Figure 8

The model of events which may lead to hyperexcitability and atrophy after SCI. Each event may represent a potential target for clinical intervention. Two pathways are posited for hypomyelination: SCI causes immediate intense activity that may initiate mechanisms that eventually lead to hypomyelination, or the period of inactivity that followed spinal cord injury called spinal shock. Either way hypomyelination (in lesion environment) would lead to upregulation of sodium channels (Na⁺ II) that will cause hyperexcitability. According to Waxman hypothesis [38] the activity of these channels would lead to reversed action of Na⁺- Ca²⁺ exchanger, followed by an increase in intracellular Ca2⁺concentration, axonal death and subsequent muscle atrophy.