Neurobiological and psychosocial risk factors, especially those acting during the period of rapid brain growth during fetal development and early in life, may cause AD-HKD by disrupting the neural networks supporting executive function and related processes. These factors include fetal exposure to the mother's use of alcohol, drugs, or cigarettes, and the adverse effects of perinatal obstetrical complications or prematurity (for more information about these neurobiological and psychosocial risk factors see elsewhere(777 and 79,)). AD-HKD occurs after traumatic brain injury in 25 per cent of cases.(8 81) or after exposure to environmental toxins such as zinc.(82) Maternal stress during pregnancy and poor quality of caregiving(8 ,84> are also implicated in the origin of AD-HKD.
Environmental risk factors probably interact, making the accurate assessment of the specific role of any single factor difficult. For example, genetic and environmental risks may interact in the case of a genetically predisposed infant and an affected parent. The results of twin studies (85) indicate that both shared and non-shared environmental effects contribute modestly to the incidence of the disorder.
Abnormal thyroid function may also be connected to AD-HKD. There is evidence of mutations in the thyroid receptor-b gene (86> in a subset of patients with generalized resistance to the thyroid hormone. This rare disorder is associated with an increased risk of AD-HKD. However, the prevalence of a thyroid hormone abnormality among children who have AD-HKD is exceedingly low.(87>
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