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The causes and pathogenesis of schizophrenia are still poorly understood, but new research aimed to find answers by looking at childhood milestones.
The causes and pathogenesis of schizophrenia are still poorly understood, but new research aimed to find answers by looking at childhood milestones.
Many researchers believe that schizophrenia is neurodevelopmental condition while others hypothesize that it is neurodegenerative. If the disease is in fact neurodevelopmental in nature, it may be possible to find genetic mechanisms — or abnormal expressions of certain genes – that lead to altered brain development in schizophrenia.
The authors of a recent study in Neuropsychiatric Disease and Treatment posit that such genetic mechanisms may significantly interact with prenatal and/or perinatal environmental insults to enhance the risk of developing schizophrenia. If this is the case, early neurodevelopmental anomalies may interact with typical brain maturation processes throughout a patient’s adolescence, causing some relatively benign markers of developmental disruption. This possibility hasn’t been studied much previously, due in part to the rarity of childhood-onset schizophrenia. Childhood-onset schizophrenia has a prevalence rate of only one child in 10,000 before age 12, and a remarkable increase around puberty and early adolescence.
The main objective of the study was to assess early childhood neurodevelopmental milestones, general intellectual ability, and neurological soft signs (NSS) in a sample of patients with early-onset schizophrenia spectrum psychosis compared to a control sample of patients with migraine. The researchers assessed early childhood neurodevelopmental milestones using a modified version of the General Developmental Scale, general intellectual ability using the Wechsler Intelligence Scale for Children—Revised or Leiter International Performance Scale-Revised for patients with speech and language abnormalities, and neurological soft signs with specific regard to subtle motor impairment. The analysis included 36 patients with early-onset psychosis. Experienced child psychiatrists made a diagnosis of EOP on the basis of the patient’s clinical evaluations, information obtained from family members, and a review of the patient’s past medical records.
Results of the study indicated that subjects with early-onset psychosis had a higher rate of impaired social development (P=0.001), learning difficulties (P=0.04), enuresis (P=0.0008), a lower intelligence quotient (P<0.001), and subtle motor impairments (P=0.005) than control subjects.
“This suggests that neurodevelopment in early-onset psychosis is characterized by a global impairment of functional and adaptive skills that manifests from early childhood, rather than a delay or limitation in language and motor development,” the researchers noted.
It is well-understood that children who become schizophrenic later in life have more developmental problems than controls, but the question remains: which developmental factors are more specifically associated with the illness? The study results suggested that childhood neurodevelopment in EOP is characterized by a global impairment of functional and adaptive skills, rather than a specific limitation or delay in the age of achievement of some developmental landmarks, such as learning to stand, walk, or speak.
“One of the main findings of this study, in fact, is that an impairment of social skills evident before the age of 6 years was significantly associated with EOP rather than migraine,” the authors wrote.
One limitation of the study is the small sample size. The researchers hope that larger longitudinal studies will be undertaken, noting that a better understanding of the evolutionary trajectories of neurodevelopment would have applicability for other neurodevelopmental disorders, including attention deficit hyperactivity disorder and autism spectrum disorders.