Studies have shown people with PTSD demonstrate reduced levels of NPY, possibly indicating their increased anxiety levels.Other studies indicate that people with PTSD have chronically low levels of serotonin, which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity. Serotonin also contributes to the stabilization of glucocorticoid production. Dopamine levels in a person with PTSD can contribute to symptoms: low levels can contribute to anhedonia, apathy, impaired attention, and motor deficits; high levels can contribute to psychosis, agitation, and restlessness.Several studies described elevated concentrations of the thyroid hormone triiodothyronine in PTSD. This kind of type 2 allostatic adaptation may contribute to increased sensitivity to catecholamines and other stress mediators. Hyperresponsiveness in the norepinephrine system can also be caused by continued exposure to high stress. Overactivation of norepinephrine receptors in the prefrontal cortex can be connected to the flashbacks and nightmares frequently experienced by those with PTSD. A decrease in other norepinephrine functions (awareness of the current environment) prevents the memory mechanisms in the brain from processing the experience, and emotions the person is experiencing during a flashback are not associated with the current environment.There is considerable controversy within the medical community regarding the neurobiology of PTSD. A 2012 review showed no clear relationship between cortisol levels and PTSD. The majority of reports indicate people with PTSD have elevated levels of corticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone.
The newer term "generalised hypermobility spectrum disorder" includes people with generalised joint hypermobility, often determined using the Beighton Score, and other symptoms. Those who do not meet the Beighton Score criteria may be diagnosed with historical joint hypermobility spectrum disorder, peripheral hypermobility spectrum disorder, or localised hypermobility spectrum disorder.In comparison to the diagnostic criteria of hypermobile Ehlers-Danlos syndrome, the criteria for hypermobile spectrum disorder are less strict. However, these criteria are differentiated from criteria of other EDS types and therefore its less-strict criteria are only comparable to the criteria of hEDS. As those with HSD experience a considerable amount of discomfort, it is important to focus on the treatment, not the labels. The severity of each condition can be equivalent. In particular, musculoskeletal involvement is a requirement for diagnosis with any form of hypermobility spectrum disorder but not for hypermobile Ehlers-Danlos syndrome. Like hypermobile Ehlers-Danlos syndrome, hypermobility spectrum disorders are associated with orthostatic tachycardia, gastrointestinal disorders, and pelvic and bladder dysfunction. Treatment
Treating hypermobility syndrome can be difficult. The condition has no direct cure, but its symptoms can be treated. Physiotherapy, particularly exercise, is the main treatment for the condition, although there is only limited evidence for its effectiveness.Treatments for pain include:

Bandaging the affected area;
Placing an ice pack on the affected area;
Taking over the counter pain killers such as paracetamol or ibuprofen. Prevalence
Prevalence of the condition is unknown, but can be high in those attending musculoskeletal services. == References ==