What is the pathophysiology of seizures?
The seizure occurs when part of the brain is too excited or when the nerves in the brain begin to shoot together in an abnormal way. Seizure activity may occur in areas of the brain that are malformed from congenital defects or genetic disorders or disturbed before infection, injuries, tumors, moves or insufficient oxygence. The pathophysiology of seizures is the result of a sudden imbalance between forces that excite and inhibit nerve cells so that the excitation forces have priority. This electrical signal then spreads to the surrounding normal brain cells that begin to shoot in accordance with abnormal cells. With long -term or recurring seizures in the short period, the risk of future seizures increases when nerve cells are death, scar tissue formation and germination of new axons.
nerve cells between discharge usually have an internally negative charge due to active drawing of positively charged sodium ions from the cell. Drain or launching cell includes sudden fluctuation of negativeThe charges for a positive charge, because the ions channels into open and positive ions such as sodium, potassium and calcium, flow into the cell. Both excitation and inhibitory control mechanisms work to allow appropriate burning and prevent inappropriate cell excitation. Pathophysiology of seizures may occur due to increased excitation nerve cells, reduced nerve cell inhibition or combination of both influences.
normally after firing nerve cells inhibitory influences prevent the second shooting of the neuron until the inner charge of the neuron returns to its resting state. Gamma-amino-butlic acid (GABA) is the main inhibition of chemicals in the brain. Gaba opens the channels for negatively charged chloride ions to flood the excited neuron, reducing the inner charge and preventing the other firing cell. Most of the anti -tour drugs reduce the pathophysiology of seizures by increasing the frequency of the openings of the chloride channel orBy extending the duration during which the channels are open. If the cells that give Gaba or the receptor for the GABA are disrupted, chloride channels are opened and the nervous cell excitability is alleviated.
Equally important for the pathophysiology of seizures are mechanisms that lead to increased excitation of neurons. Glutamate is the main excitation chemical mediator in the brain that binds to receptors that open channels for sodium, potassium and calcium into the cell. Some inherited forms of seizures include predilection for excessively frequent or permanent activation of glutamate receptors, which increases brain excitability and a view of seizure activity. In addition, continuous propagation of electrical activity along the laminated parts of the brain from the cell to Cell, a non-chemical form of promotion, which is not subject to regulation by inhibitory mechanisms may be continuously spread.
Treatment of pathophysiology of seizures focuses not only on molecular abnormalities including ion channels in nerve cells, but also non-chemical ŠSiling excitation in the brain. Benzodiazepines, such as Valium, and barbiturates such as phenobarbital, act to open inhibitory chloride channels. Phenytoin or dilantin prevents recurring neuron shooting by turning off sodium channels into nerve cells. In situations with poorly managed recurring seizures, halothan can prevent the transmission of nerve impulses. In addition, insulin and steroids change the function of glutamate receptors and suppress brain excitability.