Tutorial for New-Extern Survival Neurology

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

Neurology extern should know

Medical coma and Acute stroke Tonic-clonic seizure and

status epilepticus
confusional state

COMA
and ACUTE CONFUSIONAL STATE

Wakefulness and ascending reticular activating system(ARAS)

>> level <<

drowsiness stuporous semi-coma coma

VARIOUS STATE OF CONSCIOUSNESS

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

GCS

CPOMR

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: dolls eye, eye deviation, nystagmus, ocular bobbbing Respiratory pattern:

The pupil

Parasympathetic control

Sympathetic control

Pupillary pattern

Dolls 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?

COMA
Localizing sign-no Meningeal sign-yes
Severe meningitis
or
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 Externs 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

GCS=E1VTM1

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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: elyte 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)
Cardioembolism(high-risk/mediumrisk)

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
sensitivity
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

3-4.5

Anti-coagulant in acute ischemic stroke

: heparin IV drip , LMWH (enoxaparin) SC

acute ischemic stroke

Extracranial carotid or vertebral dissection

Cerebral venous sinus thrombosis Unstable large vessel infarction Cardioembolic clot 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

20-30 (Jugular vein)

osmotherapy: Mannitol* 0.25-0.5 g/kg 20 46 10% Glycerol 250 ml 30-60 4 50% Glycerol 50 ml 4 / Furosemide 1 mg/Kg

Treatment IICP

hypotonic solution

Hyperventilation Pco2 30-35 mmHg steroid

Hemicraniectomy in malignant MCA infarction

Keep in Externs 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
Hypoxia

Status Epilepticus

How to define status...

The Epilepsy Foundation of

continuous seizure > 30 minutes > 2 seizures with impaired

consciousness

Americas 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

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

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,

thiopental

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

Phenytoin

Vial: 250 mg/5 ml/vial

0.9% NaCl (dont 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

Midazolam

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

Propofol

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 is required

Thiopentone

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 is required

Phenobarbital

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

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

Slow tapering off AED if seizure recur, increase AED dose

enough to control seizure

Keep in Externs 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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