People with schizophrenia who hear voices in their head may be experiencing the results of “noisy” signaling produced by the brain’s motor system. As counterintuitive as this seems, the new discovery could be a gamechanger for scientists working on treatments for auditory hallucinations as it suggests that the target may lie outside of the auditory system itself.
Though not everyone with schizophrenia has such hallucinations, some patients do struggle to differentiate between their own thoughts and external voices, thus leading to the belief that some of their mental narratives are being spoken by an unseen individual. Previous research has suggested that part of the problem may be related to a type of brain signal known as the corollary discharge (CD), which usually suppresses the sound of a person’s voice when they are talking but is often “broken” in schizophrenia patients.
However, the authors of a new study point out that a misfiring CD is unlikely to tell the whole story, since the absence of inhibition doesn’t explain the appearance of positive hallucinatory symptoms. They therefore hypothesized the phenomenon to be mediated by another type of signal called the efference copy (EC).
Explaining the function of the EC, study author Dr Xing Tian told IFLScience that “when you want to speak, your motor system will generate a very precise signal that indicates what it wants to say.” Typically, this signal is accurately targeted at the neurons within the auditory system that reflect the exact sounds a person intends to make.
However, Tian says that some individuals with schizophrenia may have a “noisy” EC, giving rise to auditory hallucinations. “‘Noisy’ means that in those patients, those signals are not targeted on the auditory output. They are not precise,” he says.
To test their hypothesis, the study authors used electroencephalography (EEG) to monitor the brain activity of 40 schizophrenia patients, half of whom “hear voices” while the other half do not. Results indicated that auditory responses were not inhibited in either group while preparing to speak, confirming that all participants had a “broken” CD.
However, the EC was found to be correctly mapped onto the appropriate neural representations for each syllable spoken in those participants that lacked auditory hallucinations. In contrast, those who reported experiencing illusory sounds displayed a noisy EC, which activated neural responses to sounds other than those being spoken, thus confirming the researchers’ hypothesis.
“Even though they’re called auditory hallucinations, the cause is not all in the auditory system,” says Tian. “Maybe the cause is in the network connections from motor to auditory. If we are right, then the treatment should not always target the auditory system,” he adds.
Furthermore, while research on auditory hallucinations has generally focused on neuro-structural mechanisms such as morphological deficits, Tian says that his team has “put the cognition back into mental illness” by identifying the cause in motor-sensory processes.
“That means we have a paradigm shift”, he says.
The study is published in the journal PLOS Biology.
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