Primary injury (Acute compression)

ACTH4-10
Administration
Acute phase Vascular damage
Ion imbalance
Accumulation of
neurotransmitters
Free radical formation
Lipid peroxidation
Inflammatory
Edema
Cell death (Necrosis)

Excess levels of Damage to phospholipid

Ca2+ in cell membranes
mitochondria NADPH oxidase via
electron transport chain
Formation Formation of free Formation of esterified
superoxide arachhidonic acid arachhidonic acid

COX-1, COX-2
Lipid
peroxidation
Prostalglandin G2 Hydrolysis
Polyunsaturated fatty acids
Secondary Injuries

PG endoperoxide
+ OH+ synthase
15(S)-PGF2a
Unsaturated lipid radical Prostalglandin H2
Lipid hydroperoxides
15(S)-8-iso-
Peroxylradicals Thromboxane PGF2a
(F2 isoprostan)

Malondialdehyde PGE2
PGF2a
PGD2
4-hydroxyl-2-nonenal

Subacute Cell death (Apoptosis)

phase Demyelination of axons
Wallerian degeneration
Axonal dieback
Matrix remodeling
Evolution of glial scar cells

Chronic Formation of cystic cavity

phase Progressive axonal dieback
Maturation of glial scar cells