begins in childhood, potentially impeding education, em-
ployment, social relationships and development of a sense of
self-worth. Prompt, accurate diagnosis with appropriate so-
cial and medical management will optimize the situation. A
family physician, in conjunction with a neurologist, can as-
certain (a) if the episodes represent epileptic seizures and
(b) if so, which epileptic syndrome they represent.
A harmonized partnership between family physician and
neurologist will facilitate the recognition and care of
epileptic disorders. As the role of the family physician in
the care of patients with epilepsy increases, the principles
delineated in this article will be ever more utilized.
pilepsy and stroke are the 2 most common neurologi-
cal disorders: at any one time 7 in 1000 people in the
general population have epilepsy. Epilepsy usually
Before determining whether paroxysmal events repre-
sent an epileptic disorder, one must consider 2 alternatives:
(a) nonepileptic events mimicking epileptic seizures (Table
1) and (b) true epileptic seizures caused by a nonneurologi-
cal condition (Box 1). Three conditions are common imita-
tors of epilepsy: syncope, excessive daytime sleep and pseu-
Table 2 lists several distinguishing manifestations of
syncope, which resembles a generalized tonic-clonic
(GTC) seizure in the middle of the attack but not at its on-
set or termination. Almost always while in an erect sitting
or standing position, the patient feels faint, vision may blur,
the face becomes pale, sweating may occur, and the patient
falls atonically with occasional bilaterally synchronous tonic
or myoclonic phenomena followed by rapid recovery, albeit
with fatigue. The principal differential diagnosis is a treat-
able cardiac arrhythmia, and this should be strongly sus-
pected if syncope-like attacks occur in other circumstances,
particularly upon exercise.
Excessive daytime sleep, as episodes of microsleep, oc-
curs in children at school and in adults; it superficially re-
sembles temporal lobe seizures or absence attacks. The pa-
tient stares without specific warning or appears inattentive;
automatisms may occur. Unlike seizures, episodes of mi-
crosleep can be reliably and instantly aborted with an affer-
ent stimulus. Evidence of sleep deprivation includes less
than 7 hours of sleep, hypnic jerks in drowsiness, frequent
dreaming, prominent snoring, morning arousal only with
stimuli, morning irritability, excessive caffeine intake and
prolonged sleeping on weekends.
Psychogenic nonepileptic events may be defined as “a
paroxysmal behavioural pattern mimicing epileptic seizures
and initiated by psychological mechanisms”.1Diagnosis de-
pends principally on symptomatology (Table 2). A physician
should suspect such events in any patient with an apparently
intractable cryptogenic “seizure disorder,” except in infants
or elderly people. Psychogenic events may mimic any type of
epileptic seizure and may occur as a pseudostatus epilepticus.
Distinguishing between psychogenic and frontal lobe epilep-
tic seizures may be difficult although the latter are shorter
and occur principally at night. Psychogenic events may su-
pervene in some truly epileptic patients. Electroencephalo-
gram (EEG) monitoring may be required. However, epilep-
tic seizures that arise from mesial or inferior cortical surfaces
may demonstrate no interictal or ictal EEG abnormality. At
the Epilepsy Programme in London, Ont., we have devel-
oped a system for identifying suspected psychogenic attacks
that consists of taking a detailed description of the attack, 24-
hour telemetered EEG recordings over 2–3 days and a clini-
cal psychological consultation including the Minnesota Mul-
tiphasic Personality Inventory-2 (MMPI-2). The MMPI-2
contains profiles of significant sensitivity and specificity for
anxiety, somatization and hysteria, components that predis-
pose a person to pseudoseizures. The evaluation concludes
with an interview with the patient, one or more close rela-
tives, the clinical psychologist and the neurologist.
An erroneous diagnosis of epilepsy carries serious conse-
quences. Missing a cardiac arrhythmia could be fatal. The pa-
tient could be unnecessarily exposed to side effects of
antiepileptic medications; this occurs principally in emergent
situations with pseudostatus epilepticus. Potentially treatable
psychiatric conditions could be overlooked. The patient could
unnecessarily lose his or her driver’s licence and occupation.
Diagnosis and management of epilepsy
Warren T. Blume
THIS ARTICLE CONCISELY DESCRIBES the more common epilepsy con-
ditions and will enable physicians to efficiently evaluate and
manage these disorders. Salient aspects of the history and exami-
nation, together with electroencephalography, will usually deter-
mine the epilepsy syndrome (category), forming the basis for any
further investigation and possible antiepileptic therapy. Imaging
may be required in some circumstances.
CMAJ • FEB. 18, 2003; 168 (4)
© 2003 Canadian Medical Association or its licensors
Principal epilepsy syndromes
The first step in epilepsy management is identification
of the syndrome. A syndrome is a constellation of factors
that defines each epileptic disorder and influences manage-
ment. Syndrome determination hinges on seizure descrip-
tion and frequency, age at onset, neurological history and
functional enquiry, neurological examination and one or
more EEGs. The neurological functional enquiry (review
of systems) seeks areas of cognitive and other neurological
dysfunctions that may lead to syndrome identification.
Neuroimaging may aid in evaluation, but most syndromes
are defined by the afore-mentioned means. Most epileptic
disorders that a general physician will see will be manifesta-
tions of a syndrome. The following describes the most
Absence seizures begin in childhood or early adoles-
cence, with 5–20-second episodes of sudden arrest of activ-
ity, staring straight ahead or upward, occasionally with
myoclonic activity of the eyelids, face or upper extremities,
and ending abruptly without postictal confusion. General-
ized tonic-clonic (GTC; “grand mal”) seizures occur in
about one-third of such patients, usually in adolescence.
Findings from the neurological functional enquiry and ex-
amination, including cognition, are normal. Prognosis
varies such that “growing out of it” cannot be assured.
The EEG shows sudden bursts of bilaterally synchro-
nous 3-Hz spike-waves, whose quantity usually reflects the
frequency of absence seizures.
Complete eradication of absence attacks may require ex-
cess medication, and therefore a compromise between ade-
quate dosage and attack frequency may be required. Val-
proate and lamotrigine act against absence and GTC
seizures, whereas ethosuximide, although equally effective,
only acts against absence seizures (Table 3).2–10
Juvenile myoclonic epilepsy and generalized
tonic-clonic seizures upon awakening
These adolescents usually present with a history of
GTC seizures in sleep, within 1 hour of awakening or late
in the evening. Anxiety, sleep loss and alcohol ingestion
are precipitants. Absence attacks occur in about 30% of
such patients. Myoclonus of the arms may occur shortly
after awakening or in the evening. The history of myo-
clonus is often difficult to obtain, leaving one with a diag-
nosis of GTC seizures on awakening.11Otherwise the syn-
dromes are identical.
The EEGs may show 3–4-Hz bisynchronous spike-
waves but may be normal.
Treatment options are (a) none, if precipitants can be
avoided, (b) valproate, the most effective, (c) lamotrigine, if
valproate gives side effects, or (d) phenytoin, at a low dose
(e.g., about 200 mg/d) (Table 3).
Benign focal epilepsy of childhood
with “rolandic spikes”
This benign focal epilepsy has no identifiable brain le-
sion. It accounts for 10%–16% of all patients with seizures
under the age of 15 years and is 3–4 times more common
than childhood absence seizures.12,13An otherwise healthy
child has episodes of a unilateral unusual sensation in the
mouth, face or one arm, with hypersalivation. Focal tonic
or clonic phenomena involving the mouth, tongue or arm
may occur, and speech may arrest. Most of such attacks be-
gin during sleep, awakening the patient. This syndrome
may present as nocturnal GTC seizure followed by a brief
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.
This benign syndrome cannot be diagnosed without
demonstration of typical “rolandic” spikes on an EEG of a
nonsedated patient, whether awake or asleep, but 2 EEGs
may be required to disclose their presence. Lack of such
spikes draws into question this diagnosis and may prompt
further evaluation, including imaging. The seizure ten-
dency ends by adolescence in 98% of cases, and medication
can then be omitted.
No treatment may be necessary if the seizures occur
rarely and do not disrupt the child’s activities. Alternatively,
a low dose of carbamazepine, lamotrigine, valproate or
phenytoin will often suffice.
JAMC • 18 FÉVR. 2003; 168 (4)
Table 1: Seizure-like phenomena and possible interpretations
TemporalDaytime microsleep, narcolepsy, night terrors,
panic attacks, fugue states, transient global
amnesia, pseudoseizures, hyperventilation
Pseudoseizures, TIAs, movement disorders
Syncope, cardiac arrhythmias, cataplexy,
Syncope, cardiac arrhythmias
Pseudoseizures, syncope, hyperventilation
Note: TIAs = transient ischemic attacks.
Temporal lobe seizures
The temporal lobe is the most common site of focal
seizures, and the seizures most often begin in childhood or
adolescence. Aurae include an epigastric sensation, fear and
various types of visual, olfactory or auditory experiential
phenomena. Cognition may be impaired during the
seizure, manifesting as confusion, a receptive or expressive
dysphasia, apraxia, distraction
by an experiential phenome-
non or amnesia. Thus, the
term “dyscognitive” will re-
place “complex partial” for this
Unilateral or bilateral man-
ual automatisms may occur
when cognition is impaired.
Dystonic posturing should be
sought by observation or his-
tory-taking, as it almost always
occurs in the arm contralateral
to seizure origin. Chewing and
swallowing may occur. Ictal
speech, even if nonsensical,
suggests involvement of the
temporal lobe nondominant
for language. A GTC seizure
may evolve immediately from a
dyscognitive one and is often
heralded by contralateral head
and eye deviation. Alterna-
tively, GTC seizures may appear independently.
Prolonged febrile seizures may have occurred in infancy.
Memory may be impaired if the epilepsy and pathology re-
side in both temporal lobes or principally in the temporal
lobe dominant for language. Subtle or overt signs of unilat-
eral motor dysfunction in the face, hand or leg should be
sought on neurological examination.
Temporal lobe interictal EEG spikes should be sought
to confirm the clinical diagnosis, but more than one EEG
may be required. The lack of temporal lobe epileptiform
activity on about 3 routine EEGs suggests the need to re-
assess the diagnosis. MRI scanning is clearly warranted to
determine the side and nature of the abnormality and
Generally favoured medications include carbamazepine,
phenytoin, lamotrigine and topiramate.14However, tempo-
ral lobe epilepsy may not respond adequately to antiepilep-
tic drugs. In fact, the need to use a second medication ei-
ther as monotherapy or dual therapy reflects the severity of
the disorder, reducing somewhat the chances that adequate
control will ever be obtained. In this instance, epilepsy
surgery should be considered.
The first seizure
Management of a patient with a first epileptic seizure
depends primarily on clinical analysis and EEG findings.
Imaging may be required for (a) seizures not associated
with a benign syndrome, (b) focal seizures, (c) nonprecipi-
tated attacks, (d) an associated
central nervous system disor-
der and (e) subsequent unex-
pectedly refractory seizures.
Box 1: Conditions that can cause a single
seizure or transient epileptic disorder
Look for avoidable precipi-
tants. Sleep loss, stress and
alcohol withdrawal may pro-
voke GTC seizures.15Only
about 3% of patients with such
“stress-induced” attacks will
develop spontaneous seizures.
About 8% of patients with
a first seizure may have a
brain tumour.16This drops to
1% among patients with a
normal neurological func-
tional enquiry. Such would
include any personality or
cognitive change, or newly ac-
quired motor, somatosensory
or visual change. In this group
the chance diminishes to
0.6% if the findings on neu-
rological examination are normal, and to 0.3% if the EEG
shows no focal abnormality.
In both adults and children, the following augment the
risk of recurrence from about 33% to at least 50%: focal
seizures, abnormal findings on neurological examination,
pre-existing neurological disorder and focal spikes or gen-
eralized spike-waves on EEG.17–19
Although antiepileptic drugs reduce the risk of early
seizure recurrence, their early use apparently does not af-
fect longer term remission rates.20,21Moreover, compliance
with antiepileptic drug therapy after a single seizure varies
Catamenial epilepsy refers to the appearance or worsen-
ing of seizures in the perimenstrual period or, rarely, in the
entire second half of the menstrual period if no proges-
terone is secreted (“inadequate luteal phase” syndrome).22
This relates to a shift of the ratio between estrogen (pro-
epileptogenic) and progesterone (anti-epileptogenic).
Serum levels of antiepileptic drugs may drop perimenstru-
ally, at which time a slight dose increase may be required.
CMAJ • FEB. 18, 2003; 168 (4)
• Febrile seizure in early childhood
• Sleep deprivation
• Metabolic encephalopathy
• Central nervous system infection
• Alcohol or drug withdrawal
• Drug abuse (e.g., amphetamines, cocaine)
• Pharmacological agents (e.g., aminophylline,
phenothiazines and some analgesics)
• Acute traumatic seizures (mild–moderate
head trauma followed immediately by a
Enzyme-inducing drugs such as carbamazepine, oxcar-
bazepine, phenytoin, phenobarbital, primidone and topira-
mate may accelerate the metabolism of both estrogen and
progesterone, thereby reducing their concentrations by up
to 50%. This increases the risk of pregnancy in patients
taking oral contraceptives23and suggests the need to in-
crease the dose of estradiol from 35 µg to 50 µg if an en-
zyme-inducing antiepileptic drug is given. Midcycle bleed-
ing may indicate that estrogen levels are too low to block
ovulation. Drugs that do not increase the risk of oral con-
traceptive failure include valproate, lamotrigine and gaba-
pentin. Oral contraceptives do not impair seizure control.
JAMC • 18 FÉVR. 2003; 168 (4)
Table 2: Differentiation of generalized tonic-clonic seizures from pseudoseizures and syncope
Situation Awake or asleepAwake Usually upright; any position if
Emotion, injury, heat, crowds;
none if cardiogenic
Sleep loss, alcohol
withdrawal, flashing lights
Presence of others Usual
Location of motor component
At onset, if any
Tonic, then clonicTonic; flailing; struggling or
thrashing, or both
Side to side
Occasional, including avoidance
Lips, arms, other people
Usually atonic; if syncope lasts
> 20 seconds: tonic, then clonic
Tongue biting rare
Partial flexion or straight
To one side or none
Tongue, inside mouth
Dilated or hippus during
Cyanotic or grey
Rubor or normal
Slow if vasovagal, weak if
vasodepressor; that of
arrhythmias if cardiogenic
Cognitive and behavioural aspects
To prevent injury; 1 person
To control violence; many people
Lost or impaired
Gradual; possibly sudden if
Sequence of symptoms
Spontaneous or induced by supra-
orbital pressure, suggestion
InjuryFrequent, mild; scalp, face,
Tired, confused, sleeps
Rare, but multiple bruises
possible; scalp, face, rare
Alert, emotional outburst
If sudden onset
PostictalRegains consciousness in
2–3 min; alert but tired
The following considerations derive from 2 funda-
mental questions: Do seizures or antiepileptic drugs
harm the fetus?
A prolonged GTC seizure may produce fetal distress or
death.24However, nonconvulsive seizures are apparently
innocuous.25There is no evidence that seizures create de-
formities. Seizures remain unchanged in 60%, are in-
creased in 30% and decreased in 10% of pregnancies.23
Poor preconception seizure control predicts incomplete
control in pregnancy.
In preparing a patient with an apparent seizure disorder
for pregnancy, the treating physician should ask 3 questions:
Are the events epileptic seizures? Does the epilepsy still
require treatment? Can any polytherapy be changed to
Antiepileptic medication levels may decline during preg-
nancy because of increases in drug metabolism, excretion
and volume of distribution, and decreases in absorption,
CMAJ • FEB. 18, 2003; 168 (4)
Table 3: Some aspects of principal antiepileptic drugs
Drug*; side effectIncidence AvoidanceManagement
Carbamazepine (focal and generalized seizures)
Rash, maculopapular5%Introduce drug
Transient dose reduction
Stevens–Johnson syndrome Very rare (case reports only)Admit to hospital; stop drug
Interaction with other antiepileptic drugs
Possible dosage adjustments
Complete blood count every
3–6 mo in first year
Complete blood count at intervals
or change drug
Aplastic anemia 1 in 200 000–
Lamotrigine (focal and generalized seizures, including absence seizures)
Rash, mild 3%–5% Introduce drug very
Introduce drug very
Rash, severe 0.1% in adults, 1%–2% in
Admit to hospital; stop drug
Diplopia Dose reduction
Phenytoin (Dilantin) (focal and generalized seizures)
Augments metabolism of oral
contraceptives, anticoagulants, other
antiepileptic drugs and dexamethasone
Common–Dosage adjustment of affected
–Reduce dose or stop drug
Dosage adjustment Meticulous dental
– Mild hirsutism75%Stop drug if female patient
Topiramate (focal and generalized seizures)
Weight loss 10%–Reassure patient as levels out;
Very rare (case reports only)
Valproate (focal and generalized seizures, including absence seizures)
0.16% in children < 3 yr; lower
in older patients
None (side effect usually transient)
Ethosuximide (absence seizures only)
Depression, psychosis, leukopenia
20%–33%, usually transient
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.
protein binding and compliance. It is prudent to measure
antiepileptic serum levels before conception, at the begin-
ning of each trimester and during the last month in patients
with moderately severe seizure disorders.
The risk of major malformations in babies of mothers
taking antiepileptic drugs is about 4%–8% as compared
with a baseline of 1%–3%.25Most of this increased risk can
be attributed to unfavourable lifestyle, inadequate nutri-
tion, high antiepileptic drug levels and polypharmacy.24,25
Therefore, if possible, change gradually to monotherapy,
which is usually a safe procedure.
As no single antiepileptic drug has been shown to be more
teratogenic than another, a pregnant woman should keep tak-
ing her current drug, which is pre-
sumably the best antiepileptic
drug for her epilepsy. Barbitu-
rates, phenytoin and ethosuximide
have been associated with con-
genital heart, cleft lip and palate
carbamazepine may produce
neural tube defects and hydro-
cephalus, with an incidence of
neural tube defects of 1%–2% for
valproate and 0.5%–1% for
carbamazepine.24,25Effects of ox-
carbazepine, topiramate and lam-
otrigine are unknown. Minor mal-
formations such as hypertelorism,
low-set ears and nail-bed hypopla-
sia may occur, but these usually do
not cause serious medical or cos-
Adequate nutrition and folic
acid supplementation by about
4–5 mg/d in any sexually active
woman of childbearing age low-
ers the risk of major fetal malfor-
mations, especially neural tube
defects in babies of young women
taking antiepileptic drugs.23,24,26As
neural tube and cardiac malfor-
mations occur during the first 5
weeks of pregnancy, adequate folic acid levels should be es-
tablished before conception.
Because of high fetal demand, folic acid levels decline
in pregnancy, reaching a nadir at term.23Women who
smoke have lower folic acid levels than those who do not
smoke. High folic acid levels do not appear to exacerbate
a seizure disorder.
An expert obstetric opinion is needed to monitor for
congenital defects. This may involve α-fetoprotein screen-
ing: that of amniotic fluid is apparently more reliable than
that of maternal serum.24Ultrasonography at 16–18 weeks’
gestation may be necessary as well.
Hemorrhagic disease of the newborn may occur in an in-
fant whose mother has lower than normal levels of vitamin
K–dependent clotting factors. This can be prevented with
10–20 mg per day of vitamin K orally in the last month of
pregnancy23,25(Dr. Renato Natale, Associate Chief, St.
Joseph’s Health Centre and London Health Sciences Cen-
tre — University Campus, London, Ont.: personal commu-
nication, 2002). Oral vitamin K can be obtained in Canada
through the Special Access Programme.27,28
Although antiepileptic drugs are detectable in breast
milk, their concentrations are usually lower than those in
maternal serum. Breast-feeding
should not be discouraged in
women with epilepsy, because
its advantages appear to out-
weigh the rare (5%–10%) ad-
verse effects to the baby of seda-
tion, hypotonia and feeding
difficulty. Drug withdrawal
symptoms have been reported
drug levels may gradually in-
crease over the first few weeks
after birth as enzymatic induc-
tion will have decreased.
Mothers with incompletely
controlled seizures should avoid
bathing an infant in the bathtub
without another person present
and should change the infant on
Effectiveness and side effects both depend
on dosage. Small changes in dosage can
produce dramatic effects.
Traditional antiepileptic drugs may be as
effective as new ones.
Fatigue is the most common side effect of
most antiepileptic drugs.
Phenytoin is the only antiepileptic drug
that can be started at full dose.
Epilepsy in elderly patients
Unfortunately, the incidence
and prevalence of epilepsy in-
creases in elderly people because
hemorrhagic and ischemic
stroke, primary or secondary tu-
mours, trauma, dementia and
metabolic disorders occur com-
monly in this population. Fortunately, such epilepsy is sel-
dom intractable. The consequences of uncontrolled
seizures may be greater in elderly patients: a fall may frac-
ture a hip or create a subdural hematoma, whereas a GTC
seizure may crush a vertebra, giving back pain. A postictal
state may manifest as memory loss, cognitive impairment,
or an increase in a hemiparesis or dysphasia.
The principal differential diagnoses are syncope, sudden
falls of elderly people, transient ischemic attacks or even
sleep disturbances. Nonconvulsive status epilepticus ap-
JAMC • 18 FÉVR. 2003; 168 (4)
Antiepileptic drug therapy: key points
• Monotherapy suffices for most seizure dis-
Twice-daily dosing is most practical except
in pregnancy, when dosing 4 times daily
prevents a serum level surge and therefore
has less effect on the fetus.
The severity of the seizure disorder, not the
laboratory numbers, determines the “thera-
peutic range.” Whatever serum drug level
renders the patient seizure free is adequate
for that patient, even if it is below the labo-
Dual therapy with most antiepileptic drugs at
serum levels in the middle of the laboratory
range impairs cognition.
pears more often in elderly people, manifesting as mild
confusion and forgetfulness or total unresponsiveness for
hours or days.
Diagnostic tests include EEG, CT scanning and meta-
bolic studies. The need for antiepileptic drugs and ongo-
ing medication should be reviewed to diminish polyphar-
macy and its complications. The choice of any needed
antiepileptic drug is guided by efficacy, ease of introduc-
tion and administration, potential drug interactions and
likelihood of significant side effects. As most seizure disor-
ders in elderly patients are focal with possible secondary
generalization, carbamazepine and phenytoin would be ap-
The loss or suspension of a driving licence significantly
disrupts life, but the medical, emotional and legal impacts of
a medically related driving injury to others or self potentially
produce greater anguish. These opposing considerations
have led to the development by the Canadian Medical Asso-
ciation of guidelines for physicians (Table 4).30Although
studies have shown the risk of motor vehicle crashes to be
CMAJ • FEB. 18, 2003; 168 (4)
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
• Get neurological assessment, including EEG and CT
After epilepsy diagnosisDrive 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
Seizures in sleep or immediately
• Drive if seizures only occur in sleep or upon
awakening for at least 5 years (can reduce period if
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
• Resume driving if take medication according to the
physician’s instructions and
• Seizure free for 6 months (can reduce period if
• Drive any vehicle if seizure free off medication for
(b) If seizures recur after withdrawal
(c) Long-term withdrawal and
discontinuation of medication
Auras (simple partial seizures)Drive if
• No impairment in level of consciousness or
• Seizures are unchanged for more than 12 months
• Neurologist approves
• Remain alcohol free and seizure free for 12 months
• completed a recognized rehabilitation program for
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
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.
only equal or one-third greater among drivers with epilepsy
as compared with the general population,31this near equality
may have been achieved by the implementation of the
CMA’s guidelines. Risk assessment should include seizure
frequency and loss of awareness or other faculty during the
events. Legal responsibility for failing to report possibly in-
capable drivers is being placed ever more upon physicians.
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This article has been peer reviewed.
Competing interests: None declared.
Dr. Blume is Professor, Department of Clinical Neurological Sciences, Epilepsy
and Clinical Neurophysiology, London Health Sciences Centre — University
Campus, London, Ont.
Correspondence to: Dr. Warren T. Blume, London Health Sciences
Centre — University Campus, 339 Windermere Rd., London ON
N6A 5A5; fax 519 663-3753; email@example.com