Basic auditory processing deficits and their association with auditory emotion recognition in schizophrenia.

BACKGROUND: Individuals with schizophrenia are impaired in their ability to recognize emotions based on vocal cues and these impairments are associated with poor global outcome. Basic perceptual processes, such as auditory pitch processing, are impaired in schizophrenia and contribute to difficulty identifying emotions. However, previous work has focused on a relatively narrow assessment of auditory deficits and their relation to emotion recognition impairment in schizophrenia. METHODS: We have assessed 87 patients with schizophrenia and 73 healthy controls on a comprehensive battery of tasks spanning the five empirically derived domains of auditory function. We also explored the relationship between basic auditory processing and auditory emotion recognition within the patient group using correlational analysis. RESULTS: Patients exhibited widespread auditory impairments across multiple domains of auditory function, with mostly medium effect sizes. Performance on all of the basic auditory tests correlated with auditory emotion recognition at the p < .01 level in the patient group, with 9 out of 13 tests correlating with emotion recognition at r = 0.40 or greater. After controlling for cognition, many of the largest correlations involved spectral processing within the phase-locking range and discrimination of vocally based stimuli. CONCLUSIONS: While many auditory skills contribute to this impairment, deficient formant discrimination appears to be a key skill contributing to impaired emotion recognition as this was the only basic auditory skill to enter a step-wise multiple regression after first entering a measure of cognitive impairment, and formant discrimination accounted for significant unique variance in emotion recognition performance after accounting for deficits in pitch processing.

Quantitative levels of aripiprazole parent drug and metabolites in urine.

OBJECTIVE: The aim of this study is to assess urine levels of aripiprazole and metabolites among patients receiving steady-state dosing of aripiprazole. METHODS: One hundred fifty adults, judged compliant with a stable aripiprazole regimen, had observed dosing for 5 consecutive days. Urine specimens, obtained on days 1, 4, and 5, were analyzed for pH, creatinine, specific gravity, and for aripiprazole, OPC3373, and dehydroaripiprazole. Linear regression was used to assess the association between unadjusted urine levels of each drug/metabolite and dose taken, and linear stepwise multiple regression was performed to identify variables that added to the explanation of the variance. RESULTS: OPC3373 was found in 97 % of urine samples, whereas unchanged aripiprazole and dehydroaripiprazole were found in only 58 and 39 % of samples, respectively. Variance in urine metabolite levels accounted for by medication dose was relatively low for each individual drug/metabolite, r (2) only 0.13 to 0.23. However, when OPC3373 was adjusted for age, weight, sex, and urine creatinine values, the r (2) improved to 0.63, and further improved to 0.70, when height, urine specific gravity, and the presence of dehydroaripiprazole were added in a stepwise multiple regression model. CONCLUSIONS: Unadjusted urine levels of aripiprazole and metabolites are not strongly related to aripiprazole dosing, however, accounting for key variables yields a strong relationship between measurable urine parameters and dose taken. By defining the expected range of adjusted urine levels for each dose, the potential exists for a clinical test to identify partially nonadherent individuals who would not have been identified by conventional "present vs. absent" urine drug testing.

Effects of milnacipran on neurocognition, pain, and fatigue in fibromyalgia: a 13-week, randomized, placebo-controlled, crossover trial.

OBJECTIVE: To investigate whether milnacipran is safe and effective in improving cognitive function in patients with fibromyalgia. METHOD: Patients were randomly assigned to receive milnacipran or placebo for 6 weeks, followed by a 1-week washout and then crossover to the other arm for another 6 weeks. The overall trial lasted 13 weeks and was conducted between July 2011 and May 2013. Assessments were performed at each visit. Neurocognition was measured by the Brief Assessment of Cognition (BAC) and MATRICS. Pain was assessed by the visual analog scale (VAS) for pain. Global assessment of fibromyalgia symptoms was measured by the Fibromyalgia Impact Questionnaire (FIQ) and tender point examination. Depression was assessed by the Beck Depression Inventory (BDI). Fatigue was assessed by the Fatigue Severity Scale. Functional outcome was evaluated by the Health Assessment Questionnaire. The Clinical Global Impressions-Severity of Illness (CGI-S) and Improvement (CGI-I) scales and the Patients Clinical Global Impression of Change were used to measure the global impression of severity and improvement. RESULTS: 26 subjects were screened, and 20 subjects completed the trial. The change in verbal memory (P = .001) and the composite T score (P = .044) of the BAC and the change in the attention-vigilance domain T score (P = .042) were significantly improved, but there were no differences between the drug and placebo groups. The changes in the CGI-S scores were not significant, but the changes in the Clinical Impression-Improvement (CGI-I) scores showed worsening in the placebo group at week 1 (P = .032), week 2 (P = .024), week 4 (P = .024), and week 6 (P = .60) compared to baseline. The change in FIQ scores was not significant. CONCLUSIONS: Milnacipran may have a potential role in the improvement of pain, disability, and mood. The effect of milnacipran on cognition in fibromyalgia needs further research. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT01829243.