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Stroke and Seizures

One of the many sequellae of stroke is the development of an epileptic-type seizure, or of recurrent seizures. Among elderly people in whom seizures occur as a new-onset disorder, stroke is most often the underlying cause. In order to understand the relationship between these two neurological disorders, it is necessary to define them. I will assume that the reader is already familiar with the definition and physiological mechanisms of strokes. I will merely remind that there are two major stroke types: ischemic, resulting from blockage of a blood vessel and death of brain tissue in that blood vessel's domain; and hemorrhagic, resulting from rupture or leak of a blood vessel and extravasation of blood into brain tissue or the fluid surrounding it.

The word "seizure" is applied loosely and often erroneously to a variety of physiological phenomena ranging from strokes to heart attacks to muscle cramps. True medical seizures are phenomena that occur in the brain. Brain cells, or neurons, normally send out electrical signal pulses through long wire-like extensions called axons. For neurons in the motor areas of the brain, these signal pulses are relayed to muscles. When a muscle receives appropriate signals, it contracts, producing movement of the corresponding body part. Other neurons, in areas of the brain responsible for recognizing sensory information, receive relayed information such as touch sensation or pain from the body through their axons.

Most neurons are constantly sending out and/or receiving low levels of electrical signal pulses through their axons. When a group of neurons becomes provoked or irritated by a pathologic process or agent, it may become hyperactive and begin discharging a high level of electrical signals. If the timing of such strong signal pulses becomes synchronized among all neurons in the group, a motor or sensory seizure can occur. For example, if the electrical hyperactivity were occurring on the left side of the brain, focally in the motor area for the arm, it would produce tight contraction or violent convulsion of the right arm. If the seizure occurs in a sensory area of the brain, then the patient may notice a sudden tingling, numbness, or other ambiguous sensation in the corresponding body part.

The synchronous electrical hyperactivity from a group of neurons can spread to adjacent or distant areas of the brain, producing a more generalized seizure. Other limbs and body parts can become involved, and various degrees of impairment of consciousness can occur. In a generalized seizure involving many areas on both sides of the brain, complete loss of consciousness accompanied by violent convulsion of all the limbs occurs. This is called a generalized tonic-clonic seizure, also known as a "grand mal" seizure. Focal motor or sensory seizures and generalized tonic clonic seizures are the most common types encountered as a result of stroke.

Seizures can be precipitated by strokes by a number of mechanisms. We will first discuss seizures that occur immediately during or shortly after a stroke. Such seizures most often result from hemorrhagic strokes in which a stream of blood squirts out of an artery under pressure into brain tissue. The blood produces a ripping and tearing effect in the tissue as it forces a space for itself. Additionally, it pushes aside adjacent brain tissue causing a compression effect. The compressed tissue also becomes deprived of oxygen (a state known as anoxia). The tearing, compression, and anoxia all act as provocative factors that can precipitate epileptic electrical discharges from neurons, resulting in a seizure.

Less commonly, immediate seizures can occur in an ischemic stroke. In this case, blockage of a blood vessel deprives a portion of the brain of blood flow, and hence oxygen, producing anoxia. Large ischemic strokes can produce local swelling of brain tissue in their vicinity, producing a compressive effect. Either or both of these mechanisms may precipitate a seizure during or shortly after an ischemic stroke. As the bolus of blood in a hemorrhagic stroke is reabsorbed, or as the dead swollen tissue of an ischemic stroke subsides, the provocation for seizures usually resolves.

The most common seizures resulting from strokes are those that occur weeks or months after the initial event. When a region of brain tissue dies during a stroke, it begins to degenerate into scar tissue after a few weeks. The dead area contracts into a fibrous nodule of scar tissue. The presence of this scar tissue acts a provocative irritant to the normal neurons adjacent to it, precipitating a seizure months or even years later. The likelihood of any stroke producing such delayed seizures is dependent on its size and location. Small strokes deeper in the brain, such as lacunar strokes, are unlikely to cause seizures. Larger strokes and those involving the outer surface of the brain known as the grey matter, or cortex, are more likely to cause delayed seizures. Most neurons are located in the cortex. Because scar tissue is permanent, delayed-onset seizures have greater chance for recurrence.

As a general rule, seizures that first occur immediately during or shortly after a stroke have a low chance of heralding the development of a permanent recurrent seizure disorder. On the other hand, seizures which first occur weeks or months after a stroke have a much greater likelihood of heralding the onset of a permanent disorder characterized by episodically recurring seizures and requiring long-term or lifelong medication therapy. Some physicians will prescribe a temporary anti-seizure medication as a preventative measure immediately after a stroke even if no seizure has occurred. This is most often done in the case of hemorrhagic stroke. The use of seizure medication in other cases is a complex medical decision based on the occurrence of seizure, type and location of the stroke, information from other diagnostic tests such as the electroencephalogram (EEG), and the desires of the patient.

Mayank Pathak, M.D.

SAFE (Stroke Awareness for Everyone, Inc.) has been given permission to reproduce this article by its author, Mayank Pathak, M.D. Dr. Pathak is Staff Physician, at The Parkinson's and Movement Disorders Institute, Fountain Valley, California.

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