Epilepsy - Overview and Common Facts
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Epilepsy is a common neurological disorders in which there will be an abnormal electrical activities in the brain causing a brief disruption in the communication system of the brain cells. Epilepsy has a very common symptoms of seizures. A seizure is a sudden rise in electrical activity of the brain. It can involve a part of the brain or the entire brain. To know more details --> https://www.icliniq.com/articles/neurological-health/what-exactly-is-epilepsy
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Epilepsy - Overview and Common Facts
- 1. Overview īŽSeizure (Convulsion) âĸ Clinical manifestation of synchronised electrical discharges of neurons īŽEpilepsy âĸ Present when 2 or more unprovoked seizures occur at an interval greater than 24 hours apart
- 2. Seizure Types īŽProvoked seizures īŽ Seizures induced by somatic disorders originating outside the brain īŽ E.g. fever, infection, syncope, head trauma, hypoxia, toxins, cardiac arrhythmias
- 3. Types īŽ Status epilepticus (SE) īŽ Continuous convulsion lasting longer than 30 minutes OR occurrence of serial convulsions between which there is no return of consciousness īŽ Idiopathic SE īŽ Seizure develops in the absence of an underlying CNS lesion/insult īŽ Symptomatic SE īŽ Seizure occurs as a result of an underlying neurological disorder or a metabolic abnormality
- 4. Aetiology of seizures ī§ Epileptic ī§ Idiopathic (70-80%) ī§ Cerebral tumor ī§ Neurodegenerative disorders ī§ Neurocutaneous syndromes ī§ Secondary to ī§ Cerebral damage: e.g. congenital infections, HIE, intraventricular hemorrhage ī§ Cerebral dysgenesis/malformation: e.g. hydrocephalus
- 5. Aetiology of seizures ī§ Non-epileptic ī§ Febrile convulsions ī§ Metabolic ī§ Hypoglycemia ī§ HypoCa, HypoMg, HyperNa, HypoNa ī§ Head trauma ī§ Meningitis ī§ Encephalitis ī§ Poisons/toxins
- 6. Aetiology of Status Epilepticus īŽ Prolonged febrile seizure īŽ Most common cause īŽ Idiopathic status epilepticus īŽ Non-compliance to anti-convulsants īŽ Sudden withdrawal of anticonvulsants īŽ Sleep deprivation īŽ Intercurrent infection īŽ Symptomatic status epilepticus īŽ Anoxic encephalopathy īŽ Encephalitis, meningitis īŽ Congenital malformations of the brain īŽ Electrolyte disturbances, drug/lead intoxication, extreme hyperpyrexia, brain tumor
- 7. Pathophysiology īŽ Still unknown īŽ Some proposals: īŽ Excitatory glutamatergic synapses īŽ Excitatory amino acid neurotransmitter (glutamate, aspartate) īŽ Abnormal tissues â tumor, AVM, dead area īŽ Genetic factors īŽ Role of substantia nigra and GABA
- 8. Pathophysiology īŽ Excitatory glutamatageric synapses īŽ And, excitatory amino acid neurotransmitter (glutamate, aspartate) īŽ These are for the neuronal excitation īŽ In rodent models of acquired epilepsy and in human temporal lobe epilepsy, there is evidence for enhanced functional efficacy of ionotropic N-methyl-D-aspartate (NMDA) and metabotropic (Group I) receptors Chapman AG. Glutatmate and Epilepsy. J Nutr. 2000 Apr; 130(4S Suppl): 1043S-5S
- 9. Pathophysiology īŽAbnormal tissues â tumor, AVM, dead area īŽ These regions of the brain may promote development of novel hyperexcitable synapses that can cause seizures
- 10. Pathophysiology īŽGenetic factors īŽ At least 20 % īŽ Some examples īŽ Benign neonatal convulsions--20q and 8q īŽ Juvenile myoclonic epilepsy--6p īŽ Progressive myoclonic epilepsy--21q22.3
- 11. Pathophysiology īŽ Role of substantia nigra īŽ Studies with 2-deoxyglucose indicate that a marked increase in metabolic activity in SN is a common feature of several types of generalized seizures; it is possible that some of this increased activity is associated with GABAergic nerve terminals that become activated in an attempt to suppress seizure spread. īŽ Because GABA has been shown to inhibit nigral efferents, it is likely that GABA terminals inhibit nigral projections that are permissive or facilitative to seizure propagation From Gale K. Role of the substantia nigra in GABA- mediated anticonvulsant actions. Adv Neurol.1986;44:343-364
- 12. Pathophysiology īŽ Premature brain īŽ It is more susceptible to specific seizures than is the brain in older children and adults īŽ Kindling īŽ Repeated subconvulsive stimulation (e.g. to the amygdala) will lead to generalized convulsion īŽ This may explain the development of epilepsy after injury to the brain īŽ One temporal lobe seizure -> contralateral lobe
- 14. Seizures Partial â Electrical discharges in a relatively small group of dysfunctional neurones in one cerebral hemisphere â Aura may reflect site of origin â + / - LOC Generalized â Diffuse abnormal electrical discharges from both hemispheres â Symmetrically involved â No warning â Always LOC
- 15. Simple Complex Partial Seizures 1. w/ motor signs 2. w/ somato- sensory symptoms 3. w/ autonomic symptoms 4. w/ psychic symptoms 1. simple partial --> loss of consciousnes s 2. w/ loss of consciousnes s at onset Secondary generalized 1. simple partial --> generalized 2. complex partial --> generalized 3. simple partial --> complex partial --> generalized
- 16. Simple partial seizures with motor signs īŽ Focal motor w/o march īŽ Focal motor w/ march īŽ Versive īŽ Postural īŽ Phonatory
- 17. Simple partial seizures with motor signs īŽ Sudden onset from sleep īŽ Version of trunk īŽ Postural īŽ Left arm bent īŽ Forcefully stretched fingers īŽ Looks at watch īŽ Note seizure
- 18. Simple partial seizures with sensory symptoms īŽSomato-sensory īŽVisual īŽAuditory īŽOlfactory īŽGustatory īŽVertiginous
- 19. Simple partial seizures with sensory symptoms īŽ Vertiginous symptoms âSudden sensation of falling forward as in empty spaceâ īŽ No LOC īŽ Duration: 5 mins
- 20. Simple partial seizures with autonomic symptoms īŽVomiting īŽPallor īŽFlushing īŽSweating īŽPupil dilatation īŽPiloerection īŽIncontinence
- 21. Simple partial seizures with autonomic symptoms īŽ Stiffness in L cheek īŽ Difficulty in articulating īŽ R side of mouth is dry īŽ Salivating on the L side īŽ Progresses to tongue and back of throat
- 22. Simple partial seizures with psychic symptoms īŽDysphasia īŽDysmnesic īŽCognitive īŽAffective īŽIllusions īŽStructured hallucinations
- 23. Simple partial seizure with pyschic symptoms īŽ Dysmnesic symptoms īŽ âdÊjà -vuâ īŽ Affective symptoms īŽ fear and panic īŽ Cognitive īŽ Structured hallucination īŽ living through a scene of her former life again
- 24. Complex Partial Seizures īŽSimple partial onset followed by impaired consciousness īŽ with or without automatism īŽWith impairment of consciousness at onset īŽ with impairment of consciousness only īŽ with automatisms
- 25. Simple Partial Seizures followed by Complex Partial Seizures īŽ Seizure starts from awake state īŽ Impairment of consciousness īŽ Automatisms īŽ lip-smacking īŽ right leg
- 26. Complex Partial Seizures with impairment of consciousness at onset īŽ Suddenly sit up īŽ Roll about with vehement movement
- 27. Partial Seizures evolving to Secondarily Generalised Seizures īŽ Simple Partial Seizures to Generalised Seizures īŽ Complex Partial Seizures to Generalised Seizures īŽ Simple Partial Seizures to Complex Partial Seizures to Generalised Seizures
- 28. Simple Partial Seizures to Generalised Seizures īŽ Turns to his R with upper body and bends his L arm īŽ Stretches body īŽ LOC īŽ Tonic-clonic seizure īŽ Relaxation phase īŽ Postictal sleep
- 29. Simple Partial Seizures to Complex Partial Seizures to Generalised Seizures īŽ Initially unable to communicate but understands īŽ Automatism īŽ Smacking īŽ Hand-rubbing īŽ Abolished communication īŽ Generalised tonic- clonic seizure
- 31. Absence seizures īŽ Sudden onset īŽ Interruption of ongoing activities īŽ Blank stare īŽ Brief upward rotation of eyes īŽ Duration: a few seconds to 1/2 minute īŽ Evaporates as rapidly as it started
- 32. Absence seizures īŽ Stops hyperventilating īŽ Mild eyelid clonus īŽ Slight loss of neck muscle tone īŽ Oral automatisms
- 33. Myoclonic seizures īŽ Sudden, brief, shock-like īŽ Predominantly around the hours of going to or awakening from sleep īŽ May be exacerbated by volitional movement (action myoclonus)
- 35. Clonic seizures īŽ Repetitive biphasic jerky movements īŽ Repetitive vocalisation synchronous with clonic movements of the chest (mechanical) īŽ Venous injection of diazepam īŽ Passes urine
- 36. Tonic seizures īŽ Rigid violent muscle contraction īŽ Limbs are fixed in strained position īŽ patient stands in one place īŽ bends forward with abducted arms īŽ deep red face īŽ noises - pressing air through a closed mouth
- 37. Tonic seizures īŽ Elevates both hands īŽ Extreme forward bending posture īŽ Keeps walking without faling īŽ Passes urine
- 38. Tonic-clonic seizures (grand mal) Tonic Phase īŽ Sudden sharp tonic contraction of respiratory muscle: stridor / moan īŽ Falls īŽ Respiratory inhibition cyanosis īŽ Tongue biting īŽ Urinary incontinence Clonic Phase īŽ Small gusts of grunting respiration īŽ Frothing of saliva īŽ Deep respiration īŽ Muscle relaxation īŽ Remains unconscious īŽ Goes into deep sleep īŽ Awakens feeling sore, headaches
- 39. Tonic-clonic seizures īŽ Tonic stretching of arms and legs īŽ Twitches in his face and body īŽ Purses his lips and growls īŽ Clonic phase
- 40. Atonic seizures īŽ Sudden reduction in muscle tone īŽ Atonic head drop
- 41. Epilepsy syndrome īŽ Epilepsy syndromes may be classified according to: īŽ Whether the associated seizures are partial or generalized īŽ Whether the etiology is idiopathic or symptomatic/ cryptogenic īŽ Several important pediatric syndromes can further be grouped according to age of onset and prognosis īŽ EEG is helpful in making the diagnosis īŽ Children with particular syndromes show signs of slow development and learning difficulties from an early age
- 42. Category Localization-related Generalized Idiopathic Benign epilepsy of childhood with centrotemporal spikes (benign rolandic epilepsy) Benign occipital epilepsy Benign myoclonic epilepsy in infancy Childhood absence epilepsy Juvenile absence epilepsy Juvenile myoclonic epilepsy Symptomatic (of underlying structural disease) Temporal lobe Frontal lobe Parietal lobe Occipital lobe Early myoclonic encephalopathy Cortical dysgenesis Metabolic abnormalities West syndrome Lennox-Gastaut syndrome Cryptogenic Any occurrence of partial seizures without obvious pathology Epilepsy with myoclonic absences West syndrome (with unidentified pathology) Lennox-Gastaut syndrome (with unidentified pathology) Table 1. Modified ILAE Classification of Epilepsy Syndromes
- 43. Special syndromes Febrile convulsions Seizures occurring only with toxic or metabolic provoking factors Neonatal seizures of any etiology Acquired epileptic aphasia (Landau-Kleffner syndrome) Table 1. Modified ILAE Classification of Epilepsy Syndromes (condâ)
- 44. Three most common epilepsy syndromes: 1. Benign childhood epilepsy 2. Childhood absence epilepsy 3. Juvenile myoclonic epilepsy Three devastating catastrophic epileptic syndromes: 1. West syndrome 2. Lennox-Gastaut syndrome 3. Landau Kleffner Syndrome
- 45. Benign childhood epilepsy with centrotemporal spike (Benign Rolandic Epilepsy) 1. Typical seizure affects mouth, face, +/- arm. Speech arrest if dominant hemisphere, consciousness often preserved, may generalize especially when nocturnal, infrequent and easily controlled 2. Onset is around 3-13 years old, good respond to medication, always remits by mid-adolescence
- 46. Childhood absence epilepsy 1. School age ( 4-10 years ) with a peak age of onset at 6-7 years 2. Brief seizures, lasting between 4 and 20 seconds 3. 3Hz Spike and wave complexes is the typical EEG abnormality 4. Sudden onset and interruption of ongoing activity, often with a blank stare. 5. Precipitated by a number of factors i.e. fear, embarrassment, anger and surprise. Hyperventilation will also bring on attacks. Juvenile myoclonic seizure 1. Around time of puberty 2. Myoclonic ( sudden spasm of muscles ) jerks â generalized tonic clonic seizure without loss of consciousness 3. Precipitated by sleep deprivation
- 47. Westâs syndrome (infantile spasms) Triad: 1. infantile spasms 2. arrest of psychomotor development 3. hypsarrhythmia īŽ Spasms may be flexor, extensor, lightning, nods, usually mixed. Peak onset 4-7 months, always before 1 year. Lennox-Gastaut syndrome Characterized by seizure, mental retardation and psychomotor slowing Three main type: 1. tonic 2. atonic 3. atypical absence Landau- Kleffner syndrome ( acquired aphasia )
- 48. Diagnosis in epilepsy īŽAims: īŽ Differentiate between events mimicking epileptic seizures īŽ E.g. syncope, vertigo, migraine, psychogenic non-epileptic seizures (PNES) īŽ Confirm the diagnosis of seizure (or possibly associated syndrome) and the underlying etiology
- 49. Diagnosis in epilepsy īŽApproach: īŽ History (from patient and witness) īŽ Physical examination īŽ Investigations
- 50. History īŽ Event īŽ Localization īŽ Temporal relationship īŽ Factors īŽ Nature īŽ Associated features īŽ Past medical history īŽ Developmental history īŽ Drug and immunization history īŽ Family history īŽ Social history
- 51. Physical Examination īŽGeneral īŽ esp. syndromal or non-syndromal dysmorphic features, neurocutaneous features īŽNeurological īŽOther system as indicated īŽ E.g. Febrile convulsion, infantile spasm
- 52. Investigations īŽ I. Exclusion of differentials: īŽ Bedside: urinalysis īŽ Haematological: CBP īŽ Biochemical: U&Es, Calcium, glucose, ABGs īŽ Radiological: CXR, CT head īŽ Toxicological: screen īŽ Microbiological: LP (Always used with justification)
- 53. Investigations īŽII. Confirmation of epilepsy: īŽ Dynamic investigations : result changes with attacks īŽ E.g. EEG īŽ Static investigations : result same between and during attacks īŽ E.g. Brain scan
- 54. Electroencephalography (EEG) īŽEEG indicated whenever epilepsy suspected īŽUses of EEG in epilepsy īŽ Diagnostic: support diagnosis, classify seizure, localize focus, quantify īŽ Prognostic: adjust anti-epileptic treatment
- 55. International 10-20 System of Electrode Placement in EEG
- 56. Electroencephalography (EEG) īŽ EEG interpretation in epilepsy īŽ Hemispheric or lobar asymmetries īŽ Periodic (regular, recurring) īŽ Background activity: īŽ Slow or fast īŽ Focal or generalized īŽ Paroxysmal activity: īŽ Epileptiform features â spikes, sharp waves īŽ Interictal or ictal īŽ Spontaneous or triggered
- 57. Electroencephalography (EEG) īŽ Certain epilepsy syndromes have characteristic or suggestive features īŽ E.g. Infantile spasms Hypsarrhythmia Childhood absence epilepsy Generalized 3-Hz spike-wave Juvenile myoclonic epilepsy Generalized/ multifocal 4-5 Hz spike- wave and polyphasic-wave Benign occipital epilepsy Unilateral/ bilateral occipital sharp/ sharp-slow activity that attenuates on eye opening Lennox-Gastaut syndrome Generalized/ bianterior spike-wave activity at <2.5 Hz
- 58. Electroencephalography (EEG) īŽ E.g. Brief absence seizure in an 18-year-old patient with primary generalized epilepsy
- 59. Electroencephalography (EEG) īŽNote: īŽ Normal in 10-20% of epileptic patients īŽ Background slowed by: īŽ AED, diffuse cerebral process, postictal state īŽ Artifact from: īŽ Eye rolling, tremor, other movement, electrodes īŽInterpreted in the light of proximity to seizure
- 61. Structural Neuroimaging īŽWho should have a structural neuroimaging? īŽ Status epilepticus or acute, severe epilepsy īŽ Develop seizures when > 20 years old īŽ Focal epilepsy (unless typical of benign focal epilepsy syndrome) īŽ Refractory epilepsy īŽ Evidence of neurocutaneous syndrome
- 62. Structural Neuroimaging īŽ Modalities available: īŽ Magnetic Resonance Imaging (MRI) īŽ Computerized Tomography (CT) īŽ What sort of structural scan? īŽ MRI better than CT īŽ CT usually adequate if to exclude large tumor īŽ MRI not involve ionizing radiation īŽ I.e. not affect fetus in pregnant women (but nevertheless avoided if possible)
- 63. Functional Neuroimaging īŽPrinciples in diagnosis of epilepsy: īŽ When a region of brain generates seizure, its regional blood flow, metabolic rate and glucose utilization increase īŽ After seizure, there is a decline to below the level of other brain regions throughout the interictal period
- 64. Functional Neuroimaging īŽ Modalities available: īŽ Positron Emission Tomography (PET) īŽ Single Photon Emission Computerized Tomography (SPECT) īŽ Functional Magnetic Resonance Imaging (fMRI) īŽ Mostly used in: īŽ Planning epilepsy surgery īŽ Identifying epileptogenic region īŽ Localizing brain function
- 65. Venn Diagram
- 66. Seizure Therapy Anticonvulsant Surgery Specific Treatments Reassurance and Education General Treatment Seizure
- 67. Education & Support īŽ Information leaflets and information about support group īŽ Avoidance of hazardous physical activities īŽ Management of prolonged fits īŽ Recovery position īŽ Rectal diazepam īŽ Side effects of anticonvulsants
- 68. Anticonvulsants īŽ Suppress repetitive action potentials in epileptic foci in the brain īŽ Sodium channel blockade īŽ GABA-related targets īŽ Calcium channel blockade īŽ Others: neuronal membrane hyperpolarisation
- 69. Anticonvulsants Cabamazepine Phenytoin Valproic acid Tonic-clonic and partial Ethosuximide Valproic acid Clonazepam Absence seizures Valproic acid Clonazepam Myoclonic seizures Diazepam Lorazepam Short term control Phenytoin Phenobarbital Prolonged therapy Status Epilepticus Corticotropin Corticosteroids Infantile Spasms Drugs used in seizure disorders
- 70. Adverse Effects īŽ Teratogenicity īŽ Neural tube defects īŽ Fetal hydantoin syndrome īŽ Overdosage toxicity īŽ Life-threatening toxicity īŽ Hepatotoxicity īŽ Stevens-Johnson syndrome īŽ Abrupt withdrawal
- 71. Medical Intractability īŽ No known universal definition īŽ Risk factors īŽ High seizure frequency īŽ Early seizure onset īŽ Organic brain damage īŽ Established after adequate drug trials īŽ Operability
- 72. Surgery īŽ Curative īŽ Catastrophic unilateral or secondary generalised epilepsies of infants and young children īŽ Sturge-Weber syndrome īŽ Large unilateral developmental abnormalities īŽ Palliative īŽ Vagal nerve stimulation
- 73. Surgical Outcome īŽ Medical Intractability īŽ A well-localised epileptogenic zone īŽ EEG, MRI īŽ Low risk of new post-operative deficits
Editor's Notes
- Prolonged febrile seizure: -lasting for more than 30min, particularly in a child younger than 3, is the most common cause of SE Sudden withdrawal of anticonvulsants: -Especially benzodiazepines and barbiturates
- Simple partial In simple partial seizures, consciousness is not impaired. Patients can present with motor, somatosensory, special sensory, autonomic or psychic symptoms complex A complex partial seizure describes a seizure where consciousness is impaired. A partial seizure may begin with a simple seizure, conversely, its onset may coincide with the impairment of consciousness. It may be presented with or without an aura. 2ndary generalized Partial sezure evolve to secondarily generalized seizures May be gen. Tonic-clonis, tonico or clonic
- Focal motor may remain strictly focal OR they may spread to contiguous cortical areas producing a sequential involvement of body parts in an epileptic march - Jacksonian seizure Versive : head turning to one side usually contraversive to the discharge
- Simple partial seizure with versive motor signs and postural motor signs usually arising from sleep; version of trunk to R L arm bent at elbow, finger forcefully stretched R arm beats on arm of chair to warn the nurse tonic contraction of face and eyes jerking of head and L shoulder turns back to normal position support head with R hand look at watch for note seizure in calender
- Areas of cortex subserving sensory function, described as pins and needles / numbness Visual: flashing lights - structured visual hallucinatory phenomena e.g. persons, scenes. Auditory: crude aud sensations - highly integrated functions e.g. music Olfactory: unpleasant odours Gustatory sensations: pleasant / odious taste often described as metallic Vertiginous: sensations of falling in space, floating
- borborygmi
- Psychic: disturbance of higher mental function Dysmnesic symptoms: deja-vu or jamais-vu, forced thinking - panoramic vision ( a rapid recollection of episodes from his/her past life) Cognitive: dreamy states, distorsions of time sense. Detachment or depersonalisation Affective: Anger and Fear which is apparently unprovoked and abates rapidly
- Talking b4 sezure take off spectacles and tell others a seizure is coming turn to the R with upper body and bends his L arm âitâs getting strongerâ he turns to his L , stretches his body, loses consciousness the seizure develops into a tonic-clonic seizure with relaxation a=phase and postictal sleep
- Begins with an epigastric rising sensation, which the patient signals later, unable to speak, waving her L hand, canât communicate followed by smacking and hand-rub
- Generalized seizure: Atonic1: lack of normal tone Tonic1: under continuous tension Clonic1: rhythmic contractions and relaxations of a muscle in rapid succession Myoclonic1: single or repetitive sudden twitching or spasm of a muscle or a group of muscles
- Slight impairment of mental performance: Heard what was spoken to her before the seizure stopped, but has probably not understood it qte right âare you thereâ and âis it thereâ sound very close to each other in Danish
- Usually: patient stands in one place bends forward with abducted arms deep red face noises - pressing of air through a closed mouth
- EEG show generalized sharp waves spikes decrease in frequency
- Idiopathic (with age-related onset) â normal neuro exam, development and neuroimaging, typically nocturnal, usually stop in adolescence, family history 40% 1. Benign childhood epilepsy with centrotemporal spike (aka benign rolandic epilepsy) a. Age of onset 2-13 yrs, accounts for 11.5-25% of childhood epilepsy (autosomal dominant with variable penetrance). Always remits by mid-adolescence. b. Typical seizure affects mouth, face, +/- arm. Speech arrest if dominant hemisphere, consciousness often preserved, may generalize especially when nocturnal, infrequent and easily controlled c. Interictal EEG normal background, midtemporal and central high-amplitude spikes and sharp waves, increased in sleep, can be unilateral (less often) or bilateral but independent (more often). Ictal EEG shows unilateral sharps which can occasionally be bilateral. Sharps can be occipital in &lt;5 yo.
- Prognosis related to underlying cause, response to treatment. ACTH or steroids West Prognosis related to underlying cause, response to treatment. ACTH or steroids Lennox-Gastaut syndrome Three main type: tonic atonic atypical absence Begins age 1-8 yo, seizures can be tonic-axial, atonic, absence, myoclonic, GTC, usually frequent sz, frequent status epilepticus, seizures difficult to control. EEG abnormal background, slow spike and wave (&lt;3Hz), often multifocal abnormalities. Usually has mental retardation.
- Localization: aspects involved e.g. motor, sensory? Any specific site e.g. one limb involved, or generalized involvement? Temporal relationship: number of episode? Diurnal pattern? Duration? Onset and offset? Progression? Persistency? Factors: precipitating? Nature: consciousness impaired? Type of sensory/ motor/ psychic/ emotional disturbances observed/ experienced? Associated features: Prodrome? Aura? Postictal state? Colour of patient? Focal neurological sign?
- Na channel blockade: phenytoin, carbamazepine, lamotrigine GABA-related targets: benzodiazepines interact with specific receptors on GABAa receptor-chloride ion channel macromolecular complex Ca channel blockade: ethosuxamide inhibits low-threshold Ca currents especially in thalamic neurons that act as pacemakers to generate rhythmic cortical discharge Other mechanisms: Valproic acid - neuronal membrane hyperpolarisation possibly by enhancing K channel permeability
- Infantile spasms: corticotropin and corticosteroids are commonly used but cause cushingoid side effects.
- Neural tube defects (spina bifida) associated with valproic acid Fetal hydantoin syndrome - phenytoin Overdosage: most of the commonly used anticonvulsants are CNS depressants - respiratory depression Life threatening toxicity fatal hepato. - valproic acid greatest risk to children &lt;2 yrs of age and patients taking multiple anticonvulsant drugs Lamotrigin - skin rashes and life-threatening Stevens Johnsons syndrome Abrupt withdrawal - increased seizure frequency and severity
- Intractability can be established after: 2-3 of the established newer first and second line AED, as monotherapy at least one in combination max tolerated dose High seizure frequency: daily / weekly episode brain damage: the more severe the brain damage, the greater the likelihood of seizure persistence Assess operability using imaging studies
- Large unilateral developmental abnormalities such as cortical dysplasias and porencephalic cysts