Figure 1.

Acute and chronic events initiated after spinal cord injury: anatomical and temporal events.

Contusion or compression injury to the vertebral column causes a traumatic impact which breaks vertebrae and compresses the spinal cord initiating injury to the central nervous system (CNS). During the acute stages, the broken bones and the contusion will compress the spinal cord, causing mechanical damage which will lead to necrosis, axotomy, blood-brain barrier (BBB) disruption, vascular damage, ischemia, and reactive oxygen species generation. The BBB and vascular damage leads to the infiltration of immune cells into the spinal cord followed by a simultaneous inflammatory cascade. The initiation of these events will lead to apoptosis, demyelination, and reactive gliosis during the chronic stages after SCI. Reactive gliosis initiates a process of lesion encapsulation from the lesion epicenter and will begin to spread toward rostral and caudal levels while the injury extends. Immune cells enter a repair and clearance stage while astrocytic cells continue to design a glial scar that will become a cystic fluid filled cavity a month after the injury. In addition, a non-permissive environment for neurite extension will develop since axonal demyelination and astrocytes will produce repellent substances into the spinal cord that will block axonal regeneration, worsening the prognosis of recovery. Together, the inhibitory signals from the astrocytes, myelin, and pro-inflammatory cytokines create a non-permissive environment for axonal regeneration, neuronal survival, and locomotor recovery.