TA OGUNLESI (FWACP)1 CHILDHOOD SEIZURES. TA OGUNLESI (FWACP)2 SEIZURES Seizure defined as –A...

TA OGUNLESI (FWACP) 1

CHILDHOOD SEIZURES

CHILDHOOD SEIZURES


SEIZURES• Seizure defined as

– A paroxysmal involuntary disturbance of brain function that may be manifested as• an impairment or loss of consciousness, • behavioral abnormalities, • sensory disturbance, • or autonomic dysfunction.

— Many seizures are characterized by abnormal movements or abnormal motor activity (convulsion).


SEIZURESSeizures may be broadly classified

as:(1) Acute Recurrent (usually related to

episodes of rapid rise in core body temperature)

Non-recurrent (usually related to acute intra-cerebral infections OR to metabolic derangements)

(2) Chronic – also known as seizure disorders or epilepsy.


SEIZURESThe terms seizure and

convulsion may be incorrectly used interchangeably with epilepsy.

Convulsion is a seizure with MOTOR manifestation.

Epilepsy is a chronic disorder of the brain with a tendency to have recurrent seizures unrelated to fever or acute cerebral insults.


BURDEN OF SEIZURES

• Seizures are a common neurologic disorder in the paediatric age group and occur in 3–5% of children.

• Epilepsy occurs in 0.5–1.0% of the population and begins in childhood in 60% of cases.

• Seizures do not constitute a diagnosis but are a symptom of an underlying disorder often in the CNS.


BURDEN OF SEIZURES

• In most children, a cause of the seizure cannot be determined.

• Outcome for most uncomplicated seizures in children is good.

• 10–20% may have persistent seizures refractory to drugs and these pose a diagnostic and management challenge.


PATHOPHYSIOLOGY• Seizures are a paroxysmal

manifestation of the disturbances of electrical properties of the cerebral cortex.

• A seizure results when a sudden imbalance occurs between the excitatory and inhibitory forces within the network of cortical neurons in favour of a sudden-onset net excitation.


PATHOPHYSIOLOGY• An internal or external stimulus causes

abnormal hyper-synchronous neuronal discharges in a focal area in the cerebrum that spread throughout the cerebrum.

• The clinical manifestation depends on the location of the affected cortical network.


PATHOPHYSIOLOGY• Extracellular concentrations of

potassium are increased, and concentrations of calcium are decreased.

• This results in depolarisation of neuronal membranes.

• Changes occur in pH and utilization of glucose increases.

• Seizures cease when the neuronal cell membrane hyperpolarizes and causes the neuronal cells to cease firing, suppressing the surface potentials of the cerebrum.


PATHOPHYSIOLOGYGABA (gamma butyric acid) is the

major inhibitory neurotransmitter in the brain. It binds to 2 receptors GABA-A and GABA-B.

Glutamine is the major excitatory neurotransmitter in the brain.

Disturbance of the balance in the activities of these two neurotransmitters result in seizures.


AETIOLOGIES• Most seizures are IDIOPATHIC. • Identified causes include

–Metabolic disturbances – • Febrile states.• Hypoglycaemia.• Hypocalcaemia• Hypomagnessaemia• Hyponatraemia• Hypernatraemia


AETIOLOGIES– Pathologic processes in the brain –

• Trauma – Intracranial haemorrhages.• Neuronal injury –

– Chemical e.g. Asphyxia, Hyperbilirubinaemia.

– Physical e.g. concussions, contussions, brain laceration.

• Cerebral edema


AETIOLOGIES• Infections

– e.g. Meningitis, encephalitis.• Hypertension.• Vascular anomalies or lesions.• Space-occupying lesions –

– tumours, abscesses, cysts.• Degenerative states –

– SSPE, Mucopolysacchridoses, Sphingolipidosis


AETIOLOGIES– Endo/ - Exogenous toxic substances –

• Alcohol Intoxication• Uraemia• Hepatic Encephalopathy • Lead toxicity

– Drugs/ Medications (Use or Withdrawal Effects of hard drugs)

– Neurocutaneous syndromes (Neurofibromatosis, Tuberose sclerosis, Sturge Weber syndrome)

– Congenital brain malformations.


CLASSIFICATION OF SEIZURES

• It may give a clue to the likely aetiology.• It may be used to pick the most appropriate

drug treatment.• It may also be used to prognosticate.Clinical classification of seizures may be difficult

because the manifestations of different seizure types may be similar (absence seizures Vs complex partial epilepsy). An electroencephalogram (EEG) is a useful adjunct to the classification of epilepsy.

A system of classification combining the clinical and the EEG features has improved the delineation of childhood epilepsy.


CLASSIFICATION OF SEIZURES

In 1981, the International League Against Epilepsy (ILAE) developed an international classification of epileptic seizures that divides seizures into 2 major classes:

(1) Partial-onset seizures begin in one focal area of the cerebral cortex.

(2) Generalized-onset seizures have an onset recorded simultaneously in both cerebral hemispheres.

(3) Unclassified seizures belong to neither of the former two.


PARTIAL SEIZURES(1)Simple partial seizures: The key

defining element of simple partial seizures is the occurrence of a seizure with preservation of consciousness.

It manifests with specific sensory, motor, autonomic and psychic features.

The EEG shows focal changes.


PARTIAL SEIZURES(2) Complex partial seizures:

Consciousness is impaired during a complex partial seizure. They may follow simple partial seizures (which manifest as aura) or be complex right from onset.

Typically, a complex partial seizure begins with behavioral arrest and is followed by staring, automatisms, and postictal confusion.

Frequently, the automatisms consist of chewing, lip smacking, mumbling, and fumbling with the hands.


PARTIAL SEIZURES(3) Partial with secondarily

generalized seizures: These seizures often begin with an aura that evolves into a complex partial seizure and then into a generalized tonic-clonic seizure. However, a complex partial seizure may evolve into a generalized tonic-clonic seizure, or an aura may evolve into a generalized tonic-clonic seizure without an obvious complex partial seizure.


GENERALIZED SEIZURES

(1) Absence seizures (Petit mal): These are brief episodes of impairment of consciousness and cessation of activity with NO aura or postictal confusion. No motor involvement.

They typically last less than 20 seconds.Absence seizures are often precipitated by

hyperventilation or photic stimulation. The classic ictal EEG correlate of absence

seizures consists of 3.5-Hz generalized spike and slow wave complexes.

May be TYPICAL or ATYPICAL (when it co-exists with other types of generalized seizure. Occurs as part of Lennox – Gastaut syndrome.)



(2) Myoclonic seizures: This seizure type consists of brief, arrhythmic, jerking, motor movements that last less than a second.

Myoclonic seizures often cluster within a few minutes. If they evolve into rhythmic jerking movements, they are classified as evolving into a clonic seizure.

Myoclonus is not always epileptic in origin. For example, the myoclonic jerks during phase I of sleep are normal “release” phenomena.

The classic ictal correlate of myoclonic seizures in the EEG consists of fast polyspike and slow wave complexes.



(3) Clonic seizures: This seizure type consists of rhythmic, motor, jerking movements with impairment of consciousness.

Clonic seizures also could have a focal origin with or without impairment of consciousness. The focal seizures are classified as simple or complex partial seizures.

Typically, generalized clonic seizures simultaneously involve the upper and lower extremities.

The ictal EEG correlate consists of bilateral rhythmic epileptiform discharges.



(4) Tonic seizures: This seizure type consists of sudden-onset tonic extension or flexion of the head, trunk, and/or extremities for several seconds.

Typically, they occur in relation to drowsiness, shortly after falling asleep, or just after awakening. They often are associated with other neurologic abnormalities.

The ictal correlate of tonic seizures in the EEG includes a high-frequency electrographic discharge in the beta frequency and may evolve into slow spike-and-wave complexes or diffuse polyspikes.



(5) Tonic-clonic seizures (Grand mal): This is the most common form of generalized seizure.

They consist of several motor behaviours including generalized tonic extension of the extremities lasting for few seconds followed by clonic rhythmic movements and prolonged postictal confusion.



Typically, a loud cry and upward rolling of the eyes occur at the onset of seizure. Drooling of saliva with faecal and urinary incontinence may occur during the clonic phase.

The ictal correlate of generalized tonic-clonic seizures on EEG consists of generalized (bilateral) spike or polyspike and slow wave complexes.



(6) Atonic seizures: This occurs in people with significant neurologic abnormalities.

These seizures consist of brief loss of postural tone, often resulting in falls and injuries.

The ictal EEG correlate is similar to abnormalities observed in tonic seizures.


EPILEPTIC SYNDROMESINTERNATIONAL CLASSIFICATION OF

EPILEPSIES AND EPILEPTIC SYNDROMES 1989

• Epilepsy in children has also been classified by syndrome.

• About 50% of childhood seizures can be classified into syndromes using the:

age at onset of seizures cognitive developmentspecific neurologic deficitsdescription of seizure typethe EEG findings including the

background rhythm.


EXAMPLES OF EPILEPTIC SYNDROMESFebrile Convulsions Infantile spasms (West syndrome)Benign myoclonic epilepsy of infancy Lennox-Gastaut syndrome Landau-Kleffner syndromeBenign childhood epilepsy with

centrotemporal spikes (Rolandic epilepsy)

Juvenile myoclonic epilepsy (Janz syndrome)


FEBRILE SEIZURE• Defined as seizures occurring in

children aged 6mo – 5 years as a result of fever which has an extra-cranial origin.

• An acute, recurrent benign seizure.• Peak age: 14 to 18 months• Incidence:

– Community:• Europe/ USA: 2 – 5% (3%).• Urban NGR: 8.1%• Rural NGR: 11.6%

– CHER: 4.6 – 20.0%


FEBRILE SEIZURE• Sex:

– Slight male preponderance1.2 – 1.5: 1 (M: F ratio).– Females also have increased incidence of sequelae.

• Aetiology:– Any febrile illness without CNS involvement (URTI,

otitis media, pneumonia, tonsillitis, measles, UTI, gastroenteritis, arthritis, osteomyelitis).

– Rapid rise in temp by 4 – 5 0 F (2.2 – 2.7 o C).• Familial trends

– ? Autosomal Dominance inheritance.– May elicit positive family history in 12 – 69%– Febrile seizure gene identified on chromosomes 19p

and 8q13–21.


SIMPLE FEBRILE SEIZURE

• Duration: <15 Minutes.• Pattern: Generalized (Tonic, Clonic,

Tonic-clonic) from onset.• Brief post-ictal sleep (<30 minutes

without sedation)• Non-recurrence in 24 hours or in the

same febrile illness.• Occurs in previously neurologically

normal child.• EEG usually not required.


COMPLEX FEBRILE SEIZURES

– Duration: >15 Minutes.– Post Ictal Sleep: > 30 Minutes.– Pattern: Partial or Focal onset.– Recurrence in 24 hours/ same

febrile illness.– Usual in children with pre-existing

neurologic deficits.– EEG is indicated and usually

abnormal.


RISK OF RECURRENCE

• About 33% of children with febrile seizure will have one recurrence.

• 17% will have multiple recurrences.• Risk factors for recurrence:Age at onset <1 yearFamily history of afebrile seizureComplex febrile seizures in the first

episodePre-existing neurologic deficitsPersistent post-ictal neurologic

disorders


RISK OF DEVELOPING EPILEPSY

• 3% will develop subsequent AFEBRILE seizures• Risk factors for development of epilepsy as a

complication of febrile seizures: A positive family history of epilepsy Initial febrile seizure before 9mo of age A prolonged or complex febrile seizure Delayed developmental milestones Abnormal neurologic findings. • Chances of developing epilepsy is

approximately 9% when several risk factors are present.

• Chances of developing epilepsy is approximately 1% in the absence of risk factors.


INVESTIGATIONS IN FEBRILE SEIZURES

– CSF usually Normal.– EEG:

• Immediate EEG not beneficial: Generalized post-ictal slowing.

• Not indicated in simple FC: Cannot Predict recurrence risk or risk of development of Epilepsy.

– CT Scan: If • Focal motor seizures.• Post-ictal lateralized deficits.

– Motor paresis.– Unilateral sensory or Visual Loss.– Sustained eye deviation.– Aphasia.


MANAGEMENT• Fever control with tepid sponging and fanning.• With temp >39.1OC, give oral paracetamol 10-

15mg/kg/dose q 4hrly. AVOID ASPIRIN!!!!!.• Usually abates spontaneously, hence, most of

them will get to the hospital WITHOUT seizures

• When they present with seizures: Resuscitate (clear airways, ensure breathing,

support circulation) Abort seizures with medications (Deep IM

Paraldehyde 1ml/year of life OR 0.1ml/kg to a maximum of 5mL; IV Diazepam 0.3-0.5mg/kg stat; IV or IM Phenobarbitone 10-20mg/kg stat).


PREVENTION OF RECURRENCE

• Diazepam Rectally at onset of febrile episodes and continued over the duration of illness (usually 2-3 days).

• Long term Phenobarbitone or phenytoin prophylaxis controversial:– Decreased cognitive functions.– Does not reduce the risk of Epilepsy.

• Sodium Valproate acceptable in recurrent complex FC in kids > 2years. (CAUTION: risk of hepatotoxicity).


HOME REMEDIES• Exposure of limbs to naked flame :Risk

of burns and tetanus• Using spoon/ sticks as mouth gag: Oral

ulcers, tooth dislocation, risk of aspiration

• Instillation of pepper into the eyes: Conjunctivitis, keratitis, risk of blindness

• Incisions and scarifications: Risk of tetanus

• Use of Cow’s urine concoction (alligator pepper, garlic, tobacco leaves): Risk of hypoglycaemia

• Alcohol administration: Risk of hypoglycaemia


DIAGNOSTIC TESTS IN SEIZURE DISORDERS

• Diagnosis by clinical history and examination.

• Serum– Glucose – Hypoglycemia.– E & U – Electrolyte imbalances,

increased blood urea nitrogen.– Increased blood alcohol/ ammonia

levels. • Urine

– To detect medication toxicity.– To detect Organic & Amino – aciduria.



• Skull x-ray: Evidence of fractures. Evidences of space occupying lesions (shift in

calcified pineal gland, bony erosions, separated sutures, calcifications).

• EEG: Tonic-clonic: high, fast voltage spiked in all

leads. Absence: 3/s, rounded, spiked wave

complexes in all leads. Infantile spasms: Hypsarrythmias. Complex partial: square-topped, 4-6/s spike

wave complexes over involved lobe.



• CT/ MRI: show Structural changes– Indicated in

• Focal seizures.• Neonatal or Early Infancy onset.• Status Epilepticus• Focal Slowing/ paroxysmal EEG Activity.

• Echoencephalography– Midline shifts in brain structures

• Cerebral Angiography– Vascular abnormalities; subdural

hematoma


DIFFERENTIAL DIAGNOSES

• Syncopes• Global amnesia• Cardiogenic (arrhythmia, ischemia, aortic

stenosis)• Breath-holding attacks• Benign paroxysmal vertigo• Migraine• Panic attack• Psychogenic or Pseudoepileptic attacks• Narcolepsy• Cataplexy• Sleep apnoea


MANAGEMENT• During fits outside the hospital,

the following are important:Place patient on the LEFT LATERAL

position.If febrile, tepid sponge and expose

to cold air.Loosen tight clothings around the

neck.Put a soft mouth gag in between

the jaws to prevent biting of the tongue.


MANAGEMENT• The drug of choice depends on the

classification of the seizure, determined by the history and EEG findings.

• The goal for every patient should be monotherapy with the fewest possible side effects.

• The drug is increased slowly until seizure control is accomplished or until undesirable side effects develop.


MANAGEMENT• The child's serum anticonvulsant

level should be monitored during this stage, and the dose should be altered accordingly.

• Ketogenic diet. Not commonly used in children.

• Surgery for refractory focal seizures un-responsive to anti-convulsants.


COMMONLY USED ANTICONVULSANTS

• CARBAMAZEPINE for generalized tonic-clonic or partial. Begin with 10 mg/kg/24 hr & increase to 20–30 mg/kg/24 hr tid

• CLONAZEPAM for absence, myoclonic, infantile spasms, partial. Begin with 0.05 – 1.5mg mg/kg/24 hr & increase by 0.05 mg/kg/wk

• PHENOBARBITONE for generalized tonic-clonic, partial & status epilepticus (3–5 mg/kg/24 hr bid to 20 mg/kg)



• PHENYTOIN for generalized tonic-clonic, partial & status epilepticus ( 3–9 mg/kg/24 hr bid to 20 mg/kg)

• ETHOSUXIMIDE for absence. Begin with 20 mg/kg/24 hr & increase to maximum of 40 mg/kg/24 hr.

• NITRAZEPAM for absence, myoclonic, infantile spasms. Begin with 0.2 mg/kg/24 hr & increase slowly to 1 mg/kg/ 24 hr tid.



• PARALDEHYDE for generalized & status epilepticus. 1mL/year of life to a maximum of 5mL.

• PRIMIDONE for generalized tonic-clonic & partial. 10–25 mg/ kg/24 hr tid (NOT TO BE COMBINED WITH PHENOBARBITONE)

• TOPIRAMATE used as adjunctive therapy for poorly controlled seizures or refractory complex partial seizures.1–9 mg/kg/24 hr bid



• VALPROIC ACID for generalized tonic-clonic, absence, myoclonic & partial. Begin 10 mg/kg/24 hr & increase by 5–10 mg/kg/wk

• VIGABATRIN for infantile spasms & as an adjunctive therapy for poorly controlled seizures. Begin 30 mg/kg/24 hr once daily or bid.

• GABAPENTIN for adjuntive therapy when seizures poorly controlled. 20–50 mg/kg/24 hr tid.



• LAMOTRIGINE for adjunctive therapy when seizures poorly controlled

• PYRIDOXINE 10-25mg/day for adjunctive therapy when seizures poorly controlled because of the possibility of pyridoxine dependency.


DISCONTINUATION OF ANTICONVULSANT

THERAPY• If complete seizure control is

accomplished by an anticonvulsant, a minimum of 2 seizure-free years is an adequate and safe period of treatment for a patient with no risk factors.

• Prominent risk factors include age greater than 12yr at onset, neurologic dysfunction and numerous seizures before control is achieved. onvulsant.

• The weaning process should be done over 3 – 6mo, because abrupt withdrawal may cause status epilepticus.


STATUS EPILEPTICUS• Defined as a continuous

convulsion lasting longer than 30 min or the occurrence of serial convulsions between which there is no return of consciousness.

• It is a medical emergency.• It may be generalized (tonic-

clonic, absence) or partial (epilepsia partialis continua).


RISK FACTORS FOR STATUS EPILEPTICUS

• Sudden withdrawal of anticonvulsants (especially benzodiazepines and barbiturates)

• Sleep deprivation• Intercurrent infections• Electrolytes & metabolic derangements

(hypoglycaemia, hypocalcaemia, lead intoxication, reye syndrome).

• Severe hypoxia (co-existing very severe anaemia)

• Extreme hyper-pyrexia


MANAGEMENT OF STATUS EPILEPTICUS

• Assessment of the respiratory and cardiovascular systems.

• Resuscitation • Nasogastric tube intubation • Venous cannulation• Take blood samples for RBS, CBC, E&U,

Serum Calcium, Phosphorus, Lactate• Toxicology screening.• Arterial blood gases monitoring• CSF analysis to rule out meningitis



• Start 10% Dextrose infusion to prevent and combat hypoglycaemia

• Start oxygen therapy preferably by face mask or endotracheal intubation

• Start therapy with IV Diazepam 0.1-0.3mg/kg infused at 2mg/min for 3 doses

• IV Paraldehyde as an infusion. A 5% solution of paraldehyde is prepared by adding 1.75mL of paraldehyde (1g/mL) to D5W to a total volume of 35mL. The loading dose is 150–200mg/kg IV slowly for 15–20min, and then seizure control is maintained with an infusion of 20mg/kg/hr in a 5% concentration



• If seizures persist, phenobarbitone 20mg/kg stat IV is given & maintained with 5mg/kg infusion.

• If seizures persist, phenytoin is given as 15 - 30mg/kg IV infusion at the rate of 1mg/kg/min. It may be safely added to half-normal or normal saline but not to glucose solutions.

• If seizures persist, induce anaesthesia, paralyse and commence assisted ventilation in an ICU.

TA OGUNLESI (FWACP)1 CHILDHOOD SEIZURES. TA OGUNLESI (FWACP)2 SEIZURES Seizure defined as –A...

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