The idea that this set of symptoms forms a distinct entity began to attain greater recognition in the latter part of the 19th century. John Erichsen, a surgeon from London, played an important role in developing the study of PCS. The controversy surrounding the cause of PCS began in 1866 when Erichsen published a paper about persisting symptoms after sustaining mild head trauma. He suggested that the condition was due to "molecular disarrangement" to the spine. The condition was originally called "railroad spine" because most of the injuries studied had happened to railroad workers. While some of his contemporaries agreed that the syndrome had an organic basis, others attributed the symptoms to psychological factors or to outright feigning. In 1879, the idea that a physical problem was responsible for the symptoms was challenged by Rigler, who suggested that the cause of the persisting symptoms was actually "compensation neurosis": the railroads practice of compensating workers who had been injured was bringing about the complaints. Later, the idea that hysteria was responsible for the symptoms after a mild head injury was suggested by Charcot. Controversy about the syndrome continued through the 20th century. During World War I many soldiers with puzzling symptoms after being close to a detonation but without any evidence of a head wound. The illness was called shell shock, and a psychological explanation was eventually favoured. By 1934 the current concept of PCS had replaced ideas of hysteria as the cause of post-concussion symptoms.
if a primary protein is not functioning properly then maybe another protein could take its place by augmenting it. Upregulation of compensatory proteins has been done in models of transgenic mice. Future developments
There is no cure for any type of muscular dystrophy group. Several drugs designed to address the root cause are under development, including gene therapy (Microdystrophin), and antisense drugs (Ataluren, Eteplirsen etc.). Other medications used include corticosteroids (Deflazacort), calcium channel blockers (Diltiazem) to slow skeletal and cardiac muscle degeneration, anticonvulsants to control seizures and some muscle activity, and immunosuppressants (Vamorolone) to delay damage to dying muscle cells. Physical therapy, braces, and corrective surgery may help with some symptoms while assisted ventilation may be required in those with weakness of breathing muscles. Outcomes depend on the specific type of disorder. Prognosis
The progression of Becker muscular dystrophy is highly variable—much more so than Duchenne muscular dystrophy. There is also a form that may be considered as an intermediate between Duchenne and Becker MD (mild DMD or severe BMD). Severity of the disease may be indicated by age of the patient at the onset of the disease. One study showed that there may be two distinct patterns of progression in Becker muscular dystrophy. Onset at around age 7 to 8 years of age shows more cardiac involvement and trouble climbing stairs by age 20, if onset is around age 12, there is less cardiac involvement.The quality of life for patients with Becker muscular dystrophy can be impacted by the symptoms of the disorder.