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Presentation on theme: "CHILDHOOD SEIZURES TA OGUNLESI (FWACP)."— Presentation transcript:


2 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). TA OGUNLESI (FWACP)

3 SEIZURES Seizures 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. TA OGUNLESI (FWACP)

4 SEIZURES The 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. TA OGUNLESI (FWACP)

5 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. TA OGUNLESI (FWACP)

6 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. TA OGUNLESI (FWACP)

7 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. TA OGUNLESI (FWACP)

8 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. TA OGUNLESI (FWACP)

9 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. TA OGUNLESI (FWACP)

10 PATHOPHYSIOLOGY GABA (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. TA OGUNLESI (FWACP)

11 AETIOLOGIES Most seizures are IDIOPATHIC. Identified causes include
Metabolic disturbances – Febrile states. Hypoglycaemia. Hypocalcaemia Hypomagnessaemia Hyponatraemia Hypernatraemia TA OGUNLESI (FWACP)

12 AETIOLOGIES Trauma – Intracranial haemorrhages. Neuronal injury –
Pathologic processes in the brain – Trauma – Intracranial haemorrhages. Neuronal injury – Chemical e.g. Asphyxia, Hyperbilirubinaemia. Physical e.g. concussions, contussions, brain laceration. Cerebral edema TA OGUNLESI (FWACP)

13 AETIOLOGIES Infections Hypertension. Vascular anomalies or lesions.
e.g. Meningitis, encephalitis. Hypertension. Vascular anomalies or lesions. Space-occupying lesions – tumours, abscesses, cysts. Degenerative states – SSPE, Mucopolysacchridoses, Sphingolipidosis TA OGUNLESI (FWACP)

14 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. TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

17 PARTIAL SEIZURES 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. TA OGUNLESI (FWACP)

18 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. TA OGUNLESI (FWACP)

19 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. TA OGUNLESI (FWACP)

20 GENERALIZED SEIZURES 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.) TA OGUNLESI (FWACP)

21 GENERALIZED SEIZURES (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. TA OGUNLESI (FWACP)

22 GENERALIZED SEIZURES (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. TA OGUNLESI (FWACP)

23 GENERALIZED SEIZURES (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. TA OGUNLESI (FWACP)

24 GENERALIZED SEIZURES (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. TA OGUNLESI (FWACP)

25 GENERALIZED SEIZURES 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. TA OGUNLESI (FWACP)

26 GENERALIZED SEIZURES (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. TA OGUNLESI (FWACP)

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 development specific neurologic deficits description of seizure type the EEG findings including the background rhythm. TA OGUNLESI (FWACP)

Febrile Convulsions Infantile spasms (West syndrome) Benign myoclonic epilepsy of infancy Lennox-Gastaut syndrome Landau-Kleffner syndrome Benign childhood epilepsy with centrotemporal spikes (Rolandic epilepsy) Juvenile myoclonic epilepsy (Janz syndrome) TA OGUNLESI (FWACP)

29 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% TA OGUNLESI (FWACP)

30 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. TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

33 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 year Family history of afebrile seizure Complex febrile seizures in the first episode Pre-existing neurologic deficits Persistent post-ictal neurologic disorders TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

36 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 mg/kg stat; IV or IM Phenobarbitone 10-20mg/kg stat). TA OGUNLESI (FWACP)

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). TA OGUNLESI (FWACP)

38 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 TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

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 TA OGUNLESI (FWACP)

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 TA OGUNLESI (FWACP)

43 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. TA OGUNLESI (FWACP)

44 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. TA OGUNLESI (FWACP)

45 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. TA OGUNLESI (FWACP)

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) TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

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 TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

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. TA OGUNLESI (FWACP)

52 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). TA OGUNLESI (FWACP)

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 TA OGUNLESI (FWACP)

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 TA OGUNLESI (FWACP)

Start 10% Dextrose infusion to prevent and combat hypoglycaemia Start oxygen therapy preferably by face mask or endotracheal intubation Start therapy with IV Diazepam mg/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 TA OGUNLESI (FWACP)

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


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