Although most injury responses include a calcium influx signaling to promote resealing of severed parts, axonal injuries initially lead to acute axonal degeneration (AAD), which is rapid separation of the proximal (the part nearer the cell body) and distal ends within 30 minutes of injury.[8] After separation, dystrophic bulb structures form at both terminals and the transected membranes are sealed.[9] A brief latency phase occurs in the distal segment during which it remains electrically excitable and structurally intact.[10] Degeneration follows with swelling of the axolemma, and eventually the formation of bead-like axonal spheroids.