The majority of patients with transverse myelitis are not systemically ill and the neurological disorder usually evolves over a few days (Section 20.4.5). Pain at the site of the lesion may be the initial symptom, followed by weakness in the legs and positive sensory symptoms with sphincter involvement. With time, the weakness increases and may spread to involve one or both arms, usually in an asymmetric pattern and showing the flaccid areflexia characteristic of spinal shock. These features are infrequently seen when cord inflammation occurs in the context of multiple sclerosis, and have been used to distinguish monophasic from relapsing disease. Sensory loss replaces the paraesthesia and there is often a band of unpleasant hyperaesthesia at the upper sensory level; as in other cases of incomplete focal spinal disease, this may not accurately reflect the site of spinal affection, due to lamination of fibres in the spinothalamic pathways. Sphincter control is lost; unlike patients with multiple sclerosis, the patient is usually unable to empty rather than fill the bladder. The need to exclude a structural cause for subacute cord injury occurring as a manifestation of transverse myelitis means that many patients undergo radiological investigation. This may demonstrate mild cord swelling, which is rarely sufficient to cause spinal block, but imaging usually shows a longitudinal rather than transverse area of increased signal (Fig. 29.4c). Lumbar puncture should be carried out in cases investigated by magnetic resonance imaging. The spinal fluid shows an increased mononuclear cell count, numerically intermediate between the marked pleocytosis of acute necrotizing myelitis and the abnormalities seen in patients with multiple sclerosis. The total protein is raised and oligoclonal bands may be present on electrophoresis, but the glucose is usually normal. Multiple sclerosis and transverse myelitis cannot reliably be distinguished on the basis of changes in cerebrospinal fluid, but oligoclonal bands are more frequent and a cell count in excess of 100 lymphocytes/cm less likely in the former.
Some clinical guidelines can be used to distinguish transverse myelitis from multiple sclerosis. The most reliable indicator is the presence of spinal shock in acute monophasic lesions. Scott et al. (1998) emphasize that symmetry of the motor and sensory manifestations of acute inflammatory spinal cord disease usefully identifies patients with transverse myelitis, whereas spinal involvement in multiple sclerosis is almost invariably asymmetric. Defined in this way, they report a low conversion rate from transverse myelitis to multiple sclerosis. Unlike acute disseminated encephalomyelitis, transverse myelitis is more common in adults than children, and in women than men. Since it is a diagnosis of exclusion, in which laboratory abnormalities and bacteriological findings may be unhelpful, the probability arises that a heterogeneous collection of cases has been included in most large series. Transverse myelitis differs from acute disseminated encephalomyelitis in the peak age of onset and its more frequent occurrence as a manifestation of systemic vasculitis, immunodeficiency, and greater range of specific infectious causes. It has a low rate of conversion to multiple sclerosis, and in this respect resembles bilateral rather than unilateral optic neuritis in adults.
The series reported by Berman et al. (1981) is probably representative with respect to prognosis: 22 of 59 (68 per cent) of patients in whom follow-up information was available made an adequate recovery over the ensuing 3 months; 3 died and 14 were left with significant persistent disability. A high proportion of a population-based sample of cases originally designated as transverse myelitis had later to be excluded from their study. In the remainder, incidence peaked in the second and third decades, with a further bimodal increase in patients aged over 70 years. Only one patient subsequently developed multiple sclerosis. Preceding infection was reported in one-third of patients, the majority of whom had upper respiratory infection, other causes being herpes zoster or simplex virus infection, hepatitis, and smallpox vaccination. Identifiable infection was more common in young patients, suggesting that cases with spinal stroke, including examples due to collagen vascular disease, are sometimes erroneously diagnosed as having transverse myelitis, and this is especially problematic in patients with sensory signs indicating an anterior cord lesion. Tyler et al. (1986) have collated the viral causes of transverse myelitis, listing picornaviruses, togaviruses, retroviruses, orthomyxoviruses, paramyxoviruses, bunyaviruses, arenaviruses, rhabdoviruses, hepatitis viruses, herpes viruses, and poxviruses. More recent single case reports emphasize the occurrence of transverse myelitis after infection with hepatitis A, cytomegalovirus, herpes simplex type 2, toxoplasmosis, and schistosomiasis.