cell nuclei virtually devoid of other cell elements such as the cytoplasm), wisps of collagen, atrophic, degenerating muscle fibers, regenerating muscle fibers, and intact skeletal muscle cells containing multiple nuclei. There is no evidence of inflammation, hemorrhage, cell necrosis, or rapidly dividing and/or proliferating cells. Etiology
It has been postulated that the FMC tumor mass itself is a remnant of a hematoma caused by tissue injury occurring during delivery. However, there are no features of hematomas (e.g. hemosiderin released by dying red blood cells) in theses lesions at diagnosis and no evidence of trauma (e.g. overlying skin changes or discolorations) at birth in infants who later present with FMC tumors. It has also been suggested that venous outflow obstruction occurring in the fetus while in the uterus or during delivery leads to degeneration of sternocleidomastoid muscle fibers and subsequent fibrosis of the damaged areas. Finally, it has been suggested that an injury due to poor fetal head positioning in the uterus produces a compartment syndrome-like pressure-induced injury to the sternocleidomastoid muscle that results in muscle cell death followed by tissue fibrosis and the usual pathology of FMC tumors. Diagnosis
The recommended first step after clinically detecting a sternocleidomastoid mass in a newborn infant is Doppler ultrasonography combined with duplex ultrasonography. This method commonly reveals diagnostic (up to 100% sensitivity rates) findings of diffuse or focal enlargement of sternocleidomastoid muscle that has no cysts or other ultrasonography-detected abnormalities. If these imaging findings are not diagnostic, magnetic resonance imaging may clarify the  diagnosis.
If the findings still remain unclear, microscopic examination of fine needle asperates taken from the tumor will, when combined with the imaging findings, the lesion’s natural history, and its clinical presentation, likely confirm the diagnosis of FMC in virtually all cases. Treatment and prognosis
Prompt diagnosis and treatment of FMS is crucial for avoiding the impairments that may follow long-term mal-positioning of infants head such as permanent facial asymmetry, flattened head, loss of neck mobility, and scoliosis. About 95% of infants with minimal limitations in their heads mobility show improvements in this mobility after 4 weeks of an active home stimulation program (i.e. observation, massage, and active and passive stretching) while ~91% of infants with more severe movement limitations show good results after 3 sessions of targeted physiotherapy over a 3–4 month period. The recommended treatment for infants who show no improvements in mobility after 1 year of physical therapy or who initially present at >12 months of age is surgical tenotomy (i.e. cutting) of one of the tendons on the involved sternocleidomastoid muscle. Tenotomy may use the open surgical (i.e. cutting of skin) approach or endoscopic (i.e. percutaneous) approach. The overall prognosis of FMS tumors is good using these treatment measures.Infants presenting with FMS should be examined for the presence of hip dysplasia. See also
Skin lesion


== References ==