1. This document provides guidance on the evaluation and management of patients presenting with coma, transient ischemic attack (TIA), and ischemic stroke. 2. For patients presenting with coma, the assessment involves a detailed history, physical and neurological examination to localize the lesion. Coma etiologies are categorized based on presence of focal signs or meningism. 3. For TIA patients, risk stratification using the ABCD2 score helps determine short term risk of stroke. Acute ischemic stroke is managed with thrombolytic therapy if within 4.5 hours of onset, following strict inclusion/exclusion criteria. 4. Secondary stroke prevention focuses on antiplatelet/anticoagulant drugs based

1. Emergency in
Neurology
Narongrit Kasemsap, MD
Neurology unit, Internal Medicine Department,
Khonkaen University

2. Objectives
Localization Patient with Coma.
Evaluation and Management TIA and
Ischemic Stroke Patient.
Management Patient with Status
Epilepticus.

3. Approach to Patient with Coma

4. Consciousness
Awareness
(content of consciousness)
Arousal
(level of consciousness )
“ State of awareness of self and the environment ”

5. Reticular activating system

6. Neuroanatomical
Basis of Coma
Diffuse
Extensive bilateral hemisphere
Bilateral thalamic lesion
Hypothalamus

7. Categorized Coma
Coma without focal signs or meningism
Anoxic-ischemic, metabolic, toxic,
drug-induced, infection, post-ictal state
Coma with meningism
SAH, meningitis, meningoencephalitis
Coma with focal signs
Intracranial hemorrhage, infarction, tumour,
abscess

8. Multifocal Lesion
Mimic toxic or metabolic causes
Venous sinus thrombosis
Bilateral subdural hematoma
Vasculitis
Meningitis

9. Causes of Alteration
of Conscious
Structural causes
Metabolic causes

10. Assesment
History
General examination
Neurological examination
Where is the lesion ?
What is the nature ?

11. History
Difficult and sometime impossible.
Patient past health and illness.
seizure, diabetes, hypertension
substance abuse
depression, suicide attempts
etc..
Current medication.

12. Physical Examination
General examination
General Neurological examination
Level of consciousness
Motor function
Brain stem function
Respiratory pattern

13. Abnormal Respiratory Pattern
Cheyne-Stroke
Central Neurogenic
Hyperventilation
Apneusis
Ataxic breathing
Cluster breathing
lower pons
middle pons
low midbrain and upper pons
RAS at medulla

14. Pupillary Finding in Comatose
Lesions above the thalamus and below the pons preserve pupillary reactions

15. Ocular motility
Resting position.
Spontaneous eye movements.
If blinking is present : intact pontine reticular
formation.
Bell’s phenomenon : intact pons and midbrain.
Reflex eye movements.

16. Eye deviation
Disconjugate eye movement : CN III, CN
VI, brainstem lesion.
Upward deviation : poor localising value
Downward deviation : poor localising value
Skew deviation : posterior fossa lesion

17. Disconjugate eye
CN III
CN VI
Brainstem

18. Spontaneous Eye
Movement
Purposeful eye movements : locked-in
syndrome, catatonia, and pseudo-coma.
Roving eye movements : toxic,
metabolic, bilateral hemisphere.
Contralateral conjugate eye deviation :
epilepsy.

19. Normal /
Metabolic encephalopathy
Bilateral CN VI palsy
Oculocephalic (Doll’s eye)

20. Right CN III, INO
Absent response
Oculocephalic (Doll’s eye)

21. RightLeft
MLF

22. Caloric response
COWS : Cold Opposite Warm Same
Check tympanic membrane before testing
Fast phase nystagmus

23. Painful Stimuli

24. Motor
Response
to Pain
Decerebrate rigidity
Decorticate posture

25. Clinico-Anatomical
Correlation in Coma

26. Bilateral hemisphere
damage/dysfunction
Symmetrical signs
May have fits or myoclonus
Normal brain stem reflexes
Normal oculocephalic and calorics response
Normal pupils

27. Supratentorial mass lesion with
secondary brain stem compression
ipsilateral third nerve palsy
contralateral hemiplegia
Brain stem lesion
Abnormal OCR, calorics
Asymmetrical motor responses

28. Toxic/metabolic
Normal pupils: single most important criterion
(except opiate poisoning)
Ocular motility: rove randomly in mild coma and
come to rest in primary position with deepening
coma
Absent OCR and calorics
Decorticate and decerebrate rigidity or flaccidity,
multifocal myoclonus

29. Mimic of Coma

30. Maintain airway, breathing, and circulation
(ABC’s)
Urgently correct any hypothermia, if
profound.
If trauma has occurred or is strongly
suspected
Stability of the cervical spine before
moving the head.
Initial Management of
Coma

31. Initial Management of
Coma
Rule out hypoglycemia esp DM.
Check basic blood work (blood
count, E’lyte, BS, BUN, Cr, LFT, PT,
PTT, ABG, possibly CO level if
suspected) and urine drug screen.

32. Coma Cocktail
50 ml of 50%glucose IV
100 mg of thiamine IV
Naloxone or Flumazenil for opiate or
BZP overdose.

33. Comatose patient with
suspected SAH
Rule out SAH : brain CT scan without contrast.
Lumbar puncture if SAH is still strongly suspected
but not seen on brain CT scan.
If SAH : neurosurgical consultation and urgent
cerebral angiography.

34. Generally delay CSF examination in CT-negative patients with sudden headache
by 12 h from the onset to ‘allow’ the yellow colour to develop.

35. Comatose patient with
fever or septic syndrome
Examine for any likely systemic focus (abscess,
peritonitis) of infection.
Panculture blood and urine, CXR.
Perform LP to exclude meningitis and begin initial
broad-spectrum antibiotic coverage.
If LP is contraindicated : brain CT scan with and
without contrast.
Brain MRI if suspect Herpes simplex encephalitis

36. CT brain of Increased ICP
Lateral midline shift
Loss of suprachiasmatic or basal cisterns
Fourth ventricle effacement
Obliteration of supracerebellar or quadrigeminal
plate cisterns with patent ambient cisterns

41. Cerebrovascular disease

42. Transient
Ischemic Attack
(TIA)
“A transient episode of neurological dysfunction
caused by focal brain, spinal cord, or retinal
ischemia, without acute infarction”
Stroke. 2009;40:2276-2293.

43. Risk Stratification
• ABCD2 score
• Age >60 years (1)
• BP>140/ 90 mmHg (1)
• Clinical symptoms :
• focal weakness with the spell
(2)
• speech impairment without
weakness (1)
• Duration
• <60 minutes (2)
• 10 to 59 minutes (1)
• Diabetes (1)
The 2-day risk of
strokeScore Risk
0-1 0%
2-1 1.3%
4-5 4.1%
6-7 8.1%
Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals. Stroke.
2009 Jun;40(6):2276–93.

44. Risk Stratification
Johnston SC, Rothwell PM, Nguyen-Huynh MN, Giles MF, Elkins JS, Bernstein AL, et al.Validation and refinement of scores to predict
very early stroke risk after transient ischaemic attack. Lancet. 2007 Jan 27;369(9558):283–92.

45. Stroke
“Sudden loss of blood circulation to an area
of the brain, resulting in a corresponding
loss of neurologic function”

46. Etiology
Diagnosis

47. Baseline laboratory
FBS, CBC, Lipid, BUN, Cr, Electrolytes,
Coagulogram ,Urine exam
Cardiac work up : CXR, EKG
Non-contrast CT brain
Work up for Etiology of Stroke

48. Cardio-embolic stroke
Echocardiogram : TTE, TEE
Holter monitoring : paroxysmal AF
Work up for Etiology of Stroke

49. Stroke in the young <45 yr
No evidence of Cardio-embolism or
atherosclerosis risk factor
ESR, ANA, anti-HIV, VDRL, LFT.
Protein C, Protein S, Antithrombin III, factor V
laiden, prothrombin gene, Homocysteine.
Antiphospholipid syndrome : anticardiolipin,
Lupus anticoagulant

50. Suspected of intra or extra-cranial
artery stenosis
Carotid bruit, Amouroxis fugax
Lacunar infarction with mRS>2
Vascular Work up

51. Carotid duplex ultrasonography
Transcranial Doppler ultrasonography
Vascular Work up

52. Magnetic resonance angiography
Computerized angiography
Vascular Work up

54. Onset of stroke
Sudden onset of focal neurological deficit
Basic life support and capillary blood
glucose to exclude hypoglycaemia
Onset <4.5 hr
Stroke Fast Track
Emergency Lab
CBC, BS, BUN, Cr
Cogulogram, E’lyte, EKG
Emergency
Non-Contrast CT
Acute Ischemic Stroke
Start Thrombolytic Treatment
within 4.5 hr of Stroke onset
Normal or Hypodensity
Onset 4.5-72 hr
Emergency Lab and
Non-Contrast CT
Acute Ischemic Stroke
Treatment

55. N Engl J Med 1995;333:1581-7
Treatment with iv t-PA within 3 hours of the onset of
ischemic stroke improved clinical outcome at 3 months.
National Institute of Neurological Disorders and Stroke (NINDS) study group

56. Significantly improved clinical outcomes in
patients with acute ischemic stroke
N Engl J Med 2008;359:1317-29.
ECASS III
mRS

57. Inclusion
Criteria
&
Exclusion
Criteria
(0-3 hr)
Inclusion Criteria
Exclusion Criteria
Stroke 2013

58. Exclusion
Criteria
(0-3 hr)
Relative Exclusion Criteria
Stroke 2013

59. Additional Exclusion Criteria for
IV rtPA Within 3 to 4.5 Hours
Stroke 2013

60. Intravenous Thrombolytic Therapy
Indication
• Onset < 4.5 hours.
• Age >18 yrs.
• CT brain : no intracerebral /
subarachnoid haemorrhage.
0.9 mg/kg (ไม่เกิน 90 mg)
แบ่งให้ 10% iv in 1 นาที ส่วนที่
เหลือ drip ใน 60 นาที
ขวดละ 50 mg

61. ตัวอย่างการคำนวน
• น้ำหนัก 62.5 kgs x 0.9 mg = 56.25 mg
• ให้ 5.6 mg in 1 min then 50.6 mg in 60 mins.
• ใช้ยา 2 ขวด
• น้ำหนัก 58 kgs x 0.9 mg = 52.2 mg
• ให้ 5 mg in 1 min then 45 mg in 60 mins.
• ใช้ยา 1 ขวด (ไม่เกิน 55 mg ใช้ 50 mg แทนได้)
• น้ำหนัก 120 kgs x 0.9 mg = 108 mg
• ให้ไม่เกิน 90 mg : 9 mg then 81 mg in 60 mins.

62. Acute Treatment
Anti-platelets
• Aspirin 160-325 mg/d ภายใน 48 ชั่วโมง
• กรณีที่ได้รับ thrombolytic therapy ห้ามให้ anti-
platelets ภายใน 24 ชั่วโมง

63. Acute Treatment
Anticoagulants
แนะนำให้ใน Cardio-embolic stroke ยกเว้นมีข้อห้าม ได้แก่
Large infarction size, Brain edema.
กรณีอื่นๆ ยังมีหลักฐานไม่เพียงพอ เช่น crescendo TIA,
extracranial arterial dissection, basilar artery
thrombosis
INR 2-3, 2.5-3.5 (mechanical prosthetic heart valve)
AF, AMI with LV thrombus,
Cardiomyopathy,
Rheumatic MV disease
Mechanical Prosthetic heart valve

64. Massive MCA
territory
Ischemic Stroke

65. Anticoagulant in AIS
Early administration of UFH or LMWH
does not lower the risk of early recurrent
stroke including among people with
cardioembolic sources.
Not recommended for treatment of patients with
acute ischemic stroke (Class III; Level of Evidence A).

66. General Management
NPO : drowsiness, large infarction
Swallowing evaluation
Early mobilization

67. General Management
1. ควรให้ยาลดความดันโลหิตเมื่อ
• SBP>220 หรือ DBP>120 mmHg
• SBP <220 หรือ DBP <120 mmHg ร่วมกับ
• SBP>180 หรือ DBP>105 (thrombolytic treatment)
2. Anti-hypertensive
• Captropril, Nicardipine, Nitroglycerine, Nitroprusside
3. ในกรณีที่ความดันโลหิต <100/70 mmHg ให้หาสาเหตุและแก้ไข
Congestive heart failure
Aortic dissection
Acute Myocardial Infarction
Acute renal failure
Don’t Use Nifedipine sublingual or oral

68. ป้องกันภาวะ hypoxemia (keep O2sat>92%)
ควบคุมระดับน้ำตาลในเลือดที่ 80-140 mg/dl และ 140-180
mg/dl ในรายที่เป็นเบาหวาน
ควรให้สารน้ำเป็น 0.9%NaCl, หลีกเลี่ยงการใช้ free water
หรือสารน้ำที่มีน้ำตาล
ควบคุมอุณหภูมิร่างกายให้ปกติ ถ้ามีไข้ให้หาสาเหตุและรักษา
ให้ยากันชักเมื่อมีอาการ ไม่ควรให้เพื่อป้องกัน
General Management

69. Management of Stroke
Complication
ICH after Thrombolytic treatment
Suspect : acute neurological deterioration,
acute headache, severe hypertension, nausea/
vomiting
Stop thrombolytic + CT brain Emergency.
Check PT, aPTT, platelet count.
Cross match for FFP 10 mg/kg

70. Management of
Stroke Complication
Increased Intracranial Pressure
Intubation and Hyperventilation if alteration of consciousness.
Avoid hypervolemia, hypotonic solution, dextrose in iv fluid.
Osmotherapy
20% mannitol
10% glycerol
Consult Neurosurgeon : decompressive craniectomy.

71. Secondary Stroke Prevention
Drugs Dosage
Aspirin 60-325 mg/d
Clopidogrel 75 mg/d
Cilostazol 200 mg/d
Aspirin + dipyridamole 25+200 mg/d
Antiplatelet drugs

72. Secondary Stroke Prevention
Anticoagulant : use in cardio-embolic stroke.
Warfarin
New oral anticoagulant :
Dabigatran
Apixaban
Rivaroxaban

73. Asesment Stroke Risk :
CHA2DS2-VASc
0 : Low risk
1 : Moderate risk
2 : High risk
Better at identifying “truly low-risk”

74. Assessing Bleeding Risk :
HAS-BLED 0-2 : Low risk
>3 : High risk

75. Stroke. 2011

76. Secondary
Stroke Prevention
Carotid endarterectomy
Carotid stenosis 70-99% ในรายที่มีอาการไม่มาก
ควรทำภายใน 2 สัปดาห์ หรือกรณีที่อาการคงที่อาจ
พิจารณาผ่าตัดภายในระยะเวลาไม่เกิน 6 เดือน

77. Secondary Stroke Prevention
ความดันโลหิตสูง: keep BP <140/90 mmHg, <130/80 (DM)
เบาหวาน : goal HbA1C <7.0%
ไขมันในเลือดสูง : LDL <100 mg/dl, <70 mg/dl (DM), HDL
>40 (male), HDL>50 (female), TG<150 mg/dl
ดัชนีมวลกาย (BMI) <23
รอบเอวชาย <36 นิ้ว (90 เซนติเมตร), รอบเอวหญิง <32 นิ้ว (80
เซนติเมตร)
แนะนำเลิกสูบบุหรี่, งดดื่มสุราและให้ออกกำลังกาย

78. Status Epilepticus

79. ≥ 5 minutes of continuous
seizures
≥2 discrete seizures between
which there is incomplete recovery
of consciousness
Definition
Neurocrit Care (2012) 17:3–23

80. Convulsive Status Epilepticus
Focal motor SE and EPC not included in these definition
Non-Convulsive Status Epilepticus (NCSE)
Electrographic seizure without clinical GCSE
Two distinct phenotype : “Wandering confused”,
“Subtle status”
Classified by Semiology
Neurocrit Care (2012) 17:3–23

81. Cause of SE : Acute Process
Neurocrit Care (2012) 17:3–23
Metabolic disturbances: E’lyte, hypoglycemia, renal failure
Sepsis
CNS infection: meningitis, encephalitis, abscess
Stroke: ischemic stroke, ICH,SAH, CVST
Head trauma with or without epidural or subdural hematoma
Drug : toxicity, withdrawal (opioid, BZP, barbiturate, alcohol),
Non-compliance with AEDs
Hypoxia, cardiac arrest
Hypertensive encephalopathy, PRES
Autoimmune encephalitis : anti-NMDA, anti-VGKC,
paraneoplastic syndrome

82. Cause of SE : Chronic Process
Neurocrit Care (2012) 17:3–23
Preexisting epilepsy: breakthrough
seizures or discontinuation of AEDs
Chronic ethanol abuse in setting of
ethanol intoxication or withdrawal
CNS tumors
Remote CNS pathology (stroke,
abscess, TBI, cortical dysplasia)

83. Diagnostic Work up
Neurocrit Care (2012) 17:3–23
Monitor vital signs.
CT scan of brain.
DTx, BS, CBC, basic metabolic panel, Ca,
Mg, AED levels.
Continuous EEG monitoring
Consider : Brain MRI, CSF study,
toxicology (INH, TCA, CsA, theophylline, cocaine,
sympathomimetics, alcohol, organophosphates)

84. Complication of
Status Epilepticus
Metabolic acidosis
Brain edema
Hypoglycemia
Others : arrhythmia, hyperthermia/
hypothermia, hyperkalemia, DIC,
rhabdomyolysis, myoglobinuria, renal
failure

85. Stage of Status
Epilepticus
Current Opinion in Neurology 2011, 24:165–170
Rapid action, Parenteral, Lipid soluble
Early 0 - 30 min Lorazepam, Diazepam
Establish 30 - 60 min Phenytoin, Phenobarbital,
Valproate, Levetiracetam
Refractory > 60 min Propofol, Thiopental, Midazolam

86. Drugs use in Stage of
Early Status Epilepticus
Route of administration Adult dose
Diazepam i.v. bolus ( <2-5 mg/min) 10-20 mg
Lorazepam i.v. bolus 4 mg
Midazolam Buccal or intranasal, i.m. 5-10 mg
Clonazepam i.v. bolus (<2 mg/min) 1-2 mg at 2 mg/min
Current Opinion in Neurology 2011, 24:165–170

87. Drugs use in Stage of
Established Status Epilepticus
Route of
administration
Loading Dose Continuous dose
Phenytoin
i.v. bolus
(<50 mg/min)
15-20 mg/kg
after 8 hr 300-500
mg/d q8h
Fosphenytoin
i.v. bolus
(<100 mg PE/min)
15-20 mg PE/kg
after 8 hr 300-500
mg/d q8 h
Phenobarbital
i.v. bolus
(<100 mg/min)
10-20 mg/kg
after 8 hr 180-240
mg/d q12h
Valproate
i.v. bolus
(<50mg/min)
15-30 mg/kg 1-2 mg/kg/hr
Levetiracetam
i.v. bolus
in 15 min
Optimal dose not known,
often use 2000-4000 mg
10-30 mg/kg q12h
Topiramate * naso / orogastric 500 mg q 12h x 2days
150-750 q 12h
usual effective
300-1600
Current Opinion in Neurology 2011, 24:165–170
แนวทางรักษาโรคลมชัก
* small report

88. Drugs use in Stage of
Established Refractory Epilepticus
Route of administration
Midazolam
Bolus : 0.1–0.3mg/kg at 4mg/min
Infusion : 0.05–0.4mg/kg/h
Thiopentone
Bolus : 100–250 mg bolus over 20s then
further 50mg boluses every 2–3min until controlled
Infusion : 3–5mg/kg/h to maintain burst suppression
Pentobarbital
Bolus : 10–20mg/kg bolus at 25mg/min
Infusion : 0.5–1mg/kg/h increasing to 1–3mg/kg/h to
maintain burst suppression
Propofol
Bolus : 2mg/kg
Infusion : 5–10mg/kg/h to maintain burst suppression
Current Opinion in Neurology 2011, 24:165–170

89. Suggest
reading

90. The End