CONSENSUS GUIDELINES ON THE MANAGEMENT OF EPILEPSY 2005

Epilepsy Council, Malaysian Society of Neurosciences

Statement of Intent This guideline is not intended to be construed or to serve as a standard of medical care. Standards of medical care are determined on the basis of all clinical data available for an individual case and are subject to change as scientific knowledge and technology advance and patterns evolve. These parameters of practice should be considered guidelines only. Adherence to them will not ensure a successful outcome in every case, nor should they be construed as including all proper methods of care aimed at the same results. The ultimate judgement regarding a particular clinical procedure or treatment plan must be made by the health care provider in the light of the clinical data presented by the patient and the diagnostic and treatment options available.

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Panel of experts:
Professor Dr Raymond Azman Ali (Chairman) Senior Consultant Neurologist Department of Medicine Universiti Kebangsaan Malaysia Professor Dr Tan Chong Tin Senior Consultant Neurologist Department of Medicine Universiti Malaya Datuk Dr. Raihanah Abdul Khalid Consultant Neurologist and Head Department of Neurology Kuala Lumpur Hospital Professor Dr Benedict Selladurai Senior Consultant Neurosurgeon Department of Surgery Universiti Kebangsaan Malaysia Professor Dr Ong Lai Choo Senior Consultant Paediatric Neurologist Department of Paediatrics Universiti Kebangsaan Malaysia Dr Azmi Abdul Rashid Consultant Neurologist Damansara Specialist Centre Dr Vimalan Rama Neurologist Department of Medicine Universiti Malaya Dr Kathleen Yeap Neurologist Department of Neurology Ipoh Hospital Dr Tan Hui Jan Neurologist Department of Medicine Universiti Kebangsaan Malaysia

Panel of reviewers:
Dr Hussain Imam bin Hj Muhammad Ismail Senior Consultant Paediatric Neurologist and Head Institute of Paediatrics Hospital Kuala Lumpur Dr Khoo Teik Beng Consultant Paediatric Neurologist Institute of Paediatrics Hospital Kuala Lumpur Dr Wong Sau Wei Paediatric Neurologist Department of Paediatrics Universiti Kebangsaan Malaysia Dr Haniffah Abdul Gafoor Consultant Neurologist Island Medical Centre Penang

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7. 4.27 21 21 22 25 26 27 28 – 35 28 28 32 33 34 34 35 . DIFFERENTIAL DIAGNOSIS OF EPILEPSY INVESTIGATIONS IN EPILEPSY Purpose of investigations Electroencephalography Video-EEG monitoring Invasive EEG recording/sphenoidal electrodes Neuroimaging Other investigations GENERAL PRINCIPLES OF THE TREATMENT OF EPILEPSY Prophylactic treatment Single seizures Recurrent seizures Decision to withdraw AEDs Driving and epilepsy Education and epilepsy LONG-TERM PHARMACOLOGICAL TREATMENT Introduction Initiation and continuation of treatment of AEDs Drug monitoring Choice of first line therapy AED toxicity Stopping treatment SURGICAL TREATMENT OF EPILEPSY Introduction Early diagnosis of seizure intractability and timing of surgery Surgically remediable epilepsy syndromes Presurgical investigations and patient selection Establishment of a resection strategy 4 6 7 .10 7 9 10 11 .39 35 35 36 36 37 5.Table of Contents 1.13 14 . 6.20 14 14 16 17 17 19 21 . 2. INTRODUCTION DEFINITION AND CLASSIFICATION OF EPILEPSY Introduction Idiopathic epilepsies Non-idiopathic epilepsies 3. .

5 .66 67 9. EMERGENCY TREATMENT OF EPILEPSY Introduction Initial supportive management Postictal care in uncomplicated seizures Treatment of prolonged seizures Treatment of convulsive status epilepticus Emergency treatment of other prolonged seizure types SPECIAL ISSUES Epilepsy in women Epilepsy in children Epilepsy in the elderly CONCLUSION REFERENCES Appendix 1: Counselling checklist 39 40 .Results of Surgical Treatment 8. 11.47 40 40 40 40 43 49 50-57 50 55 57 58 59 . 10.

regional and/or international recognition in the field of epilepsy. and a chapter has also been dedicated to special issues pertaining to women. 6 . neurologists. calls for a reappraisal of how we manage our patients with epilepsy. There is a large chapter on epilepsy surgery. This guidelines is the first of its kind in Malaysia.0 INTRODUCTION The Epilepsy Council of Malaysia was established in February 2002 to complement the activities organised by the already well established lay personbased Malaysian Epilepsy Society. there have been more antiepileptic drugs introduced and more epilepsy surgery candidates operated than in the last 100 years.1. The chapters in this consensus guidelines have been written by local specialists who have national. In the last decade or so. paediatricians. together with advances in epilepsy surgery and neuroimaging. This exponential growth in new drugs. and all relevant healthcare providers pertaining to the management of epilepsy. is only a set of guidelines. physicians. It had sufficient expertise to make strong recommendations to general practitioners. psychiatrists. Nevertheless the recommendations made are based on recent publications as well as consensus of a panel of experts. and as its name suggests. Its members agreed that one of the most important early tasks of the council was to come up with a set of guidelines for the management of epilepsy in the country. children and the elderly.

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DEFINITION AND CLASSIFICATION OF EPILEPSY Introduction

An epileptic seizure is defined as a paroxysmal stereotyped disturbance of consciousness, motor function, sensation, emotion, behaviour or perception that on clinical grounds results from cortical neuronal discharge. Epilepsy can be defined as recurrent, usually unprovoked epileptic seizures that result from excessive synchronous and abnormal firing patterns of the cerebral cortical neurons. Therefore, epileptic seizures may be viewed as the symptoms of the disease, epilepsy. Epileptic seizures are classified on the basis of their clinical features alone (table 1) whereas the classification of the epilepsies and epileptic syndromes is based on electroclinical criteria (International Classification of Epilepsies and Epileptic syndromes) (table 2). The latter also provides information about the possible aetiology, anatomical basis, precipitating factors, age of onset, severity, chronicity, diurnal and circadian cycling, and sometimes prognosis of the epilepsies.
TABLE 1: The International Classification of Epileptic Seizures 1. Partial seizures 1.1 Simple partial seizure 1.1.1 Motor signs 1.1.2 Sensory symptoms 1.1.3 Autonomic symptoms or signs 1.1.4 Psychic symptoms 1.2 Complex partial seizure 1.2.1 Simple partial at onset (with or without automatism) 1.2.2 With impairment of consciousness (with or with automatism) 1.3 Partial seizures evolving into generalized seizures 2. Generalized seizures 2.1 Absence seizure 2.1.1 Typical 2.1.2 Atypical 2.2 Myoclonic seizure 2.3 Clonic seizure 2.4 Tonic seizure 2.5 Tonic-clonic seizure 2.6 Atonic seizure 3. Unclassified epileptic seizures
Consciousness is maintained in simple partial seizures but impaired in complex partial seizures. The symptomatology of partial seizures (seizure semiology) reflects the anatomical origin of the seizures. Hence, partial seizures may be characterised by motor, special sensory, autonomic or psychic symptoms. In addition, complex partial seizures are typically accompanied by automatisms; consisting of involuntary movements, e.g. lip smacking, chewing, fidgeting and wandering.

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TABLE 2: International Classification of Epilepsies and Epileptic Syndromes 1. Localisation-related (focal, local, partial) epilepsies and syndromes 1.1 Idiopathic (with age-related onset)
• • • Benign childhood epilepsy with centrotemporal spikes Childhood epilepsy with occipital paroxysms Primary reading epilepsy

1.2 Symptomatic 1.2.1 Characterised by simple partial seizures* 1.2.2 Characterised by complex partial seizures* 1.2.3 Characterised by secondarily generalised seizures* 1.3 Unknown as to whether the syndrome is idiopathic or symptomatic 2. Generalised epilepsies and syndromes 2.1 Idiopathic
• • • • • • • • • • • Benign neonatal familial convulsions Benign neonatal convulsions Benign myoclonic epilepsy in infancy Childhood absence epilepsy (pyknolepsy) Juvenile absence epilepsy Juvenile myoclonic epilepsy Epilepsy with generalised tonic-clonic seizures on awakening West syndrome Lennox-Gastaut syndrome Epilepsy with myoclonic-astatic seizures Epilepsy with myoclonic absences

2.2 Cryptogenic or symptomatic

2.3 Symptomatic 2.3.1 Non-specific aetiology
• • Early myoclonic encephalopathy Epileptic seizures complicating disease states

2.3.2 Specific syndromes 3. Epilepsies and syndromes undetermined, whether focal or generalised 3.1 With both generalised and focal seizures
• • • Neonatal seizures Severe myoclonic epilepsy in infancy Epilepsy with continuous spike and wave EEG during slow-wave sleep

• Acquired epileptic aphasia (Landau-Kleffner syndrome) 3.2 Without unequivocal generalised or focal features 4. Special syndromes 4.1 Situation-related seizures
• • •

Febrile convulsions Isolated seizures or isolated status epilepticus Seizures occurring only when there is an acute metabolic or toxic event

*With the characteristics of seizures arising from frontal, parietal, temporal, occipital, or multiple lobes; or the locus of onset is unknown.

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In addition to their distinct seizure semiologies, generalised seizures are also distinguished by their characteristic EEG features (table 3). TABLE 3: EEG features of generalised epileptic seizures • • • • • • Absence seizures - generalised 3Hz spike-wave activity Myoclonic seizures - generalised polyspikes or polyspike and wave activity Clonic seizures - generalised spike-wave activity Tonic seizures - paroxysmal fast activity Tonic-clonic seizures - combination of the two seizure types Atonic - spikes or spike-wave activity or abrupt flattening of EEG

In the classification of the epilepsies and epileptic syndromes, the terms “idiopathic”, “symptomatic” and “cryptogenic” are often misunderstood. The idiopathic epilepsies are genetically determined and have no structural cause, no associated clinical signs, normal brain imaging and normal EEG background. The symptomatic epilepsies have known causes and cryptogenic epilepsies have an underlying cause that cannot be documented objectively. Thus, the cryptogenic epilepsies are more likely to be symptomatic than idiopathic.

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Idiopathic epilepsies:

2.2.1 Idiopathic localisation-related epilepsy: The two common types of benign focal epilepsy of childhood are those with centrotemporal spikes (BCECTS) and those with occipital paroxysms (table 2). Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is a newly described epilepsy syndrome. 2.2.2 Idiopathic generalised epilepsies:

These syndromes are genetically determined, and patients have a normal neurological examination and normal intelligence. The EEG shows generalised epileptiform discharges and may show photosensitivity (table 3). Childhood absence epilepsy, previously known as petit-mal epilepsy, is characterised by an age of onset between 4 and 10 years, typical absences, generalised tonic-clonic seizures (GTCS) in about 50% of patients, myoclonic seizures in a minority of patients, and generalised 3Hz spike-wave activity on EEG. A variant of this epilepsy is juvenile absence epilepsy characterised by a later age of onset. 9

and rarely.3. The causes of temporal. a metabolic derangement or chromosomal defect. they are cryptogenic.3 2. these epilepsies are symptomatic and if the cause is not found. 2. The clinical and EEG findings are usually abnormal and age-dependent. 10 . go into remission.2 Symptomatic and cryptogenic generalised epilepsies These epilepsies (table 3) are associated with diffuse brain dysfunction. The common causes are low-grade tumours. and include traumatic scars. infarcts. generalised bilateral symmetrical polyspikes and generalised spike-wave complexes on their EEG. consisting of simple partial or complex partial seizures. If the cause is found. occipital. 2. psychic auras and complex partial seizures with orofacial and manual automatisms with or without secondary generalisation.Patients with juvenile myoclonic epilepsy (JME) tend to be older (onset in adolescence).3. is characterised by epigastric (abdominal). neoplasms. haemorrhages and cortical malformations.1 Non-idiopathic epilepsies: Symptomatic and cryptogenic localisation-related epilepsies Seizures arise from a localised region of the brain. vascular malformations. Seizure semiology. frontal and parietal neocortical epilepsy are more diverse. depends upon the area of neocortex affected. and have myoclonic jerks usually in the morning on awakening with or without GTCS. Mesial temporal lobe epilepsy. There is usually clinical evidence of intellectual deficiency and/or developmental delay. most commonly caused by hippocampal sclerosis in adults and cortical dysgenesis and low-grade tumours in children. hippocampal sclerosis and cortical dysgenesis. Common causes include anoxic birth injury.

Seizure and syncope usually rank high on the list of diagnostic possibilities. clinicians are faced with the dilemma of making a diagnosis of epilepsy in a patient who presents with unexplained loss of consciousness. TABLE 4: Differential diagnosis of seizures Neonates and infants • Jitteriness and benign myoclonus • Apnoea • Shuddering attacks • Gastro-oesophageal reflux • Hyperekplexia Young children • Breath holding spells • Reflex syncope • Parasomnias • Benign paroxysmal vertigo • Tics and ritualistic movements • Rage attacks Adults • Syncope • Migraine • Transient global amnesia • Transient ischaemic attacks • Narcolepsy • Paroxysmal movement disorders and ataxias Any age • Endocrine. the history from a reliable eyewitness and the associated symptoms and signs. a few factors need to be determined.3. namely. In the evaluation of a patient with a lapse of consciousness. the setting in which the event occurred. The differential diagnosis of seizures may be subdivided according to different age groups (table 4).0 DIFFERENTIAL DIAGNOSIS OF EPILEPSY Often. metabolic and toxic causes • Drug induced dystonia • Cardiac dysrhythmias • Delirium 11 .

calcium channel blockers. TABLE 5: Causes of syncope (Adapted from Rowland. antihypertensives. beta-blockers and lithium. levodopa. reversible global reduction in cerebral blood flow. 2000) Neurocardiogenic syncope • • • • • Vasovagal Carotid sinus syndrome Micturition syncope Cough and other Valsalva-induced syncope Emotional states Vasomotor syncope • • • • • • Medications* Postural changes Autonomic neuropathies Peripheral vascular disease Neurodegenerative disease with orthostatic hypotension Blood loss/hypovolaemia Cardiac syncope • • • • Tachyarrhythmias Asystole and heart block Outflow obstruction Failing myocardium Psychogenic syncope • • • Panic attacks Anxiety Hyperventilation Note: *Medication frequently implicated include phenothiazines.In adults. The causes of syncope are diverse (table 5). syncope is the most common cause of altered consciousness. arterial vasodilators. tricyclic antidepressants. 12 . diuretics. Syncope refers to the transient alteration of consciousness accompanied by loss of muscular tone that results from an acute.

and mislead bystanders into thinking that the attack is epileptic. Peripheral vasoconstriction imparts a pale appearance. and the pulse is rapid. shortness of breath or other features of cardiovascular insufficiency. Syncopal attacks typically begin with the premonitory phase where the person feels light-headed. 13 . remaining pink and breathing. In transient ischaemic attacks (TIAs) paraesthesiae do not show the same kind of segmental spread typically seen in epilepsy with focal sensory symptoms that spread from one part of the body to another. The absence of clonic motor activity and confusion favours focal ischaemia rather than epilepsy. Profuse sweating is accompanied by nausea. duration (often very prolonged). Vision blurs and characteristically fades out before consciousness is lost. there are often prodromal features of palpitations. The patient loses muscle tone of the legs and may fall. Psychogenic or pseudoseizures (non-epileptic attack disorder) can usually be distinguished both clinically and by video-EEG recording. In both vasovagal and cardiac syncope. Other clues to cardiac syncope include attacks with little relation to posture. resisting eye opening and eye contact. position or specific triggers. etc. the fall may be accompanied by brief myoclonic twitches of the extremities. frightening. and often prompt recovery. consciousness is preserved and patients may perform complex activities but have no recollection of the events. In transient global amnesia. brief period of unconsciousness. Features useful in distinguishing pseudoseizures from epileptic convulsions are the triggers (frustration.Important features in the history that favour vasovagal syncope rather than epileptic seizures include a clear precipitating stimulus or situation. ataxia. Identifiable precipitants are getting up quickly. the fall that often occurs in stages.). In the absence of other focal clinical features (dysarthria. urinary incontinence and tongue biting. Both tachyarrhythmias and bradyarrhythmias can produce syncope. in company). Rapid recovery occurs if the patient is allowed to lie flat. and Valsalva manoeuvres. diplopia. chest pain. episodes of loss of consciousness alone are not usually due to TIAs. painful stimuli. emotional or unpleasant scenes. rapid recovery and absence of any true postictal phase. In cardiac syncope. erratic movements (flailing. presence of prodromal symptoms. suggestion. pelvic thrusting). prolonged standing.

rather than confirm. 4. These features of the epilepsy require careful selection of certain key investigations. A complete diagnosis is necessary for proper treatment. a rational approach to requesting investigations in epilepsy is needed. Several types of EEG may be requested: 14 . the diagnosis of epilepsy.2 Electroencephalography Except for adult patients with a clear metabolic or structural abnormality on brain imaging.0 4. on the other hand. both neurological and general Monitor the progression of the condition. is incomplete without knowing its aetiology and prognosis. Several factors have changed the way we investigate patients with epilepsy. the diagnosis of epilepsy (epilepsy syndrome). The main objectives of investigating patients with epilepsy are to: a) b) c) d) e) f) Clarify the diagnosis of epilepsy and non-epileptic attacks Determine the nature of the seizure types and epilepsy syndrome Identify the laterality and localization of seizure onset (partial seizures) Identify the aetiology of epilepsy Identify concomitant problems.4. the introduction of more sophisticated and clearer neuroimaging techniques and better understanding of epilepsy syndromes and their response to pharmacological and surgical treatment have either obviated or augmented the need for certain investigations. neuropsychological assessment and other investigations (including blood tests and muscle biopsy). all patients with epilepsy will require an EEG.1 INVESTIGATIONS IN EPILEPSY Purpose of investigations Although the diagnosis of epileptic seizures is still based on a good history derived from the patient and witness. and the consequences of the epilepsy and its treatment These objectives are achieved through the electroencephalogram (EEG). To avoid requesting unnecessary. The general acceptance of epilepsy surgery. The aim of the EEG is to clarify. neuroimaging. or to omit essential investigations.

1 Routine interictal scalp EEG Technique: In general. A period of relative sleep deprivation the previous night by a few hours may enhance the chance of natural sleep. Additional focal spikes may be present in IGE. A sleep record reveals epileptic discharges in about 70-80% of patients with epilepsy. 15 . a routine interictal scalp EEG must be requested for ALL patients. epileptiform abnormalities not related to clinical epilepsy occur more commonly. intermittent photic stimulation and a period of natural sleep (particularly in temporal lobe epilepsy) to maximize the detection of interictal epileptic activity.4. The routine EEG requires placement of at least 21 electrodes on the scalp. The key EEG features in partial epilepsy are: • • • Focal or multifocal epileptic discharges Abnormal background in many cases Rarely. Findings in certain epilepsy syndromes: Epileptiform abnormalities are seen in less than 1% of healthy individuals. based on the international 10-20-electrode placement system. The detection of epileptic spikes from a single awake record is only about 30-40%. and in 50% of patients with unhelpful awake records. photosensitivity Focal spikes may propagate to produce bilaterally synchronous discharges mimicking IGE. Natural sleep can be obtained in children.2. The key EEG features in idiopathic generalised epilepsy (IGE) are: • • • Bilaterally synchronous. Both the EEG background and the characteristics (distribution and activation method) of the epileptic spikes (when present) help to clarify the epilepsy syndrome. sleep deprivation may rapidly put patients in deep sleep or precipitate potentially harmful GTCS. anteriorly predominant 3-5 Hz spike-wave activity Normal background Photosensitivity in many cases Overnight sleep deprivation may help activate the epileptic discharges in IGE. However. In the presence of a structural lesion. and chloral hydrate is only used in the occasional child who is anxious or combative. The recording should be performed during wakefulness and incorporate hyperventilation.

with the addition of simultaneous video recording. The patient is usually immediately responsive after the attack. and always abruptly following the attack. Often. the principal aim of which. but “normal” alpha rhythm is often seen “through” or in between.5-3 Hz spike and slow wave discharges that attenuate with eye opening Abnormal 1-2. absence seizures and non-epileptic disorders are best recorded this way. slow waves.5 Hz generalised. the EEG will show the characteristic 3-5 Hz bilaterally synchronous spike and slow wave activity.Characteristic EEG features of some other common epilepsy syndromes are shown in table 6. the recording may reveal additional or only non-epileptic attacks. pelvic thrusting and partial responsiveness are common clinical features that can be recorded on video. triphasic large amplitude spikes maximal in the central or centrotemporal region Normal Posterior 1. During an absence seizure. The former is similar to the routine scalp EEG. periods of attenuation) Normal Unilateral or bilateral. the main purpose of which is to localise the epileptic focus. which can usually be induced by hyperventilation. Long-term monitoring is usually a presurgical investigation. however. The recording is performed over several 16 . anteriorly predominant spike and slow wave discharges Benign childhood epilepsy with centrotemporal spikes Benign occipital epilepsy Lennox-Gastaut syndrome 4. flailing movements. TABLE 6: EEG features of common epilepsy syndromes EPILEPSY SYNDROME West syndrome EEG EPILEPTIC DISCHARGES BACKGROUND Abnormal Hypsarrhythmia – disorganised high voltage pattern (spikes. the EEG is often obscured by movement and muscle artefact.3 Video-EEG monitoring The purpose of recording the EEG and video of the patient simultaneously is to record the ictal EEG and to correlate it with the clinical behaviour of the patient during the attack(s). is to establish the diagnosis. This may be done on a short term (outpatient) or long term (inpatient) basis. In a non-epileptic seizure. Asymmetric thrashing.

The risk of infection and their invasiveness limit their use. MRI would be the initial investigation of choice. being superior to the CT with regards to the detection and delineation of epileptogenic lesions and lack of ionising radiation.5. The ictal onset is usually electrographic (preceding the change in clinical behaviour). and occasionally. in centres where it is available. 4. if this does not have a clear explanation such as omission of medication Acutely. Localisation of this activity correlates with the epileptic focus.5 4. and takes several forms. subdural and depth electrodes are inserted for long-term recording in selected patients to enhance the localisation of the ictal onset. after significant head trauma 17 . This will enable the recording of several attacks so that the localisation of the ictal onset can be determined with greater confidence. namely.4 Invasive EEG recording/sphenoidal electrodes Sphenoidal. and this to be correlated with the change in clinical behaviour. attenuation of the background. These electrodes have the advantage of detecting the first electrographic change before any spread of electrographic activity can be detected on the scalp.1 Neuroimaging Structural neuroimaging The skull radiograph is now obsolete and X-ray computed tomography of the brain is now the initial investigation of choice if structural imaging is deemed necessary. rhythmic theta activity that evolves in amplitude and frequency. Structural neuroimaging of the brain is mandatory in the following circumstances: • • • • • • Partial seizures based on the history and/or EEG Fixed or progressive neurological or psychological deficit Onset of generalised seizures before the age of 1 year and after 20 years Difficulty obtaining seizure control with AED Loss of seizure control or status epilepticus.days. and are no longer used in most centres. up to a fortnight. 4. However. The usual contraindications to MR imaging must be observed. or spikewave activity.

polymicrogyria). post-traumatic scars and dysembryoplastic neuroepithelial tumours. such as a possible intracerebral haemorrhage or infection The following MRI protocol is recommended for patients being evaluated for epilepsy surgery: • • 1. The decision to subject a patient to epilepsy surgery is greatly influenced by what is seen on the MRI. increased signal intensity on T2-weighed images.Imaging may be deferred in the following circumstances: • • • There is a clear provoking factor. such as measurement of hippocampal volumes and T2 relaxation times. may be employed. a small ipsilateral posterior fornix. apart from detecting gross lesions (such as large vascular malformations. including focal cortical malformations (e. such as alcohol withdrawal Children with benign epilepsy with centrotemporal spikes Pregnant women with no acute problems. cavernous haemangiomas. In cases where the hippocampal sclerosis is not clear or the possibility of bilateral disease cannot be excluded. Many subtle or additional lesions may be missed on a brain CT.2 Functional neuroimaging 18 . is characterised by loss of volume (compared with the normal side). the most common cause of temporal lobe epilepsy. This MRI protocol. and often. not visible on CT.5. etc) is capable of detecting other subtle lesions. allowing reformatting in any orientation or plane. and may be required for better delineation of subtle neocortical lesions prior to surgery. tumours.5 mm-thick slices using IRPF SPGR (GE) or MPRAGE (Siemens) sequences. quantitative MRI. decreased signal intensity on T1-weighted images. requiring special post-processing techniques or software.g.5 Tesla magnet A volume acquisition (contiguous) T1-weighted coronal data set of the whole brain in 1. 3D reconstruction and surface-rendering An oblique (heavily) T1-weighted coronal inversion recovery sequence orientated perpendicular to the long axis of the hippocampus (parallel to a line joining the base of the splenium of the corpus callosum to the inferior posterior border of the frontal lobe) An oblique (heavily) T2-weighted coronal spin echo (VEMP) (GE) or doubleecho STIR (Siemens) or a FLAIR sequence orientated perpendicular to the long axis of the hippocampus • • Hippocampal sclerosis. Surface coils provide better definition of the cortical ribbon. 4.

6. the patient should be investigated for an underlying endocrinopathy. a full biochemical profile is probably not necessary at initial patient evaluation other than a liver profile and full blood count prior to starting sodium valproate. 4. Hypoglycaemia.3 Investigations for inborn errors of metabolism 19 .6.2 Cardiac assessment As cardiac arrhythmias and obstruction to cardiac output may cause generalised (tonic) seizures.Functional imaging includes single photon emission computerised tomography (SPECT). In patients with typical absences and a characteristic EEG. functional MRI may also help localise specific functional areas (e. Only the former is available in a few centres in the country. These techniques are expensive and are used to further localise the epileptogenic lesion prior to surgery in cases where structural imaging is equivocal. such as an insulinoma. the recommended biochemical profile includes: • • • • Random blood glucose Renal profile Liver profile Serum calcium and magnesium (especially in children) If hypoglycaemic attacks are strongly suspected. may cause attacks that mimic complex partial seizures. a chest radiograph. In other patients. sensory or motor cortex) prior to the surgical excision of lesions in eloquent areas of the brain. the following investigations should be considered: 4.6 Other investigations At the initial evaluation of the patient. The presence of heart block is also a relative contraindication to using carbamazepine. In addition. for instance. ECG and often an echocardiogram are mandatory in all elderly patients and in those suspected of having cardiac disease. 4. 4.6.g.1 Blood biochemistry A serum biochemical profile is performed to identify possible metabolic causes or factors in certain seizure types as well as prior to starting certain AEDs. positron emission tomography (PET) and functional MRI.

repeat full blood count annually or before surgical procedures Monitoring of serum AED concentrations is discussed in Section 6. 4. and hence.6. If non-epileptic seizures are suspected. in children it is important to periodically assess cognitive function as its decline may be subtle but often greatly influences prognosis. it is less helpful for complex partial seizures and unhelpful for simple partial seizures. appropriate investigations must then be done to exclude rare neurodegenerative disorders such as progressive myoclonic epilepsy. repeat the full blood count. the decision to repeat these investigations or perform other investigations must be individualised: • Repeat EEG and neuroimaging if there is a need to reassess the cause of the epilepsy or suspicion that there is progression of the underlying disease.3. CSF studies. metabolic disorders and progressive structural disorders Repeat biochemical and haematological profiles to detect adverse effects of AED treatment or to further evaluate adverse events that have already developed In patients taking enzyme-inducing AEDs. demonstration of a normal serum prolactin level performed within 20 minutes of an apparent GTCS may be diagnostic.These investigations are usually only requested for infants and children. • • • • 20 .4 Other specific investigations Investigations such as serum or CSF VDRL. liver profile and serum calcium every 1-2 years In patients on valproate. who often have other neurological manifestations. must be individualised and ordered judiciously. HIV serology and connective tissue screening must be individualised and ordered judiciously. During subsequent follow up.

and the highest risk (65%) is in those with a remote neurological insult and epileptiform abnormalities in the EEG. While immediate treatment may reduce the risk of early post-traumatic seizures (within one week of injury). Drawbacks of therapy include potential drug side effects. occupation and family support. Few decisions are more critical in the management of epilepsy than the decision to initiate drug therapy. severity of seizures. Studies done in neurological conditions with high prospective risk of epilepsy have failed to show any evidence of benefit. Careful consideration must be given to several factors. A meta-analysis of prospective studies indicates an overall two-year risk of further seizures of 30-40%. Treatment after a first GTCS halves the two-year risk of seizures from about 40% to 20%. social relationships. cost. it does not influence the risk of late post-traumatic epilepsy. notably in patients with head injuries or large haemorrhagic strokes. This includes the need for treatment and choice of AEDs. starting an AED confirms the state of ‘epilepsy’. stigmatisation and inconvenience. include lower risk of seizure recurrence and of death or injuries. As far as the patient is concerned. which can affect self-esteem. The lowest risk (24%) is in patients with no identified cause who have a normal EEG.5.2 Single seizures Patients presenting with a first single unprovoked seizure present a common clinical dilemma. However. employment. 21 . The decision to treat essentially depends on the balance between benefits and drawbacks of therapy. The benefits of therapy on the other hand. level of function. Effective treatment also includes proper education and counselling. and advice must be individualised. 5. this is not associated with any improvement in longer-term outcomes such as proportion of patients achieving a one-year remission. education and employment. including the certainty of the diagnosis of epilepsy. schooling. 5. Important issues like driving. pregnancy and compliance must be discussed. its treatment must be individualised.1 Prophylactic treatment Prophylactic treatment has sometimes been advocated.0 GENERAL PRINCIPLES IN THE TREATMENT OF EPILEPSY Once the diagnosis of epilepsy has been established.

g. most patients would seek treatment after at least two seizures have occurred. The patient or physician considers the risk of recurrence unacceptable (e. patients with a high risk of recurrence should be given the option to start treatment. 2. There is a further 9% 22 . Seizures due to alcohol withdrawal or other metabolic or drug-related causes or sleep deprivation should not be treated with AEDs. 5.Given the potentially significant social and physical implications.1 Newly diagnosed epilepsy Factors influencing the decision to treat include: 1. There is no place at all for a ‘trial of treatment’ to clarify the diagnosis. the greatest risk being in the first 6 months.3. All patients developing seizures within a week of head injury should be treated. Treatment should be considered only if there are recurrences suggestive of epilepsy.3 Recurrent seizures The decision is more straightforward in patients with recurrent seizures and a clear-cut diagnosis of epilepsy. Recommendations: • Patients with a certain diagnosis of unprovoked GTCS should be treated after the first seizure if: 1. The seizures are associated with a previous absence and/or myoclonic seizures. if there is an underlying structural brain abnormality) • The decision to treat simple and complex partial seizures will depend on the seizure frequency and severity and patient preference. Patients should not be treated if there is uncertainty about the diagnosis. About 50-80% of all patients who have a non-febrile seizure will have further seizures. • • • 5. but AED withdrawal should subsequently be considered. and/or 2. Generally. A firm diagnosis of epilepsy based on a good first-hand witnessed account of the attacks.

seizures precipitated only under specific circumstances e. Epilepsy syndrome .some benign epilepsy syndromes have an excellent prognosis without treatment e. less than once every 2 years. Reflex seizures and acute symptomatic seizures. In those with pre-existing learning disability or cerebral damage. the risk approaches 100%. 7. Formulation of a treatment plan at the time of the patient’s initial evaluation would include: 1. the goal of therapy is to achieve complete seizure control. The risk is influenced by the following factors: • Aetiology: the risk is greatest with structural cerebral lesions and least in acute symptomatic epilepsy.g.g. Patients’ wishes-the final decision is left to the patient. simple partial. and decision to treat is established. the decision to treat will need to be re-considered. Some seizure types have a minimal impact on quality of life e. and should probably not be prescribed. 6. 23 . obviating the need for drug therapy. benign childhood epilepsy with centrotemporal spikes. alcohol or photosensitivity. Seizure type: partial seizures are more likely to recur than generalized seizures. Identifying precipitating factors such as drug abuse. 5. Seizures must be sufficiently troublesome. In circumstances where compliance is doubtful. may be treated by avoiding these precipitants. and do not require long term therapy. The risk in idiopathic epilepsy is about 50%. 4. the disadvantages of chronic drug therapy may be high. the physician’s role is to explain the relative advantages and disadvantages of therapy. Once the diagnosis is clear.g. Patients and their care-giver should be counselled about their avoidance. The benefits of AEDs in such seizures may be outweighed by their disadvantages.g. with a drug taken once or twice a day with minimal or no side-effects. absence or nocturnal seizures. Age: the risk is greater in those under the age of 16 and over 60 years.risk in the next 6 months and 8% in the following 12 months. Compliance –AEDs need to be taken reliably and regularly to be effective. alcohol. excessive fatigue and photosensitivity. • • 3. If the baseline seizure frequency is very low e.

history. titrating the dose upwards to a higher maintenance dose.sequence of drug changes. The possibility of pseudoseizures must be considered. particularly when the syndrome is unclear. Re-classify the epilepsy (seizure type(s) and syndrome). 4.3. fewer side effects. Review compliance. and has the advantages of better tolerability and compliance. EEG. the patient is considered to have chronic epilepsy (accounting for about 10-20% of all epileptic patients). etc.2 Treatment of chronic active epilepsy If seizures continue beyond 2-3 years. Set a treatment plan . 5. 3. Review drug history . Commencing the patient on a low dose of one (monotherapy) of the 1st line AEDs recommended for their type of seizures/epilepsy syndrome (table 8). serum level monitoring.2. A detailed documentation of seizure type/types should be made. which have not been tried.which AEDs have or have not been useful in the past. 5. The ideal dose for a patient is that dose that gives good seizure control without significant adverse side effects. limitations and likely duration of therapy. Counselling the patient and/or caregiver with respect to the reasons for starting therapy. Recognise limitations of therapy. 5. 7. drug and blood levels of previous therapy. 3. and lower teratogenic risk. patients with intractable epilepsy must be able to accept their disability and continue with life. This will avoid aggravation/worsening of certain syndrome/ seizures with incorrect medication. Review the diagnosis and aetiology. expectations. need for good compliance and potential risks of therapy. There are limits to the 24 . Syndromically classifying each patient's epilepsy. neuroimaging. Consider surgical therapy. 2. If seizures continue. Single drug therapy provides optimal seizure control in about 70% of patients. 4. 6. and the following management steps must be taken: 1. simpler regime.

although a normal EEG is reassuring. JME. The risk of relapse is higher in patients: • > 16 years of age • whose age at seizure onset was < 3 . • • 5. If the first AED is poorly tolerated at low dosage or fails to improve seizure control. side effects from AEDs. combination therapy may be tried.effectiveness of AEDs available and it is important to create a balance between seizure frequency. Work up for epilepsy surgery should be considered after failure of 2 welltolerated treatment regimes. and quality of life. Exceptions occur in certain epilepsy syndromes e. drug withdrawal may be considered. If needed. There is a 40. For both newly diagnosed and chronic epilepsy.g.) • with a past history of status epilepticus • with a history of afebrile or atypical febrile seizures in childhood • experiencing one or more seizures after the start of treatment • with a short duration of seizure-freedom • whose duration of treatment exceeds 10 years • with a known aetiology of seizures (symptomatic epilepsy) and associated neurological handicap • with a fast rate of drug withdrawal 25 . Although the mechanisms of action of many AEDs are not fully understood. or > 30 years • with tonic-clonic (primary or secondary) or myoclonic seizures • with partial onset seizures • with seizures needing > 1 AED for good control at the time of discontinuation • with an abnormal EEG. an alternative should be substituted. this remains a logical basis for choosing combination therapy. If the first well-tolerated AED greatly improves but does not completely abolish seizures.50% risk of relapse within the 1st year of cessation. Evidence is emerging that certain combinations offer better efficacy than others. (The EEG is not helpful in predicting seizure recurrence. subsequent combinations of 2 or at most 3 AEDs may be effective. No guarantee of seizure freedom can ever be given when a drug is withdrawn. a staged approach is advised: • • • Tolerability and long-term safety are the most important factors in choosing the first drug. which has a high relapse rate.4 Decision to withdraw AEDs When freedom from seizures has been achieved for a period of at least 2 years.

5 Driving and epilepsy. a worldwide variability. most countries and states have some laws or guidelines governing fitness to hold both ordinary and vocational licences. and states: • Under Section 30 (2) and (3) APJ 1987. the Pengarah can revoke this licence under Seksyen 30 APJ 1987 based on a medical report from any medical officer stating the level of disease/disability.Patients in whom seizure recurrence is less likely include: • those who have been seizure. Although they do not contribute greatly to the totality of road safety. and is on treatment 26 . and may be a necessity for continued employment. the doctor is not duty bound to notify JPJ. • Legally. The possession of a driver’s licence is an important contributor to health-related quality of life in epilepsy. or between three and five years at least • those with benign Rolandic and familial neonatal convulsions Discussion of whether to withdraw AEDs should take into account: • the patient’s need to work and drive a motor vehicle • the patient’s fear of seizures and attitude to prolonged AED therapy 5.free for five or more years. Generally. which allows for this inequitable variability in regulations. through to systems of individual driver’s risk assessment. If a licensee has obtained a licence before developing this condition. the decision to drive or not to drive is a choice best made after discussions between the treating physician and patient. however. the Akta Pengangkutan Jalan (APJ) 1987 and Kaedah-Kaedah Kenderaan Motor (Lesen Memandu) 1992 applies. Some conditions that may allow for safe driving include: • Well-controlled epilepsy. from some nations imposing a blanket lifelong prohibition. epileptic seizures can result in road traffic accidents by causing sudden incapacity at the wheel. especially denoting independence. the Pengarah of JPJ may refuse an application for a licence if the licensee is found to have a condition (disease or disability) that may endanger other road users. However. There is. this applies to all and any forms of licences. There is a lack of adequately researched data on relative accident risk in epilepsy compared to a non-epileptic population. In Malaysia. In this context. Kaedah 18 dan Kaedah-Kaedah Kenderaan Motor (lesen memandu) 1992 clearly states ‘epilepsy’ as one such condition.

off or on treatment. If a patient’s epilepsy is against him/her obtaining a driver’s licence. auras may not occur with every seizure.g. 27 . until the seizures have stabilized. 5. including people with epilepsy. use of public transport or carpooling is encouraged. Certain occupations are prohibited for people with epilepsy –these include driving heavy machinery e. Driving is considered a privilege. not a right. Someone who is a newly diagnosed epileptic and is being started on medication is advised to stop driving for 6 – 12 months. As such. tractors and public buses. obtaining driving licences in these situations is clearly not possible.6 Education and epilepsy The Kementerian Pendidikan Malaysia has confirmed that there are no discriminatory policies or action against any person with epilepsy who wishes to pursue higher education. Preceding aura –however. so as to facilitate any modification to their surroundings or courses as necessary.• • • Seizure freedom for at least 1 year. Purely nocturnal seizures. There are no specific disciplines which are barred for people with epilepsy. as well as flying commercial or military airplanes. People with epilepsy and any other chronic medical conditions are advised to inform the authorities of their condition. Any person who wishes to enrol in an Institute of Higher Learning (Institut Pendidikan Tinggi Awam or IPTA) is required to undergo a medical check up. and any drug-related side effects have settled. or the driver may not have enough space on the road to pull over despite an aura signalling an impending seizure.

6. 8. measures to prevent seizure recurrence are of paramount importance. 7. The decision to treat with AEDs should be made after extensive discussion with the patients or parents about the risks and benefits of treatment. 3.6. psychological. Counsel and educate the patient and caregivers about his/her epilepsy and treatment.1 Introduction Epilepsy is a chronic disease associated with physical. In about 60-70% of patients. If the seizures are not controlled and there are no side effects. 4. side effects and seizure control (table 9). introduce an alternative AED slowly (table 7) without tapering the first. If the AED fails to control seizures: • Review the diagnosis and seizure pattern. Therefore. 28 . The goal should be the restoration of a normal life through complete control of seizures with the use of a single drug that has little or no side effects. • Ensure that the maximum tolerated dosage has been used. Review every 6 to 8 weeks. and socioeconomic consequences that may compromise the quality of life. Review the patient within a month to assess compliance. The information can be given by doctors treating the patient or a nurse trained in epilepsy care (appendix 1) 5. Establish the diagnosis of epilepsy and the need for long term AEDs (chapter 5). 2. Start with a single first line AED after deciding on the type of seizure(s) and the epilepsy syndrome (table 7).0 LONG TERM PHARMACOLOGICAL TREATMENT 6. If the first AED continues to be ineffective at the maximum tolerated dose. these steps are sufficient to achieve good seizure control. Begin with a low dose and increase gradually over 2 to 3 weeks (table 8). increase the dose appropriately. 6.2 Initiation and continuation of AEDs A systematic approach to the long-term pharmacological treatment of epilepsy is recommended: 1. • Review compliance (see also “drug monitoring”).

tonic Myoclonic Valproate (M/A) Infantile spasms ACTH (M) Corticosteroids (M) Vigabatrin (M)* M = monotherapy A = adjunctive therapy *Currently not registered in Malaysia 29 .TABLE 7: List of commonly used AEDs and their indications: FIRST CHOICE Carbamazepine (M/A) Valproate (M/A) Oxcarbazepine (M/A) SECOND CHOICE Phenytoin (M/A) Lamotrigine (A) Topiramate (A) Levetiracetam (A) Gabapentin (A) Phenobarbitone (A) Acetazolamide (A) Clonazepam (A) Phenytoin (M/A) Lamotrigine (A) Topiramate (A) Phenobarbitone (A) Acetazolamide (A) Lamotrigine (M/A) Clonazepam (A) Acetazolamide (A) Lamotrigine (A) Topiramate (A) Clonazepam (A) Phenytoin (M/A) Acetazolamide (A) Clonazepam (M/A) Phenobarbitone (M/A) Piracetam (A) Acetazolamide (A) ?Lamotrigine (A) Clonazepam (A) Valproate (A) SEIZURE TYPE Partial seizures Simple partial Complex partial Secondarily generalised Generalised seizures Tonic-clonic. atonic. clonic Valproate (M/A) Carbamazepine (M/A) Absence Valproate (M/A) Ethosuximide (M/A) Valproate (M/A) Atypical absences.

of doses/day 2-3 Carbamazepine Clonazepam 2-3 Ethosuximide 2-3 Gabapentin 2-3 Lamotrigine 1-2 Levetiracetam 2 Oxcarbazepine 2 1-2 Phenobarbitone Phenytoin Topiramate Valproate 30 .2 mg/kg (children). 20-40 mg/kg (children under 20 kg). Initial: 600 mg (adults). Maintenance: 200-400 mg (adults). 20-40 mg/kg (children) Initial: 30 mg. No. 10 – 20 mg/kg (children). 0. 10-20 mg/kg (children). Maintenance: 100-200 mg (adults).25 mg (adults). 30-60 mg/kg (children). 20-50 mg/kg (children). 20-40 mg/kg (children). 35mg/kg (children). Initial: 25 mg (adults). Initial: 300 mg (adults). 0. 10 mg/kg (children). Initial: 500 mg.TABLE 8: AED Dosages of commonly used AEDs Usual daily dose Initial: 100 mg at night (adults).5-4 mg (adults). 5 mg/kg (children). 0.1-0.02 mg/kg (children). 1 Initial: 200-300 mg. Maintenance: 750-2000 mg (adults). Adjunctive therapy with valproate: gradual increment in the dose over one month (adults). 3-9 mg/kg (children). Maintenance: 300-400 mg (adults). 1-5 mg/kg (with valproate). 2 Initial: 400-600 mg (adults). 5 mg/kg (children) 2 Initial: 25-50 mg (adults). 5-15 mg/kg (without valproate) (children). Initial: 0. Initial: 250 mg (adults).15 mg/kg (with valproate). 10 mg/kg (children). 0. Maintenance: 1000-3000 mg. Maintenance: 400 – 1600 mg (adults). Maintenance: 0. 20-30 mg/kg (children over 20 kg). 10mg /kg (children) Maintenance: 1200-2400 mg (adults).5-1 mg/kg (children). Maintenance: 900-3600 (adults). Maintenance: 400-2500 mg (adults). 0.6 mg/kg (without valproate) (children). Maintenance: 30-180 mg (adults).

dizziness. and headache. headache. ataxia. and weight loss.TABLE 9: Common and important side effects of AEDs AED Side effects (acute and chronic) Carbamazepine Drowsiness. and blurring of vision. dizziness. drowsiness. and hyperactivity in children. gingival hypertrophy. tremor. dizziness. and somnolence. and hirsutism. nephrolithiasis. and thrombocytopaenia. ataxia. and hyponatraemia. dizziness.finding difficulties. hypohidrosis (children). ataxia. ataxia. tremor. leucopaenia. Dizziness. menstrual irregularities. cognitive dysfunction. hair thinning and hair loss. sedation. Sedation. lethargy. open angle glaucoma. paraesthesiae. weight gain. dizziness. Sedation. Ataxia. rash and other skin reactions. ataxia. fatigue. and myoclonus. emotional lability. word. Valproate 31 . diplopia. Somnolence. somnolence. Drowsiness. asthenia. Clonazepam Gabapentin Lamotrigine Levetiracetam Phenobarbitone Phenytoin Topiramate Drowsiness. Rash (sometimes severe). blurring of vision. dizziness.

topiramate and gabapentin are not available and generally unnecessary. Review the diagnosis if seizures continue despite the above logical approach. or produces undesirable side effects. given its narrow therapeutic range and zero order kinetics. 15. Serum assays for valproate are unhelpful due to large fluctuations in levels and lack of correlation with efficacy. 6. When employed as a guide to dosing. and benzodiazepines are moderately helpful. The possibility of pseudoseizures or poor compliance should be considered. If the patient has a good response to the second AED. Assays of carbamazepine. during pregnancy. This process can be repeated for other possible add-on AEDs. and status epilepticus 32 . Consider long-term two-drug therapy if monotherapy has not achieved remission or good seizure control.3 Drug monitoring AED concentrations are over-requested and often misinterpreted.g. Serum assays for the newer drugs such as lamotrigine. some patients may benefit from an additional third AED. and surgery may be considered. Their views on treatment such as achieving the right balance between side effects and seizure control should be taken into account when considering changes in medication. serum concentrations of phenytoin are the most useful. especially if the patient has partial seizures. 10. Patients and care-givers must be fully involved in decisions about their treatment. 11. leading to injudicious alteration of treatment. and simultaneously replace it with a second add-on AED from the remaining choices. withdraw it slowly. phenytoin) • To monitor pharmacokinetic interactions • As a guide in certain situations e. consider withdrawing the original AED gradually. and a period of 2-3 years has elapsed. When these possibilities have been excluded the patient should be evaluated for a possible progressive structural lesion. 13. 14. 12.9. If the seizures are still not adequately controlled on two AEDs. If the first add-on AED is ineffective. The importance of compliance should be stressed to patients and care-givers. The major indications for assaying serum AED levels are: • To check compliance • To determine if signs or symptoms are the result of AED toxicity • As a guide to dosing of certain AEDs (in particular. phenobarbitone. pre-pregnancy planning.

Carbamazepine and phenytoin are not only ineffective for. If drug toxicity is suspected.As a general rule.4. with or without secondary generalisation) The choice of first-line treatment for partial seizures is either carbamazepine or valproate. primary generalised tonicclonic. • Primary GTCS: carbamazepine. the following steps should be observed: 33 . phenytoin. For drugs with significant variation in serum concentrations during the dosing interval (e. serum AED levels should be measured at steady state. Blood should be drawn in the morning before the first daily dose.4.4 6. but may exacerbate absence and myoclonic seizures. The appropriate choice of AED in an individual patient is a balance of efficacy. a second sample should be taken a few hours later.g. the following drugs may be tried: phenytoin. phenobarbitone.4. 6. i. If first-line treatment is ineffective or unacceptable. clonazepam or topiramate. If first-line treatment is ineffective or unacceptable. topiramate.1 • • • Choice of first line therapy Treatment of partial seizures (simple. The time of sampling is unimportant for AEDs with long half-lives like phenobarbitone. lamotrigine.e. lamotrigine. 6. gabapentin or levetiracetam. and myoclonic seizures) • The recommended first-line treatment is sodium valproate. tolerability and cost. when the concentration is usually at its trough. Treatment of chronic epilepsy 6. In instituting long-term pharmacological treatment in such patients. gabapentin. ethosuximide or lamotrigine.3 The principles of treatment in chronic active epilepsy are covered in chapter 5. the next choice of AED depends on the seizure type and syndrome: • Absence and myoclonic seizures: clonazepam. peak levels should be taken.2 • Treatment of generalised seizures (absence. when at least 5 elimination half-lives have elapsed since the last dose change. sodium valproate and carbamazepine). complex.

lamotrigine and topiramate produce non-specific central nervous system manifestations. including lamotrigine. etc. Consider using the newer AEDs. This may occur even after a few weeks of starting treatment. gabapentin. the various AEDs tried including drug dosages. Chronic toxicity may affect any system. With polytherapy.• • • • Review previous treatment history i. with a gradual reduction over a 6 month . phenobarbitone.1 year period. loss of driving license. • 6. phenytoin. The decision to stop medication involves a balance of the risks of continuation (chronic toxicity. • • 34 . manifested initially by rash occur in 2-4% of patients exposed to carbamazepine. Intermittent usage of rectal diazepam (after the first seizure) can be considered in patients with predictable clustering.) with the implication of relapse (injury. effectiveness. especially perimenstrually. topiramate. AEDs should be withdrawn slowly. The side effects are quite specific for each AED (table 9). Allergic reactions. in particular drowsiness. starting with the least useful one. drug withdrawal and side effects.5 AED toxicity Important points pertaining to AED toxicity include: • • • • Acute dose-related toxicity is common and predictable although the dose required to produce symptoms varies between individuals. and levetiracetam after the standard AEDs have been used. unemployment. teratogenicity. death. Review compliance to AEDs. with the peak incidence at 10-21 days (table 9). Inappropriate rapid introduction of AEDs is a common reason for toxicity and apparent drug failure. and lamotrigine.6 Stopping treatment Important points pertaining to the withdrawal of AEDs include: • • In more than 60% of patient who remain free of seizures. 6.). one drug at a time should be withdrawn. Carbamazepine. etc. the medication can eventually be withdrawn successfully.e. Withdrawal of AEDs can be discussed with patients after 2 years of seizure freedom.

some low grade tumours. when: • • • Patients present with more than 20 seizures before treatment is initiated. Patients with medically intractable seizures are candidates for surgical treatment with the aim of achieving better seizure control. These include the recognition of “surgically remediable epileptic syndromes” which have a clearly defined clinical presentation and natural history. However. and There is an underlying well defined structural cerebral abnormality on imaging studies Patients who have persistent seizures despite adequate therapy with an appropriate initial AED have only a 12% to 14% chance of complete seizure control with alternate AED monotherapy and a 3% to 11% chance with AED polytherapy.g. particularly electrophysiological studies (long-term video-EEG monitoring) and high resolution MRI that allow reliable. and improvement in surgical techniques that have greatly increased the efficacy and safety of surgical procedures for the control of seizures. non-invasive identification of these syndromes. Another group of patients who might benefit from surgery are those whose seizures may be relatively well controlled but who have lesions that strongly suggest that surgical intervention might be curative (e.2 Early diagnosis of seizure intractability and timing of surgery Traditionally.7.1 SURGICAL TREATMENT OF EPILEPSY Introduction In well developed health care systems with dedicated epilepsy management programmes and easy access to AEDs. The diagnosis of intractability should be individualized with consideration given to the following: 35 . vascular malformations). In less developed health care systems. therapeutic failure of 3 AEDs has defined medical intractability. refractory epilepsy may be suspected at the outset.0 7. recent advances in diagnostic procedures. 7. Several developments have contributed to the increasingly prominent role of surgery in control of refractory seizures. it is likely that a substantial number of patients with a potential for surgical cure of seizures do not have the benefit of surgical treatment. about 30% of patients continue to have seizures despite appropriate drug therapy. There is inadequate response to the first AED prescribed.

presence of unpleasant auras. tailored resection Lesionectomy (single tuber) Lesionectomy Functional hemispherectomy 7. Table 10 summarizes the surgical options currently used. TABLE 10: Surgical options for various epilepsy syndromes Epilepsy syndrome Mesial temporal lobe epilepsy Discrete focal lesions Tuberous sclerosis Infantile spasms secondary to discrete cortical lesion Intractable seizures associated with diffuse.3 Surgically remediable epilepsy syndromes The preferred surgical technique for each syndrome may vary from centre to centre and from case to case. In adolescents and adults. dizziness. at least 1 year of non-remitting seizures should elapse before surgery is considered. education and employment Adverse effects of AED polytherapy (extreme fatigue. Detailed information regarding each syndrome and the technical details of each surgical option are beyond the scope of this guidelines.• • • Seizure type – major seizure type. seizures with risk of injury Seizure burden – number of refractory seizures. e. several months of frequent seizures might be sufficient. selective amygdalohippocampectomy Lesionectomy. given the deleterious effects of refractory seizures on the developing brain. significant postictal disability. unilateral hemispheric pathology in children Surgical options Anterior temporal lobectomy. 36 . unpredictable occurrence. in infants.4 Presurgical investigations and patient selection The single most important determinant of a successful surgical outcome is patient selection. degree of interference with quality of life. The presurgical evaluation of potential candidates should preferably be carried out at a multi-disciplinary centre experienced in the investigation and treatment of epilepsy. etc) How long epilepsy should be present before surgery is considered depends on the natural history of the epilepsy syndrome. 7. clouded thinking.g.

4.e. degree of interference with psychosocial functioning and development) Presurgical Evaluation 7.1 Selection of patients for presurgical evaluation Prior to embarking on presurgical evaluation it is important to ascertain that: • • • The epilepsy syndrome is accurately identified (i.7.4.2 The aims of the presurgical evaluation of patients in whom resection of an epileptogenic zone is planned are to: • • • accurately localise the epileptogenic zone establish a resection strategy establish definite goals once seizure control is achieved by surgery Accurate localisation of the epileptogenic zone is achieved by examining and correlating data acquired from the seizure semiology and a series of investigations: • • • Routine scalp EEG and continuous video-EEG monitoring High-resolution (preferably volumetric) brain MRI Full psychometric analysis by a trained clinical neuropsychologist 7.5 Establishment of a resection strategy Several adjunct investigations may be performed prior to surgery to maximise the benefit and minimise the risk from the operative procedure: • • • • • • Functional MRI Intracarotid amylobarbital test Intraoperative EEG mapping with electrocorticography (ECoG) Awake craniotomy and cortical stimulation Image guided surgery Ultrasonic aspirator 37 . identification of a surgically remediable syndrome) The seizures are indeed intractable to appropriate medical therapy The seizure burden is such that surgical treatment is a reasonable consideration (seizure frequency .

The objectives of these investigations are to: • • • Identify the proximity of eloquent brain tissue to the epileptogenic zone Minimise the risk of injuring adjacent eloquent brain tissue (speech. In some instances. the persistence of minor seizures postoperatively is acceptable. there is a greater potential for functional recovery following resection of eloquent cortex due to greater plasticity of the developing brain in this age group. hand motor. consideration should be given to corpus callosotomy. Patients in whom there is a risk of injury from intractable sudden akinetic seizures (drop attacks). disabling seizures and reverse an epileptic encephalopathy.and postoperative morbidity may be higher in infants and younger children than in older children and adults. Control of severe. and memory centres) To identify dual pathology Division of the corpus callosum (corpus callosotomy) and multiple subpial resection are some of the disconnection procedures in current use for palliation (in intractable patients without a surgically remediable lesion). 38 .6 Results of Surgical Treatment Surgical outcome in terms of seizure control and operative risks for different epilepsy surgery procedures are shown in table 11. However. Complications related to large cortical resections. disabling seizures and a decrease in the consumption of AEDs have been shown to result in an improvement in the rate of neurodevelopment. visual. 7. and intra. The goals of resection in children are often to stop severe. and an enhanced quality of life for both the patients and their families.

SAH) Seizure free rate of about 70% Lesionectomy Seizure free rates of 40-60% Seizure free rates of 56-82% Functional hemispherectomy Corpus callosotomy for akinetic seizures Significant seizure reduction in 50-80% 39 . increased ICP.Major permanent neurologic morbidity variable (determined by location. hemiplegia) .Complications (haemorrhage. meningitis) .Mortality .Minor hemianopic deficit in 50% (non-disabling) .Significant neurological deficit <5% .Mortality risk < 1% .Some degree of decline of verbal memory with dominant hemisphere resections (only in some patients) .Mortality Risk < 1% .Disconnection syndrome is usually transient (hemineglect. hydrocephalus. mutism. cerebral oedema.Major permanent neurologic morbidity <2% ( coma.Table 11: Results of surgical treatment for control of seizures Postoperative seizure outcome Epilepsy surgery procedure Risks of complications . thoroughness of presurgical selection) . and motor coordination deficits) Surgery for hippocampal sclerosis (ATL.Mortality risk < 1% .

vital parameters. 8. serious injury. 8. In most cases of GTCS. treatment is usually supportive and patients will recover fully after a period of rest of about 30-60 minutes. An arterial blood gas analysis must be performed if the seizures are persistent. including the blood pressure. oxygen is given via nasal prongs during the postictal phase. Stay with the patient until he or she recovers fully. and place the head on a soft support (bundle of cloth or pillow). Loosen tight clothing. including calcium and magnesium assessment. oxygen saturation and ECG must be monitored. if possible.1 EMERGENCY TREATMENT OF EPILEPSY Introduction Most seizures are self-limiting.8. heart rate.0 8. The airway must be patent and the possibility of rapid sequence endotracheal 40 . The patient is maintained in a left lateral position and intravenous access is established. and gather information about the patient’s background and epilepsy history. or there is no recovery of consciousness after 30 minutes. Turn the patient to the left lateral position. Avoid placing any objects in the patient’s mouth. Rapid blood glucose estimation via a glucometer is done and blood is drawn for urea and serum electrolytes. 8. or a recent increase in seizure frequency.4 Treatment of prolonged seizures In the event that the seizure does not stop.2 Initial supportive management During an acute epileptic seizure. Remove any harmful objects. Studies show that the mean time for a GTCS is 62 seconds and a complex partial seizure is about 120 seconds. Get the patient to the nearest hospital if the seizure persists beyond 10 minutes. significant fever.3 Postictal care in uncomplicated seizures Once the patient is in a hospital. the following measures should be taken: • • • • • • • Place the patient on a smooth surface.

The onset of action is marginally slower (2-5 minutes) compared to the intravenous route (< 2 minutes). In the former. 8. The respiratory rate and pattern is observed. Prolonged seizures may be aborted with the following AEDs: 8. rectal.intubation considered.2 Alternative parenteral benzodiazepines When intravenous access is difficult. In addition. 8. Paramedical personnel can be trained to use parenteral lorazepam or diazepam at a reduced dose to control seizures in up to 56% of patients. if Wernicke’s encephalopathy is suspected. The efficacy of intranasal midazolam is equivalent to that of rectal diazepam. namely.3 Pre-hospital treatment The duration and recurrence rate of seizures may be reduced by proper prehospital treatment. 41 . buccal or intranasal. midazolam at a dose of 0. lorazepam results in lower seizure recurrence (due to its longer redistribution and elimination half-life). Similar doses are used for buccal midazolam. 50 ml of 50% glucose should be given intravenously. an intravenous bolus of thiamine 100 mg should be given prior to the glucose administration.4. and better response rates (see table 12). Intravenous midazolam (5 mg/ml) solutions may be given intranasally or onto the buccal mucosa. alternative routes for BDZ administration may be used. Rectal diazepam is the recommended alternative route (table 14). Oxygen is delivered through a high flow mask. lower rate of respiratory depression (inactive metabolites). If there is any suspicion of hypoglycaemia as the cause of the seizures. Caregivers of patients with recurrent clusters of seizures or prolonged seizures may be trained to administer rectal diazepam at doses predetermined by their medical practitioner. The response rate is estimated at 76-100% for lorazepam and 50% for diazepam.4. Compared with diazepam. which is rapidly absorbed into the circulation in the absence of an upper respiratory tract infection.2mg/kg is dropped into the nasal cavity.1 Benzodiazepines (BDZ) Intravenous lorazepam and diazepam are the principal first line AEDs used for prolonged seizures. The former is not available in Malaysia but there is good evidence in favour of lorazepam as the drug of first choice.4.

2mg/kg adults 42 .15 mg/kg Administration Distribution Elimination Metabolites Time half life half life < 5 minutes 1-2 minutes 15-90 minutes 4-6 hours 36 hours 16 hours Active Inactive TABLE 13: Rectal diazepam dosing Rectal diazepam dosing according to age 2.1-0.5mg/kg 0.TABLE 12: Comparison of the pharmacokinetics of lorazepam and diazepam Maximal Loading dosing Diazepam 0.3mg/kg > 11 years and 0.15 mg/kg Lorazepam 0.5 years 6-11 years 0.

The capacity for spontaneous resolution falls. An additional dose of phenytoin at 5-10 mg/kg can be given if the first loading dose is unproductive. and efficacy of these AEDs in acute overt and chronic subtle SE are summarized in tables 14 and 15. and the risk of mortality and morbidity rises with time. Seizures that last longer have a higher mortality and recurrence rate. (adults) or 0.v.v. however.2 ml/kg i. diazepam 10 mg repeated once after 15’ i. In the management of established SE. phenytoin 15-18 mg/kg at ≤50 mg/min. intravenous diazepam. Even seizures lasting from 10-29 minutes have a better prognosis than those lasting more than 30 minutes. sodium valproate.5 Treatment of convulsive status epilepticus Convulsive status epilepticus (SE) is defined conventionally as a seizure or a series of seizures lasting more than 30 minutes. or i. Fosphenytoin is a relatively new and expensive AED that is safer to use than phenytoin. 4 mg) bolus i. lorazepam 0. However. Phenytoin is the preferred AED because it is widely available and is less sedating than the other AEDs. phenytoin. Sodium valproate has been shown to be useful in acute repetitive seizures and early SE in children. lorazepam. Its role in the treatment cascade is.m. and are more resistant to conventional treatment (table 7). Their role is probably in the acute phase while awaiting definite therapy.v.4 ml/kg diluted with equal volume of olive oil rectally (children) 43 . push in 30 minutes) followed by an infusion at 1 mg/kg/hour has proven to be haemodynamically safe and not arrhythmogenic.07 mg/kg (usu. debatable. sodium valproate 15-25 mg/kg slow bolus (over ½ hour).v. The dosages of. or paraldehyde may be used. without recovery of full consciousness. followed by infusion at 1 mg/kg/hr for 6 hours Paraldehyde 0. Time appears to be of the essence and an increasing number of authors are redefining the time frame for SE to any convulsion lasting more than 5 minutes or a series of seizures without recovery of consciousness. or i.8. but is currently not available in Malaysia (table 16).v. Intravenous lignocaine and ketamine may be used but their effectiveness is not proven. TABLE 14: Dosages of AEDs used in the initial phase of acute seizures • • • • • • i. most seizures abate within 2 minutes.v. phenobarbitone. phenobarbitone 20 mg/kg at ≤100 mg/min. The intravenous formulation administered at a bolus of 1525mg/kg (slow i.

7 Lorazepam Phenobarbitone Diazepam/Phenytoin 55.9 58. General anaesthesia should be induced and maintained in an intensive care unit and the patient should be connected to an EEG monitor. and the principal goal will be to achieve EEG background suppression. The administration of barbiturates or other anaesthetic agents may compound the problem and intubation will be necessary. The drugs that can be used include one of the barbiturates (table 17). Inotropes and fluid resuscitation will be needed. At this point. midazolam or propofol.1-2. The underlying aetiology will usually need to be treated.2 8.About 60-90 minutes into the seizure. 0. 2-15 mg/kg/hr infusion) infusions are usually used at this stage. Midazolam (0. There is no difference in terms of achieving this goal between the agents. respiratory depression and hypotension from the seizure or effects of the phenytoin or BDZ are of prime concern.9 24.3 7. Refractory SE is defined as seizures unresponsive to BDZ. TABLE 15: Response rates of acute overt and chronic subtle SE to various AEDs Overt SE (%) 64.5 mg/kg bolus at < 4 mg/min. the patient should be subjected to general anaesthesia.2 Subtle SE (%) 17.0 mg/kg/hr infusion) and propofol (1-2 mg/kg bolus at < 25 mg/min. phenytoin and barbiturates.6 TABLE 16: Comparison of phenytoin and fosphenytoin Phenytoin Fosphenytoin Loading dose 15-18mg/kg 20mg/kg Infusion rate 50mg/min 150mg/ min Ingredient Active moiety Prodrug Elimination half -Life 20-40 hours Converted to phenytoin 44 .8 Phenytoin 43.2-0.

it is recommended that each hospital develops its own protocol. However. 45 . The flow chart below is a useful step-by-step guide to the management of convulsive status epilepticus in adults.TABLE 17: Barbiturate dosing Loading dose Administration rate Maintenance Elimination dose half life (hours) 3-6 mg /kg / hr 200-320mg/ day 1-5 mg/kg/ hr 2-8 mg /kg / hr 53-180 Phenobarbitone 20 mg/kg max 600 mg 60mg/min (adult) 30mg/min (paediatric) Pentobarbitone Thiopentone 5 mg/kg 2-4 mg/kg Titrate to EEG/vital signs Titrate to EEG/vital signs 21-42 3-8 Other than monitoring the adequacy of general anaesthesia. require augmentation of AED therapy. which if present. continuous EEG recording will also help detect electrographic seizures.

1.v. : Blood urea & electrolytes : Full blood count : Serum calcium / magnesium. Give oxygen by nasal cannula or face .v. (ABC’s of resuscitation ). Fluids: 0. 46 . 2. thiamine 100mg followed by 50 ml of 50% glucose (direct push into the i. 1. : Serum drug levels (AEDs & toxicology.20 minutes. 3.8 minutes.2 mg/kg at 5 mg/min. administer i. 6. ( Emergency Dept) PROCEDURE. Draw arterial blood for arterial blood gas and apply Pulse oximeter (if available ).10 minutes. access. If hypoglycaemia is established. 10 . Assess cardiorespiratory status and vital signs at onset and periodically thereafter.v. through large veins. line). Establish i. diazepam 0.mask 15L/min. 4. Ensure airway patency and oxygenation at all times. 5. 8 . or a blood glucose determination is unavailable. Diagnose status epilepticus by observing continued seizure activity or one additional seizure.v.9% NaCl. 7. preferably 2 lines (branula size 18 G).MANAGEMENT OF CONVULSIVE STATUS EPILEPTICUS IN ADULTS TIME FROM START OF TREATMENT 0 . Blood investigations: Glucose level / dextrostix. Administer i.

2. If seizures persist :Additional dose of phenytoin at 5 mg/kg at rate 50 mg/min. phenytoin 100 mg 8 hourly after 12 hours of loading dose.18 mg/kg infusion (diluted in 100 ml of normal saline). phenytoin 15 . > 60 minutes. OR Phenobarbitone 10 mg/kg I/V at 100 mg/min. a 24-hour seizure-free period) 47 . 1.v. and start ORAL ANTIEPILEPTICS via Ryles tube (patient’s regular drugs) if known epileptic on medication.v. at least. whilst arranging to TRANSFER patient to ICU.60 minutes. (Total dose = 20 mg ) ED 20 . Monitor ECG and BP throughout. followed by 50 mg every 2 . Followed by :[MAINTENANCE DOSE] : i.200 mg bolus over 20 seconds. Repeat after 15 minutes if seizures persist.3 days : infusion based on blood levels or decrease dose if systolic BP < 90 mmHg Slowly discontinue once seizure controlled (reduce by 25 mg/hr every 6 hours after.5 mg/kg/hr Monitor thiopentone blood level ~ 40 ug/L After 24 hours: infusion based on blood levels After 2 . thiopentone 100 .3 minutes until seizure controlled or EEG shows burst suppression Thiopentone maintenance: 3 . Assisted ventilation : i. if seizures persist 3.v. at a rate not exceeding 50 mg/min. If seizures persist:- WARD [LOADING DOSE] : i. 1. and EEG monitoring.

2 mg/kg) at < 50 mg/min with ECG monitoring followed by i.v.4 mg/kg maintenance dose. phenobarbitone at 1 . followed. 30 minutes later.v.OR i. infusion at 50 .v. by maintenance dose of 1 mg/kg/min for 6 hours 48 . sodium valproate : loading dose 15 mg/kg.100 mg in 250 ml Dextrose 5% at rate of 3-4 mg/kg/hr OR i.5 . lignocaine 100 mg bolus (1.v. If anaesthetist / ICU bed not immediately available : In ward: i.

The first line of treatment is an infusion of a BDZ. and the eventual prognosis will depend on the underlying cause. and the simultaneous introduction of oral treatment like carbamazepine.6 Emergency treatment of other prolonged seizure types 8.6.1 Myoclonic status In hospital practice. Patients present with a change in behaviour or detachment from the environment. Treatment should be aimed at. In the event that BDZ infusion does not work. More rapid resolution can be obtained with intravenous BDZ like midazolam or sodium valproate. The condition carries a risk of convulsive SE recurrence and it must be treated aggressively as for convulsive SE. midazolam or diazepam.3 Non-convulsive SE (NCSE) This condition may present de novo. infusion of phenytoin or sodium valproate may be tried.6. i. phenytoin. The de novo form of NCSE may occur as a complex partial SE or absence SE.2 Tonic status Treatment should proceed as for GTCS.8. or sodium valproate. These must also be treated expeditiously but not as aggressively as above.e. 8.6. The incidence of NCSE in SE is estimated at 14%. after which the patient is slow to recover consciousness. 49 . Resistant patients may need a barbiturate for control. The risk of brain damage is minimal in comparison to convulsive SE. or as a sequel to convulsive SE. 8. Levetiracetam is also useful for anoxia-induced myoclonus. anoxic brain damage and acute renal deterioration are the commonest causes of myoclonic seizures.

2 Menstruation Juvenile myoclonic epilepsy and photosensitive epilepsy tend to develop at puberty whereas childhood absence epilepsy and BCECTS tend to remit at puberty. 9.1 SPECIAL ISSUES Epilepsy in women Introduction There are special issues when managing women with epilepsy.1. Between 5% and 12% of women experience catamenial exacerbation of their seizures.0 9. in particular.3 Fertility The fertility of men and women with epilepsy has been estimated to be 85% and 80% of the expected levels.1 9. has been reported to be associated with reduced sperm production and motility.9. Women of child-bearing age must be made aware of these issues. Either intermittent clobazam or acetazolamide given over the menstrual period may alleviate catamenial exacerbation of seizures. and the attending physician needs to take these into account when planning management strategies. 50 .1. 9.1. These include: • • • • • • • • • Menstruation Fertility Contraception Pregnancy Pre-conception management and counselling Labour Foetal malformations Breast feeding and the puerperium Bone health These issues arise because of the hormonal changes that take place during different phases of a woman’s life. Phenytoin. respectively.

Patients on the OCP need to be advised about additional contraceptive measures. carbamazepine. Although the increased seizure frequency in some women may be due to pregnancy-related fall in plasma drug concentrations. carbamazepine and phenobarbitone serum levels should be measured every 2-3 months through gestation so that dose increments can be made without delay to return the concentrations to the levels that gave optimum seizure control pre-conception should there be an increase in seizures. and oxcarbazepine).1. There are only anecdotal reports of miscarriage following GTCS. There is no evidence that hormonal contraception adversely affects seizure control. magnesium sulphate is often advocated by obstetricians but this is a poor anticonvulsant.9. sleep deprivation. however. However. Of special note is the treatment of eclamptic seizures. Dose adjustments should not. If a woman wishes to rely on the OCP alone. Certain underlying causes need specific treatment. phenytoin. certain special causes must be considered and appropriately ruled out because they are more common in pregnancy (table 18).5 Pregnancy Sixty percent of women will experience no change in seizure frequency during pregnancy. 51 . be based on AED concentrations alone. Pregnancy does not increase the risk of developing new epileptic seizures for the first time. Whether epilepsy is associated with an increased risk of obstetric complications remains controversial. A brain MRI or CT with lead shielding will often be required. The principles of treatment of new epileptic patients in pregnancy are the same as for the non-gravid state. and phenytoin or benzodiazepines are probably better alternatives. There is little evidence that seizures adversely affect pregnancy other than increasing the risk of trauma on the developing foetus. Intramuscular DepoProvera at a dose of 150 mg every 12 weeks is an acceptable alternative as it is not affected by enzyme-inducing AED. particularly in the first and third trimesters. she should be prescribed a preparation containing 50 µg of oestradiol.1. along with specific treatment of the eclampsia.4 Contraception There is an increased risk of oral contraceptive pill (OCP) failure with AEDs that induce hepatic microsomal enzymes (barbiturates. Serum AED concentrations often fall during pregnancy. poor compliance. 30% increased frequency and 10% decreased frequency. inappropriate reduction in AED therapy and vomiting may also be contributory. Penytoin. 9. if seizures do develop de novo in pregnancy.

7 Labour 52 . in all women with childbearing potential. If the epilepsy is still active but seizure control has been deemed optimal. The latter risk is low if the patient has been seizure-free for more than 2 years and tapering is done gradually. facial and Ultrasound limb anomalies 9.1. this is seldom possible or practical.TABLE 18: Special causes of epilepsy developing in pregnancy • • • • • • • Enlarging meningioma Enlarging arteriovenous malformation Ischaemic stroke Cerebral venous or venous sinus thrombosis Vasculitides Subarachnoid haemorrhage Eclampsia Women on AEDs should be monitored throughout pregnancy to detect foetal malformations so that their view on a possible termination of pregnancy can be sought early. the risk of teratogenicity while on AEDs and the risk of recurrent seizures if AEDs were to be withdrawn must be discussed long before they wish to conceive. 9. However. women should be advised against getting pregnant until they become seizure free and are off AEDs. Recommended investigations are listed in table 19. TABLE 19: Prenatal diagnosis of malformations Malformation Neural tube defects (NTDs) NTDs Investigation Serum alpha-fetoprotein in maternal blood Serum alpha-fetoprotein in amniotic fluid Sensitivity/timing 80% at 16 weeks >80%. Hence. but reserved when ultrasound cannot reliably exclude a NTD 94% at 16-18 weeks 20-24 weeks NTDs Ultrasound Major cardiac. However. for various personal.1.6 Pre-conception management and counselling Ideally. the AED should not be changed. cultural or religious reasons. if seizure control is poor. therapy should be adjusted until a single drug at the lowest effective dose delivers the best seizure control.

patients should be given 20 mg/day of oral vitamin K1 in the last month of pregnancy. via a nasogastric tube or intravenously. If frequent GTCS or complex partial seizures do occur during labour. if necessary. has been associated with up to a 50% risk of foetal malformation. but there is growing evidence that they are safe in pregnancy. Valproate doses exceeding 1000 mg daily carry the greatest risk. There is insufficient evidence that one AED has a higher teratogenic risk than another AED. The combination of valproate. In a large retrospective cohort study. a caesarean section is indicated. Data for most of the newer AEDs is still limited. intravenous fresh frozen plasma should be given. 9. The patient’s regular AEDs must be continued through labour.8 Foetal malformations The risk of foetal malformations is 4-8% if one AED is taken (compared with 13% in the general population) and 15% if more than one AED is taken.2-0. emotional stress and hyperventilation may increase the risk of seizures. at a dose of at least 4 mg daily. An elective caesarean section is also recommended if frequent GTCS or complex partial seizures occur during the last weeks of pregnancy. Owing to the risk of potentially fatal bleeding in infants born to mothers on AEDs (particularly hepatic enzyme-inducing drugs). carbamazepine and phenytoin.5% in the general population). lamotrigine. 53 . however. However.The risk of seizures is greatest during the delivery period. 1-2% of epileptic women suffer a GTCS during labour.1. starting before conception. Folic acid supplementation has been shown to have a protective role in the prevention of NTDs. and is recommended for all women of child-bearing age taking AEDs. The reported teratogenic effects of commonly used AEDs are summarised in table 20. As pain. in particular. If there is evidence of bleeding in the newborn. phenytoin monotherapy has not been shown to be associated with an increased risk of major congenital abnormalities. of greatest fear is the association of valproate with NTDs (1-2% risk compared with 0. epidural anaesthesia should be considered early during labour. the treatment of the seizure itself should proceed in the usual manner. and/or their newborns given 1 mg of vitamin K1 intramuscularly at birth. This must be made known to the patient and her obstetrician so that necessary precautions can be taken.

IMPORTANT STEPS IN THE MANAGEMENT OF PREGNANT WOMEN WITH EPILEPSY • Preconception counselling of patient about risks of teratogenesis and possible adverse effects of uncontrolled seizures to maternal health and pregnancy • Preconception review of AEDs. urogenital malformations NTDs Cleft palate Cleft palate Cleft palate NTDs? Recent evidence suggests no increased risk 9. craniofacial defects.1. As most AEDs are secreted in breast milk.1. cardiac defects. aim for minimal effective monotherapy if active epilepsy.5) • Vitamin K1 in last month of pregnancy. or for neonate • Reassure patient that >90% pregnancies proceed with no problem in women with epilepsy 54 . If this happens. digital hypoplasia? Recent evidence suggests no increased risk NTDs.TABLE 20: Teratogenic effects of AEDs AED Phenytoin Valproate Carbamazepine Ethosuximide Barbiturates Vigabatrin Lamotrigine Reported teratogenic effects Cleft lip and palate.9 Breast feeding and the puerperium The dose of the AEDs should be reduced to pre-conception levels over the few weeks following delivery if the dose has been increased during pregnancy to avoid drug toxicity. cardiac defects. Mothers should breastfeed their babies whilst seated on floor cushions and should not be allowed to bathe their babies in a bathtub unless assisted to avoid dropping their babies in case a seizure occurs. the infant may become sedated or hypotonic if breast-fed (occurring in 5-10% of babies). consider drug withdrawal if seizurefree • Commence folic acid supplements preconception • Screen for malformations • Monitor condition and AED concentrations through pregnancy (refer to section 9. the breastfeeds can be reduced and supplemented with bottle feeds.

adequate sunlight exposure.1.2 Epilepsy in children Most epilepsies begin in childhood. resulting in the child being mislabelled as "epileptic" and subjected to unnecessary treatment. an initial screen (blood glucose. osteoporosis and osteomalacia. The long term prognosis depends 55 . and treated with calcium and vitamin D supplementation as necessary. and phenobarbitone) as well as sodium valproate. cessation of smoking. but AEDs should be used if the seizures are recurrent. carbamazepine. If the history is not suggestive of perinatal asphyxia. Conversely. Weight-bearing exercises. Care should be taken to avoid misdiagnosis. family history and physical examination. Simultaneous video-EEG recording of these events might resolve some of this difficulty.9. not all movements are seizures. A trial of pyridoxine (and perhaps folinic acid) is warranted if seizures are resistant to standard AEDs. and avoidance of caffeine should be encouraged. cranial ultrasound and basic workup for sepsis and cerebrospinal fluid analysis) should be done. with and without altered consciousness. calcium. Neonatal seizures are often either under. and most seizures are fragmented and subtle. mainly because the pharmacokinetics of other drugs has not been worked out in the neonate. preceding antenatal and intrapartum events. magnesium and acid-base balance. followed by more specific investigations for metabolic disorders and underlying brain malformations. 9. There are many paroxysmal events.10 Bone health Women are more likely than men to develop bone health abnormalities. including osteopenia. metabolic disorder or infection. but there is still the issue of "electroclinical dissociation".or over-diagnosed. electrolytes. It is important to make the correct diagnosis and syndromic classification. All patients who have been taking these drugs for more than 5 years should be subjected to a bone densitometry. for appropriate counselling and treatment. Early treatment of metabolic bone disease will reduce morbidity and mortality from long bone fractures. from the hepatic enzyme inducing AEDs (namely phenytoin. The aetiologies are varied and may be determined by a careful history of the age of onset. Phenobarbitone and phenytoin are the first line AEDs. that mimic seizures (chapter 3). usually before 15 years of age. Large doses of BDZ should be used with caution in very premature infants or those with severe unconjugated jaundice as bilirubin can be displaced from its binding site. Generalised tonic clonic seizures do not occur in neonates. Treatment is targeted at correcting the underlying electrolyte disturbance.

The additional problems of polypharmacy (producing increased side effects).more on the underlying aetiology than the severity of the seizures during the neonatal period itself. Teachers need specific instructions on the measures that need to be taken when the child has a seizure at school. Acute fatal liver failure has been reported with the use of sodium valproate in infants who have developmental delay and are on multiple AEDs. the inheritance (if any). and the care-giver given specific guidance on the treatment of prolonged seizures (rectal diazepam) and intercurrent illnesses in situations where the seizures are exacerbated during febrile illnesses. this appears to be related more to an undiagnosed inborn error of metabolism than to the direct effect of the drug itself. Uncontrolled seizures with onset in early childhood are associated with a higher incidence of mental retardation. very often it is the underlying brain pathology that leads to both mental retardation and epilepsy. The EEG tends to be more useful in predicting recurrence of seizures than in adults. Schooling and leisure activities also need to be discussed. The need for good communication between the school teacher. Rapid growth in the preschool age has important effects on the dose requirements and drug metabolism. family and doctor cannot be overemphasised. Parent and patient education is a vital but often neglected aspect of management. Once the diagnosis of epilepsy is made. Teacher and peer group acceptance are crucial for the child's self esteem. pseudoseizures. children tend to outgrow their seizures. Sandifer's syndrome) often complicate the picture. However. an explanation of what epilepsy and seizures are. in most epilepsies. While it is likely that uncontrolled seizures contribute to intellectual impairment. Generally. and recommended doses based on weight are often 2-4 times higher than adults. Hence. concurrent use with other medication like antipyretics and antibiotics) are discussed. the arbitrary period for AED therapy is until the patient has been seizure free for two years. Phenobarbitone is known to cause hyperactive behaviour.g. and non-epileptic episodic movements (e. Some AEDs have specific adverse effects in children that are not common in adults. especially with concomitant sodium valproate therapy. Treatment considerations (purpose and objectives. and prognosis is necessary. and appears related to the rate at which the drug is escalated. possible adverse effects. learning difficulties and behavioural problems. there are some intractable epilepsy syndromes that begin in childhood and carry a poor prognosis. There is a tendency to 56 . The incidence of rashes with the use of lamotrigine is higher in children than adults. compliance and dosing schedule.

olfactory hallucinations. Drug interactions are also more important among the elderly. For example. Unlike the complex partial seizures seen in younger patients. Most AEDs are metabolised by the liver and excreted by the kidney. as the elderly often take many other medications. Nevertheless. As far as treatment is concerned. and thus mistaken for a TIA. orofacial and limb automatisms.5% as compared to 0. degenerative diseases of the CNS (10%). On the other hand. The EEG changes are often non-specific. the epileptic focus in the elderly more often involves the parietal and frontal lobes rather than the temporal lobe. differentiation from cardiac syncope may be difficult. Tonic posturing may be interpreted as paralysis. one should note the many differences in pharmacodynamics. blackouts. The principal causes of epilepsy among the elderly include cerebrovascular disease (30-40%)."overprotect" the child with epilepsy. and appropriate advice on the type of physical activities that the child can participate is needed. a large proportion of cases remain cryptogenic (3040%). elderly patients with epilepsy often have a good response to AED treatment. Generalised convulsions and complex partial seizures are the main clinical manifestations of the seizures in the elderly. and “dizziness” are common presentations. Thus. Proper counselling and advice for both child and family goes a long way towards improving the quality of life in these children. the required total dose of AED may be lower. It is thus not surprising that the elderly have increased side effects to AEDs.3 Epilepsy in the elderly The prevalence of active epilepsy in those >70 years is 1. As hepatic and renal functions diminish with age. Epilepsy may adversely affect family relationships and lead to further psychosocial disturbances.5% for the general population. and tumours (10%). 9. Thus. Postictal confusion may be quite prolonged. 57 . altered cognition. and déjà vu are less common among the elderly. aspirin may compete with phenytoin and valproic acid for proteinbinding and cause toxicity. which are common in the elderly. periods of staring and unresponsiveness.

In this regard.g. epilepsy surgery may be an option. and the neurosurgeon the contractor. The onus is on the neurologist to ensure that the epileptogenic zone is correctly identified. As this guidelines is being prepared and published. treatment must now be tailored to the individual patient. CONCLUSION The management of epilepsy is a rapidly evolving area of neurology. and understand that the patient’s seizure is only one of several possible manifestations or symptoms of the entire epilepsy syndrome. Greater efficacy in comparison with the older AEDs is unlikely to be the reason for the change in clinical practice. An individual patient may have several seizure types. The choice of AED will depend on several factors. The mode of action of most of the newer AEDs is poorly understood. and not all patients are amenable to epilepsy surgery. and education must feature prominently in the physician’s management plan. the newer AEDs are being tested in large monotherapy trials. initial AED therapy was based on personal preference and availability. pregnancy. In cases where AEDs fail to control the seizures. require a brain scan. which may change the order in which we choose AEDs for a particular epilepsy syndrome in the future. and that the operation produces a good seizure as well as neurological outcome. most importantly. employment. The number of cryptogenic cases of epilepsy will continue to decline as the quality of neuroimaging improves and our knowledge about the genetics of seizure generation expands. the epilepsy syndrome and psychosocial factors. He or she must also be sensitive to the special needs of children and the elderly. the neurologist may be viewed as the architect. or a brain tumour with malignant potential). but these drugs have proven efficacy in large randomised trials. Not all patients.10. 58 . Pharmacogenomics in the future may allow us to identify the AED that has the greatest efficacy and least side effects for an individual patient. a vascular malformation. Whereas previously. Correct diagnosis of the epilepsy syndrome will guide the physician to select investigations judiciously. non-pharmacological issues. Long-term. including driving. The attending physician must be able to differentiate epileptic seizures from other paroxysmal events that may mimic an epileptic attack. Epilepsy surgery should be considered early in patients where the MRI-identified lesion per se may be lethal (e. or when the side effects are intolerable despite good seizure control. for instance. The presurgical evaluation of a patient is the single most important pre-requisite of epilepsy surgery. albeit as add-on therapy in refractory cases. but rather the better safety and tolerability profile of the newer AEDs. but only one epilepsy syndrome.

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etc? Parenthood Has advice been given on: • fertility. fires.g. bathing. stairs. cycling.g. insurance companies. swimming. reviewing medication and seizure control)? Ongoing dialogue Has the parent/care-giver been encouraged to: • ask questions during clinic follow-up? • keep a record of the seizures (seizure diary)? • report any changes in seizure pattern and general health to own doctor? 67 . riding)? • informing schools. employers.g.Appendix 1: Counselling checklist The diagnosis Does the patient/care-giver know/understand: • that the diagnosis is epilepsy? • what epilepsy is? • what the seizures are like ? The medication Does the patient/care-giver know: • the purpose of the medication? • the importance of compliance? • about possible side effects? • about drug interactions e. pregnancy and parenthood? • the importance of pregnancy planning (e. with oral contraceptive pills? • the dose of the AED? Life-style Has guidance been given on: • leading an active and independence life? • regular and sufficient sleep? • safety at home (e.g. cooking)? • safety/risk for sport and recreation (e.