Publication details

Loss of normal facial asymmetry in schizophrenia and bipolar disorder: Implications for development of brain asymmetry in psychotic illness

Authors

SUKNO Federico M. KELLY Brendan D. LANE Abbie KATINA Stanislav ROJAS Mario A. WHELAN Paul F. WADDINGTON John L.

Year of publication 2024
Type Article in Periodical
Magazine / Source Psychiatry Research
MU Faculty or unit

Faculty of Science

Citation
Web https://www.sciencedirect.com/science/article/pii/S0165178124004980?via%3Dihub
Doi http://dx.doi.org/10.1016/j.psychres.2024.116213
Keywords Psychosis; Neurodevelopment; Craniofacies; Frontal lobes; 3D Laser surface imaging; Geometric morphometrics
Description Development of the craniofacies occurs in embryological intimacy with development of the brain and both show normal left-right asymmetries. While facial dysmorphology occurs to excess in psychotic illness, facial asymmetry has yet to be investigated as a putative index of brain asymmetry. Ninety-three subjects (49 controls, 22 schizophrenia, 22 bipolar disorder) received 3D laser surface imaging of the face. On geometric morphometric analysis with (x, y, z) visualisations of statistical models for facial asymmetries, in controls the upper face and periorbital region, which share embryological intimacy with the forebrain, showed marked asymmetries. Their geometry included: along the x-axis, rightward asymmetry in its dorsal-medial aspects and leftward asymmetry in its ventral-lateral aspects; along the z-axis, anterior protrusion in its right ventral-lateral aspect. In both schizophrenia and bipolar disorder these normal facial asymmetries were diminished, with residual retention of asymmetries in bipolar disorder. This geometry of normal facial asymmetries shows commonalities with that of normal frontal lobe asymmetries. These findings indicate a trans-diagnostic process that involves loss of facial asymmetries in both schizophrenia and bipolar disorder. Embryologically, they implicate loss of face-brain asymmetries across gestational weeks 7–14 in processes that involve genes previously associated with risk for schizophrenia.

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