Siderophages Brain Demyelinating Injury

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Fig. 10.6a-f. Contusion injuries of the spinal cord. a Edema immunohistochemistry in longitudinal sections (magnification

(H&E, magnification X100); b emigrating leukocytes as demon- c x30, d X300); e, f axonal injury as seen in cross sections (e p-APP, strated by means of naphthol AS-D chloroacetate esterase (mag- f H&E; magnification X500) nification X300); c, d axonal injury as demonstrated by p-APP

3. Proliferation of resident cells (mesenchymal and glial reaction) and/or resolution

4. Scarring process including production of glial and collagenous fibers

The phase of hemorrhage and neuronal necrosis is characterized by axonal injury. The hemorrhages occur mainly in the gray matter and produce a hemato-mylia as a result of hemorrhage and necrosis within the axial center of the cord. The zone of necrosis soon spreads, apparently due to edema. Neutrophilic leukocytes emigrate within 1 h, lymphocytes and mac rophages appear after 12 h or more. Macrophages scavenge the tissue debris.

The hallmark of the early blood cell reaction phase is an incipient astrocytic reaction (gliosis) occurring at the margins of the lesion 24-36 h post impact. De-myelination spreads and macrophages invade. Lipo-phages and siderophages appear within the necrotic tissue, which gradually diminishes and is replaced by proliferating gliomesenchymal tissue. Endothe-lial proliferation develops at the margins; this is associated with a fibroblastic and collagenous reaction (granulation tissue, as in the rest of the body tissues) and gliotic changes (unique to CNS tissue) constitut

Demyelinating Process The Brain
Fig. 10.7a-d. Loss of dendrites and demyelination. a, b Dendritic loss as demonstrated by a loss of MAP2 expression; c, d demyelin-ation as demonstrated by a loss of myelin basic protein expression (magnification Xl,000)

ing the so-called gliomesenchymal scarring process, which originates in the mesenchymal tissue components of the perivascular tissue, the leptomeninges, and the local glia. The mechanical insult to the axons causes axonal injury at the margins, which resembles that seen in MBI (Fig. 10.6c-f).

During the proliferation phase the myelin sheaths are destroyed (Fig. 10.7c, d) and removed by macrophages; the dendrites are lost as well as MAP2-reac-tivity of spinal neurons (Fig. 10.7a, b). Signs of secondary (Wallerian) degeneration in distal ascending and descending long tracts appear: above the lesion (rostral or cranial part of the cord to the injury), fiber loss occurs in the posterior columns. This will occur in the fasciculus gracilis and, to a variable degree, the fasciculus cuneatus, depending on whether the interruption is above, at, or below the cervical enlargement. Spinothalamic and spinocerebellar tract degeneration is more difficult to discern. Caudal to the lesion, the corticospinal tracts degenerate. At the level of the lesion, secondary degeneration of the neurons then begins, with central chromatolysis (axonal reaction) after spinal root transection (Fig. 3.1c).

The final (scarring) phase commences 3-6 weeks after wounding in some cases and involves mechanically induced syringomyelia, which leaves a cavity surrounded by glial tissue within the center of the spinal cord. In a few cases the cavity extends rostral and/or caudal to involve regions unaffected by the initial trauma. Clinically the patient develops sy-ringomyelic symptoms (central cord syndrome). In some patients, the cord is completely converted into a dense fibrous band and the surrounding dura becomes thickened with remnants of hemorrhage. In others, tissue fluid flow is impeded from the spinal cord, and the syrinx within the cord enlarges progressively over time (post-traumatic syringomyelia).

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