The diarrhea-causing bacteria Campylobacter jejuni is also a reported cause of transverse myelitis.Other associated causes include the helminth infection schistosomiasis, spinal cord injuries, vascular disorders that impede the blood flow through vessels of the spinal cord, and paraneoplastic syndrome. Pathophysiology
This progressive loss of the fatty myelin sheath surrounding the nerves in the affected spinal cord occurs for unclear reasons following infections or due to multiple sclerosis. Infections may cause TM through direct tissue damage or by immune-mediated infection-triggered tissue damage. The lesions present are usually inflammatory. Spinal cord involvement is usually central, uniform, and symmetric in comparison to multiple sclerosis which typically affects the cord in a patchy way and the lesions are usually peripheral. The lesions in acute TM are mostly limited to the spinal cord with no involvement of other structures in the central nervous system. Longitudinally extensive transverse myelitis
A proposed special clinical presentation is the "longitudinally extensive transverse myelitis" (LETM), which is defined as a TM with a spinal cord lesion that extends over three or more vertebral segments. The causes of LETM are also heterogeneous and the presence of MOG auto-antibodies has been proposed as a diagnostic biomarker. Diagnosis
Diagnostic criteria
In 2002, the Transverse Myelitis Consortium Working Group proposed the following diagnostic criteria for idiopathic acute transverse myelitis:

Investigations
Individuals who develop TM are typically transferred to a neurologist who can urgently investigate the patient in a hospital. If breathing is affected, particularly in upper spinal cord lesions, methods of artificial ventilation must be on hand before and during the transfer procedure.
The final third experience no recovery at all. Epidemiology
The incidence of TM is 4.6 per 1 million per year, affecting men and women equally. TM can occur at any age, but there are peaks around age 10, age 20, and after age 40. History
The earliest reports describing the signs and symptoms of transverse myelitis were published in 1882 and 1910 by the English neurologist Henry Bastian.In 1928, Frank Ford noted that in mumps patients who developed acute myelitis, symptoms only emerged after the mumps infection and associated symptoms began to recede. In an article in The Lancet, Ford suggested that acute myelitis could be a post-infection syndrome in most cases (i.e. a result of the bodys immune response attacking and damaging the spinal cord) rather than an infectious disease where a virus or some other infectious agent caused paralysis. His suggestion was consistent with reports in 1922 and 1923 of rare instances in which patients developed "post-vaccinal encephalomyelitis" subsequent to receiving the rabies vaccine which then was made from brain tissue carrying the virus. The pathological examination of those who had died from the disease revealed inflammatory cells and demyelination as opposed to the vascular lesions predicted by Bastian.Fords theory of an allergic response being at the root of the disease was later shown to be only partially correct, as some infectious agents such as mycoplasma, measles and rubella were isolated from the spinal fluid of some infected patients, suggesting that direct infection could contribute to the manifestation of acute myelitis in certain cases.