CONVULSION IN INFANCY AND

CHILDHOOD

DR. WOROMA WONODI

FWACP
SENIOR LECTURER/CONSULTANT CHILD
NEUROLOGIST
OBJECTIVES
• By the end of the lecture, students should know the
following
1. Definition of convulsion
2. Aetiology
3. Pathophysiology
4. Clinical symptoms and signs
5. Investigation
6. Treatment
7. Prevention
OUTLINE
• Introduction/Definitions
• Epidemiology
• Aetiology
• Pathophysiology
• Classification
• Approach to management of convulsions in children
• Conclusion
• References
INTRODUCTION
• Paediatric neuro-emergencies are life-threatening conditions
that can lead to secondary brain lesions and poor functional
recovery if the appropriate treatments are not instituted timely.
• The CNS is exquisitely vulnerable to ischaemia and hypoxia
• The CNS heals poorly
• Tissues that die are not replaced
• The aim of emergency management is to stop these self-
aggravating processes as soon as possible
• TIME IS BRAIN
DEFINITIONS
• The terms seizure, epileptic seizure and convulsion are often
used interchangeably but do not mean exactly the same thing.
• The term SEIZURE can be used to denote any sudden attack
from any cause. Such an attack might be applied to a faint,
attacks due to cardiac problems, a severe headache or a
manifestation of epilepsy, so, it is not precise.
• An EPILEPTIC SEIZURE is defined as an event characterized
by excessive, hypersynchronous discharge of cortical neurones
whose manifestations may be motor, sensory, autonomic or
psychic ± alteration of consciousness.
DEFINTIONS II

Psychic manifestations include fear anxiety, dread, deja vu,

faster heart rate and or breathing while autonomic
manifestations include flushing, sweating, pallor,
piloerection, sensation of warmth, coolness or discomfort,
mydriasis, ptosis and miosis

• CONVULSION = seizure with involuntary motor activity.

• Convulsions can be febrile or afebrile
EPIDEMIOLOGY OF CONVULSION
• It is one of the most common life-threatening events in
children
• Convulsions account for a significant number of
admissions in the Children’s Emergency Room (CHER)
• Higher prevalence rate in children under the age of 5 yrs
• In developed countries - Non-infectious causes account
for majority of cases
• In developing countries -Infectious causes predominate
CAUSES OF CONVULSION
• Trauma- Traumatic Head Injuries, child abuse
 Infection- Malaria, encephalitis, meningitis
 Psychiatric disorders
• Space occupying lesion, stroke
 Alcohol and drugs/toxins
• Endocrine, epilepsy, encephalopathy
 hypo/hyperglycemia)
 Hypoxia
 Uremia
 Febrile convulsions
FEBRILE CONVULSION
 Common in infancy and childhood. Affects 2-4% of
children
 Occurring b/w 3months and 5 years.
 Convulsion accompanied by fever (temperature ≥
100.4°F or 38°C) without central nervous system
infection
 Very few children will present with the first febrile
convulsion @ >5years
9
CLASSIFICATION OF FEBRILE CONVULSION II

• Neurologically abnormal children are more likely to

experience complex febrile seizures and have a higher
risk of subsequent afebrile seizures
• Febrile convulsions are usually brief, generalised tonic,
clonic and occur in conjunction with a rapid rise in body
temperature. 25% cases have a positive family history.
CAUSES OF FEBRILE CONVULSION
• Malaria
• Bronchopneumonia
• UTI - urinary tract infection
• URTI - upper respiratory tract infections
• Pharyngitis
• Tonsilitis
• Otitis media
• Measles
MANAGEMENT OF FEBRILE SEIZURES
• ABC of resuscitation
• Check blood sugar
• Abort seizure with a rapidly acting anticonvulsant - Rectal Diazepam <3yr
5mg stat, >3yr 10mg stat, Buccal Midazolam give between outer gum &
inner cheek, IM Paraldehyde -1ml/year of life max 5mls
• Control fever - tepidsponge
• Take a detailed history & do a thorough physical examination to ascertain
cause of fever
• Relevant investigations to exclude meningitis & possibly determine cause
of fever – Lumbar Puncture, Blood Film for mp, urine m/c/s, CXR
• Explain to parents
CRITERIA FOR HOSPITAL ADMISSION IN
FEBRILE CONVULSION
• Age < 1yr
• Glasgow Coma Scale (GCS)<15 one hour after seizure
• Meningeal signs
• Raised ICP
• Child acutely ill
• Signs of aspiration
• High parental or carer anxiety
• Complex febrile seizure
RISKS OF FURTHER FEBRILE CONVULSIONS

• Overall risk 30-40%

• Risk factors for recurrence:
Early age at onset <18months
Family history of febrile seizures
Lower temperature <40oC
• Complex febrile convulsion is not a risk factor for further
febrile convulsion
Risk of developing epilepsy in Febrile convulsion
• Overall risk 6X the average person
• Risk factors:
Abnormal neurology prior to first febrile convulsion
Family history of afebrile seizure/convulsion
Complex febrile convulsion
 EPILEPSY
• Defined as recurrent unprovoked seizures or two or more
unprovoked seizures, occurring > 24hours apart.
Other definitions
• One unprovoked seizure with a probability of further seizures
• Diagnosis of an epilepsy syndrome
• Specific provoking factors leading to reflex seizures are permitted
– flashes of light from TV/video games, stress, sleep deprivation.
• Recurrent seizures immediately after a head injury, acute phase of
intracranial infections or following drug intoxication do not qualify
for the diagnosis of epilepsy
EPIDEMIOLOGY OF EPILEPSY
• About 80 million people with epilepsy worldwide, two
thirds are children and majority(>80%) are in the
developing countries
• Incidence & Prevalence differ from one country to another
• Incidence lowest in the UK & Canada.
• Higher by a factor of 20 - 50% in developing countries
 PATHOPHYSIOLOGY OF EPILEPSY I
• At the molecular level different pathways can induce epilepsy
for example, oxidative stress due to an increased circulating
reactive oxygen species (ROS), which results in imbalanced
inflammatory cytokines. The latter stimulates inflammation and
subsequently leads to neuroinflammation.
• Similarly, ROS can impair calcium ion metabolism, resulting in
neural hyperexcitability.
• The loss of mitochondrial adenosine-triphosphate (ATP) has
also been implicated in the pathogenesis of epilepsy.
 PATHOPHYSIOLOGY OF EPILEPSY II
• This seems to occur in three different pathways; for instance,
the alteration of neurotransmitters due to the lack of ATP can
induce neural hyperexcitability by increasing glutamate and the
reduction of gamma-aminobutyric acid (GABA) in a
mitochondrion.
• Secondly, less ATP impairs the sodium and potassium ion
channels, resulting in nerve depolarisation. On the other hand,
the impaired brain–blood barrier (BBB) also triggers
neuroinflammation, causing neural degeneration. Altogether,
these mechanisms cause neuronal degeneration, which
facilitates the pathogenicity of epilepsy
 PATHOPHYSIOLOGY OF EPILEPSY II
• This seems to occur in three different pathways; for instance,
the alteration of neurotransmitters due to the lack of ATP can
induce neural hyperexcitability by increasing glutamate and the
reduction of gamma-aminobutyric acid (GABA) in a
mitochondrion.
• Secondly, less ATP impairs the sodium and potassium ion
channels, resulting in nerve depolarisation. On the other hand,
the impaired brain–blood barrier (BBB) also triggers
neuroinflammation, causing neural degeneration. Altogether,
these mechanisms cause neuronal degeneration, which
facilitates the pathogenicity of epilepsy
PATHOPHYSIOLOGY OF EPILEPSY
• This has been the subject of extensive research.
• The neurons are interconnected through synapses
• A small electrical current is discharged by neurons to
release neurotransmitters at synaptic levels to
communicate with one anothers
• Neurotransmitters can be inhibitory(y-aminobutyric
acid(GABA)) or excitatory (glutamate) thereby inhibiting or
exciting neurons connected to it respectively
PATHOPHYSIOLOGY OF EPILEPSY II
• A normal neuron discharges repetitively at low baseline
frequency and it is the integrated electrical activity by the
neurons of the superficial cortex that is recorded in a
normal EEG
• If the neurons are injured, damaged or suffer a chemical
or metabolic insult, a change in the discharge pattern may
develop
• In case of epilepsy regular low frequency are replaced by
bursts of high frequency discharges followed by a period
of inactivity.
PATHOPHYSIOLOGY OF EPILEPSY III
• A single neuron discharging in an abnormal manner
usually has no significance. It is only when a population of
neurons discharge synchronously in an abnormal way
that a seizure may be triggered.
• The abnormal discharge may remain localized or it may
spread to adjacent areas recruiting more neurons as it
expands
• It may also generalize throughout the brain via cortical
and subcortical routes including collosal and
thalamocortical pathways
PATHOPHYSIOLOGY OF EPILEPSY IV
• The area from which an abnormal discharge originates is
known as the ‘epileptic focus’
• An EEG recording carried out during these abnormal
changes may show a variety of atypical signs depending
on the part of the brain that is involved.
CLASSIFICATION OF EPILEPSY

• Several. Latest is ILAE 2017 classification

• A multilevel classification designed to cater for classifying
epilepsy in different clinical environments with varying
resources
• Level of classification influenced by amount of resources
available. Where possible, a diagnosis at all three levels
should be sought as well as the aetiology of the individual’s
epilepsy
 ILAE 2017 CLASSIFICATION OF SEIZURE TYPES
EXPANDED VERSION
ILAE 2017 CLASSIFICATION
Level 1: seizure type classification - based on onset (eye
witness)/seizure semiology
-focal onset
-generalized onset
-unknown onset
Level 2: epilepsy type classification - based on clinical type and
EEG findings
-focal epilepsy
-generalized epilepsy
-combined generalized and focal epilepsy
-unknown
NORMAL EEG RECORDING IN A CHILD
EEG - GENERALIZED EPILEPSY
LEFT FOCAL EPILEPSY
CHILDHOOD ABSENCE EPILEPSY
ILAE 2017 CLASSIFICATION
• Level 3 - Epilepsy syndrome - an epilepsy syndrome
refers to a cluster of features incorporating seizure types,
EEG and imaging features that tend to occur together
• It often has age-dependent features (eg age of onset and
remission where applicable), seizure triggers, diurnal
variations and prognosis.
• It may have distinctive co-morbidities eg intelellectual
disabilities
EPILEPSY SYNDROMES I
• Rolandic (age of onset 3-12 yrs, attacks mainly occur at
night, EEG- spikes in centrotemporal area)
• West (infantile spasm, hypsarrythmias on EEG and devtal
arrest or delay). seen in young infants)
• Landau Kleffner (onset 3-8yrs, gradual or sudden loss of
language, seizures usually resolve by teenage ages and
language may be restored)
EPILEPSY SYNDROMES II
• Lennox Gastaut (onset 1-14yrs, seizures difficult to
control,mental retardation, develomental delay)
• Childhood Absence (onset 3-8yrs, hyperventilate for
3mins initiates attacks, EEG- 2.5-3 spike per second
discharges, multiple episodes per day)
• Panayiotopoulos syndrome = early onset childhood
occipital epilepsy
• Juvenile Absence epilepsy - onset around puberty
• Juvenile Myoclonic epilepsy -3.5-4 spike per second
discharges on eeg, rarely remits, treatment usually for life
Aetiology of epilepsy - 6 main classes
1) Structural - stroke, brain tumuors, lissencephaly
2) Genetic - known or presumed genetic mutation
3) Infectious – NNS, Meningitis
4) Metabolic – hypoglycaemia, hyperglycaemia
5) Immune disorders like SLE, Ulcerative colitis, Grave’s dx,
Rheumatoid Arthritis etc
6) unknown
A patient’s epilepsy may be classified into more than one group eg
tuberous sclerosis(TSC)- genetic and structural
COMORBIDITIES OF EPILEPSY
• worldwide about 50% of PLWE have comorbidies which
are medical conditions that co-exist with the epilepsy.
• Mood disorders
• Learning disorders
• Depression
• Anxiety
• ASD
• personality disorder
• ADHD
CLINICAL SYMPTOMS AND SIGNS
• Sudden fall • Tingling sensation
• Jerking of the limbs- • Headache
generalized or focal • Generalised stiffening
• Blank stare • Floppiness
• Fecal/Urinary incontinence • Feeling of unfamiliarity
• Feeling of fear • Sudden stiffness of the
• Thrashing movements of whole or parts of the body
the limbs • poor school
• Seeing coloured spots performance- ? absence
• Vomiting sz etc
INVESTIGATIONS
• Electroencephalogram (EEG) - very important and may
show the pattern of electrical activity abnormality.
Others as needed include
• brain MRI/CT scan
• Elecrolytes, urea and creatinine
• serum calcium, phosphate and magnesium
• CBC- complete blood count
• genetic studies
• assays for amino acids, etc
TREATMENT MODALITIES FOR EPILEPSY
• Pharmacotherapy - mainstay of treatment. Use of drugs
known as antiepileptic drugs (AED) (antiseizure
medications (ASM)
• Surgery
• Ketogenic diet - low carbohydrate, high fat diet.
PHARMACOTHERAPY
1ST LINE 2NDLINE
• Phenobarbitone • Clonazepam
• Phenytoin • Felbamate
• Carbamazepine • Lamotigine
(Tegretol) • Gabapentin
• Sodium Valproate
• Topiramate
(Epilim)
• Levetiracetam (Keppra)
• Ethosuximide
SURGERY

In patients with intractable seizures

• Temporal lobestomy
• Hemisperectomy
• Corpus callostomy
• Vagus nerve stimulation - implanting a device surgically
DIET
• Vitamin B6 (pyridoxine) in infants and neonates with
intractable seizures
• Ketogenic diet - high fat, low protein, low carbohydrate
diet. it is not palatable and leads to weight loss. Leads to
production of ketones. The exact mechanism of action is
not understood but the ketones produced may reduce
excitability of the neurones leading to seizure control.
STATUS EPILEPTICUS
 Condition characterized by prolonged seizure lasting >
30mins or repeated seizures, such that the child does not
regain consciousness in between attacks of seizure
 Operational definition puts the duration as more than
5mins, to emphasize the risks of longer duration
 Convulsive status epilepticus (generalized tonic, clonic, or
tonic–clonic)
 Most common type
CAUSES OF SE
• Acute pathology/Acute symptomatic
– Acute CNS infection (meningitis or encephalitis), Anoxic
injury, Metabolic derangement (hypoglycemia,
hyperglycemia, hyponatremia, hypocalcemia), fever,
Traumatic injury
– Drug-related -AED non-compliance or sudden
withdrawal, AED drug overdose, Non-AED drug
overdose
CAUSE OF SE II
 Remote pathology
• Cerebral dysgenesis
• Perinatal hypoxic-ischemic encephalopathy
• Progressive neurodegenerative disorders
• Prior brain injury (meningitis, stroke, trauma)
 Idiopathic/cryptogenic
MANAGEMENT OF SE
• The objectives in acute management of SE are to:
 Maintain adequate airway, breathing, and circulation (the
‘ABCs’).
 Terminate the seizure and prevent recurrence.
 Manage refractory status epilepticus (RSE).
 Diagnose and initiate therapy for life-threatening causes
of SE (e.g., hypoglycemia, meningitis, and cerebral
space-occupying lesions).
SE MANAGEMENT PROTOCOL
 Step 1. ABC of Resuscitation. Give Oxygen. Check Blood sugar
 Step 2. Rectal / IV Diazepam. Secure IV access. If seizures
continue after 10mins,
 Step 3. IM Paraldehyde 1ml/year of life. If seizures continue after
10mins
 Step 4. IV Phenytoin 18-20mg/kg slowly over 20 mins. If no
response
 Step 5. IV Phenobarbitone 15-20 mg/ kg over 10mins. If no
response
 Step 6. Induction of anaesthesia with sodium thiopentone.
MANAGEMENT OF SE III
 Reposition the patient on their back and apply a chin lift or
jaw thrust to help open the airway
 Administer oxygen
 Bradycardia, hypotension, and poor perfusion are
ominous signs
 Hypotension or dehydration should be treated with
isotonic fluid resuscitation
MANAGEMENT OF SE IV

 Correct hypoglycaemia if present using IV dextrose

 Hypotension or dehydration should be treated with
isotonic fluid resuscitation
 Antibiotics should be administered empirically to all
patients at risk of bacterial infection, as well as to those
who present with new-onset SE and fever
 Empiric acyclovir should also be considered for patients
who present with new onset SE and fever and who are at
risk for herpetic infections
GOALS OF TREATING A CHILD WITH CONVULSION
 Adhere to the principles of neuroresuscitation, the A,B,C
Identification and treatment of immediately reversible aetiologies
eg hypoglycaemia
 Identify signs of intracranial pathology: ↑ICP or a focal neurologic
sign, head trauma
 Identify and treat the underlying cause of convulsion
 Investigation
 Continue treatment upon identifying the cause
 Determine the prognosis
 Plan appropriate long term therapy
History & physical examination

History
 Premorbid state :
• Ingestion of drug
• Abnormal behaviour
• Metabolic derangement
 Associated symptoms of CNS
• Fever –infections
• Headache, vomiting, Diplopia, convulsions -↑ ICP
History & physical examination II

 Neck Pain –meningitis , subarachnoid haemorrage (SAH)

 Skin Rash – Meningococcemia , viral exanthema
 skin exam to look for signs of a neurocutaneous disorder
 History of excessive crying, irritability, enlarging head in infants-
meningitis , hydrocephalus
 History of head trauma
 Failure to thrive , vomiting, peculiar skin odour - metabolic causes
 Recurrent episodes: Epilepsy, inborn errors of metabolism
History & physical examination III

 Jaundice, abdominal distension, hematemesis, melena

stool, bleeding- Hepatic encephalopathy
 Reduce urine output, body swelling, periorbital puffiness,
nausea, vomiting, loss of appetite –Uremic
encephalopathy
 History of loose stool- HUS, electrolyte imbalance, toxins
 Birth history- birth asphyxia, hypoglycemia, NNJ,
Infections, others
PREVENTION -Using the five levels of prevention

 General health promotion- health education, environmental

mainpulations,
 Specific protection- immunization,
 Prompt diagnosis and treatment - training and retraining of health
care providers so they can recognize seizures, parents to bring
child promptly to the hospital, drugs available to treat
 Limitation of disability = eye glasses, occupational therapy.
psychotherapy
 Rehabilitation -support groups, glasses, hearing aids, special
homes, individualized education,psychotherapy,
COMPLICATIONS OF EPILEPSY
• Physical - different injuries including fractures, burns,
dislocations
• Emotional - personality changes, low self-esteem, mood
changes, anxiety,
• Mental retardation/ poor academic performance
• Aspiration if a person vomits during seizures
• Permanent brain damage from Status Epilepticus
• Sudden Unexplained Death from Epilepsy
• Cardiac - arrythmias, infarctions
FIRST AID DURING A SEIZURE /CONVULSION/
EPILEPTIC SEIZURE (ADAPTED).
• Most seizures start outside a health facility hence the need for a
first aid management of seizures
• In case a person falls and starts to jerk outside a hospital
setting, you can give the following support:
• 1.Stay CALM. Don’t PANIC. Don’t run away
• 2.Remove any harmful objects from near the person or move the
person away from the immovable danger
• 3.Support or place something soft beneath the head
• 4.Loosen any tight clothing at the neck, waist or any part of the
body
FIRST AID DURING A SEIZURE /CONVULSION/
EPILEPTIC SEIZURE (ADAPTED) contd

• 5.Roll the person onto their side (recovery position) when

jerking stops
• 6.Time the seizure
• 7.Seek medical help immediately to stop the seizure if the
seizure lasts more than 5 minutes
• 8.Stay with the person until fully recovered and oriented
first aid mgt of seizure (contd)
• DON’TS – WHAT NOT TO DO DURING A SEIZURE AT HOME
• 1.Do not restrain the person when they are jerking
• 2.Do not push anything into their mouth (spoon, finger, etc)
• 3.Do not give food or drinks before the person is fully recovered
• 4.Do not burn the person’s feet with fire
• 5.Do not put anything into their eyes, anus or ears.
• 6.Do not hit/slap the child
• 7.Do not squeeze the child
GENERAL ADVICE
• 1.Take treatments/medications as prescribed
• 2.Do not run out of drugs - make sure you always have drugs
available
• 3.Avoid shortage of sleep
• 4.Alcohol may trigger seizures, avoid it
• 5.Do not drive without doctor’s permission
• 6.If you take family planning pills, tell your doctor about your
epilepsy (these pills can reduce the efficacy of seizure drugs
• 7.Do not change or stop your treatment without consulting with
your doctor, even when the number of seizures has reduced or
increased.
WHEN TO DISCONTINUE YOUR MEDICATION
• 1.Your doctor asks you to stop after treatment and review
• 2.If you notice jaundice(yellowness of the eyes and body)-
report back to your doctor
• 3.Abnormal rashes – report to your doctor and take child
to see the doctor immediately
CONCLUSION
• Convulsion is a neurological emergency with varied
aetiologies ranging from benign causes to life-threatening
conditions which can put patients at risk of poor
functional recovery, and even death, if not promptly
treated.
REFERENCES
• Nelson Textbook of Pediatrics. 20th Edition
• ILAE: https://www.ilae.org/journals/epigraph/epigraph-vol-
20-issue-2-fall-2018/time-is-brain-treating-status-
epilepticus
• Online sources
DID WE ACHIEVE OUR OBJECTIVES?

1. Definition of convulsion
2. Aetiology
3. Pathophysiology
4. Clinical symptoms and signs
5. Investigation
6. Treatment
7. Prevention