Neural Mechanisms Underlying Affective Theory of Mind in Violent Antisocial Personality Disorder and/or Schizophrenia

Abstract

Among violent offenders with schizophrenia, there are 2 sub-groups, one with and one without, conduct disorder (CD) and antisocial personality disorder (ASPD), who differ as to treatment response and alterations of brain structure. The present study aimed to determine whether the 2 groups also differ in Theory of Mind and neural activations subsuming this task. Five groups of men were compared: 3 groups of violent offenders-schizophrenia plus CD/ASPD, schizophrenia with no history of antisocial behavior prior to illness onset, and CD/ASPD with no severe mental illness-and 2 groups of non-offenders, one with schizophrenia and one without (H). Participants completed diagnostic interviews, the Psychopathy Checklist Screening Version Interview, the Interpersonal Reactivity Index, authorized access to clinical and criminal files, and underwent functional magnetic resonance imaging while completing an adapted version of the Reading-the-Mind-in-the-Eyes Task (RMET). Relative to H, nonviolent and violent men with schizophrenia and not CD/ASPD performed more poorly on the RMET, while violent offenders with CD/ASPD, both those with and without schizophrenia, performed similarly. The 2 groups of violent offenders with CD/ASPD, both those with and without schizophrenia, relative to the other groups, displayed higher levels of activation in a network of prefrontal and temporal-parietal regions and reduced activation in the amygdala. Relative to men without CD/ASPD, both groups of violent offenders with CD/ASPD displayed a distinct pattern of neural responses during emotional/mental state attribution pointing to distinct and comparatively successful processing of social information.

Keywords: conduct disorder; functional magnetic resonance imaging; psychotic disorders; social cognition; types of violent offenders.

Fig. 1.

Theory of Mind performance^a. ^aSignificant differences between test conditions (F = 89.7, df = 78, P < .001) and condition × group interaction (F = 3.9, df = 78, P = .006).

Fig. 2.

Foci and contrast estimates of brain regions, that distinguished between groups on Theory of Mind related brain activation^a. ^aP < .05 corrected for multiple comparisons after Family-Wise-Error at cluster-level. Significant clusters of activation differences include the medial PFC (Brodman areas [BAs] 8,9,32; MNI: −10, 28, 40; k = 407; z = 4.26), left ventrolateral PFC (BAs 10,46,47; MNI: −44, 50, 6; k = 1095; z = 4.78), extending into the left superior temporal gyrus (STG, BA 38; MNI = −46, 14, −20; z = 4.52), left supplementary motor area (SMA, BA 6; MNI: −24, 12, 60; k = 413; z = 4.25), right dorsolateral PFC (BA 46; MNI: 48, 32, 24; k = 705; z = 4.64), left pSTS/TPJ (BA 39,40; MNI: −26, −66, 44; k = 1330; z = 4.69), the bilateral precuneus (BA 7, MNI: −2, −72, 56; k = 557; z = 4.63) and lingual/fusiform gyrus (BAs 18,19; MNI: 24, −84, −20; k = 812; z = 5.09). The color or b/w bar indicates F-value.

Fig. 3.

Location, and contrast estimates of in Theory of Mind related activation of the left amygdala^a, and associations between amygdala activation and Theory of Mind performance. ^aMNI coordinates: x = −18, y = −2, z = −20; cluster-size = 43 voxels; z value = 3.52; P_FWE–SVC = .032. Scale bar depicts the uncorrected T-statistic.