Almost invariably, the CSF contains lymphocytes and other mononuclear cells in the range of 10 to 50/mm3 (sometimes higher), with slightly raised protein and normal glucose content. However, there may be only 3 or 4 cells/mm3, or none, making the inflammatory aspect less clear. Oligoclonal bands are usually absent. In most instances that have come under our care, the MRI has shown slight T2 signal abnormalities and minimal gadolinium enhancement extending over 2 or 3 spinal segments. Although the cord may be swollen in these regions (Fig. 42-4), several of our patients with mild and partial myelitis have had normal MRI studies.
Clinical variants of this syndrome are frequent in our experience, including an almost pure paresthetic illness with posterior column dysfunction and the converse; a symmetrical paraparesis with analgesia below a level on the trunk but without involvement of deep sensation (a syndrome more typically associated with infarction in the territory of the anterior spinal artery); a syndrome of variable sensory loss involving the leg and groin on one side or both; a purely lumbosacral or sacral myelopathy (conus syndrome with saddle analgesia and sphincter disturbances); and a partial Brown-Séquard syndrome.
In the past, postinfectious myelitis was most often observed in relation to the common exanthems (rubella, rubeola, varicella). The neurologic signs appeared as the rash was fading, often with a slight recrudescence of fever. Practically all human viruses have at one time or another been found to have preceded acute myelitis; however, the DNA viruses such as Epstein-Barr and cytomegalovirus are most common, and hepatitis B, varicella, and enteroand rhinoviruses have been detected from time to time. Mycoplasma is almost unique in being a bacterial trigger of the disease, but as noted earlier, there is some uncertainty regarding its ability to cause direct infection rather than a postinfectious immune reaction. Our interpretation of the existing information still favors a postinfectious etiology. In most instances of postinfectious myelitis, the connection to a preceding infection is presumed but cannot be proved. Only the associations with EBV, CMV, and Mycoplasma seem fairly certain based on the regularity of their occurrence, but it may simply reflect the relative ease with which a recent infection can be documented by serologic tests. The list of antecedent infections is otherwise much the same as for the Guillain-Barré syndrome with the notable difference of Campylobacter jejuni, which has not led to myelitis and is a frequent precedent to acute polyneuropathy. It can be reasonably assumed that, for example, pharyngitis, respiratory infection, and conjunctivitis, with or without fever, was a likely trigger for myelitis and the finding of abnormal liver function tests or severe pharyngitis with cervical adenopathy usually indicates EBV or, less often, CMV infection.
More difficult to understand are the large number of cases of myelitis, including autopsy-proven ones, in which the disease develops without an apparent antecedent infection. There is understandable uncertainty in such cases as to whether the illness is the opening phase of multiple sclerosis of the type described below under “Acute Demyelinating Myelitis of Multiple Sclerosis.” In the numerous cases of transverse myelitis under our care, fewer than half have shown other signs of MS after 10 to 20 years (this is a far lower incidence than disseminated multiple sclerosis following a bout of optic neuritis). There is also an isolated form of relapsing myelitis, sometimes but not always triggered by an infection that does not manifest lesions elsewhere in the neuraxis and therefore has an ambiguous relationship to MS. Further discussion of acute transverse myelitis in relation to other demyelinating diseases can be found below and in Chap. 35.