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Auditory hallucinations are among the most disabling symptoms in patients with schizophrenia (SZ) and frequently persist despite antipsychotic treatment. Converging imaging and neurochemical evidence implicates striatal subregions, particularly the nucleus accumbens and caudate, and their abnormally elevated functional coupling with superior temporal cortex (STC) in hallucination pathophysiology1–5. However, causal tests of striatal circuit involvement have been limited because these deep targets are not accessible with conventional noninvasive neuromodulation.
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Subramaniam et al. (2026) studied this question.
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