WELL COME TO OUR

SEMINAR PRESENTATION
Approach to a patient
with seizure
presenter
Tewodros Tsidu
Haider Mamo
Bruk Wolde
Modulator Dr. RODAS (MD,
INTERNIST)
 OUTLINE
•Definition
•Epidemiology
•Classifications
•Etiology/causes of seizure
•Mechanism of seizure
Differential Diagnosis
•Patient Approach
•Investigations
•Management
 INTRODUCTION

• A seizure (from the Latin sacire, "to take possession of")

is a paroxysmal event due to abnormal excessive or
synchronous neuronal activity in the brain.

• Depending on the distribution of discharges, this abnormal

brain activity can have various manifestations, ranging from
dramatic convulsive activity to experiential phenomena not
readily discernible by an observer.

• Although a variety of factors influence the incidence and

prevalence of seizures,5–10% of the population will have
at least one seizure,

• The highest incidence occurring in early childhood and late adulthood.

 INTRODUCTION….

• The meaning of the term seizure needs to be

carefully distinguished from that of epilepsy.

• Epilepsy describes a condition in which a person has

recurrent seizures due to a chronic, underlying process.

• This definition implies that a person with a single seizure,

or recurrent seizures due to correctable or avoidable
circumstances, does not necessarily have epilepsy.
 INTRODUCTION…

• Epilepsy refers to a clinical phenomenon rather than a

single disease entity, since there are many forms and
causes of epilepsy.

• However, among the many causes of epilepsy there are various

epilepsy syndromes in which the clinical and pathologic
characteristics are distinctive and suggest a specific underlying
etiology.

• Using the definition of epilepsy as two or more

unprovoked seizures, the incidence of epilepsy is 0.3–
0.5% in different populations throughout the world, and
the prevalence of epilepsy has been estimated at 5–10
persons per 1000.
 CLASSIFICATION OF SEIZURE

• Why is classification of seizure important?

Determining the type of seizure that has occurred is
essential for focusing the diagnostic approach on
particular etiologies, selecting the appropriate
therapy, and providing potentially vital information
regarding prognosis.
The International League Against Epilepsy (ILAE)
Commission on Classification and Terminology
provided an updated approach to classification of
seizures in 2017
This system is based on the clinical features of
seizures and associated electroencephalographic
findings
 CLASSIFICATION….

• According to ILAE, seizure disorders are

classified into:

• Focal seizure
• Generalized seizure
• Unclassified seizure

• Focal seizure
Focal Seizures with Impaired Awareness
Focal Seizures with Intact Awareness
 CLASSIFICATION….

• Generalized seizures

• Absence seizure Tonic Clonic seizure

• Tonic seizure Clonic seizure
• Atonic seizure Myoclonic seizure

• Unclassified seizures

• Neonatal seizures
• Infantile spasms

• Absence seizures are further classified as typical vs

atypical
 CLASSIFICATION….
Focal seizures
• Focal seizures arise from a neuronal
network either discretely localized within
one cerebral hemisphere or more broadly
distributed but still within the
hemisphere.
• Could have no cognitive defect or have
it.
• Focal seizures can also evolve into
generalized seizures.
 CLASSIFICATION…
The routine inter ictal (i.e., between seizures)
clinical finding or electroencephalogram (EEG) in
patients with focal seizures is often normal or may
show brief discharges termed epileptiform spikes,
or sharp waves.
• Since most focal seizures can arise from the
medial temporal lobe or inferior frontal lobe (i.e.,
regions distant from the scalp), the EEG
recorded during the seizure may be non
localizing.
• However, the seizure focus is often detected
using sphenoidal or surgically placed intracranial
electrodes.
 CLASSIFICATION….

• Focal Seizures with Intact Awareness

• Focal seizures
• can cause motor, sensory, autonomic, or psychic
symptoms without impairment of cognition. Focal
motor seizure arising from the right primary motor
cortex near the area controlling hand movement
will note the onset of involuntary movements of
the contralateral, left hand.
• These movements are typically clonic (i.e., repetitive,
flexion/extension movements) at a frequency of 2–3 Hz;
pure tonic posturing may be seen as well.
• Since the cortical region controlling hand movement is
immediately adjacent to the region for facial expression,
the seizure may also cause abnormal movements of the
face synchronous with the movements of the hand.
 CLASSIFICATIONS…
The EEG recorded with scalp electrodes during the
seizure (i.e., an ictal EEG) may show abnormal
discharges in a very limited region over the
appropriate area of cerebral cortex if the seizure
focus involves the cerebral convexity
• Three additional features seen in
focal motor seizures
• JACKSONIAN MARCH
• TODD’S PARALYSIS
• EPILEPSIA PARTALIS CONTINIUA
• Focal Seizures with Impaired Awareness
Focal seizures may also be accompanied by transient
impairment of the patient’s ability to maintain normal
contact with the environment
The patient is unable to respond appropriately to
visual or verbal commands during the seizure and has
impaired recollection or awareness of the ictal phase

• The seizures frequently begin with an aura (i.e., a

focal seizure without cognitive disturbance) that is
stereotypic for the patient
• The start of the ictal phase is often a sudden behavioral
arrest or motionless stare, which marks the onset of the
period of impaired awareness.
• The behavioral arrest is usually accompanied by
automatisms,which are involuntary, automatic behaviors
that have a wide range of manifestations.
• Automatisms may consist of very basic behaviors
such as chewing, lip smacking, swallowing, or
"picking" movements of the hands, or more
elaborate behaviors such as a display of emotion or
running
The patient is typically confused following the seizure, and
the transition to full recovery of consciousness may range
from seconds up to an hour.

Examination immediately following the seizure may show

an anterograde amnesia or, in cases involving the dominant
hemisphere, a postictal phase
• Ictal EEG shows continuous focal Epds
infrontal and temporal areas
 CLASSIFICATION….

EVOLUTION OF FOCAL SEIZURES TO GENERALIZED

SEIZURES

• Focal seizures can spread to involve both cerebral hemispheres and

produce a generalized seizure, usually of the tonic-clonic variety.

• This evolution is observed frequently following focal seizures arising

from a focus in the frontal lobe, but may also be associated with
focal seizures occurring elsewhere in the brain.

• A focal seizure that evolves into a generalized seizure is often difficult

to distinguish from a primary generalized-onset tonic-clonic seizure.

• Bystanders tend to emphasize the more dramatic, generalized

convulsive phase of the seizure and overlook the more subtle, focal
symptoms present at onset.
• Focal seizure stays for only short time
 CLASSIFICATION….

• In some cases, the focal onset of the seizure becomes

apparent only when a careful history identifies a
preceding aura.

• Often, however, the focal onset is not clinically evident and

may be established only through careful EEG analysis.

• Nonetheless, distinguishing between these two entities is

extremely important, as there may be substantial
differences in the evaluation and treatment of epilepsies
associated with focal versus generalized seizures.
 GENERALIZED SEIZURE

• Generalized seizures are thought to arise at some

point in the brain but immediately and rapidly
engage neuronal networks in both cerebral
hemispheres.

• Bilateral clinical & EEG events without any

detectable focal onset
 1.ABSENCE SEIZURE(TYPICAL VS ATYPICAL)

• Typical absence seizures

• are characterized by sudden, brief lapses of consciousness
without loss of postural control.

• The seizure typically lasts for only seconds

• consciousness returns as suddenly as it was lost, and there is

no postictal confusion.

• usually accompanied by subtle, bilateral motor signs such as:-

 rapid blinking of the eyelids

 chewing movements,
 clonic movements of the hands.
 Patient is unaware of the attack.
May occur hundreds of times a day

 Main seizure type in children (4-8 yr)

• Accounts for 15-20%

• First clue-day dreaming or decreased school

performance

 EEG is diagnostic ( 3HZ Spike-and-wave)

Spontaneous remission: 60-70% during
adolescence
• Atypical absence seizure

 Gradual in onset, longer duration

 Less abrupt to resolve
 accompanied by more obvious motor signs
 EEG: generalized slow spike-wave
pattern<2.5 sec
 Less responsive to AED
 Cause: diffuse multifocal structural lesion
 Seen with mental retardation
 2 . GENERALIZED TONIC-CLONIC
SEIZURE(GTCS)
• 10 % of epilepsy
• The most common seizure type resulting from metabolic
derangements
• Usually begins abruptly without warning.
Ictal phas (tonic-clonic)
• The initial phase of the seizure is usually tonic contraction
of muscles throughout the body

• Tonic contraction of the muscles of expiration and the

larynx at the onset will produce a loud moan or "ictal cry.“

- impaired respiration, Increased secretion, Cyanosis, biting

of tongue,
Increase sympatatic activity (HR,BP,pupilary size)
• Clonic phase: beginning of muscle relaxation
• Takes 40-50 sec
Post ictal phase
• Immediate: Lethargy, confusion,
flaccidity, strider, incontinence-lasting
15-30 min
• Period of unconsciousness lasts 1 hr
• Head ache, muscle cramps, mental
dullness, lack of energy, mood
change-lasting 24 hrs
 3. ATONIC SEIZURE (DROP
ATTACK)
 Loss of postural muscle tone:1-2 sec
• Quick head drop, nodding, collapse
 Brief loss of consciousness
 No post ictal confusion
 EEG: Brief generalized spike-wave then
diffuse slow waves
 Cause: diffuse encephalopathy
 Seen in children with developmental
delay
 Uncommon
 4 .MYOCLONIC SEIZURE
 Sudden brief muscle contraction
 Brief, unpredictable jerks
 Any limb, eyes, head, trunk
 Sometimes alone; often associated with other
generalized seizure types
 Focal, multi-focal, generalized
 Predominant feature of JME
 EEG: Bilateral spikes-wave synchronous with
myoclonus
 Cause: metabolic, degenerative, anoxic brain
damage (physiological during sleep)
 EPILEPSY SYNDROME:

• Disorders in which epilepsy is a predominant

feature and there is sufficient evidence to
suggest a common underlying mechanism.
• Three most common epilepsy syndromes are
Juvenile myclonic epilepsy
• Lennox- Gastaut syndrome
• Mesial temporal lobe epilepsy
• Juvenile myoclonic epilepsy (JME)= is a
generalized seizure disorder of unknown cause is usually
characterized by bilateral myoclonic jerks most frequent
in the morning.
• Lennox-Gastaut syndrome occurs in children and
is defined by the following triad:
• (1) multiple seizure types ( tonic-clonic,
atonic, and atypical absence seizures)
• (2) an EEG showing slow (<3 Hz) spike-and-
wave discharges and other abnormalities;
• (3) impaired cognitive function in most but not
all cases.
• Mesial temporal lobe epilepsy (MTLE) is the most
common syndrome associated with focal seizures
with dyscognitive features and is an example of
an epilepsy syndrome with distinctive clinical,
electroencephalographic, and pathologic features
 ETIOLOGIES OF SEIZURE AND
EPILEPSY

In practice, it is useful to consider the etiologies of

seizures based on the age of the patient, because age
is one of the most important factors determining both
the incidence and the likely causes of seizures or
epilepsy
 ETIOLOGIES…

• During the neonatal period and early infancy, potential

causes include hypoxic-ischemic encephalopathy, trauma, CNS
infection, congenital CNS abnormalities, and metabolic disorders.

• Babies born to mothers using neuro-toxic drugs such as cocaine,

heroin, or ethanol are susceptible to drug-withdrawal seizures in the first
few days after delivery.

• Hypoglycemia and hypocalcemia, which can occur as secondary

complications of perinatal injury, are also causes of seizures early after
delivery.

• Pyrodoxime (B6) deficiency an important inborn error of metabolism

which causes seizure
 ETIOLOGIES…

• The most common seizures arising in late infancy and

early childhood are febrile seizures, which are
seizures associated with fevers but without evidence
of CNS infection or other defined causes.

• The overall prevalence is 3–5% and even higher in some parts

of the world such as Asia.

• Patients often have a family history of febrile seizures or

epilepsy.

• Febrile seizures usually occur between 3 months and 5 years

of age and have a peak incidence between 18 and 24 months.
 ETIOLOGIES…

• The causes of seizures in older adults include

cerebrovascular disease, trauma (including subdural
hematoma), CNS tumors, and degenerative diseases.

• Cerebro-vascular disease may account for 50% of new

cases of epilepsy in patients older than age 65.

• Acute seizures (i.e., occurring at the time of the stroke) are

seen more often with embolic rather than hemorrhagic or
thrombotic stroke.

• Chronic seizures typically appear months to years after the

initial event and are associated with all forms of stroke.
 ETIOLOGIES…

• Metabolic disturbances such as electrolyte

imbalance, hypo- or hyperglycemia, renal failure, and
hepatic failure may cause seizures at any age.

• Similarly, endocrine disorders, hematologic

disorders, vasculitides, and many other systemic
diseases may cause seizures over a broad age range.

• A wide variety of medications and abused

substances are known to precipitate seizures as well
 MECHANISM OF
SEIZURE

• Mechanism of seizure initiation and propagation

• Focal seizure activity can begin in a very discrete region of cortex

and then spread to neighboring regions.

• Seizure initiation phase and a seizure propagation phase.

• The initiation phase is characterized by two concurrent events in an

aggregate of neurons:

(1) High-frequency bursts of action potentials and

(2) Hyper-synchronization
 MECHANISM….

• 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 after potential mediated by

-aminobutyric acid (GABA) receptors or potassium (K+) channels,
depending on the cell type.

• The synchronized bursts from a sufficient number of

neurons result in a so-called spike discharge on the EEG.
 MECHANISM….

• Normally, the spread of bursting activity is prevented by

intact hyper-polarization and a region of "surround" inhibition
created by inhibitory neurons.

• With sufficient activation there is a recruitment of

surrounding neurons via a number of synaptic and non
synaptic mechanisms, including:

(1) An increase in extracellular K+, which blunts hyper-

polarization and depolarizes neighboring neurons;

(2) Accumulation of Ca2+ in pre-synaptic terminals, leading to

enhanced neurotransmitter release;
 MECHANISM….

(3) Depolarization-induced activation of the N-methyl-D-

aspartate (NMDA) subtype of the excitatory amino
acid receptor, which causes additional Ca2+ influx
and neuronal activation; and

(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 local cortical connections, and
to more distant areas via long commissural
pathways such as the corpus callosum
 MECHANISM….

• Mechanism of Epileptogenesis

• Epileptogenesis refers to the transformation of a normal neuronal

network into one that is chronically hyper excitable.

• There is often a delay of months to years between an initial CNS

injury such as trauma, stroke, or infection and the first seizure.

• The injury appears to initiate a process that gradually lowers the

seizure threshold in the affected region until a spontaneous seizure
occurs.

• In many genetic and idiopathic forms of epilepsy, epileptogenesis

is presumably determined by developmentally regulated
events.
 DIFFERENTIAL DIAGNOSIS

1. Syncope

2. Psychological Disorders
- Psychogenic seizure, panic attack

3. Metabolic Disturbances
- Alcoholic blackouts, Hypoglycemia &
Hypoxia

4. Psychoactive Drugs (E.g. hallucinogens)

5. Transient Ischemic Attack

6. Sleep Disorders

7. Movement Disorders

8. Special Considerations in Children

-Apnea, night terror . . .
PATIENT APPROACH
 APPROACH TO A PATIENT WITH
SEIZURE
History
o an indepth history is essential, for in
many cases the diagnosis of a seizure is
based solely on clinical grounds—the
examination and laboratory studies are
often normal.
o Focus on the symptoms before, during, and after the
episode:-in order to differentiate a seizure from other
paroxysmal events
o Interview witnesses to the event
o The history should also focus on the risk factors
and predisposing enents

44
Risk factors
• History of febrile seizures; unrecognized earlier auras or
brief seizures; family history of seizures
• Epileptogenic factors : Identify prior head trauma, stroke,
tumor, or vascular malformation
Precipitating factors
• sleep deprivation, systemic diseases, electrolyte or
metabolic derangements, CNS infection, drugs that lower
the seizure threshold, or alcohol or illicit drug use.

45
 PHYSICAL EXAMINATION
• Signs of infection or systemic illness
• Skin: signs of neurofibromatosis, tuberous sclerosis,
chronic liver or renal disease
• Organomegaly: metabolic storage disease
• Limb asymmetry: developmental brain injury
• Signs of head trauma, alcohol or drug abuse
• Auscultation of the heart and carotid arteries:
cerebrovascular disease

46
• Complete neurologic examination
• Required in all patients
• Focus on cerebral hemisphere signs.
• Assess mental status (including memory, language
function, and abstract thinking) for suggestion of lesions
in the anterior frontal, parietal, or temporal lobes.

47
• Test visual fields to screen for lesions in the optic
pathways and occipital lobes.
• Motor function testing: Pronator drift, deep tendon
reflexes, gait, and coordination may suggest lesions in
motor (frontal) cortex.
• Cortical sensory testing (e.g., double simultaneous
stimulation) may detect lesions in the parietal cortex

48
• search for signs of infection or systemic
illness
• HEENT – head trauma
• CVS - auscultation of the heart and carotid
arteries
• GIS- HSM - a metabolic storage disease
• INTEGU- neurocutaneous disorders, such as
tuberous sclerosis or neurofibromatosis, or
chronic liver or renal disease
• MSK - limb asymmetry may provide a clue to
brain injury early in development
• CNS - All patients require a complete
neurologic examination
49
 INVESTIGATIONS

Laboratory studies
 to identify the more common metabolic
causes of seizures such as abnormalities in
electrolytes, glucose, calcium, or magnesium, and
hepatic or renal disease.
 A screen for toxins in blood and urine should also
be obtained from all patients in appropriate risk
groups, especially when no clear precipitating
factor has been identified.

50
 A lumbar puncture(LP) is indicated if there is any
suspicion of meningitis or encephalitis, and it is
mandatory in all patients infected with HIV, even
in the absence of symptoms or signs suggesting
infection.
 Complete blood count
• To help identify infectious causes

51
Electrophysiologic studies
 All patients who have a possible seizure disorder
should be evaluated with an EEG as soon as
possible.
 Electrographic seizure activity during an event
clearly establishes diagnosis.

 Absence of electrographic seizure activity does

not exclude a seizure disorder.

52
 EEG is used for classifying seizure disorders and
aiding in the selection of anticonvulsant
medications.
 in general, a normal EEG implies a better
prognosis, whereas an abnormal background or
profuse epileptiform activity suggests a poor
outlook

53
 BRAIN IMAGING

Almost all patients with new-onset seizures should have

a brain imaging study to determine whether there is an
underlying structural abnormality that is responsible.

54
 MRI
• MRI > CT : cerebral lesions
• In some cases MRI will identify lesions such as
tumors, vascular malformations, or other
pathologies that need immediate therapy
 CT
• CNS infection and mass lesion,if MRI is not
available

55
 PET & SPECT
for medically refractory seizure
Serum prolactin level
organic Vs psychogenic seizure
elevate in generalized seizure and complex
partial seizure but not in psychogenic seizure

56
 TREATMENT OF SEIZURE AND
EPILEPSY
Based on the patient’s presentation, we should
act accordingly
• Airway management as indicated
• Pulse oximetry, oxygen with suction available
The goal of treatment is to improve the quality of
life of patients and controlling seizures is the first
step.
i. Stop seizure
ii. Reduce frequency of attack
iii. Treat underlying cause
iv. Avoiding treatment side effects
 TREATMENT….

• Therapy for a patient with a seizure disorder is

almost always multimodal and includes

1. Treatment of underlying conditions that cause or

contribute to the seizures,
2. Avoidance of precipitating factors,
3. Suppression of recurrent seizures by prophylactic
therapy with antiepileptic medications or surgery,
and
4. Addressing a variety of psychological and social
issues.
5. Continuous follow ups
I. Treatment of the underlying
disease
If the sole cause of a seizure is a metabolic disturbance such as an
abnormality of serum electrolytes or glucose, then treatment is aimed at
reversing the metabolic problem and preventing its recurrence. Therapy
with antiepileptic drugs is usually unnecessary unless the metabolic
disorder cannot be corrected promptly and the patient is at risk of
having further seizures

If the apparent cause of a seizure was a medication (e.g., theophylline)

or illicit drug use (e.g., cocaine), then appropriate therapy is avoidance
of the drug; there is usually no need for antiepileptic medications unless
subsequent seizures occur in the absence of these precipitants

Seizures caused by a structural CNS lesion such as a brain tumor,

vascular malformation, or brain abscess may not recur after appropriate
treatment of the underlying lesion
 TREATMENT….
II. Avoidance of the precipitating factor
 Some patients can identify particular
situations that appear to lower their
seizure threshold; these situations should
be avoided.
• sleep deprivation
• alcohol intake
• highly specific stimuli such as
• a video game monitor,
• music, or
• an individual's voice ("reflex
epilepsy").
 III. ANTI EPILEPTC DRUGS

• The first step in designing a treatment plan is to

classify the patient's seizure type(s)
• Antiepileptic drug therapy is the mainstay of
treatment for most patients with epilepsy.
• The overall goal is to
• completely prevent seizures
• without causing any untoward side effects,
• preferably with a single medication and
• a dosing schedule that is easy for the patient to
follow.
 AED…
When do you start AED?
 Antiepileptic drug therapy should be started in
any patient with
 recurrent seizures of unknown etiology or
 a known cause that cannot be reversed.
 Whether to initiate therapy in a patient with a
single seizure is controversial.
 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.
 AED…
AED treatment is generally started after two or more
unprovoked seizures,
 because the recurrence proves that the patient has a
substantially increased risk for repeated seizures, well
above 50 percent.
Generally accepted risk factors associated with
recurrent seizures include the following:
(1) An abnormal neurologic examination,
(2) Seizures presenting as status epilepticus,
(3) Post-ictal Todd's paralysis,
(4) A strong family history of seizures, or
(5) An abnormal EEG.
(6) Social indications such as occupation.
Most patients with one or more of these risk
factors should be treated
 INITIATION AND
MONITORING OF THERAPY
 Because the response to any antiepileptic drug is unpredictable,
patients should be carefully educated about the approach to
therapy.
The goal is as mentioned in previous slide
 to prevent seizures and
 minimize the side effects of therapy;
 determination of the optimal dose is often a matter of trial and
error.
Seizure calendar: Patients and family members should
be asked to record
 seizures and
 AED doses
 Triggers like stress, sleep deprivation, alcohol, menses on a
calendar.
This process may take months or longer if the baseline
seizure frequency is low.
 INITIATION AND
MONITORING OF THERAPY
Most anticonvulsant drugs need to be
introduced relatively slowly to minimize side
effects, and
patients should expect that minor side effects
such as mild sedation, slight changes in
cognition, or imbalance will typically resolve
within a few days.
Starting doses are usually the lowest value.
Subsequent increases should be made only
after achieving a steady state with the previous
dose (i.e., after an interval of five or more half-
lives).
 INITIATION AND MONITORING OF
THERAPY

Monitoring of serum antiepileptic drug levels can be

very useful for establishing the initial dosing schedule.
However, the published therapeutic ranges of serum
drug concentrations are only an approximate guide for
determining the proper dose for a given patient.
The key determinants are the clinical measures of
 seizure frequency and
 presence of side effects, …..not the laboratory values.
 INITIATION AND
MONITORING…
Conventional assays of serum drug levels measure the
total drug (i.e., both free and protein bound).
However, it is the concentration of free drug that reflects
extracellular levels in the brain and correlates best with
efficacy.
In practice, other than during the initiation or
modification of therapy,
 monitoring of antiepileptic drug levels is most useful for
documenting compliance.
 INITIATION AND
MONITORING…

If seizures continue despite gradual increases to the

maximum tolerated dose and documented compliance,
 then it becomes necessary to switch to another
antiepileptic drug.
This is usually done by maintaining the patient on the
first drug while a second drug is added.

The dose of the second drug should be adjusted to

decrease seizure frequency without causing toxicity.
 WHEN DO YOU STOP AED?
When to discontinue therapy-this should be decided
by a specialist only!
Overall, about 60% of adults who have their seizures
completely controlled with antiepileptic drugs can
eventually discontinue therapy.
The following patient profile yields the greatest chance of
remaining seizure free after drug withdrawal:
(1) Complete medical control of seizures for 1–5
years;
(2) Single seizure type, either focal or generalized;
(3) Normal neurologic examination, including
intelligence; and
(4) Normal EEG.
The appropriate seizure-free interval is unknown and
undoubtedly varies for different forms of epilepsy.
• However, it seems reasonable to attempt
withdrawal of therapy after 2 years in a patient
who
• Meets all of the above criteria,
• Is motivated to discontinue the medication, and
• Clearly understands the potential risks and benefits.
• 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,
• Patients should be advised to avoid potentially
dangerous situations such as driving or swimming
during this period.
 ……. REFRACTORY
EPILEPSY
In most cases the initial combination therapy
combines first-line drugs (i.e.,
carbamazepine, oxcarbazepine, lamotrigine,
valproic acid, and phenytoin).
If these drugs are unsuccessful, then the
addition of a newer drug such as levetiracetam,
topiramate, and zonisamide is indicated.
Patients with myoclonic seizures resistant to
valproic acid may benefit from the addition of
clonazepam, and
Those with absence seizures may respond to a
combination of valproic acid and ethosuximide.
Always check for drug interaction and
adeherence if seizure occurs in polyparmacy
 …….REFRACTORY EPILEPSY
Surgery for Refractory epilepsy
 Approximately 20–30% of patients with epilepsy continue to have
seizures despite efforts to find an effective combination of antiepileptic
drugs.
 For some, surgery can be extremely effective in substantially reducing
seizure frequency and even providing complete seizure control.
 Understanding the potential value of surgery is especially important
when a patient's seizures are not controlled with initial treatment, as
such patients often fail to respond to subsequent medication trials.
 Rather than
 submitting the patient to years of unsuccessful medical therapy
 psychosocial trauma and
 increased mortality associated with ongoing seizures,
 the patient should have an efficient but relatively brief attempt at
medical therapy and then be referred for surgical evaluation.
 …….REFRACTORY EPILEPSY

Pre surgical evaluation

Surgical options
 Temporal lobectomy
 Amygdelo-hippocampectomy
 Lesionectomy
 Multiple sub-pial resection
 Hemispherectomy
 Corpus callosumectomy
 Vagus nerve stimulation
 BEYOND SEIZURES

• Depression occurs in 20% of patients, and the incidence of

suicide is higher in epileptic patients than in the general
population.

• Depression should be treated through counseling or medication.

• The selective serotonin reuptake inhibitors (SSRIs) typically have no effect

on seizures, while high doses of tricyclic antidepressants may lower the
seizure threshold.

• Anxiety can appear as a manifestation of a seizure, and anxious

or psychotic behavior can sometimes be observed as part of a
post-ictal delirium.

• Post-ictal psychosis is a rare phenomenon that typically occurs

after a period of increased seizure frequency
 BEYOND SEIZURES
Psycho social issues
There continues to be a cultural stigma about
epilepsy, although it is slowly declining in societies
with effective health education programs.
Many patients with epilepsy harbor fears such as
the fear of becoming mentally retarded or dying
during a seizure.
These issues need to be carefully addressed by
educating the patient about epilepsy and by
ensuring that family members, teachers, fellow
employees, and other associates are equally well
informed
Employment, driving and other activities
 BEYOND SEIZURES

• Mortality of epilepsy

• Patients with epilepsy have a risk of death that is roughly two to

three times greater than expected in a matched population without
epilepsy.

• Most of the increased mortality is due to the underlying etiology of

epilepsy (e.g., tumors or strokes in older adults).

• However, a significant number of patients die from accidents, status

epilepticus, and a syndrome known as sudden unexpected death in
epileptic patients (SUDEP), which usually affects young people with
convulsive seizures and tends to occur at night.

• Depression and suicide

 SEQUELAE OF SEIZURE AND
EPILEPSY

• Neuropsychiatric complications

• Cognitive disturbances including memory, intellect, attention and

abstract thinking
• Depression and suicide
• Psychosis and anxiety

• SUDEP
• Seizure ‘be gets’ seizure
• Focal deficits,
• Metabolic disturbances like SIADH
• Physical injury and Psycho-social issues
• Side effects of the drugs
REFERENCE
THANK YOU