Status epilepticus, a continuous seizure or multiple seizures in rapid succession, is especially strongly correlated with the development of PTE; status seizures occur in 6% of all TBIs but are associated with PTE 42% of the time, and quickly halting a status seizure reduces chances of PTE development. Pathophysiology
For unknown reasons, trauma can cause changes in the brain that lead to epilepsy. There are a number of proposed mechanisms by which TBI causes PTE, more than one of which may be present in a given person. In the period between a brain injury and onset of epilepsy, brain cells may form new synapses and axons, undergo apoptosis or necrosis, and experience altered gene expression. In addition, damage to particularly vulnerable areas of the cortex such as the hippocampus may give rise to PTE.Blood that gathers in the brain after an injury may damage brain tissue and thereby cause epilepsy. Products that result from the breakdown of hemoglobin from blood may be toxic to brain tissue. The "iron hypothesis" holds that PTE is due to damage by oxygen free radicals, the formation of which is catalyzed by iron from blood. Animal experiments using rats have shown that epileptic seizures can be produced by injecting iron into the brain. Iron catalyzes the formation of hydroxyl radicals by the Haber-Weiss reaction; such free radicals damage brain cells by peroxidizing lipids in their membranes.
Spondylopathies are disorders of the vertebrae. When involving inflammation, it can be called spondylitis. In contrast, a spondyloarthropathy is a condition involving the vertebral joints, but many conditions involve both spondylopathy and spondyloarthropathy. Examples include ankylosing spondylitis and spondylosis. See also
Dorsopathies
Spondyloarthropathy
Spondylolisthesis
Spondylosis
Spondylitis
Spondylolysis

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