How to prevent epilepsy caused by brain trauma?

Epilepsy is what we often call epilepsy. There are many causes of epilepsy. Changes in cerebral blood circulation and electrophysiological changes in the body will lead to epileptic discharges, glial hyperplasia, destruction of glial relationships between neurons, brain scars, etc. can all cause epilepsy. Epilepsy patients will experience headaches, drowsiness, paralysis, convulsions, pupil dilation and other symptoms. Prevention is important in normal times.

Pathogenesis

The mechanism of post-traumatic epilepsy is still not fully understood. Penfield and Erickson believed that a series of biochemical, electrophysiological and brain structural changes may occur after brain injury, leading to the formation of epileptic foci. Primary or secondary brain damage caused by trauma can cause changes in the neurons themselves or their surrounding glial cells and blood vessels, thereby promoting excessive discharge and abnormal hyperassimilation of individual brain cells. The changes can be local or widespread. From the perspective of pathophysiology, the main mechanisms of epilepsy are as follows:

Changes in cerebral blood circulation

Changes in blood circulation lead to subtle chemical and electrophysiological changes in the nerve cells themselves, causing epileptic discharges. During the acute phase, there is extensive intracranial hemorrhage and cerebral blood circulation disorder, which stimulates nerve cells and causes excessive abnormal discharges. As a result, the oxygen and glucose supply to brain cells is reduced, metabolic products accumulate, and the blood-brain barrier is destroyed, aggravating the damage to nerve cells, which can manifest clinically as epilepsy. Severe local damage can cause chronic ischemia and gliosis around nerve cells, forming chronic epileptic foci. Similarly, ischemia and sclerosis of the amygdala-hippocampus area caused by cerebral edema or brain herniation often form chronic epileptic foci.

Mechanical effects of meningeal scarring and gliosis

The normal cortex has pial arteries and a rich capillary network. The intermediate zone between the brain scar and the normal cortex lacks capillaries and shows the destruction of nerve cells and the regeneration of neuronal processes. This cell regeneration phenomenon is an important factor in the occurrence of epilepsy. The intermediate zone is in an ischemic state, and due to the slow atrophy of gray matter, it is also one of the causes of epileptic foci. Glial hyperplasia and brain scars, especially meningeal-cerebral scars, pull brain tissue toward the center of the scar due to their contractile effect. Combined with the pulsating stimulation of blood vessels, this exerts mechanical tension on the neuronal dendrites in the intermediate zone, increasing the possibility of the intermediate zone becoming an epileptic focus.

Disruption of the blood-brain barrier and disruption of neuron-glia relationships

The blood-brain barrier has the function of transporting and diffusing some chemical substances between the blood and brain tissue. The blood-brain barrier is often damaged after trauma, which becomes a factor in the generation of epileptic foci. Studies have shown that the neuron-glia system can serve as an ion buffer system to control the balance of ions inside and outside the nerve cell membrane. The disruption of this normal relationship after injury will cause serious and persistent membrane potential imbalance and produce epileptic foci.

Disruption of the axonal collateral inhibitory system

The collateral branches of the axons of cerebral cortical neurons can in turn inhibit the excitability of the neurons themselves through a feedback loop composed of interneurons. Various pathological factors produced during brain trauma affect axonal collaterals, causing them to lose their inhibitory control function, resulting in neuronal hyperexcitability and cell membrane repolarization disorders, causing epileptic discharges.

Biochemical changes

For example, impaired binding ability to acetylcholine, loss of glutamate metabolism, and impaired ability to restore and maintain intracellular potassium concentration may all become factors that promote abnormal cortical discharges.

Treatment principles

Except for a few cases that require surgical treatment, traumatic epilepsy is generally treated with medical therapy. The principles are as follows:

⑴ Medical treatment first determines the type of epilepsy, and then selects appropriate anti-epileptic drugs based on the electroencephalogram. The principles of medication are as follows:

① Use commonly used drugs first, start with one drug and sufficient dose, and gradually increase the dose if it is ineffective. If it is still ineffective, you can use a combination of drugs;

②The time of taking medicine should be determined according to the time of onset;

③Drug treatment should be continuous, otherwise it will be ineffective; changes, increases and decreases should be made gradually, and sudden discontinuation of medication can often lead to severe epileptic seizures;

④ During medication, it is necessary to test whether the effective blood drug concentration has been reached, and check blood count and liver function regularly. If allergic or poisoning symptoms occur, the drug should be stopped or changed in time.

⑵Surgical treatment refers to the removal of epileptic lesions, and patient selection is particularly important. Preoperative EEG screening is of great significance. Indications for surgery are:

① Multiple electroencephalogram examinations confirmed that there was a fixed and localized epileptic focus in one cerebral hemisphere;

② The lesions should generally be in non-functional areas;

③Cases that meet the above conditions have not responded to systemic drug treatment.

The effectiveness of surgery is related to strict case selection, accurate localization of epileptic lesions, and complete resection. The overall success rate of surgery is usually around 85%. It is worth mentioning that some patients still need to take medication after surgery, but the number of epileptic seizures is significantly reduced. In addition, patients and families should consider the possible complications of surgical treatment.

Dangerous phenomenon

1. Headache: The degree is quite severe, general analgesics are ineffective, and it is often accompanied by frequent nausea and vomiting.

2. Paralysis: Limb movement is normal when injured, but gait becomes unstable gradually, or one upper limb becomes weak and difficult to lift.

3. Coma: If a person who was awake becomes deeply asleep or difficult to wake up, do not assume that he or she has fallen asleep. Be alert to the possibility that the coma is deepening.

4. Convulsion: Limb convulsion is called paralysis attack, which is a specific manifestation of brain cells being stimulated and discharged.

5. Mydriasis: Normally, the pupils on both sides are equal in size and round, but they shrink when exposed to light. In abnormal cases, one pupil is larger than the other and the light response is slow.

6. Bedwetting: Bedwetting indicates that the brain's urination center is compressed. Bedwetting in adults may be the first sign of intracranial hematoma.

7. Slow heartbeat: A normal adult's heartbeat slows down to below 40-50 beats per minute, accompanied by increased blood pressure and slowed breathing, indicating that intracranial hematoma or cerebral edema has occurred.

8. Agitation: Extreme restlessness, accompanied by profuse sweating, indicates that the intracranial pressure has risen to a level that is difficult to compensate.

9. Mental abnormality: confusion, lack of concentration, and inability to do things as usual.

10. Dizziness: Patients in the early stages of brain trauma all complain of dizziness, often accompanied by nausea and vomiting. If the dizziness reaches an unbearable level, you should also be alert to the possibility of intracranial hematoma.