USMLE – Seizures
A seizure is any abnormal clinical event caused by an electrical discharge from the brain, while epilepsy is a tendency to have seizures. Major seizures cause loss of consciousness, with the patient falling to the ground and presenting with a history of ‘blackouts’. Minor seizures causing alteration of consciousness, without the patient falling to the ground, may also be described as ‘blackouts’.
In the normally functioning cortex, synchronous discharge amongst neighboring groups of neurons is limited by recurrent and collateral inhibitory circuits. The inhibitory transmitter gamma-aminobutyric acid (GABA) is particularly important in this role and drugs which block GABA receptors provoke seizures. There are also a large number of excitatory neurotransmitters, of which acetylcholine and the amino acids glutamate and aspartate are examples. ‘Epileptic’ cerebral cortex exhibits hypersynchronous repetitive discharges involving large groups of neurons. Intracellular recordings show bursts of rapid-action potential firing, with reduction of the transmembrane potential (paroxysmal depolarization shift). It is likely that both reduction in inhibitory systems and excessive excitation play a part in the genesis of seizure activity. Cells undergoing repetitive ‘epileptic’ discharges undergo morphological and physiological changes which make them more likely to produce subsequent abnormal discharges (‘kindling’).
The chief division of seizure types on physiological grounds is between partial (focal) seizures in which paroxysmal neuronal activity is limited to one part of the cerebrum, and generalized seizures where the electrophysiological abnormality involves both hemispheres simultaneously and synchronously. If partial seizures remain localized, the symptomatology depends on the cortical area affected. If consciousness (the awareness of, and ability to respond to the environment) is preserved, the attack is termed ‘simple’. If, however, the activity involves some parts of the brain dealing with awareness (such as the temporal or frontal lobes), then consciousness is affected and a ‘complex partial seizure‘ results. Further spread into the diencephalon and thence throughout the remainder of the cortex leads to a secondarily generalized seizure.
In primary generalized seizures, the abnormal activity is seen to begin synchronously throughout the cortex without an initial partial onset. It probably originates in the central diencephalic mechanisms controlling cortical activation. This is recognizable on an EEG which shows spikes and waves of abnormal activity and quite often provocation of abnormalities with hyperventilation and/or photic stimulation. This may cause a major seizure identical to a secondarily generalized seizure, or a more restricted clinical manifestation if the abnormal electrical activity fails to affect muscle tone. In this case there is an ‘absence’, in which consciousness is lost but the patient remains standing or sitting in an attack which may be difficult to distinguish clinically from a complex partial seizure in the temporal lobe.
Tonic clonic seizures
A tonic clonic seizure may be preceded by a partial seizure (the ‘aura’) which can take various forms, described below. However, a history of such an ‘aura’ is commonly not obtained, probably because the subsequent seizure causes some retrograde amnesia for immediately preceding events. The patient then goes rigid and becomes unconscious, falling down heavily if standing, often sustaining injury. During this phase, respiration is arrested and central cyanosis may be witnessed. After a few moments, the rigidity is periodically relaxed, producing clonic jerks. Some patients do not have a clonic phase and the rigidity is replaced by a flaccid state of deep coma which can persist for some minutes. The patient then gradually regains consciousness, but is in a confused and disorientated state for half an hour or so after regaining consciousness. Full memory function may not be recovered for some hours. During the attack urinary incontinence may occur, as may tongue-biting. (A severely bitten, bleeding tongue after an attack of loss of consciousness is pathognomonic of a generalized seizure.) After a generalized seizure the patient usually feels terrible, may have a headache and will want to sleep. Witnesses of a seizure are usually frightened by the events, often believing the person to be dying, and may not give a clear account; this is in itself a helpful diagnostic pointer since syncope seldom produces such fear in onlookers.
Patients may have no tonic or clonic phase, and may not become cyanosed or bite their tongue. However, postictal confusion or headache and a period of subsequent malaise and/or confusion are usually seen, and this is useful in differentiating seizures from faints. Psychogenic nonepileptic attacks (‘pseudo-seizures’) may be accompanied by dramatic flailing of the limbs and arching of the back; however, these usually are not followed by the same degree of postictal confusion and never cause cyanosis.
Complex partial seizures
Partial seizures may cause episodes of altered consciousness without the patient collapsing to the ground, especially if arising from the temporal or, less frequently, the frontal lobe. These may be referred to as ‘blackouts’. The patient stops what he or she is doing and stares blankly, often making rhythmic smacking movements of the lips or displaying other automatisms, such as picking at their clothes. After a few minutes the patient returns to consciousness but may be initially muddled and feel drowsy. Immediately before such an attack the patient may report alterations of mood, memory and perception such as undue familiarity (deja vu) or unreality (jarnais vu), complex hallucinations of sound, smell, taste, vision, emotional changes (fear, sexual arousal), or visceral sensations (nausea, epigastric discomfort). If these changes of memory or perception occur without subsequent alteration in awareness the seizure is said to be a simple partial seizure.
A type of minor seizure which resembles a complex partial seizure occurs in the generalized absence epilepsy of childhood, and is known as ‘petit mal’. The attacks in petit mal are usually briefer and very much more frequent (20 or 30/day) than complex partial seizures and are not associated with postictal confusion. Absence attacks are caused by a generalized discharge which does not spread out of the hemispheres and so does not cause loss of posture.
Partial motor seizures
Epileptic activity arising in the precentral gyrus causes partial motor seizures affecting the contralateral face, arm, trunk or leg. Seizures are characterized by rhythmical jerking or sustained spasm of the affected parts. They may remain localized to one part, or may spread to involve the whole side. Some attacks begin in one part (e.g. mouth, thumb, great toe) and spread gradually; this is Jacksonian epilepsy. Attacks vary in duration from a few seconds to several hours. More prolonged episodes may leave paresis of the involved limb lasting for several hours after the seizure ceases (Todd’s palsy).
Partial sensory seizures
Seizures arising in the sensory cortex cause unpleasant tingling or ‘electric’ sensations in the contralateral face and limbs. A spreading pattern like a Jacksonian seizure may occur, the abnormal sensation spreading much faster over the body (in seconds) than the ‘march’ of a migrainous focal sensory attack, which spreads over 10-15 minutes.
A frontal epileptic focus may involve the frontal eye field, causing forced deviation of the eyes to the opposite side. This type of attack often becomes generalized to a tonic clonic seizure.
Partial visual seizures
Occipital epileptic foci cause simple visual hallucination such as balls of light or patterns of color. Formed visual hallucinations of faces or scenes arise more anteriorly in the temporal lobes.
Factors precipitating seizures
Sometimes specific trigger factors can be identified.