Changes that occur during<unk>  are poorly understood but are thought to include cell death, axonal sprouting, reorganization of neural networks, alterations in the release of neurotransmitters, and neurogenesis. These changes cause neurons to become hyperexcitable and can lead to spontaneous seizures. Brain regions that are highly sensitive to insults and can cause<unk>  include temporal lobe structures such as the hippocampus, the amygdala, and the piriform cortex. Neural reorganization In addition to chemical processes, the physical structure of neurons in the brain may be altered. In acquired epilepsy in both humans and animal models, pyramidal neurons are lost, and new synapses are formed. Hyperexcitability, a characteristic feature of<unk>  in which the likelihood that neural networks will be activated is increased, may be due to loss of inhibitory neurons, such as GABAergic interneurons, that would normally balance out the excitability of other neurons. Neuronal circuits that are epileptic are known for being hyperexcitable and for lacking the normal balance of glutamatergic neurons (those that usually increase excitation) and GABAergic ones (those that decrease it). In addition, the levels of GABA and the sensitivity of GABAA receptors to the neurotransmitter may decrease, resulting in less inhibition. Another proposed mechanism for<unk>  in TBI is that damage to white matter causes hyperexcitability by effectively undercutting the cerebral cortex. Glutamate receptor activation It is believed that activation of biochemical receptors on the surfaces of neurons is involved in<unk> ; these include the TrkB neurotrophin receptor and both ionotropic glutamate receptors and metabotropic glutamate receptors (those that are directly linked to an ion channel and those that are not, respectively). Each of these types of receptor may, when activated, cause an increase in the concentration of calcium ions (Ca2+) within the area of the cell on which the receptors are located, and this Ca2+ can activate enzymes such as Src and Fyn that may lead to<unk> . Excessive release of the neurotransmitter glutamate is widely recognized as an important part of<unk>  early after a brain injury, including in humans. Excessive release of glutamate results in excitotoxicity, in which neurons are excessively depolarized, intracellular Ca2+ concentrations increase sharply, and cellular damage or death results. Excessive glutamatergic activity is also a feature of neuronal circuits after epilepsy has developed, but glutamate does not appear to play an important role in<unk>  during the latent period. Another factor in hyperexcitability may include a decrease in the concentration of Ca2+ outside cells (i.e. in the extracellular space) and a decrease in the activity of ATPase in glial cells. Blood brain barrier disruption Blood brain barrier (BBB) disruption occurs in high prevalence following all brain lesions that may cause post injury epilepsy such as stroke, traumatic brain injury, brain infection or brain tumor. BBB disruption was shown to underlay<unk>  by several experimental models. Furthermore, it was shown that albumin, the most frequent protein in the serum is the agent that leaks from the blood into the brain parenchyma under BBB disruption conditions and induces<unk>  by activation of the transforming growth factor beta receptor on astrocytes. Additional investigation exposed that this process is mediated by a unique inflammatory pattern and the formation of excitatory synapses. Pathogenic influence was attributed also to the extravasation of other blood born substances such as hemosiderin or iron. Iron from hemoglobin, a molecule in red blood cells, can lead to the formation of free radicals that damage cell membranes; this process has been linked to<unk> .
Epileptogenesis
Cortical spreading depression
Excited delirium
Stimulant psychosis
Decompensation
Hypnoid state
Body substance isolation
Ischemic cascade