The origin of auditory hallucinations, which are one of the core symptoms
of schizophrenia, is still a matter of debate. It has been hypothesized that
alterations in connectivity between frontal and parietotemporal speech-related
areas might contribute to the pathogenesis of auditory hallucinations. These
networks are assumed to become dysfunctional during the generation and monitoring
of inner speech. Magnetic resonance diffusion tensor imaging is a relatively
new in vivo method to investigate the directionality of cortical white matter
To investigate, using diffusion tensor imaging, whether previously described
abnormal activation patterns observed during auditory hallucinations relate
to changes in structural interconnections between the frontal and parietotemporal
A 1.5 T magnetic resonance scanner was used to acquire twelve 5-mm slices
covering the Sylvian fissure. Fractional anisotropy was assessed in 13 patients
prone to auditory hallucinations, in 13 patients without auditory hallucinations,
and in 13 healthy control subjects. Structural magnetic resonance imaging
was conducted in the same session. Based on an analysis of variance, areas
with significantly different fractional anisotropy values between groups were
selected for a confirmatory region of interest analysis. Additionally, descriptive
voxel-based t tests between the groups were computed.
In patients with hallucinations, we found significantly higher white
matter directionality in the lateral parts of the temporoparietal section
of the arcuate fasciculus and in parts of the anterior corpus callosum compared
with control subjects and patients without hallucinations. Comparing patients
with hallucinations with patients without hallucinations, we found significant
differences most pronounced in the left hemispheric fiber tracts, including
the cingulate bundle.
Our findings suggest that during inner speech, the alterations of white
matter fiber tracts in patients with frequent hallucinations lead to abnormal
coactivation in regions related to the acoustical processing of external stimuli.
This abnormal activation may account for the patients' inability to distinguish
self-generated thoughts from external stimulation.