Case presentation on seizure and status epilepticus

Out line of presentation
Case presentation on seizure and status epilepticus.
Defination of seizure,status epilepticus and epilepsy.
Pathophysiology,etiology and epidemology of seizure.
Classification of seizure and epileptic syndromes.
Differential diagnosis and investigation of seizures.
Class and choice of anticonvulsant for specific type of
seizure.
Seizure management and seizure effect on specific
population.
PTE pathophysiology and its management.
Management of seizure in children and neonates

Objective of presentation
To be able to approach patient with seizure and
status epilepticus on specific case presentation.
To have good knowledge on seizure and status
epilepticus classification and management.
To be able to know about anticonvulsant choice in
each specific seizure type and specific population.
To know about PTE and pathophysiology and its
management.
To be able to know how seizure is different in
children and neonates.

Case presentation
 28 year/f patient from Addis ababa lafito k/ketema refered
from CMC general hospital after loading phenytoin and
diazepam was given
 MRN=078763 presented to RED side for diagnosis of status
epileptics + ?ICSOL r/o cerebral vein thrombosis +
aspiration pneumonia on 05/08/13 E.C at 3:00 NLT.
1 survey A=patent and protected
 Oral air way inserted and no secretion
B=RR=20 pso2=98 0n INO2
 bilateral good air entry
C=BP=112/70 PR=88 BPM
 IV line secured and investigation sent

Conti……
D=GCS=E2V2M5=9/15
 Eye- mid size and reactive
 RBS-165 mg/dl
 u/s- no collection and IVC was 2cm
-good cardiac contractility
 2 survey=28yr/f patient who presented with abnormal
body movement of 6 episode with out regain of
consciousness which is tonic clonic type for about 3
hours.she has globalized headache for which she slept to
relive it.

Conti….
 O ASL BP=112/70 PR=88 RR=20 PSO2=98 on INO2
 Pink and non icteric sclera
 No LAP clear resonant chest
 S1 and s2 well heard
 Soft abdomen move with respiration
 No CVAT no deformity and no edema
 Plan –keep oral air way
-put on INO2
-keep on lateral position
-CBC,OFT,PICT,VIRAL MARKER
- Catheterize her

Conti…..
 Treament= phenytoin 100mg po tid
=diazepam 10mg IV PRN
=omeprazole 40mg iv day
= put on m.fluid
 On 06/8/13 she was seizure free and discharged home with
phenytoin and and appointed to neuroside after one month
to come with brain MRI result.
 On 07/08/13 she presented to ST paul ED for about 6
episode of abnormal body movement with out regain of
consciousness for about 6 hours

Conti….
1 survey A=patent and not protected
 oral air way inserted and secretion sucked out
B=RR-48 pso2-88 with 15L face mask o2
 Bilateral transmitted sound
C= BP-140/90 PR=122
 full palpable peripheral pulse
D=post ictal and bilaterally mid size reactive pupil
 RBS=166mg/dl
 u/s= no fluid collection,no consolidative change,IVC full

Conti….
 O ASL BP=140/90 PR=122 RR=48 PSO2=88 on face mask
o2
 Transmitted sound bilaterally
 Catheter inserted
 No pertinent physical finding
 Plan=intubation and intubated with ETT size of 7 and fixed
at depth of 22 and transferred to Aabet ICU after
communication.
 On Aabet ICU acceptance note
 1 survey A=protected with ETT size 7 and fixed at 22cm
 No secretion and on ETT care

Conti……
B=RR-20 pso2=94 on MV
Good air entry bilaterally
C=BP=130/80 PR=130
D=sedated with Diazepam
Pupil mid size and reactive and RBS=184mg/dl
Plan= To continue and escalate phenytoin 200mg po
tid
Diazepam 10mg iv PRN
Omeprazole 40 mg iv day
Put on m.fluid and suctioning
Sedated with propofol and when BP becomes 90/50
changed to ketamine and fluid bolus was given

Conti…
 At 7:30 pm on 07/08/13 the patient suddenly arrested for
possible cause cardio respiratory arrest 2 to brain hernation
2 to ?ICSOL r/o cerebral vein thrombosis.
 CPR done no ROSC achieved and death care given
day WBC NEU HCT PLT CREA UREA Na k cl
7/8/13 21 K 92% 49.5 454 K 0.4 18 135 3.7 98
5/8/13 22K 91% 44 435K 0.6 10 135 4.4 104
5/8/13 HCG= negati
ve
and U/A=4
-6
RBC
2-4
pus
cell
Nitrite
=+!
PH=6 SG=1.0
2

Case summary
 Strength in the patient management:
 Pheyntoin and Diazepam was given before referral.
 Detailed evaluation and treatment plan on RED side.
 Worked up by available investigation in our hospital.
 Better air way management and transfer to ICU
 Pit fall in the patient management:
 MRI should be done immediately even though patient can
not afford.
 Phenytoin should be reloaded and other 2nd line
anticonvulsant should be considered.
 Should be observed for long period in the hospital before
discharge.
 The hypotension may be due to propoful so
discontinuation may be important.
 Causes of sudden death in epilepsy should be considered.

Defination of Terms
 Seizures are sudden, abnormal electrical discharges from
the brain that result in changes in sensation, behavior,
movements, perception, or consciousness.
 The clinical signs or symptoms of seizures depend on the
location of the epileptic discharges in the cerebral cortex
and the extent and pattern of the propagation of the
epileptic discharge in the brain.
 Status epilepticus: is any prolonged seizure or recurrent
seizures lasting >5 minutes without return to full
consciousness.
 medically refractory epilepsy: individuals who have tried 2
adequate doses of AED without a clinical response.

Defination of Terms
 Epilepsy is a medical disorder marked by recurrent
unprovoked seizures or one seizure with future further
recurrence risk.
 Epileptic seizures are only one manifestation of neurologic
or metabolic diseases.
 Epileptic seizures have many causes
 genetic predisposition
 head trauma or stroke or brain tumor
 alcohol or drug withdrawal
 metabolic insults, such as hypoglycemia.

Pathophysiology
 A seizure results when a sudden imbalance occurs between
the excitatory and inhibitory forces within the network of
cortical neurons in favor of a sudden-onset net excitation.
 The pathophysiology of focal-onset seizures differs from
the mechanisms underlying generalized-onset seizures.
 Mechanism to cause focal onset seizure
 Decreased inhibition
 Defective activation of GABA neurons
 Increased activation

Pathophysiology of
generalized seizures
 Pathophysiologic mechanisms of generalized seizures is
the thalamocortical interaction that may underlie typical
absence seizures.
 The thalamocortical circuit has normal oscillatory rhythms
with periods of relatively increased excitation and periods
of relatively increased inhibition.
 Altered thalamocortical rhythms may result in primary
generalized-onset seizures.
 The thalamic relay neurons receive ascending inputs from
the spinal cord and project to the neocortical pyramidal
neurons.

Etiology
 In a substantial number of cases the cause of epilepsy
remains unknown.
 Identified causes tend to vary with patient age.
 Leading causes in children are:
 Inherited syndromes
 congenital brain malformations
 infection and head trauma
 Head trauma is the most common known cause in young
adults.

Etiology
 Frequent causes in middle age are:
 Strokes
 Tumors
 head trauma
 In elderly the most common cause are stroke ,Alzheimer
disease and degenerative conditions.
 Categories of genetic disorder that cause seizure:
 Genetic Syndromes with seizure disorder
 Chromosomal deletion or duplication syndromes
 Metabolic diseases
 Mitochondrial diseases
 Seizure disorders caused by single-gene mutations

Etiology
 Genetic syndromes with seizure disorder
 Angelman syndrome
 About 90% of angelman syndrome patients have seizure
 Rett syndrome
 About 70 to 90% of patients have seizure
 Pitt-Hopkins syndrome
 Prader-Willi syndrome
 Sturge-Weber syndrome

Etiology
 Chromosomal deletion or duplication syndromes with
seizures
 Chromosomal 22q deletion syndrome
 Wolf-Hirschhorn syndrome is caused by deletions of
chromosome 4p16.3
 Chromosomal 1p36 deletion syndrome
 Mitochondrial diseases
 Mitochondrial encephalomyopathy
 lactic acidosis
 stroke like episodes syndrome

Etiology
 Metabolic disorders that can cause seizures
 Hypoglycemia or acidosis
 Certain vitamin deficiencies like thiamine
 Congenital disorders of glycosylation
 Neuronal ceroid lipofuscinosis
 Disorders of metal and metal cofactor deficiency
 Disorders of neurotransmitter metabolism
 Lysosomal storage diseases

Etiology
 Seizure disorders caused by single-gene mutations
 Autosomal dominant nocturnal frontal lobe epilepsy is
caused by mutations in the CHRNA4, CHRNB2,
or CHRNA2 genes.
 Autosomal dominant juvenile myoclonic epilepsy is caused
by a mutation in one of a number of genes.
 Benign familial neonatal seizures are caused by mutations
in the KCNQ2 or KCNQ3 genes and are inherited in an
autosomal dominant manner.

Etiology
Mutations in SCN9A, GPA6, and GPR98 are known
to cause familial febrile seizures.
Mutation in GABRG2 is known to cause
generalized epilepsy with febrile seizures and
familial febrile seizures.
Mutations in SCN2A and SCN1B are known to
cause generalized epilepsy with febrile seizures.

Epidemiology
 The lifetime likelihood of experiencing at least one
epileptic seizure is about 9%.
 The lifetime likelihood of receiving a diagnosis of epilepsy
is almost 3%.
 The prevalence of active epilepsy is only about 0.8%.
 The annual incidence of recurrent non febrile seizures in
Minnesota
 about 100/100,000 persons aged 0–1 year
 40/100,000 persons aged 39–40 years
 140/100,000 persons aged 79–80 years

Prognosis
 The patient's prognosis for disability and for a recurrence of
epileptic seizures depends on the type of epileptic seizure
and the epileptic syndrome in question.
 Impairment of consciousness during a seizure may
unpredictably result in morbidity or even mortality.
 Regarding mortality, seizures cause death in a small
proportion of individuals.
 Most deaths are accidental and result from impaired
consciousness.

Prognosis
 The mechanism of death in sudden unexpected death in
epilepsy ( SUDEP ) is controversial.
 suggestions include
 cardiac arrhythmias
 neurogenic pulmonary edema
 suffocation during an epileptic seizure with impairment of
consciousness.
 Treatment with anticonvulsants and successful epilepsy
surgery decreases the risk of SUDEP to that of the general
population.

Seizure classification
 International classification of Epileptic seizures based on
clinical seizure type and on EEG findings during the ictal
period and the interictal period.
 There are two major categories:
 PARTIAL SEIZURES: the neurologic abnormality may be
limited to a specific part or focus of brain.
 GENERALIZED SEIZURES: additionally the seizure may
involve the entire cortical surface (cerebral cortex).

Phases of seizure
 Depending on the types seizure may progress through
several phases:
 The prodromal phase :
 with signs or activity which precede a seizure.
 The aural phase :
 is an unusual sensations of smell / taste/ butterflies in
stomach / feeling of opposite or unfamiliar and intense
feeling.
 The ictal phase :
 with full seizure.
 The postictal phase :
 period of recovery after seizure.

Partial or focal seizure
 These are most common type of epilepsy.
 The first clinical & electroencephalographic changes
indicate initial activation of neurons in one part of cerebral
hemisphere.
 Simple partial seizure
 no impairment of consciousness.
 These arise from a focus in motor cortex.
 It has 4 types that do not impair consciousness.

Simple partial seizure
 1 ) Motor manifestation
 Because the hand and fingers have largest cortical
representations many focal motor seizures begin with
convulsive movement in the upper extremity.
 Involuntary movements may spread centrally & involve the
entire limb including one side of face & lower extremity.
 This progression or spread is known as the Jacksonian
march.
 The client also may exhibit changes in posture or spoken
utterances.
 If the epileptogenic focus is in the parietal region the client
experiences sensory phenomena such as numbness &
tingling in the affected area.

 2 ) Somato –sensory manifestation
If the focus is in the occipital region, the client
may experience bright, flashing lights in the field
of vision opposite the side of focus.
The client can have changes in speech or taste with
involvement of the posterior temporal area of
dominant hemisphere.

 3) Autonomic manifestation
 Seizures of the autonomic system produce epigastric
sensations, pallor sweating, flushing , piloerection,
pupillary dilation, tachycardia, and tachypnea.
 4 ) psychic types
 sub classified into affective, cognitive, dysmnesic seizures.
 Psychic seizures are prone to be missed because they are
subjective symptoms that are diverse and subtle.

Complex partial seizure
 1) Complex partial seizures with automatisms:
The most characteristics features of a complex
partial seizures are accompanying automatisms
which is an action performed unconsciously or
involuntarily.
 These automatic behaviors include purposeless
repetitive activities such as lip-smacking , chewing
, patting a part of the body (touching someone to
tell something).

Complex partial seizure
 Partial seizures evolving to secondary generalized
seizure
These seizures start from a particular focus & then the
electrical discharges spread throughout the brain .
Clinically one side of the face moves and then the
whole body becomes involved
 Consciousness is lost if the discharges spread
throughout the brain.
Corpus callosotomy is a palliative procedure
performed to reduce the severity of drug-resistant
epilepsy and to treat focal seizure with secondary
generalization.

Generalized seizure
 These seizures lead to a loss of consciousness.
 They can be convulsive or non convulsive
 Generalized seizures involve both hemispheres.
 About one third of seizures are generalized.
 1) Absence seizures
 These are abruptperiods of staring and lapses of
awareness lasting a few seconds to a few minutes.

Generalized seizures
 2) myoclonic seizures:
 involves sudden uncontrolled jerking movements of either
a single muscle group or multiple groups sometimes
causing the client to fall.
 The client loses consciousness for a moment and then is
confused post ictally.
 These seizures often occur in morning.
 Clients often report that they spill their coffee with their
seizures.

 3 )CLONIC SEIZURES :
 The clinical manifestations of clonic seizures include
rhythmic muscular contraction & relaxation lasting several
minutes.
 Distinct phases of clonic seizures are not easily observed.
 4 )TONIC SEIZURES:
 These include an abrupt increase in muscular tone &
muscular contraction.
 In addition with tonic seizures there is a loss of
consciousness and the presence of autonomic
manifestations.
 Tonic seizures may last from 30 seconds to several
minutes.

 5 )Generalized Tonic Clonic Seizures: (10%)
 Formerly known as grandmal seizures.
 Tonic clonic seizures are the type of seizures most closely
associated with epilepsy.
 Respirations are interrupted temporarily and the
client may become cyanotic.
 The jaw is fixed and the hands are clenched.
 The eyes may be opened wide and the pupils are
dilated & fixed.

 TONIC PHASE
 lasts 30-60 seconds.
 At the end of this phase the client breathes deeply.
 CLONIC PHASE
 Is phase begins next with rhythmic jerky contraction
and relaxation of all body muscles especially those of
extremities
 The client is usually incontinent and may bite the lips ,
tongue , or inside of the mouth.
 Excessive saliva is blown from the mouth, which creates
frothing at lips.

 The entire tonic clonic phase may last from 2-5 minutes,
after which the client enters the post ictal phase.
 During which the client relaxes & remains totally
unresponsive for a time.
 The client may awake briefly & then go into a post ictal
sleep lasting 30 minutes to several hours.
 This sleep may be followed by general fatigue, depression ,
confusion , or headache , all of which gradually resolve.
 The client has complete amnesia for the seizure episode
and may feel nauseated, stiff, and sore.
 Bruising may occur as the result of falls.

 Petechial hemorrhages may develop on the face & chest
due to vasovagal responses.
 The tonic clonic seizure vary in frequency from many times
daily to once or twice a year.
 Tonic only and clonic only seizure may also occur.
 6 ) ATONIC SEIZURES or DROP ATTACKS :
 These are associated with a total loss of muscle tone.
 They may be mild, with the client briefly nodding the
head or the client may fall to the floor.
 Consciousness is impaired only briefly.

Classification of
Epileptic Syndromes
 1 ) Localization-related epilepsies and syndromes include:
 Idiopathic with age-related onset
 Benign childhood epilepsy with centro temporal spikes
 Childhood epilepsy with occipital paroxysms
 Symptomatic
 Mesial temporal lobe sclerosis
 2 ) Generalized epilepsies and syndromes include :
 Idiopathic, with age-related onset
 Benign neonatal familial convulsions
 Benign neonatal convulsions
 Benign myoclonic epilepsy of infancy

Classification of
Epileptic Syndromes
 Childhood absence epilepsy
 Juvenile absence epilepsy
 Juvenile myoclonic epilepsy (JME)
 Epilepsy with grand mal seizures on awakening
 Idiopathic and/or symptomatic infantile spasms
 Lennox-Gastaut syndrome
 Epilepsy with myoclonic astatic seizures
 Epilepsy with myoclonic absences
 Symptomatic

Differential Diagnosis
 Syncope (eg, vasovagal syncope, dysautonomia).
 Syncope is the most common condition that may be
mistaken for seizures.
 Hypoglycemia or Hyponatremia
 Migrainous aura or migraine equivalent
 Transient ischemic attacks
 Sleep disorders (eg, cataplexy, narcolepsy, night terror)
 Movement disorders (eg, paroxysmal dyskinesia)
 Esophageal reflux in neonates and infants
 Psychiatric conditions (eg,panic attacks, malingering)

Investigation
 Diagnosis is by analyzing detailed clinical history and by
performing ancillary tests for confirmation.
 Electroencephalogram
Locating the focus of abnormal electrical discharge.
Establishing a diagnosis of epilepsy.
Identifying the specific type of seizures
 Measuring serum electrolytes (Ca,Mg and Na)
 Abnormalities on an EEG may include:
 Epileptiform discharges
 Focal slowing
 Diffuse background slowing
 Intermittent diffuse intermixed slowing

Investigation
 Lab studies in seizures: RBS, CBC, KFT, LFT, Lumbar
puncture and urea.
 CT scan & MRI are used to rule out brain lesions that can
trigger seizures.
 PET & SPECT may be helpful to measure cerebral
blood in clients undergo surgery for epilepsy.
 CSF examination has a role in the patient with obtundation
or meningitis, encephalitis, or subarachnoid hemorrhage
is suspected.
 Prolactin levels obtained shortly after a seizure (within 20
min) have been used to assess the etiology.
 levels are typically elevated 3- or 4-fold.
 elevations are more likely to occur with generalized tonic-
clonic seizures than with other seizure types.

Investigation
 Serum Studies of Anticonvulsant Agents
 Baseline measurements
 Toxicity and efficacy
 Medication noncompliance
 To know pharmacokinetic change in patients who are
unusual metabolizers of a medication.
 Work up for fever in children suspected of febrile seizure.
 Complication of seizure
 Fracture of bone.
 Impair intelligence.
 Socially stigmated.
 Reduced quality of life.
 sudden unexpected death in epilepsy

management
 Goals of management:
 To prevent injury during seizures.
 To eliminate factors that precipitate seizure.
 To control seizures to allow a desired lifestyle.
 major goals during seizure are :
 To maintain the airway.
 To prevent injury to client.
 To observe the seizure activity.
 To administer appropriate anticonvulsant drugs.

management
 In a hospital setting suction equipment should be readily
available.
 Any tight clothing around the person’s neck is loosened.
 Put a pillow or folded blanket under the affected person’s
head, but not flex the neck sharply or close the airway.
 Turning the client to his/her side displaces the tongue and
usually opens the airway once the tonic phase has ceased.
 Do not attempt to open the airway with your fingers.
 Use jaw thrust maneuver or head tilt - chin lift to open the
airway to avoid harm the client.

management
• Eliminate the factors that precipitate seizure.
 Eating a balanced diet
 restricting excessive cafeine
 Avoid alcohol intake
 sleeping well
 minimizing emotional stress.
 The goal of treatment in patients with epileptic seizures is
to achieve a seizure-free status without adverse effects.
 Monotherapy is desirable because it decreases the
likelihood of adverse effects and avoids drug interactions
and less expensive.

management
 For patients who had more than one unprovoked seizure
treatment with an anticonvulsant is recommended.
 A care for a single unprovoked seizure is avoidance of
typical precipitants.
 anticonvulsants are not recommended unless the patient
has risk factors for recurrence.
 The risk of recurrence in the 2 years after a first
unprovoked seizure is 15-70%.
 Principal factors that increase the risk of recurrence are
 abnormal MRI study.
 abnormal EEG study.
 a partial-onset seizure.

Anticonvulsant classification
 Blockers of repetitive activation of the sodium channel:
 Phenytoin, carbamazepine, oxcarbazepine,
eslicarbazepine, lamotrigine,topiramate, cenobamate.
 Enhancers of slow inactivation of the sodium channel:
 Lacosamide, rufinamide.
 Gamma-aminobutyric acid –receptor enhancers:
 Phenobarbital, benzodiazepines, clobazam.
 N -methyl-D-aspartic acid receptor blockers:
 Felbamate.
 Alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic
acid receptor blockers:
 Perampanel, topiramate.

Anticonvulsant classification
 T-calcium channel blockers:
 Ethosuximide, valproate.
 N- and L-calcium channel blockers:
 Lamotrigine, topiramate, zonisamide, valproate.
 H-current modulators:
 Gabapentin, lamotrigine.
 Blockers of unique binding sites:
 Gabapentin, levetiracetam, perampanel.
 Carbonic anhydrase inhibitors:
 Topiramate, zonisamide.
 Neuronal potassium channel opener:
 Ezogabine.

Anti convulsant classification

Anticonvulsants for
Specific Seizure Types
 Absence seizures
 If only absence seizures are present most neurologists treat
them with ethosuximide.
 If absence seizures are present along with generalized
tonic-clonic seizures or myoclonic seizures the choices are
valproic acid, lamotrigine, or topiramate.
 Do not use carbamazepine, gabapentin or tiagabine they
may exacerbate absence seizures.
 Tonic or atonic seizures are treated by valproic acid,
lamotrigine, topiramate or felbamate.

Anticonvulsants for
 juvenile myoclonic epilepsy are treated by valproic acid,
lamotrigine, and topiramate and Levetiracetam.
 Primary generalized tonic-clonic seizures respond to
valproic acid, topiramate, or lamotrigine.
 Levetiracetam and perampanel are indicated as adjunctive
therapy for these seizures.
 Generalized and unclassified epilepsies
 valproate should remain the drug of first choice for many
patients with generalized and unclassified epilepsies.
 valproate has better tolerated than topiramate and more
efficacious than lamotrigine.

Anticonvulsants for
 Focal-onset seizures
 monotherapy indications, including carbamazepine,
cenobamate, lacosamide, lamotrigine, oxcarbazepine, and
topiramate.
 Adjunctive therapy with levetiracetam, tiagabine,
gabapentin, pregabalin, lacosamide, cenobamate, or
ezogabine may be considered if the first-line treatments
fails.
 carbamazepine and phenytoin were tolerated better by
men than women.

Anticonvulsants for
 for complex focal seizures carbamazepine may be a better
choice than valproate.
 If carbamazepine fails to control the seizures, lamotrigine,
topiramate, tiagabine, gabapentin, levetiracetam,
oxcarbazepine, pregabalin, and zonisamide are considered
for second or third line therapy.
 Neonates, children, and elderly patients.
 neonate and children they tend to metabolize the drugs
faster than adults.
 This younger population also has rapid increases in the
total volume of distribution.

Anticonvulsants in Specific
Patient Populations
 elderly patients need lower initial and maintenance doses
due to :
 Slowed hepatic metabolism
 Decreased renal clearance
 Decreased volumes of distribution
 Patients with hepatic and renal insufficiency
 Gabapentin, pregabalin, levetiracetam, and lacosamide are
excreted mostly by means of renal clearance, and their
doses can be adjusted for renal insufficiency.
 phenytoin, carbamazepine, valproic acid, and felbamate
have been associated with acute hepatic injury.

Anticonvulsants in
Specific Patient Populations
Women on contraceptive agents
 Drugs such as carbamazepine, phenytoin, phenobarbital,
primidone, felbamate, lamotrigine, topiramate, and
oxcarbazepine, decrease the efficacy of oral contraceptive
pills.
 Women of childbearing age and pregnant women
 Switching medications during pregnancy is not
recommended because it exposes the fetus to
polypharmacy.

Seizure during pregnancy
Eclampsia - serious condition where high blood
pressure results in seizures during pregnancy.
Eclampsia affects about one in every 200 women with
preeclampsia.
symptoms of eclampsia are seizures,loss of
consciousness and agitation.
Management of eclampsia is lowering blood
pressure,deliverind the baby and prophylactic
anticonvulsant like magnesium sulphate.
 Cerebral venous sinus thrombosis is potentially life-
threatening cause of seizure during pregnancy in 12% -
31.9% of cases.

Effect of pregnancy on Epilepsy
 Seizure frequency may remain unchanged or decreases in
2/3 of Women with epilepsy.
 Pregnancy does not cause epilepsy but in known epileptic
patient increased frequency of seizures in pregnancy is 17-
33%.
 Seizure frequency may also vary between pregnancies in
the same woman.
 Frequency of seizure can be differed in different trimester.

Effect of Epilepsy on pregnancy
 Maternal:
 Miscarriage due to trauma experienced during seizures.
 Pre-eclampsia
 Premature separation of placenta
 Pre-term labour
 Fetal:
 Fetal malformation
 Fetal injury

Effect of Epilepsy on pregnancy
 FETAL
 Fetal heart rate deceleration
 IUGR and Still birth
 Fetal anticonvulsant syndrome :
 Occur in children born to mothers who have taken some
AEDs during pregnancy.
 such as spina bifida, heart abnormalities,cleft lip, Lower
intellectual abilities ,Poor language skills,Autistic spectrum
disorders,Delayed walking & talking.

Effect of Drugs in
pregnancy with Epilepsy
 Most of the antiepileptic drugs are teratogenic.
 Carbamazepine and Lamotrigine have the lowest incidence
of major fetal malformations.
 Sodium valproate and Phenytoin are found to be most
teratogenic.
 Levetiracetam may be safe but we should avoid other newer
drugs.

Counseling pregnant
with Epilepsy
 To initiate Monotherapy replacing Polytherapy.
 Discuss about the outcome of pregnancy
 Chance of 90% of having Normal Child
 Risk of Epileptic child : 2-5%
 Congenital Malformation: 1-2%
 Pregnancy complication : 1-2%

During Antenatal care
 INVESTIGATION:
 Serum AFP Level- at 16 weeks.
 Screening for congenital anomalies:
 Detailed fetal anomaly scan with USG including fetal
echocardiography at 18 weeks.
 Serial growth scans are required for detection of small for
gestational age.
 Choose the safest anticonvulsant drug and follow for drug
adherence.

During Antenatal care
 Take Vit K about 10-20 mg daily from 36 week until delivery
for patients who take hepatic enzyme inducing drugs.
 Folic acid 5 mg daily prior to conception throughout the
pregnancy.
 Contraception in EPILEPSY
 Contraceptive failure is more marked with
Carbamazepine, Phenytoin, Phenobarbital.
 If the AED can not be changed we can give higher dose
preparations of the oral contraceptive to avoid failure.

Discontinuing
Anticonvulsant Agents
 After seizure free for typically 2-5 years the physician may
consider discontinuing that patient’s medication.
 increased risk of seizure recurrence after discontinuation
include :
 Several seizure types (eg, worse if tonic or atonic seizures
are present)
 High number and frequency of seizures
 Long duration of epilepsy before the seizures were
controlled
 Short duration of seizure freedom

Discontinuing Anticonvulsant
agents
 Seizure relapse
 About 75% of seizure relapses after medication
discontinuation occur in the first year.
 50% of patient have relapse seizure in the first 3 months.
 all anticonvulsants except primidone, phenobarbital, and
benzodiazepines be gradually discontinued over 6-10 weeks
if they were used for a long period.
 Discontinue primidone, phenobarbital, and
benzodiazepines over 10-16 weeks.

Non pharmacologic
Management of seizures
 Ketogenic diet and modified Atkins diet.
 About 40% to 50% of children who start the keto diet have
50% fewer seizures.
 Vagal nerve stimulation.
 Prevent seizures by sending regular mild pulses of
electrical energy to the brain via the vagus nerve .
 Implantable neuro stimulator.
 implanted device in brain with 2 leads that can both
record intracranial electric activity and provide dynamic
electric stimulation to prevent seizure.

Non pharmacologic
Management of seizures
 Lobectomy and Lesionectomy.
 The goal of lesionectomy is to remove the seizure focus
while preserving vital functions such as speech, sensation,
movement, and memory.
 Temporal lobectomy is a surgery that can lower the number
of seizures or make them less severe or even stop them
from happening.
 The surgen removes some of the part of your brain where
most seizures start.
o Vagal nerve stimulation,implantable neuro stimulator and
lobectomy and lesionectomy are used for treatment of drug
refractory epilepsy.

Post traumatic Epilepsy
 Posttraumatic epilepsy - is a recurrent seizure disorder that
apparently results from injury to the brain.
 Seizures that occur within 24 hours after brain injury are
called immediate PTS.
 PTS that occur within one week after injury are termed
early PTS.
 seizures that occur more than one week after injury are
termed late PTS.
 PTS is a provoked seizure it is different than unprovoked
seizure.
 late PTS may be hard to differentiate from PTE.

Pathophysiology of PTE
 Cortical lesions with cortical dysfunction seem important
in the genesis of the epileptic activity.
 Early seizures are likely to have a different pathogenesis
than late seizures.
 Early PTS are thought to be a nonspecific response to the
physical insult.
 The PTE kindling model of epilepsy postulates that iron
deposition from extravasated blood leads to damage by free
radicals, and the accumulation of glutamate leads to
damage by excitotoxicity.

Pathophysiology of PTE
 Animal studies suggest that disruption of the blood-brain
barrier is likely to contribute to the generation of seizures
in PTE.
 New information suggests that inflammation and
immune system alteration may be contributing to the
development of seizures and epilepsy.
 This offers an opportunity to intervene with therapry to
decrease the developement of PTE.

Etiology
 Patient factors that increase susceptibility to PTE :
 Age younger than 5 years
 Age older than 65 years
 Chronic alcoholism
 Injury-related factors that increase the risk of PTE :
 Severe trauma
 Penetrating head injuries
 Intracranial hematoma

Etiology
 Linear or depressed skull fracture
 Hemorrhagic contusion
 Coma lasting more than 24 hours
 Early PTS
 History of prior TBI as it tends to be cumulative
 Focal neuro imaging or EEG abnormalities in the acute
post injury period

Epidemiology
 The incidence of PTS for all types of head injuries is 2-2.5%
in civilian populations.
 It is higher in the military ( 50 % ) due to higher-velocity
projectiles.
 This incidence increases to 5% in hospitalized
neurosurgical patients.
 In severe head injuries the incidence is 10-15% for adults
and 30-35% for children.
 Early PTS are more common in children while late PTS are
more common in older adults.

Epidemology
 Clinical feature
 Most early PTS are partial seizures and most late PTS are
partial-onset with and without secondarily generalized
seizures.
 Posttraumatic status epilepticus is a complication of PTE.
 It is more common in children than in adults.

Management
 Early posttraumatic seizure should be treated earily as
seizure activity is likely to further damage the already
compromised brain.
 For active seizures :
 IV phenytoin and sodium valproate are the antiepileptic
drugs of choice and are usually effective in stopping the
seizure along with IV benzodiazepine.
 Some patients isolated of seizure may choose not to take
regular medication.

management
 Patients with PTE should be on seizure medications.
 Surgical treatment is an option for PTE refractory to
medication.
 Treatment of posttraumatic epilepsy does not require
hospitalization.
 Admission may be needed for the treatment of status
epilepticus or for video-EEG telemetry to assist in the
diagnosis.

Anticonvulsant Therapy
 Any anticonvulsant except ethosuximide can be prescribed
for PTE.
 Phenytoin seems to increase the risk of impairing cognitive
function.
 Newer AEDS—particularly, topiramate and
levetiracetam—are showing promise in this regard.
 An AED that also may be useful for some of the symptoms
of TBI such as headaches, anxiety can be taken into
consideration when selecting AED.

Anticonvulsants therapy
 Sodium Valproate
 mechanism - potentiate postsynaptic GABA responses,
affect the potassium channel or have a direct membrane-
stabilizing effect.
 As adjunctive therapy valproate may be added to the
regimen at 10-15 mg/kg/d.
 The dosage may increase by 5-10 mg/kg/wk for optimal
clinical response.
 Optimal clinical response is usually achieved at a dose of
less than 60 mg/kg/d.

Anticonvulsant therapy
 Carbamazepine
 is indicated for complex partial seizures.
 It may block posttetanic potentiation by reducing
summation of temporal stimulation.
 After therapeutic response the dose can be reduced to the
minimum effective level or discontinued at least once every
3 months.
 Phenytoin
 may act in the motor cortex inhibiting spread of seizure
activity.
 it may inhibit activity of brainstem centers responsible for
the tonic phase of grand mal seizures.
 Direct IV injection may cause severe hypotension or CNS
depression.

Anticonvulsant therapy
 Topiramate
 is a sulfamate-substituted monosaccharide with a broad
spectrum of antiepileptic activity that may have state-
dependent sodium channel blocking action.
 potentiating the inhibitory activity of the neurotransmitter
gamma-amino butyrate .
 It may block glutamate activity.
 Levetiracetam
 is used as adjunctive therapy for partial seizures and
myoclonic seizures.
 It is also indicated for primary generalized tonic-clonic
seizures.

Surgical Care
 Surgical treatment of PTE has the goal of excision of the
epileptogenic focus.
 Precise identification and excision of the focus is can be
more difficult in PTE.
 But in other types of epilepsy depending on the severity
and location of TBI.

Prevention of PTE
 Prevention of PTE starts with prevention of head trauma.
 In adult patients with severe traumatic brain injury,
prophylaxis with phenytoin is effective in decreasing the
risk of early PTS.
 AED prophylaxis is probably not effective in decreasing the
risk of late PTS.
 A study of seizure prophylaxis in patients with severe
traumatic brain injury or subarachnoid hemorrhage found
that intravenous levetiracetam appeared to be an
alternative to fosphenytoin in that setting.

Prevention of PTE
 Administration of AEDs for the first week after
neurosurgery is a routine practice.
 Phenytoin has most often been used for this purpose.
 But levetiracetam is gaining popularity and appears to be as
effective with fewer adverse effects.
 Some natural antioxidants such as alpha-tocopherol and
condensed tannins have been demonstrated to be
prophylactic for the occurrence of epileptic discharge in the
iron-injected animal brain.

Prevention of PTE
 Predictors of PTE include:
 lesion location (particularly in the left parietal lobe)
 lesion size
 lesion type
 retained ferric metal fragments.
• Medication
 Administering the medication via the intravenous route is
prefered.
 phenytoin or fosphenytoin is the drug of choice for IV
administration for acute seizures.
 The main drugs used for PTE are valproate and
carbamazepine.

Seizures in Infants and Children
 There are many different causes of pediatric seizures.
 Febrile seizures are the most common type of pediatric
seizure.
 It affecting 2% to 5% of all children between 6 months and
5 years of age.
 Epilepsy is diagnosed when a patient has one or more
unprovoked seizures.

PATHOPHYSIOLOGY
 The same to adults but Incomplete myelination of the
brain may limit secondary generalization of seizure activity
in young infants.
 a relative imbalance between glutamate and gamma-
aminobutyric-acid with paradoxical excitation from
gamma-aminobutyric-acid makes younger children more
susceptible to seizure activity.
 Seizures can be primary (intrinsic) or secondary (the result
of another process).

PATHOPHYSIOLOGY
 Primary seizures are often idiopathic or may be caused by
 congenital developmental abnormalities
 in utero central nervous system insult (e.g., infection,
infarct)
 genetic factors.
 Secondary seizures may result from
 trauma or injury
 Infection
 metabolic abnormalities (e.g. hypoglycemia)
 electrolyte abnormalities
 inborn errors of metabolism)
 toxins, or systemic illness.

clinical features
 Generalized seizures involve both hemispheres of the brain
and lead to loss of consciousness usually followed by a
period of post ictal drowsiness.
 In convulsive generalized seizures or grand mal seizures,
rhythmic motor activity affects both sides of the body.
 Non convulsive generalized seizures produce loss of
consciousness without motor activity and can only be
recognized on electroencephalogram.
 Young children with new-onset focal seizures are at
increased risk for structural anatomic abnormalities, and
neuroimaging is more likely to be abnormal in these
children.

management
 Benzodiazepines (Diazepam, Midazolam, Lorazepam)
 are the first-line treatment for prolonged seizures because
of their rapid onset and effectiveness.
 are effective and act by binding to gamma-aminobutyric-
acid receptors.
 The use of a paralytic with intubation obscures the ability
to assess ongoing seizure activity.
 Nonconvulsive status epilepticus may present as a
prolonged postictal state and must be considered in any
patient with altered mental status.
 Lorazepam is preferred over other benzodiazepines
because of its longer duration of action and has fewer side
effects.

management
 Second- and Third-Line Treatments
 If a seizure persists after two doses of a benzodiazepine
have been given, fosphenytoin, levetiracetam,
phenobarbital, or valproic acid are preferred second-line
treatment choices.
 From all this fosphenytoin is safe and effective.
 advantage of levetiracetam over fosphenytoin is that it is
commonly used for maintenance therapy for multiple
seizure types.

management
 Phenobarbital is most commonly used in neonates who
are often maintained on daily phenobarbital for
subsequent seizure control.
 pentobarbital coma or continuous infusion has been used
for refractory status epilepticus not responsive to multiple
anticonvulsant treatments with reported efficacy between
74% and 100%.
 Valproic acid used for treatment of status epilepticus and is
also effective for partial and generalized seizures.

management
 Fourth-Line Treatment
 Propofol is an IV anesthetic agent shown to effectively
treat refractory status epilepticus better than
pentobarbital.
 Treatment of Glucose and Electrolyte Abnormalities
 Abnormal glucose, sodium, calcium, and magnesium,
especially low levels, can cause seizures.

Febrile seizures
 Simple Febrile seizure:
 is a generalized tonic-clonic seizure lasting < 15 minutes
with a fever 38 ̊c or 100.4 F in child 6 month to 5 year that
occurs only once in 24 hour period.
 no blood studies, neuroimaging, or electroencephalogram
is necessary for most simple febrile seizures and the
evaluation should focus on identifying the source of fever.

Febrile seizures
 Factors that increase the risk to 2% to 4% include
 family history of seizures
 multiple febrile seizures
 first febrile seizure before 12 months of age.
 factors that increase the risk of recurrence include
 developmental delay
 focal seizures
 Todd’s paralysis
 focal neurologic findings on examination
 abnormal findings on EEG, CT, or MRI.

Febrile seizures
 Complex Febrile Seizures
 are seizures with fever that last >15 minutes that recur
within a 24-hour period.
 They are focal and occur in children 5 years of age without
any signs of serious infection.
 Routine blood tests and imaging are not indicated if the
child returns to baseline in the ED.
 Treatment anticonvulsant therapy is not recommended for
simple febrile seizures since side effects outweigh the
minor risks of seizure recurrence.

Neonatal seizures
 Neonates do not have a fully developed neurologic system,
and seizures in this age group can be subtle.
 They are more likely to be focal and often carry a poor
prognosis.
 Neonates with seizures are more likely to have electrolyte
abnormalities than older children.
 Consider head CT for concerns of non accidental trauma,
intracranial hemorrhage, infarction, or mass.

Types of neonatal seizures
 Subtle seizures : 50%
 are more often encountered in the full term infant.
 include chewing, pedaling, or ocular movements.
 Clonic seizures : 25%
 The rhythm of the clonic movements is usually slow at 1-3
movements per second
 Tonic seizures : 5%
 often manifest with tonic extension of the upper and lower
limbs.
 Myclonic seizures : 20%
 Are rapid single or arrhythmic repetitive jerks.
 Neonatal spasms : rare
 sudden stiffening of muscles of arm and legs.

Etiology of neonatal seizures
 Hypoxic-ischemic encephalopathy
 an important and common cause of neonatal seizure.
 Hemorrhage
 more frequently in premature than in term infants.
 Metabolic disorders
 hypoglycemia, hypocalcemia, and hypomagnesemia.
inborn errors of metabolism.
 Genetic disorders
 Intracranial infections
 Brain Malformation syndromes

Etiology of neonatal seizures
 Most seizures in the neonate are focal but
generalized seizures have been described in rare
instances.
 SEIZURES IN CHILDREN WITH
VENTRICULOPERITONEAL SHUNTS
 causes include underlying epilepsy, shunt
malfunction, and central nervous system infection.
So management is treating the underlying cause
after controllnig the active seizure.

Neonatal seizures treatment
 Treat the actively seizing neonate with benzodiazepines as
with older children.
 But for comatose neonate Initial treatment with
phenobarbital should be considered.
 If seizures persist phenytoin should be added.
 Persistent seizures may require the use of an intravenous
benzodiazepine, such as lorazepam or midazolam.
 Identify and treat hypoglycemia and electrolyte
abnormalities.
 Pyridoxine may be effective in seizures that are refractory
to all anticonvulsant medications.

Reference
 patient card from medical recording unit for the
case presentation.
Tintinallis Emergency medicine 8th edition book.
Medscape

Case presentation on seizure and status epilepticus

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