Viral causes of myelitis include:
- coxsackie viruses,
- herpes zoster,
- herpes simplex,
- human immunodeficiency virus (HIV),
- Epstein–Barr virus (EBV),
- cytomegalovirus (CMV), and
Although a number of the former viruses cause an acute infective myelitis, they may also be associated with a post-infectious myelitis, which is likely not to be the result of viral infection but rather to an immune-mediated response triggered by the viral antigens.
Poliomyelitis and coxsackie viruses produce an acute inflammatory meningomyelitis with cord involvement predominantly affecting the anterior horn cells, leading to patchy, multifocal, or sometimes extensive muscle weakness and wasting, with corresponding reflex loss but no sensory abnormality. Acutely, there is a CSF mononuclear pleocytosis and elevation of protein. Varicella zoster usually produces a sensory dermatomal deficit, often with marked pain, due to predominant involvement of the dorsal root ganglion. The associated dermatomal vesicular rash will normally establish the diagnosis. More extensive involvement of the adjacent cord or roots can lead to features of myelopathy or segmental myotomal deficits.
A transverse myelitis due to viral infections such as those above, although much rarer, may be indistinguishable from a post-infectious transverse myelitis. Such infections are more likely to occur in immunocompromised states, including those with HIV infection. The diagnosis is confirmed by the isolation of portions of viral antigen from the CSF by polymerase chain reaction. High-dose aciclovir is indicated for cord infections due to herpes simplex or zoster.
In patients with AIDS, a vacuolar myelopathy sometimes develops. The tempo is subacute with symptoms typically evolving over a number of weeks. Motor, sensory, and sphincter abnormalities all appear, sometimes asymmetrical and predominantly in the legs, although the arms may also be involved. Pathologically, there is vacuolation in the spinal cord white matter which is most marked in the thoracic region. As this manifestation is seen in patients with AIDS rather than in asymptomatic HIV-positive individuals, its appearance should be delayed or prevented by the use of effective antiretroviral therapies.