This document discusses the evaluation of acute seizures in the emergency department. It outlines the basic steps in evaluation including determining if it was a seizure, the seizure type, identifying any underlying causes, and assessing for epilepsy. Taking a detailed history is emphasized as the most important step in managing patients with seizures. Two patient cases are then presented and discussed in detail to demonstrate the evaluation process. Various diagnostic tests and their appropriate use are also outlined.

1. EVALUATION OF ACUTE
SEIZURE IN THE EMERGENCY
Dr Pramod Krishnan
Consultant Neurologist and Epileptologist
Manipal Hospital, Bengaluru.

2. Basic steps in evaluation of seizures
• Is it a seizure?
• What are the types of seizures in the patient?
• Is there a treatable underlying cause?
• Are there specific precipitating/ predisposing factors?
• Does the clinical features constitute epilepsy?

3. THE MOST IMPORTANT STEP IN MANAGING A PATIENT WITH
SEIZURE/ EPILEPSY IS ELUCIDATING A CLEAR, DETAILED, RELIABLE
HISTORY.
IT TAKES SOME TIME, BUT SAVES A LOT OF TROUBLE FOR YOU AND
YOUR PATIENT.

4. Patient 1
• 20 year old lady is brought to the Emergency with h/o seizures 1 hour
ago. She never had seizures before. She is on treatment for Type 1
diabetes. There is h/o mild fever for 2 days and intermittent headache.
The semiology is of jerking of all limbs with uprolling of eyes lasting 2-5
minutes with frothing at the mouth. She is drowsy since then and has
bitten her tongue.
• ?DKA ?Neuroinfection ?Systemic infection with sepsis. ?Epilepsy

5. Is the patient seizing?
Convulsive
seizures
NCSE
Focal
Generalised
Look for subtle clinical features:
• Twitching of face, limbs
• Tonic eye deviation
• Tachycardia, hypertension
0-5 min:
• ABC, GRBS, ABGA
• IV Access
• Inj Lorazepam, Midazolam
• Labs: RBS, Electrolytes, CBC
NEAD
Look for atypical features:
• Arrhythmic head/ limb
movements.
• Distractibility,
suggestibility
• Partial/ full
responsiveness inspite
of generalised jerking
• Side-to-side head
movements, pelvic
movements.
Continuous EEG
monitoring

6. Patient not seizing/ post-ictal
Was it a seizure?
Interview of patient:
• Aura, prodromal
symptoms
• Focal symptoms
• Myoclonus
• Post-ictal symptoms
• Triggering factors
• Past history of seizures
Interview of eye-witness
• Circumstances, Aura
• GTCS
• POS
• Myoclonus
• NEAD
• Post-ictal symptoms
Examination:
• Tongue bite
• Incontinence
• Vomitus
• Odour
• Joint dislocation,
Injuries
Labs:
• CPK
• Prolactin

7. • Lateral tongue bite is characteristic of seizures.
• Injury to the tip of the tongue may be seen in other causes of LOC like
syncope.

8. History and findings suggest seizures.
Over next 5-20 min assess:
Seizure description:
Prodromal symptoms
Aura
POS
SGTCS
GTCS, myoclonus
Incontinence
Tongue bite
Joint dislocation
Triggers:
Sleep deprivation
Metabolic
Substance abuse
Comedications
Menses
Post-ictal symptoms:
Confusion
Headache
Vomiting
Myalgia
Reactive automatism
Combative behaviour
Focal deficits- Todds
paralysis, aphasia
Age of onset
Birth history, development
Antecedent illness, injury
Febrile seizure
Progression
AED history:
All AEDS used, in order.
Max dose tried.
Combinations tried.
Benefit/ adverse effects.
Misc:
Comorbidities
Comedications
Family history
Substance abuse
Psychosocial history
Disability assessment

9. Patient 1
• Had seizures, but no h/o Epilepsy.
• Semiology: GTCS.
• Was drowsy, arousable, obeying commands.
• No lateralising signs.
• GRBS of 580 mg/dl.
• Urine ketones positive.
• Had UTI due to E.coli.
• Normal EEG, MRI brain and CSF analysis.
ACUTE SYMPTOMATIC SEIZURE

10. 60 year old male, with acute onset right facio-brachial weakness and dysarthria. Continuous right focal
seizures since stroke onset lasting 4 days. MRI brain showed left sided watershed territory infarcts.

12. Patient
• 45 year old male, brought to Emergency with h/o LOC while on the way to the
toilet. Few jerks of the limbs were noted, with up-rolling of eyes and
incontinence. Injury to the tongue and lips were noted, along with scalp
swelling. He recovered over 5 minutes and had fatigue thereafter. He is on
treatment for HTN. CABG in the past. H/o postural giddiness in the past.
• ABGA, Vitals, ECG, CBC normal.
• Normal neurological examination. Injury to tip of tongue and lower lip noted.
• Right Carotid was not palpable.

13. Distinguishing GTCS from Syncope
Features Seizure Syncope
Immediate precipitating factors. Usually none. Photic
stimulation.
Emotional stress, orthostatic
hypotension, intense pain.
Premonitory symptoms. Usually none. Aura in some. Dizziness, tunnelling of vision,
fatigue, light-headedness, sweating.
Posture at onset. Variable. Usually upright.
Transition to unconsciousness Usually immediate. Over seconds.
Duration of unconsciousness Minutes. Seconds.
Duration of tonic-clonic
movements
30-60 sec or more. Never more than 15 sec.
Facial appearance during event Cyanosis, frothing. Pallor.
Post-ictal drowsiness,
disorientation
Several minutes to hours. Less than 5 min
Post-ictal myalgia, headache. Common Infrequent.
Tongue bite. Common. Lateral tongue bite. Rare. Tip of tongue.
Incontinence Common. Rare. Due to full bladder.

14. Causes of NEAD
Systemic disturbances Neurologic disturbances
Syncope TIA, VBI
Breath holding TGA
Hyperventilation Migraine with aura
Toxic and metabolic disturbances Parasomnias, RBD,
PNES Narcolepsy, microsleep
Panic attacks PKD and related disorders
Tetanus Dystonia, hemiballismus, chorea
Hyperekpleksia
Hemifacial spasms
Hydrocephalic attacks

15. CTA neck showing >70% stenosis of left ICA and non-visualisation of right ICA, CCA (total occlusion)

16. Patient
• 39 year old lady with recurrent right focal seizures since 2 years, along with
inability to speak during the attack. No significant injuries despite numerous
falls during the attacks. Poor response to multiple trials of AEDs. Significant
stressors. Attacks are more during periods of stress.
• MRI brain shows left frontal gliosis. EEG normal.
• Ictal SPECT, inter-ictal PET: inconclusive.
• Diagnosis: Psychogenic attacks.

17. MRI brain (axial T2F and T1W contrast): Left anterior frontal ill-defined hyperintensity with volume loss and
no enhancement consistent with gliosis.

18. Features Seizures PNES
Background history Epilepsy or disorders known to cause
seizures.
Psychiatric illness.
Immediate precipitants AED default, febrile illness, metabolic or
toxic disturbance.
Emotional stressors.
Onset Almost always sudden. Gradual or sudden
Duration, recovery. Few minutes. Recovery is gradual Can be prolonged. Recovery variable.
Semiology Focal/ generalised/ tonic-clonic etc. Asynchronous limb movements, side-
to-side head movements, variation in
amplitude, pelvic thrusting, pauses.
Vocalisation Ictal cry at onset. May cry any time during the event,
shouting, screaming.
Tongue bite. Lateral, if present. Unlikely.
Eyes Usually open, uprolled, tonically
deviated, nystagmoid jerks.
Forcefully closed, fluttering.
Stereotyped Yes. Variable.
Vital signs Cyanosis, desaturation, tachycardia. None.
EEG Ictal rhythm, post-ictal slowing, IEDs Normal or artefacts.

19. EXAMINATION

20. Patient
• 14 year old male, with seizures since early childhood, refractory, along
with mild mental subnormality and marked skin changes. Brought to
Emergency due to increase in seizure frequency. On OXC, CLB and LEV.
• Semiology: brief behavioural arrest, unresponsiveness, head and face
deviation to one side, fall, generalised tonic-clonic movements.
• No family history.

21. Ash leaf macules Shagreen patch
Adenoma sebaceum Tuberous Sclerosis

22. Nevus Anemicus
Multiple café-au-lait spots
Axillary freckling Neurofibromatosis

23. Facial angiomatosis in Sturge-
Weber syndrome
Multiple injection marks in patients with substance abuse

24. Dysmorphic features in Downs syndrome
Microcephaly (above) Megalencephaly (below)

25. Gingival hypertrophy with AED use
Facial Hirsutism with AED use

26. MRI brain (axial T2): Multiple cortical tubers and white matter hyperintensities.

27. Patient
• 24 year old male with right focal seizures since 2 months. Brought to
Emergency due to secondary generalised seizures. Not on treatment.
• He had right facio-brachial weakness lasting 2 hours along with
dysarthria.
• EEG was unremarkable.

28. Neurological examination
Usually normal.
Altered sensorium Post-ictal, medications, metabolic, infective, toxic causes.
Mental subnormality Diffuse cerebral insult: perinatal, genetic- metabolic/
degenerative
Visual impairment, nystagmus,
squint, field defects
Parieto-occipital insult.
Language disturbances Dominant hemisphere, peri-sylvian region
Todds paralysis Contralateral peri-Rolandic region. Lasts < 48 hours.
Repeat the examination to differentiate post-ictal from static deficits.

29. MRI brain (axial T2F): left frontal ill-defined lesion extending to midline. ?Glioma.

30. History and
examination
Lateralisation Localisation
Non-dominant
Dominant Lt Hemisphere
Rt hemisphere
Temporal Extra-temporal
Mesial
temporal
Temporal
Neocortical
Frontal
Parietal
Occipital

31. INVESTIGATIONS

32. Common causes of seizures/ epilepsy by age
Early neonatal (0-3 days) Intracranial infection
Perinatal asphyxia
Intracranial haemorrhage
Drug withdrawal
Late neonatal (after 3 days) Metabolic causes
Developmental defects
Infancy and Childhood Trauma
Intracranial infection
Developmental defects (MCDs, vascular malformations)
Inherited CNS disorders (phakomatoses, metabolic)
Hippocampal sclerosis
Adolescence Trauma, MTS, FCD.
Intracranial infection
Substance abuse
Adulthood Intracranial infection
Neoplasm, metabolic, toxic causes.
Trauma, Vascular

33. Laboratory tests Laboratory tests
ABGA Urinalysis
RBS CSF analysis
Electrolytes: Na, K, Cl, Ca, Mg CPK
Serum creatinine, BUN LFT, Ammonia
CBC, ESR Work up for systemic and neuro infections
AED levels Work up for autoimmune encephalitis
Toxicology Work-up for systemic autoimmune diseases
ECG Genetic tests
Elevated CSF glutamine levels can indicate VPA induced hyperammonemia if serum ammonia is
normal.
Serum prolactin is elevated in GTCS and focal dyscognitive seizures. Sample should be drawn within 20
minutes of ictus and compared to levels drawn at the same time on another day.

34. EEG
• Most important diagnostic test for epilepsy.
• Easily misused, misinterpreted leading to misdiagnosis.
• All patients with first seizure/ epilepsy require EEG for:
1. Characterisation of the event.
2. Classification of epilepsy, epilepsy syndromes.
3. Localisation
4. Assessment of therapy, esp in status epilepticus, CAE.
5. To diagnose NCSE.

35. In Acute seizures,
• EEG is not a priority except to exclude NCSE, NEAD, epilepsy syndrome.
• EEG is not required if patient has epilepsy which has been evaluated and
classified adequately.
• EEG is not essential in acute symptomatic seizures (due to a definite
immediate or remote cause).
• Occurrence of seizures while on adequate AED therapy is reason to
consider changes in treatment rather than IED burden on EEG.

36. However,
• Beware of benign variants on EEG.
• 2-3% of the population have epileptiform discharges even without history
of seizures.
• 50% of patients with epilepsy do not show epileptiform discharges on
one routine EEG.
• 20% of patients with epilepsy do not show epileptiform discharges even
on serial EEGs.

37. Patient
• 24 year old lady, with first seizure in life, was brought to the Emergency.
Semiology was GTCS. There was history of sleep deprivation. H/o
occasional myoclonus with sleep deprivation since 5 years.
• Neurological examination was normal.
• MRI brain was normal.

38. EEG: Frontally dominant generalised polyspike and wave discharges consistent with JME.

39. Patient 7
• 16 year old boy, with h/o neonatal hypoglycaemia and seizures, followed
by developmental delay, has frequent CPS and SGTCS since 3-4 years of
age which is refractory to medical therapy.
• He was brought to Emergency with h/o prolonged GTCS.

40. EEG showing non-specific slowing of background activity and diffuse slowing, with frequent left posterior head
region spikes.

41. MRI brain (axial T2): Bilateral mesial occipital gliosis with hyperintensity consistent with perinatal insult.

42. EEG showing non-specific slowing of background activity and intermittent theta- delta range slowing
suggesting bihemispheric dysfunction as in metabolic encephalopathies.

43. LF1.6Hz/HF50Hz/15μV
Right sided PLEDS in a 32 year old gentleman with HSV and recurrent seizures. Diffuse slowing noted.

44. LF1.6Hz/HF50Hz/5μV
Bilateral independent PLEDS (BIPLEDS) in a 68 year old lady with HSV and recurrent seizures. Diffuse slowing
noted.

45. GPEDs in an EEG of a 72-yr-old lady with epilepsy, presenting with altered mental status due to NCSE.

46. Triphasic NCSE in a 40 year old male, rhythmic, 2Hz, maximum frontal, with subtle eye movements.
LF 1Hz, HF 70Hz, Sen 7 uv

47. Triphasic NCSE: initial component is small and of short duration. Abolished by BZD, with
improvement in responsiveness.
LF 1Hz, HF 70Hz, Sen 7 uv

48. Neuroimaging
• All patient with first seizure in life or epilepsy require neuroimaging.
• MRI brain (3T, 1.5T), epilepsy protocol is the test of choice.
• Contrast study is recommended.
• CT brain should be considered only if MRI is not feasible.
• CT may suffice in traumatic brain injury.
• MRI can be avoided in:
1. Certain benign epilepsy syndromes like CAE, BRE, JME.
2. Acute symptomatic seizures due to metabolic encephalopathies,
intoxications, substance abuse and withdrawal.

49. 28 year old lady with first episode of seizure in life. Right UL paresthesias with jerking, followed by GTCS. EEG
was normal. MRI brain (axial T2F, TW1 contrast) showed left frontal ring enhancing lesion with perilesional
edema in the grey-white matter junction consistent with NCC.

50. 34 year old lady with first episode of seizure in life. Left focal with secondary generalisation. EEG showed right
hemispheric slowing. MRI brain (axial T2, TW1 contrast) showed right temporal large ring enhancing lesion
with marked perilesional edema consistent with tuberculoma.

51. 33 year old male with first episode of seizure in life with right hemiparesis. EEG showed left frontal slowing.
MRI brain (GRE) and CT brain showed left frontal ICH with subdural and subarachnoid extension. ?CVT.

52. 65 year old male, with acute right hemiplegia developed
recurrent right focal seizures since the stroke onset.
Required 2 AEDs. MRI showed large left MCA territory
infarct. MRA showed left ICA occlusion was noted and
mechanical thrombectomy was done.

54. Right Mesial temporal sclerosis characterised
by hippocampal atrophy and hyperintensity
on T2/T2F
Left Mesial temporal sclerosis
with temporal neocortical focal
cortical dysplasia.

55. 11 year old boy with h/o perinatal insult, followed by developmental delay, refractory epilepsy, visual
impairment and squint. MRI brain (T2F coronal and axial) shows b/l parieto-occipital gliosis, with ulegyria,
more on the right side.

56. Is it a seizure?
Diagnose and treat
systemic, neurologic or
psychogenic disorders
First seizure in life?
Abnormalities on
evaluation?
Is there a definite
cause?
Is specific treatment of
the cause successful in
curing seizures?
Acute seizure.
Treatment +/-
Patient has epilepsy.
Evaluate and treat.
NO
YES
NO
NO
YES
NO
YES
NEAD
NO
YES
Acute symptomatic
seizures
YES

57. Clinical Stages and management of Status Epilepticus
Stage Definition Management
Premonitory Variable Clobazam- oral
Incipient 0-5 min Airway, breathing, circulation, GRBS.
Large bore IV access. Start IVF.
Collect blood for ABGA, RBS, electrolytes, CBC,
toxicology, AED levels.
Administer Thiamine and Dextrose if hypoglycemic.
Inj. Lorazepam/ Midazolam/ Diazepam.
Cardiac monitoring.
Early 5-30 min Inj Lorazepam/ Midazolam/ Diazepam, followed by PHT/
LEV.
Established 30-60 min Second line: LEV/ PHT/ VPA/ PB
Start EEG monitoring.
Refractory >60 min Anesthetic agents, LCM, TPM, CLB, CLZ
Super-refractory >24 hrs of anesthetic use Same as refractory, ketogenic diet, immunomodulation,
surgery, ECT

58. Status epilepticus
BZD:LOR/ DZP/ MDZ
LOR and DZP can be repeated once.
MDZ can be repeated multiple times.
Other seizure types Genetic epilepsy syndromes, elderly,
cardiac comorbidity
LEV/ PHT/ VPA/ PB LEV/ VPAStill seizing- refractory SE
Intubation, ICU, Anesthetic agents Another 2nd line AED
LCM, TPM, CLB, CLZ, Ketogenic diet,
Immunomotherapy, ECT, Surgery
Seizing

59. THANK YOU