It has been proposed that BCS lesions may not denote a single disease, but a final pathway of various demyelinating diseases, reflecting the presence of intralesional hypoxia as recently proposedRecently it has been reported that pattern III lesions are responsive to Mitoxantrone. On the other hand, this pattern is the less responsive to plasmapheresisPattern III lesions can be diagnosed without a biopsy because these patients show a high reactivity to AQP1 (without antibody) and varicella zoster virus (VZV). Origin of the lesions
Pattern III lesions were for sometime thought to be a MS nascent lesion, though it is not likely anymore. A strain of bacterium Clostridium perfringens has been found in Pattern III lesions. Tests in mice found that a toxin made by a rare strain of C. perfringens caused MS-like damage in the brain, and earlier work had identified this strain of C. perfringens in a human with MS. MS patients were found to be 10 times more immune-reactive to the epsilon toxin than healthy people.Later reports state that Balós patients showed loss of AQP1 and AQP4 in demyelinating lesions without binding auto-antibodies but with high reactivities to AQP1 peptides, which probably reflect astrocytic damage

History
Though the disease carries the name of József Baló, it was first described by Otto Marburg in 1906. Later, in 1928, József Baló studied the encephalitis periaxialis concentrica in a Hungarian patient, showing also demyelination of the peripheral nervous system. See also
Multiple sclerosis
The Lesion Project
Tumefactive multiple sclerosis

References

Khonsari RH, Calvez V (September 2007). "Concentric demyelination by self-organization: a new hypothesis for Balós sclerosis".
Authors review the previous pathogenic theories, discuss the link between concentric sclerosis and Liesegangs periodic precipitation phenomenon and propose a new mechanism based on self-organization. Clinical courses
It that the clinical course is primary progressive, but a relapsing-remitting course has been reported. It seems that the course gets better with prednisone therapy, although evidence of this is anecdotal and such conclusions are difficult to accept given that there are cases where patients spontaneously recover whether the patient was on steroid therapy or not.Baló lesions can disappear over time, but it has also been reported that the disease can convert to RRMSThe clinical course of Balo-like lesions also depends to the context in which they appear. Balo-like lesions have been reported in aquaporin-4 seropositive and seronegative NMOSD, and also in children, as part of an ADEM-like presentation

Diagnosis
Lesions under MRI are distinctive due to their natural concentric shape.Under a lumbar puncture CSF test, with Balós concentric sclerosis, as well as patients with pattern III lesions, were recently shown to be mostly negative for CSF-restricted oligoclonal bands. Also pattern III patients tend to be negative under the MRZ-reaction (measles, rubeola and zoster viruses)

Paediatric cases
Balós concentric sclerosis in children has been reported to behave different from adults

Lesions in autopsy and biopsy
A report comparing 1H-magnetic resonance spectroscopy, magnetization transfer and diffusion tensor imaging with histopathology in a patient with Balós concentric sclerosis, found that inflammation was traced by fractional anisotropy and increased lactate.