seizure

1. Approach to
seizure/epilepsy
Dr Biplave Karki

2. Introduction
 Seizure
 an abnormal, excessive, paroxysmal discharge of the
cerebral neurons
 5–10% of the population will have at least one
seizure, with the highest incidence occurring in
early childhood and late adulthood
 Epilepsy
 a chronic condition characterized by recurrent,
unprovoked seizures
 if a patient has 2 or more seizures, he/she is diagnosed
as having epilepsy
 Incidence 0.3–0.5%
 Prevalence 5–30 persons per 1000.

3. Differential Diagnosis of Seizures
 Benign positional vertigo
 Breath holding spells in children
 Cardiac arrhythmia
 Hypoglycemia
 Migraine
 Narcolepsy/Cataplexy
 Night terrors
 Nightmares
 Nocturnal myoclonus
 Panic attacks
 Periodic paralysis
 Pseudoseizures/Hysterical seizures
 Sleep apnea
 Syncope
 Transient ischemic attacks

4. Syncope
 A transient loss of consciousness due to brief interruption of blood
supply to the brain.
 Convulsive movements of the extremities may follow some prolonged
episodes.
 Vasovagal syncope
 secondary to fear, pain or unpleasant sights such as blood or
medical procedures.
 Reflex syncope
 coughing, micturition, defecation or Valsalva’s maneuver.
 Other causes, especially in the elderly,
 orthostatic hypotension and cardiac arrhythmias.
 Clinical presentation
 dizzy/light-headed
 fullness in ears
 Nauseous
 often gradual graying or blurring of the vision.

5. Syncope contd..
 Patients who fall tend to go down more “gracefully” than those
with seizures
 Stereotypical provoking factors such as
 prolonged periods of standing in the heat,
 sight of blood,
 micturition, or
 abruptly assuming an erect posture after prolonged
recumbence.
 The absence of an aura , tongue bite, urinary incontinence and
prolonged tonic-clonic activity in the presence of a provoking
factor would be more suggestive of syncope.

6. Transient Ischemic Attacks
 TIA result from temporary interruption of blood
supply in the distribution of a cerebral vessel.
 “Negative symptoms” such as numbness and
weakness are more likely to manifest as compared
to the “positive symptoms” (stiffness and twitching)
seen with seizures.
 Patients will likely have risk factors for
cerebrovascular disease such as hypertension,
diabetes and/or coronary artery disease.

7. Migraines
 A classic migraine with visual aura, nausea/vomiting and
pounding hemicranial headache can be differentiated easily from
a seizure based on history alone.
 However, migraines presenting with isolated symptoms such as
vertigo, episodic vomiting (cyclic vomiting), visual changes and
aphasia with/without headaches can be a challenge.
 A detailed history of previous attacks
 Certain triggers (caffeine, sleep withdrawal, chocolate)
 Family history of migraines
 Empirical treatment with antiepileptic/anti-migraine medications
may clarify the diagnosis in some instances

8. Pseudoseizures and Hysterical
Seizures
 Pseudoseizures are paroxysmal attacks of non-
epileptic etiology
 waxing and waning movements during a single attack
 prolonged tonic-clonic activity without postictal
disorientation
 non-rhythmic pelvic thrusting
 non-physiological evolution of symptoms such as motor
activity spreading from one hand to the other without first
affecting the ipsilateral face or leg.

9. Classification of seizure
 Seizures may be either focal or generalized.
 Focal seizures
 originate within networks limited to one cerebral hemisphere
 Focal seizures with or without impairment of cognition
 Generalized seizures
 arise within and rapidly engage networks distributed across both
cerebral hemispheres.
 Focal seizures are usually associated with structural
abnormalities of the brain.
 In contrast, generalized seizures may result from cellular,
biochemical, or structural abnormalities that have a more
widespread distribution.

11. FOCAL SEIZURES
 Arise from a neuronal network either discretely
localized within one cerebral hemisphere or more
broadly distributed but still within the hemisphere
 Focal seizures with or without dyscognitive features
(“simple focal seizures” and “complex focal seizures”)
 Focal seizures can also evolve into generalized seizures
(focal seizures with secondary generalization)
 Interictal EEG
 often normal or may show brief discharges termed
epileptiform spikes, or sharp waves.

12. Focal Seizures Without
Dyscognitive Features
 Focal seizures can cause motor, sensory, autonomic, or psychic
symptoms without impairment of cognition
 Ictal EEG
 abnormal discharges in a very limited region over the appropriate area of
cerebral cortex if the seizure focus involves the cerebral convexity
 Focal motor seizures
 abnormal motor movements may begin in a very restricted region such as
the fingers and gradually progress (over seconds to minutes) to include a
larger portion of the extremity
 “Jacksonian march”
 spread of seizure activity over a progressively larger region of motor cortex.
 Localized paresis (Todd’s paralysis) may occur for minutes to many hours in
the involved region following the seizure
 Seizure may continue for hours or days
 epilepsia partialis continua

13. Focal Seizures Without
Dyscognitive Features
 Focal seizures may also manifest as changes in
 somatic sensation (e.g., paresthesias)
 Vision (flashing lights or formed hallucinations)
 Equilibrium (sensation of falling or vertigo), or
 Autonomic function (flushing, sweating, piloerection).
 Focal seizures arising from the temporal or frontal cortex may also
cause alterations in hearing, olfaction, or higher cortical function
(psychic symptoms)
 sensation of unusual, intense odors (e.g., burning rubber or kerosene) or
 sounds (crude or highly complex sounds)
 epigastric sensation that rises from the stomach or chest to the head
 Fear
 sense of impending change, detachment, depersonalization, déjá vu
 illusions that objects are growing smaller (micropsia) or larger (macropsia).
 These subjective, “internal” events that are not directly observable by
someone else are referred to as auras.

14. Focal Seizures with
Dyscognitive Features
 Transient impairment of the patient’s ability to maintain normal contact with the
environment
 unable to respond appropriately to visual or verbal commands during the seizure
 impaired recollection or awareness of the ictal phase
1. Aura (i.e., a focal seizure without cognitive disturbance)
2. Sudden behavioral arrest or motionless stare
3. Automatisms
 involuntary, automatic behaviors
 very basic behaviors such as chewing, lip smacking, swallowing, or “picking”
movements of the hands
 more elaborate behaviors such as a display of emotion or running.
4. The patient is typically confused following the seizure
 Transition to full recovery of consciousness may range from seconds up to an hour.
 Anterograde amnesia
 Postictal aphasia

15. EVOLUTION OF FOCAL SEIZURES
TO GENERALIZED SEIZURES
 Tonic-clonic variety
 Focal seizures arising from a focus in the
frontal lobe
 H/O of preceding aura

16. GENERALIZED SEIZURES
 Arise at some point in the brain but
immediately and rapidly engage neuronal
networks in both cerebral hemispheres

17. Typical Absence Seizures
 Sudden, brief lapses of consciousness without loss of postural control
 Typically lasts for only seconds
 No postictal confusion
 Subtle, bilateral motor signs such as
 rapid blinking of the eyelids
 chewing movements
 small-amplitude, clonic movements of the hands.
 Associated with a group of genetically determined epilepsies
 onset usually in childhood or early adolescence
 main seizure type in 15–20% of children with epilepsy
 EEG
 generalized, symmetric, 3-Hz spike-and-wave discharge that begins and
ends suddenly, superimposed on a normal EEG background

18. Atypical Absence Seizures
 Lapse of consciousness
 longer duration
 less abrupt in onset and cessation
 More obvious motor signs
 EEG
 generalized, slow spike-and-wave pattern with a frequency
of ≤2.5 Hz
 Diffuse or multifocal structural abnormalities of the
brain
 signs of neurologic dysfunction such as mental retardation
 Less responsive to anticonvulsants

19. Generalized, Tonic-Clonic
Seizures
 Main seizure type in ~10% of all persons with epilepsy
 Most common seizure type resulting from metabolic derangements
 The seizure usually begins abruptly without warning,
 Vague premonitory symptoms in the hours leading up to the seizure
 distinct from the stereotypic auras associated with focal seizures that
generalize.
 Tonic contraction of muscles throughout the body
 muscles of expiration and the larynx
 loud moan or “ictal cry.”
 Respirations are impaired
 Secretions pool in the oropharynx
 Cyanosis
 jaw muscles
 biting of the tongue
 Marked enhancement of sympathetic tone
 increases in heart rate, blood pressure, and pupillary size

20. Generalized, Tonic-Clonic
Seizures
 After 10–20 s
 Clonic phase
 superimposition of periods of muscle relaxation on the tonic
muscle contraction.
 periods of relaxation progressively increase until the end of the
ictal phase, which usually lasts no more than 1 min.
 Postictal phase
 Unresponsiveness, muscular flaccidity, and excessive salivation
that can cause stridorous breathing and partial airway obstruction
 Bladder or bowel incontinence
 Postictal confusion
 Headache, fatigue, and muscle ache

21. Generalized, Tonic-Clonic
Seizures
 EEG
 tonic phase
 progressive increase in generalized low-voltage fast
activity, followed by generalized high-amplitude, polyspike
discharges
 clonic phase
 high-amplitude activity is typically interrupted by slow waves
to create a spike-and-wave pattern
 postictal EEG
 diffuse slowing that gradually recovers as the patient
awakens
 Brief tonic seizures lasting only a few seconds
 Lennox-Gastaut syndrome

22. Atonic Seizures
 Sudden loss of postural muscle tone lasting 1–2 s
 Consciousness is briefly impaired
 No postictal confusion
 EEG
 brief, generalized spike-and-wave discharges followed
immediately by
 diffuse slow waves that correlate with the loss of muscle
tone
 Atonic seizures are usually seen in association with
known epilepsy syndromes.

23. Myoclonic Seizures
 Myoclonus is a sudden and brief muscle contraction that may involve
one part of the body or the entire body.
 Physiologic form of myoclonus
 sudden jerking movement observed while falling asleep.
 Pathologic myoclonus
 metabolic disorders
 degenerative CNS diseases
 anoxic brain injury
 Myoclonic seizures are considered to be true epileptic events because
they are caused by cortical dysfunction.
 EEG
 bilaterally synchronous spike-and-wave discharges synchronized with the
myoclonus
 Myoclonic seizures
 juvenile myoclonic epilepsy

25. Epilepsy syndromes
 Epilepsy syndromes are disorders in which
epilepsy is a predominant feature
 There is sufficient evidence (e.g., through
clinical, EEG, radiologic, or genetic
observations) to suggest a common
underlying mechanism

29. Juvenile myoclonic epilepsy
(JME)
 Generalized seizure disorder of unknown cause
 Appears in early adolescence
1. Bilateral myoclonic jerks that may be single or repetitive
 most frequent in the morning after awakening and can be provoked by
sleep deprivation.
 Consciousness is preserved unless the myoclonus is especially severe.
2. Many patients also experience generalized tonic-clonic seizures
3. Up to one-third have absence seizures.
 Although complete remission is relatively uncommon, the seizures
usually respond well to appropriate anticonvulsant medication.
 There is often a family history of epilepsy, and genetic linkage studies
suggest a polygenic cause

30. Lennox-Gastaut syndrome
 Occurs in children
 Triad:
1. Multiple seizure types
 generalized tonic-clonic, atonic, and atypical absence seizures
2. EEG
 slow (<3 Hz) spike-and-wave discharges and a variety of other
abnormalities; and
3. Impaired cognitive function in most but not all cases.
 Associated with CNS disease or dysfunction from a variety of causes
 De novo mutations
 Developmental abnormalities
 Perinatal hypoxia/ischemia
 Trauma
 Infection
 Unfortunately, many patients have a poor prognosis
 underlying CNS disease
 severe, poorly controlled epilepsy.

31. Mesial temporal lobe epilepsy
(MTLE)
 Most common syndrome associated with
focal seizures with dyscognitive features
 High resolution MRI
 hippocampal sclerosis
 Refractory to treatment with anticonvulsants
but responds well to surgical intervention

32. History
1. When did you experience the first seizure in your life?
2. Do you experience some kind of a warning or unusual feeling at
the onset, or immediately preceding the seizure?
3. What happens during the seizure?
4. What happens immediately following the seizure?
5. Is there a diurnal variation?
6. Are there any known triggering factors?
7. What is the seizure frequency?
8. What has been the maximum seizure-free period since the
seizure onset?
9. Is there more than one kind of seizure?
10. Has the patient sustained injuries related to the seizures?
11. What is the frequency of visits to the emergency department?

33. 1. When did you experience
the first seizure in your life?
 Early neonatal period
 perinatal insults
 metabolic disorders, and
 congenital malformation.
 Generalized seizures tend to present in early
childhood or teenage years
 Elderly with new onset seizures
 structural pathology such as a stroke or brain
tumor

36. 2. Do you experience some kind of a
warning or unusual feeling at the
onset, or immediately preceding the
seizure?
 The warning symptoms that are perceived at the onset
of a seizure are called “aura.”
 An aura actually indicates that the seizure is focal in
origin.
 Temporal lobe epilepsy
 déjà vu
 epigastric sensation,
 Parietal lobe epilepsy
 Paresthesias
 Occipital lobe epilepsy
 visual distortions
 transient blindness

37. 3. What happens during the
seizure?
 Is there head or eye deviation to one side?
 Seizures originating from the frontal eye fields may cause head and eye
deviation to the contralateral side
 Is there excessive eye blinking at the onset?
 Occipital lobe seizures can present with excessive blinking at the onset,
negative visual symptoms or visual distortions
 If automatisms (defined as involuntary, organized sequences of
movement that are not causally related to the external environment)
occur, are these more pronounced on one side?
 Temporal lobe seizures are often manifested with lip smacking and other
oral and alimentary automatic behavior
 most pronounced in the ipsilateral extremity, along with dystonic posturing of
the contralateral arm
 Does the patient bite his tongue or lose control of the bladder function?
 more often seen with generalized seizures

38. 4. What happens immediately
following the seizure? Postictal
period
 Generalized tonic-clonic seizure
 postictal sleep
 disorientation and lack of awareness of the surroundings
 Hemiparesis or hemiplegia following a seizure
(Todd’s paralysis)
 focal seizure
 Aphasia with otherwise normal awareness
 language areas in the dominant hemisphere.
 Absence seizures
 brief or no postictal disorientation

39. 5. Is there a diurnal variation?
 Tonic-clonic and myoclonic seizures seen in
primary generalized epilepsies
 more common on awakening or in early morning.
 Temporal lobe seizures
 occur any time.
 Certain frontal lobe seizures
 nocturnal presentation

40. 6. Are there any known
triggering factors?
 Sleep deprivation
 Flickering lights
 Menses
 Alcohol consumption
 Non-compliance of medication
 Use of antihistamines
 Stress
 Fever
 Exercise

41. 7. What is the seizure
frequency?
 Response to treatment

42. 8. What has been the maximum
seizure-free period since the
seizure onset?
 To determine if any specific antiepileptic drug
was more efficacious than the others.

43. 9. Is there more than one kind
of seizure?
 Different seizure types

44. 10. Has the patient sustained
injuries related to the seizures?
 do not have auras
 do not have enough time after the aura to
take preventive measures

45. 11. What is the frequency of visits
to the emergency department?
 Degree of seizure control

46. PAST MEDICAL HISTORY
 Central nervous system infections such as
meningitis, encephalitis, Lyme disease,
cysticercosis.
 Head injuries, especially associated with
 depressed skull fracture,
 intracerebral hemorrhage,
 loss of consciousness
 prolonged amnesia
 Brain tumor
 Cerebrovascular accident

47. SOCIAL HISTORY
 Level of education
 Job description
 construction worker, heavy equipment mechanic, driver
 Planning pregnancy in the near future
 Teratogenicity of antiepileptic drugs
 Lower efficacy of oral contraceptives with enzyme-inducing
medication (phenytoin, carbamazepine, and phenobarbital),
 Alcohol use
 risk factor for a first generalized tonic-clonic seizure
 interact with the metabolism of the antiepileptic drugs
 seizure exacerbation, especially after continued or binge
drinking.

48. FAMILY HISTORY
 Specific epilepsy syndromes and Genetically
mediated neurological disorders that have
seizures as one manifestation.
 Juvenile myoclonic epilepsy (JME),
 Familial neonatal convulsions,
 Benign rolandic epilepsy

50. Examination
 Asymmetries in the size of limbs or one half of the body (hemiatrophy)
 perinatal cerebral insult
 Marks or ulcerations on the side of tongue or oral mucous membranes
 Gingival hyperplasia
 Phenytoin
 Dupytrens contractures
 chronic use of barbiturates
 Dystonic posturing of one arm on stressed gait, such as walking on the
sides of the feet
 remote insult to the corticospinal tracts
 Multiple bruises or injuries
 falls secondary to seizures
 End gaze nystagmus, diplopia and difficulty in tandem walking
 toxicity related to antiepileptic medications such as carbamazepine,
phenytoin, and lamotrigine

51. Examination
Stigmata of neurocutaneous syndrome
 Neurofibramatosis
 café au lait spots
 iris hamartoms
 Tuberous sclerosis
 Ash leaf spots
 shahgreen patches
 subungal fibromas
 adenoma sebaceum
 Sturge-Weber syndrome
 port-wine stain (capillary hemangioma)

52. INVESTIGATING THE FIRST
SEIZURE
 A seizure is a symptom of an underlying
pathology.
 Investigations are directed at identifying the
precipitating etiology and conditions that can
be arrested, reversed, or treated.
 A detailed history and physical examination
can provide direction to the extent of
investigations

54. Laboratory Investigations
 Hyponatremia, hypoglycemia,
hypomagnesemia, uremia and hepatic
encephalopathy
 Serum and urine toxicology should be done
when substance abuse or drug overdose is
suspected.
 In newborns and young children appropriate
metabolic screen can be requested

55. Neuroimaging
 CT scan
 subdural hematoma, subarachnoid hemorrhage, abscess,
neoplastic processes, and other space occupying lesions.
 MRI
 cerebral dysplasia
 mesial temporal scleroses
 when history and physical examination is suggestive of
focal pathology and the CT does not show the cause

56. Electroencephalogram (EEG)
 EEG tests the cerebral function rather than
structure.
 Epileptiform discharges on the EEG can help
classify the seizure types
 Focal and generalized slowing is reflective of focal
and generalized disturbance of cerebral function
respectively.
 Focal disturbance
 strokes, tumors, and abscess.
 Generalized disturbance
 toxic, metabolic, or diffuse structural abnormalities

57. Treatment
 Treatment of underlying condition
 Avoidance of precipitating factors
 Antiepileptic drugs
 Refractory epilepsy

58. Antiepileptic drugs
Appear to act primarily by blocking the initiation or spread of
seizures
1. Inhibition of Na+-dependent action potentials in a frequency-
dependent manner
 (e.g., phenytoin, carbamazepine, lamotrigine, topiramate,
zonisamide, lacosamide, rufinamide),
2. Inhibition of voltage-gated Ca2+ channels
 (phenytoin, gabapentin, pregabalin),
3. Facilitating the opening of potassium channels
 (ezogabine),
4. Attenuation of glutamate activity
 (lamotrigine, topiramate, felbamate),

59. Antiepileptic drugs
5. Potentiation of GABA receptor function
 (benzodiazepines and barbiturates),
6. Increase in the availability of GABA
 (valproic acid, gabapentin, tiagabine),
7. Modulation of release of synaptic vesicles
 (levetiracetam).
8. Inhibiting T-type Ca2+ channels in thalamic
neurons.
 ethosuximide and valproic acid

60. When to Initiate Antiepileptic
Drug Therapy
 Recurrent seizures of unknown etiology or a known cause that
cannot be reversed
 Patients with a single seizure due to an identified lesion such as
a CNS tumor, infection, or trauma, in which there is strong
evidence that the lesion is epileptogenic, should be treated.
 Most patients with one or more of these risk factors should be
treated
 an abnormal neurologic examination,
 seizures presenting as status epilepticus,
 postictal Todd’s paralysis,
 a strong family history of seizures,
 an abnormal EEG.

63. Antiepileptic Drug Selection
for Focal Seizures
 Carbamazepine (or oxcarbazepine), lamotrigine, phenytoin, and levetiracetam
 drugs of choice approved for the initial treatment of focal seizures
 Carbamazepine
 first-order pharmacokinetics
 leukopenia, aplastic anemia, or hepatotoxicity
 Oxcarbazepine
 avoids an intermediate metabolite
 fewer drug interactions
 Lamotrigine
 skin rash
 Stevens-Johnson syndrome
 low initial doses and slow titration
 Phenytoin
 long half-life
 once or twice daily dosing
 nonlinear kinetics
 Long-term use of phenytoin
 untoward cosmetic effects (e.g., hirsutism, coarsening of facial features, gingival hypertrophy) and
 effects on bone metabolism

64. Antiepileptic Drug Selection
for Focal Seizures
 Levetiracetam
 no known drug-drug interactions
 irritability, anxiety, and other psychiatric symptoms
 Topiramate
 focal and generalized seizures
 significant psychomotor slowing and other cognitive problems
 Avoid in glaucoma or renal stones
 Valproic acid
 is an effective alternative for some patients with focal seizures, especially when the seizures
generalize.
 Gastrointestinal side effects are fewer when using the delayed-release formulation
 Reversible bone marrow suppression
 Hepatotoxicity
 Zonisamide, tiagabine, gabapentin, lacosamide, and ezogabine
 additional drugs currently used for the treatment of focal seizures with or without evolution into
generalized seizures.
 Phenobarbital and other barbiturate compounds
 were commonly used in the past as first-line therapy for many forms of epilepsy
 sedation in adults
 hyperactivity in children
 subtle cognitive changes

65. Antiepileptic Drug Selection
for Generalized Seizures
 Lamotrigine and valproic acid
 DOC for primary generalized, tonic-clonic seizures
 Topiramate, zonisamide, phenytoin, carbamazepine, and oxcarbazepine
 suitable alternatives
 Valproic acid
 absence, myoclonic, and atonic seizures
 DOC in patients with generalized epilepsy syndromes having mixed seizure types
 Carbamazepine, oxcarbazepine, and phenytoin
 worsen certain types of generalized seizures, including absence, myoclonic, tonic, and
atonic seizures.
 Ethosuximide
 uncomplicated absence seizures
 not useful for tonic-clonic or focal seizures
 bone marrow suppression.
 Lamotrigine
 epilepsy syndromes with mixed, generalized seizure types such as JME and Lennox-Gastaut
syndrome.
 Topiramate, zonisamide, and felbamate
 similar broad efficacy

66. Guidelines for antiepileptic
therapy
 Start with one first-line drug
 Start at a low dose; gradually increase dose until effective control of seizures is
achieved or side-effects develop
 Optimise compliance
 If first drug fails
 start second first-line drug, followed if possible by gradual withdrawal of first
 If second drug fails
 start second-line drug in combination with preferred first-line drug at maximum
tolerated dose
 If this combination fails
 replace second-line drug with alternative second-line drug
 If this combination fails
 check compliance and reconsider diagnosis
 (Are events seizures? Occult lesion? Treatment compliance/alcohol/drugs confounding
response?)
 Consider alternative, non-drug treatments (e.g. epilepsy surgery, vagal nerve
stimulation)
 Use minimum number of drugs in combination at any one time

67. Definition of drug resistant
epilepsy
 The International League Against Epilepsy (ILAE)
has proposed the following definition of drug
resistant epilepsy and suggests that this term be
used instead of the term 'refractory epilepsy'.
 Drug resistant epilepsy occurs when a person has failed to
become (and stay) seizure free with adequate trials of two
seizure medications (called AEDs).
 These seizure medications must have been chosen
appropriately for the person’s seizure type, tolerated by the
person, and tried alone or together with other seizure
medications

68. Surgical treatment
 Temporal lobe epilepsy
 resection of the anteromedial temporal lobe (temporal lobectomy)
 limited removal of the underlying hippocampus and amygdala
(amygdalohippocampectomy)
 Focal seizures arising from extratemporal regions
 focal neocortical resection with precise removal of an identified
lesion (lesionectomy).
 When the cortical region cannot be removed
 multiple subpial transection
 Hemimegalencephaly or other dysplastic abnormalities
 Hemispherectomy or multilobar resection
 Disabling tonic or atonic seizures, usually when they are part of a
mixed-seizure syndrome (e.g., Lennox-Gastaut syndrome).
 corpus callosotomy

69. Surgical treatment
 Vagus nerve stimulation (VNS)
 Implantable device
 can detect the onset of a seizure and deliver an
electrical stimulation
 Responsive NeuroStimulation
 Stereotactic radiosurgery,
 Laser thermoablation
 Deep brain stimulation (DBS)

70. When to Discontinue Therapy
 Withdrawal of therapy can be attempted after 2
years of seizure free interval in a patient who meets
all of the following criteria
 complete medical control of seizures for 1–5 years
 single seizure type, either focal or generalized
 normal neurologic examination, including intelligence
 normal EEG
 In most cases, it is preferable to reduce the dose of
the drug gradually over 2–3 months
 Most recurrences occur in the first 3 months after
discontinuing therapy

71. Epilepsy in pregnancy
 Pre-conception counselling
 folic acid 5 mg daily for 2 mths before conception
 Fetal malformation
 Single drug
 Carbamazepine and lamotrigine have the lowest incidence of major fetal malformations
 Sodium valproate has relatively higher risk
 Levetiracetam may be safe
 Learning difficulties in children
 Lower IQ with valproate
 Haemorrhagic disease of the newborn
 oral vitamin K 20 mg daily to the mother during the last month of pregnancy
 IM vitamin K 1 mg to the infant at birth
 Increased frequency of seizures
 carbamazepine levels may fall in the third trimester.
 Lamotrigine and levetiracetam levels may fall early in pregnancy
 adjust the dose regimen

78. References
 Davidsons principle and practice of medicine,
22nd edition
 Harrisons principle of internal medicine 19th
edition
 Wisconsin Medical Journal 2004
An Approach to the Evaluation of a Patient for
Seizures and Epilepsy
S. Nizam Ahmed, MD, FRCPC; Susan S.
Spencer, MD

79. Thank you