Pretreatment anterior cingulate activity predicts antidepressant treatment response in major depressive episodes.

Major depressive disorder leads to substantial individual and socioeconomic costs. Despite the ongoing efforts to improve the treatment for this condition, a trial-and-error approach until an individually effective treatment is established still dominates clinical practice. Searching for clinically useful treatment response predictors is one of the most promising strategies to change this quandary therapeutic situation. This study evaluated the predictive value of a biological and a clinical predictor, as well as a combination of both. Pretreatment EEGs of 31 patients with a major depressive episode were analyzed with neuroelectric brain imaging technique to assess cerebral oscillations related to treatment response. Early improvement of symptoms served as a clinical predictor. Treatment response was assessed after 4 weeks of antidepressant treatment. Responders showed more slow-frequency power in the right anterior cingulate cortex compared to non-responders. Slow-frequency power in this region was found to predict response with good sensitivity (82 %) and specificity (100 %), while early improvement showed lower accuracy (73 % sensitivity and 65 % specificity). Combining both parameters did not further improve predictive accuracy. Pretreatment activity within the anterior cingulate cortex is related to antidepressive treatment response. Our results support the search for biological treatment response predictors using electric brain activity. This technique is advantageous due to its low individual and socioeconomic burden. The benefits of combining both, a clinically and a biologically based predictor, should be further evaluated using larger sample sizes.

Delusions and the role of beliefs in perceptual inference.

Delusions are unfounded yet tenacious beliefs and a symptom of psychotic disorder. Varying degrees of delusional ideation are also found in the healthy population. Here, we empirically validated a neurocognitive model that explains both the formation and the persistence of delusional beliefs in terms of altered perceptual inference. In a combined behavioral and functional neuroimaging study in healthy participants, we used ambiguous visual stimulation to probe the relationship between delusion-proneness and the effect of learned predictions on perception. Delusional ideation was associated with less perceptual stability, but a stronger belief-induced bias on perception, paralleled by enhanced functional connectivity between frontal areas that encoded beliefs and sensory areas that encoded perception. These findings suggest that weakened lower-level predictions that result in perceptual instability are implicated in the emergence of delusional beliefs. In contrast, stronger higher-level predictions that sculpt perception into conformity with beliefs might contribute to the tenacious persistence of delusional beliefs.

Cannabis induces different cognitive changes in schizophrenic patients and in healthy controls.

It is known that 60 to 80% of schizophrenic patients show deficits in cognition. There may be an increase in these deficits as a result of additional regular use of cannabis. The aim of the study was to evaluate the effect of chronic cannabis consumption on the cognitive functions of schizophrenic patients and healthy control subjects after a minimum abstinence time of 28 days. The study sample consisted of 39 schizophrenics (19 cannabis-abusers and 20 non-abusers) and 39 healthy controls (18 cannabis-abusers, 21 non-abusers). In a 2x2-factorial design (Diagnostic Groups [healthy controls, schizophrenic patients]xCannabis abuse [without, with]) with diagnostic group and cannabis consumption considered between-subject factors) we tested the hypothesis that dually diagnosed patients (i.e. suffering both from schizophrenia and cannabis abuse) perform worse in neuropsychological tests than schizophrenic patients without cannabis abuse. On the whole, schizophrenic patients performed worse than healthy control subjects. Surprisingly, rather than deteriorating neuropsychological performance, regular cannabis abuse prior to the first psychotic episode improved cognition in some tests. This was even more pronounced when regular consumption started before the age of 17. On the other hand, cannabis use deteriorated test performance in healthy controls, especially in cases when regular consumption started before the age of 17. To sum up, regular cannabis abuse has a different effect on cognitive function in schizophrenic patients and healthy controls.

Differential impact of heavy cannabis use on sensory gating in schizophrenic patients and otherwise healthy controls.

Cannabis abuse may precipitate the onset of schizophrenia and a dysfunction of the endocannabinoid system may be involved in the pathology of schizophrenia. Nevertheless, only few studies have addressed the neurobiological consequences of cannabis abuse for the development and course of schizophrenia. We measured the long-term effect of chronic cannabis abuse on the inhibitory function of the brain by the auditory P50 sensory gating in schizophrenic (n=15) and otherwise healthy chronic cannabis abusers (i.e. cannabis controls; n=11) and compared it to that of schizophrenic patients (n=12) and healthy controls (n=18) without cannabis or other drug abuse. All study subjects had to be abstinent from cannabis for at least 28 days. The main finding of our study was a P50 sensory gating deficit in cannabis controls that was correlated with the number of years with daily consumption (r=0.81; p=0.003). In contrast, we found no differences in P50 sensory gating between schizophrenic cannabis-abusers and non-abusers or healthy controls and no correlation with the number of years with daily consumption in those groups. To our knowledge this is the first study comparing the influence of chronic cannabis abuse in schizophrenic and otherwise healthy abusers on the inhibitory function of the brain. Our data provide some evidence that chronic cannabis abuse may affect sensory cortical circuits even after prolonged abstinence and they point to a possible differential effect in schizophrenic and otherwise healthy users.