(See also Overview of Spinal Cord Disorders.)
Acute transverse myelitis is most commonly due to multiple sclerosis; however, it can occur in patients with vasculitis, systemic lupus erythematosus (SLE), antiphospholipid syndrome, other autoimmune disorders, mycoplasmal infections, Lyme disease, syphilis, tuberculosis (TB), or viral meningoencephalitis or in patients taking amphetamines, IV heroin, or antiparasitic or antifungal drugs. Transverse myelitis occurs with optic neuritis in neuromyelitis optica (Devic disease), once considered a variant of multiple sclerosis but now considered a distinct disorder.
The mechanism of transverse myelitis is often unknown, but some cases follow viral infection or vaccination, suggesting an autoimmune reaction. Inflammation tends to involve the spinal cord diffusely at one or more levels, affecting all spinal cord functions.
Symptoms of acute transverse myelitis may include pain in the neck, back, or head. A bandlike tightness around the chest or abdomen, weakness, tingling, numbness of the feet and legs, and difficulty voiding develop over hours to a few days. Deficits may progress over several more days to a complete transverse sensorimotor myelopathy, causing paraplegia, loss of sensation below the lesion, urinary retention, and fecal incontinence. Occasionally, position and vibration sensation are spared, at least initially.
Acute transverse myelitis occasionally recurs in patients with multiple sclerosis, SLE, or antiphospholipid syndrome.
Diagnosis of acute transverse myelitis is suggested by transverse sensorimotor myelopathy with segmental deficits. Guillain-Barré syndrome can be distinguished because it does not localize to a specific spinal segment.
Diagnosis requires MRI and CSF analysis. MRI typically shows cord swelling if transverse myelitis is present and can help exclude other treatable causes of spinal cord dysfunction (eg, spinal cord compression). CSF usually contains monocytes, protein content is slightly increased, and IgG index is elevated (normal, ≤ 0.85).
A test for a marker for neuromyelitis optica IgG (NMO-IgG)—an autoantibody that targets the astrocyte water channel protein aquaporin-4—is highly specific and helps distinguish neuromyelitis optica from multiple sclerosis.
Tests for treatable causes should include chest x-ray; PPD (purified protein derivative) for tuberculosis; serologic tests for mycoplasma, Lyme disease, and HIV; erythrocyte sedimentation rate (ESR); antinuclear antibodies; and CSF and blood Venereal Disease Research Laboratory (VDRL) tests. History may suggest a drug as a cause.
The differential diagnosis of acute transverse myelitis includes other transverse myelopathies due to nutritional deficiencies (eg, deficiency of vitamin B12, folate, zinc, or copper), vascular insufficiency, and intraspinal tumors.
Brain MRI is done; multiple sclerosis develops in 50% of patients who have multiple periventricular T2 bright lesions and in 5% who do not have them.
Generally, the more rapid the progression is, the worse the prognosis. Pain suggests more intense inflammation. About one third of patients recover, one third retain some weakness and urinary urgency, and one third are bedbound and incontinent.
Multiple sclerosis eventually develops in about 10 to 20% of the patients in whom the cause is initially unknown.
Treatment of acute transverse myelitis is directed at the cause or associated disorder but is otherwise supportive.
In idiopathic cases, high-dose corticosteroids are often given and sometimes followed by plasma exchange because the cause may be autoimmune. Efficacy of such a regimen is uncertain.
Autoimmune and demyelinating disorders, infections, and drugs can inflame tissues in spinal cord segments, causing transverse myelitis, which may progress to complete transverse sensorimotor myelopathy.
Do MRI of the spinal cord, CSF analysis, testing for neuromyelitis optica IgG, and other tests for treatable causes (eg, infections).
Treat the cause if identified, and if no cause is evident, consider corticosteroids and plasma exchange.