The pathology of the<unk>  demyelinating lesion (TDL) is heterogeneous. There are several conditions can produce<unk>  lesions. This is known because in some special cases the etiology can be identified. For example, there are some cases of NMO, misidentified as MS and treated with interferon-beta by mistake. Some of these patients developed<unk>  lesions. Anyway, it is important to have into account that NMO itself can also produce them Some other cases have been found related to viral infection, some others related to NMOSD, others could be paraneoplastic, Also some cases could be related to hormonal treatments Other possible cause are immunomodulatory combinations. In particular, it has been found that switching from standard MS therapies to fingolimod can trigger<unk>  lesions in some MS patients While standard<unk>  sclerosis process has an autoimmune response after the breach of the blood-brain barrier, in<unk>  MS things do not process in the same way, and demyelinating lesions do not always show antibody damage. Subjects with<unk>  display elevated levels of choline (Cho)/creatine ratio and increased lactate which is associated with demylinating diseases. Cases also display oligoclonal bands in the cerebrospinal fluid. The disease is heterogeneous and the lesions do not always comply with the requirements for<unk>  sclerosis diagnosis (dissemination in time and space). In these cases it is only possible to speak about<unk>  demyelination (TD). In general, it is accepted that the two main causes of pseudo-tumoral lesions are Marburg<unk>  sclerosis and acute disseminated encephalomyelitis (ADEM).<unk>  demyelination of the spinal cord is rare but it has been reported Damage is not confined to the demyelinating area. Wallerian degeneration outside the lesions has been reported. In general, during the acute phase, the plaques of lesions were characterized by massive demyelination with relatively axonal preservation associated with reactive astrocytosis and infiltration of macrophages. In plaques of chronic lesions, demyelinated lesions with relative axonal preservation and sharply defined margins were major findings. And myelin-laden macrophages accumulate at the edges of plaques and stay inactive
Tumefactive multiple sclerosis
CMV polyradiculomyelopathy
Paraneoplastic cerebellar degeneration
Post viral cerebellar ataxia
Juvenile primary lateral sclerosis
Malignant multiple sclerosis
Viliuisk encephalomyelitis
Chronic inflammatory demyelinating polyneuropathy