Epilepsy in Adults

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

An epileptic seizure is the transient occurrence of signs or symptoms due to abnormal electrical activity in the brain, leading to a disturbance of consciousness, behaviour, emotion, motor function or sensation.[1] Epilepsy is not a single diagnosis but is a symptom with many underlying causes.[2] 

Adults presenting with a suspected seizure should be seen by a specialist in the diagnosis and management of the epilepsies within two weeks of presentation.[3] A wrong diagnosis of epilepsy can cause severe restrictions on a patient's lifestyle as well as unnecessary side-effects from long-term medication.

Epileptic seizures and epilepsy syndromes should be classified according to the description of seizure, the seizure type, the epilepsy syndrome and the aetiology. The seizure type(s) and epilepsy syndrome, aetiology and comorbidity should be accurately determined because failure to classify the epilepsy syndrome correctly can lead to inappropriate treatment and persistence of seizures.[4] 

In 2014 the International League Against Epilepsy task force for the definition of epilepsy proposed that epilepsy be considered a disease of the brain defined by any of the following conditions:

  • At least two unprovoked (or reflex) seizures occurring more than 24 hours apart.
  • One unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk after two unprovoked seizures (at least 60% over the next 10 years); or
  • Diagnosis of an epilepsy syndrome.

International classification of epileptic seizures

l. Focal seizures (focal is now preferred to partial): originate within networks limited to one hemisphere, discretely localised or more widely distributed. They may be divided into simple focal (motor or sensory) with retained awareness or focal dyscognitive seizures (impaired awareness). Focal seizures may progress into generalised seizures. See also the separate Temporal Lobe Epilepsy article:

A. Simple focal seizures (no loss of consciousness).
B. Focal dyscognitive seizures:

  1. With impairment of consciousness at onset.
  2. Simple focal onset followed by impairment of consciousness.

C. Focal seizure evolving to generalised tonic-clonic (GTC) convulsions.

II. Generalised seizures (convulsive or non-convulsive with bilateral discharges involving subcortical structures); associated with impairment of consciousness and distortion of the electrical activity of the whole or a large part of both sides of the brain. May be tonic-clonic (the term generalised tonic-clonic is now preferred to 'grand mal'), isolated tonic or clonic, myoclonic (brief, shock-like muscle contractions) or absence ('petit mal').

A. Absence
B. Myoclonic
C. Clonic
D. Tonic
E. Tonic-clonic
F. Atonic

III. Unclassified epileptic seizures (usually used when an adequate description is not available).

Focal and generalised epilepsies are subdivided into idiopathic syndromes (have a presumed genetic basis) and cryptogenic/symptomatic syndromes (a structural lesion is known or suspected). The terms 'simple partial seizure' and 'complex partial seizure' have been replaced by the term 'focal seizure'. Focal seizures in which consciousness is impaired are described as 'focal dyscognitive seizures'. The terms 'idiopathic', 'symptomatic' and 'cryptogenic' have been replaced by the terms 'genetic', 'structural-metabolic' and 'unknown'.

There are a number of other forms of epilepsy, especially in children. See the separate Epilepsy in Children and Young People article for further information.

  • Diagnosis of epilepsy in patients with learning difficulties can be difficult. Confusion may arise between stereotypical or other behaviours and seizure activity.
  • Particular attention should be paid to the possibility of adverse cognitive and behavioural effects of anti-epileptic drug (AED) therapy.
  • All adults with epilepsy and learning disabilities should have a risk assessment - eg, bathing and showering, preparing food, using electrical equipment, the suitability of independent living.

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  • The prevalence of active epilepsy is 5-10 cases per 1,000 - but with 5-30% of these misdiagnosed as having epilepsy.[2]
  • Epilepsy most commonly starts in children or in people older than 60 years of age.
  • Epilepsy is much more common in people with a learning disability.
  • Epilepsy is a feature of over 200 genetic disorders, accounting for approximately 2% of people with epilepsy. Approximately 30% of people with epilepsy have a first-degree relative with the condition.
  • Approximately a third of people with epilepsy in the UK have an anatomically identifiable cause (symptomatic epilepsy) - eg, cerebrovascular disease, cerebral tumour, head injury. This is the most common cause of epilepsy occurring in the elderly - see the separate Epilepsy in Elderly People article.
  • Most are idiopathic; seizures due to underlying diseases affecting the brain are more likely to have a focal onset.
  • Cerebrovascular disease such as cerebral infarction, cerebral haemorrhage and venous thrombosis.
  • Head injury: head trauma is more significant when it occurs with loss of consciousness lasting longer than 30 minutes, post-traumatic amnesia lasting longer than 30 minutes, focal neurological findings or neuro-imaging findings suggesting a structural brain injury.
  • Following cranial surgery.
  • CNS infections such as meningitis or encephalitis.
  • Neurodegenerative diseases: epilepsy is more common in people with Alzheimer's disease or multi-infarct dementia.
  • Autoimmune disease.
  • Brain neoplasm.
  • Genetic diseases.
  • Drugs: for example, phenothiazines, isoniazid, tricyclic antidepressants; binge alcohol drinking; drug (eg, benzodiazepines) or alcohol withdrawal.
  • Metabolic medical disorders such as uraemia, hypoglycaemia, hyponatraemia, hypernatraemia, hypercalcaemia and hypocalcaemia.

Epilepsy may be difficult to diagnose in the early stages, especially in the absence of a witnessed account. A clear history from the patient and an eyewitness to the attack provide the most important diagnostic information.

Generalised seizures cause a disturbance in consciousness. The classic GTC seizure progresses through tonic, clonic and postictal phases. The postictal phase is often associated with headache and drowsiness. GTC seizures are often associated with tongue-biting and incontinence. Whatever the cause, the patient may have amnesia for both the event and its exact circumstances.

Absence seizures cause an interruption to mental activity for less than 30 seconds. They rarely persist into adulthood.

Features suggesting genetic generalised epilepsies include:[5] 

  • Childhood or teenage onset.
  • Triggered by sleep deprivation and alcohol.
  • Early morning tonic-clonic seizures or myoclonic jerks.
  • Short absence seizures photoparoxysmal response on electroencephalography (EEG).
  • Generalised 3 per second spike and wave or polyspike and wave on EEG.

Features suggesting focal epilepsies include:[5] 

  • History of potential cause.
  • Aura.
  • Focal motor activity during seizure.
  • Automatisms.

Complex focal seizures may have features of:

  • Motor: automatism, lip-smacking, plucking at clothes, hair.
  • Sensory: transient paraesthesiae.
  • Autonomic: odd epigastric sensation, nausea, abnormal taste or smell.
  • Psychiatric: unreality, déjà vu, fear.

Symptoms

  • There may be a clear precipitating cause - eg, inadequate sleep, alcohol abuse or medications such as tricyclic antidepressants, which lower the seizure threshold.
  • It is common for seizure frequency to vary throughout the menstrual cycle. In ovulatory cycles, peaks occur around the time of ovulation and in the few days before menstruation. In anovulatory cycles, there is an increase in seizures during the second half of the menstrual cycle.[6]
  • Possible seizure-related symptoms include:
    • Sudden falls.
    • Involuntary jerky movements of limbs whilst awake.
    • Blank spells.
    • Unexplained incontinence of urine with loss of awareness, or in sleep.
    • Odd events occurring in sleep - eg, fall from bed, jerky movements, automatisms.
    • Episodes of confused behaviour with impaired awareness.
    • Possible simple focal seizures.
    • Epigastric fullness sensation.
    • Déjà vu.
    • Premonition.
    • Fear.
    • Elation, depression.
    • Depersonalisation, derealisation.
    • Inability to understand or express language (written or spoken).
    • Loss of memory, disorientation.
    • Olfactory, gustatory, visual, auditory hallucinations.
    • Focal motor or somatosensory deficit, or positive symptoms (jerking, tingling).

Signs

  • Examination is usually unremarkable.
  • Check for any neurological or cerebrovascular signs.
  • Skin examination may reveal café-au-lait spots (neurofibromatosis), port-wine stain (Sturge-Weber syndrome) or adenoma sebaceum (tuberous sclerosis).

Sudden unexpected death in epilepsy (SUDEP) is defined as sudden, unexpected, unwitnessed, non-traumatic, non-drowning death of a person with epilepsy, with or without a seizure, excluding documented status epilepticus, and in whom post-mortem examination does not reveal a structural or toxicological cause of death.

The reported incidence of SUDEP depends on the populations studied but community-based studies give incidences of between 0.09 and 0.35/1,000 patient years.

Seizure type and frequency: GTC seizures are the principal risk factor for SUDEP. Early identification of treatment-resistant epilepsy and referral for assessment for epilepsy surgery to reduce seizure frequency may reduce incidence of SUDEP.

  • SUDEP is the most common cause of death directly related to epilepsy and most frequently occurs in people with chronic epilepsy.[7]
  • Information provided to people with epilepsy and carers should take account of the small but definite risk of SUDEP.[4]
  • SUDEP seems to occur more commonly during sleep and more often affects young adults with medically intractable epilepsy (especially tonic-clonic seizures), those with neurological comorbidity and patients receiving AED polytherapy.[8]
  • The risk of SUDEP can be minimised by optimising seizure control and being aware of the potential consequences of nocturnal seizures.[4]

Misdiagnosis of epilepsy is common. The conditions most frequently confused with epilepsy include vasovagal syncope, cardiac syncope and non-epileptic attack disorder. Conditions that may mimic seizures include migraine, parasomnias, movement disorders, metabolic disturbances and panic disorder.[5] 

  • Appropriate blood tests (eg, glucose, electrolytes, calcium, renal function, liver function, and urine biochemistry) to identify potential causes and/or to identify any significant comorbidity should be considered.
  • EEG:
    • An EEG should be performed only to support a diagnosis of epilepsy when the clinical history suggests that the seizure is likely to be epileptic in origin. The EEG should not be used in isolation to make a diagnosis of epilepsy.
    • If an EEG is considered necessary, it should be performed after the second epileptic seizure but may, in certain circumstances, as evaluated by the specialist, be considered after a first epileptic seizure. Following a first unprovoked seizure, unequivocal epileptiform activity shown on EEG can be used to assess the risk of seizure recurrence.
    • Photic stimulation and hyperventilation should remain part of standard EEG assessment but the patient should be made aware that such activation procedures may induce a seizure.
    • An EEG should not be performed in the case of probable syncope because of the possibility of a false positive result.
    • An EEG may be used to help to determine seizure type and epilepsy syndrome.
    • Repeated standard EEGs may be helpful when the diagnosis of the epilepsy or the syndrome is unclear. However, if the diagnosis has been established, repeat EEGs are not likely to be helpful. Repeated standard EEGs should not be used in preference to sleep or sleep-deprived EEGs.
    • When a standard EEG has not contributed to diagnosis or classification, a sleep EEG should be performed.
    • Long-term video or ambulatory EEG may be used in the assessment when there are diagnostic difficulties after clinical assessment and standard EEG.
  • Neuroimaging:
    • Neuroimaging should be used to identify structural abnormalities that cause certain epilepsies. MRI is the imaging investigation of choice. MRI is particularly important in those:
      • Who have any suggestion of a focal onset on history, examination or EEG (unless clear evidence of benign focal epilepsy).
      • In whom seizures continue in spite of first-line medication.
    • Neuroimaging should not be routinely requested when a diagnosis of idiopathic generalised epilepsy has been made.
    • CT should be used to identify underlying gross pathology if MRI is not available or is contra-indicated. CT may be used to determine whether a seizure has been caused by an acute neurological lesion or illness.
  • Short-term video-EEG, preferably with suggestion, should be available for the investigation and diagnosis of suspected epilepsy and non-epileptic attack disorder. Inpatient video-EEG monitoring may be useful for patients who present diagnostic difficulties.[5] 
  • Polysomnography may be used to confirm a diagnosis of sleep-related epilepsy.[5] 
  • Handheld video: asking family members or friends to video record events should be considered in patients with uncertain diagnosis. Consent from the patient should always be sought in advance.[5] 
  • Electrocardiography (ECG) should be carried out in the assessment of all patients with altered consciousness, particularly those in older age groups, when disorders of cardiac rhythm may simulate epilepsy. 24-hour ambulatory ECG and other cardiovascular tests (including implantable loop devices) may also be helpful.[5] 

Neuropsychological assessment[4]

Neuropsychological assessment should be considered when it is important to evaluate learning disabilities and cognitive dysfunction, particularly in regard to language and memory. Referral for a neuropsychological assessment is indicated:

  • When the person with epilepsy is having educational or occupational difficulties.
  • When an MRI has identified abnormalities in cognitively important brain regions.
  • When there are reported memory or other cognitive deficits and/or cognitive decline.

Genetic testing[5] 

Most genetically acquired epilepsies show a complex inheritance pattern. However, an increasing number of monogenic epilepsy syndromes (caused by a mutation in a single gene) are recognised. A comprehensive history with particular focus on the family history is required. In most cases reassurance can be given that the risk of epilepsy developing in the children of parents with epilepsy is low but a clinical genetics service, with expertise in the genetics of epilepsy, should be available if required.

  • All adults with epilepsy should have a comprehensive care plan, which should include lifestyle issues as well as medical issues.
  • Epilepsy specialist nurses (ESNs) should be an integral part of the network of care.
  • A Cochrane review found that two types of intervention (ESNs and self-management education) showed some evidence of benefit; there was no clear evidence that other service models substantially improved outcomes for adults with epilepsy.[10]
  • One study showed that patient access to primary care appointments and being seizure-free for 12 months were associated with lower hospital admission rates.[11] 
  • People with epilepsy, particularly those with a genetic epilepsy, should be advised that sleep deprivation may precipitate seizures and be provided with advice to obtain sufficient sleep with a regular sleep pattern.[5] 

The decision whether or not to start AED treatment must be based on the relative risks of recurrent seizures and the commitment to long-term medication with potential adverse effects. AEDs should not be given until the diagnosis of epilepsy has been confirmed.[5] 

Management of provoked seizures[5] 

Provoked seizures are defined as occurring within seven days of an acute condition such as encephalitis, head injury, cerebral infarction, craniotomy and cerebral haemorrhage. Seizures can be provoked by:

  • Acute metabolic disturbances, treatment with certain drugs and drug withdrawal (eg, alcohol, benzodiazepines, barbiturates).
  • Drug misuse (alcohol, heroin, cocaine, methadone, amfetamine, ecstasy).

The risk of recurrence of such provoked seizures can be reduced by correction or withdrawal of the provocative factor. Following an acute brain insult, AEDs used to treat the provoked seizures should be withdrawn (unless unprovoked seizures occur later). Longer-term AED treatment is only indicated if unprovoked seizures occur.

Patients with seizures provoked by alcohol or substance misuse may benefit from referral to addiction services and other support agencies.

Drug treatment

See also separate articles Anticonvulsants used for Generalised Seizures and Anticonvulsants used for Focal Seizures.

  • The AED treatment strategy should be individualised according to the seizure type, epilepsy syndrome, co-medication and comorbidity, lifestyle and the preferences of the person and their family and/or carers as appropriate.
  • The diagnosis of epilepsy needs to be critically evaluated if events continue despite an optimal dose of a first-line AED.
  • Consistent supply to the adult with epilepsy of a particular manufacturer's AED preparation is recommended. Different preparations of some AEDs may vary in bioavailability or pharmacokinetic profiles.
  • Treatment should be with a single AED wherever possible. If the initial treatment is unsuccessful then monotherapy using another drug can be tried.
  • If an AED has failed because of adverse effects or continued seizures, a second drug should be started and built up to an adequate or maximum tolerated dose and then the first drug should be tapered off slowly.
  • Combination therapy should only be considered when attempts at monotherapy with AEDs have not resulted in seizure freedom. If trials of combination therapy do not bring about worthwhile benefits, treatment should revert to the regimen (monotherapy or combination therapy) that has proved most acceptable.
  • If using carbamazepine, offer controlled-release carbamazepine preparations.
  • Epilepsy is resistant to drug treatment in a third of patients.[12] Of the newer drugs, the broad-spectrum AEDs levetiracetam, topiramate and zonisamide have multiple mechanisms of action and are often chosen in drug-resistant epilepsy.[13]

Initiation of drug treatment

  • AED therapy should only be started once the diagnosis of epilepsy is confirmed, except in exceptional circumstances. AED therapy should be initiated by a specialist.
  • Treatment with AED therapy is generally recommended after a second epileptic seizure. AED therapy should be considered and discussed after a first unprovoked seizure if:
    • There is a neurological deficit.
    • The EEG shows unequivocal epileptic activity.
    • The patient considers the risk of having a further seizure unacceptable.
    • Brain imaging shows a structural abnormality.

Continuation of drug treatment

  • Maintain a high level of vigilance for adverse effects of treatment.
  • Continuing AED therapy should be planned by a specialist but part of an agreed treatment plan and the needs of the patient and their family and/or carers as appropriate should be taken into account.
  • If management is straightforward, continuing AED therapy can be prescribed in primary care if local circumstances and/or licensing allow.
  • Adherence to treatment can be optimised with the following:
    • Educating patients and their families and/or carers in the understanding of their condition and the rationale of treatment.
    • Reducing the stigma associated with the condition.
    • Using simple medication regimens.
    • Positive relationships between healthcare professionals, the adult with epilepsy and their family and/or carers.
  • Regular blood test monitoring is not recommended as routine and should be done only if clinically indicated. Indications for monitoring of AED blood levels are:
    • Detection of non-adherence to the prescribed medication.
    • Suspected toxicity.
    • Adjustment of phenytoin dose.
    • Management of pharmacokinetic interactions (eg, changes in bioavailability, changes in elimination, co-medication with interacting drugs).
    • Specific clinical conditions - eg, status epilepticus, organ failure and certain situations in pregnancy.
  • Examples of blood tests include:
    • Before surgery - clotting studies in those on sodium valproate.
    • FBC, electrolytes, liver enzymes, vitamin D levels and other tests of bone metabolism (eg, serum calcium and alkaline phosphatase) every 2-5 years for patients taking enzyme-inducing drugs.
    • Asymptomatic minor abnormalities in test results are not necessarily an indication for changes in medication.

Withdrawal of drug treatment

  • The decision to continue or withdraw medication should be taken after a full discussion of the risks and benefits of continuing or withdrawing AED therapy. Withdrawal of AEDs must be managed by, or be under the guidance of, the specialist.
  • The risks and benefits of continuing or withdrawing AED therapy should be discussed when the person with epilepsy has been seizure-free for at least two years.
  • Withdrawal of AED treatment should be carried out slowly (at least 2-3 months) and one drug should be withdrawn at a time.
  • Particular care should be taken when withdrawing benzodiazepines and barbiturates (may take up to six months or longer) because of the possibility of drug-related withdrawal symptoms and/or seizure recurrence.
  • There should be an agreed plan that if seizures recur, the last dose reduction is reversed and medical advice is sought.

Psychological interventions

  • Psychological interventions have not been proven to affect seizure frequency and are not an alternative to pharmacological treatment.
  • Psychological interventions (relaxation, cognitive behavioural therapy, biofeedback) may be used in conjunction with AED therapy in patients when seizure control is inadequate with optimal AED therapy.[14]

Complementary therapy[5] 

There is no consistent evidence to support, or definitively exclude, the use of any particular type of complementary therapy to improve seizure frequency in patients with epilepsy. Some aromatherapy preparations (eg, hyssop, rosemary, sweet fennel, sage and wormwood) may have an alerting effect on the brain and so may exacerbate seizures.

  • Adults with epilepsy should have a regular structured review and be registered with a general medical practice.
  • Adults with epilepsy should have a regular structured review with their GP but depending on the person's wishes, circumstances and epilepsy, the review may be carried out by the specialist.
  • The maximum interval between reviews should be one year but the frequency of review will be determined by the patient's epilepsy and their wishes. The interval is usually between 3 and 12 months.
  • Treatment should be reviewed at regular intervals to ensure that the patient is not maintained for long periods on treatment that is ineffective or poorly tolerated and that concordance with prescribed medication is maintained.
  • Annual review should include an enquiry about side-effects and a discussion of the treatment plan to ensure concordance and adherence to medication.
  • At the review, there should be access to written and visual information, counselling services, information about voluntary organisations, epilepsy specialist nurses, appropriate investigations and referral to tertiary services, including surgery, when indicated.

Referral for complex or refractory epilepsy

  • If seizures are not controlled, there is diagnostic uncertainty or there is treatment failure, adults with epilepsy should be referred to tertiary services soon for further assessment. Referral should be considered when one or more of the following criteria are present:
    • The epilepsy is not controlled with medication within two years.
    • Management is unsuccessful after two drugs.
    • A patient experiences, or is at risk of, unacceptable side-effects from medication.
    • There is a unilateral structural lesion.
    • There is psychological and/or psychiatric comorbidity.
    • There is diagnostic doubt as to the nature of the seizures and/or seizure syndrome.
  • Behavioural or developmental regression or inability to identify the epilepsy syndrome should result in immediate referral to tertiary services.
  • Patients with specific syndromes such as Sturge-Weber syndrome, the hemispheric syndromes, Rasmussen's encephalitis and hypothalamic hamartoma should be referred to a tertiary epilepsy service.
  • Psychiatric comorbidity and/or negative baseline investigations should not be a contra-indication for referral to a tertiary service.

Vagus nerve stimulation (VNS) and deep brain stimulation (DBS)

  • VNS is indicated for use as an adjunctive therapy in reducing the frequency of seizures in adults who are refractory to anti-epileptic medication but who are not suitable for resective surgery. This includes adults whose epileptic disorder is dominated by focal seizures (with or without secondary generalisation) or generalised seizures.[4]
  • The National Institute for Health and Care Excellence (NICE) states that the evidence on the efficacy of DBS for refractory epilepsy is limited and that there are potentially serious side-effects. Therefore, DBS is currently not recommended.[15]

Surgery

The introduction of newer AEDs with better tolerability and fewer drug-drug interactions has made a significant impact on the treatment of epilepsy. However, a significant proportion of patients still have intractable epilepsy.[16] Surgery is increasingly used as treatment for refractory focal epilepsy.[17][18]

Some neurosurgical procedures involve resection of part of the brain and the aim is to obtain complete seizure freedom. For the most commonly performed procedures, involving anterior and medial temporal lobe resection, about 70% of patients will become seizure-free. Other procedures are palliative and include callosotomy, subpial transection, VNS and DBS.[5] 

  • Modern techniques for the accurate localisation of epileptic discharge and the recognition of specific seizure patterns have increased the role of surgery in the management of drug-resistant epilepsy.[18]
  • Neurosurgical treatment has particular benefit for selected people with refractory focal epilepsy.[19]
  • Surgical operations for epilepsy include anteromedial temporal resection (the most frequently performed operation for medial temporal lobe epilepsy), corpus callosotomy (for generalised epilepsy syndromes), functional hemispherectomy and multiple subpial transection.
  • Doctors and patients can use Decision Aids together to help choose the best course of action to take.
  • Compare the options  

Driving legally can be affected by epilepsy, see Neurological Disorders - DVLA Guide for more details.

  • Social stigmatisation and occupational issues.
  • Psychosocial problems: anxiety, depression and suicide rates are more common than in the general population.[5] 
  • Developmental problems in children with early-onset seizures. Specific cognitive and learning difficulties impacting on education if not recognised.
  • AED side-effects; risk of fetal malformation associated with AEDs.
  • Accidents resulting from a seizure often cause injuries - eg, head injuries, lacerations, fractures and burns.
  • Studies have suggested that women with epilepsy are at increased risk of fractures, osteoporosis and osteomalacia.[6]
  • Increased mortality rate:
    • SUDEP.
    • Deaths due to accidents during seizures.
    • Deaths due to status epilepticus.
  • Remission becomes less likely with longer persistence of seizures.
  • Factors suggesting a poorer prognosis include a combination of focal dyscognitive seizures and tonic-clonic seizures, clustering of seizures, abnormal physical signs and the presence of learning difficulties.
  • Studies report premature death in adults with epilepsy compared to the general population. The majority of these deaths occur in people under 55 years of age.
  • Premature death in epilepsy has a wide variety of causes including alcohol misuse, drowning, falls, drug poisoning and motor vehicle accidents.
  • Another significant cause of premature mortality is suicide. A population-based study of suicide in epilepsy reported a suicide rate in people with epilepsy three times higher than in the general population, with rates increased further in people with epilepsy who had a comorbid psychiatric condition.

Further reading & references

  1. Epilepsy; NICE CKS, December 2014 (UK access only)
  2. Nunes VD, Sawyer L, Neilson J, et al; Diagnosis and management of the epilepsies in adults and children: summary of BMJ. 2012 Jan 26;344:e281. doi: 10.1136/bmj.e281.
  3. The epilepsies in adults, NICE Quality Standard, February 2013
  4. The epilepsies: the diagnosis and management of the epilepsies in adults and children in primary and secondary care; NICE Clinical Guideline (January 2012)
  5. Diagnosis and management of epilepsy in adults; Scottish Intercollegiate Guidelines Network - SIGN (2015)
  6. Crawford PM; Managing epilepsy in women of childbearing age. Drug Saf. 2009;32(4):293-307. doi: 10.2165/00002018-200932040-00004.
  7. Surges R, Thijs RD, Tan HL, et al; Sudden unexpected death in epilepsy: risk factors and potential pathomechanisms. Nat Rev Neurol. 2009 Sep;5(9):492-504. Epub 2009 Aug 11.
  8. Asadi-Pooya AA, Sperling MR; Clinical Features of Sudden Unexpected Death in Epilepsy. J Clin Neurophysiol. 2009 Aug 24.
  9. Transient loss of consciousness ('blackouts') management in adults and young people; NICE Clinical Guideline (August 2010)
  10. Bradley PM, Lindsay B; Care delivery and self-management strategies for adults with epilepsy. Cochrane Database Syst Rev. 2008 Jan 23;(1):CD006244.
  11. Calderon-Larranaga A, Soljak M, Cowling TE, et al; Association of primary care factors with hospital admissions for epilepsy in England, 2004-2010: National observational study. Seizure. 2014 Sep;23(8):657-61. doi: 10.1016/j.seizure.2014.05.008. Epub 2014 May 23.
  12. Kwan P, Schachter SC, Brodie MJ; Drug-resistant epilepsy. N Engl J Med. 2011 Sep 8;365(10):919-26.
  13. Brodie MJ, Kwan P; Newer drugs for focal epilepsy in adults. BMJ. 2012 Jan 26;344:e345. doi: 10.1136/bmj.e345.
  14. Ramaratnam S, Baker GA, Goldstein LH; Psychological treatments for epilepsy. Cochrane Database Syst Rev. 2008 Jul 16;(3):CD002029.
  15. Deep brain stimulation for refractory epilepsy; NICE Interventional Procedure Guidance, January 2012
  16. Kawai K; Epilepsy surgery: current status and ongoing challenges. Neurol Med Chir (Tokyo). 2015 May 15;55(5):357-66. doi: 10.2176/nmc.ra.2014-0414. Epub 2015 Apr 28.
  17. de Tisi J, Bell GS, Peacock JL, et al; The long-term outcome of adult epilepsy surgery, patterns of seizure remission, Lancet. 2011 Oct 15;378(9800):1388-95.
  18. Balabanov A, Rossi MA; Epilepsy surgery and vagal nerve stimulation: what all neurologists should know. Semin Neurol. 2008 Jul;28(3):355-63. Epub 2008 Jul 24.
  19. Rossetti AO, Hurwitz S, Logroscino G, et al; Prognosis of status epilepticus: role of aetiology, age, and consciousness J Neurol Neurosurg Psychiatry. 2006 May;77(5):611-5.
  20. At a glance guide to the current medical standards of fitness to drive; Driver and Vehicle Licensing Agency

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
Current Version:
Peer Reviewer:
Prof Cathy Jackson
Document ID:
2107 (v25)
Last Checked:
08/06/2015
Next Review:
06/06/2020