Any of these muscles can be involved or spasm with a painful and dysfunctional sacroiliac joint. The SI joint is a pain-sensitive structure richly innervated by a combination of unmyelinated free nerve endings and the posterior primary rami of spinal segments L2-S3. The wide possibility of innervation may explain why pain originating from the joint can manifest in so many various ways, with different and unique referral patterns (see "referred pain") for individual patients. Patients with sacroiliac joint dysfunction can also develop tightness and dysfunction in the hamstring, quadriceps, iliotibial tract (see "iliotibial band syndrome") and hip flexors, including the psoas muscle. Individuals with severe and long-standing sacroiliac joint dysfunction can develop muscle deconditioning and atrophy throughout the body due to limitation of activities and exercise that bring about pain in the low back. Diagnosis
Perhaps the biggest reason for misdiagnosis or lack of diagnosis of sacroiliac joint dysfunction is based on the inability of common radiological imaging to discern the disorder. Diagnostic testing, such as X-ray, CT scan, or MRI, do not usually reveal abnormalities; therefore, they cannot reliably be used for diagnosis of sacroiliac joint dysfunction. There is a new imaging test SPECT/CT which can sometimes detect sacroiliac joint dysfunction. There is also a lack of evidence that sacroiliac joint mobility maneuvers (Gillet, Standing flexion test, and Seated Flexion test) detect motion abnormalities. Given the inherent technical limitations of the visible and palpable signs from these sacroiliac joint mobility maneuvers another broad category of clinical signs have been described called provocative maneuvers.
People with variations in this gene can have kyphoscoliosis, tapered fingers, osteoporosis, aortic aneurysms, and problems with the lungs. Other cases can be caused by the SLC39A13 gene. Those with variations in this gene have protuberant eyes, wrinkled palms of the hands, tapering fingers, and distal joint hypermobility. Musculocontractural EDS
Musculocontractural EDS is characterized by congenital multiple contractures, characteristically adduction-flexion contractures and/or talipes equinovarus (clubfoot), characteristic craniofacial features, which are evident at birth or in early infancy, and skin features such as skin hyperextensibility, bruising, skin fragility with atrophic scars, and increased palmar wrinkling. It can be caused by variations in the CHST14 gene. Some other cases can be caused by variations in the DSE gene. Myopathic EDS
Myopathic EDS (mEDS) is characterized by three major criteria: congenital muscle hypotonia and/or muscle atrophy that improves with age, proximal joint contractures of the knee, hip, and elbow, and hypermobility of distal joints (ankles, wrists, feet, and hands). Four minor criteria may also contribute to a diagnosis of mEDS. This disorder can be inherited through either an autosomal dominant or an autosomal recessive pattern. Molecular testing must be completed to verify that mutations in the COL12A1 gene are present; if not, other collagen-type myopathies should be considered. Periodontal EDS
Periodontal EDS (pEDS) is an autosomal-dominant disorder characterized by four major criteria of severe and intractable periodontitis of early-onset (childhood or adolescence), lack of attached gingiva, pretibial plaques, and family history of a first-degree relative who meets clinical criteria. Eight minor criteria may also contribute to the diagnosis of pEDS.