Depending on where the demyelination takes place and its severity, patients with tumefactive MS have different clinical symptoms.
The more common symptoms include spasticity, visual loss, difficulty in walking and paresthesia which is a feeling of tickling or numbness of the skin.
[citation needed] Subjects have been reported to suffer from a decreased motor control resulting in a 'foot drop',[9] or significantly reduced leg movement.
Spasticity is not as prevalent in tumefactive cases, because in standard MS it is caused by demyelination or inflammation in the motor areas of the brain or the spinal cord.
MS patients may show signs of cognitive impairment where there is a reduction in the speed of information processing, a weaker short-term memory and a difficulty in learning new concepts.
Subjects with tumefactive multiple sclerosis display elevated levels of choline (Cho)/creatine ratio and increased lactate which is associated with demyelinating diseases.
[11] The disease is heterogeneous and the lesions do not always comply with the requirements for multiple sclerosis diagnosis (dissemination in time and space).
[31] In general, it is accepted that the two main causes of pseudo-tumoral lesions are Marburg multiple sclerosis and acute disseminated encephalomyelitis (ADEM).
[34] 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.
And myelin-laden macrophages accumulate at the edges of plaques and stay inactive[35] Diagnosis of tumefactive MS is commonly carried out using magnetic resonance imaging (MRI) and proton MR spectroscopy (H-MRS).
Diagnosis is difficult as tumefactive MS may mimic the clinical and MRI characteristics of a glioma or a cerebral abscess.
[38] MRI diagnosis is based on lesions that are disseminated in time and space, meaning that there are multiple episodes and consisting of more than one area.
Subjects with tumefactive multiple sclerosis may see a reduction of diffusion of the white matter in the affected area of the brain.
[11] Proton (H+) MR spectroscopy (H-MRS) identifies biochemical changes in the brain such as the quantity of metabolic products of neural tissue including choline, creatine, N-acetylaspartate (NAA), mobile lipids and lactic acid.
[citation needed] When demyelination is occurring, there is breakdown of cell membranes resulting in an increase in the level of choline.
[13] No standard treatment exists, but practitioners seem to apply intravenous corticosteroids, followed by plasmapheresis and cyclophosphamide in non-responsive cases[43] Plasmapheresis has been reported to work even in the absence of response to corticosteroids[44] Pharmacologic treatments for MS include immunomodulators and immunosuppressants which reduce the frequency and severity of relapses by about 35% and reduce the lesion growth.
The main ones are Interferon beta (IFN-beta), Glatiramer acetate and Mitoxantrone[citation needed] Plasma exchange has been reported to work at least in some cases[46] Due to the wide range of symptoms experienced by people with MS, the treatment for each MS patient varies depending on the extent of the symptoms.
One hypothesis is that aspirin has an effect on the hypothalamus and can affect the perception of fatigue through altering the release of neurotransmitters and the autonomic responses.
This means that only around 2000 people in the world suffer of tumefactive MS. Of those cases, there is a higher percentage of females affected than males.
When the demyelinating lesion appears alone it has been termed "solitary sclerosis"[citation needed] This variant was first proposed (2012) by Mayo Clinic researches.