<P> Due to neuroferritinopathy's genetic etiology, the disorder is not currently curable . Furthermore, progression of the disorder is unable to be effectively halted . Therefore current treatment focuses on managing symptoms of the disorder . No medication is available to treat all symptoms . Botox has been shown to help with focal dystonia . The dopamine depleter Tetrabenazine shown to help with involuntary movements . 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 . </P> <P> 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 disease's general location of Northern and Northeast England, multiple more cases of neuroferritinopathy have been diagnosed around the rest of the world in recent years . </P> <P> New potential treatment options being researched are Venesection (removing red blood cells), Iron chelation with deferiprone, and Coenzyme Q10 (ubiquinone). </P>

What does iron deposition in the brain mean