Therapeutic intervention
Children in the child welfare system have often experienced significant and repeated traumas and having a background in foster homes—especially in instances of sexual abuse—can be the precipitating factor in a wide variety of psychological and cognitive deficits it may also serve to obfuscate the true cause of underlying issues. The foster care experience may have nothing to do with the symptoms, or on the other hand, a disorder may be exacerbated by having a history of foster care and attendant abuses. The human brain however has been shown to have a fair degree of neuroplasticity. and adult neurogenesis has been shown to be an ongoing process.Multidimensional Treatment Foster Care (MTFC), also referred to as Treatment Foster Care Oregon (TFCO) and Treatment Foster Care (TFC) is a community-based intervention that was created in 1983 by Dr. Patricia Chamberlain and her associated colleagues with the initial design intended to offer a replacement for group facilities. MTFC has differing approaches for different age groups. Preschoolers receive “a behavior-management approach and intensively trains, supervises, and supports foster caregivers to provide positive adult support and consistent limit setting” coupled with “coordinated interventions with the child’s biological parents.” MTFC for adolescence consists of individual placement with an intensely trained foster family providing “coordinated interventions in the home, with peers, [and] in educational settings.” MTFC has been shown to provide better results than group facilities and proves to be more cost effective.
Thus, it has been suggested that free radicals, oxidative stress, and reactive oxygen species may play some role in the neuropathology of LNS.However, some evidence suggests against a role for uric acid in the neuropathology of Lesch–Nyhan syndrome:

Hyperuricemia associated with classic primary gout, which is caused by low uric acid renal clearance rather than uric acid overproduction, is not associated with neuropathology. Hypouricemia occurs in a number of purine disorders, in particular xanthinuria. Despite having complete absence of blood uric acid, xanthinuria patients do not have any neuropathology, nor any other disease states – other than the kidney stones caused by accumulation of insoluble xanthine in lieu of uric acid.Similarly,  uric acid does not penetrate the blood–brain barrier well. However, oxidative stress due to uric acid is now thought to figure in metabolic syndrome, atherosclerosis, and stroke, all syndromes associated with high uric acid levels. Similarly, Superoxide dismutase ( "SOD" ) and SOD-mimetics such as TEMPOL ameliorate the effects of hyperuricemia. Likewise, 6-hydroxydopamine (the putative animal model for Lesch–Nyhans neuropathy) apparently acts as a neurotoxin by generation of reactive oxygen species. It may be that oxidative stress induced by some other oxypurine such as xanthine causes the disease. Diagnosis
When an affected individual has fully developed the three clinical elements of uric acid overproduction, neurologic dysfunction, and cognitive and behavioral disturbances, diagnosis of LNS is easily made. Diagnosis is less easy in the early stages, when the three features are not yet obvious.