Recovery from TM may be absent, partial or complete and generally begins within 1 to 3 months after acute treatment. Historic data, not controlling for treatment, suggested that approximately 1/3 of individuals recover with little or only minor symptoms, 1/3 are left with a moderate degree of permanent disability and 1/3 have virtually no recovery and are left severely functionally disabled. These data, however, predate a number of more aggressive treatment protocols and are likely inaccurate. In present day experiences the outcomes seem to be better than this distribution. Most show good to fair recovery. Some studies have shown that the rapid progression of clinical symptoms, the presence of back pain, and the presence of spinal shock, as well as para-clinical evidence, such as absent central conduction on evoked potential testing and the presence of 14-3-3 protein in the cerebrospinal fluid (CSF) during the acute phase are often indicators of a less complete recovery. These markers are imperfect and do not assume aggressive rehabilitation or treatment strategies.
TM can be the presenting feature of Multiple Sclerosis. In individuals with acute partial transverse myelitis and normal brain MRI, about 10-33 percent develop MS over a five to ten-year period. If the brain MRI shows lesions, the transition rate to clinically definite MS is known to be quite high, in the range of 80 to 90 percent within a few years. Those who are ultimately diagnosed with MS are more likely to have asymmetric clinical findings, predominant sensory symptoms with relative sparing of motor systems, MR lesions extending over fewer than 2 spinal segments, abnormal brain MRI, and oligoclonal bands in the CSF.
Although typically a monophasic disease, in a subset of cases that manifest a history of systemic autoimmune disease, TM can be recurrent. Recurrence can often be predicted at the initial acute onset based on multifocal lesions in the spinal cord, lesions in the brain, presence of anti-Rho antibody, underlying mixed connective tissue disease, the presence of oligoclonal bands in the cerebrospinal fluid, and/or NMO-IgG antibodies.