Neuropsychological evidence for abnormal neurodevelopment associated with early-onset psychoses.

BACKGROUND: The longitudinal neuropsychological study of first-episode early-onset psychosis (EOP) patients, whose brain maturation is still in progress at the time of illness onset, provides a unique opportunity to compare their cognitive development with that of healthy subjects, in search of specific patterns resulting from the interaction between neurodevelopmental processes and the presence of psychotic disorders. Method Seventy-five first-episode EOP patients (schizophrenia n = 35; bipolar disorder n = 17; other forms of psychosis n = 23) with a mean age of 15.53 years were assessed with a neuropsychological battery that included measures of attention, working memory, memory and executive functions within 6 months following the onset of the first psychotic symptom (baseline) and 2 years later. Psychotic symptoms were assessed at both times with the Positive and Negative Symptom Scale (PANSS). Seventy-nine healthy subjects matched for age and education served as controls. RESULTS: EOP patients showed significant cognitive impairment at both baseline and the 2-year follow-up, with no significant differences between diagnostic groups at either time. Both healthy controls and EOP patients improved in all cognitive measures, except for patient working memory. Improvement in patient attention lost significance after controlling for psychotic symptom reduction. No significant time/diagnosis interaction was found among patients (p > 0.405). CONCLUSIONS: Cognitive impairment in EOP is already present at the first episode, and cognitive development seems to be arrested early in EOP patients compared to their healthy peers, at least for some cognitive functions. These and previous similar results support the neurodevelopmental hypothesis of psychosis.

Insight correlates in child- and adolescent-onset first episodes of psychosis: results from the CAFEPS study.

BACKGROUND: The correlates of insight in early-onset psychosis have received little previous attention. METHOD: We studied clinical correlates of insight in a sample of 110 adolescent recent-onset psychosis patients (mean age 15.53 years; psychotic symptoms present for <6 months). Insight was measured with the Scale to Assess Unawareness of Mental Disorder (SUMD) at baseline, 6 months and 12 months follow-up. RESULTS: Insight improved over the early phases of the illness, in parallel with psychopathological improvement. Poor insight at baseline and 6 months correlated with poor functioning at 6 and 12 months respectively. Schizophrenia patients had poorer insight than patients with bipolar disorder at 6 and 12 months but not at baseline. Logistic and linear regressions were used to predict 12-month diagnoses and functioning based on insight measurements. Baseline awareness of illness was a significant predictor for diagnosis [odds ratio (OR) 1.4, 95% confidence interval (CI) 1.05-1.97]. Treatment compliance at 6 months did not correlate with baseline SUMD subscores, but correlated with insight into having a disorder (Spearman's rho=0.21, p=0.039), its consequences (Spearman's rho=0.28, p=0.006) and the need for treatment (Spearman's rho=0.26, p=0.012) at 6 months. The 'attribution of symptoms' dimension of insight is poorly correlated with other insight dimensions and with other clinical variables. CONCLUSIONS: Poor insight correlates with symptom severity and global functioning but also has some trait value for schizophrenia, which is apparent once acute psychotic symptomatology is not prominent. A multi-dimensional approach to the assessment of insight is necessary, as different dimensions are influenced by different factors.

Visual hallucinations induced by the combination of prolintane and diphenhydramine.

The case of a young man is presented who developed visual hallucinations following two months of concomitant use of prolintane and diphenhydramine at therapeutic dosages. An increase in dopaminergic brain activity is proposed as the causal mechanism for hallucinations--whereas prolintane can induce the release of dopamine at the synaptic cleft, diphenhydramine can act inhibiting the reuptake of dopamine and inducing a potentiation of its effects. The psychiatric complications appearing two months after starting the use of both drugs could be attributed to a phenomenon of pharmacological kindling.

Regional cerebral blood flow in obsessive-compulsive patients with and without a chronic tic disorder. A SPECT study.

The main goal of the present study was to explore whether regional cerebral blood flow (rCBF) differs between obsessive-compulsive disorder (OCD) patients without chronic motor tic disorder and those OCD patients with a comorbid chronic tic disorder. Twenty-seven patients suffering from OCD (DSM-IV criteria), including 7 OCD patients who met DSM-IV criteria for simple chronic motor dic disorder, and 16 healthy volunteers were examined at rest using a high resolution SPECT. Seven regions of interest (ROIs) were manually traced and quantified as a percentage of the mean cerebellar uptake. Severity of obsessive-compulsive symptoms (OCS), anxiety and depressive symptoms and presence of motor tics were assessed with the Y-BOCS, HRS-A, HRS-D, MADRS, and Yale Global Tics Severity Scale, respectively. We found a significant relative decrease in rCBF in OCD patients without motor tics compared to healthy volunteers in the right orbitofrontal cortex (OCD without tics = 0.87; healthy volunteers = 0.94; p = 0.02). No significant differences in rCBF were seen when OCD patients with and without chronic tics were directly compared. A lower severity of OCS in OCD patients with chronic tics was found. These results are consistent with previous functional neuroimaging studies at rest that have widely involved the orbitofrontal cortex in the pathophysiology of the OCD. However, our results do not support the idea that OCD patients with chronic tics may constitute a biological subgroup within the OCD.