The Medical Explanation About Epilepsy

Epilepsy is functionally characterized by the abnormal recurrent excessive electric discharge of cerebral origin, and clinically characterized by loss of excess of motor, sensory or autonomic functions with or without alteration in consciousness. Epilepsy may be primary where there is no anatomically demonstrable abnormality of secondary when a local or diffuse lesion is present.

Classification of epilepsy: Epilepsies have been classified in several ways.

I. Primary generalized epilepsies: Tonic-clonic seizures (grand mal), Absence seizures (Petit mal), Myoclonic epilepsy, Infantile spasms, Atonic seizures.

II. Partial seizures: Simple- Motor, sensory (somatic, visual, auditory, olfactory), Affective. Complex- Temporal lobe or psychomotor seizure.

III. Partial seizure with secondary generalization.

Pathogenesis

The cortical neuron is abnormally excitable due to differentiation. The cytoplasmic cell membrane of such cells has increased permeability rendering it susceptible to activation by hyperthermia, hypoxia, hypoglycemia and hyponatremia. Deficiency of the inhibitory neurotransmitter gamma-amino benzioc acid (GABA) and disturbance of local regulation of extracellular Potassium ions, Sodium ions, calcium ions or Magnesium ions are probably responsible for the membrane instability. This abnormal electrical discharge, if unchecked, spreads to the contralateral hemisphere across the interhemispheric pathways and also to the subcortical structures like basal ganglia and brain stem reticular nuclei, from where the excitatory activity is fed back to the rest of the cortex. Most of the so-called idiopathic forms of epilepsy do not have any demonstrable lesions in the brain. However, the secondary types of epilepsy may have definable morbid lesions. These include areas of neuronal loss and gliosis (scars), hamatomas, tumors and vascular malformations. One major clinical feature is the Grand Mal epilepsy.

Grand Mal epilepsy: The paroxysm occurs in different stages sequentially. The stages may be subdivided into the prodromal phase, aura, tonic phase, clonic phase and the postictal phase. The prodromal phase may start several hours before the ictus (fit). It consists of several subjective phenomena like depressed or apathetic mood, irritability, vague abdominal cramps or other funny sensations, which are easily recognized by the patient in many cases, stereotyped movements like rotation of the head or movement of the eyes, gripping sensation in the epigastriun or an unnatural sensation in some part of the body occur just before consciousness is lost. This is called just before consciousness is lost. This is called the “aura” and it often indicates activation of the epileptic focus in the brain. In many instances, there is no aura and the patient gets the attack without any forewarning.

The tonic phase consists of opening of mouth and eyes associated with abduction of the arms followed by snapping closure of the jaws, often resulting in injury to the tongue and a cry as the entire musculature goes into spasm forcing air through the closed vocal cords. The patient becomes cyanosed and there may be voiding of Urine. This phase lasts for 10-15 secs. The tonic phase is followed by the clonic phase characterized by alternate to and fro movements of all the four limbs, sweating, frothing of the mouth and excess salivation. Urine and feces may be voided. The clonic phase lasts for 1-2 minutes. This is followed by a deep comatose states which lasts for about 5 minutes. The pupils slowly begin to react and the patient then resumes speech, but still remains confused. If left undisturbed, he goes into sleep for several hours and often wakes up with severe headache. This is the postictal phase and the patient does not remember anything that happened except the aura.

Electroencephalogram (EEG) taken during the attacks or sometimes even during the intervals shows abnormal electrical activity.