NIHSS (National Institutes of Health Stroke Scale, 15 item, 0-42 score)
1a. Level of Consciousness: 0 – alert, 1 – not alert, but responds to mild stimuli, 2 – not alert, requires significant stimuli, 3 – only reflex motor, flaccid.
1b. LOC questions: Ask month and patient’s age: 0 – answers both, 1 – answers 1 correctly, 2 – answers both incorrectly.
1c. LOC commands: ask them to open/close eyes and grip/release hand: 0 – performs both, 1 – performs 1 correctly, 2 – performs neither.
2. Best Gaze: Only horizontal eye movements are tested. 0 – normal, 1 – partial gaze palsy, pt able to deviate away from gaze, 2 – forced gaze, unable to break it.
3. Visual: visual fields tested. 0 – no vision loss, 1 – partial hemianopsia, 2 – complete hemianopsia (half of vision on both eyes gone), 3 – bilateral hemianopia (blind).
4. Facial Palsy: show teeth and raise eyebrows/close eyes. 0 – normal symmetry, 1 – minor paralysis, 2 – total or near paralysis, 3 – complete paralysis of one/both sides – no movement of facial muscles at all.
5. Motor Arm: raise limp palms down for 10 seconds. 5a and 5b (left/right). 0 – no drift, 1 – drift eventually before 10s, 2 – some effort, but limb cannot get to fun 90 degrees, 3 – no effort against gravity, 4 – no movement.
6. Motor Leg: raise leg to 30 degrees for 5 seconds. 6a/6b (left/right). Same as Motor Arm.
7. Limb Ataxia: finger to nose and heel-shin test on both sides. Tests of unilateral cerebellar lesion. 0 – None. 1 – Present in 1 limb. 2 – present in two limbs (assuming both arm and leg).
8. Sensory: you can test as many spots as possible to get a better score. 0 – no sensory loss, 1 – mild to moderate sensory loss, 2 – severe to total sensory loss, patient not aware of being touched.
9. Best Language: Describe what is happening in picture (mother with cookies and overflowing water). 0 – no aphasia, 1 – mild-to-moderate aphasia – some obvious loss of fluency/facility of comprehension, 2 – severe aphasia, very fragmented expression, lots of guessing by listener, 3 – mute, global aphasia.
10. Dysarthria: read or repeat words. 0 – normal, 1 – mild to moderate dysarthria, slurs at least some of the words, 2 – severe dysarthria, speech is so slurred its hard to comprehend.
11. Extinction and Attention: Looking for neglect. 0 – none, 1 – visual, tactile, auditory, personal inattention to bilateral simultaneous stimuli, 2 – profound heme-attention or extinction.
Ischemic: 87% of all strokes, 3 types: thrombotic (sometimes waxing and waning prior to stroke, common cause of TIA), embolic (usually sudden onset, only 20% of ischemic strokes), and hypoperfusion (usually cardiac failure).
Hemorrhagic: intracerebral (10% of all strokes) and nontraumatic SAH (3% of all strokes). Usually sudden onset as well.
Anterior Cerebral Artery Infarctions: uncommon, contralateral sensory/motor in the lower extremity with hand/face sparing. If on right leg, sometimes akinetic mutism (unable to speak) where as on left leg, confusion or motor hemineglect can be apparent.
Middle Cerebral Artery Infarctions: most common, since left hemisphere is usually dominant (in all right handed people and 80% of left handed people), aphasia usually with right sided weakness where as inattention/neglect, dysarthria would be left sided weakness. Deficits in face/upper extremity more than lower. A homonymous hemianopsia and gaze preference toward the side of the lesion can be seen regardless of the side of the lesion.
Posterior Cerebral Artery Infarctions: visual field defects (contralateral homonymous hemianopsia and unilateral cortical blindness), most common symptom though is unilateral headache. Light touch and pinprick deficits, alexia (unable to read), inability to name colors, recent memory loss. Motor deficits are minimal.
Vertebrobasiliar Infarctions: multiple simultaneous symptoms: usually vertigo, headache, nausea, visual disturbances, oculomotor disturbances, ataxia. Hallmark of posterior circulation stroke is crossed neuro disorders (ipsilateral CN deficits with contralateral motor).
Basilar Artery Infarctions: severe coma, quadriplegia, locked-in syndrome. Due to pontine tectum lesions – complete muscle paralysis except for upward gaze.
Cerebellar Infarctions: vertigo, gait instability, limb ataxia, headache, dysarthria, nausea/vomting, CN abnormalities. CT of posterior fossa artifact usually not accurate so usually needs MRI or MRA. Looking for obstructing hydrocephalus – would need emergent NSGY consult.
Lacunar Infactions: pure motor or sensory deficits.
Cervical Artery Dissection: 10-20% of all strokes in patients young and middle-aged. Peaks at 5th decade. Risks: history of neck trauma (major or trivial), family history or genetic factors, recent respiratory infections, hx/o migraines or connective tissue disorder. Both anterior and posterior can cause transient/persistent symptoms. Anterior (internal carotid) symptom generally is unilateral anterior headache or neck pain. Usually frontotemporal though can be varied. Partial Horners has been linked. Vertebral artery dissection usually presents with posterior neck pain and occipital headache as well as unilateral facial paresthesia, dizziness, vertigo, nausea/vomiting, diplopia, ataxia, limb weakness, numbness, dysarthria, hearing loss. Median time between neck pain and neuro symptoms is 14 days. MRI/MRA and CT/CTA are the way to check for it.
General Management: ABCs, IV access, bedside glucose, check Hgb, platelets, pulse ox, ECG, CT noncontrast, cardiac enzymes, strict bedrest with head of bed to 30 degrees.
Hypertension: If patient not candidate for tPa, permissive hypertension with no active attempts to lower BP unless SBP > 220 or diastolic BP is > 120. If going to reduce, reduce only 10-25%. If receiving or had received tPa, need to keep SBP < 185 or DBP < 110. Use Labetolol 10-20mg IV over 1-2min, may repeat x 1 (prior to receiving tPa though if already received, can go up to 300mg total) or nitro paste 1-2inch (C/I with viagra), nicardipine infusion (5mg/h, can increase by 2.5 up to max 15mg/h.
NINDS: 1996 trial, tPa within 3 hours. Only 624 pts, showed no difference in treatment at 24 hours, though did show favorable outcome at 3 months. Symptomatic ICH occurred in 6.4% compared to 0.6% in placebo.
ECASS (European Cooperative Acute Stroke Study III): expanded upon NINDS to tPa treatment within 3-4.5hr in 18-80yos. AHA/ASA endorsed it, but FDA has not approved it.
tPa: 0.9mg/kg, max dose of 90mg, 10% bolus, rest remaining over 60 minutes. No anticoagulation/antiplatelets given in first 24 hours. NINDS exclusion: SAH concerns, initial seizure, previous head trauma or stroke within last 3 months, previous MI in last 3 months, previous GI/GU hemorrhage in last 3 weeks, major surgery in last 2 weeks, prior ICH, SBP > 185/DBP > 110, active bleeding or acute major fracture, glucose < 50, INR > 1.7, use of heparin recently with elevated PT, Platelets < 100. Needs ICU admission if received for neuro checks, looking for possible side effect of angioedema as well.
Antiplatelet Therapy: Dipyridamole + Aspirin after TIA showed possible better benefit; still well received to just start aspirin only after TIA, though can consider plavix if already on aspirin. After acute stroke, 324mg aspirin should be started within 24-48hrs after.
Warfarin/Coumadin: Atrial fibrillation with acute stroke: increased risk of hemorrhagic conversion so consensus is to withhold heparin/lovenox/warfarin initially and have it started while in the hospital, but not in the ED.
Hemorrhage Stroke Treatment: If ICP elevation suspected, head of bed up 30 degrees, head midline, analgesics/sedation, osmotic therapy with mannitol vs hypertonic saline, mild hyperventilation, barb coma.
Cervical Artery Dissection: treated with IV heparin with conversion to warfarin.
TIA (Transient Ischemic Attack)
Transient episode of neuro dysfunction without acute infarction. Typically less than 1-2 hours, should be considered to be like unstable angina. 90-day overall stroke risk after TIA is > 10%, 50% of subsequent events occurred within 2 days.
ABCD2: risk stratify low-risk patients for possible outpatient workup for TIA. Varied results from external validity still showing increased risk with even the low risk group. A – Age > 60, B – BP > 140, C – Clinical Features: 1- Speech Impairment, 2 – unilateral weakness, D – Duration: 1 – 10-60 min, 2 – > 60 min, D – Diabetes. Low Risk is 0-3, Moderate 4-5, High 6-7.
References / Resources
Tintinalli, Chapter 161 – Stroke, Transient Ischemic Attack, and Cervical Artery Dissection
NIHSS Video Tutorial/Simulation – FREE 3.0 CME Hours
Acute Stroke is clinical diagnosis. Sudden onset of neuro deficits explained by vascular cause.
Glucose is the only absolute requirement before tPa lab wise. If on anticoagulants coumadin, need INR or if considering platelet issue, then need that checked otherwise. No labs required.
CT brain noncontrast is only needed.
Early signs of infarction (blurry of gray/white), hyperdense MCA sign – can be candidate for endovascular repair).
Needs BP less than 185/110
Exclusion criteria: basically risk factors for patient bleeding bad if got tPa (head trauma or prior stroke in less 3 months, concerns for SAH, previous ICH, intracranial neoplasm/AV malformation, aneurysm, intracranial or intraspinal surgery, active internal bleeding, acute bleeding diathesis, platelet < 100, Heparin within last 48 hours, INR > 1.7, current use of direct thrombin inhibitors or direct factor Xa inhibitor, glucose < 50, CT shows hypodensity > 1/3.
Seizure is no longer in exclusive criteria (though it is relative C/I, minor).
3-4.5 window exclusions: > 80, severe stroke (NIHSS>25), taking oral anticoagulant, hx/o DM and prior stroke.
Use short acting titratable IV agents: labetolol, nicardipine, clevidipine.
If not candidates, perimissive HTN up to 220.
tPa (0.9mg/kg – max 90), 10% over 1 min, remainder over 1 hour.
Risk of ICH with tPa: NIHSS 0-10 2-4%, 11-20 4-5%, >20 17%. ECASS 7.9%. 6.4% for NINDS total.
IV tPa: ICA-T: 4-8%, MCA-M1 24-32%, MCA-M2: 31-44%. Sometimes clot is too big.
SYNTHESIS/IMSII/MR RESCUE – first generation. Achieved recanalization at 25-41%, no clinical benefit.
MR CLEAN/ESCAPE/SWIFT/PRIME/EXTEND IA/REVASCAT – used stent retrievers, recanalization at 59-88%, all showed clinical benefit.
2015 AHA/ASA Update: Meet all following criteria: prestroke mRS score 0-1, acute ischemic stroke receiving IV tPA within 4.5 hours according to regular guidelines, causative occlusion of ICA or proximal MCA M1 (hyperdense MCA, CTA (best way), angio if high suspicion, MRI), age > 18, NIHSS > 6, ASPECTS > 6 (Alberta Stroke Program Early CT score – don’t want to repervuse brain that’s already dead – , Tx can be initiated (groin puncture) within 6 hours of symptom onset.
Deterioration after tPa: 6-8 units of cryoprecipitate, 6-8 units of platelets, consider 40-80 ug/kg of rFVII – depends on circumstances.
Noncontrast CT: sensitive for acute hemorrhage.
MRI: Gradient echo, T2 susceptibility weighted, and FLAIR MRI are as sensitive for detection of acute blood, more sensitive for prior hemorrhage (more in T2W and GRE).
Acute ischemic present? 4-60% for 6-hour time window.
NCCT: insular ribbon sign (hyperdense vessel), basal ganglia sign (make out internal capsule, thalasmus – should be able to make out demarkation of lines) loss of gray-white differentiation.
DWMRI (measures net movement of water in tissue): accurate within minutes. To differenitae acute from subacute, DWI is used with conjunction with older MRI modalities.
Posterior fossa: NCCT terrible at seeing ischemic stroke. DWMRI better.
Posterior fossa stroke: misses posterior circulation ischemia up to 20% of the time. Can’t completely rely on it.
CTA: covers entire brain, can assess carotid/vertebrobasiliar system, sensitive for detection of IC aneurysms > 4mm. Helps show the collaterals. If you’re looking for aneurysm > 4mm, its 100% sensitive. Pro CT/LP: aneurysm < 4mm can rupture, CTA diagnoses the potential cause, not the hemorrhage itself. CTA will not diagnosis meningitis, IIH, or CVST (venous sinus thrombosis).
Salvageable brain tissue
Infarction (dead, not coming back) vs penumbra (hypoperfusion, likely ready to die) vs benign oligemia (hypoperfused, though likely not going to die).
Core Infarct: NCCT normal, DWMRI sees it.
CT Perfusion: inject dye, and tracts dye as it goes thru brain parenchyma. Allows quantitative assessment of CBV and CBV. Tech dependent. Scan thru in rapidedly. Radiation dose is higher. CT Perfusion only get 4 slices of brain – doesn’t do the whole brain.
MTT: Artery to Vein Mean Transit Time. Looking for mismatched. – able to see areas of hypoperfusion – might need intervention. Does this mean all the areas that would die without intervention – unsure of this at this time (could be benign oligemia though). Sort of like a VQ scan. You can get close to same radiation for NCCT for CTP with the correct settings.
LA Motor Scale: used to find big, meanful strokes. 3 things: facial droop, arm drift, grip strength.
MR-CLEAN: tPa alone vs mechanical/IA + tPa (most, not all). Median time from time of onset to tPa was 88 minutes. Groin puncture at 260 minutes ( 4-5 hrs) median time in 84%. Ideally cath lab by 4.5 hrs.
IMS-3: Similar to MR-CLEAN. Better outcomes in tPa + cath lab.
ED and Early Management of Large Vessel Occlusion, William Meurer, 2016 MCEP Critical Care in the ED, eMedHome.