why symptoms can vary greatly between different individuals, depending on where their lesions occur. lesion recovery under laboratory conditions, stem cells are quite capable of proliferating and differentiating into remyelinating oligodendrocytes; it is therefore suspected that inflammatory conditions or axonal damage somehow inhibit stem cell proliferation and differentiation in affected areas it is possible to predict how much and when lesion will recover related to this, it was found in 2016 that neural cells of primary progressive patients (ppms) do have some kind of problem to protect neuroprotection against demyelination or oligodendrocytes, compared to healthy subjects. some genetics seem to underlie the problem as this was shown using induced pluripotent stem cell (ipsc) as neural progenitor cells (npc) demyelination patterns in standard ms four different damage patterns, known as lassmann patterns, have been identified by her team in the scars of the brain tissue in multiple sclerosis, and they are used sometimes as a basis for describing lesions in other demyelinating diseases. pattern ithe scar presents t-cells and macrophages around blood vessels, with preservation of oligodendrocytes, but no signs of complement system activation. pattern iithe scar presents t-cells and macrophages around blood vessels, with preservation of oligodendrocytes, as before, but also signs of complement system activation can be found. though this pattern could be considered similar to damage seen in nmo, some authors report no aqp4 damage in pattern ii lesions pattern iiithe scars are diffuse with inflammation, distal oligodendrogliopathy and microglial activation. there is also loss of myelin-associated glycoprotein (mag). the scars do not surround the blood vessels, and in fact, a rim of preserved myelin appears around the vessels. there is evidence of partial remyelinization and oligodendrocyte apoptosis. for some researchers this pattern is an early stage of the evolution of the others. pattern ivthe scar presents sharp borders and oligodendrocyte degeneration, with a rim of normal appearing white matter. there is a lack of oligodendrocytes in the center of the scar. there is no complement activation or mag loss. the meaning of this fact is controversial. for some investigation teams it means that ms is a heterogeneous disease. others maintain that the shape of the scars can change with time from one type to other and this could be a marker of the disease evolution. anyway, the heterogeneity could be true only for the early stage of the disease. some lesions present mitochondrial defects that could distinguish types of lesions. currently antibodies to lipids and peptides in sera, detected by microarrays, can be used as markers of the pathological subtype given by brain biopsy. after some debate among research groups, currently the heterogeneity hypothesis looks like accepted