Tuesday, November 15, 2016

Pathophysiology of Secondary Generalized Seizures

To understand the pathophysiology of seizures in brief, lets take the following case.

Two brothers, Ram and Shyam were playing chess. When all of  a sudden Ram noticed that his 40-year old brother seemed to be daydreaming  and seemed to be confused and having a petrified stare for about 20 seconds. Then suddenly his right hand began to bend into an awkward position and then to shake. The shaking grew worse, progressing gradually from the hand to the arm and then to the entire right side of the body. Then his body stiffened for about 15 seconds, followed by shaking movements of all four limbs that lasted another 30 seconds or so. Then he became limp and unconscious.

1. Now here Rob first showed the symptoms of daydreaming, confusion and petrified stare, this is known as Aura. Since its a behavioural disturbance, we can guess that the foci of this seizure activity is in the temporal lobe(hippocampus, amygdala etc).

2. So there is abnormal synchronous electrical activity(ASET) somewhere in the temporal lobe which could have been due to any pathology like tumour, tuberculoma, stroke, viral encephalitis, neurocysticercosis etc.

3. It took the seizure activity 20 seconds to override the Surround inhibition  of the temporal lobe and then spread to the neighbouring areas.

4. Next there is contraction of muscles followed by shaking first in his right hand, then arm, then the complete right side. This means now the abnormal synchronous electrical activity(ASET) has spread to the left motor cortex and progressively involved the entire homunculus.

5. Next this tonic-clonic activity involves the entire body. This means that ASET has spread to the contralateral hemishphere via corpus callosum and other commissures and that it has involved Thalamus, which is the gateway to the entire cerebral cortex. Now since it is bilateral, we can call it a Generalized seizure.

6. Lets learn the mechanism of Tonic-Clonic seizure(Grand Mal seizure) activity.

A: First there is sudden inhibition of all GABAergic activity leading to overriding       of the Surround Inhibition, causing contraction of both agonist and antagonist group of muscles, referred to as the Tonic phase.

B: Then the GABA-mediated inhibition is gradually restored and while increasing it starts      oscillating with the excitatory activity mediated by Glutamate via its NMDA and AMPA receptors. If this oscillation involves the motor cortex, there is shaking movements, referred to as Clonic phase.

C: Ultimately the GABA-mediated inhibition prevails, resulting in all the muscles               becoming flaccid and the patient becomes unconscious until normal brain function is restored.   


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