Rosens Notes – Chapter 99 – Stroke, Tia, And Tga

Front 1

BREAK DOWN of strokes?

Back 1

· Thrombosis (1/3) or embolic (2/3) (carotid or heart)

Front 2

Types of ischemic strokes

Back 2

Large vessel - 16%

small vessel ie lacunar 25%

-internal capsule, BG, thalamus, pons

-HTN,DM

-syndromes

=>20 types

=>main

o Pure motor
o Pure sensory
o Ataxic hemiparesis
o Clumpsy hand syndrome

Embolic ( 25% of all strokes)

Front 3

Clues to a lacunar infarct

Back 3

No cognitive deficits
o No language deficit
o No LOC
o NO simultaneous motor and sensory findings
o No visual loss
o No loss of cortical sensory function (graphesthesia, stereognosis)

Front 4

Embolic

Back 4

Cardioembolic in 25% of all strokes
o Sources:
§ Afib: MCC, more like to be big, large vessel CVA and higher mortality
§ Mural thrombi also seen with severe LV dysfunction: post MI (1-2% will have CVA), cardiomyopathy, CHF, myocarditis
§ Carotid artery source of emboli also common

Front 5

CVA in the young person

Back 5

o Hypercoagulable states: APC-resistance, Prot C def, Prot S def, antiphospholipid Ab syndrome, oral contraceptives, SLE
o Polycythemia
o DVT/PE with PFO
o Vasculitis
o Fibromuscular hyperplasia of cerebral vessel
o Prolonged vasoconstriction from Migraine
o Drugs: cocaine, amphetamines (more likely to cause hemorrhagic)

Front 6

· Transient Ischemic Attacknhhhhhhhh

Back 6

o Sudden onset = key aspect
o Neurologic deficit completely resolves in 24 hours (AHA definition = <1hr)
o Focal neuro deficit
o Important WARNING sign of impending CVA
§ 10% will stroke within 3 months, of these half within 2 days
o Majority last less than 30 min
o Crescendo TIAs = three or more TIA w/i 72hrs
· Anterior circulation TIA: 50% will have carotid disease on angio
· First TIA > 65yo: 50% have evidence of previous infarct on MR --------> silent infarcts are common
· PROGNOSIS: see Johson’s article in JAMA
· (Wu – archives internal med 2007 - paper also good)
· Incidence of TIA in Canada = 15000-20000
· ~25-30% of strokes are preceded by TIA

Front 7

Risk Factors for Ischemic CVA

Back 7

Modifiable: HTN, smoking, TIAs, heart disease, DM, hypercoagulopathy, carotid bruit, sickle cell anemia, polycythemia, hypercholesterolemia, inactivity

· Nonmodifiable: age, sex, race, prior stroke, fhx, previous MI

Front 8

PATHOPHYSIOLOGY

Back 8

Ischemic brain cells become neurologically silent and thus lose function
· Ischemic penumbra is the area surrounding the primary injury where small amounts of blood flow are maintained by collateral circulation
· Time of vessel occlusion is KEY to determining
o < 2hrs usually reversible
o 2 - 6 hrs may or may not be reversible
§ 6 hrs definitely NOT reversible

Front 9

· Completed stroke

Back 9

= neurologic deficit persists longer than 3 weeks even if some improvement has occurred

Front 10

· Stroke in evolution

Back 10

= focal deficits worsen over the course of minutes to hours (20% of anterior and 40% of posterior circulation strokes have evidence of progression; anterior progress over 24hrs, posterior can progress over 3 days)

Front 11

Anterior Circulation Stroke

Back 11

· Anterior cerebral artery. Carotid --> ACA and MCA territories
· Rarely present with loss of consciousness (can occur if patient has had many previous strokes)
· Rare b/c of collateral supply
· Frontal Lobe function
o Altered mentation, Impaired judgement and insight
o Presence of primitive reflexes (suckle, grasp)
o Bowel and bladder incontinence
o Weakness and sensory loss of LEG > ARM is characteristic (contralateral side; shouldn’t involve arm unless MCA involved)
o Apraxia or gait clumsiness can occur

Front 12

Middle Cerebral Artery

Back 12

· Contralateral weakness and sensory loss in FACE/ARM > LEG is characteristic
· Weakness may be fairly focal in a part of the face or arm but is almost always accompanied by sensory loss in the area of weakness
· Ipsilateral Hemianopsia is common
· Agnosia common (inability to recognize previously known subjects)
· Gaze preference TOWARD the lesion
o Gaze center in each side of the brain pushes eyes away. So gaze center on L pushes eyes to right. Thus if you lose that in a stroke the eyes look toward the lesion whereas in a seizure the center is hyperactive and eyes are pushed away from lesion
· Neglect if involves nondominant hemiphere
· Aphasia common if affects the dominant hemisphere
o Aphasia = disturbance in language function (comprehension, repetition, naming, fluency)
o Dysphasia = Aphasia
o Dysphagia = difficulty swallowing
o Dysarthria = normal language function but slurred speech due motor deficit of muscles involved in speech
o Wernicke’s aphasia = receptive aphasia
o Broca’s aphasia = expressive aphasia

Front 13

MCA eye signs?

Back 13

- ipsilateral hemianopsia

- neglect(if involves non dominant hemisphere)

- gaze preference towards lesion

Front 14

Posterior Circulation Stroke

Back 14

· Vertebrobasillar system
· Can present with loss of consciousness b/c RAS is in brain stem
· Nausea and vomiting common b/c of emesis center in BS
· Parietal lobes: neglect, visual neglect, visual agnosia (unable to recognize known objects), alexia (unable to understand writing)
· Occipital lobes: homonymous hemianopsia
· Cranial nerves of BS: diplopia, IIIrd nerve palsy, vertigo, nystagmus, facial droop, dysphagia
· Cerebellum: ataxia
· Sensory and motor deficits
· Crossed deficits = disruption of sensation/power on one side of face but opposite side of body

Front 15

DDX OF ISCHEMIC STROKE

Back 15

· Vascular: ICH, AVM, Carotid dissection, Vertebral dissection

· Infection: Brain abscess, Meningitis, Encephalitis,Bell’s palsy

· Traumatic: EDH, SDH, SAH,

· Metabolic (hyperglycemia, hypoglycemia, wernike’s encephalopathy (DOA),
· Conversion d/o
· Inflammation: GCA, PAN
· Brain tumor
Contusion/hemorrhage
· Toxic: sympathomimetics,

· Neurologic: Seizure, Migraine, Peripheral vertigo
· Enviromental: Air embolism (diving, during procedures)

Front 16

o Early findings in 1/3 (w/i 3hrs)

Back 16

§ Localized Hypodensity
§ Loss of Grey - White differentiation
§ Hyperdense MCA sign
§ Disappearing Basal Ganglia sign
§ Sulcal effacement (due to edema)
§ Loss of insular ribbon
§ Mass effect (due to edema)
§ Majority do not have findings until 6 - 12 - 24hrs

Front 17

other imaging available for stroke?

Back 17

o Contrast CT is not indicated unless noncontrast is abnormal and you want contrast to look for tumor, abscess, AVM
· Echocardiogram
· Mural thrombus, tumor, PFO, valvular dz, valvular veggies,
· Consider in all patients < 65 with no obvious source of CVA
· Carotid Dopplers
· Known or suspected lesions in carotids
· May identify candidates for heparin or emergency carotid endarterectomy
· May require angiography to further delineate lesion
Other
· Angiography
· CTA
· MRI
o Better for early detection
o Better for posterior circulation infarcts/lesions
· MRA: identifies large vessel occlusions well, may miss small vessel occlusion; is replacing angiography for identifying occlusion or stenosis in selected pts
· New MRI techniques: diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) may be able to differentiate reversible lesions

Front 18

What should you avoid?

Back 18

overhydration - b/c edema

hyperglycaemia-a/c worse outcome

Front 19

BP Management with ischemic CVA or TIA

Back 19

· Controversial b/c of limited data
· More aggressive control if getting tPA (table 95-5)
· Generally leave BP alone b/c brain does a better job of autoregulation
· Labetolol or nitroprusside iv favored (avoid nifedipine b/c big drops in BP)
· Leave BP alone unless (i) severe HTN (>220/120) (ii) getting tPA or (iii) has one of the following....
o Aortic dissection
o Hypertensive encephalopathy
o Acute MI
o Severe CHF

Front 20

BP control

Back 20

DBP > 140 mm Hg

Sodium nitroprusside (0.5 μg/kg/min).

Aim for 10–20% reduction in DBP

SBP > 220, DBP > 120, or MAP[†] > 130 mm Hg

10–20 mg labetalol[‡] IV push over 1–2 min.

May repeat or double labetalol every 20 min to a maximum dose of 150 mg.

SBP < 220, DBP > 120, or MAP[†] > 130 mm HgEmergency antihypertensive therapy is deferred in the absence of aortic dissection, acute myocardial infarction, severe congestive heart failure, or hypertensive encephalopathy

Lowering Blood Pressure in acute Ischemic Stroke does not improve outcomes (outside of CVA Thrombolysis or sbp>220 mmHg)

1. the catis trial He (2014) JAMA 311(5): 479-89
2. Sandset (2011) Lancet 377(9767):741-50

Front 21

BP control w/ tpa?

Back 21

10 mg labetalol[‡] IV push. May repeat or double labetalol every 10–20 min to a maximum dose of 150 mg or give initial labetalol bolus, then start a labetalol drip at 2 mg/min

aim <185 <110

Front 22

ASA in acute stroke

Back 22

· Being studied
· NNT is 100 for prevention of death or non-fatal recurrence in first few weeks
· NNT is 100 for prevention of death or dependance at 6 months
· Should not be given with tPA in first 24hrs (increased bleeding rates)

Front 23

Heparin

Back 23

· Consult neurology if you are going to give it!
· Often given for ischemic strokes but benefit UNPROVEN
· No data has established the efficacy of anticoagulation
· Net balance of further thrombosis/embolism versus hemorrhagic transformation
· Consider for use: crescendo TIAs, cardioembolic source, high-grade carotid lesion, posterior circulation TIA, evolving strokes
· LMWH: benefit shown by Kay 1995 but not reproducible by larger study

Front 24

tPA dose?

Back 24

· Dose = 0.9 mg/kg (max 90mg): 10% of dose as bolus and the rest over 60 min

Front 25

Fibrinolytic Therapy for Acute Ischemic Stroke: Inclusion and Exclusion Criteria

Back 25

Inclusion Criteria

1. Age ≥18 years

2. Clinical diagnosis of ischemic stroke causing a measurable neurologic deficit

3. Time of symptom onset well established to be <4.5h before treatment would begin

Exclusion Criteria (arrange into head vs not head)

1. Evidence of intracranial hemorrhage on noncontrast head CT

2. Only minor or rapidly improving stroke symptoms

4. Active internal bleeding (e.g., gastrointestinal bleed or urinary bleeding within last 21 days)

5. Known bleeding diathesis, including but not limited to:

Platelet count <100,000/mm[3]

Patient has received heparin within 48 hours and had an elevated activated partial thromboplastin time (greater than upper limit of normal for laboratory)

Recent use of anticoagulant (e.g., warfarin sodium) and elevated prothrombin time >15 seconds OR INR > 1.7

7. Within 14 days of major surgery or serious trauma

8. Recent arterial puncture at noncompressible site

9. Lumbar puncture within 7 days

11. Witnessed seizure at stroke onset

12. Recent acute myocardial infarction

13. On repeated measurements, systolic pressure <185 mm Hg or diastolic pressure <110 mm Hg at time of treatment, requiring aggressive treatment to reduce blood pressure to within these limits

6. Within 3 months of intracranial surgery, serious head trauma, or previous stroke

10. History of intracranial hemorrhage, arteriovenous malformation, or aneurysm

3. High clinical suspicion of subarachnoid hemorrhage even with normal CT

Front 26

What to avoid if you give tpa?

Back 26

o Restrict central venous access and arterial puncture during 1st 24hrs
o Avoid placement of bladder catheter during infusion and until 30min a/f
o Avoid NG tube if possible during 1st 24hrs
o Should NOT receive asa, heparin, warfarin, ticlopidine, etc w/i 1st 24hrs
o People who have taken asa ARE eligible for tPA

Front 27

Evidence for tpa?

Back 27

o ECASS I (JAMA 1995;274:1017-25)(<6hrs)
intracranial hemorrhage, fatal cerebral edema and early mortality were more common in treated patients than in controls. If you sirvive tpa better outcomes

NINDS (N Engl J Med 1995;333:1581) (<3hrs)

t-PA recipients had a 12% absolute (32% relative) increase in the proportion with minimal or no disability.
§ But this benefit came with an attached risk: t-PA was associated with a 10-fold increase in symptomatic intracerebral hemorrhage (6.4% vs. 0.6%), and the overall intracerebral hemorrhage rate (symptomatic + asymptomatic) was 10.1%.

Front 28

ABCD2 score – evaluates 2 DAY stroke risk

Back 28

ABCD2 score – evaluates 2 DAY stroke risk
o Reference: Johnston et al. Lancet. 2007 Jan 27;369(9558):283-92
· Age ≥60 = 1 pt
· BP @ time of 1st assessment
o SBP ≥140 or DBP ≥90 = 1 pt
· Clinical symptoms
o Unilateral weakness = 2 pts
o Isolated speech impairment = 1 pt
· DM = 1 pt
· Duration
o <10 minutes = 0
o 10-59 minutes = 1 pt
o ≥60 minutes = 2 pts
· Prognosis
o Score 6 to 7: High two-day stroke risk (8.1 percent), 7d – 11.7%, 90d – 17.8%
o Score 4 to 5: Moderate two-day stroke risk (4.1 percent), 7d – 5.9%, 90d – 9.8%
o Score 0 to 3: Low two-day stroke risk (1.0 percent), 7d – 1.2%, 90d – 3.1%

Front 29

· Carotid Dopplers ?

Back 29

if hear carotid bruit arrange in ed otherwise OPD?

Front 30

ED TIA

Back 30

· Labs
o CBC, lytes, Cr, gluc, cholesterol
o PTT, INR
o ESR, syphylis serology??
o Hypercoagulable w/u if: < 50yo and no cause, hx of prior venous thrombosis, hx of hypercoaguable state
· CT head
o Should be done for all TIAs
o 1% will reveal non-vascular mimic (tumor, AVM, abscess, etc)
o 20% show hypodensities
· Carotid Dopplers
o Arrange in ED if bruit heard otherwise outpatient doppler
· Echo
o Yield low (<3%) without evidence of heart disease
o TTE arranged as an outpatient
· Counselling
o Modify risk factors
o Risk of subsequent CVA
o Do NOT d/c HRT
o D/C oral contraceptive

Front 31

· Antiplatelet Therapy tia

Back 31

o Aspirin
§ Proven benefit in preventing subsequent CVA. NNT 100
§ NO difference has been demonstrated in dosing
§ ECASA 80 - 325 mg/day

o Plavix (clopidogrel)
§ CAPRIE trial: plavix vs ASA
· intention-to-treat analysis showed that patients treated with clopidogrel had an annual 5.32% risk of ischaemic stroke, myocardial infarction, or vascular death compared with 5.83% with aspirin
· RRR of 8%, ARR 0.51%, NNT 200 compared to ASA

o Aggrenox
§ PRoFESS Trial – RCT 20,332 patients comparing aggrenox vs plavix looking at stroke recurrence. Showed no difference.
§ Thus, if patient is already on plavix you do not need switch the patient.
o Ticlid (ticlopidine)
§ Shown to be effective by CATS trial
§ Shown to be slightly better than ASA by TASS trial (20% relative risk reduction compared to ASA)
§ Diarrhea, rash, neutropenia (1%) are problematic
§ Disopyridamole
§ Phosphodiesterase inhibitor
§ Slightly better than ASA

Front 32

o Consider admission for high risk of early CVA ?

Back 32

(3 or more risk factors from Johnson article)
§ age > 60
§ DM
§ symptoms > 10 min
§ weakness with episode
§ speech impairment with episode

Front 33

Scary facts about hemorrhagic cva

Back 33

10% of strokes
· 2Xs as common as SAH
· 30 day mortality 50% (½ in 2 days)

Front 34

Etiologies of H cva

Back 34

o hypertensive hemorrhage,

o amyloid angiopathy,

o AVMs,

o hypertensive emergencies (sympathomimetics, pheo, cocaine),

o tumor/bleed,

o anticoagulants

· Hypertensive hemorrhages
o Predominantly elderly
o Degenerative changes in small penetrating arteries leading to the formation of microaneurysms (MC in MCA territory)

Front 35

· Most common sites.....

Back 35

o Putamen 44%
o Other cortical areas 25%
o Thalamus 13%
o Cerebellum 9%
o Pons 9%

Front 36

CLINICAL FEATURES

Back 36

· Sudden onset headache, vomiting, HTN, focal neuro deficit
· Motor/sensory deficit contralateral to lesion
· Agitation, lethargy and may rapidly progress to coma
· 1/3 have significant growth of hemorrhage size in first hrs
· More likely to have precipitant like exertion, sex, valsalva, labor
· Airway more of a problem b/c of decreased LOC
o Cheyne-Stokes (deep and rapid then apnea) common with large ICH
o Irregular resp pattern with putamenal hemorrhages
o Normal resp pattern with CB hemorrhages
· Pontine hemorrhage: bilateral pinpoint pupils b/c of loss of sympathetics
· Dilated pupils: putamen
· Anisocoria, miosis, poor response with thalamic bleed

Front 37

· Estimate volume of blood in cc (ABC/2 method)

Back 37

o A = largest diameter of hemorrhage
o B = largest diameter perpendicular to A
o C = number of 10mm slices hemorrhage seen in

Front 38

Transient Global Amnesia

Back 38

· Paroxysmal, transient loss of memory function for < 24h
· Immediate recall ability is preserved, as is remote memory; however, patients experience striking loss of memory for recent events and an impaired ability to retain new information.
· Attention, social skills, language, vision, motor, sensory are preserved
· Cause: unknown but thought to be multifactorial and perhaps to decreased venous outflow from the brain.
o Not thought to be caused by cerebraovascular disease like stroke or TIA
o Unlikely secondary to migraines
· No specific treatment other than neurologist follow-up.