The sequelae of transverse myelitis are variable, even after severe paralysis. One third of patients recover completely, one third does not improve from their nadir, and one third has some degree of residual symptoms (Lipton and Teasdall 1973; Ropper and Poskanzer 1978; Berman et al 1981; Dunne et al 1986). Patients with multiple sclerosis-like acute partial myelitis have a better short-term prognosis and are more likely to recover than patients with acute complete transverse myelitis. Recurrences are unusual in acute transverse myelitis compared to multiple sclerosis (Tippett et al 1991; Jeffery et al 1993). Some patients have lasting motor, sensory, or urologic complaints. Persistent genitourinary symptoms include detrusor hyperreflexia, detrusor-external sphincter dyssynergia, and erectile dysfunction (Berger et al 1990).
Bad prognostic indicators include a catastrophic onset, severe weakness, initial lancinating pain, sensory disturbance at cervical levels, spinal shock, incontinence, no recovery after 3 months, long cord lesions, and presence of 14-3-3 protein in the CSF (Irani and Kerr 2000). Favorable prognostic signs include subacute progression of sensory or motor symptoms over days or weeks, youth, retention of posterior column function and deep tendon reflexes, and early recovery (Lipton and Teasdall 1973; Ropper and Poskanzer 1978). In addition, the chance of recovery is poor when somatosensory evoked potentials show a conduction block, but good when somatosensory evoked potentials are normal or only slightly delayed (Wulff 1985; Kalita et al 1998). CSF cells or protein do not predict outcome (Altrocchi 1963; Ropper and Poskanzer 1978).
In 50 Japanese children, younger patients and those with hypotonia had a worse prognosis (Miyazawa et al 2003). Also ominous are need for respiratory support and high cord lesions (Borchers and Gershwin 2012). Many of these children (62%) had residual deficits. This contrasts with other studies with good functional outcomes in 50% (Paine and Byers 1953), 56% (Defresne et al 2003), and 62% of children with myelitis (Dunne et al 1986).
The incidence of multiple sclerosis in transverse myelitis ranges from 0% over 6.5 years (Defresne et al 2003), 1% over 15 years (Berman et al 1981), 5% over 8 years in children from Chongqing, China (Chen et al 2013), 6% over 5 years (Altrocchi 1963), 3% after 5 years (Lipton and Teasdall 1973), 3% over 6 years (Andersen 2000), or 8% to 14% after an average of 5 years (Ropper and Poskanzer 1978), 13% over 4.5 years—four fifths had brain lesions at presentation (Thomas et al 2012), 29% over 5 years (Perumal et al 2008), 40% of 20 patients over 12 to 30 months (Dalecky et al 1997), or 45% over 6 years (Debette et al 2009). The second attack, ie, multiple sclerosis, is most likely to occur 1 year later and unlikely if 2 years have passed (Perumal et al 2008).
Acute complete transverse myelitis, with long central lesions, only occasionally evolves into multiple sclerosis; acute partial transverse myelitis with short, acentric, asymmetric lesions evolves to multiple sclerosis more frequently (Scott et al 2005). Partial cord lesions with negative MRI will evolve to multiple sclerosis in 2% to 25%, partial myelitis with multiple sclerosis-like brain lesions evolves to multiple sclerosis in 44% to 85% (Scott 2007; Perumal 2008; Sellner et al 2008). Compared to patients with partial cord lesions, those with complete transverse myelitis have less frequent oligoclonal bands, relapses, and multiple sclerosis. In contrast, partial cervical myelopathy and transverse myelitis without initial brain MRI lesions often evolves into clinically definite multiple sclerosis, especially if evoked potentials and CSF are abnormal (Bashir and Whitaker 2000; Perumal et al 2008). Many of the older series are likely to have included patients with neuromyelitis optica or CNS Sjögren disease.
The following features increase the risk of developing multiple sclerosis: (1) partial, rather than complete, transverse myelopathy and more than one cord lesion; (2) cranial MRI suggestive of multiple sclerosis after a transverse myelopathy, especially with multiple lesions, infratentorial plaques, high burden of disease, and development of new brain lesions on repeat scans (these suggest the myelitis is not the first episode of demyelination); (3) CSF IgG or IgM oligoclonal bands; (4) abnormal visual or sensory evoked potentials (less helpful than MRI); (5) HLA-DR2 positive status (Bashir and Whitaker 2000); and (6) family history of multiple sclerosis.
A hemicord lesion or disseminated lesions modify prognosis. In acute partial myelitis, the unilateral cord lesion is incomplete or patchy. It appears to be an entity separate from acute complete transverse myelitis. In slightly more than 3 years, 12 of 15 (80%) patients with acute partial myelitis developed multiple sclerosis (Ford et al 1992). In a comparable study of acute partial cord syndromes, 14 of 38 patients developed multiple sclerosis within 18 months (Miller et al 1989); 13 of these had disseminated MRI lesions at the onset of myelitis. Fourteen of 25 had positive oligoclonal bands at onset; 10 of these developed multiple sclerosis, but only 1 of 11 without oligoclonal bands progressed to multiple sclerosis. In 52 patients presenting with acute partial transverse myelitis, 30 developed multiple sclerosis over 3 years (Cordonnier et al 2003). Predictors of multiple sclerosis in acute partial transverse myelitis are the following: black Afro-American descent, initial sensory symptoms, lateral-posterior lesions, Gd-positive cord lesions, abnormal brain MRI, and positive CSF oligoclonal bands.
With a normal MRI, acute partial transverse myelitis seldom leads to multiple sclerosis, despite the fact that this type of lesion (1 segment in length, acentric) is typical in multiple sclerosis. In the largest series, only 3 or 4 of 30 patients (10% to 13%) developed multiple sclerosis over 5 years (Scott et al 2005); 8 of 13 tested had oligoclonal bands, but only 1 of these developed multiple sclerosis. When the brain MRI is abnormal, however, the chance of developing multiple sclerosis is 80% to 90%. In other, smaller series in 1995 and one in 1997, 8 of 24 patients had positive bands, and 4 developed multiple sclerosis over 2 years (Scott et al 2005).
In established multiple sclerosis, when acute transverse myelitis appears, it is associated with later onset and optic neuritis, but with fewer brainstem, cerebral, or cerebellar symptoms and fewer lesions on MRI (Fukazawa et al 1990). (Note: These are Japanese patients. A Devic-like syndrome is more common in Japanese than in European patients.) In another series, 15 out of 16 patients with acute myelopathic multiple sclerosis had asymmetric motor or sensory symptoms, but 19 out of 20 acute transverse myelopathy patients had symmetric weakness and sensory symptoms (Scott et al 1998). NMO-IgG is rare with short cord lesions in the United States; only 1 of 22 in acute partial transverse myelitis, but 3 of 4 in Devic disease, and none of 6 in multiple sclerosis (Scott et al 2006).