Projects

Impaired facial affect recognition is characteristic of schizophrenia and has been related to impaired social function, but the relevant neural mechanisms have not been fully identified. The present study sought to identify the role of oscillatory alpha activity in that deficit during the process of facial emotion recognition. Neuromagnetic brain activity was monitored while 44 schizophrenia patients and 44 healthy controls viewed 5-s videos showing human faces gradually changing from neutral to fearful or happy expressions or from the neutral face of one poser to the neutral face of another. Recognition performance was determined separately by self-report. Relative to prestimulus baseline, controls exhibited a 10- to 15-Hz power increase prior to full recognition and a 10- to 15-Hz power decrease during the postrecognition phase. These results support recent proposals about the function of alpha-band oscillations in normal stimulus evaluation. The patients failed to show this sequence of alpha power increase and decrease and also showed low 10- to 15-Hz power and high 10- to 15-Hz connectivity during the prestimulus baseline. In light of the proposal that a combination of alpha power increase and functional disconnection facilitates information intake and processing, the finding of an abnormal association of low baseline alpha power and high connectivity in schizophrenia suggests a state of impaired readiness that fosters abnormal dynamics during facial affect recognition.

Deficits in social cognition including facial affect recognition and their detrimental effects on functional outcome are well established in schizophrenia. Structured training can have substantial effects on social cognitive measures including facial affect recognition. Elucidating training effects on cortical mechanisms involved in facial affect recognition may identify causes of dysfunctional facial affect recognition in schizophrenia and foster remediation strategies. In the present study, 57 schizophrenia patientswere randomly assigned to (a) computer-based facial affect training that focused on affect discrimination and working memory in 20 daily 1-hour sessions, (b) similarly intense, targeted cognitive training on auditory-verbal discrimination and working memory, or (c) treatment as usual. Neuromagnetic activity was measured before and after training during a dynamic facial affect recognition task (5 s videos showing human faces gradually changing from neutral to fear or to happy expressions). Effects on 10–13 Hz (alpha) power during the transition from neutral to emotional expressionswere assessed viaMEG based on previous findings that alpha power increase is related to facial affect recognition and is smaller in schizophrenia than in healthy subjects. Targeted affect training improved overt performance on the training tasks. Moreover, alpha power increase during the dynamic facial affect recognition task was larger after affect training than after treatment-as-usual, though similar to that after targeted perceptual–cognitive training, indicating somewhat nonspecific benefits. Alpha power modulationwas unrelated to general neuropsychological test performance, which improved in all groups. Results suggest that specific neural processes supporting facial affect recognition, evident in oscillatory phenomena, are modifiable. This should be considered when developing remediation strategies targeting social cognition in schizophrenia.

Research has linked oscillatory activity in the α frequency range, particularly in sensorimotor cortex, to processing of social actions. Results further suggest involvement of sensorimotor α in the processing of facial expressions, including affect. The sensorimotor face area may be critical for perception of emotional face expression, but the role it plays is unclear. The present study sought to clarify how oscillatory brain activity contributes to or reflects processing of facial affect during changes in facial expression. Neuromagnetic oscillatory brain activity was monitored while 30 volunteers viewed videos of human faces that changed their expression from neutral to fearful, neutral, or happy expressions. Induced changes in α power during the different morphs, source analysis, and graph-theoretic metrics served to identify the role of α power modulation and cross-regional coupling by means of phase synchrony during facial affect recognition. Changes from neutral to emotional faces were associated with a 10–15 Hz power increase localized in bilateral sensorimotor areas, together with occipital power decrease, preceding reported emotional expression recognition. Graph-theoretic analysis revealed that, in the course of a trial, the balance between sensorimotor power increase and decrease was associated with decreased and increased transregional connectedness as measured by node degree. Results suggest that modulations in α power facilitate early registration, with sensorimotor cortex including the sensorimotor face area largely functionally decoupled and thereby protected from additional, disruptive input and that subsequent α power decrease together with increased connectedness of sensorimotor areas facilitates successful facial affect recognition.

Hemodynamic and electromagnetic neuroimaging suggests a sequence of intraregional and interregional activity during emotion processing. Oscillatory activity within trials may offer insight into neural mechanisms involved in this process. MEG was measured in 24 subjects during passive viewing of neutral and unpleasant pictures and emotion regulation by cognitive reappraisal. Regulation prompted more gamma increase and alpha decrease to picture onset than did passive viewing. Source analysis confirmed differential modulation of these power changes in occipitoparietal regions during passive viewing and larger power changes in prefrontal regions during regulation. Local coupling of alpha phase to gamma amplitude within a medial prefrontal region and long-range synchrony of medial prefrontal, occipital, and temporoparietal regions index mechanisms of prefrontal top-down contribution to emotion processing.

Schizophrenia patients commonly exhibit smaller amplitudes of mismatch negativity (MMN) than in controls. It remains unclear whether this results from deficient processes indexed by MMN or 'normally' though more variable processing. The present magnetoencephalographic study addressed this question by analyzing intra-individual trial-by-trial variability and MMN amplitude.

The ratio of magnetoencephalogram-recorded brain responses occurring 50 ms after paired clicks (S2-evoked M50/S1-evoked M50) serves as a measure of sensory gating. An abnormally large ratio is commonly found in schizophrenia. Whether this abnormality indicates impaired gating is debated. Using event-related oscillations the present study sought to elucidate processes contributing to the phenomenon of altered M50 gating ratio. Schizophrenia inpatients (n=50) showed the expected large M50 gating ratio relative to 48 healthy controls, which correlated with less induced frontally generated activity in the 10–15 Hz frequency band starting 200 ms before the onset of S2. Patients also produced smaller alpha (8–12 Hz) and gamma (60–80 Hz) responses to S1. Results suggest that the deviant gating ratio in schizophrenia is a consequence of a complex alteration in the processing of incoming information that cannot be attributed to impaired gating alone.

Background: The ratio of scalp-recorded brain responses occurring 50 msec after paired clicks (S2-evoked P50/S1-evoked P50) serves as a measure of sensory gating. An abnormally large ratio is commonly found in schizophrenia and is considered as a sign of reduced sensory
gating or otherwise dysfunctional organization of the auditory/verbal system as a factor contributing to psychopathology and cognitive
dysfunction in schizophrenia. This initial randomized clinical trial compared the efficacy of two 4-week, computer-based cognitive training
methods that emphasize either auditory discrimination and verbal memory or a broader range of cognitive functions in schizophrenia.
Methods: Thirty-nine schizophrenia patients (ICD-F20.0 diagnosis) were assigned to Cognitive Exercises (CE) or Cognitive Package (Cogpack).
The M50, the magnetoencephalographic analogue of electroencephalographic P50, and performance on verbal learning and
memory tests were used to evaluate training effects.
Results: As expected, patients exhibited higher pretreatment gating ratios than 28 age-matched healthy comparison participants. Gating
ratios decreased after CE but not after Cogpack. Cognitive test performance improved more after CE than after Cogpack.
Conclusions: Appropriately specific psychological training changes the neural performance in schizophrenia, normalizing sensory and cognitive function.