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Reduced mirror neuron activity in schizophrenia and its association with theory
of mind deficits: evidence from a transcranial magnetic stimulation study
#MMPMID24214933
Mehta UM
; Thirthalli J
; Basavaraju R
; Gangadhar BN
; Pascual-Leone A
Schizophr Bull
2014[Sep]; 40
(5
): 1083-94
PMID24214933
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BACKGROUND: The "mirror-neuron system" has been proposed to be a
neurophysiological substrate for social cognition (SC) ability. We used
transcranial magnetic stimulation (TMS) paradigms to compare putative mirror
neuron activity (MNA) in 3 groups: antipsychotic-naive, medicated schizophrenia
patients, and healthy comparison subjects. We also explored the association
between MNA and SC ability in patients. METHODS: Fifty-four consenting
right-handed schizophrenia patients (33 antipsychotic naive) and 45 matched
healthy comparison subjects completed a TMS experiment to assess putative
premotor MNA. We used 4 TMS paradigms of eliciting motor-evoked potentials (MEP)
in the right first dorsal interosseous (FDI) muscle. These were applied while the
subjects observed a goal-directed action involving the FDI (actual action and its
video) and a static image. The difference in the amplitude of the MEP while they
observed the static image and the action provided a measure of MNA. Subjects also
underwent SC assessments (theory of mind [ToM], emotion processing, and social
perception). RESULTS: Two-way repeated measures ANOVA revealed significant group
× occasion interaction effect in 3 TMS paradigms, indicating deficient motor
facilitation during action observation relative to rest state in
antipsychotic-naive schizophrenia patients as compared with the other two groups.
Among patients, there were significant direct correlations between measures of
MNA and ToM performance. CONCLUSIONS: Antipsychotic-naive schizophrenia patients
have poorer MNA than medicated patients and healthy controls. Measures of
putative MNA had significant and consistent associations with ToM abilities.
These findings suggest a possibility of deficient mirror neuron system underlying
SC deficits in schizophrenia.
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