The Physiology of Auditory Hallucinations in Schizophrenia

Hearing voices in schizophrenia, clinically termed auditory verbal hallucinations (AVH), is one of the most prevalent and distressing symptoms, involving the perception of spoken speech with no actual external source. The physiology of this phenomenon involves disruptions in brain regions responsible for processing sound and speech, as well as core failures in self-monitoring brain mechanisms.
 
Auditory hallucinations are primarily linked to abnormal activation and organization of the auditory cortex, especially the superior temporal region and Heschl’s gyrus. Neuroimaging studies demonstrate that those with schizophrenia and voice-hearing show scrambled tonotopic maps in the auditory cortex, where the normal organized mapping of sound frequencies is disrupted, allowing internally generated speech and thoughts to be interpreted as external voices. Other regions including the inferior parietal cortex, prefrontal cortex, hippocampus, and insula, are commonly activated during hallucinations.
 
Auditory hallucinations in schizophrenia are underpinned by alterations in several key neurotransmitter systems, especially dopamine, glutamate, GABA, serotonin, and noradrenaline. These chemical changes disrupt normal brain signaling, resulting in abnormal perceptions and misattribution of internal thoughts as external voices. These transmitter alterations jointly contribute to the pathophysiology of AVH, suggesting why multi-target pharmacological approaches are useful for symptom management in schizophrenia.
 
Failures in self-monitoring mechanisms, especially “corollary discharge” and “efference copy,” contribute heavily to voice-hearing. Corollary discharge usually helps the brain distinguish between self-generated and external sounds by suppressing neural signals related to the former. In schizophrenia, this mechanism malfunctions, causing the brain to misidentify inner speech as coming from an outside source, effectively hearing voices.
 
The efference copy signal, which normally predicts and dampens the sensation of our own speech, becomes overly active or distorted. This makes the voices sound more vivid and external. Some studies show patients with AVH possess reduced or altered activation in response to real spoken words or tones, which may reflect early information processing deficits.
 
Recent research highlights the pulvinar nucleus of the thalamus as potentially critical. Abnormalities in its structure and function may disrupt connections to the primary auditory cortex, resulting in its hyperactivation and creating hallucinated voices without any real auditory input. This region may also explain why some patients experience both auditory and visual hallucinations. 
 
A long-held model now supported by neurophysiological evidence proposes that patients’ inner speech is incorrectly tagged by the brain as external rather than self-generated, leading to hearing voices. This disruption in self-monitoring may be rooted in developmental abnormalities present many years before schizophrenia emerges clinically and is detectable via altered auditory cortex organization from infancy.
 
References
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