The Diagnosis and Management of Epilepsy: Journal of Tropical Pediatrics January 2002

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The Diagnosis and Management of Epilepsy

Article  in  Journal of Tropical Pediatrics · January 2002


DOI: 10.1093/tropej/47.6.320 · Source: PubMed

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Review
Synthèse

Diagnosis and management of epilepsy

Warren T. Blume
Abstract pected if syncope-like attacks occur in other circumstances,
particularly upon exercise.
THIS ARTICLE CONCISELY DESCRIBES the more common epilepsy con- Excessive daytime sleep, as episodes of microsleep, oc-
ditions and will enable physicians to efficiently evaluate and curs in children at school and in adults; it superficially re-
manage these disorders. Salient aspects of the history and exami- sembles temporal lobe seizures or absence attacks. The pa-
nation, together with electroencephalography, will usually deter- tient stares without specific warning or appears inattentive;
mine the epilepsy syndrome (category), forming the basis for any automatisms may occur. Unlike seizures, episodes of mi-
further investigation and possible antiepileptic therapy. Imaging crosleep can be reliably and instantly aborted with an affer-
may be required in some circumstances.
ent stimulus. Evidence of sleep deprivation includes less
CMAJ 2003;168(4):441-8 than 7 hours of sleep, hypnic jerks in drowsiness, frequent
dreaming, prominent snoring, morning arousal only with

E
pilepsy and stroke are the 2 most common neurologi- stimuli, morning irritability, excessive caffeine intake and
cal disorders: at any one time 7 in 1000 people in the prolonged sleeping on weekends.
general population have epilepsy. Epilepsy usually Psychogenic nonepileptic events may be defined as “a
begins in childhood, potentially impeding education, em- paroxysmal behavioural pattern mimicing epileptic seizures
ployment, social relationships and development of a sense of and initiated by psychological mechanisms”.1 Diagnosis de-
self-worth. Prompt, accurate diagnosis with appropriate so- pends principally on symptomatology (Table 2). A physician
cial and medical management will optimize the situation. A should suspect such events in any patient with an apparently
family physician, in conjunction with a neurologist, can as- intractable cryptogenic “seizure disorder,” except in infants
certain (a) if the episodes represent epileptic seizures and or elderly people. Psychogenic events may mimic any type of
(b) if so, which epileptic syndrome they represent. epileptic seizure and may occur as a pseudostatus epilepticus.
A harmonized partnership between family physician and Distinguishing between psychogenic and frontal lobe epilep-
neurologist will facilitate the recognition and care of tic seizures may be difficult although the latter are shorter
epileptic disorders. As the role of the family physician in and occur principally at night. Psychogenic events may su-
the care of patients with epilepsy increases, the principles pervene in some truly epileptic patients. Electroencephalo-
delineated in this article will be ever more utilized. gram (EEG) monitoring may be required. However, epilep-
tic seizures that arise from mesial or inferior cortical surfaces
Differential diagnoses may demonstrate no interictal or ictal EEG abnormality. At
the Epilepsy Programme in London, Ont., we have devel-
Before determining whether paroxysmal events repre- oped a system for identifying suspected psychogenic attacks
sent an epileptic disorder, one must consider 2 alternatives: that consists of taking a detailed description of the attack, 24-
(a) nonepileptic events mimicking epileptic seizures (Table hour telemetered EEG recordings over 2–3 days and a clini-
1) and (b) true epileptic seizures caused by a nonneurologi- cal psychological consultation including the Minnesota Mul-
cal condition (Box 1). Three conditions are common imita- tiphasic Personality Inventory-2 (MMPI-2). The MMPI-2
tors of epilepsy: syncope, excessive daytime sleep and pseu- contains profiles of significant sensitivity and specificity for
doseizures. anxiety, somatization and hysteria, components that predis-
Table 2 lists several distinguishing manifestations of pose a person to pseudoseizures. The evaluation concludes
syncope, which resembles a generalized tonic-clonic with an interview with the patient, one or more close rela-
(GTC) seizure in the middle of the attack but not at its on- tives, the clinical psychologist and the neurologist.
set or termination. Almost always while in an erect sitting An erroneous diagnosis of epilepsy carries serious conse-
or standing position, the patient feels faint, vision may blur, quences. Missing a cardiac arrhythmia could be fatal. The pa-
the face becomes pale, sweating may occur, and the patient tient could be unnecessarily exposed to side effects of
falls atonically with occasional bilaterally synchronous tonic antiepileptic medications; this occurs principally in emergent
or myoclonic phenomena followed by rapid recovery, albeit situations with pseudostatus epilepticus. Potentially treatable
with fatigue. The principal differential diagnosis is a treat- psychiatric conditions could be overlooked. The patient could
able cardiac arrhythmia, and this should be strongly sus- unnecessarily lose his or her driver’s licence and occupation.

CMAJ • FEB. 18, 2003; 168 (4) 441

© 2003 Canadian Medical Association or its licensors


Blume

Principal epilepsy syndromes seizures, whereas ethosuximide, although equally effective,


only acts against absence seizures (Table 3).2–10
The first step in epilepsy management is identification
of the syndrome. A syndrome is a constellation of factors Juvenile myoclonic epilepsy and generalized
that defines each epileptic disorder and influences manage- tonic-clonic seizures upon awakening
ment. Syndrome determination hinges on seizure descrip-
tion and frequency, age at onset, neurological history and These adolescents usually present with a history of
functional enquiry, neurological examination and one or GTC seizures in sleep, within 1 hour of awakening or late
more EEGs. The neurological functional enquiry (review in the evening. Anxiety, sleep loss and alcohol ingestion
of systems) seeks areas of cognitive and other neurological are precipitants. Absence attacks occur in about 30% of
dysfunctions that may lead to syndrome identification. such patients. Myoclonus of the arms may occur shortly
Neuroimaging may aid in evaluation, but most syndromes after awakening or in the evening. The history of myo-
are defined by the afore-mentioned means. Most epileptic clonus is often difficult to obtain, leaving one with a diag-
disorders that a general physician will see will be manifesta- nosis of GTC seizures on awakening.11 Otherwise the syn-
tions of a syndrome. The following describes the most dromes are identical.
common ones.
Management
Absence seizures
The EEGs may show 3–4-Hz bisynchronous spike-
Absence seizures begin in childhood or early adoles- waves but may be normal.
cence, with 5–20-second episodes of sudden arrest of activ- Treatment options are (a) none, if precipitants can be
ity, staring straight ahead or upward, occasionally with avoided, (b) valproate, the most effective, (c) lamotrigine, if
myoclonic activity of the eyelids, face or upper extremities, valproate gives side effects, or (d) phenytoin, at a low dose
and ending abruptly without postictal confusion. General- (e.g., about 200 mg/d) (Table 3).
ized tonic-clonic (GTC; “grand mal”) seizures occur in
about one-third of such patients, usually in adolescence. Benign focal epilepsy of childhood
Findings from the neurological functional enquiry and ex- with “rolandic spikes”
amination, including cognition, are normal. Prognosis
varies such that “growing out of it” cannot be assured. This benign focal epilepsy has no identifiable brain le-
sion. It accounts for 10%–16% of all patients with seizures
Management under the age of 15 years and is 3–4 times more common
than childhood absence seizures.12,13 An otherwise healthy
The EEG shows sudden bursts of bilaterally synchro- child has episodes of a unilateral unusual sensation in the
nous 3-Hz spike-waves, whose quantity usually reflects the mouth, face or one arm, with hypersalivation. Focal tonic
frequency of absence seizures. or clonic phenomena involving the mouth, tongue or arm
Complete eradication of absence attacks may require ex- may occur, and speech may arrest. Most of such attacks be-
cess medication, and therefore a compromise between ade- gin during sleep, awakening the patient. This syndrome
quate dosage and attack frequency may be required. Val- may present as nocturnal GTC seizure followed by a brief
proate and lamotrigine act against absence and GTC Todd’s paresis and may be the most common cause of an
idiopathic nocturnal GTC seizure in children between 5
and 10 years of age.
Table 1: Seizure-like phenomena and possible interpretations
False seizure Management
interpretation Seizure-like events
Temporal Daytime microsleep, narcolepsy, night terrors,
This benign syndrome cannot be diagnosed without
panic attacks, fugue states, transient global demonstration of typical “rolandic” spikes on an EEG of a
amnesia, pseudoseizures, hyperventilation nonsedated patient, whether awake or asleep, but 2 EEGs
Focal sensory TIAs, hyperventilation may be required to disclose their presence. Lack of such
Focal motor Pseudoseizures, TIAs, movement disorders spikes draws into question this diagnosis and may prompt
Occipital Migraine further evaluation, including imaging. The seizure ten-
Absence Daytime microsleep dency ends by adolescence in 98% of cases, and medication
Atonic Syncope, cardiac arrhythmias, cataplexy, can then be omitted.
TIAs, hyperventilation No treatment may be necessary if the seizures occur
Myoclonic Syncope, cardiac arrhythmias rarely and do not disrupt the child’s activities. Alternatively,
Generalized Pseudoseizures, syncope, hyperventilation a low dose of carbamazepine, lamotrigine, valproate or
Note: TIAs = transient ischemic attacks. phenytoin will often suffice.

442 JAMC • 18 FÉVR. 2003; 168 (4)


Epilepsy

Temporal lobe seizures Special issues


The temporal lobe is the most common site of focal The first seizure
seizures, and the seizures most often begin in childhood or
adolescence. Aurae include an epigastric sensation, fear and Management of a patient with a first epileptic seizure
various types of visual, olfactory or auditory experiential depends primarily on clinical analysis and EEG findings.
phenomena. Cognition may be impaired during the Imaging may be required for (a) seizures not associated
seizure, manifesting as confusion, a receptive or expressive with a benign syndrome, (b) focal seizures, (c) nonprecipi-
dysphasia, apraxia, distraction tated attacks, (d) an associated
by an experiential phenome- central nervous system disor-
non or amnesia. Thus, the der and (e) subsequent unex-
term “dyscognitive” will re- Box 1: Conditions that can cause a single pectedly refractory seizures.
place “complex partial” for this seizure or transient epileptic disorder Look for avoidable precipi-
seizure type. tants. Sleep loss, stress and
• Febrile seizure in early childhood
Unilateral or bilateral man- alcohol withdrawal may pro-
ual automatisms may occur • Sleep deprivation voke GTC seizures. 15 Only
when cognition is impaired. • Hypoglycemia about 3% of patients with such
Dystonic posturing should be • Hyponatremia “stress-induced” attacks will
sought by observation or his- • Metabolic encephalopathy develop spontaneous seizures.
tory-taking, as it almost always About 8% of patients with
• Central nervous system infection
occurs in the arm contralateral a first seizure may have a
to seizure origin. Chewing and • Alcohol or drug withdrawal brain tumour.16 This drops to
swallowing may occur. Ictal • Drug abuse (e.g., amphetamines, cocaine) 1% among patients with a
speech, even if nonsensical, • Pharmacological agents (e.g., aminophylline, normal neurological func-
suggests involvement of the phenothiazines and some analgesics) tional enquiry. Such would
temporal lobe nondominant • Acute traumatic seizures (mild–moderate include any personality or
for language. A GTC seizure head trauma followed immediately by a cognitive change, or newly ac-
may evolve immediately from a tonic-clonic seizure) quired motor, somatosensory
dyscognitive one and is often or visual change. In this group
heralded by contralateral head the chance diminishes to
and eye deviation. Alterna- 0.6% if the findings on neu-
tively, GTC seizures may appear independently. rological examination are normal, and to 0.3% if the EEG
Prolonged febrile seizures may have occurred in infancy. shows no focal abnormality.
Memory may be impaired if the epilepsy and pathology re- In both adults and children, the following augment the
side in both temporal lobes or principally in the temporal risk of recurrence from about 33% to at least 50%: focal
lobe dominant for language. Subtle or overt signs of unilat- seizures, abnormal findings on neurological examination,
eral motor dysfunction in the face, hand or leg should be pre-existing neurological disorder and focal spikes or gen-
sought on neurological examination. eralized spike-waves on EEG.17–19
Although antiepileptic drugs reduce the risk of early
Management seizure recurrence, their early use apparently does not af-
fect longer term remission rates.20,21 Moreover, compliance
Temporal lobe interictal EEG spikes should be sought with antiepileptic drug therapy after a single seizure varies
to confirm the clinical diagnosis, but more than one EEG among patients.
may be required. The lack of temporal lobe epileptiform
activity on about 3 routine EEGs suggests the need to re- Women’s issues
assess the diagnosis. MRI scanning is clearly warranted to
determine the side and nature of the abnormality and Catamenial epilepsy
its cause.
Generally favoured medications include carbamazepine, Catamenial epilepsy refers to the appearance or worsen-
phenytoin, lamotrigine and topiramate.14 However, tempo- ing of seizures in the perimenstrual period or, rarely, in the
ral lobe epilepsy may not respond adequately to antiepilep- entire second half of the menstrual period if no proges-
tic drugs. In fact, the need to use a second medication ei- terone is secreted (“inadequate luteal phase” syndrome).22
ther as monotherapy or dual therapy reflects the severity of This relates to a shift of the ratio between estrogen (pro-
the disorder, reducing somewhat the chances that adequate epileptogenic) and progesterone (anti-epileptogenic).
control will ever be obtained. In this instance, epilepsy Serum levels of antiepileptic drugs may drop perimenstru-
surgery should be considered. ally, at which time a slight dose increase may be required.

CMAJ • FEB. 18, 2003; 168 (4) 443


Blume

Contraception taking oral contraceptives23 and suggests the need to in-


crease the dose of estradiol from 35 µg to 50 µg if an en-
Enzyme-inducing drugs such as carbamazepine, oxcar- zyme-inducing antiepileptic drug is given. Midcycle bleed-
bazepine, phenytoin, phenobarbital, primidone and topira- ing may indicate that estrogen levels are too low to block
mate may accelerate the metabolism of both estrogen and ovulation. Drugs that do not increase the risk of oral con-
progesterone, thereby reducing their concentrations by up traceptive failure include valproate, lamotrigine and gaba-
to 50%. This increases the risk of pregnancy in patients pentin. Oral contraceptives do not impair seizure control.

Table 2: Differentiation of generalized tonic-clonic seizures from pseudoseizures and syncope


Generalized
Characteristic tonic-clonic seizure Pseudoseizure Syncope
Circumstances
Situation Awake or asleep Awake Usually upright; any position if
cardiogenic
Precipitating factors Sleep loss, alcohol Emotion Emotion, injury, heat, crowds;
withdrawal, flashing lights none if cardiogenic
Presence of others Variable Usual Variable
Motor phenomena
Vocalization At onset, if any During course None
Location of motor component Proximal limb Proximal limb None
(if present)
Generalized motor Tonic, then clonic Tonic; flailing; struggling or Usually atonic; if syncope lasts
thrashing, or both > 20 seconds: tonic, then clonic
Tonic posture Partial flexion or straight Opisthotonic –
Head movements To one side or none Side to side –
Clonus/limb jerks Bilaterally synchronous Asynchronous Bilaterally synchronous
Purposeful movements Absent Occasional, including avoidance Absent
Biting Tongue, inside mouth Lips, arms, other people Tongue biting rare
Babinski’s sign Present Absent Absent

Autonomic features
Micturition Frequent Rare Occasional
Eyes Open Closed Open
Pupils Dilated or hippus during Normal Dilated
attacks
Colour Cyanotic or grey Rubor or normal Pale
Pulse Rapid, strong Normal Slow if vasovagal, weak if
vasodepressor; that of
arrhythmias if cardiogenic
Cognitive and behavioural aspects
Awareness Lost Preserved Lost or impaired
Talking None Occasional None
Restraint necessary To prevent injury; 1 person To control violence; many people Never
suffices required
Timing
Usual duration 1–5 min 5–60 min 1–2 min
Onset Sudden Gradual Gradual; possibly sudden if
cardiogenic
Sequence of symptoms Stereotyped Variable Stereotyped
Termination Spontaneous Spontaneous or induced by supra- Rapid
orbital pressure, suggestion

Sequelae
Injury Frequent, mild; scalp, face, Rare, but multiple bruises If sudden onset
common possible; scalp, face, rare
Postictal Tired, confused, sleeps Alert, emotional outburst Regains consciousness in
2–3 min; alert but tired

444 JAMC • 18 FÉVR. 2003; 168 (4)


Epilepsy

Pregnancy Poor preconception seizure control predicts incomplete


control in pregnancy.
The following considerations derive from 2 funda- In preparing a patient with an apparent seizure disorder
mental questions: Do seizures or antiepileptic drugs for pregnancy, the treating physician should ask 3 questions:
harm the fetus? Are the events epileptic seizures? Does the epilepsy still
A prolonged GTC seizure may produce fetal distress or require treatment? Can any polytherapy be changed to
death.24 However, nonconvulsive seizures are apparently monotherapy?
innocuous.25 There is no evidence that seizures create de- Antiepileptic medication levels may decline during preg-
formities. Seizures remain unchanged in 60%, are in- nancy because of increases in drug metabolism, excretion
creased in 30% and decreased in 10% of pregnancies.23 and volume of distribution, and decreases in absorption,

Table 3: Some aspects of principal antiepileptic drugs


Drug*; side effect Incidence Avoidance Management

Carbamazepine (focal and generalized seizures)


Rash, maculopapular 5% Introduce drug Transient dose reduction
slowly
Stevens–Johnson syndrome Very rare (case reports only) Introduce drug Admit to hospital; stop drug
slowly
Interaction with other antiepileptic drugs Common, variable – Possible dosage adjustments
Transient leukopenia 10%–20% – Complete blood count every
3–6 mo in first year
Persistent leukopenia 2% – Complete blood count at intervals
or change drug
Aplastic anemia 1 in 200 000 – Stop drug

Lamotrigine (focal and generalized seizures, including absence seizures)


Rash, mild 3%–5% Introduce drug very Dose reduction
slowly
Rash, severe 0.1% in adults, 1%–2% in Introduce drug very Admit to hospital; stop drug
children slowly
Diplopia Dose dependent – Dose reduction

Phenytoin (Dilantin) (focal and generalized seizures)


Augments metabolism of oral Common – Dosage adjustment of affected
contraceptives, anticoagulants, other medications
antiepileptic drugs and dexamethasone
Rash 5% – Reduce dose or stop drug
Gingival hypertrophy 25% Meticulous dental Dosage adjustment
hygiene
Mild hirsutism 75% – Stop drug if female patient
Topiramate (focal and generalized seizures)
Weight loss 10% – Reassure patient as levels out;
reduce dose
Mental sluggishness Dose dependent – Dose reduction
Fatigue Dose dependent – Dose reduction
Kidney stones 1%–2% – Stop drug
Glaucoma Very rare (case reports only) – Stop drug
Valproate (focal and generalized seizures, including absence seizures)
Weight gain 40%–100% Exercise Dose reduction
Hair loss 1%–3% – None (side effect usually transient)
Liver failure 0.16% in children < 3 yr; lower – Stop drug
in older patients
Ethosuximide (absence seizures only)
Gastrointestinal irritability 20%–33%, usually transient – Dose reduction
Depression, psychosis, leukopenia Very rare (case reports only) – Reduce dose or stop drug
*Cost per 100 tablets: Tegretol $34, lamotrigine $146, phenytoin $10, topiramate $219, Epival $87, ethosuximide $31.
Sources: References 2–10. This table was adapted, with permission, from Blume WT: Diagnosis and management of epilepsy. Can J Contin Med Educ 2001;12(9):162-3.

CMAJ • FEB. 18, 2003; 168 (4) 445


Blume

protein binding and compliance. It is prudent to measure that of maternal serum.24 Ultrasonography at 16–18 weeks’
antiepileptic serum levels before conception, at the begin- gestation may be necessary as well.
ning of each trimester and during the last month in patients Hemorrhagic disease of the newborn may occur in an in-
with moderately severe seizure disorders. fant whose mother has lower than normal levels of vitamin
K–dependent clotting factors. This can be prevented with
Teratogenic effects 10–20 mg per day of vitamin K orally in the last month of
pregnancy23,25 (Dr. Renato Natale, Associate Chief, St.
The risk of major malformations in babies of mothers Joseph’s Health Centre and London Health Sciences Cen-
taking antiepileptic drugs is about 4%–8% as compared tre — University Campus, London, Ont.: personal commu-
with a baseline of 1%–3%.25 Most of this increased risk can nication, 2002). Oral vitamin K can be obtained in Canada
be attributed to unfavourable lifestyle, inadequate nutri- through the Special Access Programme.27,28
tion, high antiepileptic drug levels and polypharmacy.24,25
Therefore, if possible, change gradually to monotherapy, Postpartum considerations
which is usually a safe procedure.
As no single antiepileptic drug has been shown to be more Although antiepileptic drugs are detectable in breast
teratogenic than another, a pregnant woman should keep tak- milk, their concentrations are usually lower than those in
ing her current drug, which is pre- maternal serum. Breast-feeding
sumably the best antiepileptic should not be discouraged in
drug for her epilepsy. Barbitu- women with epilepsy, because
rates, phenytoin and ethosuximide Antiepileptic drug therapy: key points its advantages appear to out-
have been associated with con- weigh the rare (5%–10%) ad-
genital heart, cleft lip and palate • Monotherapy suffices for most seizure dis- verse effects to the baby of seda-
abnormalities. 24 Valproate and orders. tion, hypotonia and feeding
• Twice-daily dosing is most practical except
carbamazepine may produce difficulty. Drug withdrawal
in pregnancy, when dosing 4 times daily
neural tube defects and hydro- symptoms have been reported
prevents a serum level surge and therefore
cephalus, with an incidence of sporadically. 23 Antiepileptic
has less effect on the fetus.
neural tube defects of 1%–2% for • The severity of the seizure disorder, not the drug levels may gradually in-
valproate and 0.5%–1% for laboratory numbers, determines the “thera- crease over the first few weeks
carbamazepine.24,25 Effects of ox- peutic range.” Whatever serum drug level after birth as enzymatic induc-
carbazepine, topiramate and lam- renders the patient seizure free is adequate tion will have decreased.
otrigine are unknown. Minor mal- for that patient, even if it is below the labo- Mothers with incompletely
formations such as hypertelorism, ratory range. controlled seizures should avoid
low-set ears and nail-bed hypopla- • Dual therapy with most antiepileptic drugs at bathing an infant in the bathtub
sia may occur, but these usually do serum levels in the middle of the laboratory without another person present
not cause serious medical or cos- range impairs cognition. and should change the infant on
metic effects.23 • Effectiveness and side effects both depend the floor.
Adequate nutrition and folic on dosage. Small changes in dosage can
acid supplementation by about produce dramatic effects. Epilepsy in elderly patients
4–5 mg/d in any sexually active • Traditional antiepileptic drugs may be as
woman of childbearing age low- effective as new ones. Unfortunately, the incidence
ers the risk of major fetal malfor- • Fatigue is the most common side effect of and prevalence of epilepsy in-
most antiepileptic drugs.
mations, especially neural tube creases in elderly people because
• Phenytoin is the only antiepileptic drug
defects in babies of young women hemorrhagic and ischemic
that can be started at full dose.
taking antiepileptic drugs.23,24,26 As stroke, primary or secondary tu-
neural tube and cardiac malfor- mours, trauma, dementia and
mations occur during the first 5 metabolic disorders occur com-
weeks of pregnancy, adequate folic acid levels should be es- monly in this population. Fortunately, such epilepsy is sel-
tablished before conception. dom intractable. The consequences of uncontrolled
Because of high fetal demand, folic acid levels decline seizures may be greater in elderly patients: a fall may frac-
in pregnancy, reaching a nadir at term.23 Women who ture a hip or create a subdural hematoma, whereas a GTC
smoke have lower folic acid levels than those who do not seizure may crush a vertebra, giving back pain. A postictal
smoke. High folic acid levels do not appear to exacerbate state may manifest as memory loss, cognitive impairment,
a seizure disorder. or an increase in a hemiparesis or dysphasia.
An expert obstetric opinion is needed to monitor for The principal differential diagnoses are syncope, sudden
congenital defects. This may involve α-fetoprotein screen- falls of elderly people, transient ischemic attacks or even
ing: that of amniotic fluid is apparently more reliable than sleep disturbances. Nonconvulsive status epilepticus ap-

446 JAMC • 18 FÉVR. 2003; 168 (4)


Epilepsy

pears more often in elderly people, manifesting as mild ders in elderly patients are focal with possible secondary
confusion and forgetfulness or total unresponsiveness for generalization, carbamazepine and phenytoin would be ap-
hours or days. propriate drugs.14,29

Management Driving

Diagnostic tests include EEG, CT scanning and meta- The loss or suspension of a driving licence significantly
bolic studies. The need for antiepileptic drugs and ongo- disrupts life, but the medical, emotional and legal impacts of
ing medication should be reviewed to diminish polyphar- a medically related driving injury to others or self potentially
macy and its complications. The choice of any needed produce greater anguish. These opposing considerations
antiepileptic drug is guided by efficacy, ease of introduc- have led to the development by the Canadian Medical Asso-
tion and administration, potential drug interactions and ciation of guidelines for physicians (Table 4).30 Although
likelihood of significant side effects. As most seizure disor- studies have shown the risk of motor vehicle crashes to be

Table 4: Guidelines for determining a patient’s fitness to drive


Seizures Private drivers*
Single, unprovoked seizure before • Not drive for at least 3 mo and
a diagnosis • Get neurological assessment, including EEG and CT
scan
After epilepsy diagnosis Drive if:
• 12 months seizure free on medication† and
• Physician has insight into patient compliance
• Physician caution against fatigue, alcohol
After surgery to prevent epileptic • Resume driving if 12 months seizure free after
seizure surgery†
Seizures in sleep or immediately • Drive if seizures only occur in sleep or upon
upon awakening awakening for at least 5 years (can reduce period if
neurologist agrees)
Medication withdrawal or change
(a) Initial withdrawal or change • Not drive for a period of 3 months from the time
medication has been discontinued or changed
(b) If seizures recur after withdrawal • Resume driving if take medication according to the
or change physician’s instructions and
• Seizure free for 6 months (can reduce period if
neurologist agrees)
(c) Long-term withdrawal and • Drive any vehicle if seizure free off medication for
discontinuation of medication 5 years
Auras (simple partial seizures) Drive if
• No impairment in level of consciousness or
cognition
• Seizures are unchanged for more than 12 months
• Neurologist approves
Alcohol-withdrawal induced Drive if
seizures • Remain alcohol free and seizure free for 12 months
• completed a recognized rehabilitation program for
substance dependence
Febrile or toxic convulsion • No concern if fully recovered from illness
Syncope, sudden falls • Single, fully explained event: careful observation only
• Multiple, unexplained events: not drive until
explained, corrected
Note: EEG = electroencephalogram, CT = computed tomography.
*A private driver is one who drives less than 36 000 km a year or spends less than 720 hours a year behind the wheel, drives
a vehicle weighing less than 11 000 kg and does not earn a living by driving. For guidelines pertaining to professional drivers
with seizures, refer to reference 30.
†Most private drivers with epilepsy resume driving after being seizure free for 12 months (irrespective of the treatment
modality). This 12-month period may be reduced to 6 months on the recommendation of a neurologist.
Source: Determining medical fitness to drive: a guide for physicians.30

CMAJ • FEB. 18, 2003; 168 (4) 447


Blume

only equal or one-third greater among drivers with epilepsy 13. Loiseau P. Idiopathic and benign partial epilepsies. In: Wyllie E, editor. The
treatment of epilepsy. Principles and practice. 3rd ed. Philadelphia: Lippincott
as compared with the general population,31 this near equality Williams & Wilkins; 2001. p. 475-84.
may have been achieved by the implementation of the 14. Karceski S, Morrell M, Carpenter D. The expert consensus guideline series.
Treatment of epilepsy. Epilepsy Behav 2001;(Suppl 2):A1-50.
CMA’s guidelines. Risk assessment should include seizure 15. Friis ML, Lund M. Stress convulsions. Arch Neurol 1974;31:155-9.
frequency and loss of awareness or other faculty during the 16. Bardy AH. Decisions after first seizure. Acta Neurol Scand 1991;83:294-6.
17. Berg AT, Shinnar S. The risk of seizure recurrence following a first unpro-
events. Legal responsibility for failing to report possibly in- voked seizure: a quantitative review. Neurology 1991;41:965-72.
capable drivers is being placed ever more upon physicians. 18. Shinnar S, Berg AT, Moshe SL, Petix M, Maytal J, Kang H, et al. Risk of
seizure recurrence following a first unprovoked seizure in childhood: a
prospective study. Pediatrics 1990;85:1076-85.
This article has been peer reviewed. 19. Camfield PR, Camfield CS, Dooley JM, Tibbles JA, Fung T, Garner B. Epilepsy
after a first unprovoked seizure in childhood. Neurology 1985;35:1657-60.
Dr. Blume is Professor, Department of Clinical Neurological Sciences, Epilepsy 20. Camfield C, Camfield P, Gordon K, Dooley J. Does the number of seizures
and Clinical Neurophysiology, London Health Sciences Centre — University before treatment influence ease of control or remission of childhood epilepsy?
Campus, London, Ont. Not if the number is 10 or less. Neurology 1996;46:41-4.
21. First Seizure Trial Group. Randomized clinical trial on the efficacy of anti-
Competing interests: None declared.
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