Epilepsy
 Epilepsy (from the Ancient Greek (epilēpsia):
seizure) is a group of chronic neurological disorders
characterized by seizures, which are the result of
abnormal, excessive or hyper synchronous neuronal
activity in the brain.
 Epilepsy (sometimes referred to as a seizure disorder)
is a common chronic neurological condition that is
characterized by recurrent unprovoked epileptic
seizures.
 It affects approximately 50 million people worldwide.
 It is usually controlled, but not cured.
 A chronic disorder characterized by paroxysmal brain
dysfunction due to excessive neuronal discharge, and
usually associated with some alteration of
consciousness.
 The clinical manifestations of the attack may vary
from complex abnormalities of behavior including
generalized or focal convulsions to momentary spells
of impaired consciousness.
 It affects between 2% and 3% of the population, ¾
before adolescence.
 It can be caused by genetic, structural, metabolic or
unknown factors.
 Among the structural factors, the most common
causes in developing countries are infectious and
parasitic diseases, perinatal brain damage, vascular
disease, and head trauma.
 The prognosis of epilepsy depends on the etiology of
the illness as well as on early and sustained treatment.
 It is estimated that up to 70% of people with epilepsy
can live normal lives if they receive proper care.
 The cause of an individual's epilepsy can be divided
into two categories: symptomatic and idiopathic.
 Symptomatic epilepsies originate due to some
structural or metabolic abnormality in the brain.
 The term idiopathic means "a disorder unto itself",
and not "cause unknown".
 No other condition has been implicated as the cause
of the epilepsy.
 Idiopathic epilepsies are often but not exclusively
genetic and generalized – for example Juvenile
Absence Epilepsy.
 Certain circumstances can lead to an increased
likelihood of seizures in someone with epilepsy or in
certain syndromes.
 For example:
During sleep
The transition between sleep and awake
Tiredness
Illness
Constipation
Menstruation
Stress
 They are variously based on:
1. The clinical manifestations of the seizure (motor,
sensory, reflex or psychic)
2. The pathological substrate (hereditary, inflammatory,
degenerative, neoplastic or traumatic)
3. The location of the epileptogenic lesion (rolandic,
temporal, diencephalic regions),
4. The time of life at which the attacks occur (nocturnal,
diurnal, menstrual, etc.)
 Seizure types are organized firstly according to
whether the source of the seizure within the brain is
localized (partial or focal onset seizures) or
distributed (generalized seizures).
 Partial seizures are further divided on the extent to
which consciousness is affected.
 If it is unaffected, then it is a simple partial seizure;
otherwise it is a complex partial seizure.
 Status epilepticus (SE)
Continuous convulsion lasting longer than 30
minutes OR occurrence of serial convulsions
between which there is no return of consciousness
 Idiopathic SE
Seizure develops in the absence of an underlying
CNS lesion/insult
 Symptomatic SE
Seizure occurs as a result of an underlying
neurological disorder or a metabolic abnormality
Seizures
Partial
– Electrical discharges in a
relatively small group of
dysfunctional neurones in
one cerebral hemisphere
– Aura may reflect site of
origin
– + / - LOC
Generalized
– Diffuse abnormal
electrical discharges
from both
hemispheres
– Symmetrically
involved
– No warning
– Always LOC
Simple Complex
Partial Seizures
1. w/ motor
signs
2. w/ somato-
sensory
symptoms
3. w/ autonomic
symptoms
4. w/ psychic
symptoms
1. simple
partial --> loss
of
consciousnes
s
2. w/ loss of
consciousnes
s at onset
Secondary
generalized
1. simple partial
--> generalized
2. complex partial
--> generalized
3. simple partial
--> complex partial
--> generalized
Simple partial
– In simple partial seizures, consciousness is not
impaired.
– Patients can present with motor, somatosensory,
special sensory, autonomic or psychic symptoms
Complex partial
– A complex partial seizure describes a seizure where
consciousness is impaired.
– A partial seizure may begin with a simple seizure,
conversely, its onset may coincide with the
impairment of consciousness.
– It may be presented with or without an aura.
2nd
ary generalized
– Partial sezure evolve to secondarily generalized
seizures . May be gen. Tonic-clonis, tonico or clonic
Simple partial seizures with autonomic symptoms
• Vomiting
• Pallor
• Flushing
• Sweating
• Pupil dilatation
• Piloerection
• Incontinence
Simple partial seizures with autonomic symptoms
• Stiffness in L cheek
• Difficulty in articulating
• R side of mouth is dry
• Salivating on the L side
• Progresses to tongue and back of throat
Simple partial seizures
with psychic symptoms
• Dysphasia
• Dysmnesic
• Cognitive
• Affective
• Illusions
• Structured hallucinations
Simple partial seizure with pyschic symptoms
• Dysmnesic symptoms
– “déjà-vu”
• Affective symptoms
– fear and panic
• Cognitive
• Structured hallucination
– living through a scene of her former life
again
Complex Partial Seizures
• Simple partial onset followed by impaired
consciousness
– with or without automatism
• With impairment of consciousness at onset
– with impairment of consciousness only
– with automatisms
Simple Partial Seizures followed by Complex Partial
Seizures
• Seizure starts from awake state
• Impairment of consciousness
• Automatisms
– lip-smacking
– right leg
Complex Partial Seizures with impairment of
consciousness at onset
• Suddenly sit up
• Roll about with vehement
movement
Partial Seizures evolving to Secondarily Generalized
Seizures
 Simple Partial Seizures to Generalized Seizures
 Complex Partial Seizures to Generalized Seizures
 Simple Partial Seizures to Complex Partial Seizures
to Generalized Seizures
Simple Partial Seizures to Generalized Seizures
• Turns to his R with upper body and
bends his L arm
• Stretches body
• Tonic-clonic seizure
• Relaxation phase
• Postictal sleep
Simple Partial Seizures to Complex Partial Seizures
to Generalized Seizures
• Initially unable to communicate but
understands
• Automatism
– Smacking
– Hand-rubbing
• Abolished communication
• Generalized tonic-clonic seizure
Generalized seizures
• Absence
• Myoclonic
• Clonic
• Tonic
• Tonic-clonic
• Atonic
Absence seizures
– Sudden onset
– Interruption of ongoing activities
– Blank stare
– Brief upward rotation of eyes
– Duration: a few seconds to 1/2 minute
– Evaporates as rapidly as it started
Absence seizures
• Stops hyperventilating
• Mild eyelid clonus
• Slight loss of neck muscle tone
• Oral automatisms
Myoclonic seizures
– Sudden, brief, shock-like
– Predominantly around the hours of going to or
awakening from sleep
– May be exacerbated by volitional movement
(action myoclonus)
Myoclonic seizures
• Symmetrical
myoclonic jerks
Clonic seizures
– Repetitive biphasic jerky movements
– Repetitive vocalisation synchronous with clonic
movements of the chest (mechanical)
– Passes urine
Tonic seizures
– Rigid violent muscle contraction
– Limbs are fixed in strained position
• patient stands in one place
• bends forward with abducted arms
• deep red face
• noises - pressing air through a closed mouth
Tonic seizures
• Elevates both hands
• Extreme forward bending posture
• Keeps walking without falling
• Passes urine
Tonic-clonic seizures
(grand mal)
Tonic Phase
– Sudden sharp tonic
contraction of respiratory
muscle: stridor / moan
– Falls
– Respiratory inhibition
cyanosis
– Tongue biting
– Urinary incontinence
Clonic Phase
– Small gusts of grunting
respiration
– Frothing of saliva
– Deep respiration
– Muscle relaxation
– Remains unconscious
– Goes into deep sleep
– Awakens feeling sore,
headaches
Tonic-clonic seizures
• Tonic stretching of arms and legs
• Twitches in his face and body
• Purses his lips and growls
• Clonic phase
Atonic seizures
– Sudden reduction in muscle tone
– Atonic head drop
Change in consciousness, so that you can't
remember some period of time
Change in emotion, like unexplainable
fear, panic, joy, or laughter
Change in sensation of the skin, usually spreading
over the arm, leg, or trunk.
• Changes in vision, including flashing lights, or
(rarely) hallucinations (seeing things that aren't
there)
• Loss of muscle control and falling, often very
suddenly Muscle movement such as twitching that
might spread up an armor leg
• Muscle movement such as twitching that might
spread up an arm or leg
• Muscle tension/tightening that causes twisting of
the body, head, arms or leg
• Tasting a bitter or metallic flavor
Diagnosis in epilepsy
• Aims:
– Differentiate between events mimicking
epileptic seizures
• E.g. syncope, vertigo, migraine, psychogenic non-
epileptic seizures (PNES)
– Confirm the diagnosis of seizure (or possibly
associated syndrome) and the underlying
etiology
Diagnosis in epilepsy
• Approach:
– History (from patient and witness)
– Physical examination
– Investigations
History
• Event
– Localization
– Temporal relationship
– Factors
– Nature
– Associated features
• Past medical history
• Developmental history
• Drug and immunization history
• Family history
• Social history
Physical Examination
• General
– esp. syndromal or non-syndromal dysmorphic
features, neurocutaneous features
• Neurological
• Other system as indicated
– E.g. Febrile convulsion, infantile spasm
Investigations
• I. Exclusion of differentials:
– Bedside: urinalysis
– Haematological: CBP
– Biochemical: U&Es, Calcium, glucose, ABGs
– Radiological: CXR, CT head
– Toxicological: screen
– Microbiological: LP
(Always used with justification)
Investigations
• II. Confirmation of epilepsy:
– Dynamic investigations : result changes with
attacks
• E.g. EEG
– Static investigations : result same between
and during attacks
• E.g. Brain scan
Electroencephalography (EEG)
• EEG indicated whenever epilepsy
suspected
• Uses of EEG in epilepsy
– Diagnostic: support diagnosis, classify
seizure, localize focus, quantify
– Prognostic: adjust anti-epileptic treatment
Electroencephalography (EEG)
• EEG interpretation in epilepsy
– Hemispheric or lobar asymmetries
– Periodic (regular, recurring)
– Background activity:
• Slow or fast
• Focal or generalized
– Paroxysmal activity:
• Epileptiform features – spikes, sharp waves
• Interictal or ictal
• Spontaneous or triggered
Electroencephalography (EEG)
• Certain epilepsy syndromes have characteristic or suggestive
features
• E.g.
Infantile spasms Hypsarrhythmia
Childhood absence epilepsy Generalized 3-Hz spike-wave
Juvenile myoclonic epilepsy Generalized/ multifocal 4-5 Hz spike-
wave and polyphasic-wave
Benign occipital epilepsy Unilateral/ bilateral occipital sharp/
sharp-slow activity that attenuates on
eye opening
Lennox-Gastaut syndrome Generalized/ bianterior spike-wave
activity at <2.5 Hz
Electroencephalography (EEG)
• E.g. Brief absence seizure in an 18-year-old patient with
primary generalized epilepsy
Electroencephalography (EEG)
• Note:
– Normal in 10-20% of epileptic patients
– Background slowed by:
• AED, diffuse cerebral process, postictal state
– Artifact from:
• Eye rolling, tremor, other movement, electrodes
• Interpreted in the light of proximity to
seizure
Neuroimaging
• Structural neuroimaging
• Functional neuroimaging
Structural Neuroimaging
• Who should have a structural
neuroimaging?
– Status epilepticus or acute, severe epilepsy
– Develop seizures when > 20 years old
– Focal epilepsy (unless typical of benign focal
epilepsy syndrome)
– Refractory epilepsy
– Evidence of neurocutaneous syndrome
Structural Neuroimaging
• Modalities available:
– Magnetic Resonance Imaging (MRI)
– Computerized Tomography (CT)
• What sort of structural scan?
– MRI better than CT
– CT usually adequate if to exclude large tumor
– MRI not involve ionizing radiation
• I.e. not affect fetus in pregnant women (but nevertheless
avoided if possible)
Functional Neuroimaging
• Principles in diagnosis of epilepsy:
– When a region of brain generates seizure, its
regional blood flow, metabolic rate and
glucose utilization increase
– After seizure, there is a decline to below the
level of other brain regions throughout the
interictal period
Functional Neuroimaging
• Modalities available:
– Positron Emission Tomography (PET)
– Single Photon Emission Computerized Tomography
(SPECT)
– Functional Magnetic Resonance Imaging (fMRI)
• Mostly used in:
– Planning epilepsy surgery
– Identifying epileptogenic region
– Localizing brain function
Venn Diagram
Seizure Therapy
Anticonvulsant Surgery
Specific Treatments
Reassurance and
Education
General Treatment
Seizure
Focal with/
without secondary
generalisation
Carbamazepine
Lamotrigine
Levetiracetam
Oxcarbazepine
Generalised
tonic-clonic
Carbamazepine
Lamotrigine
Oxcarbazepine
Sodium valproate
Tonic or atonic
Sodium valproate
Absence
Ethosuximide
Lamotrigine
Sodium valproate
Myoclonic
Levetiracetam
Sodium valproate
Epilepsy with generalised
tonic-clonic seizures only
Carbamazepine
Lamotrigine
Oxcarbazepine
Sodium valproate
Idiopathic generalised
epilepsy
Lamotrigine
Sodium valproate
Topiramate
Drug Starting
dose/day
Typical
maintenance
dose/day
Dosing
interval
Commonest
side effects
Carbamazepine 200 mg 400−1800 mg Bid Rash
Diplopia
Dizziness
Headache
Nausea
Hyponatraemia
Ethosuximide 250 mg 500-2000 mg Bid Nausea
Drowsiness
Headache
Lamotrigine 25 mg 100-400 mg Bid Nausea
Dizziness
Headache
Insomnia
rash
Levetiracetam 250 mg 1000−3000 mg Bid Lethargy
Irritability
Mood disturbance
Insomnia
Drowsiness
Unsteadiness
Sodium
valproate
300 mg 600-2500 mg bid Weight gain
Tremor
Hair loss
Teratogenesis
Education & Support
• Information leaflets and information
about support group
• Avoidance of hazardous physical
activities
• Management of prolonged fits
– Recovery position
– Rectal diazepam
• Side effects of anticonvulsants
Anticonvulsants
• Suppress repetitive action potentials in
epileptic foci in the brain
– Sodium channel blockade
– GABA-related targets
– Calcium channel blockade
– Others: neuronal membrane
hyperpolarisation
Anticonvulsants
Cabamazepine
Phenytoin
Valproic acid
Tonic-clonic and partial
Ethosuximide
Valproic acid
Clonazepam
Absence seizures
Valproic acid
Clonazepam
Myoclonic seizures
Diazepam
Lorazepam
Short term
control
Phenytoin
Phenobarbital
Prolonged
therapy
Status Epilepticus
Corticotropin
Corticosteroids
Infantile Spasms
Drugs used in seizure disorders
Adverse Effects
• Teratogenicity
– Neural tube defects
– Fetal hydantoin syndrome
• Overdosage toxicity
• Life-threatening toxicity
– Hepatotoxicity
– Stevens-Johnson syndrome
• Abrupt withdrawal
Medical Intractability
• No known universal definition
• Risk factors
– High seizure frequency
– Early seizure onset
– Organic brain damage
• Established after adequate drug trials
• Operability
Surgery
• Curative
– Catastrophic unilateral or secondary
generalised epilepsies of infants and young
children
• Sturge-Weber syndrome
• Large unilateral developmental abnormalities
• Palliative
– Vagal nerve stimulation
Surgical Outcome
• Medical Intractability
• A well-localised epileptogenic zone
– EEG, MRI
• Low risk of new post-operative deficits
References
1. Stedman’s Medical Dictionary.
2. MDConsult: Nelson’s textbook.
3. Illustrated Textbook of Pediatrics.
4. Video atlas of epileptic seizures – Classical
examples, International League against epilepsy.
5. Guberman AH, Bruni J, 1999, Essentials of
Clinical Epilepsy, 2nd
edn. Butterworth
Heinemann.
6. Manford M, 2003, Practical Guide to Epilepsy,
Butterworth Heinemann.

epilepsy PPT pschiatric MENTAL HEALTH NURSING

  • 1.
    Epilepsy  Epilepsy (fromthe Ancient Greek (epilēpsia): seizure) is a group of chronic neurological disorders characterized by seizures, which are the result of abnormal, excessive or hyper synchronous neuronal activity in the brain.
  • 3.
     Epilepsy (sometimesreferred to as a seizure disorder) is a common chronic neurological condition that is characterized by recurrent unprovoked epileptic seizures.  It affects approximately 50 million people worldwide.  It is usually controlled, but not cured.
  • 4.
     A chronicdisorder characterized by paroxysmal brain dysfunction due to excessive neuronal discharge, and usually associated with some alteration of consciousness.  The clinical manifestations of the attack may vary from complex abnormalities of behavior including generalized or focal convulsions to momentary spells of impaired consciousness.
  • 5.
     It affectsbetween 2% and 3% of the population, ¾ before adolescence.  It can be caused by genetic, structural, metabolic or unknown factors.  Among the structural factors, the most common causes in developing countries are infectious and parasitic diseases, perinatal brain damage, vascular disease, and head trauma.  The prognosis of epilepsy depends on the etiology of the illness as well as on early and sustained treatment.  It is estimated that up to 70% of people with epilepsy can live normal lives if they receive proper care.
  • 6.
     The causeof an individual's epilepsy can be divided into two categories: symptomatic and idiopathic.  Symptomatic epilepsies originate due to some structural or metabolic abnormality in the brain.  The term idiopathic means "a disorder unto itself", and not "cause unknown".  No other condition has been implicated as the cause of the epilepsy.  Idiopathic epilepsies are often but not exclusively genetic and generalized – for example Juvenile Absence Epilepsy.
  • 7.
     Certain circumstancescan lead to an increased likelihood of seizures in someone with epilepsy or in certain syndromes.  For example: During sleep The transition between sleep and awake Tiredness Illness Constipation Menstruation Stress
  • 8.
     They arevariously based on: 1. The clinical manifestations of the seizure (motor, sensory, reflex or psychic) 2. The pathological substrate (hereditary, inflammatory, degenerative, neoplastic or traumatic) 3. The location of the epileptogenic lesion (rolandic, temporal, diencephalic regions), 4. The time of life at which the attacks occur (nocturnal, diurnal, menstrual, etc.)
  • 9.
     Seizure typesare organized firstly according to whether the source of the seizure within the brain is localized (partial or focal onset seizures) or distributed (generalized seizures).  Partial seizures are further divided on the extent to which consciousness is affected.  If it is unaffected, then it is a simple partial seizure; otherwise it is a complex partial seizure.
  • 10.
     Status epilepticus(SE) Continuous convulsion lasting longer than 30 minutes OR occurrence of serial convulsions between which there is no return of consciousness  Idiopathic SE Seizure develops in the absence of an underlying CNS lesion/insult  Symptomatic SE Seizure occurs as a result of an underlying neurological disorder or a metabolic abnormality
  • 11.
    Seizures Partial – Electrical dischargesin a relatively small group of dysfunctional neurones in one cerebral hemisphere – Aura may reflect site of origin – + / - LOC Generalized – Diffuse abnormal electrical discharges from both hemispheres – Symmetrically involved – No warning – Always LOC
  • 12.
    Simple Complex Partial Seizures 1.w/ motor signs 2. w/ somato- sensory symptoms 3. w/ autonomic symptoms 4. w/ psychic symptoms 1. simple partial --> loss of consciousnes s 2. w/ loss of consciousnes s at onset Secondary generalized 1. simple partial --> generalized 2. complex partial --> generalized 3. simple partial --> complex partial --> generalized
  • 13.
    Simple partial – Insimple partial seizures, consciousness is not impaired. – Patients can present with motor, somatosensory, special sensory, autonomic or psychic symptoms Complex partial – A complex partial seizure describes a seizure where consciousness is impaired. – A partial seizure may begin with a simple seizure, conversely, its onset may coincide with the impairment of consciousness. – It may be presented with or without an aura. 2nd ary generalized – Partial sezure evolve to secondarily generalized seizures . May be gen. Tonic-clonis, tonico or clonic
  • 14.
    Simple partial seizureswith autonomic symptoms • Vomiting • Pallor • Flushing • Sweating • Pupil dilatation • Piloerection • Incontinence
  • 15.
    Simple partial seizureswith autonomic symptoms • Stiffness in L cheek • Difficulty in articulating • R side of mouth is dry • Salivating on the L side • Progresses to tongue and back of throat
  • 16.
    Simple partial seizures withpsychic symptoms • Dysphasia • Dysmnesic • Cognitive • Affective • Illusions • Structured hallucinations
  • 17.
    Simple partial seizurewith pyschic symptoms • Dysmnesic symptoms – “déjà-vu” • Affective symptoms – fear and panic • Cognitive • Structured hallucination – living through a scene of her former life again
  • 18.
    Complex Partial Seizures •Simple partial onset followed by impaired consciousness – with or without automatism • With impairment of consciousness at onset – with impairment of consciousness only – with automatisms
  • 19.
    Simple Partial Seizuresfollowed by Complex Partial Seizures • Seizure starts from awake state • Impairment of consciousness • Automatisms – lip-smacking – right leg
  • 20.
    Complex Partial Seizureswith impairment of consciousness at onset • Suddenly sit up • Roll about with vehement movement
  • 21.
    Partial Seizures evolvingto Secondarily Generalized Seizures  Simple Partial Seizures to Generalized Seizures  Complex Partial Seizures to Generalized Seizures  Simple Partial Seizures to Complex Partial Seizures to Generalized Seizures
  • 22.
    Simple Partial Seizuresto Generalized Seizures • Turns to his R with upper body and bends his L arm • Stretches body • Tonic-clonic seizure • Relaxation phase • Postictal sleep
  • 23.
    Simple Partial Seizuresto Complex Partial Seizures to Generalized Seizures • Initially unable to communicate but understands • Automatism – Smacking – Hand-rubbing • Abolished communication • Generalized tonic-clonic seizure
  • 24.
    Generalized seizures • Absence •Myoclonic • Clonic • Tonic • Tonic-clonic • Atonic
  • 25.
    Absence seizures – Suddenonset – Interruption of ongoing activities – Blank stare – Brief upward rotation of eyes – Duration: a few seconds to 1/2 minute – Evaporates as rapidly as it started
  • 26.
    Absence seizures • Stopshyperventilating • Mild eyelid clonus • Slight loss of neck muscle tone • Oral automatisms
  • 28.
    Myoclonic seizures – Sudden,brief, shock-like – Predominantly around the hours of going to or awakening from sleep – May be exacerbated by volitional movement (action myoclonus)
  • 29.
  • 30.
    Clonic seizures – Repetitivebiphasic jerky movements – Repetitive vocalisation synchronous with clonic movements of the chest (mechanical) – Passes urine
  • 31.
    Tonic seizures – Rigidviolent muscle contraction – Limbs are fixed in strained position • patient stands in one place • bends forward with abducted arms • deep red face • noises - pressing air through a closed mouth
  • 32.
    Tonic seizures • Elevatesboth hands • Extreme forward bending posture • Keeps walking without falling • Passes urine
  • 33.
    Tonic-clonic seizures (grand mal) TonicPhase – Sudden sharp tonic contraction of respiratory muscle: stridor / moan – Falls – Respiratory inhibition cyanosis – Tongue biting – Urinary incontinence Clonic Phase – Small gusts of grunting respiration – Frothing of saliva – Deep respiration – Muscle relaxation – Remains unconscious – Goes into deep sleep – Awakens feeling sore, headaches
  • 34.
    Tonic-clonic seizures • Tonicstretching of arms and legs • Twitches in his face and body • Purses his lips and growls • Clonic phase
  • 36.
    Atonic seizures – Suddenreduction in muscle tone – Atonic head drop
  • 38.
    Change in consciousness,so that you can't remember some period of time Change in emotion, like unexplainable fear, panic, joy, or laughter Change in sensation of the skin, usually spreading over the arm, leg, or trunk.
  • 39.
    • Changes invision, including flashing lights, or (rarely) hallucinations (seeing things that aren't there) • Loss of muscle control and falling, often very suddenly Muscle movement such as twitching that might spread up an armor leg • Muscle movement such as twitching that might spread up an arm or leg • Muscle tension/tightening that causes twisting of the body, head, arms or leg • Tasting a bitter or metallic flavor
  • 40.
    Diagnosis in epilepsy •Aims: – Differentiate between events mimicking epileptic seizures • E.g. syncope, vertigo, migraine, psychogenic non- epileptic seizures (PNES) – Confirm the diagnosis of seizure (or possibly associated syndrome) and the underlying etiology
  • 41.
    Diagnosis in epilepsy •Approach: – History (from patient and witness) – Physical examination – Investigations
  • 42.
    History • Event – Localization –Temporal relationship – Factors – Nature – Associated features • Past medical history • Developmental history • Drug and immunization history • Family history • Social history
  • 43.
    Physical Examination • General –esp. syndromal or non-syndromal dysmorphic features, neurocutaneous features • Neurological • Other system as indicated – E.g. Febrile convulsion, infantile spasm
  • 44.
    Investigations • I. Exclusionof differentials: – Bedside: urinalysis – Haematological: CBP – Biochemical: U&Es, Calcium, glucose, ABGs – Radiological: CXR, CT head – Toxicological: screen – Microbiological: LP (Always used with justification)
  • 45.
    Investigations • II. Confirmationof epilepsy: – Dynamic investigations : result changes with attacks • E.g. EEG – Static investigations : result same between and during attacks • E.g. Brain scan
  • 46.
    Electroencephalography (EEG) • EEGindicated whenever epilepsy suspected • Uses of EEG in epilepsy – Diagnostic: support diagnosis, classify seizure, localize focus, quantify – Prognostic: adjust anti-epileptic treatment
  • 47.
    Electroencephalography (EEG) • EEGinterpretation in epilepsy – Hemispheric or lobar asymmetries – Periodic (regular, recurring) – Background activity: • Slow or fast • Focal or generalized – Paroxysmal activity: • Epileptiform features – spikes, sharp waves • Interictal or ictal • Spontaneous or triggered
  • 48.
    Electroencephalography (EEG) • Certainepilepsy syndromes have characteristic or suggestive features • E.g. Infantile spasms Hypsarrhythmia Childhood absence epilepsy Generalized 3-Hz spike-wave Juvenile myoclonic epilepsy Generalized/ multifocal 4-5 Hz spike- wave and polyphasic-wave Benign occipital epilepsy Unilateral/ bilateral occipital sharp/ sharp-slow activity that attenuates on eye opening Lennox-Gastaut syndrome Generalized/ bianterior spike-wave activity at <2.5 Hz
  • 49.
    Electroencephalography (EEG) • E.g.Brief absence seizure in an 18-year-old patient with primary generalized epilepsy
  • 50.
    Electroencephalography (EEG) • Note: –Normal in 10-20% of epileptic patients – Background slowed by: • AED, diffuse cerebral process, postictal state – Artifact from: • Eye rolling, tremor, other movement, electrodes • Interpreted in the light of proximity to seizure
  • 51.
  • 52.
    Structural Neuroimaging • Whoshould have a structural neuroimaging? – Status epilepticus or acute, severe epilepsy – Develop seizures when > 20 years old – Focal epilepsy (unless typical of benign focal epilepsy syndrome) – Refractory epilepsy – Evidence of neurocutaneous syndrome
  • 53.
    Structural Neuroimaging • Modalitiesavailable: – Magnetic Resonance Imaging (MRI) – Computerized Tomography (CT) • What sort of structural scan? – MRI better than CT – CT usually adequate if to exclude large tumor – MRI not involve ionizing radiation • I.e. not affect fetus in pregnant women (but nevertheless avoided if possible)
  • 54.
    Functional Neuroimaging • Principlesin diagnosis of epilepsy: – When a region of brain generates seizure, its regional blood flow, metabolic rate and glucose utilization increase – After seizure, there is a decline to below the level of other brain regions throughout the interictal period
  • 55.
    Functional Neuroimaging • Modalitiesavailable: – Positron Emission Tomography (PET) – Single Photon Emission Computerized Tomography (SPECT) – Functional Magnetic Resonance Imaging (fMRI) • Mostly used in: – Planning epilepsy surgery – Identifying epileptogenic region – Localizing brain function
  • 56.
  • 57.
    Seizure Therapy Anticonvulsant Surgery SpecificTreatments Reassurance and Education General Treatment Seizure
  • 58.
    Focal with/ without secondary generalisation Carbamazepine Lamotrigine Levetiracetam Oxcarbazepine Generalised tonic-clonic Carbamazepine Lamotrigine Oxcarbazepine Sodiumvalproate Tonic or atonic Sodium valproate Absence Ethosuximide Lamotrigine Sodium valproate Myoclonic Levetiracetam Sodium valproate Epilepsy with generalised tonic-clonic seizures only Carbamazepine Lamotrigine Oxcarbazepine Sodium valproate Idiopathic generalised epilepsy Lamotrigine Sodium valproate Topiramate
  • 59.
    Drug Starting dose/day Typical maintenance dose/day Dosing interval Commonest side effects Carbamazepine200 mg 400−1800 mg Bid Rash Diplopia Dizziness Headache Nausea Hyponatraemia Ethosuximide 250 mg 500-2000 mg Bid Nausea Drowsiness Headache Lamotrigine 25 mg 100-400 mg Bid Nausea Dizziness Headache Insomnia rash Levetiracetam 250 mg 1000−3000 mg Bid Lethargy Irritability Mood disturbance Insomnia Drowsiness Unsteadiness Sodium valproate 300 mg 600-2500 mg bid Weight gain Tremor Hair loss Teratogenesis
  • 60.
    Education & Support •Information leaflets and information about support group • Avoidance of hazardous physical activities • Management of prolonged fits – Recovery position – Rectal diazepam • Side effects of anticonvulsants
  • 61.
    Anticonvulsants • Suppress repetitiveaction potentials in epileptic foci in the brain – Sodium channel blockade – GABA-related targets – Calcium channel blockade – Others: neuronal membrane hyperpolarisation
  • 62.
    Anticonvulsants Cabamazepine Phenytoin Valproic acid Tonic-clonic andpartial Ethosuximide Valproic acid Clonazepam Absence seizures Valproic acid Clonazepam Myoclonic seizures Diazepam Lorazepam Short term control Phenytoin Phenobarbital Prolonged therapy Status Epilepticus Corticotropin Corticosteroids Infantile Spasms Drugs used in seizure disorders
  • 63.
    Adverse Effects • Teratogenicity –Neural tube defects – Fetal hydantoin syndrome • Overdosage toxicity • Life-threatening toxicity – Hepatotoxicity – Stevens-Johnson syndrome • Abrupt withdrawal
  • 64.
    Medical Intractability • Noknown universal definition • Risk factors – High seizure frequency – Early seizure onset – Organic brain damage • Established after adequate drug trials • Operability
  • 65.
    Surgery • Curative – Catastrophicunilateral or secondary generalised epilepsies of infants and young children • Sturge-Weber syndrome • Large unilateral developmental abnormalities • Palliative – Vagal nerve stimulation
  • 66.
    Surgical Outcome • MedicalIntractability • A well-localised epileptogenic zone – EEG, MRI • Low risk of new post-operative deficits
  • 67.
    References 1. Stedman’s MedicalDictionary. 2. MDConsult: Nelson’s textbook. 3. Illustrated Textbook of Pediatrics. 4. Video atlas of epileptic seizures – Classical examples, International League against epilepsy. 5. Guberman AH, Bruni J, 1999, Essentials of Clinical Epilepsy, 2nd edn. Butterworth Heinemann. 6. Manford M, 2003, Practical Guide to Epilepsy, Butterworth Heinemann.

Editor's Notes

  • #12 Simple partial In simple partial seizures, consciousness is not impaired. Patients can present with motor, somatosensory, special sensory, autonomic or psychic symptoms complex A complex partial seizure describes a seizure where consciousness is impaired. A partial seizure may begin with a simple seizure, conversely, its onset may coincide with the impairment of consciousness. It may be presented with or without an aura. 2ndary generalized Partial sezure evolve to secondarily generalized seizures May be gen. Tonic-clonis, tonico or clonic
  • #14 borborygmi
  • #16 Psychic: disturbance of higher mental function Dysmnesic symptoms: deja-vu or jamais-vu, forced thinking - panoramic vision ( a rapid recollection of episodes from his/her past life) Cognitive: dreamy states, distorsions of time sense. Detachment or depersonalisation Affective: Anger and Fear which is apparently unprovoked and abates rapidly
  • #22 Talking b4 sezure take off spectacles and tell others a seizure is coming turn to the R with upper body and bends his L arm “it’s getting stronger” he turns to his L , stretches his body, loses consciousness the seizure develops into a tonic-clonic seizure with relaxation a=phase and postictal sleep
  • #23 Begins with an epigastric rising sensation, which the patient signals later, unable to speak, waving her L hand, can’t communicate followed by smacking and hand-rub
  • #24 Generalized seizure: Atonic1: lack of normal tone Tonic1: under continuous tension Clonic1: rhythmic contractions and relaxations of a muscle in rapid succession Myoclonic1: single or repetitive sudden twitching or spasm of a muscle or a group of muscles
  • #26 Slight impairment of mental performance: Heard what was spoken to her before the seizure stopped, but has probably not understood it qte right “are you there” and “is it there” sound very close to each other in Danish
  • #32 Usually: patient stands in one place bends forward with abducted arms deep red face noises - pressing of air through a closed mouth
  • #34 EEG show generalized sharp waves spikes decrease in frequency
  • #42 Localization: aspects involved e.g. motor, sensory? Any specific site e.g. one limb involved, or generalized involvement? Temporal relationship: number of episode? Diurnal pattern? Duration? Onset and offset? Progression? Persistency? Factors: precipitating? Nature: consciousness impaired? Type of sensory/ motor/ psychic/ emotional disturbances observed/ experienced? Associated features: Prodrome? Aura? Postictal state? Colour of patient? Focal neurological sign?
  • #61 Na channel blockade: phenytoin, carbamazepine, lamotrigine GABA-related targets: benzodiazepines interact with specific receptors on GABAa receptor-chloride ion channel macromolecular complex Ca channel blockade: ethosuxamide inhibits low-threshold Ca currents especially in thalamic neurons that act as pacemakers to generate rhythmic cortical discharge Other mechanisms: Valproic acid - neuronal membrane hyperpolarisation possibly by enhancing K channel permeability
  • #62 Infantile spasms: corticotropin and corticosteroids are commonly used but cause cushingoid side effects.
  • #63 Neural tube defects (spina bifida) associated with valproic acid Fetal hydantoin syndrome - phenytoin Overdosage: most of the commonly used anticonvulsants are CNS depressants - respiratory depression Life threatening toxicity fatal hepato. - valproic acid greatest risk to children <2 yrs of age and patients taking multiple anticonvulsant drugs Lamotrigin - skin rashes and life-threatening Stevens Johnsons syndrome Abrupt withdrawal - increased seizure frequency and severity
  • #64 Intractability can be established after: 2-3 of the established newer first and second line AED, as monotherapy at least one in combination max tolerated dose High seizure frequency: daily / weekly episode brain damage: the more severe the brain damage, the greater the likelihood of seizure persistence Assess operability using imaging studies
  • #65 Large unilateral developmental abnormalities such as cortical dysplasias and porencephalic cysts