Baló's concentric sclerosis is a disease in which the white matter of the brain appears damaged in concentric layers, leaving the axis cylinder intact. It was described by József Mátyás Baló who initially named it "leuko-encephalitis periaxialis concentrica" from the previous definition, and it is currently considered one of the borderline forms of multiple sclerosis. Baló's concentric sclerosis is a demyelinating disease similar to standard multiple sclerosis, but with the particularity that the demyelinated tissues form concentric layers. Scientists used to believe that the prognosis was similar to Marburg multiple sclerosis, but now they know that patients can survive, or even have spontaneous remission and asymptomatic cases. The concentric ring appearance is not specific to Baló's MS. Concentric lesions have also been reported in patients with neuromyelitis optica, standard MS, progressive multifocal leukoencephalopathy, cerebral autosomal dominant arteriopathy with subcortical infarcts, leukoencephalopathy, concomitant active hepatitis C and human herpes virus 6. Pathophysiology The lesions of the Baló's sclerosis belong to the MS lesion pattern III (distal oligodendrogliopathy). Balo concentric sclerosis is now believed to be a variant of pattern III multiple sclerosis and probably due to metabolic problems. The Baló lesions show veins at their center, like those of MS, some suggestive of microhemorrhages or small ectatic venules. Unlike MS, no cortical gray matter lesions appear. Theoretical models According with Dr. Lucchinetti investigations, in Baló's concentric sclerosis, the rings may be caused by a physiological hypoxia (similar to that caused by some toxins or viruses) in the lesion, which is in turn countered by expression of stress proteins at the border. This expression and counter-expression forms rings of preserved tissue within the lesion and rings of demyelinated tissue just beyond where the previous attack had induced the protective stress proteins. Hence, subsequent attacks form concentric rings. Some other researchers maintain that, as in pattern III MS, the mitochondrial respiratory chain complex IV activity is reduced and this could be the culprit of glutamate-mediated axonal injury. Ultimately, this expanding lesion causes the progressive picture typically seen. However, in some patients, the pathology underlying the disease appears to burn out and hence the disease may halt, hence the patients who spontaneously recover. The mechanisms triggering attacks and recovery remain uncertain. Nevertheless, this model is questioned by recent reports that found astrocyte damage, similar to the one found in aquaporin-seropositive neuromyelitis optica. Though no anti-NMO antibodies have been found, the damage is similar, pointing