Epidemiology

• Up to 5% of population may experience a single seizure; incidence similar in males and females.
  
• Generalised seizure disorders usually commence in childhood or adolescence. Focal seizures can start at any age and can be related in younger patients to hippocampal sclerosis. In older patients it may be associated with cerebrovascular disease or a structural abnormality (tumour).

Aetiology

Aetiologies for the first seizure in adults include (i) idiopathic, (ii) acute or subacute neurological insult or injury due to stroke, head injury and infection (meningitis, encephalitis, subdural empyema and cerebral abscess), (iv) structural CNS diseases, including tumours (primary or metastatic), arteriovenous malformations and congenital CNS abnormalities, (iv) systemic disorders, including electrolyte disturbance (hyponatraemia or hypernatraemia, hypoglycaemia, hypercalcaemia, uraemia and magnesium level disturbances), hepatic encephalopathy and porphyria, (vi) toxin, illicit drug or medication related, including alcohol withdrawal or excess and (vii) eclampsia. In paediatric population, the first seizure may be due to a febrile episode or the so-called febrile convulsion, be it idiopathic or ‘symptomatic or provoked’ due to electrolyte disturbance, meningitis and so on.

Classification and Characteristics

This relies primarily on the mode of onset. Two main categories are primary generalised versus partial (focal) seizures with or without subsequent secondary generalisation.

Primary generalised seizures (40% of all seizures): Bilateral hemispheric symmetrical and synchronous discharge associated with loss of consciousness from the onset.

• Generalised tonic–clonic (GTC) seizure (grand mal): Sudden onset with loss of consciousness and initial tonic (stiffening of limbs) and then a clonic (jerking) phase; may be associated with urinary and/or faecal incontinence and tongue biting. In the postictal phase, patients are drowsy and confused with a gradual return of normal function.
  
• Tonic and clonic components can occur in isolation leading to tonic or clonic seizures, respectively.
  
• Absence (petit mal): Presents in childhood with episodes of transient (≤10 s) impairment of consciousness or pauses (staring episode) with minimal or no motor involvement. Three Hertz spike and wave activity on EEG. No postictal phase. Usual remission in teens.
  
• Myoclonic seizures: Characterised by sudden body jerks.
  
• Atonic seizures: Sudden transient loss of tone (flaccidity) leading to falls and high incidence of injury.

Partial seizures (around 50–60% of seizures): Attributed to seizure activity in one hemisphere or part of one hemisphere at the onset. Often occurs due to an underlying structural abnormality. Clinical features help localize area of onset, for example isolated limb jerking—contralateral motor strip arm region; lip smacking/chewing movements, olfactory or gustatory hallucination—contralateral medial temporal lobe; visual hallucination—occipital lobe and paraesthesia—contralateral somatosensory cortex. Classified as simple or complex, depending on whether consciousness is or is not impaired.

• Simple partial seizure: No impairment of consciousness, for example Jacksonian motor seizure.
  
• Complex partial seizure: With associated impairment of consciousness, often due to temporal lobe pathology; for example, hippocampal sclerosis leading to mesial temporal lobe epilepsy. Can be characterised by an aura (e.g. a rising epigastric sensation or olfactory or gustatory hallucinations) and the automatisms (e.g. lip smacking or chewing).
  
• Partial seizure with secondary generalisation: A seizure which is initially localization related (focal in onset and producing simple or complex phenomena) and then spreading to involve both hemispheres and hence evolving into, for example, a tonic–clonic episode.

Associations/Risk Factors

Refer to Section ‘Aetiology’. Certain factors can lower seizure threshold including photic stimulation (flashing lights) in certain forms of primary generalised epilepsy, hyperventilation, head injury and related posttraumatic seizures, systemic metabolic disturbances (as above) and infection of the CNS.

Pathology/Pathogenesis

Seizures may occur due to an imbalance between excitatory and inhibitory components within cortical neurone networks leading to abnormal excitation.

Possible inherited predisposition to seizures as in primary generalised seizures. Some seizure syndromes like West and Lennox–Gestaut syndrome occur in childhood in association with structural CNS disease, for example tuberous sclerosis.

History

This is extremely important! An account of the events should be sought from a witness if available. See Chapter 6 regarding key points needing clarification in the history, particularly to distinguish seizures from syncope. ‘Onset’ of the sequence of events and establishing any possible compromise of consciousness often allows a clinical classification of seizures as above. Impairment of consciousness is reflected by the patient’s partial or complete lack of memory about the episode. For example, a complex partial seizure with secondary generalisation to a tonic–clonic event may evolve as follows. A prodromal phase (not part of seizure and lasting hours to days) with a possible change in behaviour may be noted followed by an aura (part of the seizure, for example epigastric sensation and unusual smell, which is typically brief and may be associated with an altered level of awareness). With secondary generalization, patients may go on to lose consciousness with falling to the floor and witness tonic followed by clonic movements. Grunting noises, frothing at the mouth and rolling back of eyes may occur. Facial skin may be red or blue in colour (rather than deathly pale). Jerking movements may be seen usually for several minutes with possible associated urinary incontinence and tongue biting. The ‘offset’ of the seizure is typically abrupt followed by a period of marked confusion; the patient subsequently recalls that near clear memory was being in the Emergency Department. Question about any precipitating factors, for example alcohol use, with further questions directed towards other aetiological factors, for example systemic/metabolic or structural causes.

Examination

• In primary generalised epilepsy (idiopathic), clinical examination is usually normal between seizures (inter-ictal period). In partial seizures with or without generalisation, clinical examination may demonstrate a persistent focal deficit between seizures.
  
• If the seizure is witnessed by a doctor or a nurse, a detailed description (pre-event warning signs, onset, postural change, movements, colour of skin, whether eyes open or closed, duration of event, associated features (incontinence) and offset) should be noted in a seizure chart.
  
• In the immediate ‘postictal’ phase, patients may be drowsy and confused following a GTC seizure.
  
• ‘Todd’s paralysis’: Transient weakness or paralysis is observed in an affected limb following a partial seizure, for example after a Jacksonian seizure with weakness improving slowly over hours. Jacksonian seizure is related to abnormal electrical activity within the motor cortex and may start in fingers, followed by hands and then move to more proximal areas.

Investigations

In an adult presenting with a first seizure, direct tests towards establishing a possible underlying cause, particularly if no provoking factors are obvious, for example alcohol withdrawal (refer to aetiologies). Test should include the following: