ABSTRACT
Introduction: Non compressive myelopathy is defined as“spinal cord dysfunction in the absence of clinico-radiologicalevidence of spinal cord compression.” It can result fromdemyelinating, infectious, autoimmune, vascular, degenerativeand metabolic disorders in the absence of demonstrablecompression by imaging techniques. We aimed in analyzingthe etiological profile of non-compressive myelopathies in atertiary care hospital of Central Tamil nadu.Material and Methods: In the Neurology department, weconducted an observational study at Thanjavur MedicalCollege, Thanjavur, from September 2017 to September2018. Patients of non-compressive myelopathies whounderwent magnetic resonance imaging (MRI) of the spinewere segregated into two categories: Degenerative and nonDegenerative, as well as into acute, subacute and chronicmyelopathies.Results: The study had 75 patients with a median age of34.5 years and male: female ratio of 1.35:1. Presentation wasacute in 10 patients (13%), subacute in 5 (6.5%), chronic in54 (72.5%) and history of relapse and remission in 6(8%)patients. Degenerative etiology was found for 42 (56%)others were non degenerative (demyelinating, autoimmune,vascular, nutritional, or physical agent). MRI study carried outin all cases showed signal changes in 51 cases (68%) whichincluded myelomalacia, demyelination, atrophy of cord,infarction of cord. Etiological diagnosis could be establishedin 74 (97.3%) cases.Conclusion: Underlying etiology (degenerative,demyelinating, autoimmune, infectious, vascular, metabolicdisorder, or physical agent) was found in 91.3% patients ofnoncompressive myelopathy. Clinical features combinedwith MRI findings are helpful in defining the cause ofnon-compressive myelopathies. A follow-up of long termmay reveal some of the diagnosis especially degenerativemyelopathies in early stage.
ABSTRACT
Endemic fluorosis leads to dental fluorosis, skeletal fluorosis and visceral fluorosis. This case described about the crippling skeletal fluorosis with neurological manifestations in the form of myelopathy, due to exposure to high fluoride level in water for many years. The complications of fluoride deposition in bones resulted in generalised sclerosis, osteophytosis, with narrowing of inter vertebral disc spaces in vertebral column. In this case the skeletal fluorosis leads to severe spastic quadriparesis. This case had features of visceral fluorosis; the affected organs include thyroid gland with hypothyroidism, parathyroid gland with secondary hyperparathyroidism, pancreas with intra pancreatic calcification and the kidneys with chronic kidney disease.
ABSTRACT
Objective:To discuss the autoimmune response on the mechanism and clinical significance of nerve root injury induced by the non-compressive nucleus pulposus protrusion.Methods:Forty-eight female SD rats were randomly divided.Twenty-four female SD rats were recruited as model group,and the others as control.After ten days,twenty days and forty days,the pain threshold of left hind leg and the levels of TNF-α, CD4+, CD8+T cells were measured, the nerve root changes in morphology were observed by HE.Results:Compared with the control group,model group in ten days,twenty days,which left hind leg pain threshold,the proportion of CD4,CD8+T cell and the expression of TNF-αare significantly different.After forty days,these two groups have no statistical differ-ence.After ten days,lumbar nerve root cross-sectional myelin of model group was partial disintegrated.The worst damage happened in twenty days,and almost recovered to normal in forty days.Conclusion:T cell-mediated autoimmunity and TNF-αplay an important role to the nerve root injury in the early time of the non-compressive nucleus pulposus protrusion.