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Seizure new onset
1. New onset seizure in adults
-A review article
Jay R. Gavvala.MD, Stephan U.Schule .MD.Journal of american medical association , volume 316, number 24, page 2657
2. • Jay R. Gavvala.MD, Stephan U.Schule .MD.
• Journal of american medical association , volume 316, number 24, page 2657
• JAMA. 2016;316:2657-2668.DOI10.1001/JAMA .2016.18625
• Impact factor Journal Of American Medical Association 37.684
• Impact factor of The Lancet journal 44.006
• Impact factor The British Medical Journal 19.974
.Journal of American Medical Association , volume 316, number 24, page 2657
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3. Methods
• Review aricles , primary literature, metaanalysis were included
in this study
• 1976 to 2016
• And the articles were rated using oxford centre for evidence
based medicine 2009
• Grade A- best level of evidence
• Grade D – poor level of evidence
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4. Aim of the Article….
• To clear the doubts regarding definition of epilepsy
• Systematic Approach to new onset seizures
• Order of the investigations to be done as well as the sensitivity
and specificity of those investigations .
• Beginnining of therapy.
• Continuation or cessation of therapy.
• Response rates to the individual drugs, specific considerations,
comparative trials.
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6. Article index
• Introduction –Definitions & Distinguish
• Methods
• Results
Clinical presentation
Epidemiology
Risk factors for epilepsy
Assessment and diagnosis – histiory,imaging,eeg,chemistry,prolactin, lumbarpuncture
• Risk of seizure recurrence – unprowoked / prowoked
• Treatment – choice of antiepileptic
• Response rates
• Patient counselling
• Prognosis and duration of therapy
• Discussion
• Conclusion .Journal of American Medical Association , volume 316,
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7. Introduction
• Seizure – a transient occurance of signs and symptoms due to abnormal excessive or
synchronus neuronal activity in brain
• Unprowokwed seizure
• Acute symptamatic seizure – in close temporal association with a transient central
nervous system or systemic insult presumed to be an acute manifestation of the insult
• Focal seizure – one part of cerebral hemisphere
• Generalised seizure – rapidly engaging networks distributing in bilateral hemispheres
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8. Epilepsy..
Disorder of the brain characterised by an enduring predisposition to generarate
epileptic seizures i.e.
2 or more un provoked seizures occuring more than 24 hours apart
or
One un provoked seizure and a high risk ( at least 60 % ) of recurrent un
provoked seizures over the next 10 years
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10. • Rapid onset of negative symptoms such as numbness,weakness,aphasia
• Typically not a/w stiffening/ jerking
• Resulting from temporary interruption of bllod supply in the
distrriibution of certebral vessel
Transient Ischaemic Attack
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11. • Unilateral pulsating head ache , aura , nausea . vomitting
• Some times isolated, neurological symptoms without head ache .
• Duration of sisease typically lasting hours to days with a slow progression of
aura and neurological deficit.
Typical or atypical migraine
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12. • A transient loc with complete return to preexisting neuroogical function
• Some times triggered by, fear, pain, medical procedures, coughing, micturition,
defecation or valsalva maneuver
• Some tomes due to orthostasis – in case of hypovolemia and underlying sructural
heart disease
Syncope / vasovagal syncope
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13. • Abnormal body movements
• Trigger being emotional events or stressors
• Lasting longer than epileptic seizure with waxing and wanindg
quality
• Eye closure , pelvic thrusting , vocal stuttering . partial awareness
Psychogenic non epileptic seizure
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14. • Start with aura
• Loss of awareness
• Unilateral sensations
• Unilateral Motor activity
• Faster than migraine symptoms
Focal seizure
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15. • No warning
• Sudden generalised tonic – clonic activity
• Some tomes brief staring looks
• Myoclonic jerks
Generalised seizure
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16. CLINICAL PRESENTATION
• Always think that event was epileptic and rule out then proceed
• Clinical history- recollection , awareness and experience
• Any witnesses, if so , enquire seperately.
• Age of onset / family history
• Excessive sleep deprivation
• Alcohol / illicit drugs
• Certain medication that dicrease the seizure threshold- Clozapine ,
Cephalosporins, Fluoroquinolones , Bupropion, Tramadol.
• Metabolic derangement abg
• Toxin exposure
• Head injury / prior neurological disease or surgeries.
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17. • Description of all relevant physical examination findings and
classification is beyond the scope
• Lateral tongue bite - 22% of patients with all types of epileptic
seizures.
• Bruces , back pain , compression fractures
• Nuchal rigidity or asterexis – s/o underlying systemic disorder that may
have caused the acute symtmatic seizure
• Skin – signs of Neurofibromatosis , Tuberous Sclerosis, Sturge Weber
Syndrome
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18. BRAIN IMAGING
• First seizure – Neuroimaging is must
• Uncertainity remains regarding appropriate timing and type of
imaging ( grade b )
• Earier studies – CT Was The Modality – 10% of new onset
seizure had abnormality in CT
• Mri – abnormality detection increased to 30%
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19. • New neuro deficit
• persistent alterd mental status
• recent trauma and prolonged head ache
Urgent Imaging
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20. • CT is the usual first imaging modality.
• Lesions which are missed on CT
Low grade glioma
Hippocampal sclerosis
Cavernous malformation
Cortical dysplasia
Periventricular heterotopias
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21. AN EPILEPSY PROTOCOL- SPECIFIC BRAIN
MRI
• 1 -3 mm slices
• Coronal fluid attenuated inversion recovery sequences
• Best for focal cortical dysplasias , hippocampal sclerosis
• Presence of abnormalities
risk recurrence becomes 60 %
defines epilepsy
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22. Electro encephalography
• New onset seizure , but not returning to base line within 30 to 60 minutes after end of the
seizure or waxing and waning level of conciousness or have a focal dysfunction un explained
by a structural lesion
CONTINUOUS EEG .
• Subclinical seizures or acute brain inury or altred mental status persisting
LESS THAN 50 % ARE DETECTED BY 30 MIN OF EEG(GRADE B)
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23. • But 90 % are detected by 24 to 36 hours of continuous eeg
monitoring
• New onset seizure = 29% will epileptiform changes on first eeg
• Detection rate is better in opd pateints than in ipd.
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24. CHEMISTRY PANEL
• ROUTINE SCREENING IS PROPOSED IN NEW ONSET SEIZURES FOR
Hypoglycemia
Uremia
drug intoxication
Hyponatremia
Grade d
Harldly 4 % have these abnormalities
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25. PROLACTIN LEVEL
• It is actually comparison of the prolactin after seizure and base line
prolactin at least before 6 hours of the seizure event
• If already pretest probability of developing seizure is 50 % then
only proactin shows 93% sensitivity
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26. • To differentiaate from psychogenic seizures can be used .
(Gradeb )
• Impracical due to base line measurmemnts not possible
• Cannot differentiate btw sycope and seizure
• Low sensitivity and low negative predictive value ( grade a )
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27. Lumbar puncture
• In view of
• Meningitis
• Encephalitis
• SAH
• Lp in new onset sz has (grade d)
• 8 % of patients had a clinically significant findings
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28. POSSIBLE NEW ONSET SZR
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IS THE EVENT DECRIPTION AND
WITNESS S/O SZR ??
Is yes , take history and
perform a physical
examination
If no, look for ,
migrain , tia , syncope
Fever , focal deficit or mental
status change ??
29. .Journal of American Medical Association , volume 316,
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If no fever / altered mental status , look for
evidence provoking factors (sleep deprivation ,
alcohol use , drugs ) ?
If yes , urgent evaluation for acute symptamatic seizure
Lab testing
Urgent CT
And or MRI
Urgent EEG / continuos EEG
Manage as in patient admission
30. .Journal of American Medical Association , volume 316,
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If presence of provoking factors , non urgennt evaluation for acute symptamatic
seizure , work up,
Lab testing
Brain CT
Out patient EEG
Management
life style modification ,
defer anti epileptic medication
If no, then its unprovoked seizure
Do, EEG
Epilepsy protocol MRI
31. Risk of seizure recurrence
Un provoked seizures
35 % chance of recurrence within 5 years following new onset
seizures
Second seizure occurance = 75 % in 5 years
Higher risk of recurrence in patients with
Abnormal brain imaging (grade b )
Eeg positive ( grade a )
Nocturnal seizure ( grade b )
Seizures attributed to prior brain injury ( grade a)
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33. Acute symptamatic seizures( provoked seizures)
• Lower risk of subsequent un provoked seizures
• In acute brain insults 10-20% risk of recurrence
• Acute brain insults – closed head injury , acute hemorrhagic ir
ischemic stroke , sah , brain surgery , cns infections.
• Eeg with abormality increases risk of recurrence , but cannot
predict the future risk of unprovoked seizure
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34. TREATMENT
• Points to considered
Risk of recurrence
Seizure type
Etiology
Suitable choice of antiepileptic with limitted adverse effects
Anticipated duration of medication
Consider the time to therapeutic onset of antiepileptic drug , to eliminate the frequent
seizure and to decide the dose before discharge from hospital.Journal of American Medical Association , volume 316,
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35. TREATMENT ALGORITHM IN PATIENTS
WITH NEW ONSET EPILEPSY
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36. Individuals with new onset epilepsy
one seizure + abnormal eeg / mri or
two seizure
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FOCAL EPILEPSY - BEGIN ANTI EPILEPTIC
Narrow spectrum – carbamazepine , oxcarbamazepine , phenytoin , lacosamide or
Broad spectrum –lamotrigine , levitiracetam , topiramate , valproate , zonisamide
37. • GENERALISED EPILEPSY OR UNKNOWN EPILEPSY TYPE
BEGIN BROAD SPECTRUM ANTIEPILEPTIC MEDICATION ( CHOICE
DEPENDS ON SEIZURE TYPE )
lamotrigine , levitiracetam , topiramate , valproate , zonisamide
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38. Titrate to therapeutic dose
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Is the patient still having seizures?
If no, continue curent treatment untill seizure free for atleast 2 years
If yes , add a second medication ( dual therapy ) or taper then
discontinue first medication while adding a second medication
39. Do the seizure persists ?
• If yes , revisit diagnosis for seizure that persists for > 1 year ,
consider epilepsy monitiring unit admission
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If no, continue treatment , either as mono therapy or dual
therapy untill seizure free atleast for 2 years
40. • In case of insufficient evidence to prove focal seizures , use
broad spectrum drugs
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QUICK ONSET OF ACTION
Lacosamide
Phenytoin
Levitiracetam
valproate
41. CAUTION
• Phenytoin and carnamazepine cyp 450 inducers
• Valproate – enzyme inhibitor
• Patients with muliple co morbodities , like taking warfarin or
chemotherapeutic agents use – lamotrigine, levitiracetam,
lacosamide
• Rft , lft must before prescribing the anti epileptics
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42. GENERIC FORMULATIONS
• Seizure control and adrs effects vary with various generic
formulations
• But recent studies shows very less variation at plasm drug
concentartion level and one can switch over the generic and
brand names
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43. COMPARATIVE TRIALS
• Older drugs like phenytoin and carbamazepine have higher success
ratesin treatment but side effects are more with phenytoin( grade a)
• Carbamazepine = valproate in treatment of focal seizures evolving
into bilateral convulsive seizures.
• Carbamazepine has fewer side effects
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44. • Lamotrigine = Oxcarbamazepine= Carbamazepine In Efficacy
In Focal Szr Treatment
• Tolerance Wise Lamotrigine >Oxcarbamazepine=
Carbamazepine ( Grade A ) In Focal Szr Treatment
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45. • In generalised epilepsies , valproate Is more efficaccious than
lamotrigine and better tolerated than topiramate ( grade a )
• Recent studies , levitiracetam and zonisamide to be both
efficacious and well tolerated in both focal and generalised
epilepsy
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46. Adverse effects
• Individuals with first time anti epileptic drugs , side effects
were seen in 7 to 31 % of all patients
• Poly therapy = 88 % cance of developing adrs
• Adrs – somnoloscence , dizziness, blurry vision , difficulties
with cincentration and memory
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47. • Adrs are dose dependent and are prominent during first few
days of therapy
• Dose should be slowly escalated and minimum dose with
frequent administration
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48. • All antiepileptics can cause , rash raning from maculopapular variety
to TEN and SJ syndrome( 1 -10 / 10000)
• Most common are – phenytoin , carbamazepine, lamotrigine
• Risk of TEN OR SJ more commonly seen in first 60 days of initiation
of therapy
• HLA B 15.02ALLELES are more prone for SJ OR TEN – in asians
om CBZ and phenytoin FDA says , madatory screning before CBZ
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50. ANTIEPILEPTICS IN FEMALES
• Teratogenicity and intreraction with cintraception should be
considered.
• Enzyme inducers failure of contraceptives
• OC pills dicrease the plasma concentration of lamotrigine
• IUD are best for contraception
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51. • Valproate is teratogenic – 10 % risk of major congenital anomalies.
Also lower iq in born child
• Congenital malformation also seen with –phenobarbital , topiramate
, phenytoin and carbamazepine , levitiracetam and lamotrigine also
exhibit the risk
• Lacosamide and oxcarbamazepine showse limited teratogenecity
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52. Antiepileptics in older patients
• Lamotrigine and gabapentin = good efficacy , less side effects (
limitted literature )
• Levitiracetam > cbz or valproic acid
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53. Response rates
• Early initiatiation of therapy in new onset szr , only delayes the 2nd
episode of seizure but long term prognosis remains the same .( grade a)
• Diagnosed epilepsy after two or more un provoked seizures ,
50 % will become seizure with single apprppriate drug
13 % will be seizure free with second drug addition
4 % with 3 rd drug
• Declining prognosis with additon as severity increasing
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54. Counselling
• Known fact
• 15 – 19 times risk of death by drowning compared to general
population.
• Non commercial driving can be allowed 6 months after un
provoked seizure and 3 months after acute symptamatic seizure.
• Commercial driving only after 2 to 5 years of seizure free interval.
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55. DURATION OF THERAPY
• Free of seizure for 2 years with antiepileptics and normal
neurological examination then after withdrawl of drug 59 %
remained seizure free for next 2 years ( grade a )
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56. • Seizure free period of less than 4 years before withdrawl ang
longer duration of active epilepsy that is not started treatment
are independent risk factors for relapse.
• Highest risk of relapse = within 2 yrs of withdrawl
• < 1 % risk after 5 years of withdrawl.
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57. • Cautiously wean patients with persistent abnormal eeg / structural
lesion
• Patients with relatively treatable and self limitted derangements ( or
metabolic abnormalities ) = use for 7 days
• In acute brain insult – prophylactically, sometimes extend from one
month to 6 months
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