This is considered a  reliable resource for establishing if a child is going through post traumatic stress disorder due to physical, sexual, or mental abuse.In a study conducted in Oregon and Washington state, the rate of PTSD in adults who were in foster care for one year between the ages of 14–18 was found to be higher than that of combat veterans, with 25 percent of those in the study meeting the diagnostic criteria as compared to 12–13 percent of Iraq war veterans and 15 percent of Vietnam war veterans, and a rate of 4% in the general population. The recovery rate for foster home alumni was 28.2% as opposed to 47% in the general population. "More than half the study participants reported clinical levels of mental illness, compared to less than a quarter of the general population". Eating disorders
Foster children are at increased risk for a variety of eating disorders in comparison to the general population. In a study done in the United Kingdom, 35% of foster children experienced an increase in Body Mass Index (BMI) once in care. Food Maintenance Syndrome is characterized by a set of aberrant eating behaviors of children in foster care. It is "a pattern of excessive eating and food acquisition and maintenance behaviors without concurrent obesity"; it resembles "the behavioral correlates of Hyperphagic Short Stature". It is hypothesized that this syndrome is triggered by the stress and maltreatment foster children are subjected to, it was prevalent amongst 25 percent of the study group in New Zealand.
The pathologic basis of TTH is most likely derived from a combination of personal factors, environmental factors, and alteration of both peripheral and central pain pathways. Peripheral pain pathways receive pain signals from pericranial (around the head) myofascial tissue (protective tissue of muscles) and alteration of this pathway likely underlies episodic tension-type headache (ETTH). In addition to these myofascial tissue pain signals, pericranial muscle tenderness, inflammation, and muscle ischemia have been postulated in headache literature to be causal factors in the peripheral pathophysiology of TTH. However, multiple studies have failed to illustrate evidence for a pathologic role of either ischemia or inflammation within the muscles. Pericranial tenderness is also not likely a peripheral causal factor for TTH, but may instead act to trigger a chronic pain cycle in which the peripheral pain response is transformed over time into a centralized pain response. It is then these prolonged alterations in the peripheral pain pathways that lead to increased excitability of the central nervous system pain pathways, resulting in the transition of episodic tension-type headache into chronic tension type headache (CTTH). Specifically, the hyperexcitability occurs in central nociceptive neurons (the trigeminal spinal nucleus, thalamus, and cerebral cortex) resulting in central sensitization, which manifests clinically as allodynia and hyperalgesia of CTTH.