Chronic or acute narrowing of the spinal canal by more than 50% compromise of the free antero-pos-terior diameter entails the risk of compressing the cord (Scarff 1960). The acute compression caused by impact (Fig. 10.8a, b) results in an acute neurological deficit of the involved motor and/or sensory axons in the cord. Chronic lesions of the cord may be caused by survival after impact-induced compression (Fig. 10.8c, d), as well as by congenital diseases of the vertebral column (achondroplasia), by neoplastic proliferation (Schwannoma, meningioma, carcinoma), by osteogenic degeneration (spondylosis, osteoporosis), by cartilaginous degeneration (protrusion of the intervertebral disc), by inflammatory diseases (spondylitis), or by iatrogenic events (myelograph-
onstrated by an intraspinal necrosis of white and gray matter; d necrosis of the periventricular pontine tissue associated with ascending degeneration of nerve fibers (circles)
ia). A secondary ascending alteration may be a focal necrosis in the medulla or pons (Fig. 10.8d). The cord may also be displaced and compressed by chronic subdural hemorrhage (Oehmichen and Meissner 1999): a compressive myelopathy may develop as a result of relatively prolonged intrinsic compression of the cord by encroachment on the space of the vertebral canal or by protruding intervertebral discs (Fig. 10.9).
Neuropathology. The pathological changes induced by compression of the cord derive largely from impairment of the intrinsic circulation (Hughes 1992). The early phase is marked by venous compression leading to venous stasis and edema. The myelin sheaths become swollen, conferring a vacuolated appearance of the white matter. A further increase in compression leads to necrosis and cavitation of the cord, particularly in the center of the cord. The last phase is characterized by a gliotic scar involving gray and white matter, with preservation of some of the axons. Wallerian (secondary degeneration) will result in ascending and descending fiber tracts at all levels distal to the lesion (see above). If the compression is only minor, the local decrease in blood flow can be compensated by autoregulatory mechanisms involving dilation of vessels and formation of collaterals at the site of compression (Palleske et al. 1970).
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