Abstract
Auditory verbal hallucinations (AVH) in schizophrenia are typically characterized by rich emotional content. Despite the prominent role of emotion in regulating normal perception, the neural interface between emotion-processing regions such as the amygdala and auditory regions involved in perception remains relatively unexplored in AVH. Here, we studied brain metabolism using FDG-PET in 9 remitted patients with schizophrenia that previously reported severe AVH during an acute psychotic episode and 8 matched healthy controls. Participants were scanned twice: (1) at rest and (2) during the perception of aversive auditory stimuli mimicking the content of AVH. Compared to controls, remitted patients showed an exaggerated response to the AVH-like stimuli in limbic and paralimbic regions, including the left amygdala. Furthermore, patients displayed abnormally strong connections between the amygdala and auditory regions of the cortex and thalamus, along with abnormally weak connections between the amygdala and medial prefrontal cortex. These results suggest that abnormal modulation of the auditory cortex by limbic-thalamic structures might be involved in the pathophysiology of AVH and may potentially account for the emotional features that characterize hallucinatory percepts in schizophrenia.
Highlights
The pathophysiology of positive symptoms in schizophrenia remains a critical and poorly understood area of psychiatry
We aimed to investigate emotional and linguistic processing during hallucination-like auditory stimulation in remitted schizophrenia patients with Auditory verbal hallucinations (AVH) compared to healthy controls
Previous imaging studies have used auditory stimulation in the form of emotional words in chronic hallucinators and hallucination-like stimulation in remitted patients. These studies have shown that patients with schizophrenia have increased hemodynamic responses in limbic regions, among other brain regions, during auditory stimulation [14,15]
Summary
The pathophysiology of positive symptoms in schizophrenia remains a critical and poorly understood area of psychiatry. Converging evidence indicates that the mesolimbic dopaminergic system, normally involved in reward prediction and assignment of salience to environmental stimuli, may be critically altered in individuals with schizophrenia [2]. Some amygdala nuclei interact with an array of cortical and subcortical structures including the striatum, midbrain dopaminergic system, and the prefrontal cortex ( its medial and orbital parts) to modulate reward processing by dynamically updating stimulusvalue associations [4]. This physiological update of associations permits accurate predictions about the environment, and its malfunction has been proposed to lead to delusions and hallucinations [5]. Postmortem studies, in turn, indicate disturbances in amygdalocortical circuitry that are suggestive of increased excitatory afferents in the amygdalar projections to the neocortex [8]
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