A new study reveals that auditory hallucinations in schizophrenia may be caused by two faulty brain processes: a failed suppression of self-generated sounds and an overactive response to internal noises. The research showed that patients with hallucinations had a “broken” corollary discharge and an enhanced response to unintentional sounds, compared to those without hallucinations. These findings suggest that future treatments for auditory hallucinations could target these disrupted processes.
Perceptual experiences can be triggered by both sensory processing and internal mechanisms, such as memory retrieval or mental imagery. In other words, our perceptions can be generated both by the world around us and by our minds.
However, the brain must monitor these different sources to distinguish what is real from what is imagined. When this monitoring fails, hallucinations can occur.
A clear example of this is auditory hallucinations, common in patients with schizophrenia, who "hear" voices even in the absence of external sounds. These patients have difficulty distinguishing their thoughts, such as internal speech, from real voices, leading them to believe that these thoughts come from outside.
Studies suggest that auditory hallucinations can be explained by a combination of two complementary functions that modulate motor and perceptual signals in the brain. The first function, called Corollary Discharge (CD), acts as a "copy" of generic motor signals, which are sent during the execution of actions.
These signals have the role of inhibiting the connected sensory processes to warn the brain about the expected sensory consequences of its own actions.
In simple terms, the brain "predicts" the results of an action and reduces sensitivity to them so that we can differentiate between stimuli that we generate and those that come from the environment.
The second function, known as Efference Copy (EC), refers to a more specific copy of a motor plan that increases sensitivity to certain sensations directly linked to the action in question. For example, when we are preparing to speak, the brain increases its sensitivity to speech sounds, helping us focus on what we are about to say.
A recent study published by researchers at Shanghai Jiao Tong University in Plos Biology proposes that auditory hallucinations in patients with schizophrenia are caused by selective failures in these functions.
In patients with hallucinations, the DC does not properly inhibit internal stimuli, such as internal speech, and the CS ends up increasing sensitivity to internal sounds or sensations that should not be perceived as real. This creates the experience of "hearing voices" that are actually generated internally but are mistaken for external sounds.
The Figure shows schematics of distinct functions of motor signals in the motor-to-sensory transformation at temporal stages of action in normal and clinical populations. (A) Normal individuals. (B) Individuals with schizophrenia without auditory hallucinations; and (C) Individuals with schizophrenia with auditory hallucinations. doi.org/ 10.1371/journal.pbio.3002836
When this mechanism fails, especially in patients with schizophrenia, self-monitoring also fails, and auditory hallucinations may occur. However, there is an interesting point: rather than simply failing to suppress self-generated sounds, such as internal speech, there is evidence that in some patients the brain increases sensitivity to these sounds, leading to the perception of sounds that do not exist externally.
In this new study, researchers conducted electroencephalogram (EEG) experiments measuring the brain waves of twenty patients diagnosed with schizophrenia who had auditory hallucinations and twenty patients diagnosed with schizophrenia who had never experienced such hallucinations.
Normally, when people are preparing to speak, their brains send out a signal known as a “corollary discharge” that suppresses the sound of their voice.
However, the new study showed that when patients with auditory hallucinations were preparing to speak a syllable, their brains not only failed to suppress these internal sounds but had an enhanced “efference copy” response to internal sounds other than the planned syllable.
The researchers conclude that impairments in these two processes likely contribute to auditory hallucinations and that targeting them in the future could lead to new treatments for such hallucinations.
In summary, this study suggests that problems in the brain’s motor and auditory systems, which are responsible for distinguishing between internally generated sounds and external sounds, play a crucial role in auditory hallucinations in people with schizophrenia. These findings are important because they could help in the development of new treatments to improve the lives of patients with these symptoms.
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Impaired motor-to-sensory transformation mediates auditory hallucinations
Yang F, Zhu H, Cao X, Li H, Fang X, Yu L, et al.
PLoS Biol. https://doi.org/ 10.1371/journal.pbio.3002836
Abstract:
It has been hypothesized that a copy of motor signals, termed efference copy (EC) or corollary discharge (CD), suppresses sensory responses to yield a sense of agency; impairment of the inhibitory function leads to hallucinations. However, how can the sole absence of inhibition yield positive symptoms of hallucinations? We hypothesize that selective impairments in functionally distinct signals of CD and EC during motor-to-sensory transformation cause the positive symptoms of hallucinations. In an electroencephalography (EEG) experiment with a delayed articulation paradigm in schizophrenic patients with (AVHs) and without auditory verbal hallucinations (non-AVHs), we found that preparing to speak without knowing the contents (general preparation) did not suppress auditory responses in both patient groups, suggesting the absent of inhibitory function of CD. Whereas, preparing to speak a syllable (specific preparation) enhanced the auditory responses to the prepared syllable in nonAVHs, whereas AVHs showed enhancement in responses to unprepared syllables, opposite to the observations in the normal population, suggesting that the enhancement function of EC is not precise in AVHs. A computational model with a virtual lesion of an inhibitory inter-neuron and disproportional sensitization of auditory cortices fitted the empirical data and further quantified the distinct impairments in motor-to-sensory transformation in AVHs. These results suggest that “broken” CD plus “noisy” EC causes erroneous monitoring of the imprecise generation of internal auditory representation and yields auditory hallucinations. Specific impairments in functional granularity of motor-to-sensory transformation mediate positivity symptoms of agency abnormality in mental disorders.
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