The degree and type of sensory loss will depend upon the extent of the involvement of the various sensory tracts, but there is often a "sensory level" at the spinal ganglion of the segmental spinal nerve, below which sensation to pain or light touch is impaired. Motor weakness occurs due to involvement of the pyramidal tracts and mainly affects the muscles that flex the legs and extend the arms.Disturbances in sensory nerves and motor nerves and dysfunction of the autonomic nervous system at the level of the lesion or below, are noted. Therefore, the signs and symptoms depend on the area of the spine involved. Back pain can occur at the level of any inflamed segment of the spinal cord.If the upper cervical segment of the spinal cord is involved, all four limbs may be affected and there is risk of respiratory failure – the phrenic nerve which is formed by the cervical spinal nerves C3, C4, and C5 innervates the main muscle of respiration, the diaphragm.Lesions of the lower cervical region (C5–T1) will cause a combination of upper and lower motor neuron signs in the upper limbs, and exclusively upper motor neuron signs in the lower limbs. Cervical lesions account for about 20% of cases.A lesion of the thoracic segment (T1–12) will produce upper motor neuron signs in the lower limbs, presenting as a spastic paraparesis.
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.