A self-limiting spontaneously occurring form of torticollis with one or more painful neck muscles is by far the most common (stiff neck) and will pass spontaneously in 1–4 weeks. Usually the sternocleidomastoid muscle or the trapezius muscle is involved. Sometimes draughts, colds, or unusual postures are implicated; however, in many cases, no clear cause is found. These episodes are commonly seen by physicians.Most commonly this self-limiting form relates to an untreated dental occlusal dysfunction, which is brought on by clenching and grinding the teeth during sleep. Once the occlusion is treated it will completely resolve. Treatment is accomplished with an occlusal appliance, and equilibration of the dentition. Tumors of the skull base (posterior fossa tumors) can compress the nerve supply to the neck and cause torticollis, and these problems must be treated surgically. Infections in the posterior pharynx can irritate the nerves supplying the neck muscles and cause torticollis, and these infections may be treated with antibiotics if they are not too severe, but could require surgical debridement in intractable cases. Ear infections and surgical removal of the adenoids can cause an entity known as Grisels syndrome, a subluxation of the upper cervical joints, mostly the atlantoaxial joint, due to inflammatory laxity of the ligaments caused by an infection. The use of certain drugs, such as antipsychotics, can cause torticollis. Antiemetics - Neuroleptic Class - Phenothiazines
There are many other rare causes of torticollis. A very rare cause of acquired torticollis is fibrodysplasia ossificans progressiva (FOP), the hallmark of which is malformed great toes.
The thrombi which form in these individuals are unstable, tend to embolize, and may therefore lead to thromboembolic events such as pulmonary embolism. Both bleeding and thrombotic events can occur at separate times or even concurrently in the same individual with the disorder. Fibrinogen storage disease
All individuals with mutations causing fibrinogen storage disease have low blood fibrinogen levels but usually lack severe bleeding episodes, thrombotic episodes or liver disease. Individuals that do have fibrinogen storage disease often come to attention either because they have close relatives with the disease, are found to be hypofibrinogenmic during routing testing, or exhibit clinical (e.g. jaundice) or laboratory (e.g. elevated blood levels of liver enzymes) evidence of liver disease. Unlike other forms of congenital hypofibrinogenemia, a relatively high percentage of individuals with fibrinogen storage disease have been diagnosed in children of very young age. Pathophysiology
Fibrinogen is made and secreted into the blood by liver hepatocytes. The final secreted protein is composed of two trimers each of which is composed of three polypeptide chains, Aα (also termed α) encoded by the FGA gene, Bβ (also termed β) encoded by the FGB gene, and γ encoded by the FGG gene. All three genes are located on the long or "p" arm of human chromosome 4 (at positions 4q31.3, 4q31.3, and 4q32.1, respectively). The genes are ordered FGB, FGA, and FGG and are transcribed into messenger RNA in tight synchrony. The messenger RNAs associate with the endoplasmic reticulum, translated into polypeptides, and enter the endoplasmaic reticulum where they assembled together.