Tutorial for New-Extern “Survival Neurology”

Surat Tanprawate, MD, MSc(London), FRCP(T) Division of Neurology, Chiang Mai University

“เมือมีเรืองยาก หากหลีกไมได้ จงเขาใจมัน” ่ ่ ่ ้

Neurology extern should know

• Medical coma and • Acute stroke • Tonic-clonic seizure and
status epilepticus
confusional state


Wakefulness and ascending reticular activating system(ARAS)

>> level <<
drowsiness stuporous semi-coma coma

Delirium Acute confusional state

2 component of consciousness: arousal and awareness
coma, vegetative state, minimally conscious state, and locked-in syndrome.

Practical approach

History taking

• • •

as the patient can not talk, then ask their relative or witness

underlying disease is important (DM, atherosclerotic risk, HIV)
symptoms before and during coma(neurological complain)
clinical classification

• •

Physical examination
evaluate location and cause evaluate severity

coma with localizing sign
coma without localizing sign but with meningeal sign coma without both localizing and meningeal sign



coma with seizure

“CPOMR” can help us to
localize the lesion
ARAS is located mainly at the brainstem, and both hemisphere

• • •

Conscious: drowsy, stupor, semi-coma, coma Pupil: dilate, constrict, response to light, uni-bilateral abnormality Ocular movement: doll’s eye, eye deviation, nystagmus, ocular bobbbing Respiratory pattern:

The pupil

Parasympathetic control

Sympathetic control

Pupillary pattern

“Doll’s eye” “Oculocephalic reflex” “Vestibulo-ocular reflex”

Loss of VOR indicates brainstem dysfunction

Motor response and Posture in coma
Decorticate posturebilateral flexion of the upper limbs and extension of the lower limbs, usually the consequence of an diencephalic lesion(late)

Decerebrate rigiditybilateral upper and lower limb extensor posture, usually the consequence of bilateral mid-brain lesions

the Respiratory pattern
Cheyne-Srokes Central neurogenic hyperventilation Apneusis Clustering breathing Ataxic breathing

Where is it?

Localizing sign-no Meningeal sign-yes
Severe meningitis
CT with CM in bacterial meningitis

Meningitis with complication; hydrocephalus, vasculitis, infarct
CT without CM in SAH

Encephalitis Subarachnoid hemorrhage

- CT Brain with contrast - Lumbar puncture
MRI Brain in viral encephalitis

Non-structural lesion caused coma • Exogenous- drug, toxin (lead,
thallium, cyanide, methanol, CO), addict substance (heroin, amphetamine)

• Endogenous- metabolic; Ca,
Na, glucose, hypoxemia, hypercapnia, hypothyroid ::: internal toxin; uremia, hepatic encephalopathy
These causes are reversible; if no localizing sign; lab screen first Glucose, CBC with Plt, BUN, Cr, Elyte, Ca, Mg, PO, Oxygen sat

Keep in Extern’s Mind
Alter mental state 1. Ask history; if obvious history suggest cause, treat immediately (hypoglycemia in DM patient, toxin ingestion) 2. Restore vital signs (Oxygen, BP)...then taking lab (glucose immediately, and other basic lab) 3. Physical exam: “CPOMR” + “Meningeal sign”
-) if coma with no both focal or meningeal sign: metabolic, toxic, drug, diffuse intracranial lesion, SAH, brain stem stroke, stroke with brain herniation -) if coma with meningeal sign; do CT brain emergency -) if coma with focal sign; do CT brain emergency -) if coma with sign suggesting to seizure: start AED

Case exercise
• A woman with sudden coma • complain vertigo, and then sudden coma • C=coma, P=pupil 1.5 mm, O=multidirectional nystagmus, and ocular bobbing, M=quadriplegia, R=apneustic breathing


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Hypodensity lesion at pons and bilateral cerebellum : Basilar artery thrombosis

Delirium, Acute confusional state
- good wakefulness - impair orientation - fluctuation of consciousness (usually occur at night) - broader cause than coma

Cause of delirium - intracranial cause: stroke, cerebritis, etc. - extracranial cause: e’lyte imbalance, deoxygenation etc. - multiple medical/surgical condition

Please aware of aphasia that may mimic delirium

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Sensory aphasia

Acute stroke

when we suspect stroke

when the patient has sudden neurological deficit; symptoms depend on where is the brain is involved

• • • • •

weak, numb brain stem sign

cerebellar sign
cortical sign alter mental state

Stroke can be...
Ischemic 75%

TOAST classification

Large-artery atherosclerosis(emboli/thrombosis)

Hemorrhagic (25%); subarachnoid, intracerebral

• • •

Small-vessel occlusion(lacune)
Stroke of other determine etiology Stroke of undetermined etiology

HP Adams, Jr, BH Bendixen, Stroke 1993;24;35-41

TOAST, Trial of Org 10172 in Acute Stroke Treatment.

Anterior vs Posterior circulation

Condition that mimic stroke

“Acute brain attack”
ABCD, Neuro sign w/u stroke mimicker; specially hypoglycemia in DM, postseizure EKG IV NSS, Lab (CBC plt, PT, PTT, INR, BUN/Cr/elyte

clinical stroke within 2-4.5 hours

Activate Fast tract for rt-PA

CT Brain non-contrast emergency

CT Brain normal or evidence of acute ischemic stroke
IV rtPA if indicated

CT brain, non-contrast

Hemorrhagic stroke
• สามารถทาไดรวดเร็ว ใช้เวลาน้อย วินิจฉัยภาวะเลือดออกในสมองเฉียบพลันไดโดยมี sensitivity ้ ้
เกือบ 100% Minor or subtle signs : loss of lentiform nucleus, loss of insular ribbon, loss of gray-white differentiation and sulcal effacement

Ischemic stroke

Standard treatment in acute ischemic stroke • • • •
IV rtPA within 3 hrs : NNT=10 (now 3-4.5 hrs) Stroke unit : NNT = 30-40 ASA within 48 hrs : NNT 140

Early decompressive surgery for malignant MCA infarction : NNT =2 for death prevent

ขอบงชีในการให้ยาละลายลิม ้ ่ ้ ่ เลือด

• • •
อาการเขาไดกับโรคหลอดเลือดสมอง ้ ้ ขาดเลือด
อาการทางระบบประสาทไมไดหายเอง ่ ้ อาการทางระบบประสาทไมน้อยเกินไป ่ เช่น มีอาการชาอยางเดียว ่ สามารถให้การรักษาไดทันภายในเวลา ้ 3-4.5 ชัวโมง ่

Anti-coagulant in acute ischemic stroke

ยาที่ใช้ : heparin IV drip , LMWH (enoxaparin) SC
อาจพิจารณาให้ใน acute ischemic stroke กรณีตอไปนี้ ่

• • • • •

Extracranial carotid or vertebral dissection
Cerebral venous sinus thrombosis Unstable large vessel infarction Cardioembolic ทีพบ clot ในหัวใจ ่ Arterial dissection

First case rt-PA in CM
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5 Min

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25 Min

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Brain herniation
• Subfalcine (A) • Uncal (B) • Central (C) • Extradural (D) • Tonsillar (E)

Herniation syndrome

Treatment IICP
• • •
ให้นอนยกศี รษะและส่วนบนของรางกายสูง 20-30 องศา ่ จัดทาผูป่วยให้หลีกเลียงการกดทับของหลอดเลือดดาทีคอ ่ ่ ่ ้ (Jugular vein)

• •

พิจารณาให้ osmotherapy: Mannitol* 0.25-0.5 g/kg ทางหลอดเลือดดาใน 20 นาที 46 ครังตอวัน ้ ่ หรือ 10% Glycerol 250 ml ทางหลอดเลือดดาใน 30-60 นาที วันละ 4 ครัง ้ หรือ 50% Glycerol 50 ml ทางปากวันละ 4 ครัง ้ และ/หรือ Furosemide 1 mg/Kg ทางหลอดเลือดดา

• •

Treatment IICP
• • • •
หลีกเลียงการให้ hypotonic solution ่

หลีกเลียงภาวะขาดออกซิเจน พิจารณาใส่ทอ ่ ่ ช่วยหายใจในกรณีทมการหายใจผิดปกติ ี่ ี
Hyperventilation เพือให้ Pco2 30-35 ่ mmHg มีประโยชนในการลดความดันในสมอง ์ ในช่วงสั้ น ๆ กอนผาตัด ่ ่ ไมควรให้ steroid ่

Hemicraniectomy in malignant MCA infarction

Keep in Extern’s mind
Stroke 1. when the sudden neurological deficit occur; suspect stroke...every case 2. check time and onset (eligible for rt-PA??) and exclude mimicker cause (hypoglycemia, seizure)
3. if within 4.5 hours; call resident/neurologist “activate FAST TRACT” can request CT brain emergency 4. check v/s, assess severity, check and follow up neurological signs

Seizure and status epilepticus

Seizure or Not seizure
• Seizure mimicker • pseudo-seizure • convulsive syncope • movement disorder: myoclonus, • hypnic jerk
chorea, paroxysmal dyskinesia

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Identify cause of seizure

Acute processes

• • • • • •

Stroke Metabolic disturbances CNS infection Trauma

Chronic processesPreexisting epilepsyEthanol abuseOld CVARelatively long-standing tumors

Drug Toxicity

Status Epilepticus

How to define status...

• The Epilepsy Foundation of

• continuous seizure > 30 minutes • > 2 seizures with impaired

America’s Working Group on SE (1993)

New proposed definition of SE
• Status Epilepticus Cooperative Study
group (1998)

• Lowenstein DH (1999) • SE > 5 minutes

• SE > 10 minutes

Classification of status epilepticus
1.Generalized convulsive status epilepticus
2.Non-convulsive SE 3.Simple partial SE
(Treiman 1980)

1. Overt 2. Subtle 3. Electrical generalized generalized generalized convulsive SE convulsive SE convulsive SE

Generalized convulsive status epilepticus

(Treiman 1980)

Complication of SE
• Acidosis • Cerebral edema • Hypoglycemia • Other: arrhythmia, hyperthermia,
hyperkalemia, DIC, rhabdomyolysis, myoglobinuria, renal failure

Management of SE

What should we do?
• Evaluate ABCD, and check basic lab,
intubation or oxygen therapy if indicate

• Clarify: is it seizure?? • If seizure is not stop; consider AEDs • Complete general, and neuro-exam • Brain imaging if indicate

• treat early as possible • step up AED is depended on stage of

• add on therapy is needed • monitor EEG regularly, even if no
obvious seizure

Define stage of the status epilepticus

• Pre-monitory status(0-5 min) • Early status(5-30 min) • Established status(30-60 min) • Refractory status(>60 min)

Drug used
• diazepam, phenytoin(Dilantin), valproic
acid(Depakine), levetirazetam(Keppra)

• Phenobarbital, propofol, midazolam,

• Topiramate(feed)

drug use depend on stage of status
stage of status
Premonitory (0-5 min)

AED treatment
Diazepam (i.v. bolus)

Early (5-30 min)

Diazepam (i.v. bolus) followed by phenytoin (iv load) or sodium valproate (i.v. loading) or levetiracetam (i.v.)

Established (30-60 min)

half dose i.v. load of previous drug, if seizure don’t stop, load another drug

Refractory ( > 60 min)

Propofol (i.v.), or midazolam (i.v.), or thiopental (i.v.) or phenobarbital (i.v.) or topiramate (feed)

• diazepam 10 mg (2-5mg/min) • max 10 mg per dose • can be repeated 2 doses


• • •
Vial: 250 mg/5 ml/vial

0.9% NaCl (don’t use infusion pump)

starting dose: 20 mg/kg (rate < 1 mg/kg/min)

maintenance: 5-8 mg/kg/day
e.g. weight 50 kg

Dilantin 1000 mg+0.9%NSS 100 cc iv drip in 20 min. then Dilantin 100 mg+0.9%NSS 100 cc iv drip in 15 min

Valproic acid
• • • •
Vial: 400 mg/4 ml/vial

0.9% NaCl or 5% Dextrose

starting dose: 20-30 mg/kg (rate < 50 mg/min) maintenance: 1-2 mg/kg/hr (max 60 mg/kg/day) e.g. weight 50 kg

Depakine 1000 mg+0.9%NSS 100 cc iv drip in 30 min. then Depakine 100 mg/hr (10 cc/hr)

warning: hepatotoxicity


Vial: 1 mg/ml/vial, 5 mg/ml/vial, 15mg/ 3ml

0.9% NaCl or 5% Dextrose/w

• • •

starting dose: 0.1-0.3 mg/kg bolus (rate < 4 mg/min) maintenance: 0.05-0.4 mg/kg/hr e.g. weight 50 kg

Midazolam 5 mg iv bolus then + Midazolam (1:1)iv drip 5 cc/hr (0.1 mg/kg/hr)

Levetiracetam (Keppra)
• • • • •
Vial: 500 mg/5 ml 0.9% NaCl or 5% Dextrose/w 100 ml starting dose: 2,000-4,000 mg/kg in 15 min maintenance: 10-30 mg/12 hr e.g. weight 50 kg

Keppra 2000 mg iv in 15 min then 1000 mg iv q 12 hour


Vial: 10 mg/ml

5% Dextrose/w

• • •

starting dose: 2 mg/kg bolus
maintenance: 5-10 mg/kg/hr e.g. weight 50 kg

Propofol (2:1) iv 100 mg then 250 mg/hr

Consult ดมยา is required

• • •
Vial: 1 g/vial

starting dose: 100-250 mg in 20 min then 50 mg q 23 min until seizure stop
maintenance: 3-5 mg/kg/hr

Consult ดมยา is required


Vial: 200 mg/4 ml in sterile water 10 ml

5% Dextose

• •

starting dose: 20 mg/kg (rate < 100 mg/min)
maintenance: 1-4 mg/kg/day

Topiramate for SE
• Clinical trial: 500 mg every 12 hours
noso/orogastric feed for 2 days then 150 mg-750 mg every 12 hours

• Effective dose: 300-1600 mg/day

• Tapering off AED • seizure stop > 24 hours • Burst suppression on EEG > 24

• Slow tapering off AED • if seizure recur, increase AED dose
enough to control seizure

Keep in Extern’s Mind

Seizure 1. Seizure or not seizure: history, neuro exam 2. Identify cause, ABCD management 3.Start AEDs if seizure tend to be recurrent 4. if seizure is going to be status; need to be quick, and follow up the status epilepticus guideline therapy

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