Midline Brain Abnormalities Across Psychotic and Mood Disorders.

Patients with schizophrenia are known to have increased prevalence of abnormalities in midline brain structures, such as a failure of the septum pellucidum to fuse (cavum septum pellucidum) and the absence of the adhesio interthalamica. This is the first study to investigate the prevalence of these abnormalities across a large multidiagnostic sample. Presence of cavum septum pellucidum and absence of the adhesio interthalamica was assessed in 639 patients with chronic schizophrenia, delusional disorder, schizoaffective disorder, bipolar disorder, major depressive disorder, or a first episode of psychosis, mania or unipolar depression. This was compared with 223 healthy controls using logistic-regression-derived odds ratios (OR). Patients with psychotic or mood disorders showed an increased prevalence of both abnormalities (OR of cavum septum pellucidum = 2.1, OR of absence of the adhesio interthalamica = 2.6, OR of both cavum septum pellucidum and absence of the adhesio interthalamica = 3.8, all P < .001). This increased prevalence was separately observed in nearly all disorders as well as after controlling for potential confounding factors. This study supports a general increased prevalence of midline brain abnormalities across mood and psychotic disorders. This nonspecificity may suggest that these disorders share a common neurodevelopmental etiology.

Eye movement desensitization and reprocessing therapy in subsyndromal bipolar patients with a history of traumatic events: a randomized, controlled pilot-study.

Traumatic events are frequent in bipolar patients and can worsen the course of the disease. Psychotherapeutic interventions for these events have not been studied so far. Twenty DSM-IV bipolar I and II patients with subsyndromal mood symptoms and a history of traumatic events were randomly assigned to Eye Movement Desensitization and Reprocessing therapy (n=10) or treatment as usual (n=10). The treatment group received between 14 and 18 Eye Movement Desensitization and Reprocessing sessions during 12 weeks. Evaluations of affective symptoms, symptoms of trauma and trauma impact were carried out by a blind rater at baseline, 2 weeks, 5 weeks, 8 weeks, 12 weeks and at 24 weeks follow-up. Patients in the treatment group showed a statistically significant improvement in depressive and hypomanic symptoms, symptoms of trauma and trauma impact compared to the treatment as usual group after intervention. This effect was only partly maintained in trauma impact at the 24 weeks follow-up visit. One patient dropped from Eye Movement Desensitization and Reprocessing group whereas four from the treatment as usual group. This pilot study suggests that Eye Movement Desensitization and Reprocessing therapy may be an effective and safe intervention to treat subsyndromal mood and trauma symptoms in traumatized bipolar patients.

EMDR therapy modulates the default mode network in a subsyndromal, traumatized bipolar patient.

BACKGROUND: Some functional imaging abnormalities found in bipolar disorder are state related, whereas others persist into euthymia. It is uncertain to what extent these latter changes may reflect continuing subsyndromal affective fluctuations and whether those can be modulated by therapeutic interventions. METHOD: We report functional magnetic resonance imaging (fMRI) findings during performance of the n-back working memory task in a bipolar patient who showed a marked improvement in subsyndromal affective symptoms after receiving eye movement desensitization and reprocessing (EMDR) therapy in the context of a clinical trial. RESULTS: The patient's clinical improvement was accompanied by marked changes in functional imaging, as compared to 30 healthy subjects. fMRI changes were noted particularly in deactivation, with failure of deactivation in the medial frontal cortex partially normalizing after treatment. CONCLUSIONS: This case supports the potential therapeutic overall benefit of EMDR in traumatized bipolar patients and suggests a possible neurobiological mechanism of action: normalization of default mode network dysfunction.