Seizures occur when nerve cells in the brain become overly excited or fire abnormally due to various factors. The pathophysiology of seizures involves an imbalance between excitatory and inhibitory forces, and treatments target both molecular abnormalities and non-chemical spread of excitation in the brain.
A seizure occurs when one part of the brain becomes overly excited, or when nerves in the brain start firing together in an abnormal way. Seizure activity can arise in areas of the brain malformed by birth defects or genetic disorders or disrupted by infection, injury, tumor, stroke, or inadequate oxygenation. The pathophysiology of seizures results from an abrupt imbalance between the forces that excite and inhibit nerve cells such that excitatory forces take precedence. This electrical signal then spreads to surrounding normal brain cells, which begin firing in concert with the abnormal cells. With seizures that are prolonged or recur over a short period, the risk of future seizures increases as nerve cell death, scar tissue formation, and the sprouting of new axons occur.
Nerve cells between discharges normally have a negative charge internally due to the active pumping of positively charged sodium ions out of the cell. The discharge or activation of the nerve cell results in a sudden fluctuation of the negative charge to a positive charge as the ion channels in the cell open and positive ions, such as sodium, potassium and calcium, flow into the cell. Both excitatory and inhibitory control mechanisms act to allow for appropriate activation and prevent inappropriate excitation of the cell. The pathophysiology of seizures may occur due to increased nerve cell excitation, decreased nerve cell inhibition, or a combination of both influences.
Normally, after firing a nerve cell, inhibitory influences prevent a second firing of the neuron until the neuron’s internal charge returns to its resting state. Gamma-amino-butyric acid (GABA) is the main chemical inhibitor in the brain. GABA opens channels for negatively charged chloride ions to flow into the excited neuron, which reduces the internal charge and prevents a second firing of the nerve cell. Most antiepileptic drugs reduce the pathophysiology of seizures by increasing the frequency of openings of the chloride channels or by increasing the duration during which the channels are open. When there is a disruption in the GABA-emitting cells or GABA receptor sites, there is a failure of the chloride channels to open and temper the excitability of the nerve cell.
Equally significant to the pathophysiology of seizures are the mechanisms leading to increased excitation of neurons. Glutamate is the primary excitatory chemical mediator in the brain, binding to receptors that open channels for sodium, potassium, and calcium in the cell. Some inherited forms of seizures involve a predilection for excessively frequent or prolonged activation of glutamate receptors, increasing the excitability of the brain and the prospect of seizure activity. Furthermore, contiguous diffusion of electrical activity along layered parts of the brain can occur from cell to cell, a nonchemical form of propagation that is not subject to regulation by inhibitory mechanisms.
Treatments for the pathophysiology of seizures target not only the molecular abnormalities involving ion channels in nerve cells but also the non-chemical spread of excitation in the brain. Benzodiazepines, such as Valium, and barbiturates, such as phenobarbital, act to open inhibitory chloride channels. Phenytoin or Dilantin prevents repetitive firing of neurons by closing sodium channels in nerve cells. In situations with poorly managed recurring seizures, halothane can prevent the non-chemical transmission of nerve impulses. Also, insulin and steroids change the function of glutamate receptors, suppressing the excitability of the brain.
Protect your devices with Threat Protection by NordVPN
