[Merycism : when humain being starts ruminating]. / Le mérycisme : quand l'être humain se met à ruminer.

Merycism is a rare and little-known functional gastrointestinal disorder. Indeed, the diagnosis is made, on average, with a delay of 21 to 77 months. This delay can lead to dramatic consequences for the patient such as significant weight loss, ionic imbalance and social isolation. Through a clinical situation, we evoke the difficulties and the particularities of the diagnosis of merycism as well as its management, in a situation evoking a disorder of the eating habits. This pathology can be found in various specialties such as general medicine, pediatrics, gastroenterology, endocrinology, dentistry, child psychiatry, psychiatry, neonatology services or maternity.

Le mérycisme est un trouble gastro-intestinal fonctionnel rare et méconnu. En effet, le diagnostic est posé, en moyenne, avec un retard de 21 à 77 mois. Ce retard peut entraîner des conséquences dramatiques pour le patient, comme une importante perte de poids, un déséquilibre ionique et un isolement social. Au travers d'une situation clinique, nous évoquons les difficultés et les particularités du diagnostic de mérycisme ainsi que sa prise en charge, dans un tableau évoquant un trouble des conduites alimentaires. Cette pathologie peut se rencontrer dans diverses spécialités comme la médecine générale, la pédiatrie, la gastro-entérologie, l'endocrinologie, la dentisterie, la pédopsychiatrie, la psychiatrie, les services de néonatologie ou encore à la maternité.

[Treatment of sensory information in neurodevelopmental disorders]. / Traitement de l'information sensorielle dans les troubles neurodéveloppementaux.

INTRODUCTION: The processing of information coming from the elementary sensory systems conditions the development and fulfilment of a child's abilities. A dysfunction in the sensory stimuli processing may generate behavioural patterns that might affect a child's learning capacities as well as his relational sphere. The DSM-5 recognizes the sensory abnormalities as part of the symptomatology of Autism Spectrum Disorders. However, similar features are observed in other neurodevelopmental disorders. Over the years, these conditions have been the subject of numerous controversies. Nowadays, they are all grouped together under the term of Neurodevelopmental Disorders in DSM-5. The semiology of these disorders is rich and complex due to the frequent presence of comorbidities and their impact on cognitive, behavioural, and sensorimotor organization but also on a child's personality, as well as his family, his school, or his social relationships. MATERIAL AND METHODS: We carried out a review of the literature on the alterations in the treatment of sensory information in ASD but also on the different neurodevelopmental clinical panels in order to show their impact on child development. FINDINGS: Atypical sensory profiles have been demonstrated in several neurodevelopmental clinical populations such as Autism Spectrum Disorder, Attention Deficit/Hyperactivity Disorders, Dysphasia and Intellectual Disability. CONCLUSION: Abnomalies in the processing of sensory information should be systematically evaluated in child developmental disorders.

INTRODUCTION: Le traitement des informations qui provient des systèmes sensoriels élémentaires conditionne le développement et l'épanouissement des aptitudes de l'enfant. Un dysfonctionnement du traitement des stimuli sensoriels peut engendrer des patterns comportementaux qui affectent les apprentissages et la sphère relationnelle. La nouvelle classification DSM-5 reconnaît les anomalies sensorielles comme faisant partie des symptômes des Troubles du Spectre Autistique (TSA). Toutefois, des particularités du même ordre sont observées dans d'autres troubles neurodéveloppementaux. Ceux-ci font l'objet de nombreuses controverses diagnostiques depuis de nombreuses années. Actuellement, ils sont regroupés sous le terme de troubles neurodéveloppementaux dans le DSM-5 (handicaps intellectuels, troubles de la communication, trouble du spectre de l'autisme, déficit de l'attention/ hyperactivité, trouble spécifique des apprentissages, troubles moteurs, autres troubles neurodéveloppementaux). La sémiologie de ces troubles est riche et complexe par la présence fréquente de comorbidités et par le retentissement des atteintes cognitives, comportementales et sensorimotrices sur l'organisation de la personnalité de l'enfant, mais aussi sur ses relations familiales, scolaires ou sociales. Matériel et Méthode : Nous avons réalisé une revue de littérature sur les altérations du traitement des informations sensorielles dans les TSA mais aussi dans les différents tableaux cliniques neurodéveloppementaux afin de montrer leur retentissement sur le développement de l'enfant. Résultats : Des profils sensoriels atypiques ont été mis en évidence dans plusieurs troubles neurodéveloppementaux tels que le TSA, les troubles de déficit de l'attention/hyperactivité, la dysphasie et le handicap intellectuel. CONCLUSION: Les anomalies de traitement de l'information sensorielle doivent être systématiquement évaluées en présence de troubles du développement chez l'enfant.

[Transition from child and adolescent to adult mental health care]. / La transition entre soins pédopsychiatriques et soins en psychiatrie adulte.

Adolescents and young adults are at particularly at-risk population in mental health. For a large majority of patients suffering from chronic psychiatric condition, the age of onset of psychiatric symptoms is less than 24 years, while the coverage in psychiatric care is the lowest between 16 and 24. Presenting a psychiatric pathology during childhood and adolescence constitutes an independent risk factor for the occurrence of adverse life events in adulthood. Furthermore, that population is at the edge between child and adolescent mental health services (CAMHS) and adult mental health services (AMHS). Transition is the deliberate and planned movement from CAMHS to AMHS. CAMHS and AMHS struggle to achieve optimal transitions between them. Many barriers exist at the interface of the two types of structure and some young people who require continuous care during this period do not have access to it. There are also too few specific psychiatric services for the population of adolescents and young adults. Some recommendations emerge to intend to guide practices, but the literature lacks data to better define this population and build guidelines about the transition between CAMHS and AMHS and about specific services for adolescents and young adults in psychiatry.

Les adolescents et jeunes adultes constituent une population particulièrement à risque en santé mentale. Pour une grande majorité des patients souffrant d'une pathologie psychiatrique chronique, l'âge d'apparition des symptômes est inférieur à 24 ans, alors que la couverture en soin psychiatrique est la plus faible entre 16 et 24 ans. La présence d'une pathologie psychiatrique durant l'enfance ou l'adolescence constitue un facteur de risque indépendant pour la survenue d'événements de vie défavorables à l'âge adulte. Cette population se situe par ailleurs à la lisière entre soins pédopsychiatriques et soins psychiatriques adultes. La transition est le passage délibéré et planifié d'un service de pédopsychiatrie vers un service de psychiatrie adulte. Ces deux systèmes de soins peinent à s'accorder pour réaliser des transitions optimales. De nombreuses barrières existent à l'interface des deux types de structures et certains jeunes qui nécessitent une prise en charge continue durant cette période de leur vie n'y ont pas accès. Il existe également trop peu de services psychiatriques pouvant accueillir cette population de manière spécifique. Certaines pistes émergent pour tenter de guider les pratiques, mais la littérature manque de données permettant de définir cette population et de créer des guidelines en ce qui concerne la transition entre pédopsychiatrie et psychiatrie adulte ainsi que la création de dispositifs psychiatriques spécifiques pour les adolescents et jeunes adultes en psychiatrie.

[Depression in adolescents and multiculturality : a multifactorial analysis of psychological suffering inside a family in crisis]. / Dépression chez l'adolescent et multiculturalité : analyse multifactorielle de la souffrance psychique au sein d'une famille en crise.

The complexity of depressive diagnosis and other forms of expression of psychological suffering during adolescence explain why particular caution is required. The medico-psycho-social determinants of teenager's mental health enjoin us to support a holistic analysis of these situations. Different analysis spectra - symptomatic, environnemental, anthropological, cultural - allow us to understand a situation at different levels of interpretation. As we will see through a clinical case examination, the difficulty of depressive diagnosis in a multicultural background is increased by the ethnocentrical aspect of this category.

La complexité des diagnostics de type dépressif et des modes d'expression de la souffrance psychique à l'adolescence nous invitent à la prudence. Les aspects médico-psycho-sociaux des déterminants de la santé mentale à l'adolescence nécessitent de privilégier une analyse la plus holistique et complète possible dans les situations rencontrées. Différentes grilles d'analyse - symptomatique, environnementale, anthropologique, culturelle - permettent de comprendre une même situation à plusieurs niveaux d'interprétation. Comme nous le verrons dans la discussion autour d'un cas clinique, la difficulté du diagnostic dépressif en milieu multiculturel est encore majorée par le caractère ethnocentrique de cette catégorie.

[Depression in childhood and adolescence]. / Dépression de l'enfant et de l'adolescent.

Child and adolescent depression is often unknown due to its varied and heterogeneous clinical presentation that makes the diagnosis complex. Indeed, it differs from adult depression by some aspects as the absence of depressive experience. It is a major risk factor for suicide, dropping out of school and social isolation. We will identify the specific clinical signs to make a diagnosis in children and adolescents and to identify therapeutic approaches. On the other hand, we will try to highlight the risk factors of depression.

La dépression de l'enfant et de l'adolescent est souvent méconnue en raison de sa présentation clinique variée et hétérogène qui rend le diagnostic complexe. En effet, elle se différencie de celle de l'adulte de par certains aspects dont le vécu dépressif qui est souvent absent. Elle est un facteur de risque majeur de suicide, de décrochage scolaire et d'isolement social. Nous allons dégager les signes cliniques spécifiques qui permettront de poser un diagnostic chez l'enfant et l'adolescent et de dégager des pistes thérapeutiques. D'autre part, nous essaierons de mettre en évidence les facteurs de risques de dépression.

[Bariatric surgery in adolescent with morbid obesity : what role for the child psychiatrist?] / Prise en charge chirurgicale de l'obésité morbide chez l'adolescent : quel rôle pour le pédopsychiatre ?

The prevalence of obesity has grown steadily in recent years, making it almost an epidemic. Obesity is a chronic condition whose prognosis is burdened by severe comorbidities. Both the quality of life and the life expectancy are affected. The medical management of morbid obesity is still the rule, but surgical practices are developing rapidly. While bariatric surgery in adults is common and gives excellent results, in adolescents, its practice is less prevalent. Beyond issues specific to this developmental period, this question raises ethical issues. In this context, the pluridiscplinary team faces diverse determinants and challenges and the child and adolescent psychiatrist (CAP) is, the psychiatrist is summoned for psychopathological aspects but also for embarrassing questions. In this work, we are going to specify the role of the CAP in the practice of bariatric surgery.

L'obésité dont la prévalence n'a cessé de croître ces dernières années, est en passe de devenir une véritable épidémie. Affection chronique, le pronostic de l'obésité morbide est grevé de co- morbidités sévères altérant la qualité de vie des patients et amputant leur espérance de vie. Les prises en charge diététique et médicale restent les plus répandues. Cependant, les pratiques chirurgicales n'ont cessé de se développer. Alors que la chirurgie bariatrique chez l'adulte est devenue courante, sa pratique chez l'adolescent est moins fréquente et se prête moins à la banalisation. Au-delà des enjeux développe- mentaux spécifiques à la période particulière qu'est l'adolescence, cette question soulève des considérations éthiques et suscite des positionnements extrêmes. Dans ce contexte aux déterminants flous et aux enjeux tant sociétaux que médicaux, le pédopsychiatre peut être convoqué, au-delà de la question psycho- pathologique, pour statuer sur des questions relevant plus de la morale que de la science. Nous nous attèlerons donc, au long de ce travail, à définir les différents objets de soins somatiques ou psychiques qui rassemblent les praticiens de différents bords au chevet de l'obésité et à expliciter la fonction psy dans ces prises en charge.

[Early detection of autism spectrum disorders]. / Détection précoce des troubles du spectre autistique.

The evaluation of the development of young children had to consider the possible detection of neurodevelopmental disorders in particular autism spectrum disorders. When a child of 18 months has a developmental language delay or a defect in social contact, the hypothesis of autism must be considered through a clinical evaluation. We will point out some clinical guidelines and some early signs to detect the trouble and to propose early treatment interventions. This will help to develop specific skills of the child aiming at influencing positively clinical evolution and reducing mental retardation.

L'évaluation du développement du jeune enfant doit prendre en compte la détection des troubles neurodéveloppementaux et notamment celle des troubles du spectre autistique. Face à un retard de développement du langage à 18 mois ou face à un défaut de contact social, cette hypothèse doit être considérée afin de réaliser une évaluation plus approfondie. Nous donnons quelques repères cliniques ainsi que les signes précurseurs afin de permettre le cas échéant une prise en charge la plus précoce possible. Ceci permettra souvent une évolution plus favorable avec l'objectif de réduire le déficit mental et de permettre le développement des compétences spécifiques de l'enfant.

[The contagion of adolescent suicide: cultural, ethical and psychosocial aspects]. / La contagion du suicide chez les adolescents: aspects culturels, éthiques et psychosociaux.

Suicide is the second leading cause of death among adolescents. The risk factors are many and varied. The contagion of suicide was raised as a potential cause of youth suicide. In support of this argument, we did a review of the literature on the possible contagion of adolescent suicide. Several types of situations can support this hypothesis : when a youth is faced with the suicide of a relative or close friend, when he lived in a community, through the media or via the Internet. The way suicide is reported in the press shows a correlation with increased incidence of suicide among adolescents. In summary, there is evidence increasingly obvious that the contagion is the source of some youth suicides. For this reason, it seems important that preventive measures are in place. However, although this mechanism has been instrumental in initiating the act, it is important to note that suicide is always the result of several factors including the personal history of the subject.

[Suicidal attempts in adolescents]. / Les tentatives de suicide chez les adolescents.

Adolescent suicidal attempts relates on average 1 teenager out of 10. Very often the suicidal attempt is not followed by an intervention of care. Parents and sometimes doctors do not proposed professional help because it does not represent a factor of lethal risk. However, the main major risk of suicidal attempt is suicidal repetition with a risk of suicide succeeds. We thus will consider prevention and detection factors of the suicidal risk in teenagers as well as strategies for medical and psychological help after a suicide attempts. We will then approach the various associated psychopathological factors.

Brain glucose metabolism in eating disorders assessed by positron emission tomography.

OBJECTIVE: As anorectic and bulimic patients present similar clinical and neurobiological symptoms, the purpose of this study was to compare brain glucose metabolism at rest in these patients. METHODS: Positron emission tomography with (18-F)-fluorodeoxyglucose was used to evaluate cerebral glucose metabolism (CMRglu) in 10 normal-weight bulimic women, in 10 underweight anorectic patients, and in 10 age- and sex-matched healthy volunteers. RESULTS: Absolute global cortical glucose activity was significantly lower in anorectic patients compared with bulimic and control subjects. Anorectic patients compared with normal control subjects also showed higher relative CMRglu in the inferior frontal cortex and in the basal ganglia, and putamen and caudate relative hypermetabolism when compared with bulimic patients. Thus, both eating disorder groups differed from control subjects in low relative parietal values of glucose. DISCUSSION: While absolute global metabolism seems to be related to weight loss, we can hypothesize either a common parietal cortex dysfunction in eating disorders or a particular sensitivity of this cortex to consequences of eating disturbances.

Brain hypometabolism of glucose in low-weight depressed patients and in anorectic patients: a consequence of starvation?

As low-weight anorectic patients presented a global as well as a regional absolute hypometabolism of glucose, we investigated a population of ten age- and sex-matched low-weight depressed patients without anorexia nervosa to evaluate the impact of weight loss on cerebral glucose metabolism evaluated by positron emission tomography and [18F]-fluorodeoxyglucose. Ten age- and sex-matched healthy volunteers were used as controls. Absolute global and regional glucose activity was significantly lower in anorectic and low weight depressed patients than in control subjects. Anorectic patients compared with normal control subjects also showed lower relative metabolism of glucose in the parietal cortex. Within patients, absolute hypometabolism of glucose seems to be a consequence of low-weight while there is a positive correlation between absolute metabolism of glucose and body mass index.

Brain glucose metabolism in anorexia nervosa and affective disorders: influence of weight loss or depressive symptomatology.

Relationships between eating and affective disorders remain complex and unclear. Brain glucose metabolism of anorectic patients has been demonstrated to be reduced both globally and regionally, with a particular relative hypometabolism in the parietal cortex. To explore the possible influence of weight loss or depressive symptomatology on brain metabolism, we studied age- and sex-matched low-weight anorectic and depressed patients, normal-weight depressed patients, and healthy volunteers. Absolute global and regional glucose activity levels were reduced in low-weight patients, with the lowest values being found for anorectic patients. In relative values, anorectic patients showed a significant parietal hypometabolism in comparison to control subjects while they had higher metabolism in the caudate nuclei when compared with the other groups. Absolute hypometabolism of glucose seems to be a consequence of low weight as it was found in both low-weight anorectic and low-weight depressive patients. In addition, absolute glucose values were significantly correlated with body mass index in all subjects. Future positron emission tomographic studies in psychiatric patients should control for alimentary parameters.

Brain hypometabolism of glucose in bulimia nervosa.

OBJECTIVE: A cerebral function lateralization has been described in bulimic patients in positron emission tomography (PET) studies realized during a specific cognitive task. The purpose of this study was to evaluate, at rest, brain glucose metabolism in patients with bulimia nervosa. METHOD: PET with (18-F)-fluorodeoxyglucose was used to evaluate cerebral glucose metabolism in 11 normal-weight bulimic girls compared to 11 age- and sex-matched healthy volunteers. Patients were diagnosed following DSM-IV and were off psychoactive medication. RESULTS: In comparison with control subjects, bulimic patients showed global and regional absolute hypometabolism of glucose. In relative values, only parietal cortex metabolism was significantly lower in bulimic patients. No correlation was found within groups for absolute or relative cerebral glucose metabolic rates (rCMRglu) and body mass index (BMI), anxiety scores, or Hamilton scores of depression. DISCUSSION: Since previous studies have demonstrated similar disturbances in anorectic patients, we hypothesized that these observations could be a consequence of neurobiological perturbations following nutritional deficiencies or a particular cerebral dysfunction in eating disorders.

Brain hypometabolism of glucose in anorexia nervosa: normalization after weight gain.

Using positron emission tomography and (18-F)-fluorodeoxyglucose, we studied cerebral glucose metabolism in 10 anorectic girls within their underweight state and after weight gain. Ten age- and sex-matched healthy volunteers were used as controls. Both groups were scanned during rest, eyes closed and with low ambient noise. In absolute values, the underweight anorectic patients, when compared to control subjects, showed a global (p = 0.002) and regional (p < or = 0.001) hypometabolism of glucose which normalized with weight gain. In relative values, no global difference could be assessed between underweight anorectic patients and controls but a trend can, nevertheless, be observed toward parietal and superior frontal cortex hypometabolism associated with a relative hypermetabolism in the caudate nuclei and in the inferior frontal cortex. After weight gain, all regions normalized for absolute and relative values, although a trend appears toward relative parietal hypometabolism and inferior frontal cortex hypermetabolism in weight gain anorectic patients. Absolute brain glucose hypometabolism might result from neuroendocrinological or morphological aspects of anorexia nervosa or might be the expression of altered neurotransmission following deficient nutritional state. As some differences exists in relative values in underweight patients and tend to persist in weight gain states, this could support a potential abnormal cerebral functioning, a different reaction to starvation within several regions of the brain or different restoration rates according to the region.

Altered frontostriatal relationship in unmedicated schizophrenic patients.

Positron emission tomography with [18F]-fluoro-2-deoxy-D-glucose as tracer was used to investigate frontal glucose metabolism in 15 unmedicated schizophrenic patients and 15 healthy subjects under resting conditions. Although no difference in absolute frontal cerebral metabolic rates of glucose (CMRglu) were found between schizophrenic patients and control subjects, relative measures significantly differentiated the two groups. Whole frontal metabolism and frontocaudate ratio were significantly decreased in both hemispheres in the patients. The results confirm the existence of hypofrontality in unmedicated schizophrenia and indicate disturbances in metabolic relationships between the frontal cortex and the striatum in this disorder.

Brain hypometabolism of glucose in anorexia nervosa: a PET scan study.

Cerebral glucose metabolism was studied in 20 underweight anorectic girls and in 10 age- and sex-matched healthy volunteers using positron emission tomography with (18-F)-fluorodeoxy-glucose. Both groups were scanned during rest, with eye closed and with low ambient noise. Compared to controls, the underweight anorectic group showed a global hypometabolism (p = .002) and an absolute (p < .001) as well as relative (p < .01) hypometabolism of glucose in cortical regions, with the most significant differences found in the frontal and the parietal cortices. Within the underweight anorectic and the control groups, no correlations were found between absolute or relative rCMRGlu and BMI, anxiety scores, or Hamilton scores of depression. Different factors might explain this reduction of glucose metabolism in anorexia nervosa. It might be the consequence of neurophysiological or morphological aspects of anorexia nervosa and/or the result of some associated symptoms such as anxiety or depressed feelings. Supported by cognitive studies, we can also hypothesize a primary corticocerebral dysfunctioning in anorexia nervosa.

Linkage analysis of bipolar illness with X-chromosome DNA markers: a susceptibility gene in Xq27-q28 cannot be excluded.

Transmission studies have supported the presence of a susceptibility gene for bipolar (BP) illness on the X-chromosome. Initial linkage studies with color blindness (CB), glucose-6-phosphate dehydrogenase (G6PD) deficiency, and the blood coagulation factor IX (F9) have suggested that a gene for BP illness is located in the Xq27-q28 region. We tested linkage with several DNA markers located in Xq27-q28 in 2 families, MAD3 and MAD4, that previously were linked to F9 and 7 newly ascertained families of BP probands. Linkage was also examined with the gene encoding the alpha 3 subunit of the gamma-amino butyric acid receptor (GABRA3), a candidate gene for BP illness located in this region. The genetic data were analyzed with the LOD score method using age-dependent penetrance of an autosomal dominant disease gene and narrow and broad clinical models. In MAD3 and MAD4 the multipoint LOD score data suggested a localization of a BPI gene again near F9. In the 7 new families the overall linkage data excluded the Xq27-q28 region. However, if the families were grouped according to their proband's phenotype BPI or BPII, a susceptibility gene for BPI disorder at the DXS52-F8 cluster could not be excluded.

Frontal and parietal metabolic disturbances in unipolar depression.

The authors investigated brain glucose utilization using positron emission tomography (PET) in 12 normal volunteers and 12 unipolar unmedicated depressed patients (six endogenous; six nonendogenous) following injection of [18F]fluoro-deoxyglucose (FDG). Compared by analyses of variance, absolute and relative regional glucose metabolic rates appeared different in depressed patients and control subjects, especially in parietal and frontal lobes. In patients with unipolar depression, metabolic rates were increased in the orbital part of the frontal lobe and decreased in a frontal dorsolateral area. The metabolic supero-basal gradient calculated in the frontal cortex was significantly lower in depressed patients than in normal subjects. Decreased glucose metabolism was also observed in the parietal cortex of depressed patients. No differences in glucose metabolic rates have been detected between endogenous and nonendogenous patients. No correlation has been found between the metabolic data and the Hamilton Rating Scale.

Nonlinkage of bipolar illness to tyrosine hydroxylase, tyrosinase, and D2 and D4 dopamine receptor genes on chromosome 11.

OBJECTIVE: Previous linkage and allelic association studies using DNA polymorphisms, cosegregation of cytogenetic abnormalities with psychiatric illness, and assignment of genes involved in neutotransmitter metabolism suggested that chromosome 11 may harbor a gene predisposing to bipolar illness. The authors examined linkage in the families of 14 probands with bipolar illness, with the candidate genes tyrosine hydroxylase (TH), D4 dopamine receptor (DRD4) at 11p15, tyrosinase (TYR) at 11q14-q21, and D2 dopamine receptor (DRD2) at 11q22-q23, as well as with the c-Harvey-ras oncogene (HRAS) and insulin gene (INS), both located at 11p15, a region that previously showed linkage to bipolar illness. METHOD: The genetic data were analyzed with both lod score analysis (parametric) and affected-sib-pair analysis (nonparametric); both narrow and broad definitions of the clinical phenotype were used. Further influences of diagnostic uncertainties were accounted for by using diagnostic probability classes weighing the stability of each phenotype. RESULTS: Two-point linkage results excluded close linkage of bipolar illness to each candidate gene; negative results were also obtained when the narrow definition of the clinical phenotype was used. Moreover, multipoint linkage analysis of HRAS and INS excluded the 11p15 region encompassing both DRD4 and TH. In agreement with the negative linkage results, affected-sib-pair analysis did not show preferential sharing of marker alleles at any of the candidate genes. CONCLUSIONS: The negative results obtained under different genetic models exclude a frequent role for DRD4, TH, TYR, and DRD2 in the pathogenesis of bipolar illness.