Seizure and Epilepsy

Dr Manish Mittal
SRHU
 Seizure
• Defined as symptom of abnormal excessive and
synchronous neuronal activity in the brain.
• Depending on the site of abnormal activity,
seizure can manifest as an alteration in mental
state, tonic or clonic movements(convulsions)
and various other psychic symptoms such as
déjà vu or jamais vu.
• Convulsion: An intense, paroxysmal, involuntary
muscular contraction due to a seizure.
 Syncope
• or Fainting
• Defined as a transient loss of consciousness and postural
tone characterized by rapid onset, short duration, and
spontaneous recovery due to global cerebral hypoperfusion
that most often results from hypotension.
• Many forms of syncope are preceded by a prodromal state
that often includes dizziness and loss of vision ("blackout")
(temporary), loss of hearing (temporary), nausea, sweating,
palpitations and other phenomena, which, if they do not
progress to loss of consciousness and postural tone are
often denoted “presyncope”.
 Pseudoseizure
• Or Psychogenic non-epileptic seizures (PNES).
• Are events superficially resembling an epileptic seizure,
but without the characteristic electrical discharges
associated with epilepsy.
• Thus, PNES are regarded psychological in origin, and
may be thought of as similar to conversion disorder.
• The most conclusive test to distinguish epilepsy from
PNES is long term video-EEG monitoring, with the aim
of capturing one or two episodes on both videotape
and EEG simultaneously.
 Seizure Vs Pseudoseizure
Features Pseudoseizures True Seizures

Pattern Variable Same every time

Precipitant Obvious emotional precipitant May be there but less obvious

and occurrence in presence of and presence of others not
others associated

Sleep Do not occur in sleep Can occur

Response to No response Usually respond to AED

Antiepileptic drugs

Other history History of sexual abuse may be History of incontinence

present

Onset Gradual Abrupt

Duration of tonic 10-15 min or longer 1-2mins

clonic phase
 Seizures Vs Pseudoseizures
Features Pseudoseizures True Seizures
Consciousness Usually preserved with bilateral motor Lost and unresponsive
activity. May be fluctuating but usually to pain
respond to pain
Aura May complain of headache, anxiety, Aura may be present
suffocation, cocking, chest pain and
hyperventilation.
Moaning Swoon or faint, may have moan, cry, Monotonous epileptic
scream or weep cry
Movements Tonic posturing, clinching of teethes, Usually tonic- clonic
pelvic thrusting, opisthotonic posturing,
side to side head movements
Injury Seldom fall or injury Frequent self-injury,
tongue bite, hit head,
hurt limb.
Reflexes Normal Up going plantar,
constricted pupil after
the episode
 Epilepsy
• The medical syndrome of recurrent, unprovoked seizures
is termed epilepsy, but seizures can occur in people who
do not have epilepsy.Ex: Alcohol withdrawal seizure.
• The diagnosis of epilepsy requires the occurrence of
atleast 2 unprovoked seizures 24 hours apart.
• Some clinicians also diagnose epilepsy when one
unprovoked seizure occurs in the setting of a
predisposing cause such as a focal cortical injury or a
generalized interictal discharge that suggests a persistent
genetic predisposition.
 Aura
• That portion of the seizure which occurs
before consciousness is lost and for which
memory is retained afterwards.
• It is the initial sensation of a seizure, without
observable signs, that the patient is aware of
and recollects( this definition separates an
aura from a focal motor seizure).
• Somatosensory Auras: Tingling, Numbness
and electrical feeling. Seen in seizures arising
from sensory cortex( Post central gyrus)
• Visual auras: spots, stars, bars or circles of
light, colors. Seen in seizures from occipital
lobes.
• Auditory auras: Superior temporal gyrus
• Vertiginous auras: Superior temporal gyrus
Focal seizures without Dyscognitive features
or Simple Partial Sz
• Are those seizure which involve small focal area of
brain and are not associated with any impairment
of consciousness or Awareness. Patient ability to
respond is preserved.
• Presentation:
1. Focal Motor seizures: Jacksonian march, Epilepsia
partialis continua, Focal jerk of arm or leg.
2. Focal Sensory seizures: Tingling, Numbness, pain
and sensation of movements.
3. Focal Autonomic seizures: Nausea, epigastric pain,
piloerection, miosis, mydriasis, perspiration, flushing,
palpitations and tachycardia.
TODD’S Palsy: focal Weakness of limb after a partial seizure in
the same limb.
Focal seizure can sometimes go on for secondary
generalization(A Focal seizure may spread within the brain
—a process known as secondary generalization)
D/D: TIA- It’s a negative phenomenon( Focal weakness or
numbness) rather than positive phenomenon in case of
seizure( focal jerk, Paresthesia)
 Focal Sz with Dyscognitive features or
Complex Partial Seizures(CPS)
• Complex partial seizures occur when excessive and
synchronous electrical brain activity causes impaired
awareness and responsiveness. The abnormal
electrical activity might spread to the rest of the
brain causing secondary generalized tonic-clonic
seizure.
• Usually occurs in temporal tobe lesion. Ex Mesial
Temporal Lobe sclerosis
• CPS is seen with lesions of frontal or temporal
lobe(i.e. Parts of brain concerned with awareness)
 Features of CPS
• Stage of Aura: Epigastric aura, deja vu, Jamais vu, fear,
euphoria or Depersonalization.
• Stage of Absence: Patient does not respond during the
episode and do not have memory of the event later on.
• Stage of Automatisms: such as lip smacking, chewing, or
swallowing movements, Hand automatisms (picking up
cloths).
• There may or may not be secondary generalization.
• SPS/CPS may spread into the diencephalon and thence
throughout the rest of the cortex, leading to a secondarily
generalized seizures.
 Primary Generalized Epilepsy
• 10% of all epilepsies.
• Onset is almost always in childhood or adolescence(5
to 15yrs)
• CT/MRI brain normal, No structural abnormality
• Genetic predisposition present
• Background EEG is normal
• EEG may show Generalized spike wave discharges
• Mentation, IQ and school performance is normal.
• No aura
 Cont.
• The abnormal activity begins synchronously throughout the
cortex without an initial partial onset.
• It probably originates in the central diencephalic activating
system and spread simultaneously to all areas of the brain.
(By Thalamocortical pathways)
• Ex: Childhood absence epilepsy, Juvenile myoclonic
epilepsy, Juvenile Absence epilepsy and GTCS on
awakening.
• Usual provoking factors: Sleep deprivation,
Hyperventilation, Photic stimulation and alcohol
withdrawal.
 Features of GTCS(Generalized tonic clonic
seizures)
• Tonic Phase: all the limbs become rigid, pt become
unconscious, fall on the ground, respiration is arrested
and central cyanosis may occur. May last for few minutes
• Clonic phase: Jerking of limbs/clonic jerks. Lasts for few
minutes
• Patient may bite his tongue or has urine incontinence
during the tonic/clonic phase
• Postictal phase: Limbs become flaccid, post ictal
confusion may remain for minutes to hrs. Patient
complain of body ache and headache.
 Absence Seizures
• Always start in childhood
• D/D: CPS
• Short in duration
• 20 to 30 times per day
• No post ictal confusion
• Absence attacks are caused by a generalized
discharges that does not spread out of the
hemispheres and so does not cause loss of posture
 Atonic seizures
• Sz leads to brief loss of muscle tone, usually
resulting in heavy falls with or without loss of
consciousness.
• They only occur in the context of epilepsy
syndromes which involve other forms of
seizure.
• They are not a cause of collapse in patients
without epilepsy
 Myoclonic epilepsy
• Classical Eg- JME- Juvenile myoclonic epilepsy
• Myoclonus may occur before GTCS or it may occur
independently without GTCS
• Usually occur in early morning
• Increases with sleep deprivation or early morning
awakening
• Pt drops things from his hands due to myoclonus
• Myoclonus in night are physiological and non
epileptic and are known as hypnic jerks
 Pathophysiology
• In normal circumstances, recurrent and collateral inhibitory
circuits in the cerebral cortex limit synchronous discharges of
neighboring group of neurons.
• The inhibitory transmitter GABA is particularly important in this
role, and drugs that block GABA receptors provoke seizures.
• Reduction of inhibition and excessive excitation play a part in
the genesis of most seizures.
• Seizures may be partial(Focal) in which paroxysmal neuronal
activity is limited to one part of the cortex, or generalized when
the electrophysiological abnormality involves both hemispheres
simultaneously and synchronously.
 Trigger factors for Seizures
• Sleep deprivation
• Alcohol (particularly withdrawal)
• Recreation drug misuse
• Physical and mental exhaustion
• Flickering lights, TV and Computer screens( for
primary generalised epilepsies)
• Infection and metabolic disturbances
• Uncommonly: loud noises, music, reading, hot
baths
 Causes- Primary generalized epilepsies

• Childhood absence epilepsy

• Juvenile myoclonic epilepsy
• Juvenile absence epilepsy
• GTCS on early morning awakening
 Causes of Acute symptomatic seizures
• Head inury
• NCC(Neurocysticercosis)
• Tuberculoma/Brain Abcess
• Encephalitis
• CVA
• Hepatic failure
• Renal Failure
• Drug toxicity
• Alcohol withdrawal
• Hyponatremia
• Hypocalcemia
• Hypoglycaemia
• Hyperglycaemia
Causes of Remote symptomatic seizures(CNS
insult >7days)
• Old CVA
• Post traumatic gliosis
• Calcified lesion
• Operated brain tumour
• Treated Encephalitis
• Birth asphyxia
Tuberculomas
Meningioma
Old Rt MCA infarct/Gliosis
Brain abcess
Neurocysticercosis
Investigation of Suspected epilepsy
Are the attacks truly epileptic?
• Ambulatory EEG
• Video EEG
From where is the epilepsy arising?
• Standard EEG
• Sleep EEG
• EEG with special electrodes
Cont.(What is the cause of the epilepsy)
Structural lesion
• CT
• MRI
Metabolic Disorder
• LFT, RFT, Electrolytes, Ca, Mg
• RBS(Sugar)
Inflammatory or infective disorder
• ESR, CRP, Blood counts, Chest Xray, HIV, Collagen
diseases and CSF examination
3 Hz Spike Wave Discharges- Childhood
absence epilepsy
Focal spike wave Discharges
Benign epilepsy with centrotemporal spikes
 First aid for Seizures
• Move person away from danger(fire, water,
machinery, furniture)
• After convulsion cease, turn the patient into
semiprone position
• Ensure airways is clear, do not insert anything
in mouth.
• If convulsion continue for more than 5 min
than call for medical help.
 Immediate management of Seizures

• Ensure airway is patent

• Give oxygen to offset cerebral hypoxia
• Give IV diazepam only if convulsions are
continuous or repeated
• Take blood for anticonvulsant levels
• Investigate cause
 Treatment of newly diagnosed epilepsy

• AED therapy is generally recommended after a second unprovoked

epileptic seizure.
• AED therapy should be started only after the diagnosis of epilepsy
is confirmed.
• AED treatment may occasionally be deferred under the following
circumstances:
1. Infrequent seizures with extremely long / several years interval
between seizures.
2. Occurrence of brief ( and infrequent partial sensory or myoclonic)
seizures without underlying structural lesion.
3. Benign epilepsy with centro-temporal spikes (Rolandic epilepsy in
children).
Circumstances in which a single seizure may
be treated
• First seizure presenting as status epilepticus
• Presence of neurological deficit, hemiparesis, mental
retardation, cerebral palsy etc.
• Family history of seizures among parents, siblings or
children.
• EEG abnormality
• Abnormality on brain imaging (CT, MRI)
• When the patient might have had a seizure before. This
may not have been recognized by the patient and may
be brought out only by a careful history.
 Lifestyle modification
• Avoid activities involving exposure to heights,
dangerous machinery, fires or water.
• Take bath with door unlocked
• Avoid driving for atleast 6 mths after Sz.
• Take regular Diet/ Avoid fasting
• Sleep for atlest 8hrs in night/ Avoid night
duties/ sleep by 10 PM
• Avoid flickering lights
 Guidelines for anticonvulsant therapy
• Start with one first line drug
• Start at low dose, gradually increase dose until
effective control of seizures is achieved or side
effects develop(drug level may be helpful)
• Optimise compliance(use minimum number of
doses per day)
• If first drug fails(seizures continue or side effects
develop), start second first line drug whilst
gradually withdrawing first
 Cont.
• 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
• If this combination fails, consider alternative therapy eg.
Epilepsy surgery
• Do not use more than two drugs in combination at any
one time
 Guidelines for choice of AED
Epilepsy Type First Line 0thers

Partial and or Carbamazepine, Lamotrigine, Sodium valproate, Levetiracetam,

Secondary GTCS Oxcarbazepine Topiramate, Phenytoin, Phenobarbitone,
clobazam

Primary GTCS Lamotrigine, Phenobarbitone, Clonazepam

Sodium Valproate

Absence Sodium Valproate Lamotrigine, Clonazepam

Myoclonic Sodium Valproate Clonazepam, Levetiracetam, Phenobarbitone

 Choice of AEDs

• Phenytoin (PHT), Phenobarbitone (PB), Carbamazepine (CBZ),

Valproate (VPA) are usually called ‘conventional drugs’. The
other AEDs are called ‘newer’ drugs.
• It is preferable to use a conventional AED as the initial drug
since those are less expensive and the side effects with long-
term use are well known.
• The choice of AED is mainly based on the seizure type and
epilepsy syndrome. For partial seizures, the initial choice can be
CBZ, OXC. Other drugs which can be used are- Phenytoin,
Phenobarbitone and Valproate.
• For generalized onset tonic clonic seizures, the initial choice is
VPA, Lamotrigine. Others are Phenobarbitone. For absence
seizures VPA is the drug of choice. For myoclonic jerks, VPA and
benzodiazepines are generally used.
• Adult dosage of few AED’s
1. Sodium valproate(chrono)- 500mg
BID(20mg/kg/day)
2. Phenytoin- 300mg HS, 5mg/kg/day
3. Phenobarbitone- 90 to 120mg HS,
2-3mg/kg/day
4. Carbamazepine- 400mg BID, 15mg/kg/day
5. Oxcarbazepine- 600mg BID, 20mg/kg/day.
 AED and Contraception
• AED’s like carbamazepine, phenytoin, topiramate
and phenobarbitone induces hepatic
enzyme(Accelerate metabolism of Estrogen) and
can cause contraceptive failure
• Safest is to use other modes of contraception
• Or give higher dose of estrogen
• Lamotrigine and oxcarbezepine have little
interaction with OCP’s
• Sodium valproate has no interaction with OCP’s
 Epilepsy during Pregnancy
• Fetal Malformation: Due to AED- Spina bifida, cleft lip
and cardiac defects
• Safest AED in pregnancy: Gabapentin, Lamotrigine and
Levetiracetam
• Risk is greatest when treatment is given during first
trimester
• Risk of fetal malformation: increases two fold with one
AED, four fold with two AED.
• Start folic acid 5mg daily for 2 months before
conception to reduce risk
 Breast Feeding and Epilepsy
• Given the overall benefits of breastfeeding
and the lack of evidence for long term harm to
the infant by being exposed to antiepileptic
drugs, mothers with epilepsy can be
encouraged to breast-feed.
 Withdrawing Anticonvulsant therapy
• Withdrawal of AED can be considered after 2 to 4
yr of Sz free period
• Childhood absence epilepsy has best prognosis for
successful drug withdrawal
• JME(juvenile myoclonic epilepsy usually seizure
recur after drug withdrawal)
• Adults with focal lesion in brain also has less
chance of successful drug withdrawal
• Withdraw the AED gradually over 6- 12 months
 Status Epilepticus(SE)
• Common Neurological emergency with high mortality and
morbidity
• Classified as Convulsive SE(CSE) and Non Convulsive
SE(NCSE) based on the presence or absence of convulsion
• CSE: Defined as continuous convulsive seizure for more
than 5min or 2 or more convulsive seizure in which pt
does not regain consciousness in between.
• NCSE: Continuous Non convulsive seizure( change in
mental status from baseline) associated with ictal
discharges on EEG.
 Causes of status epilepticus
• Rare in primary generalised epilepsy but can occur with sudden
withdrawal of drugs
• Encephalitis and brain abscess
• Gliosis after surgery, stroke or head injury
• Brain tumors, neurocysticercosis, MTLE
• Alcohol withdrawal
• Hypoxic brain injury
• Electrolyte abnormalities: Hypoglycemia, hyperglycaemia,
HypoNa, HyperNa, HypoCa, Uraemia and Hepatic
encephalopathy.
• Cortical dysplasia
 Management of status epilepticus
• Step 1 – Maintain airway, breathing and circulation.
• Step 2 – Maintain IV line and take blood sample for
biochemical testing (CBC, Electrolytes, Ca,
Phosphorus, Mg, LFT, RFT, Toxicology and RBS. Use
normal saline, consider thiamine 100mg; followed
by 50 ml of 50% dextrose.
• Step 3 - To terminate the seizure give IV DIAZEPAM
(0.2mg/kg at 5 mg/min) or IV LORAZEPAM (0.1
mg/kg at 2mg/min.
 Cont.
• Step 4 – If seizure continues, give Fosphenytoin 15
to 20mg PE/kg or Phenytoin 15 to 20mg/kg at
50mg/min infusion in normal saline. (in children,
give a second dose of lorazepam before giving
Phenytoin)
Step 5 – If seizure continues give second loading
with half of previous dose of Phenytoin /
Fosphenytoin.
• Step 6 – If seizure continues, give Phenobarbitone
15 mg/kg at 50mg/min.
 Cont.
• Step 7 - – If seizure continues give second loading with half of
previous dose of Phenobarbitone.
• Step 8 – If seizure continues for more than 40 min give IV
anaesthesia
• Midazolam 0.2 mg/kg loading dose followed by 1 to 10
microgram/kg/min.
• Propofol 1 to 2 mg/kg loading dose.
• Thiopentone 5mg/kg.
• NOTE: If IV access is not available, Diazepam (10 to 20 mg) or
lorazepam can be administered rectally or Fosphenytoin via
the IM route.