Usable methods may include posture reeducation, muscle release, joint mobilization, trunk stabilization, and manual therapy for overworked muscles. Cognitive behavioural therapy is used in all chronic pain patients, especially those who have severe, chronic, life-controlling pain that is unresponsive to treatment. It had not been checked for efficiency in clinical trials. The state of pain management with EDS is considered insufficient. Medications
Nonsteroidal anti-inflammatory drugs (NSAIDs) may help if the pain is caused by inflammation. But long-term use of NSAIDs is often a risk factor for gastrointestinal, renal, and blood-related side effects. It can worsen symptoms of mast cell activation syndrome, a disease that may be associated with EDS. Acetaminophen can be used to avoid the bleeding-related side effects of NSAIDs.Opioids have shown efficiency in some EDS cases for the management of both acute and chronic pain.112
Lidocaine can be applied topically after subluxations and painful gums. It can also be injected into painful areas in the case of musculoskeletal pain.If the pain is neuropathic in origin, tricyclic antidepressants in low doses, anticonvulsants, and selective norepinephrine reuptake inhibitors can be used. Dislocation and subluxation management
When a dislocation or subluxation does occur, muscle spasms and stress tend to occur, increasing pain and reducing the chances of the dislocation/subluxation naturally relieving. Methods to support a joint after such an incident include usage of a sling to hold the joint in place and allow it to relax. Orthopedic casts are not advised as there could be pain if unrelaxed muscles are still trying to spasm out against the cast.
The pain may also be misdiagnosed as a behavior disorder or Munchausen by proxy.The pain associated with EDS ranges from mild to debilitating. Causes
Every type of EDS except the hypermobile type (which affects the vast majority of people with EDS) can be positively tied to specific genetic variation. Variations in these genes can cause EDS:
Collagen primary structure and collagen processing: ADAMTS2, COL1A1, COL1A2, COL3A1, COL5A1, COL5A2
Collagen folding and collagen cross-linking: PLOD1, FKBP14
Structure and function of myomatrix: TNXB, COL12A1
Glycosaminoglycan biosynthesis: B4GALT7, B3GALT6, CHST14, DSE
Complement pathway: C1R, C1S
Intracellular processes: SLC39A13, ZNF469, PRDM5Variations in these genes usually alter the structure, production, or processing of collagen or proteins that interact with collagen. Collagen provides structure and strength to connective tissue. A defect in collagen can weaken connective tissue in the skin, bones, blood vessels, and organs, resulting in the features of the disorder. Inheritance patterns depend on the specific syndrome. Most forms of EDS are inherited in an autosomal dominant pattern, which means only one of the two copies of the gene in question must be altered to cause a disorder. A few are inherited in an autosomal recessive pattern, which means both copies of the gene must be altered for a person to be affected. It can also be an individual (de novo or "sporadic") variation. Sporadic variations occur without any inheritance. Diagnosis
A diagnosis can be made by an evaluation of medical history and clinical observation. The Beighton criteria are widely used to assess the degree of joint hypermobility. DNA and biochemical studies can help identify affected people.