Self-disturbances as a possible premorbid indicator of schizophrenia risk: a neurodevelopmental perspective.
Self-disturbances (SDs) are increasingly identified in schizophrenia and are theorized to confer vulnerability to psychosis. Neuroimaging research has shed some light on the neural correlates of SDs in schizophrenia. But, the onset and trajectory of the neural alterations underlying SDs in schizophrenia remain incompletely understood. We hypothesize that the aberrant structure and function of brain areas (e.g., prefrontal, lateral temporal, and parietal cortical structures) comprising the "neural circuitry of self" may represent an early, premorbid (i.e., pre-prodromal) indicator of schizophrenia risk. Consistent with neurodevelopmental models, we argue that "early" (i.e., perinatal) dysmaturational processes (e.g., abnormal cortical neural cell migration and mini-columnar formation) affecting key prefrontal (e.g., medial prefrontal cortex), lateral temporal cortical (e.g., superior temporal sulcus), and parietal (e.g., inferior parietal lobule) structures involved in self-processing may lead to subtle disruptions of "self" during childhood in persons at risk for schizophrenia. During adolescence, progressive neurodevelopmental alterations (e.g., aberrant synaptic pruning) affecting the neural circuitry of self may contribute to worsening of SDs. This could result in the emergence of prodromal symptoms and, eventually, full-blown psychosis. To highlight why adolescence may be a period of heightened risk for SDs, we first summarize the literature regarding the neural correlates of self in typically developing children. Next, we present evidence from neuroimaging studies in genetic high-risk youth suggesting that fronto-temporal-parietal structures mediating self-reflection may be abnormal in the premorbid period. Our goal is that the ideas presented here might provide future directions for research into the neurobiology of SDs during the pre-psychosis development of youth at risk for schizophrenia.
Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA; Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA; Massachusetts Mental Health Center Division of Public Psychiatry, Boston, MA, USA; Harvard Medical School, Boston, MA, USA. Electronic address: bbrent@bidmc.harvard.edu.
Benjamin K
BK
Brent
Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA; Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA; Massachusetts Mental Health Center Division of Public Psychiatry, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Larry J
LJ
Seidman
Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA; Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA; Massachusetts Mental Health Center Division of Public Psychiatry, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Heidi W
HW
Thermenos
Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Daphne J
DJ
Holt
Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA; Massachusetts Mental Health Center Division of Public Psychiatry, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Matcheri S
MS
Keshavan
D001921:Brain / Q000098:blood supply / Q000254:growth & development* / Q000473:pathology*; D006801:Humans; D011618:Psychotic Disorders / Q000209:etiology*; D012559:Schizophrenia / Q000150:complications* / Q000473:pathology; D012565:Schizophrenic Psychology; D012649:Self Concept
Genetic high-risk; Neurodevelopment; Premorbid; Schizophrenia; Self-disturbances