Prognosis

The course of TM is highly variable.

Acute partial TM, such as is seen with multiple sclerosis (MS), has a good prognosis. The neurologic deficits typically improve over several weeks, and most patients achieve a complete or near-complete recovery. Patients with complete lesions, especially those with longitudinally extensive TM, have more variable recovery. An individual attack is typically more severe than in acute partial TM, and the degree of recovery ranges from complete to none. Some patients are left with permanent and severe motor and sensory deficits.

Acute partial TM

Acute partial TM typically improves over several weeks to months, with most recovery taking place during the first 3 months after onset, though sometimes slower improvement is noted for up to 1 year after TM onset. If no other disease is found responsible for the myelitis attack, the risk of recurrence (or other central nervous system attack) is best predicted by brain magnetic resonance imaging. The presence of one or more white matter lesions typical of demyelination predicts >80% risk for the patient having another event, and therefore developing confirmed MS, within 10 years.[7]

Complete TM

Longitudinally extensive TM has many causes, but most cases are idiopathic monophasic TM or the first event of a neuromyelitis optica spectrum disorder (NMOSD). Maximum deficit usually occurs within a few days, and sometimes within 24 hours. Recovery is highly variable, ranging from return to normal function to complete loss of motor and sensory loss below the level of the lesion. About one-third of patients experience complete or near-complete recovery, one-third have moderate residual deficits, and the remaining one-third are severely disabled.[1][79] Most recovery occurs within 3 months, but slower improvement is sometimes noted for up to 2 years after TM onset.[51][79][87] Onset with back pain, maximal progression within hours of onset, spinal shock, and sensory impairment up to the cervical level are risk factors for poorer outcome.[92]

If the patient is seropositive for aquaporin-4-IgG, he or she would be considered to have an NMOSD with the longitudinally extensive TM event representing the inaugural attack.[5][9] Such a patient is at very high risk for relapse of TM or of developing optic neuritis (thereby fulfilling NMOSD diagnostic criteria).

The risk of recurrent TM is unknown in cases associated with systemic processes such as connective tissue diseases; generally treatment for the underlying disease is recommended.[79]

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