<unk> 's symptoms result from maturation-related changes in various systems of the brain. How<unk>  occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with<unk> , and the neuropsychological linkages between brain structures and behaviors. The behaviors appear to have multiple pathophysiologies. There is evidence that gut–brain axis abnormalities may be involved. A 2015 review proposed that immune dysregulation, gastrointestinal inflammation, malfunction of the autonomic nervous system, gut flora alterations, and food metabolites may cause brain neuroinflammation and dysfunction. A 2016 review concludes that enteric nervous system abnormalities might play a role in neurological disorders such as<unk> . Neural connections and the immune system are a pathway that may allow diseases originated in the intestine to spread to the brain. Several lines of evidence point to synaptic dysfunction as a cause of<unk> . Some rare mutations may lead to<unk>  by disrupting some synaptic pathways, such as those involved with cell adhesion. Gene replacement studies in mice suggest that<unk> ic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes. All known teratogens (agents that cause birth defects) related to the risk of<unk>  appear to act during the first eight weeks from conception, and though this does not exclude the possibility that<unk>  can be initiated or affected later, there is strong evidence that<unk>  arises very early in development.
Autism
Schizophrenia
Tourettism
Reactive attachment disorder
Puberphonia
Intellectual disability
Selective mutism
Lesch–Nyhan syndrome