Transverse myelitis

Etiology
Article section 5 of 16.  Previous  Next

By Anthony T Reder MD

Two thirds of acute transverse myelitis episodes are idiopathic. Virus infections seem to trigger one third of the cases of transverse myelitis in adults and at least half of the cases in children (Lipton and Teasdall 1973; Berman et al 1981; Thomas et al 2012). In children, one half to two thirds have preceding infection (Miyazawa et al 2003). Transverse myelitis typically develops 3 to 15 days after an upper respiratory infection (Paine and Byers 1953; Jeffery et al 1993). Some reported viral triggers include adenovirus; cat scratch fever; coxsackievirus strains A and B; cytomegalovirus; dengue 2; echovirus; enterovirus; Epstein-Barr virus; enteric cytopathogenic human orphan (ECHO) virus; hepatitis A; HSV types 1, 2, and 6; Herpes zoster; influenza; lymphocytic choriomeningitis virus; mumps; poliovirus; rubeola; rubella; Russian spring-summer encephalitis; and varicella (Miller et al 1956; Knebusch et al 1998). There are occasional case reports of transverse myelitis following various immunizations, but a true disease association is not evident in controlled studies (below). Transverse myelitis with a more indolent course over several days or weeks has been described as a rare presentation of both HIV and HTLV-1 infections. In addition, some nonviral infections trigger acute transverse myelitis, including mycoplasma pneumoniae and occasionally pulmonary tuberculosis or Borrelia (Knebusch et al 1998).

A virus could cause transverse myelitis through: (1) direct damage to parenchymal cells (eg, subacute sclerosing panencephalitis and possibly AIDS myelopathy); (2) a "bystander effect" damaging the cord during an immune response against the virus, or damage from release of virus-induced cytokines or superantigens that activate immune cells (eg, heat shock protein from mycoplasma); and (3) sensitization of the host to brain antigens during an inflammatory response, eg, release of damaged myelin (processed by antigen-presenting cells) or cross-reactivity between virus and myelin antigens. Examples of the latter include postinfectious encephalomyelitis (Label and Batts 1982) and postvaccinal encephalomyelitis, especially following rabies vaccination containing duck embryo CNS components and, arguably, following recombinant hepatitis B vaccine (Tartaglino et al 1995). The latter correlation does not hold in large series (Asherio et al 2001). Viruses trigger most episodes of acute disseminated encephalomyelitis, which is a true autoimmune, delayed-type hypersensitivity response against brain antigens. Similarly, postinfectious myelitis is seen after measles infection. Here, there is a clear host response to myelin basic protein, even when the virus is no longer present in the brain (Johnson et al 1984). Virus infections precede one third of multiple sclerosis relapses (Panitch et al 1991) and one third of episodes of transverse myelitis. The mechanism of the viral association with multiple sclerosis relapses is unknown.

Mycoplasma may induce neurotoxins or cause thrombosis or transient immunosuppression. It also induces interferons and polyclonal B cell activation (Albucher et al 1995). Mycoplasma and brain antigens may cross-react and lead to anti-brain immune responses.

In This Article

Introduction
Historical note and nomenclature
Clinical manifestations
Clinical vignette
Etiology
Pathogenesis and pathophysiology
Epidemiology
Prevention
Differential diagnosis
Diagnostic workup
Prognosis and complications
Management
Pregnancy
Anesthesia
References cited
Contributors