Abstract
Adjunctive psychotherapeutic approaches recommended for patients with schizophrenia (SZ) who are fully or partially resistant to pharmacotherapy have rarely utilized biomarkers to enhance the understanding of treatment-effective mechanisms. As SZ patients with persistent auditory verbal hallucinations (AVH) frequently evidence reduced neural responsiveness to external auditory stimulation, which may impact cognitive and functional outcomes, this study examined the effects of cognitive behavioral therapy for voices (CBTv) on clinical and AVH symptoms and the sensory processing of auditory deviants as measured with the electroencephalographically derived mismatch negativity (MMN) response. Twenty-four patients with SZ and AVH were randomly assigned to group CBTv treatment or a treatment as usual (TAU) condition. Patients in the group CBTv condition received treatment for 5 months while the matched control patients received TAU for the same period, followed by 5 months of group CBTv. Assessments were conducted at baseline and at the end of treatment. Although not showing consistent changes in the frequency of AVHs, CBTv (vs. TAU) improved patients' appraisal (p = 0.001) of and behavioral/emotional responses to AVHs, and increased both MMN generation (p = 0.001) and auditory cortex current density (p = 0.002) in response to tone pitch deviants. Improvements in AVH symptoms were correlated with change in pitch deviant MMN and current density in left primary auditory cortex. These findings of improved auditory information processing and symptom-response attributable to CBTv suggest potential clinical and functional benefits of psychotherapeutical approaches for patients with persistent AVHs.
Highlights
Auditory verbal hallucinations (AVHs), defined as perceptions or subjective experiences of “hearing voices” without corresponding external auditory stimulation, occur with a high frequency of up to 60% to 80% in patients with schizophrenia (SZ) [1]
The causes of AVHs are still unclear, improved understanding of the neural basis of AVHs has been forthcoming from functional magnetic resonance imaging studies which have shown elevated activation of brain regions associated with auditory stimulus processing, speech generation, and speech perception during the experience of active hallucinations [3,4,5,6]
Evidenced in SZ patients who are prone to AVHs, diminished neural responsiveness to external auditory stimulation is believed to affect the functional cost of an auditory cortex that is thought to be tonically “tuned on” and “tuned in” to the internal channels broadcasting hallucinating stimuli, with the preferential endogenous processing of AVHs resulting in the “saturation” of neuronal resources and resulting in limited capacity for the exogenous processing of external auditory stimuli [12, 13]
Summary
Auditory verbal hallucinations (AVHs), defined as perceptions or subjective experiences of “hearing voices” without corresponding external auditory stimulation, occur with a high frequency of up to 60% to 80% in patients with schizophrenia (SZ) [1]. In sensory cortices hyper-excitable neuronal states are typically associated with enhanced exogenous induced processes [7,8,9,10], AVHs have been associated with reduced neuronal activation of the auditory cortex in response to external auditory stimulation [11] These opposing findings in hallucinating patients of increased activation of the auditory cortex in the absence of external stimulation and reduced activation of the auditory cortex in response to externally presented speech and non-speech sounds have been interpreted as evidence for competition between internally generated and externally originating neural activity in the auditory cortex for the attentional resources of the hallucinating patient [11]. Evidenced in SZ patients who are prone to AVHs (vs. patients who have never hallucinated), diminished neural responsiveness to external auditory stimulation is believed to affect the functional cost of an auditory cortex that is thought to be tonically “tuned on” and “tuned in” to the internal channels broadcasting hallucinating stimuli, with the preferential endogenous processing of AVHs resulting in the “saturation” of neuronal resources and resulting in limited capacity for the exogenous processing of external auditory stimuli [12, 13]
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