Transcript epilepsy - Government Madurai Medical College

EPILEPSY
DEPARTMENT OF GENERAL MEDICINE
MADURAI MEDICAL COLLEGE
DEFINITION
CLASSIFICATION
ETIOLOGY
MECHANISM OF SEIZURES
STAGES IN EVOLUTION GTCS
SYMPTOMS OF INDIVIDUAL SEIZURE TYPES
INVESTIGATION
MANAGEMENT
SPECIAL CONSIDERATION
REFRACTORY / INTRACTABLE SEIZURE
IN PREGNANCY AND WOMEN
STATUS EPILEPTICUS
PSEUDO SEIZURES
WHEN TO STOP ANTIEPILEPTICS
A seizure is a paroxysmal event due to abnormal excessive or
synchronous neuronal activity in the brain.
Epilepsy is condition in which a person has recurrent seizures
due to chronic underlying process.
Convulsion.
An intense paroxysm of involuntary repetitive muscular contractions.
Seizure (is a generic term)
Convulsive seizure or motor seizure.
Non convulsive seizure
sensory seizure.
Psychic seizure.
 Autonomic seizure.
All seizures are not convulsions.
Not all convulsions are seizure.
CLASSIFICATION OF SEIZURES
ILAE CLASSIFICATION (1981)
II. Generalized seizures (Convulsive and nonconvulsive)
I. Partial (Focal)seizures
A. Simple partial seizures
B. Complex Partial Seizures
C. Partial Seizures evolving to secondary
generalized seizures (tonic-clonic,
tonic or clonic)
A. Absence seizures
i) Typical
ii) Atypical
B. Myoclonic seizures
C. Clonic seizures
D. Tonic seizures
E. Tonic-Clonic seizures
F. Atonic seizures
(Combinations may occur: myoclonic and
atonic or myoclonic and tonic)
III. Unclassified epileptic seizures
Anatomical site
Cortex
Temporal
Frontal
Parietal
Occipital
Generalised (diencephalon)
Multifocal
Pathological cause
Genetic
Developmental
Tumours
Trauma
Vascular
Infections
Inflammation
Metabolic
Drugs, alcohol and toxins
Degenerative
Causes of partial seizures
Idiopathic
Benign Rolandic epilepsy of childhood •
Benign occipital epilepsy of childhood •
Focal structural lesions
Genetic
Tuberous sclerosis
von Hippel–Lindau disease
Neurofibromatosis
Cerebral migration abnormalities
infantile hemiplegia
Dysembryonic
Cortical dysgenesis
Sturge–Weber syndrome
Mesial temporal sclerosis(associated with febrile convulsions
Cerebrovascular disease
Intracerebral haemorrhage
Cerebral infarction
Arteriovenous malformation
Cavernous haemangioma
Tumours(primary and secondary)
Trauma(including neurosurgery)
Infective
Cerebral abscess (pyogenic)
Toxoplasmosis
Cysticercosis
Tuberculoma
Subdural empyema
Encephalitis
Human immunodeficiency virus (HIV)
Inflammatory
Sarcoidosis •
Vasculitis •
Causes of partial seizures
Genetic
Inborn errors of metabolism
Storage diseases
Phakomatoses (e.g. tuberous sclerosis,)
Cerebral birth injury
Hydrocephalus
Cerebral anoxia
Drugs
Antibiotics: penicillin, isoniazid, metronidazole •
Antimalarials: chloroquine, mefloquine Ciclosporin •
Cardiac anti-arrhythmics: lidocaine, disopyramide •
Psychotropic agents: phenothiazines, tricyclic antidepressants, lithium
Amphetamines (withdrawal)
Alcohol (especially withdrawal)
Toxins
Heavy metals (lead, tin) • Organophosphates (sarin) •
Metabolic disease
Hypocalcaemia •
Hypoglycaemia •
Hyponatraemia •
Renal failure •
Hypomagnesaemia •
Liver failure
Infective
Meningitis
Post-infectious encephalopathy
Inflammatory
Multiple sclerosis (uncommon)
SLE
Diffuse degenerative diseases
Alzheimer’s disease (uncommonly)
Creutzfeldt–Jakob disease (rarely) s
The Causes of Seizures and Epilepsy
Seizures are a result of a shift in the normal balance of excitation and inhibition within the CNS
The normal brain is capable of having a seizure under the appropriate circumstances, and there are differences between individuals in
differences between individuals in the susceptibility or threshold for seizures.
seizures may be induced by high fevers in children who are otherwise normal and who never develop other neurologic problems,
including epilepsy.
Normal development also plays an important role, since the brain appears to have different seizure thresholds at different maturational
stages
There are a variety of conditions that have an extremely high likelihood of resulting in a chronic
seizure disorder.
severe, penetrating head trauma
long-lasting pathologic change in the CNS that transforms a presumably normal neural network into
This process is known as epileptogenesis,
epileptogenic factors.
stroke, infections, and abnormalities of CNS development.
Seizures are episodic.
completely normal for months or even years between seizures.
important provocative or precipitating factors that induce seizures in patients with epilepsy.
Precipitants
psychological
physical stress
sleep deprivation
hormonal changes associated with the menstrual cycle.
exposure to toxic substances and certain medications.
These observations emphasize the concept that the many causes of seizures and epilepsy result from a dynamic interplay between
endogenous factors,
epileptogenic factors, and
precipitating factors.
Mechanisms of Seizure Initiation and Propagation
seizure initiation phase
The initiation phase is characterized by two concurrent events in an aggregate of neurons: (1) high-frequency bursts of action potentials
and (2) hypersynchronization.
The bursting activity is caused by a relatively long-lasting depolarization of the neuronal membrane due to influx of extracellular calcium
(Ca2+), which leads to the opening of voltage-dependent sodium (Na+) channels, influx of Na+, and generation of repetitive action
potentials.
This is followed by a hyperpolarizing afterpotential mediated by ℽ -aminobutyric acid (GABA) receptors or potassium (K+) channels,
depending on the cell type.
seizure propagation phase.
Normally, the spread of bursting activity is prevented by intact hyperpolarization and a region of
inhibitory neurons.
With sufficient activation there is a recruitment of surrounding neurons via a number of synaptic and
(1) an increase in extracellular K+, which blunts hyperpolarization and depolarizes neighboring neurons;
(2) accumulation of Ca2+ in presynaptic terminals, leading to enhanced neurotransmitter release; and
(3) depolarization-induced activation of the N-methyl-D-aspartate (NMDA) subtype of the excitatory amino acid receptor,
neuronal activation;
(4) ephaptic interactions related to changes in tissue osmolarity and cell swelling.
The recruitment of a sufficient number of neurons leads to the propagation of seizure activity into contiguous areas via
areas via long commissural pathways such as the corpus callosum
Mechanisms intrinsic to the neuron include changes
in the conductance of ion channels,
response characteristics of membrane receptors, cytoplasmic buffering,
second-messenger systems, and protein expression as determined by gene transcription, translation, and posttranslational modification.
Mechanisms extrinsic to the neuron include changes
in the amount or type of neurotransmitters present at the synapse,
modulation of receptors by extracellular ions and other molecules, and temporal and spatial properties of synaptic and non synaptic input.
Nonneural cells such as astrocytes and oligodendrocytes, have an important role in many of these mechanisms as well.
The basic mechanisms of other precipitating factors of seizures such as sleep deprivation, fever, alcohol withdrawal, hypoxia, and infection, are not as well understood
but presumably involve analogous perturbations in neuronal excitability
Mechanisms of Action of Antiepileptic Drugs
Antiepileptic drugs appear to act primarily by blocking the initiation or spread of seizures.
inhibition of Na+-dependent action potentials in a frequency-dependent manner (e.g., phenytoin, carbamazepine, lamotrigine, topiramate, zonisamide, lacosamide,
rufinamide
inhibition of voltage-gated Ca2+ channels (phenytoin, gabapentin, pregabalin),
attenuation of glutamate activity (lamotrigine, topiramate, felbamate),
potentiation of GABA receptor function (benzodiazepines and barbiturates),
increase in the availability of GABA (valproic acid, gabapentin, tiagabine), and
modulation of release of synaptic vesicles (levetiracetam).
The two most effective drugs for absence seizures, ethosuximide and valproic acid, probably act by inhibiting T-type Ca2+ channels in thalamic neurons.
SIMPLE PARTIAL SEIZURES
SIMPLEX PARTIAL SEIZURES
 No loss of consciousness
 Symptoms depend on area of brain involved:
 Motor
 Sensory
 Autonomic
 Psychosensory
 It can be the introductory phase of a complex partial or generalised tonic-
clonic seizure (‘aura’)
COMPLEX PARTIAL SEIZURES
COMPLEX PARTIAL SEIZURES
 Origin is most often in the temporal lobe
 A common seizure type in adulthood
 Can be introduced by a simplex partial psychosensory seizure:
 olfactory hallucination
 déjà vu, jamais vu
 feeling of alienation
 Loss of consciousness: stare, ‘going blank’
 Automatisms:
 oral automatisms
 fiddling with the hands
Additional
1.
features of partial motor seizures.
JACKSONIAN SEIZURE
 Motor
seizure begins in a restricted region such as the
fingers and gradually progresses over seconds to minutes
to include a larger portion of the extremity.
2.
TODDS PARALYSIS.
 Patients
may experience paresis of the involved limb for
minutes to many hours following the seizure.
3.
EPILEPSIA PARTIALIS CONTINUA.
 Rarely
the seizure may continue for hours to days when it is called
epilepsia partialis continua.
 Often
refractory to treatment.
4.
VERSIVE SEIZURES
 A frontal epileptic focus may involve the frontal eye field causing forced deviation of the eyes and sometimes
turning of the head to the opposite side.
 Such seizures often become generalised to a tonic clonic seizure.

Somatosensory seizures.

Special sensory seizures.
PARTIAL SENSORY SEIZURES
 Focus in the contralateral post rolandic convolution.
 Sensory seizures described as
 Numbness
 Tingling
 Pins and needles feeling
 Sensation of crawling (formication)
 Electric sensation,
 Sensation of movement of the part.
 Pain and thermal sensations occur occasionally.
SOMATOSENSORY SEIZURES

Visual seizures.
 Rare.
 Occur as sensation of darkness or flashes of light which may be stationary or moving.
 May appear colourless or coloured.
 There may be twinkling or pulsating lights.
 Visual hallucinations may occur with involvement of occipito-temporal or antero-medial temporal areas.
SPECIAL SENSORY SEIZURES
 Auditory hallucinations.
 Rare.
 There may be sensation of buzzing or roaring in the ears or sensation of human voice repeating unrecognisable
words.
 Vertiginous sensations.
 occur with supero posterior temporal region or parieto temporal region involvement.
 Olfactory hallucinations.
 assoc with lesions of inferior and medial parts of temporal lobe usually in the region of parahippocampal convolution
or uncus and hence the term uncinate seizures.
 patient perceives a foul smell
 Gustatory hallucinations.
 in temporal lobe disease.
 salivation and sensation of thirst is present.
 Vague and often indefinable visceral sensations arising in the thorax, epigastrium and abdomen may occur with
temporal lobe focus.
 COMPLEX PARTIAL SEIZURES

OR PSYCHOMOTOR SEIZURES
OR TEMPORAL LOBE SEIZURES.
These patients have
 Aura- in the form of a simple focal seizure or a hallucination or illusion suggestive of a temporal lobe origin.
 have a period of altered behavior, altered consciousness and amnesia to the event.
 Psychic experiences which occur in complex partial seizures.
1.
Sensory illusions and distortions

Micropsia and macropsia- objects and persons in the environment appear to shrink or recede into distance or
may enlarge
2.
Hallucinations.
 visual and auditory common.
 Olfactory and gustatory rare.
3.
Dyscognitive states.
 Dejavu- feelings of increased familiarity.
 Jamais vu- feelings of strangeness or unfamiliarity.
 Feeling of depersonalisation.
 Sudden interruption in memory.
 Fragments of old memories and scenes appear in patients mind and recur with striking clarity.
4.
Emotional experiences.
 Less commonly observed.
 sadness,loneliness,anger,happiness,sexual excitement.
 Fear and anxiety-most common affective experiences.
 Sense of rage and intense anger.
3.
Dyscognitive states.
 Dejavu- feelings of increased familiarity.
 Jamais vu- feelings of strangeness or unfamiliarity.
 Feeling of depersonalisation.
 Sudden interruption in memory.
 Fragments of old memories and scenes appear in patients mind and recur with striking clarity.
 AUTOMATISMS - occur in the form of

Lipsmacking
 Chewing
 Swallowing
 Fumbling of hands
 Shuffling of feet
 Inappropriate acts.
 OTHER AUTOMATISMS.
 Gelastic epilepsy — laughter may be the most striking feature of an automatism.
 Volvular epilepsy—patient may walk repititively in small circles.
 Epilepsia procursiva—runs repititively.
 Poriomania—wanders aimlessly as an ictal or postictal
phenomenon.
 During the episode, patient is not in contact with his surroundings.
 Patient is typically confused following the seizure.
 May take seconds to an hour for full recovery of consciousness.
 Postictally patient may show anterograde amnesia or aphasia (if dominant hemisphere)
 Interictal EEG is often normal or may show brief epileptiform spikes or sharo waves.
 Since CP seizures can arise from the medial temporal lobe or inferior lobe which are distant from the scalp, EEG during seizure may
be non localising but detected using sphenoidal or surgically placed intracranial electrodes
 CP seizures can occur at any age.
 Usually seen in adolescence and adults.
 H/o febrile seizures in childhood is often present.
 2/3rds of CP seizure pts have GTC seizures.
 Cp seizure pts may show
- features of
 Depressive illness
 Psychotic symptoms
 Paranoid delusional state and
 Abnormalities of behaviour and
 Personality during interictal period.
TONIC-CLONIC SEIZURES
GENERALISED TONIC-CLONIC SEIZURE
(GRAND MAL)
 The most common seizure
 Acute symptomatic seizures are generalised tonic-clonic seizures
 Course:
 Cry, loss of consciousness, fall
 Tonic phase- generalised muscle contraction, apnoea
 Clonic phase- rhythmic contraction of muscles, tongue bite, foaming,
enuresis
 Terminal sleep and gradual regaining of consciousness (transient
confusion)
ABSENCE SEIZURES
ABSENCE
 Cognitive dysfunction with a sudden onset and end, lasting 5-
10 seconds
 Stare, expressionless face; arrest of ongoing activity;
generally no motor phenomena
 EEG: generalised 3 Hz spike and wave activity
 Occurs in genetic (idiopathic) epilepsies, mostly in children
 Absence seizures may be accompanied by rapid blinking movements, chewing, or clonic movements of the hands.
 Begin in childhood (4-8 yrs age) or early adolescence.
 Main seizure type in 15-20% of children with epilepsy.
 May occur 100 times a day (pykno epilepsy)
 May manifest as unexplained day dreaming or poor performance.
 EEG-typically reveals characteristic generalised
3 -Hz/sec spike and wave discharges.
 Respond well to treatment.
 About 60—70% usually have a spontaneous remission during adolesence.
 May be associated with GTC seizures.
ATYPICAL ABSENCE SEIZURES
LOC
may be longer.
Focal
motor signs may be present.
EEG
not characteristic and may show generalised
slow spike and wave pattern with a frequency of
about 2.5Hz/sec.
Often
associated
with
diffuse
structural
abnormalities of the brain and patients may have
neurologic dysfunction like mental retardation.
Less
responsive to treatment.
ATONIC SEIZURE

ATONIC SEIZURES
 Sudden loss of muscle tone lasting 1—2 secs
 Brief impairment of consciousness.
 No post ictal confusion.
 EEG reveals brief generalised spike and wave discharges followed immediately by diffuse slow waves that correlate with
loss of muscle tone.
 Usually seen in association with known epileptic syndromes.
MYCLONIC SEIZURES
MYOCLONIC SEIZURE
 Sudden, quick, arrhythmic muscle contraction, twitch of a
limb; no loss of consciousness
 EEG: generalised polyspike and wave activity
 Occurs in genetic (idiopathic) epilepsies
 Not only an epileptic phenomenon- it can be the sign of
diffuse encephalopathies
CLINICAL PRESENTATIONS
Myoclonic seizures
Abrupt , very brief, involuntery flexion movements.
Involve whole body or part of the body
Occur most commonly at morning, shortly after walking.
May occur in healthy people (physiological)
Atonic Seizures
Brief loss of muscle tone.
Heavy fall , with or without loss of consciousness.
Versive seizures
A frontal epileptic foci may involve the frontal eye field.
Force deviation of the eyes and turning head to the opposite side.
Status Epilepticus
Series of recurrent Tonic-Clonic seizures occurs without regaining consciousness over 30 min.
Catamenial epilepsy: Epileptic women experienced that their seizures worsen during menstruation; due to the imbalance between
the proconvulsant estrogen and anticonvulsant progestogen
DIFFERENTIAL DIAGNOSIS
Condition mimicking Seizures:
True Seizure Vs Pseudoseizure
Features & Lab findings
True Seizure Pseudoseizure
1.
Pseudoseizure
Resemble known seizure types
Yes
No
2.
Syncope
Tongue bite
Yes
No
3.
Some sleep disorders
Duration
Short
Long
4.
Hypoperfusion in brain
Post-Ictal Phenomena
Present
Absent
5.
Cardiac Arrhythmia
Injury
Yes
No
6.
Emotional Outburst
Occurs during sleep
Yes
No
7.
Dissociative fugue
Can be precipitated by
suggestion
No
Yes
8.
Drop Attacks
EEG during attack
Abnormal
No Change
9.
Migraine
EEG after attack
No Change
10.
Hypoglycaemia
Slowing
pattern
Serum prolactin (after attack)
Raised
No change
Anti Epileptic drug usage
Suppress
seizures
No Change
(may worsen)
EPILEPTIC SEIZURE VERSUS SYNCOPE
Syncope
Tonic-clonic seizure
Position
Upright
Any
Facial colour
Paleness
Cyanosis
Onset
Gradual; introduced by
dizziness, blurring of
vision
Sudden; can start by
‘aura’ (simplex partial
seizure)
Twitchings
Rarely (‘convulsive
syncope’)
Always
Enuresis
Rarely
Often
Tongue bite
No
Often
Duration
10-20 seconds
Few minutes
Postictal
confusion
No
Yes
Perspiration
Pronounced
Not typical
DIAGNOSIS OF EPILEPSY
Thorough History taking :
From patients
From reliable valid informants
From observer (who observed seizures)
Physical Examination:
Specially neurological system
Higher Psychic function
Laboratory Investigation:
S. Electrolytes, S. Prolactin, Blood sugar, CBC, TFT, LFT, RFT, CSF
study
Imaging:
EEG, Video EEG telemetry, CT Scan of Brain, MRI of Brain,
MRS, PET, SPECT.
Polysomnography
MANAGEMENT OF EPILEPSY
Medical treatment:
Immediate care of seizures
Move persons away from danger
Recovery position (semi prone)
Ensure clear airway
Do not insert anything into mouth
Urgent medical attention- (patent airway, O2 ,
Should not be left alone after recovery
Consider about regular AED
Surgical treatment:
Indicated when seizures shown to be intractable to medical treatment.
Removal of epileptic focus (eg:mesial temporal sclerosis)
Anterior Temporal Lobectomy
Corpus callostomy
Subpial transection
Vagus Nerve stimulation
Ketogenic diet
anticonvulsant, investigate cause)
GUIDELINES FOR ANTICONVULSANT THERAPY
Start with one first line drugs
Start with low dose: Gradually increase to effective dose or until side effects.
Check compliance
If first drug fails due to side effects or continue seizures, start second line drugs whilst gradually
withdrawing first.
Try Three AED singly before using combinations
Beware about drug interactions
Do not use more than two drugs in combination at any one time
If above fails consider occult structural or metabolic lesion and whether seizures are truly epileptic.
CHOICE OF ANTI EPILEPTIC DRUGS
Epilepsy Type
Partial and /or
Secondary GTCS
First-Line
Second-Line
Third-Line
Carbamazepine
Lamotrigine
Oxcarbazepine
Topiramate
S. Valporate(in
children)
S. Valporate
Tiagabine
Gabapentin
Clobazum
Phynytoin
Phenobarbital
Vigabatrin
Acetazolamide
Primary GTCS
S. Valporate
Lamotrigine
Topiramate
Carbamazepine
Phynytoin
Gabapentin
Phenobarbital
Tiagabine
Acetazolamide
Absence
S. Valporate
Lamotrigine
Ethosuximide
Clonazepum
Acetazolamide
Myoclonic
S. Valporate
Clonazepum
Piracetam
Lamotrigine
Phenobarbital
PHARMACOLOGY OF AEDS II.
Steady state
Phenytoin
Phenobarbital
Binding to plasma proteins
7-20 days
10-30
Primidon
2-5
Valproate
2-5
Carbamazepine
3-5
Ethosuximid
7-12
Clobazam
4-5
Lamotrigine
3-10
Topiramate
3-6
Gabapentin
2-5
Vigabatrin
2-5
Pronounced
(>90%) binding
phenytoin
valproate
Moderate (30-80%)
binding
carbamazepine
clobazam
lamotrigine
No or minimal
(<20%) binding
gabapentin
vigabatrin
topiramate
ethosuximid
 When
do we start antiepileptic medication (AED)?
 Which AED
to choose?
 When
and how do we switch AEDs?
 When
is polytherapy needed?
 When
can AEDs be discontinued?
 Pregnancy
 Driver’s
licence
MEDICAL TREATMENT OF
EPILEPSY
 More
than one non-provoked, well-documented
seizure
 AEDs
are usually not started after the first seizure
(needs individual assessment)
WHEN DO WE START TREATMENT?
 Preventive
treatment is not justified
MECHANISM OF ACTION OF AEDS
Inhibition of voltage gated Na,
Ca channels
Na: phenytoin, carbamazepine,
oxcarbazepine, lamotrigine,
topiramate, felbamate, zonisamide
Ca: ethosuximid, valproate?
lamotrigine, topiramate,
zonisamide
Potentiaton of GABA mediated
inhibition
phenobarbital, benzodiazepins,
vigabatrin, tiagabine, topiramate,
valproate, gabapentin, felbamate
Decrease of glutamate mediated felbamate, topiramate
excitation
EFFICACY OF AEDS
All seizure types: absence,
myoclonic, generalised tonicclonic seizures, partial seizures
valproate, lamotrigine, topiramate
clobazam, clonazepam
phenobarbital, primidon
felbamate
levatiracetam, zonisamide
Partial seizures, generalised
tonic-clonic seizures
carbamazepine, oxcarbazepine
gabapentin, vigabatrin, tiagabine
phenytoin
Absence
ethosuximid
PHARMACOLOGY OF AEDS I.
Hepatic metabolism
valproate, carbamazepine,
oxcarbazepine, lamotrigine,
topiramate, clobazam, clonazepam,
phenobarbital, primidon, phenytoin,
ethosuximid, felbamate, tiagabin
No metabolism
gabapentin, vigabatrin
(topiramate, levatiracetam)
Hepatic enzyme induction
carbamazepine, phenytoin,
phenobarbital, primidon
(oxcarbazepine)
Hepatic enzyme inhibition
valproate, felbamate






Inadequate dose → dose escalation
Lack of compliance → measure blood AED levels
False diagnosis: the patient doesn’t have epilepsy
‘Pseudoseizures’ → precise description of seizure, EEG / video
monitoring
Inadequate selection of AED
True inefficacy of AED → AED switch

Other AED on monotherapy

AED combination
POSSIBLE CAUSES OF AED
INEFFICACY
Partial epilepsies
Juvenile myoclonic epilepsy
First AED in monotherapy: 43%
Second AED in monotherapy: 7%
Other monotherapies: 2%
First AED (valproate) in
monotherapy: 85%
AED combination: 5%
Total in remission: 57%
THERAPEUTIC SUCCESSREMISSION
RATES
Altogether
65-70%
of patients with epilepsy
respond well to AED treatment.
 Teratogenic


In normal population: 2-3%
In women on AEDs: 4-9%
 Teratogenic





risk
risk is increased
High AED dose
Fluctuating plasma levels
Polytherapy
Occurrence of spina bifida in the family
Folic acid deficiency
EPILEPSY AND PREGNANCY


Before conception:

Attain the best possible seizure control with the lowest possible AED
dose, preferably in monotherapy

Folic acid profilaction 4 mg/day
During pregnancy:

During first trimester supplement folic acid 4 mg/nap

Change medication only if seizure control worsens

Screening of fetal malformations (ultrasound on week 16 and 20, AFP)

In case of enzyme inductor AEDs, give vitamin K in the third trimester
EPILEPSY AND PREGNANCY: WHAT
TO DO?

Breast feeding is not contraindicated with women on AEDs.

Sleep deprivation can provoke seizures.
EPILEPSY AND BREAST FEEDING
 Driving
is prohibited for one year after a seizure
with loss of consciousness
 Driving
 2-3
is permitted:
years of seizure free interval with patients on AEDs
 2-3
years of seizure free interval after withdrawal of
AEDs
EPILEPSY AND DRIVING
AED: INDICATIONS AND DOSAGE
AED
Seizure type
Dose
Doses Therapeutic
range
per day
range
(mg/day)
(μmol/L)
250-2000
2-3
30-50
Carbamazepine
Partial,Secondary GTCS,
Sodium
Valporate
Primary & Secondary GTCS,
Absence, Myoclonus
400-2500
1-2
NA
Phenytoin
Partial, Secondary GTCS
150-350
1
40-80
Lamotrigine
Lorazepum
Clonazepum
25-500
4 i.v.
1-8
1-2
-2-4
NA
NA
NA
Ethosuximide
Partial, secondary GTCS
Status Epilepticus
Partial (adjunctive),
Myoclonus
Childhood Abssence
500-1500
2
200-700
Topiramate
Partial, secondary GTCS
200-600
1-2
NA
Phenobarbital
Partial, secondary GTCS
60-100
1
50-150
AED: SIDE EFFECTS
AED

Side Effects 
Neurological
Sodium
Valporate
Carbamazepine
Phenobarbital
Topiramate
Phenytoin
Ataxia,
Nystagmus,
Diplopia,
Tremor
Ataxia,
Nystagmus,
Diplopia
Ataxia,
Nystagmus,
Diplopia
Neuropathy
Ataxia
Ataxia,
Nystagmus,
Diplopia,
Tremor,
Dystonia,
Asterixis
Neuropathy
Cognitive &
behavioral
Drowsiness
Drowsiness
Drowsiness
Drowsiness
Dermatological
Rashes,
Alopecia
Rashes, SJS,
Rashes
Confusion
Drowsiness
----
Hematological
Blood
dyscrasias
Megalobastic Anaemia,
Osteomalacia
----
Blood
dyscrasias
Osteomalacia
Endocrine
Hepatology &
Kidney
Pancreatitis
Liver
damage
Blood
Dyscrasias,
Thrombo-cytopenia
-------
-------
---Nephro-lithiasis
---Liver damage
Others
Nausea,
Weight Gain
Hyponatremia
Foliate deficiency,
Depression (adults),
Excitement (Children),
SLE
SLE
Facial
Dysmorphism
Foliate
deficiency
Drug Interactions
Other AEDs,
Antimalarials
Other AEDs,
OCP,
Antimalarials,
Corticosteroids
Other AEDs,
CCB,OCP,
Digoxin,
Antidepressant,
Antimalarials
Nausea,
depression,
Taste
alteration,
Weight loss
Other AEDs,
OCP
Rashes,
Hirsutism,
Gum
Hypertrophy,
Other AEDs,
OCP, Anti
Arrythmic,
Antimalarials,
Corticosteroids
Thyroxine
WITHDRAWAL OF AED
After complete control of seizures for 2-4 years, withdrawal of Anti Epileptic drugs may be considered. But in case of special
professional group (car driver, machine man etc) withdraw the AED after keen follow-up.
AED should be tapered during the stopping of medications.
Slow reduction by increments over at least 6 months.
If the patient is taking two AEDs one drug should be slowly withdrawn before the second is tapered.
PROGNOSIS
Generalized seizures are more readily controlled than partial seizures.
Childhood onset epilepsy (particularly classical absence seizures) carries the best prognosis for successful drug withdrawal.
The presence of a structural lesion makes complete control of epilepsy less likely.
Epilepsy outcome: After 20 years
50% seizure-free, without drugs, for last 5 years
20% seizure-free, continue to take medication, for last 5 years
30% seizures continue in spite of adequate dose of AEDs.
Refractory epilepsy: When seizure control is not achieved with the first two appropriate and well tolerated AED schedules taken
PSYCHIATRIC COMORBIDITIES IN EPILEPSY
Mood variation: Nearly 1 in 3 patients of epilepsy report significant concern about their mood.
Depression: Upto 55% prevalent in patients with epilepsy.
Suicide rate: In depressed patients with epilepsy is 5 times higher than that in the general population and 25 times higher in
patients with complex partial seizures of temporal lobe origin.
Anxiety : Upto 50% prevalent in patients with epilepsy.
Psychosis: Incidence of Psychosis 3.3% in patients with idiopathic generalized epilepsy, 14% in Temporal lobe epilepsy. In the
concern of severity; Psychosis occurs in 0.6-0.7% patients with epilepsy in community and 19-27% of epilepsy patients who require
hospitalization.