UCLA

Evidence suggests that the core cognitive features of schizophrenia (SZ) include impairments in auditory and visual memory systems and that each of these deficits individually correlates with functional impairment. However, recent basic research suggests that numerous levels of cognitive processing, from perception to learning, optimally function under multisensory conditions, i.e., with multiple sensory modalities engaged at the same time by the same stimulus. Growing evidence points to the possibility that multisensory learning facilitates neuroplasticity beyond what is possible in unisensory modalities, and, what is more, multisensory information has increasingly been found to rely upon neural communication both within specific cortical modules and also across broad neural networks. In the area of SZ research, recent formulations of the disorder suggest that it is precisely in the domain of neural communication, or connectivity and plasticity, that patients are characteristically impaired. Yet, in the extant literature, one finds very few investigations of memory or other processes in which the more ecologically valid, multisensory stimuli were employed. Furthermore, while the dysconnection model of SZ is promising theoretically and supported by neurological data, very few studies seek instantiations of these effects behaviorally or the emergent properties of their biomarkers. The current study examined SZ patients' capacity to benefit from multisensory encoding of auditory memoranda relative to healthy controls. It further sought to delineate the electrophysiological substrates predictive of behavioral performance within the framework of a neuroconnectivity-based model of episodic memory function. In addition to replicating pilot data findings of benefits to auditory recognition from multisensory encoding in controls, the data also demonstrated a capacity for SZ patients to capitalize upon this same process for improvement of auditory memory deficits. In keeping with the theoretical model, results revealed that recognition of unisensory-encoded sounds were predicted by low frequency connectivity across a broad, hippocampally-centered network. Auditory memory deficits in patients were statistically mediated by impairments in the operation of this system and several measures of SZ symptomatology were associated with those same biomarkers. Increases in memory for multisensory-encoded sounds appeared to be predicted by both low- and high-frequency posterior connectivity for which no group differences were found.