logically complete injuries show some amount of tissue and axonal sparing across the site of the lesion (Bunge et al., 1997).


A spinal cord injury immediately injures or kills cells, but it also causes delayed damage and death to cells that survive the original trauma. The biological response to a spinal cord injury is divided into three phases that follow a distinct but somewhat overlapping temporal sequence: acute (seconds to minutes after the injury), secondary (minutes to weeks after the injury), and chronic (months to years after the injury). A general overview of the three phases is presented in Table 2-4. Diverse groups of cells and molecules from the nervous, immune, and vascular systems are involved in each phase. Most participating cells reside in the spinal cord, but others are summoned to the site of injury from the circulatory system (Table 2-5). To carry out many of their functions, the cells depend on changes in gene expression. As would be expected, injury triggers certain cells to up-regulate (increase expression) or down-regulate (decrease expression) genes responsible for a host of proteins involved in inflammation, neurotransmission, regrowth and repair, and other local responses to injury (Bareyre and Schwab, 2003). The final pattern of sensory and motor losses from the

TABLE 2-4 Major Features of the Three Phases of Injury

Acute (Seconds after Injury)

Secondary (Minutes to Weeks)

Chronic (Months to Years)

  • Systemic hypotension and spinal shock

  • Hemorrhage

  • Cell death from direct insult or ischemia (disruption of blood supply)

  • Edema (swelling)

  • Vasospasm (reduction in blood flow)

  • Shifts in electrolytes

  • Accumulation of neurotransmitters

  • Continued cell death

  • Continued edema

  • Continued shifts electrolytes

  • Free-radical production

  • Lipid peroxidation

  • Neutrophil and lymphocyte invasion and release of cytokines

  • Apoptosis (programmed cell death)

  • Calcium entry into cells

  • Continued apoptosis radiating from site of in injury

  • Alteration of ion channels and receptors

  • Formation of fluid-filled cavity

  • Scarring of spinal cord by glial cells

  • Demyelination

  • Regenerative processes, including sprouting by neurons

  • Altered neurocircuits

  • Syringomyelia


SOURCES: Sekhon and Fehlings, 2001; Hulsebosch, 2002.

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