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Epilepsy in later childhood and adulthood 

Epilepsy in later childhood and adulthood

Chapter:
Epilepsy in later childhood and adulthood
Author(s):

G.D. Perkin

and M.R. Johnson

DOI:
10.1093/med/9780199204854.003.240501_update_001

Update:

Definitions and classification—expanded discussion.

Pathophysiology—role of inflammatory mechanisms in focal epilepsy; enhanced discussion of genetic generalized epilepsies.

Clinical features—discussion of sudden unexpected death in epilepsy (SUDEP); comments on differential diagnosis from syncope and psychogenic nonepileptic seizures.

Management—comments on levetiracetam, and on use of valproate and carbamazepine in pregnancy.

A relevant case history from Neurological Case Histories: Case Histories in Acute Neurology and the Neurology of General Medicine has been added to this chapter.

Updated on 28 Nov 2012. The previous version of this content can be found here.
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date: 30 March 2017

An epileptic seizure is a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain. Epilepsy is defined as a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiological, cognitive, psychological, and social consequences of this condition. The definition of epilepsy requires the occurrence of at least one epileptic seizure and evidence for an enduring alteration in the brain that increases the likelihood of future seizures such as an ‘epileptiform’ EEG abnormality, an appropriate lesion on structural brain imaging (CT or MRI), or the presence of recurrent (two or more) seizures. Epilepsy is a common, serious neurological disease, with prevalence 1% and a cumulative lifetime risk of 5%.

Pathophysiology

Epileptic seizures are thought to arise at cortical sites. Focal (also referred to as partial) seizures begin focally; generalized seizures infer widespread, bilateral cortical involvement from the beginning. Underlying mechanisms have been best defined for generalized absence seizures, where a thalamocortical circuit is responsible for generating synchronous burst-firing of neurones. In different types of epilepsy, roles for specific ion channels (e.g. voltage-dependent calcium channel, (T-channel)), receptors (e.g. GABAA receptors), and neurotransmitters (e.g. serotonergic) have been suggested, but modern genetic research is increasingly implicating other aspects of synaptogenesis in the aetiology of epilepsy. Epilepsy may occur solely as the result of an inherited predisposition (formally referred to as ‘idiopathic epilepsy’ but increasingly referred to as ‘genetic epilepsy’), or as a result of an inherited or environmentally acquired brain injury. Genetic inheritance is complex for most genetic epilepsies, although important mendelian disorders are recognized.

Clinical features—partial seizures

Epilepsy seizures can be variously classified in terms of their anatomical substrate (focal or generalized, lobar) or according to the extent of functional impairment, ‘complex partial’ referring to impairment of consciousness and ‘simple partial’ referring to the absence of impairment. Complex partial seizures are not synonymous with temporal lobe seizures and may occur with focal seizures arising from lobes other than temporal lobes. Examples of simple partial seizures include focal sensory or motor seizures, occipital lobe seizures with visual hallucinations, mesial temporal seizures including transient disturbances of memory such as déjà vu or other psychic phenomena, or lateral temporal seizures involving simple auditory hallucinations. Complex partial seizures imply altered or loss of conscious awareness and in the case of temporal lobe complex partial seizures various automatic activity or movement (automatisms) may occur (of which the patient is unaware). Temporal lobe complex partial seizures usually evolve slowly over seconds to minutes, whereas other focal seizures such as those arising from frontal lobes may have abrupt onset.

Clinical features—generalized seizures

These include (1) tonic-clonic seizures (‘grand mal’ epilepsy)—the tonic phase is associated with contraction of axial and then limb muscles; clonic movements appear and slowly increase in amplitude; finally all movements cease and the patient is flaccid. Injury is common; urinary and/or faecal incontinence may occur. Confusion and disorientation are usual when the patient wakes. (2) Absence seizures (petit mal)—activity suddenly ceases for 10 to 20 s, but without loss of posture. (3) Myoclonic seizures—brief, shock-like contractions of muscle, occurring either in a generalized or focal distribution. (4) Atonic seizures—result in sudden loss of muscle tone.

Status epilepticus—defined as a single seizure lasting more than 30 min or successional seizures without recovery of consciousness between.

Investigation

First seizures should be assessed from a general medical perspective, with urgent and careful consideration given to the possibility of the presence of an underlying life-threatening condition such as encephalitis. After exclusion of acute underlying medical emergencies (stroke, encephalitis, metabolic precipitants, most particularly hypoglycaemia etc), key investigations are often electroencephalography (EEG) and structural imaging (usually MRI). The diagnosis of epilepsy confers important implications, and should be made by an epilepsy-competent service.

Treatment

Whether the patient requires anticonvulsants or not is judged on the basis of their likelihood of having further seizures. For a patient with a single generalized tonic–clonic seizure and normal EEG and MRI brain imaging, their chance of further seizures is approximately 50% over the next 2 years, with the bulk of the risk falling within the first 6 months after the first seizure. If all such patients with a first seizure are treated, then approximately 50% of patients will have been treated unnecessarily as they were not destined to have a further seizure. However, if a first seizure is associated with a clearly epileptiform abnormality on the EEG, or occurred in the presence of an appropriate structural brain lesion (such as a tumour), treatment with antiepilepsy drug (AED) therapy may be indicated. Epidemiological studies have shown that the presence of two or more seizures indicates a high risk of further seizures, and it is this epidemiological principle that informs the usual practice to treat following two epileptic seizures. Treatment decisions should be made by an epilepsy-competent service, and carefully weighed and discussed with the patient. Patients with first seizures or epilepsy must be informed of driving regulations.

Choice of anticonvulsant is informed by individual patient circumstances, as well as national and local guidelines such as those from the UK National Institute of Health and Clinical Excellence (NICE). Broadly, for generalized epilepsy (tonic-clonic, absence, or myoclonic) sodium valproate is an appropriate first choice (but special considerations apply such as those relating to women of childbearing potential) and for partial seizures, with or without generalization—carbamazepine and lamotrigine are probably the drugs of choice. Status epilepticus is a medical emergency and special considerations apply.

Newer anticonvulsants and problems with anticonvulsants—many new antiepileptic drugs have been introduced over the last 20 years: each has an individual role and profile of unwanted effects. Antiepilepsy drug therapy poses specific problems in relation to pregnancy, breastfeeding, drug withdrawal, driving and long-term adverse effects (such as increased fracture risk) requiring expert management.

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