Although self-injurious behavior is a common comorbid behavior problem among individuals with neurodevelopmental disorders, little is known about its etiology and underlying neurobiology. Interestingly, it shows up in various forms across patient groups with distinct genetic errors and diagnostic categories. This suggests that there may be shared neuropathology that confers vulnerability in these disparate groups. Convergent evidence from clinical pharmacotherapy, brain imaging studies, postmortem neurochemical analyses, and animal models indicates that dopaminergic insufficiency is a key contributing factor. This chapter provides an overview of studies in which animal models have been used to investigate the biochemical basis of self-injury and highlights the convergence in findings between these models and expression of self-injury in humans.
Keywords: Animal model; Dopamine; Lesch-Nyhan syndrome; Prader-Willi syndrome; Self-injurious behavior; Striatum.