In the 1950s, the term "benign myalgic encephalomyelitis" was used in relation to a comparable outbreak at the Royal Free Hospital in London. The descriptions of each outbreak were varied, but included symptoms of malaise, tender lymph nodes, sore throat, pain, and signs of encephalomyelitis. The cause of the condition was not identified, although it appeared to be infectious, and the term "benign myalgic encephalomyelitis" was chosen to reflect the lack of mortality, the severe muscular pains, symptoms suggesting damage to the nervous system, and to the presumed inflammatory nature of the disorder. Björn Sigurðsson disapproved of the name, stating that the illness is rarely benign, does not always cause muscle pain, and is possibly never encephalomyelitic. The syndrome appeared in sporadic as well as epidemic cases. In 1969, benign myalgic encephalomyelitis appeared as an entry to the International Classification of Diseases under Diseases of the nervous system. In 1986, Ramsay published the first diagnostic criteria for ME, in which the condition was characterized by: 1) muscle fatiguability in which, even after minimal physical effort, three or more days elapse before full muscle power is restored; 2) extraordinary variability or fluctuation of symptoms, even in the course of one day; and 3) chronicity. By 1988, the continued work of Ramsay had demonstrated that, although the disease rarely resulted in mortality, it was often severely disabling. : 28–29  Because of this, Ramsay proposed that the prefix "benign" be dropped.
Symptoms affecting movement (dystonia) have also been treated with L-Dopa, orphenadrine, benzhexol, sulpiride, diazepam, clonazepam, and deanol. Parkinsonian symptoms were not decreased by L-Dopa. Iron supplements should be avoided. Epidemiology
Neuroferritinopathy was first discovered in 2001, with its first case being reported in Cumbria from Northern England. The discovery of neuroferritinopathy was mediated by a study done on a large family suffering from a dominantly inherited basal ganglia disease. The disease was reported to be instigated by a mutation on the ferritin light chain polypeptide, (FTL1), and was found to cause iron accumulation in the brain and neurodegeneration. Following in suit of the location of the first case of Neuroferritinopathy, the majority of patients diagnosed with the disease have also been found in Northern and Northeast England. The localization of the majority of cases to Northern and Northeast England suggests that a common ancestor may be responsible for many or possibly all cases. Despite there being fewer than 100 cases reported and the diseases general location of Northern and Northeast England, multiple more cases of neuroferritinopathy have been diagnosed around the rest of the world in recent years. Research
New potential treatment options being researched are Venesection (removing red blood cells), Iron chelation with deferiprone, and Coenzyme Q10 (ubiquinone). References


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