• Sudden discharge of cerebral neurons characterized by alteration in brain function
• Epilepsy condition with no underlying cause for the seizure
Causes of Seizures
• Genetic predisposition
• Perinatal injury
• Postnatal trauma
• Brain tumor
• Vascular disease
• Drug or alcohol abuse
• Fatigue or lack of sleep
• Emotional or physical stress
• Large amounts of water ingestion
• Hyperventilation(resp alkalosis)
• Environmental stimuli
• Epileptogenic focus
• Oxygen consumption
Types of seizures
– Secondary generalized
• Generalized seizures
– Absence tonic tonic-clonic
– Myclonic atonic
• Unclassified epileptic seizures
INCREASED INTRACRANIAL PRESSURE
• Intracranial pressure may increase with increases in
• cranial blood,
• CSF, or
• A significant increase in intracranial pressure is called intracranial hypertension.
• Intracranial hypertension causes neurons and capillaries in the brain to become compressed, leading to hypoxia, neuronal injury and death, and progressive deterioration of brain function.
• If intracranial pressure reaches systemic mean arterial pressure, blood flow to the brain will stop and the individual will die.
• Edema and Swelling of the Interstitial Space:
• Infection and inflammation are associated with interstitial swelling and edema as a result of the release of vasoactive mediators of inflammation that stimulate increased capillary blood flow and increased capillary permeability
• Severe hypertension may increase intracranial pressure by causing filtration of plasma into the interstitial space, again leading to edema and swelling.
• Severe trauma to the head, a burst aneurysm, or a hemorrhagic stroke all cause bleeding in the brain.
The Stages of Intracranial Hypertension
• Stage 1
• An increase in one of the three volumes in the brain (blood, CSF, or tissue) is normally compensated for by a decrease in one or both of the other volumes. If there is increased volume in one compartment, but near normal intracranial pressure due to compensation, the brain is said to be in stage 1 of intracranial hypertension.
• Usually, this stage first involves decreased CSF production or increased CSF reabsorption, if possible, followed by venous constriction to increase blood flow out of the brain. Individuals in stage 1 may demonstrate only subtle behavioral changes, primarily drowsiness and slight confusion.
• Stage 2
– If the volume continues to increase, intracranial pressure begins to rise significantly.
• This stage would occur with the progression of a tumor or continual bleeding from a severed artery or vein.
• During stage 2, the brain responds by constricting cerebral arteries in an attempt to further reduce pressure by reducing blood volume.
• However, reduced blood flow causes development of cerebral hypoxia and hypercapnea, and deterioration of brain function.
• Obvious clinical signs include decreased level of consciousness, alterations in breathing pattern, and pupillary changes
• Stage 3
– Brain hypoxia and deterioration of brain function cause the cerebral arteries to respond with reflex dilation and blood volume increases.
• Intracranial pressure increases further and worsens the situation.
• This is called decompensation. With the onset of decompensation, the individual is said to enter stage 3 of intracranial hypertension.
• Fast-rising pressure compresses the arterioles and capillaries, worsening the hypoxia and the hypercapnea, and damaging the neural cells.
• The result is pronounced decreased consciousness, altered respiratory pattern, and loss of pupillary reflexes.
• As the brain senses worsening hypoxia and hypercapnia, it responds with reflexes geared toward increasing systemic mean arterial pressure in an attempt to increase its own oxygenation.
• A dramatic rise in systemic blood pressure only serves to further increase intracranial pressure, accelerating the destruction of the brain cells. Cerebral blood flow slows, and consciousness and reflexes are usually lost.
• Stage 4
• herniation (bulging) into another compartment occurs. When intracranial pressure reaches mean systolic pressure, cerebral perfusion stops.
Treatment of Intracranial Hypertension
• Treatment of intracranial hypertension includes osmotic diuretics (mannitol) to reduce blood volume and steroids to decrease inflammation.