Seizure Disorder Management classification .pptx

power point on seizure disorder, medicine on anti epileptic drugs and management of seizures in ER settings and admitted, presented for doctors with medicine and dosages according to current guidelines. specifically presented for pediatric doctors for management of seizures and epilepsy classifications.

1. Seizure Disorder By: Dr Eyob

2. Introduction A seizure is a convulsion or transient abnormal event resulting from a paroxysmal discharge of cerebral neurones Epilepsy is the continuing tendency to have seizures, even if a long interval separates attacks. generalized convulsion is the most common recognized event. Epilepsy is common. Over 2% of the population have two or more seizures during their lives in 0.5% epilepsy is an active problem and hence a common one in general practice. Often no clear cause is found for seizures. Neurosurgery (temporal lobectomy) is also valuable in carefully selected cases.

3. Mechanisms Spread of electrical activity between neurones is normally restricted and synchronous discharge of neurones takes place in restricted groups producing the normal EEG rhythms. During a seizure, large groups of neurones are activated repetitively, unrestrictedly and hyper-synchronously. Inhibitory synaptic activity between neurones fails. This produces high-voltage spike-and-wave EEG activity, the electrophysiological hallmark of epilepsy. A partial seizure is epileptic activity confined to one area of cortex with a recognizable clinical pattern This activity either remains focal or spreads to generate epileptic activity in both hemispheres - and thus a generalized seizure. This spread is called secondary generalization. The focal onset of a seizure may not be apparent. This means that a generalized tonic- clonic seizure may either have started as a focal seizure, or be a primary generalized major convulsion. Brain becomes epileptogenic either because neurones have a predisposition to be hyperexcitable, for example following abnormal neuronal migration patterns in utero, or because the cells acquire this hyperexcitable tendency. Trauma or brain neoplasms are examples of acquired conditions that alter neuronal seizure threshold.

4. Seizure threshold Each individual has a seizure threshold. Experimentally some chemicals (e.g. pentylenetetrazol, a toxic gas) induce seizures in everyone. People who are more likely to have seizures in response to flashing lights, for example, have low seizure thresholds - a concept, not a measurement.

5. Classification Tonic- clonic seizures (grand mal seizures, generalized major convulsions) Following a vague warning, the tonic phase commences. The body becomes rigid, for up to a minute. The patient utters a cry and falls, sometimes suffering serious injury.  The tongue is usually bitten. There may be incontinence of urine or faeces. The clonic phase then begins, a generalized convulsion, with frothing at the mouth and rhythmic jerking of muscles. This lasts from a few seconds to several minutes. Seizures are usually self-limiting, followed by drowsiness, confusion or coma for several hours. Generalized Seizure Types

6. Generalized Seizure Types Ty pical absences (petit mal) This generalized epilepsy almost invariably begins in childhood. Each attack is accompanied by 3 Hz spike-and-wave EEG activity Activity ceases, the patient stares and pales slightly for a few seconds. The eyelids twitch; a few muscle jerks may occur. After an attack, normal activity is resumed. T T ypical absence attacks are never due to acquired lesions such as tumours. They are a developmental abnormality of neuronal control. Children with typical absence attacks tend to develop generalized tonic-clonic seizures in adult life (known as primary generalized epilepsy). Petit mal describes only these 3 Hz absence seizures. Clinically similar absence attacks are also caused by partial seizures of temporal lobe origin, a source of some confusion.

7. Generalized Seizure Types Other generalized seizure types Myoclonic seizures describe isolated muscle jerking Tonic seizures describe intense stiffening of the body not followed by convulsive jerking. Atonic seizures cause sudden loss of tone, with falling and loss of consciousness.

8. Partial Seizure Types Partial seizures (focal seizures) A partial or focal seizure implies that an area of brain (e.g. a temporal lobe) has generated abnormal electrical activity. The seizure frequently has clinical features that provide evidence of its site. An aura describes the effects of initial focal electrical events, such as an unusual smell, tingling in a limb or a strange inner feeling often recognized as a warning of an impending seizure.

9. Partial Seizure Types Jacksonian ( focal motor seizures ) These simple partial seizures originate in the motor cortex. Jerking movements typically begin at the angle of the mouth or in the hand spreading to involve the limbs on the side opposite the epileptic focus. Clinical evidence of this spread of activity is called the march of the seizure. With a frontal lesion, conjugate gaze and the head deviate away from the irritative epileptic focus - known as an a d versive seizure. Weakness of the convulsing limbs for several hours sometimes follows a seizure - Todd's paralysis.

10. Partial Seizure Types Temporal lobe seizures These partial seizures, either simple or complex, describe feelings of unreality (jamais vu) undue familiarity ( de ja v u) with the surroundings. Absence attacks, ve rtigo other visual hal 00000 lu c i nations die. Visions o f faces are o th er examples of temporal lobe seizures. Many other types of partial seizure occur, such as autonomic disturbances with piloerection, flushing, and over breathing, strange smells (frontal cortex), sensory disturbances (parietal cortex), crude visual shapes (occipital cortex), or strange sounds (auditory cortex)

11. Aetiology and precipitants A definite cause for epilepsy is found in under a third of cases cerebrovascular disease accounts for some 15% cerebral tumours for 6% a alcohol-related seizures for 6% post-traumatic epilepsy 2%. Rarer causes include hippocampal sclerosis (resection may be possible), malformations of cortical development, vascular malformations, hematomas, brain abscesses and tuberculomas.

12. Genetic predisposition and developmental anomalies Over 200 genetic disorders list epilepsy among their features, giving rise to complex syndromic classifications. About 30% of epilepsy patients have first-degree relatives with seizures. Usually the mode of inheritance is uncertain. A low seizure threshold appears to run in some families. Generalized typical absence seizures petit mal, 3 Hz spike-and-wave) and primary generalized epilepsy are often inherited as an autosomal dominant trait with variable penetrance. Primary epilepsies are due to complex developmental abnormalities of neuronal control. There are abnormalities in synaptic connections, a and anomalies in neurotransmitter distribution and R elease . Neuronal migration defects in utero, dysplastic areas of cerebral cortex and hamartomas contribute to seizures both in infancy and adult life.

13. Trauma, hypoxia and surgery Perinatal trauma (cerebral contusion and haemorrhage) and foetal anoxia are common causes of childhood seizures. Hypoxic damage to the hippocampi (mesial temporal sclerosis) is another childhood cause of epilepsy. Brain injury is sometimes followed by epilepsy within the first week (early epilepsy) or many months or years later (late epilepsy). To cause epilepsy, the injury must (usually) be sufficient to cause coma. a depressed skull fracture penetrating brain injury cerebral contusion, dural tear or intracranial haematoma increases the incidence of late post-traumatic epilepsy. Seizures follow some 10% of neurosurgical operations on the cerebral hemispheres.

14. Pyrexia Convulsions sometimes occur when children under 5 years have high fevers (febrile convulsions). In the majority there is no recurrence. Partly for social reasons, febrile convulsions are not usually labelled as “ epilepsy ”

15. Brain tumours (and abscesses) Mass lesions in the cortex cause epilepsy either partial or secondary generalized seizures. If epilepsy develops in adult life, the chance of finding an unsuspected tumour is around 3%. Hydrocephalus also lowers seizure threshold.

16. Vascular Seizures sometimes follow cerebral infarction Seen especially in the elderly - there is a peak in incidence late in life. A brain arteriovenous malformation may present with seizures occasionally a subarachnoid bleed.

17. Alcohol, drugs and drug withdrawal Chronic alcohol abuse is a common cause of seizures. These occur either while drinking heavily or during periods of withdrawal. Alcohol-induced hypoglycaemia also provokes attacks Phenothiazines, monoamine oxidase inhibitors, tricyclic antidepressants, amfetamines , lidocaine, propofol and nalidixic acid sometimes provoke fits, either in overdose or at therapeutic doses in individuals with a low seizure threshold. Withdrawal of anticonvulsant drugs (especially pheno -barbital) and benzodiazepines may provoke seizures.

18. Alcohol, drugs and drug withdrawal Chronic alcohol abuse is a common cause of seizures. These occur either while drinking heavily or during periods of withdrawal. Alcohol-induced hypoglycaemia also provokes attacks Phenothiazines, monoamine oxidase inhibitors, tricyclic antidepressants, amfetamines , lidocaine, propofol and nalidixic acid sometimes provoke fits, either in overdose or at therapeutic doses in individuals with a low seizure threshold. Withdrawal of anticonvulsant drugs (especially pheno -barbital) and benzodiazepines may provoke seizures.

19. Encephalitis and inflammatory conditions Seizures are frequently presenting features of encephalitis cortical venous thrombosis neuro-syphilis. chronic meningitis TB rarely be the first sign of bacterial meningitis. neurocysticercosis is a frequent cause of seizures where tapeworm is prominent like Eswatini

20. Encephalitis and inflammatory conditions Seizures are frequently presenting features of encephalitis cortical venous thrombosis neuro-syphilis. chronic meningitis TB rarely be the first sign of bacterial meningitis. neurocysticercosis is a frequent cause of seizures where tapeworm is prominent like Eswatini

21. Metabolic abnormalities hypocalcaemia hypoglycaemia hyponatraemia acute hypoxia uraemia hepatocellular failure

22. Degenerative brain disorders Seizures can occur in Alzheimer's disease and in many degenerative diseases. Epilepsy is three times commoner in multiple sclerosis patients than in the general population.

23. Provoked seizures Seizures are occasionally precipitated by flashing lights or a flickering television screen. Photosensitivity can be recorded on occipital EEG electrodes. Rarely other stimuli (e.g. music) provoke attacks.

24. Sleep deprivation A convulsion sometimes follows missing a nights sleep in a susceptible person

25. Diagnosis The history from a witness is crucial, and usually enables one to distinguish other causes of disturbed consciousness The onset, setting, and stages of attacks are of importance. Neurological examination may be normal or point to a clinical diagnosis (e.g. hemiparesis and papilloedema in a hemisphere tumour). General medical screening, including serum calcium and an ECG should be carried out.

26. Electroencephalography The EEG remains a useful test, despite limitations. It should be performed after a first fit. During a seizure the EEG is almost invariably abnormal, because spikes reach the brain surface. EEG evidence of seizure activity is shown typically by focal cortical spikes (e.g. over a temporal lobe) or by generalized spike-and-wave activity. Epileptic activity is continuous in status epilepticus.

27. Electroencephalography * A normal EEG between attacks (interictal) does not in any way exclude epilepsy. Many people with epilepsy have normal interictal EEGs. * An abnormal interictal EEG does not prove that one particular attack was epileptic

28. Electroencephalography * A normal EEG between attacks (interictal) does not in any way exclude epilepsy. Many people with epilepsy have normal interictal EEGs. * An abnormal interictal EEG does not prove that one particular attack was epileptic

29. CT and/or MR I imaging The trend is towards sophisticated imaging of all new cases of epilepsy when resources permit. In practice, CT is a reasonable screening test for tumours in adults but MR I is used routinely if available.

30. Treatment Emergency measures When faced with a seizure it is best simply to ensure that the patient comes to as little harm as possible, and that the airway is maintained both during a prolonged seizure and in post-ictal coma. Wooden mouth gags, tongue forceps and physical restraint cause injury. Most seizures last only minutes and end spontaneously. A prolonged seizure - longer than 3 minutes - or repeated. seizures outside hospital are best treated with rectal diazepam (10 mg), or intravenous diazepam. If there's any suspicion of hypoglycaemia, take blood for glucose and give i.v. glucose. Serial epilepsy describes repeated seizures with brief periods of recovery. These may lead to status epilepticus. Sudden death in a seizure is unusual but does occur.

31. Status epilepticus This medical emergency means continuous seizures without recovery of consciousness. It should be considered if prolonged serial seizures (two or more) occur with incomplete recovery of consciousness. Status has a mortality of 10-15%. Over 50% of cases occur without a previous history of epilepsy. Focal status also occurs. In absence status, for example, status is non-convulsive - the patient is in a continuous, distant, stuporous state. Epilepsia partials continua is continuous seizure activity in one part of the body, such as a finger or a limb, without loss of consciousness. This is often due to a cortical neoplasm or, in the elderly, a cortical infarct.

32. Acute Management of Seizures Time (min) Intervention* 0-5 min Stabilise the patient to Assess airway, breathing, circulation, and vital signs Administer oxygen Obtain intravenous or intraosseous access Consider hypoglycaemia, thiamine deficiency, intoxication (dextrose, thiamine, naloxone may be given immediately if suspected) Obtain laboratory studies: Consider glucose, electrolytes, calcium, magnesium, blood gas, CBC, BUN, creatinine, and LFTs, toxicology screen, anticonvulsant levels, blood culture (if the infection is suspected) Initial screening history and physical examination

33. Acute Management of Seizures Time (min) Intervention * 5-15 Begin pharmacotherapy Lorazepam IV 0.05-0.1mg/kg up to 4-6mg repeat in 5-10mins Diazepam IV 0.2-0.5mg/kg (0.5mg/kg rectally) repeat in 5-10mins  if seizure persists, load with Fosphenytoin IV/IM 15-20 mg PE/kg IV/IM at 3 mg PE/kg/min. via peripheral IV live (max. 150 mg PE/min). If given IM, may require multiple dosing sites Phenytoin IV 15-20mg/kg at rate not to exceed 1 mg/kg/min via central line Or Phenobarbital IV 15-20 mg/kg IV at rate not to exceed 1mg/kg/min for 7 days

34. Acute Management of Seizures Time (min) 25-40 mins Levetiracetam IV 20-30mg/kg plus Sodium valproate IV 20mg/kg

35. Acute Management of Seizures Time (min) 25-40 mins phenobarbital can be given if s till convulsing at 5 minutes and (Fos) phenytoin previously used Additional phenytoin or fosphenytoin 5 mg/kg over 12 hours. for goal serum level of 10 mg/L Additional phenobarbital 5mg/kg/dose every 15-30 min (maximum total dose of 30 mg/kg; be prepared to support respirations) If seizure persists, consider pentobarbital, midazolam, or general anaesthesia in the Intensive Care Unit. Avoid paralytics.

36. Long term Management Generalised Tonic and/or Clonic: 1 st line Valproate OR Phenobarbital (< 6 months old) 2 nd line Lamotrigine(Specialist advice) Partial: 1 st Line Carbamazepine 2 nd line Rx Lamotrigine Absence: 1 st line Valproate 2 nd line Lamotrigine

37. Anticonvulsants Valproate: Oral 5 mg/kg/dose, 8-12 hourly Increase to 15-20mg/kg/dose: 8-12 hourly -Maximum total daily dose: 40mg/kg/day Exclude liver dysfunction prior to initiating therapy in children under 2 years Carbamazepine : oral, 2 mg/kg/dose (starting dose) Increase slowly at 2 weekly intervals to 5-10 mg/kg/dose 8-12 hourly -Usual maintenance total daily dose: 10-20 mg/kg Maximum total daily dose: 20 mg/kg/day Dosage intervals: Syrup 8 hourly, tablets 12 hourly. Exacerbates myoclonic seizures and absence seizures.

38. Anticonvulsants Lamotrigine: oral, 3-5 mg/kg/dose starting daily dose (specialist initiated) Increase slowly at 2 weekly intervals to 1-5 mg/kg/dose 12-24 hourly Maximum dose when given with valproate: 5 mg/kg/day Lamotrigine is given as add-on therapy for different seizure types Double the dose of lamotrigine when using carbamazepine or Phenobarbitone and halve the dose when using valproate. Phenobarbitone : oral, 3-5 mg/kg/dose as a single dose at night. May be used in children under six months of age. It’ s not recommended as maintenance therapy for children older than 2 years due to undesirable side effects such as sedation, behaviour disturbances, hyperkinesia's and dependence, except in situations where there is poor adherence to other drugs. Exacerbates absence seizures.

39. Reference Medscape Kumar and Clark clinical medicine Sixth edition STG Paediatric guidelines 2021