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convulsions in
children
Prepared by:
ANCY ANTO
M.Sc. Nursing
History...
 3000 yrs ago ......Babylonians wrote
about the symptoms and causes of
epilepsy
 caused by demons attacking the person
 The word epilepsy is derived from the
Greek word for "attack’’
Patron of epilepsy.........

 St.valentine
World epilepsy day
National epilepsy day
November 17
Did you know that:
 Epilepsy is not a form of mental illness
 Epilepsy can begin at any age from birth to
99+
 Epilepsy can & does affect memory and
learning.
 NOTHING should be put in the mouth of a
person having a seizure
 Medication does not stop all seizures .
 Epilepsy is not contagious
 The tongue cannot be swallowed during a
seizure
 Most seizures are not medical emergencies
Seizures...
 It is a transient occurrence of signs and / or
symptoms resulting from abnormal excessive or
synchronous neuronal activity in the brain
 A sudden paroxysmal electrical discharge from the
CNS resulting in involuntary motor, sensory or
autonomic disturbances with or without alteration
in sensorium
Epilepsy....
 Is a disorder of the brain characterised by an
enduring predisposition to generate seizures
& by the neurological cognitive, psychological
& social consequences.
Epileptic syndrome..
 Is a disorder that manifests one or more
specific types and a specific age of onset and
a specific prognosis.
Disorders mimicking
seizures...
 Jitteriness
 Benign neonatal sleep myoclonus
 Breath holding spells
 Shuddering attacks
 Syncopal attacks
 Night terror
 pseudo seizures
Provoked vs. Unprovoked
seizures..
 Provoked = occurs during the course of acute
illness
 Common causes
 Febrile seizures
 Metabolic events (b. sugar <36mg/dl)
 Acute CNS infections
 Drug intoxification
 Head trauma
Incidence
 72-80 / 1lak under 9 yrs of age
 46-83 / 1lak under 14 yrs of age
 Prevalence
 Seizure disorders: 360/100,000 (India, Saha
SP 2003).
 350/1lak in India
 Greater in neonatal period
Classification of Epileptic
Seizures.
 Partial seizures:
 Simple partial (consciousness retained)
Motor
Sensory
Autonomic
Psychic
 Complex partial (consciousness impaired)
Simple partial, followed by impaired consciousness
Consciousness impaired at onset
 Partial seizures with secondary generalization
 Generalized seizures
 Absences
 Typical
 Atypical
 Generalized tonic clonic
 Tonic
 Clonic
 Myoclonic
 Atonic
 Infantile spasms
 Unclassified seizures
ILAE classification
Self limited
 Focal
 Generalised
Continuous
Classification of epilepsy syndromes
•Idiopathic-focal & general
•Familial
•Symptomatic
•reflex
Common causes
Infection to the central nervous system
1. Acquired bacterial meningitis
 tuberculus meningitis
 aseptic
 encephalitis
 cerebral malaria
2. Intrauterine infections
Post infectious or post vaccinal encephalopathy
 Pertussis vaccination
 Pan encephalitis
 Post measles encephalopathy
 Chickenpox encephalopathy
 Disseminated encephalomyeolopathy
Metabolic causes
 Dehydration
 Dyselectrolytemia
 Acidosis/ alkalosis
 Hypocalcaemia/ hypomagnesaemia
 Inborn errors of metabolism
Space occupying lesions in the brain
 Neoplasm
 Brain abscess
 Tuberculoma
 Cysticercosis
Vascular
 Arterio venous malformations
 Intracranial thrombosis/ haemorrhage
 Coagulopathies
Congenital malformations
Migration defects
Miscellaneous
 Birth trauma
 Birth asphyxia
 Heat stroke
 Brain swelling
 Poisoning
 Lead encephalopathy
 Breath holding spells
 Gray matter degeneration
Drugs and poisons
 Toxic doses of phenothiazine
 Salicylate
 Diphenylhydantoin
 Carbon monoxide
Causes
Early neonatal
period
Neonatal period 1m - 3 yrs
Birth asphyxia
Obstructed labour
IVH
Hypoglycaemia
IEM
Hypocalcaemia
Kernicterus
Developmental
malformations
Meningitis
Metabolic errors
Febrile
convulsions
Neurologic
infections
Metabolic causes
Lesions
drugs
Mechanisms of seizure
1. Underlying aetiology
2. Epileptogenesis
3. Excitability
4. Neuronal injury after prolonged febrile &
afebrile status epilepticus
Neuron – action potential
Basic mechanisms of
epileptogenesis
Neurophysiology and
neurochemistry
Epileptogenic neurons + disinhibition + circuit
PDS trigger Ca channel (Mg)
synchronization
Opens sp. K+ channel
Hyperpolarisation
Hyperpolarisation
Disappear depolarisation
seizure
Kindling
 Process by which brief trans of electrical
stimuli are repeatedly delivered at
appropriate intervals to a susceptible area of
brain.
 Prolonged generalised seizure
Factors determine focal –
generalised
 Excitability of epileptic neurone
 The ease with which the electric discharge
can be propagated from focus
 Threshold of brain stem for disseminating an
electrical discharge
Excitatory & inhibitory
neurotransmitters
 Glutamate & aspartate – Excitatory
neurotransmitters
Induces Ca + ion current
Depolarisation
seizure
Inhibitory neurotransmitters
GABA Hyperpolarisation
GABA receptors are coupled with Cl- channel
stabilises cell in
resting potential
 Pyridoxine deficiency
 Adenosine- inhibit the release of excitatory
neurotransmitters
Catecholamine's &
indolamines
 ↓ in nor epinephrine -↑ seizure susceptibility
 ↑ in nor epinephrine- ↓ seizure severity
Biochemical alterations
induced by seizure
epilepsy syncope
Precipitating factors
Occurrence
Onset
Duration
Jerking limbs
Facial colour
Perspiration
Post ictal recovery
Post ictal confusion
EEG & prolactin
Rare
Awake , sleep
Abrupt
60-90 sec
Yes
Flushed
Hot, sweaty
Slow
Common
Positive
Common
Awake
Gradual
10-15 sec
Occasional
Pale
Cold, clammy
Rapid
Uncommon
Negative
Partial seizures.
 Simple partial
Localised motor symptoms
Somatosensory, psychic, autonomic symptoms
 Manifestations
- aversive seizure- eyes and head turn away
from focus & loss of consciousness
- rolandic seizure - tonic–clonic movements
involving face, salivation, arrested speech
 Jacksonian march
- Sequential progression of Clonic movements
Simple partial seizures with
sensory signs..
 Numbness
 Tingling
 Pricking
 Paresthesia/ pain originating in one area
 Visual sensations
 Motor phenomena – posturing / hypertonia
- Uncommon < 8yrs
Complex partial seizures(psychomotor
seizures)
 3yrs – adolescence
 Characterised by
- Period of altered behaviour
- Amnesia
- Inability to respond to environment
- Impaired consciousness during event
- Drowsiness / sleep
- Confusion & amnesia
aura
 odd or pleasant odours
 Auditory or visual hallucinations
 Ill defined feelings (de javu)
 Strong feelings of fear and anxiety
 In small children
- emission of cry
- attempt to run
Patterns of motor behaviour
 Stereotypic
 May suddenly cease activity , appear dazed
stare into space
 Confused & apathetic
 Become limp or stiff
 automatisms
 Post ictal confusion
 Exhibit oropharyngeal activities –smacking
chewing , drooling etc
 Rarely exhibit – temper tantrums or rage
Generalised seizures
 Tonic clonic seizures (grandmal )
- Most common
- Occur without warning
Tonic phase clonic phase post ictal phase
Tonic phase
 10- 20 sec
 Eyes roll upward
 Immediate loss of consciousness
 Stiffness
 Contraction of entire body
 Arms flexed
 Legs, head & neck
flexed
 May utter a peculiar cry
 Apnoeic
 Increased salivation
 Loss of swallowing reflex
 If standing, falls to floor or ground
Clonic phase
 30 sec
 Violent jerking movements
 Foams at mouth
 Incontinent of urine and faeces
Post ictal state
 Appears relaxed
 Remain semiconscious
 May awake in few minutes
 Confused for several hours
 Poor coordination
 Mild impairment in fine motor movements
 Visual & speech difficulties
 Vomit or complain of severe headache
 Usually sleeps for several hours
 Feels tired
 No recollection of event
Absence seizures (petit mal/
lapses)
 4-12 years of age
 common in girls than boys
 Ceases at puberty
 Brief / no loss of consciousness
 No alteration in muscle tone
 May go unrecognised
 Abrupt in onset
Manifestations:
 Brief loss of consciousness
 Without aura
 5-10 sec
 Slight loss of muscle tone
 Minor movements
 No incontinence
 Amnesia
 Need reorientation
Atonic & akinetic seizures
(drop attacks )
 2-5 yrs
 Sudden momentary loss of muscle tone &
postural control
 Recurrent frequently
Manifestation :
- Loss of tone causing child to fall down
Myoclonic seizures
 Seizure episodes
 Sudden brief contractions of a muscle
 No post ictal state
 May / not LOC
Infantile spasms
 Infantile myoclonus / massive spasms /
hypsarrhythmia / salaam episodes / Infantile
myoclonic spasms
 6- 8 months of life
 Twice common in boys
 Numerous without post ictal drowsiness
Manifestations
 Series of sudden muscular contractons
 Head flexed arms extended & legs drawn up
 Eyes rolling
 Preceded / followed by cry
 May / not LOC
 Flushing / pallor / cyanosis
 Jack-knife seizure – sudden dropping forward
of the head & neck with trunk flexed forward
 Single momentary shock like contractions
Comparison of simple, complex partial
& absence seizure
Clinical features Simple complex Absence
Age of onset Any age Uncommon before
3 yrs
Uncommon before
3 yrs
Freq /day Variable 1- 2 times Multiple
Duration < 30 sec >60 sec <10 sec
Aura May be sole
manifestation
Frequently never
Impaired
consciousness
Never always Always
Automatisms never frequent frequent
Clinical
features
Simple complex Absence
Clonic
movements
Frequent Occasional Occasional
Post ictal
impairment
Rare Frequent Never
Mental
disorientation
Rare Common Unusual
Video game related epilepsy
 Flicker frequency of video games
 Type – generalised , simple / complex /
absence
 Treatment – abstain from video games
 Factors – screen brightness, sleep
deprivation, fatigue, fever, short distance
from screen
Epilepsy syndromes
 The Major Benign Partial Syndromes
1. Benign Rolandic Epilepsy
- Male preponderance 60%
- Onset 2 - 13 years (peak: 9-10 years)
- Older children- motor & somatosensory
symptoms, usually nocturnal.
 Younger children- Hemiclonic / GTCS
(especially at night).
 Rx: None if seizures are mild and rare.
 Most AEDs very effective.
 Evolution: Recovery before 15 - 16 years.
Benign Occipital Epilepsy
 Frequency- rare
 Genetic 37%, migraine 17%
 Male = female
 Onset 2 - 17 years (peak:7 - 8 years)
 Initial visual symptoms, often followed by a
hemiclonic seizure or by automatism
 Postictal migrainous cephalgia in a quarter of
the cases.
 Rx: Most AEDs with control in 60%.
 Recovery by end of adolescence.
The Major Primary Generalized
Syndromes
Childhood Absence Epilepsy (True Petit Mal
Epilepsy)
 Frequency 8%
 Genetic predisposition- strong 20%
 Female preponderance 75%
 Onset 3 - 12 years (peak: 6 - 7 years)
 Very frequent simple absences.
 Rx: VPA or ESM with control in 70 - 80%.
Evolution: Remission- 95%.
- Rare persistence of absences only- 6%.
- GTCS during adolescence or later- 40%.
Juvenile Myoclonic Epilepsy (JME)
 Frequency 5%
 Genetic predisposition- strong >25%
 Male = female
 Onset: 8-26 years (peak: 16 - 17)
 Myoclonus , GTCS often also occur,
occasionally absence.
 Rx: VPA with control in 60 - 100%
 Evolution: Rarely remits (<10%)
Grand Mal on Awakening
(GMA)
 Genetic predisposition- strong >10%
 Male > female
 Onset 6-24 (peak: puberty)
 GTS exclusively or predoninantly (90%)
 Myoclonic or absence may occur.
 Rx: VPA with control in 60 - 100%
 Evolution: Rarely remits (<20%)
The Major Secondary
Generalized Syndromes
Infantile Spasms (West Syndrome)
Lennox Gastaut Syndrome (LGS)
 Frequency 3 - 10%
 Genetic predisposition- no
 Male preponderance
 Onset 1 - 8 years (peak: 3 - 5 years)
 Poor prognosis in most cases
 Tonic, atypical absence, drop attacks, other
generalized or partial seizures.
 Rx: VPA,rarely with complete control.
 persisting seizures.
DIAGNOSTIC EVALUATION
 History collection
 Physical examination
 Laboratory investigations
- Serum glucose & calcium levels
• Lumbar puncture – Ist febrile seizures
protein content – increased
Imaging studies:
 CT
 MRI- structural lesions
 PET-demonstrate perfusion,O2 & glucose intake
 SPECT scan- perfusion in ictal & inter ictal state
 Cerebral angiography
 Magneto encephalography
 Telemetry
Electroencephalogram
Electric activity of brain.
 Fast activity – beta rhythm(14 - 20 Hz)
 Alpha rhythm – 8 -13 Hz
 Theta rhythm – 4 - 7 Hz
 Slow rhythm- 1 - 3 Hz
Absence seizure
Abnormalities.
 Slow/ abnormal rhythm-generalised ,localised
or lateralised to one side thus helps to
anatomic lesions
 Spikes
 Sharp waves
 Poly spikes
 Slow waves (hypsarrhythmia)
Tests consider in the evaluation of
patients with seizures
Type Test Comments
Simple partial
Complex partial
GTC
Absences
MRI
MRI
MRI
None required
Rule out
structural lesions
Rule out
structural lesions
Rule out
structural lesions
Management of child with
seizures
Goals:
1. Ensure adequate vitals & oxygenation
2. Terminate seizure activity
3. Prevent seizure recurrence
4. Establish the diagnosis & treat the
underlying
steps
 Step I – confirm diagnosis
 Step II – establish seizure type & syndrome
 Step III – evaluate the need for treatment
 Step IV – select AED
 Step V – start monotherapy (start slow go
slow policy)
 Step VI – switch to another monotherapy
add on therapy
Treatment of a newly diagnosed case of
epilepsy
Newly diagnosed case
Ist monotherarpy seizure therapy
IInd monotherapy/ combination therapy seizure
free
Intractable epilepsy
Combination therapy ketogenic diet , VNS
Choice of AED
Seizure First line second line
partial CBZ, PHT, SVA , PB OXC, LTG, TPM
2nd gen GTCS SVA, ESM, CZP,
CLB
LTG , TPM , LEV
GTCS SVA, CBZ, PHT, PB TPM, LTG, OXC,
LEV
Absence SVA, CZP, CLB LTG , TPM , LEV
Myoclonic SVA LTG , TPM , LEV
Atonic / tonic SVA CBZ, CLB , NTZ,
LTG, TPM
mixed SVA
ILAE GUIDELINE FOR DRUG
LEVEL MONITORING
 Check compliance once or twice YEARLY
 Suspect toxicity after each AED change
DURATION:
 Withdrawal – if seizure free for 2 YEARS
 Gradually over 6-12 wks
Ketogenic diet
 A very strict diet that involves fluid restriction,
high fat and low carbohydrate + protein
intake.
 The goal: alter the body’s fuel source from
glucose to fat.
 The basis of the diet – fasting
 The encounter with a faith healer
 Duration – 2yrs
Sample Meals:
 Meal 1:
 melted butter
 heavy whipping
cream
 chicken
 apple
 sugar free Jell-O
Problems that may arise:
 Low blood sugar
 Lethargy
 Nausea
 Vomiting
 Elevated cholesterol
 Kidney stones
 Constipation
 Weight loss or gain
 Dehydration
 Cheating
Vagus nerve stimulation
 >12 years
 50% reduction in
seizures
Types of surgery
1. Resection
Removal of the area causing the seizures
2. Disconnection
Corpus callosotomy
Multiple subpial transections
3.Hemispherectomy
procedure Type
Temporal lobectomy
nonTemporal
lobectomy
Corpus callostomy
Hemispherectomy
Simple/ complex
partial
Partial
Partial, tonic ,clonic
Unilateral , partial ,
hemiparesis
Nursing management
 Seizure precautions
 Relieving anxiety
 Managing treatment
 Providing family support & education
Febrile seizures
 Occurrence of seizure activity in
neurologically healthy infants & children
between 6 months & 5 yrs of age associated
with fever >38c without evidence of
intracranial infection & with no history of prior
afebrile seizures
 Common in 18- 22 months
 Provoked seizures
 Causes:
- Infections of middle ear
- URTI
- Urinary tract & GI infections
Types
 Simple febrile seizures:
- 85%
- Generalised seizures
- Lasting less than 15 min
- No post ictal neurologic abnormalities
 Complex febrile seizures
- Recurrent within 24 hrs
 Febrile status
- A seizure with duration of 30 min
- Without regaining consciousness interictally
Risk factors
 Age <18 months
 Family history
 Shorter duration
Recurrence
75% within 1 yr
Risk of subsequent epilepsy – 2- 2.5 %
Diagnostic evaluation
 History
 Serum electrolytes – calcium , magnesium
 Blood glucose
LUMBAR PUNCTURE
 abnormal neurological examination
 Ongoing seizure
Management
 During the seizure
- Manage as for any other acute seizure
- Should hospitalise
o Lethargy
o Complex features
o Unclear follow up
Long term management
 Primary goal – to prevent recurrences
 Antipyretics – to reduce fever
INTERMITTENT PROPHYLAXIS
 Diazepam – 0.3 – 0.5 mg/ kg orally / rectally
 clobazem - 1mg /kg / day
Continuous prophylaxis
 Indications :
- Recurrent complex seizures
- Abnormal neurodevelopment
- Positive family history
 Sodium valproate is preferred
Status epilepticus
 A seizure that persists for a sufficient length
of time / is repeated frequently enough that
recovery between attacks does not occur
Early status established status
Epilepticus Epilepticus
A condition characterised by an epileptic
seizure that is sufficiently prolonged or
repeated at sufficiently brief intervals so as to
produce an unvarying and enduring epileptic
condition
(dictionary of epilepsy )
Etiology
 Recurrent neonatal seizures
 Traumatic subarachnoid haemorrhage
 HIE
 IEM
Classification
 Generalised status epilepticus
 Partial status epilepticus
 Refractory status epilepticus
 Super refractory status epilepticus
Generalised status epilepticus
 Convulsive seizures
1. Tonic clonic
2. Tonic
3. Clonic
4. Myoclonic
 Non convulsive
Refractory status epilepticus
 Persistent seizure beyond 120 min
 Despite of therapy with benzodiazepine,
phenytoin, phenobarbitone or valproate
 Treatment :
- Midazolam
- Thiopentone
- Magnesium
- Ketogenic diet
Intractable epilepsy
 It is defined as an at least one seizure every
2 months for the first 5 years of treatment &
subsequently as at least one seizure per year
with failure of at least 3 Ist line AEDs
 Rx: surgery
 Ketogenic diet
 VNS
Misconceptions about
childhood epilepsy
 Children with epilepsy are brain injured
 Has mental handicaps
 Only SE will harm child's brain
 An EEG will determine if child has epilepsy
 Abnormal EEG -↑ AED dose
 Child has twitches of legs & arms while
asleep. Are these seizures ?
 Blood level AED ↑ - change the dose ?
 AED – only way of treatment
 Surgery – after a attempting all AED
 Life will never be the same
Nursing diagnosis
 Risk for injury related to CNS dysfunction &
inability to control self secondary to the type of
seizure.
 Risk for aspiration & ineffective breathing
pattern related to impaired motor activity, LOC.
 Risk for injury related to impaired
consciousness & automatisms
 Anxiety / fear related to child having life
threatening seizure activity
 Ineffective tissue perfusion
 Interrupted family processes
 Self esteem disturbances
pediatric convulsion

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pediatric convulsion

  • 2. History...  3000 yrs ago ......Babylonians wrote about the symptoms and causes of epilepsy  caused by demons attacking the person  The word epilepsy is derived from the Greek word for "attack’’
  • 4. World epilepsy day National epilepsy day November 17
  • 5. Did you know that:  Epilepsy is not a form of mental illness  Epilepsy can begin at any age from birth to 99+  Epilepsy can & does affect memory and learning.  NOTHING should be put in the mouth of a person having a seizure
  • 6.  Medication does not stop all seizures .  Epilepsy is not contagious  The tongue cannot be swallowed during a seizure  Most seizures are not medical emergencies
  • 7. Seizures...  It is a transient occurrence of signs and / or symptoms resulting from abnormal excessive or synchronous neuronal activity in the brain  A sudden paroxysmal electrical discharge from the CNS resulting in involuntary motor, sensory or autonomic disturbances with or without alteration in sensorium
  • 8. Epilepsy....  Is a disorder of the brain characterised by an enduring predisposition to generate seizures & by the neurological cognitive, psychological & social consequences.
  • 9. Epileptic syndrome..  Is a disorder that manifests one or more specific types and a specific age of onset and a specific prognosis.
  • 10. Disorders mimicking seizures...  Jitteriness  Benign neonatal sleep myoclonus  Breath holding spells  Shuddering attacks  Syncopal attacks  Night terror  pseudo seizures
  • 11. Provoked vs. Unprovoked seizures..  Provoked = occurs during the course of acute illness  Common causes  Febrile seizures  Metabolic events (b. sugar <36mg/dl)  Acute CNS infections  Drug intoxification  Head trauma
  • 12. Incidence  72-80 / 1lak under 9 yrs of age  46-83 / 1lak under 14 yrs of age  Prevalence  Seizure disorders: 360/100,000 (India, Saha SP 2003).  350/1lak in India  Greater in neonatal period
  • 13. Classification of Epileptic Seizures.  Partial seizures:  Simple partial (consciousness retained) Motor Sensory Autonomic Psychic  Complex partial (consciousness impaired) Simple partial, followed by impaired consciousness Consciousness impaired at onset  Partial seizures with secondary generalization
  • 14.  Generalized seizures  Absences  Typical  Atypical  Generalized tonic clonic  Tonic  Clonic  Myoclonic  Atonic  Infantile spasms  Unclassified seizures
  • 15. ILAE classification Self limited  Focal  Generalised Continuous Classification of epilepsy syndromes •Idiopathic-focal & general •Familial •Symptomatic •reflex
  • 16. Common causes Infection to the central nervous system 1. Acquired bacterial meningitis  tuberculus meningitis  aseptic  encephalitis  cerebral malaria 2. Intrauterine infections
  • 17. Post infectious or post vaccinal encephalopathy  Pertussis vaccination  Pan encephalitis  Post measles encephalopathy  Chickenpox encephalopathy  Disseminated encephalomyeolopathy
  • 18. Metabolic causes  Dehydration  Dyselectrolytemia  Acidosis/ alkalosis  Hypocalcaemia/ hypomagnesaemia  Inborn errors of metabolism
  • 19. Space occupying lesions in the brain  Neoplasm  Brain abscess  Tuberculoma  Cysticercosis
  • 20. Vascular  Arterio venous malformations  Intracranial thrombosis/ haemorrhage  Coagulopathies Congenital malformations Migration defects
  • 21. Miscellaneous  Birth trauma  Birth asphyxia  Heat stroke  Brain swelling  Poisoning  Lead encephalopathy  Breath holding spells  Gray matter degeneration
  • 22. Drugs and poisons  Toxic doses of phenothiazine  Salicylate  Diphenylhydantoin  Carbon monoxide
  • 23. Causes Early neonatal period Neonatal period 1m - 3 yrs Birth asphyxia Obstructed labour IVH Hypoglycaemia IEM Hypocalcaemia Kernicterus Developmental malformations Meningitis Metabolic errors Febrile convulsions Neurologic infections Metabolic causes Lesions drugs
  • 24. Mechanisms of seizure 1. Underlying aetiology 2. Epileptogenesis 3. Excitability 4. Neuronal injury after prolonged febrile & afebrile status epilepticus
  • 25. Neuron – action potential
  • 26.
  • 28. Neurophysiology and neurochemistry Epileptogenic neurons + disinhibition + circuit PDS trigger Ca channel (Mg) synchronization Opens sp. K+ channel Hyperpolarisation
  • 29.
  • 31. Kindling  Process by which brief trans of electrical stimuli are repeatedly delivered at appropriate intervals to a susceptible area of brain.  Prolonged generalised seizure
  • 32. Factors determine focal – generalised  Excitability of epileptic neurone  The ease with which the electric discharge can be propagated from focus  Threshold of brain stem for disseminating an electrical discharge
  • 33. Excitatory & inhibitory neurotransmitters  Glutamate & aspartate – Excitatory neurotransmitters Induces Ca + ion current Depolarisation seizure
  • 34.
  • 35. Inhibitory neurotransmitters GABA Hyperpolarisation GABA receptors are coupled with Cl- channel stabilises cell in resting potential  Pyridoxine deficiency  Adenosine- inhibit the release of excitatory neurotransmitters
  • 36. Catecholamine's & indolamines  ↓ in nor epinephrine -↑ seizure susceptibility  ↑ in nor epinephrine- ↓ seizure severity
  • 38. epilepsy syncope Precipitating factors Occurrence Onset Duration Jerking limbs Facial colour Perspiration Post ictal recovery Post ictal confusion EEG & prolactin Rare Awake , sleep Abrupt 60-90 sec Yes Flushed Hot, sweaty Slow Common Positive Common Awake Gradual 10-15 sec Occasional Pale Cold, clammy Rapid Uncommon Negative
  • 39. Partial seizures.  Simple partial Localised motor symptoms Somatosensory, psychic, autonomic symptoms  Manifestations - aversive seizure- eyes and head turn away from focus & loss of consciousness - rolandic seizure - tonic–clonic movements involving face, salivation, arrested speech
  • 40.  Jacksonian march - Sequential progression of Clonic movements
  • 41.
  • 42. Simple partial seizures with sensory signs..  Numbness  Tingling  Pricking  Paresthesia/ pain originating in one area  Visual sensations  Motor phenomena – posturing / hypertonia - Uncommon < 8yrs
  • 43. Complex partial seizures(psychomotor seizures)  3yrs – adolescence  Characterised by - Period of altered behaviour - Amnesia - Inability to respond to environment - Impaired consciousness during event - Drowsiness / sleep - Confusion & amnesia
  • 44. aura  odd or pleasant odours  Auditory or visual hallucinations  Ill defined feelings (de javu)  Strong feelings of fear and anxiety  In small children - emission of cry - attempt to run
  • 45. Patterns of motor behaviour  Stereotypic  May suddenly cease activity , appear dazed stare into space  Confused & apathetic  Become limp or stiff  automatisms  Post ictal confusion
  • 46.  Exhibit oropharyngeal activities –smacking chewing , drooling etc  Rarely exhibit – temper tantrums or rage
  • 47.
  • 48. Generalised seizures  Tonic clonic seizures (grandmal ) - Most common - Occur without warning Tonic phase clonic phase post ictal phase
  • 49. Tonic phase  10- 20 sec  Eyes roll upward  Immediate loss of consciousness  Stiffness  Contraction of entire body  Arms flexed  Legs, head & neck flexed
  • 50.  May utter a peculiar cry  Apnoeic  Increased salivation  Loss of swallowing reflex  If standing, falls to floor or ground
  • 51. Clonic phase  30 sec  Violent jerking movements  Foams at mouth  Incontinent of urine and faeces
  • 52. Post ictal state  Appears relaxed  Remain semiconscious  May awake in few minutes  Confused for several hours  Poor coordination  Mild impairment in fine motor movements
  • 53.  Visual & speech difficulties  Vomit or complain of severe headache  Usually sleeps for several hours  Feels tired  No recollection of event
  • 54. Absence seizures (petit mal/ lapses)  4-12 years of age  common in girls than boys  Ceases at puberty  Brief / no loss of consciousness  No alteration in muscle tone  May go unrecognised  Abrupt in onset
  • 55. Manifestations:  Brief loss of consciousness  Without aura  5-10 sec  Slight loss of muscle tone  Minor movements  No incontinence  Amnesia  Need reorientation
  • 56. Atonic & akinetic seizures (drop attacks )  2-5 yrs  Sudden momentary loss of muscle tone & postural control  Recurrent frequently Manifestation : - Loss of tone causing child to fall down
  • 57. Myoclonic seizures  Seizure episodes  Sudden brief contractions of a muscle  No post ictal state  May / not LOC
  • 58. Infantile spasms  Infantile myoclonus / massive spasms / hypsarrhythmia / salaam episodes / Infantile myoclonic spasms  6- 8 months of life  Twice common in boys  Numerous without post ictal drowsiness
  • 59. Manifestations  Series of sudden muscular contractons  Head flexed arms extended & legs drawn up  Eyes rolling  Preceded / followed by cry  May / not LOC  Flushing / pallor / cyanosis
  • 60.  Jack-knife seizure – sudden dropping forward of the head & neck with trunk flexed forward  Single momentary shock like contractions
  • 61. Comparison of simple, complex partial & absence seizure Clinical features Simple complex Absence Age of onset Any age Uncommon before 3 yrs Uncommon before 3 yrs Freq /day Variable 1- 2 times Multiple Duration < 30 sec >60 sec <10 sec Aura May be sole manifestation Frequently never Impaired consciousness Never always Always Automatisms never frequent frequent
  • 62. Clinical features Simple complex Absence Clonic movements Frequent Occasional Occasional Post ictal impairment Rare Frequent Never Mental disorientation Rare Common Unusual
  • 63. Video game related epilepsy  Flicker frequency of video games  Type – generalised , simple / complex / absence  Treatment – abstain from video games  Factors – screen brightness, sleep deprivation, fatigue, fever, short distance from screen
  • 64. Epilepsy syndromes  The Major Benign Partial Syndromes 1. Benign Rolandic Epilepsy - Male preponderance 60% - Onset 2 - 13 years (peak: 9-10 years) - Older children- motor & somatosensory symptoms, usually nocturnal.
  • 65.  Younger children- Hemiclonic / GTCS (especially at night).  Rx: None if seizures are mild and rare.  Most AEDs very effective.  Evolution: Recovery before 15 - 16 years.
  • 66. Benign Occipital Epilepsy  Frequency- rare  Genetic 37%, migraine 17%  Male = female  Onset 2 - 17 years (peak:7 - 8 years)
  • 67.  Initial visual symptoms, often followed by a hemiclonic seizure or by automatism  Postictal migrainous cephalgia in a quarter of the cases.  Rx: Most AEDs with control in 60%.  Recovery by end of adolescence.
  • 68. The Major Primary Generalized Syndromes Childhood Absence Epilepsy (True Petit Mal Epilepsy)  Frequency 8%  Genetic predisposition- strong 20%  Female preponderance 75%  Onset 3 - 12 years (peak: 6 - 7 years)  Very frequent simple absences.
  • 69.  Rx: VPA or ESM with control in 70 - 80%. Evolution: Remission- 95%. - Rare persistence of absences only- 6%. - GTCS during adolescence or later- 40%.
  • 70. Juvenile Myoclonic Epilepsy (JME)  Frequency 5%  Genetic predisposition- strong >25%  Male = female  Onset: 8-26 years (peak: 16 - 17)  Myoclonus , GTCS often also occur, occasionally absence.  Rx: VPA with control in 60 - 100%  Evolution: Rarely remits (<10%)
  • 71. Grand Mal on Awakening (GMA)  Genetic predisposition- strong >10%  Male > female  Onset 6-24 (peak: puberty)  GTS exclusively or predoninantly (90%)  Myoclonic or absence may occur.  Rx: VPA with control in 60 - 100%  Evolution: Rarely remits (<20%)
  • 72. The Major Secondary Generalized Syndromes Infantile Spasms (West Syndrome) Lennox Gastaut Syndrome (LGS)  Frequency 3 - 10%  Genetic predisposition- no  Male preponderance  Onset 1 - 8 years (peak: 3 - 5 years)
  • 73.  Poor prognosis in most cases  Tonic, atypical absence, drop attacks, other generalized or partial seizures.  Rx: VPA,rarely with complete control.  persisting seizures.
  • 74. DIAGNOSTIC EVALUATION  History collection  Physical examination  Laboratory investigations - Serum glucose & calcium levels • Lumbar puncture – Ist febrile seizures protein content – increased
  • 75. Imaging studies:  CT  MRI- structural lesions  PET-demonstrate perfusion,O2 & glucose intake  SPECT scan- perfusion in ictal & inter ictal state  Cerebral angiography  Magneto encephalography  Telemetry
  • 76. Electroencephalogram Electric activity of brain.  Fast activity – beta rhythm(14 - 20 Hz)  Alpha rhythm – 8 -13 Hz  Theta rhythm – 4 - 7 Hz  Slow rhythm- 1 - 3 Hz
  • 77.
  • 78.
  • 79.
  • 81. Abnormalities.  Slow/ abnormal rhythm-generalised ,localised or lateralised to one side thus helps to anatomic lesions  Spikes  Sharp waves  Poly spikes  Slow waves (hypsarrhythmia)
  • 82. Tests consider in the evaluation of patients with seizures Type Test Comments Simple partial Complex partial GTC Absences MRI MRI MRI None required Rule out structural lesions Rule out structural lesions Rule out structural lesions
  • 83. Management of child with seizures Goals: 1. Ensure adequate vitals & oxygenation 2. Terminate seizure activity 3. Prevent seizure recurrence 4. Establish the diagnosis & treat the underlying
  • 84. steps  Step I – confirm diagnosis  Step II – establish seizure type & syndrome  Step III – evaluate the need for treatment  Step IV – select AED  Step V – start monotherapy (start slow go slow policy)  Step VI – switch to another monotherapy add on therapy
  • 85.
  • 86. Treatment of a newly diagnosed case of epilepsy Newly diagnosed case Ist monotherarpy seizure therapy IInd monotherapy/ combination therapy seizure free Intractable epilepsy Combination therapy ketogenic diet , VNS
  • 87. Choice of AED Seizure First line second line partial CBZ, PHT, SVA , PB OXC, LTG, TPM 2nd gen GTCS SVA, ESM, CZP, CLB LTG , TPM , LEV GTCS SVA, CBZ, PHT, PB TPM, LTG, OXC, LEV Absence SVA, CZP, CLB LTG , TPM , LEV Myoclonic SVA LTG , TPM , LEV Atonic / tonic SVA CBZ, CLB , NTZ, LTG, TPM mixed SVA
  • 88.
  • 89.
  • 90. ILAE GUIDELINE FOR DRUG LEVEL MONITORING  Check compliance once or twice YEARLY  Suspect toxicity after each AED change DURATION:  Withdrawal – if seizure free for 2 YEARS  Gradually over 6-12 wks
  • 91. Ketogenic diet  A very strict diet that involves fluid restriction, high fat and low carbohydrate + protein intake.  The goal: alter the body’s fuel source from glucose to fat.  The basis of the diet – fasting  The encounter with a faith healer
  • 93. Sample Meals:  Meal 1:  melted butter  heavy whipping cream  chicken  apple  sugar free Jell-O
  • 94. Problems that may arise:  Low blood sugar  Lethargy  Nausea  Vomiting  Elevated cholesterol  Kidney stones  Constipation  Weight loss or gain  Dehydration  Cheating
  • 95. Vagus nerve stimulation  >12 years  50% reduction in seizures
  • 96.
  • 97. Types of surgery 1. Resection Removal of the area causing the seizures 2. Disconnection Corpus callosotomy Multiple subpial transections 3.Hemispherectomy
  • 98. procedure Type Temporal lobectomy nonTemporal lobectomy Corpus callostomy Hemispherectomy Simple/ complex partial Partial Partial, tonic ,clonic Unilateral , partial , hemiparesis
  • 99. Nursing management  Seizure precautions  Relieving anxiety  Managing treatment  Providing family support & education
  • 100. Febrile seizures  Occurrence of seizure activity in neurologically healthy infants & children between 6 months & 5 yrs of age associated with fever >38c without evidence of intracranial infection & with no history of prior afebrile seizures
  • 101.  Common in 18- 22 months  Provoked seizures  Causes: - Infections of middle ear - URTI - Urinary tract & GI infections
  • 102. Types  Simple febrile seizures: - 85% - Generalised seizures - Lasting less than 15 min - No post ictal neurologic abnormalities
  • 103.  Complex febrile seizures - Recurrent within 24 hrs  Febrile status - A seizure with duration of 30 min - Without regaining consciousness interictally
  • 104. Risk factors  Age <18 months  Family history  Shorter duration Recurrence 75% within 1 yr Risk of subsequent epilepsy – 2- 2.5 %
  • 105. Diagnostic evaluation  History  Serum electrolytes – calcium , magnesium  Blood glucose LUMBAR PUNCTURE  abnormal neurological examination  Ongoing seizure
  • 106. Management  During the seizure - Manage as for any other acute seizure - Should hospitalise o Lethargy o Complex features o Unclear follow up
  • 107.
  • 108. Long term management  Primary goal – to prevent recurrences  Antipyretics – to reduce fever INTERMITTENT PROPHYLAXIS  Diazepam – 0.3 – 0.5 mg/ kg orally / rectally  clobazem - 1mg /kg / day
  • 109. Continuous prophylaxis  Indications : - Recurrent complex seizures - Abnormal neurodevelopment - Positive family history  Sodium valproate is preferred
  • 110. Status epilepticus  A seizure that persists for a sufficient length of time / is repeated frequently enough that recovery between attacks does not occur Early status established status Epilepticus Epilepticus
  • 111. A condition characterised by an epileptic seizure that is sufficiently prolonged or repeated at sufficiently brief intervals so as to produce an unvarying and enduring epileptic condition (dictionary of epilepsy )
  • 112. Etiology  Recurrent neonatal seizures  Traumatic subarachnoid haemorrhage  HIE  IEM
  • 113. Classification  Generalised status epilepticus  Partial status epilepticus  Refractory status epilepticus  Super refractory status epilepticus
  • 114. Generalised status epilepticus  Convulsive seizures 1. Tonic clonic 2. Tonic 3. Clonic 4. Myoclonic  Non convulsive
  • 115. Refractory status epilepticus  Persistent seizure beyond 120 min  Despite of therapy with benzodiazepine, phenytoin, phenobarbitone or valproate  Treatment : - Midazolam - Thiopentone - Magnesium - Ketogenic diet
  • 116.
  • 117. Intractable epilepsy  It is defined as an at least one seizure every 2 months for the first 5 years of treatment & subsequently as at least one seizure per year with failure of at least 3 Ist line AEDs  Rx: surgery  Ketogenic diet  VNS
  • 118. Misconceptions about childhood epilepsy  Children with epilepsy are brain injured  Has mental handicaps  Only SE will harm child's brain  An EEG will determine if child has epilepsy  Abnormal EEG -↑ AED dose
  • 119.  Child has twitches of legs & arms while asleep. Are these seizures ?  Blood level AED ↑ - change the dose ?  AED – only way of treatment  Surgery – after a attempting all AED  Life will never be the same
  • 120. Nursing diagnosis  Risk for injury related to CNS dysfunction & inability to control self secondary to the type of seizure.  Risk for aspiration & ineffective breathing pattern related to impaired motor activity, LOC.  Risk for injury related to impaired consciousness & automatisms
  • 121.  Anxiety / fear related to child having life threatening seizure activity  Ineffective tissue perfusion  Interrupted family processes  Self esteem disturbances