Contusional Injury of the Cord

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Commonly the term "contusio spinalis" designates all primary mechanical alterations of the cord and its coverings caused by blunt violence to the cord. Spinal cord contusion injuries also include all non-disruptive injuries without evidence of continuing compression but those more severe than reversible functional disturbances are referred to as concussion injuries (Jellinger 1976).

Fig. 10.5a-d. Fracture of the dens axis (arrows in a, b) and in- cipito-cervical junction and fracture of the dens axis; c epidural traspinal hemorrhage as a result of a combined retroflexion and hemorrhage and intraspinal hemorrhage; d intraspinal hemor-rotation around the z-axis: a Spine and spinal cord in situ; b oc- rhage

Fig. 10.5a-d. Fracture of the dens axis (arrows in a, b) and in- cipito-cervical junction and fracture of the dens axis; c epidural traspinal hemorrhage as a result of a combined retroflexion and hemorrhage and intraspinal hemorrhage; d intraspinal hemor-rotation around the z-axis: a Spine and spinal cord in situ; b oc- rhage

This type of SCI features intramedullary hemorrhage and/or edema (Fig. 10.6a). The histological alterations extend the lesion for several segments both above and below the original site of injury. The bleeding involves the central gray matter, particularly the ventral portion of the posterior horn and the central canal, i.e., central cord necrosis or myelomalacia. Most cases exhibit a combination of hemorrhage and necrotic liquefaction of the central parts of the cord.

During the first 2 h after the impact, the first reactive changes arise: congestion, edema, and homog-enization of vessel walls with leakage of plasma into the perivascular spaces (Wolman 1965) as well as leukocyte reaction (Fig. 10.6b). The periphery of the primary injury is characterized by rostral and caudal axonal swelling and axonal bulbs (Fig. 10.6c-f). Dendrite injury (Fig. 3.2) is also seen as marked by the absence of immunoreactivity to microtubule-as-sociated protein 2 (Map2 - see Fig. 10.7a, b) (Li et al. 1997). An extensive demyelination occurs (Fig. 10.7c, d). Retrograde and Wallerian (= anterograde) degenerations are evident (Hughes 1978). The adjacent neuropil features a pronounced spongy gliosis. Four inflammatory phases are seen:

1. Hemorrhage and neuronal necrosis

2. Blood cell reaction

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