BackgroundDespite the devastating impact of anxiety disorders (ADs) worldwide, long-lasting debates on causes and remedies have not solved the clinician’s puzzle: who should be treated and how? Psychiatric classifications conceptualize ADs as distinct entities, with strong support from neuroscience fields. Yet, comorbidity and pharmacological response suggest a single “serotonin dysfunction” dimension. Whether AD is one or several disorders goes beyond academic quarrels, and the distinction has therapeutic relevance. Addressing the underlying dysfunctions should improve treatment response. By its own nature, neurophysiology can be the best tool to address dysfunctional processes.PurposeTo search for neurophysiological dysfunctions and differences among panic disorder (PD), agoraphobia-social-specific phobia, obsessive–compulsive disorder (OCD) and generalized anxiety disorder.MethodsA sample population of 192 unmedicated patients and 30 aged-matched controls partook in this study. Hypothesis-related neurophysiological variables were combined into ten independent factors: 1) dysrhythmic patterns, 2) delta, 3) theta, 4) alpha, 5) beta (whole-head absolute power z-scores), 6) event-related potential (ERP) combined latency, 7) ERP combined amplitude (z-scores), 8) magnitude, 9) site, and 10) site of hyperactive networks. Combining single variables into representative factors was necessary because, as in all real-life phenomena, the complexity of interactive processes cannot be addressed through single variables and the multiplicity of potentially implicated variables would demand an extremely large sample size for statistical analysis.ResultsThe nonparametric analysis correctly classified 81% of the sample. Dysrhythmic patterns, decreased delta, and increased beta differentiated AD from controls. Shorter ERP latencies were found in several individual patients, mostly from the OCD group. Hyperactivities were found at the right frontorbital-striatal network in OCD and at the panic circuit in PD.ConclusionsOur findings support diffuse cortical instability in AD in general, with individual differences in information processing deficits and regional hyperactivities in OCD and PD. Study limitations and the rationale behind the variable selection and combination strategy will be discussed before addressing the therapeutic implications of our findings.

If behavior results from brain function, some evidence of dysfunction could be expected in children with major behavioral problems. Yet, neurophysiologic studies in these children are frequently normal. We hypothesized a relationship between maturational asymmetry and behavior, given the role of hemispheric imbalance in adult psychopathology. The purpose of this study was to investigate whether age-sensitive neurophysiologic measures could identify behaviorally relevant maturational asymmetries in otherwise healthy children. Ninety-five children were studied; reasons for testing were behavioral (19), academic (12), medical nonneurologic (16), and mixed (28), along with 20 control subjects. Academic, behavioral (Child Behavioral Checklist), and psychometric (Wechsler Intelligence Scale for Children-Revised; WISC-R) measures were analyzed in relation to four neurophysiologic parameters: P300 Latency, P300 Latency Asymmetry, Maturational Z-score, and Maturational Z-score Asymmetry, within a canonical design. The highest correlation was behavior with Maturational Z-score Asymmetry. Academic scores were predicted by the three-variable interaction of P300 Latency,Maturational Z-score, and Maturational Z-score Asymmetry. We concluded that behavior was strongly influenced by maturational asymmetry, while academic performance depended on both global maturation and maturational asymmetry. Our results suggest that behavioral disturbances can have a neural substrate despite apparently normal electroencephalograms (EEGs) and event-related potentials (ERPs). They open the possibility for specific therapeutic interventions to improve behavior and performance, and, perhaps, prevent major psychopathology in later life.

Los Trastornos de la Conducta Alimentaria (TCA) son problemas relevantes de salud mental que afectan principalmente a mujeres adolescentes y jóvenes. En su etiología convergen factores biológicos, psicológicos y sociales y por lo tanto, el tratamiento debe considerar esta multicausalidad. La enfermera de Salud Mental tiene un papel fundamental mediante la actuación sobre los factores de riesgo y así prevenir la enfermedad. La insatisfacción corporal constituye un importante factor de riesgo y de mantenimiento de las patologías alimentarias. Las influencias socioculturales (sobre todo los medios de comunicación, familia y compañeros) contribuyen al desarrollo de la insatisfacción y, en consecuencia, aumentar la probabilidad de trastornos de la alimentación. El objetivo es demostrar la eficacia de intervenciones grupales para mejorar la imagen corporal, la autoestima, la alfabetización mediática y otros factores que influyen en comportamientos y actitudes relacionados con la alimentación y poder prevenir la aparición de Trastornos de la conducta alimentaria en adolescentes de entre 13 y 15 años mediante un estudio pre/post.

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