Pathology of Spinal Cord in Leprosy

The pathologic aspects and distribution of lesions resulting from leprosy have been extensively investigated in the peripheral nerves, but little attention has been paid to the spinal cord. The spinal lesions are mentioned briefly or not at all in most neuropathology text-books. Although there are reports on acute stage of lesions and young cases, the distribution of old lesions in the spinal cord-treated is not well known. This report describes the neuropathologic findings in the spinal cord of 12 patients who has old lesions and survived for an extended period.The pattern of dorsal column degeneration was observed in all patients, with degeneration of the posterior funiculi and survival of few axons without lepra bacilli. Most often, the degeneration was limited to the fasciculus gracilis, occured bilaterally, and extended from thoracic through cervical segment to the nucleus gracilis, while sparing lumbar and sacral cord. Only rarely was the slightless pallor demonestrable in the posterior funicli in the rostal lumbar spinal cord. The site of degeneration was marked by cellular and fibrillary astrogliosis. The presence and amount of macrophages were variable. The cross-sectional areas of the degenerated fasciculus gracilis was larger in the upper cervical than in the lower cervical spinal cord.The gray matter of the spinal cord as well as the fasciculus cuneatus and the anterior and lateral funiculi were normal. No cribriform degeneration was noted, and the destruction did not resemble that of combined degeneration. Dystrophic axons were found in the gracile and cuneate nuclei. Whether or not there was a degeneration of the fasciculus gracilis. Dorsal roots and ganglia were abnormal in all checked-patients who had degeneration of the posterior column. The other, no other lesions were seen in the remaining portions of central nervous system in these patients except for cerebral softening.Of the 12 patients in our sample, one patient died at 30 years of age. The male: female ratio for these with the degeneration was 7:5.Clinically, the posterior column lesion was not suspected. Of the entire population, most of all had clinical evidence recorded of psychoneurological signs of the leprosy. The spinal cords dying with leprosy after advanced age showed posterior column degeneration. Advanced age did not to be appear a increased risk. None of these patients had findings of pericious anemia or spino-cerebellar degeneration. It is possible that nutritional, toxic or bacteric factors may be play role in producing this lesion. Such limited damage cannot account for the dissociated deficit of the sensory system.The selective involvement of the posterior funiculi in our patients with leprosy may be a better explanation of the neurologic deficit following neuropathy.