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Literature Supports Trigger-Dispersion Theory

Carly Cenedella

Having seen epileptic seizures and talking qualitatively about the experience with people who have epilepsy, I made five basic hypotheses about epilepsy. I collectively call these hypotheses my trigger dispersion theory of epilepsy. My five hypotheses are:

1 There is an area in the brain where abnormal firing associated with seizures begins. I will call this area the trigger area. From the trigger area, abnormal firing spreads to other areas of the brain compromising the function of the affected area.

2 There is a stimulus either external or internal which excites the trigger area. I will call this stimulus the trigger. The trigger can be very specific.

3 The first area affected after the trigger area is sensory.

4 The abnormal firing spreads from the sensory area to an area for motor control.

In this paper, I will go through the hypotheses of the trigger-dispersion theory and discuss literature that supports each hypothesis.

Hypothesis 1- There is an area in the brain where abnormal firing associated with seizures begins. I will call this area the trigger area. From the trigger area, abnormal firing spreads to other areas of the brain compromising the function of the affected area.

During a seizure, certain cells (a seizure focus) begin to fire rapidly. In fact, nerve cells in the brain fire electrical impulses at a rate of up to four times higher than normal during a seizure (5) .

This abnormal firing is spread this to other neighboring cells. In the brain of an epileptic, there is not enough inhibitory neurotransmitters to stop the spread of the abnormal firing (2) .

In the 1800s, it was noted by Jackson that epileptic seizures begin in isolated parts of the body such as the thumb and from there spread to neighboring regions perhaps the arm and then to the rest of the body. He hypothesized that there were areas in cerebral cortex that controlled isolated movements and that the areas that were adjacent in the brain were anatomically adjacent as well. Therefore, a seizure began in one area and spread to the rest of the cortex. His hypothesis was later substantiated by Fritsch and Hittig's excitation experiments on motor cortex or area 4. It is a band of neural tissue on the cerebral cortex lying on precentral fissure. The body's movements are mapped out on this band giving rise to the spreading fashion that Jackson described during seizures (6) .

Hypothesis 2- There is a stimulus either external or internal which excites the trigger area. I will call this stimulus the trigger. The trigger can be very specific.

The normal brain is capable of seizing in response to a variety of stimuli. The triggers for seizures may be divided into two categories, extracranial and intracranial. Extracranial triggers are those that arise outside of the nervous system. Intracranial triggers arise within the nervous system, such as brain tumors (2) .

An example of an extracranial trigger is that of a strobe light on a photosensitive epileptic. Extensive EEG studies have shown that a flicker stimuli with the frequency of 10 to 30 flashes per second induces generalized epileptiform discharges and the clinical characteristics of an epileptic seizure(3) .

The specificity of this stimulus for this particular type of epilepsy suggests that all epilepsy have a certain trigger. Additionally, individuals with epilepsy may have an increased risk for having a seizure if the following triggers are present; stress, sleep deprivation, fatigue, or insufficient food intake (4) .

Hypothesis 3- The first area affected after the trigger area is sensory.

The onset of a seizure called aura is characterized by a certain smell or hallucination (7) or by an uncomfortable feeling (1) . Given that the first stage of a seizure is strongly altered perception of sensory information, it seems to follow that the sensory area is affected first. In fact, epilepsy is strongly associated with sensory (and motor discussed next) cortex, which lies just behind the central fissure on each side of the brain. Posttraumatic epilepsy, a common complication of severe head injuries, may be the result of scar tissue formation near the sensory cortex (8) .

Hypothesis 4- The abnormal firing spreads from the sensory area to an area for motor control.

The second stage of a seizure is ictus and is characterized by convulsions. This suggests that the abnormal firing in the sensory cortex must move to the motor cortex (2) . Additionally, sensory and motor cortex are interdependent. Many sensory inputs that reach sensory cortex give rise to a signals in the motor cortex. (8) . As mentioned above, motor cortex plays a central role in epilepsy. Tumors growing in motor cortex may irritate the neurons causing them to discharge and cause seizures (8) .

All in all, the trigger-dispersion theory seems viable. The literature supports is hypotheses. The Serch for this information confrimed many of my hypotheses and also teught me a lot about epilepsy and the brain.

WWW Sources

1) The National Institutes of Health Homepage: Research in the News , written by Ruth Lew Guver

2)Seizures in Dogs , written by Teri Dickinson, DVM

3) Trenite, D.G.A. Video Game Epilepsy. The Lancet. October 22, 1994.

4) The National Institute of Neurological Disorders and Stroke: What is Epilepsy?

5) The National Institute of Neurological Disorders and Stroke: Epilepsy

6) Houssay M.D., Bernando A. Human Physiology. McGraw-Hill Book Company: 1955.

7) Eleftheriou, Basil E. The Neurobiology of the Amygdala. Plenum Press: 1972.

8) Gardner M.D., Ernest. Fundamentals of Neurology, 4th Edition. W.B.Saunders Company: 1963.




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