Percutaneous recording of the electrical potentials associated with cerebral activity confirms that an epileptic attack is associated with a sudden abnormal electrical discharge form cerebral neuroses. Sub threshold paroxysms may be demonstrable between clinical attacks. The EEG phenomena indicate that the differences in type of seizure are due to the site of the initial abnormal discharge of cerebral neurons and the mode of spread. One group originates in the upper brain stem (termed the cent encephalon by Penfield) the simultaneously disturbed function in both cerebral hemispheres; the site of discharge is believed to be the upper reticular formation because in grand mal and petit mal suspension of consciousness is invariable.

Fits of identical type may occur in either group and the response to drug treatment tends to be related to types of fit rather than to etiology. For this reason it is desirable to adopt a double classification of the epilepsies, one based on causation and the second on the clinical features of the fit. The latter is based on clinical observation correlated with the finding of electro encephalography.

An epileptic fit is associated with sudden paroxysmal discharges form neutrons. In some cases the instability is constitutional and the tendency may be familial but the factors precipitating the attack are usually obscure. Epilepsy is not a mental disease though it may be associated with cerebral disorder coursing mental symptoms. Psychological reactions of resentment and aggression may occur if the patient is deprived of a normal place in school and social life. Emotional disturbances may precipitate an attack in the predisposed. In other case it is clear those irrigative factors are involved such as cortical scars, ischemia, infecting, toxemia, alkalaemia, hypoglycemia, water retention or hypertension. On this basic but us possible to classify epilepsy into two etiological groups. Idiopathic where there is no apparent cause, Symptomatic, where there is an apparent cause.

Antibiotics should not be given as a routine. It is perdurable, f good nursing conditions and close medical supervision can be assured to with hold antibiotics until necessary in order to reduce the risk of infection by resistance organisms. Food: When coma is prolonged it is essential to maintain nutrition by giving a high calorie fluid diet by means of a nasal tube. Care of the skin bladder and bowel is also required although these are last to be mentioned the preventions of pressure sores begin from the earliest moment. Earl catheterizations necessary to obtain urine for analysis when the case of coma is unknown.

The stomach may be emptied early to avoid aspiration pneumonia and the fluid should be retained for examination. It a poison is identified the antidote may be placed in the stomach after ravage. Poisoning by narcotic is common and may be fatal if treatment is delayed. If, however, the diagnosis is not in doubt it is advisable to delay gastric aspiration until respiration is adequate and a cough reflex is present but if unconsciousness lasts more than a few hours a nasal tube should be passed for administration of fluid to prevent dehydration

The unconscious patient is exposed to special hazards as the is dependant on reflexes auto protect his body and maintain respiratory and cardiovascular function and the reflexes are progressively lost as coma deepens. Until full consciousness returns the patient must be protected form these hazards in addition to those of the causative disease. The airway: Maintenance of a clear airway is the first essential. The tongue should be kept forward by a tube if necessary and the pharynx free mucus, if respiration is shallow or irregular it must be assisted. Peroration should be made immediately.

There may be a history of a drinking bout and the odor of alcohol may be detected in the breath but the possibility of illness or injury occurring to a patient ego has taken a harmless amount of alcohol must be considered or the alcohol may have been administered after the onset of illness. The patient is often stupor us with flushed skin full pulse deep respiration and dilated pupils which react sluggishly to light. In severe alcoholic poisoning there may be deep coma with respiratory depression. The pupils then become very small but if the patient is hake nth pupils dilate though he cannot be roused and again constrict what he is left at rest. This sign is highly characteristic of alcoholic coma. It is sometimes seen in narcotic poisoning but never after head injury or apoplexy.

Coma is associated with body temperature lower than 96 f. thermometers is essential for accurate measurement in this race. It may be due to exposure to severe climate condition or form normal loss of body heat if a poorly clad person lies hapless or unconscious in an unheated room for one or more days especially if he is elderly and thin. Hypothermic coma may occur in the absence of cold if the metabolic rate is depressed by myxoedema or hypopituitarism.

Virus encephalitis as a cause of coma is rare. It is important to bear in mind cerebral malaria in the tropics so in any comatose patient who has recently returned form a country in which malaria is prevalent. Early treatment is completely effective. Coma also occurs in African try panosomiasis, but is a late complication. Cerebral: Tumor an other causes of raised intracranial pressure. As pressure rises the brain becomes displaced and ischemic. Consciousness is lost slowly and signs of pressure coning and papilloedema develop.