Schizophrenia, Not Depression, Linked to Subcortical Auditory Deficits

Through the use of functional magnetic resonance imaging of the whole brain, researchers found that in patients with schizophrenia a reduction of the mismatch negativity within the auditory modality is a potential biomarker; specifically, they detected deficits propagated from subcortical nodes to cortical nodes.

Schizophrenia and major depression exhibit different neural profiles related to auditory detection deficits, in which the auditory mismatch in schizophrenia is propagated along the auditory pathway from subcortical levels to the cortical stage, according to study results published in Schizophrenia Bulletin.

The investigators of this study sought to examine exactly where in the auditory hierarchy the schizophrenic deficit can first be detected, and if the well-known cortical deficit is a direct consequence of dysfunction at lower hierarchical (subcortical) levels. In addition, the investigators sought to characterize the differences between auditory mismatch profiles in schizophrenia and major depressive disorder with auditory processing deficits.

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The study included 29 patients with schizophrenia, 27 patients with major depressive disorder, and 31 healthy controls matching patient groups by age, gender, and education. The investigators assessed auditory mismatch processing using functional magnetic resonance imaging, which has been demonstrated to show localized disturbances of functional connectivity in cortical as well as subcortical responses. Whole-brain activation analysis was used to define 5 different mismatch conditions as predictors of interest. Regions of interest analyses characterized processing differences along the auditory hierarchy among patient groups, and path and connectivity analysis explored the causal relationships between subcortical and cortical deficits.

In whole-brain activation analysis, mismatch deficits in patients with schizophrenia were observed at all stages of the auditory pathway, including the inferior colliculus, thalamus, auditory cortex, and prefrontal cortex; however, in patients with depression, significant deficits were observed only in the prefrontal cortex. In path analysis, activation deficits observed in schizophrenia fit a feed-forward model, in which deficits were propagated from subcortical nodes to cortical nodes. Reduced connectivity along this processing stream was exhibited by both patients with schizophrenia and with major depression, indicating there was no significant group effect on condition-dependent connectivity.

Limitations to the study include the small number of participants and the absence of a patient group with bipolar disorder; in addition, all participants received psychotropic medication and had higher nicotine consumption than the general population. Future studies with large samples should test the effects of medication and nicotine use on sensory deficits.

The investigators suggest that auditory change detection deficits already begin to manifest at the subcortical level and contribute to well-known cortical deficits specific to schizophrenia, whereas depression is associated only with cortical dysfunction.

Gaebler AJ, Zweerings J, Koten JW Jr, et al. Impaired subcortical detection of auditory changes in schizophrenia but not in major depression [published online April 11, 2019]. Schizophr Bull. doi:10.1093/schbul/sbz027