. The mental needs of these patients should be focused in addition to the well-established somatic care.