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Stroke and TIA Flashcards

1
Q

How common are strokes in US?

A
  • 3rd leading cause of death in US
  • major cause of adult disability
  • about 800,000 people in US have a stroke each year
  • on avg, one American dies from a stroke q 4 minutes
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2
Q

Definition of a stroke?

2 main types?

A
  • alteration of cerebral blood flow
    either from:
    brain ischemia: thrombosis, embolism, or systemic hypo perfusion
    or
    brain hemorrhage: intracerebral hemorrhage or SAH
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3
Q

source of anterior circulation of the brain?

A
  • from internal carotid

- majority of blood flow to the brain

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4
Q

Source of posterior circulation of the brain?

A
  • verterbal-basilar
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5
Q

Cardiac sources of ischemic stroke?

A
  • a fib
  • ASD/VSD
  • recent AMI
  • endocarditis
  • cardiac tumor
  • valvular disorder
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6
Q

What is the most common stroke type?

A
  • ischemic stroke
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7
Q

Other etiologies of strokes?

A
  • atherosclerotic plaques (emboli from rupture, lack of perfusion from stenosis of vessels)
  • vasculitis
  • prothrombotic state
  • cerebral hemorrhage (20% of strokes)
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8
Q

How is a-fib a source of a stroke?

- how does anticoag help this? aspirin?

A
  • embolization of intracardiac thrombi
  • most commonly from left atrial appendage
  • anticoagulation decreases the risk of stroke by up to 70%
  • aspirin decreases risk by 20-25%
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9
Q

Atrial and ventricular septal defects - source of stroke?

A

atrial:

  • if assoc with R to L shunt can cause stroke
  • patent foramen ovale: present in about 25% of general population, surgical or percutaneous closure

ventricular:
if assoc with R to L shunt can cause stroke

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10
Q

MI - as source of stroke?

A
  • most common in pts after anterior wall infarction
  • left ventricular wall mural thrombi:
    large infarctions, LV dilation, CHF
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11
Q

Endocarditis source of stroke?

A
  • emboli from vegetations
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12
Q

Cardiac tumor as a source of stroke?

A
  • obstruction of blood flow
  • can lead to arrhythmias (like a-fib)
  • embolization of tumor fragments
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13
Q

Valvular disorders as a source of a stroke?

A
  • native valves: rheumatic mitral stenosis is most commonly assoc with stroke
  • MVP: may have fibrinious deposits on valve
  • prosthetic heart valves: mechanical valves require lifelong anticoag
  • repaired cardiac valves: require only anticoag short term
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14
Q

How common is hemorrhagic stroke?

A

20% of al strokes
- spontaneous intracerebral hemorrhage (10%)
- SAH - other 10%:
intracranial aneurysm, and arteriovenous malformations

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15
Q

What are the causes of spontaneous intracerebral hemorrhage?

A
  • assoc with poorly controlled HTN: commonly located in basal ganglia and less commonly in pons, thalamus, cerebellum or cerebral white matter
  • lacunar infarcts are assoc with HTN or DM
  • bleeding disorders
  • amyloid angiopathy: amyloid deposits lead to weakening of cerebral blood vessels resulting in a stroke
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16
Q

Causes of SAH?

A
  • trauma
  • spontaneous SAH is usually related to a ruptured AVM or aneurysm
  • abnorm vascular composition (amyloid angiopathy or dissection)
  • illict drug use such as cocain or amphetamines
  • intracranial arterial dissections
  • 20% may have no ID cause
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17
Q

Most common site for intracranial aneurysm? What determines the risk of rupture?

A
  • most commonly located in circle of willis
  • aneurysm is usually asx until rupture
  • size and location determine risk of rupture: in general size over 1 cm carries a high risk of rupture
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18
Q

What is an arteriovenous malformation (AVM)?

A
  • abnormal arterial to venous connection
  • arteries and veins are tangled up - veins are under high pressure which leads to rupture
  • also assoc with risk of seizure
  • occurs in 0.01% of population, 1-2% of all strokes and 9% of SAH
  • may be assoc with heredirary hemorrhagic telangiectasia (HHT; osler-weber-rendu syndrome)
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19
Q

Subtypes of strokes?

A
  • hemorrhagic:
    intracerebral hemorrhage
    SAH
  • ischemic:
    anterior circulation
    posterior circulation
    lacunar
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20
Q

What is an intracerebral hemorrhage? Major causes?

A
  • arterial bleeding directly into the brain parenchyma
  • major causes:
    HTN, trauma, bleeding disorder, amyloid angiopathy, illicit drug use, AVMs
  • accum of blood over minutes to hours forming a localized hematoma
  • *** neuro sxs increase gradually as hematoma grows
  • brain tissue is destroyed as hematoma enlarges, pressure created by blood and surrounding brain edema is life-threatening
  • large hematomas have a high mortality and morbidity
  • goal of tx is to contain and limit the bleeding
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21
Q

2 main causes of SAH? What is happening?

A
  • ruptured aneurysm (most common) or AVM
  • bleeding into CSF and space surrounding brain
  • aneurysm bleeds into CSF under arterial pressure and increased the ICP (this causes sxs)
  • bleeding lasts a few seconds but rebleeding is common
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22
Q

Main tx goal of SAH?

A
  • Identification of source of bleeding and tx before rebleeding occurs
  • other goal of tx is to prevent brain damage due to delayed ischemia related to vasoconstriction of intracranial arteries: blood within the CSF induces vasoconstriction which can be intense and severe (can cause another stroke!)
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23
Q

2/3 of all ischemic strokes affect what circulation in the brain? 2 main arteries of this circulation?

A
  • anterior circulation

- MCA and ACA

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24
Q

What is the most commonly affected vessel in ischemic strokes?

A
  • MCA: 96% of all anterior circulation strokes (due to direct flow from internal carotid artery and its large size)
  • 3% in ACA
  • 1% in entire ICA distribution
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25
Q

What arteries would be involved in posterior circulation stroke?
What areas of the brain does this supply?

A
  • verterbral artery
  • basilar artery
  • posterior cerebral artery
  • blood supply to posterior portion of brain, including occipital lobes, cerebellum, and brainstem
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26
Q

Outcomes of posterior circulation strokes?

A
  • terrible!
  • 20% of all strokes
  • 20-60% have unfavorable outcomes
  • basilar artery occlusion: 90% mortality, 8-14% of all posterior circulation strokes
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27
Q

What are lacunar strokes?

A
  • small lesions (less than 5 mm) that occur in penetrating arterioles in basal ganglia, pons, cerebellum, internal capsule, thalamus, and deep cerebral white matter
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28
Q

Outlook of lacunar strokes?

How do these appear on CT?

A
  • less morbidity and mortality than other strokes

- on CT sometimes seen as “punched out hypodense areas” but sometimes no abnormalities can be seen

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29
Q

Anterior strokes occur from occlusion off of what artery?

A
  • internal carotid artery or its branches
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30
Q

Posterior strokes occur from occlusion off of what artery?

A
  • vertebral artery or its branches
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31
Q

HTN may cause what tpye of strokes?

A
  • intracerebral hemorrhages or lacunar infarcts from small vessel occlusion
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32
Q

Stroke RFs?

A
  • HTN
  • DM
  • hyperlipidemia
  • cigarette smoking
  • cardiac disease
  • elevated blood homcysteine levels
  • AIDs
  • recreational drug abuse
  • heavy alcohol consumption
  • family hx of stroke
  • overweight
  • ischemic heart disease
  • PVD
  • sedentary lifestyle
  • men older than 45 and women older than 55
  • OCPs combined with smoking
  • hypercoagulopathy
  • polycythemia
  • prior stroke
  • sleep apnea (causes pro-thrombotic state while sleeping)
  • bleeding disorders
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33
Q

What is aphasia?

A
  • acquired communication disorder
  • impairs ability to process language but doesn’t affect intelligence
  • impairs ability to speak and understand others
  • experience diffciculty reading and writing
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34
Q

Types of aphasia?

A
  • global
  • anomic
  • broca’s
  • wernicke’s
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35
Q

Global aphasia?

A
  • most severe form
  • produce few recognizable words
  • understands little or no spoken speech
  • can neither read or write
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36
Q

Anomic aphasia?

A
  • persons who are left with persistent inability to supply words for the things that they want to talk about.
  • sig in nouns and verbs
  • understand speech well
  • read adequately
  • poor writing ability
37
Q

Broca’s aphasia (expressive)?

A
  • broca’s area supplied by superior division L MCA
  • speech output severely reduced limited mainly to short utterances of less than 4 words: formation of sounds often laborious/clumsy, and comprehension fair, and cognitively intact
  • reading and writing also affeted
  • AKA expressive aphasia
38
Q

Wernickes aphasia (receptive)?

A
  • wernickes area supplied by inferior division of L MCA
  • fluent but meaningless spontaneous speech - jargon of real words and nonwords
  • individual unaware of language errors unlike in broca’s aphasia
  • comprehension is poor
  • writing, reading also poor
  • AKA receptive aphasia
39
Q

Dysarthria?

A
  • problem with muscles that produces speech
40
Q

Dysconjugate gaze?

A
  • failure of eyes to turn together in the same direction
41
Q

Apraxia?

A
  • difficulty with motor planning to perform tasks or movements when asked
    (ex: being asked to put on shoes and tie them)
42
Q

Dystaxia?

A
  • lack of muscle coordination
43
Q

Agnosia?

A
  • inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes or smells
44
Q

FAST campaign?

A

F- facial droop
A - arm weakness
S - speech difficulties
T - time to call 911

45
Q

Diff sxs of a stroke?

A
  • typical: right sided facial droop with weakness of R arm and leg
  • sudden onset severe HA
  • severe dizziness, N/V
  • acute speech deficit
  • sudden onset impaired consciousness w/o focal neuro deficits
46
Q

Sxs of a SAH?

A
  • Sxs begin abruptly
  • sudden increase in ICP may cause a cessation of activity (knees may buckle, loss of memory)
  • sudden, severe HA “thunderclap” followed by vomiting
  • usually no focal neuro signs
  • may have signs of meningeal irritation
  • sxs may be preceded by heavy physical exertion or sex
47
Q

Sxs of an intracerebral hemorrhage?

A
  • sxs slower onset than SAH and increase over minutes to hours
  • sxs worsen as hematoma enlarges
  • HA and vomiting occur in about half of pts
  • sxs may be preceded by heavy physical exertion or sex
  • neuro sxs will vary depending on location and size of bleed and may be similar to ischemic sxs
  • with large hematoma - may have decreased LOC
48
Q

Differences and similarities b/t SAH and ICH strokes?

A
  • SAH: sxs at max intensity at onset
    • ICH: sxs increase with intensity as bleed worsens
  • both have HA but much worse at onset and more common in SAH
  • both may lack focal deficits
  • may have meningeal signs
  • both may rapidly deteriorate clinically
49
Q

What side of the body is affected by a stroke?

A
  • brain damage in one side results in neuro deficits on opposite side of body
50
Q

General sxs of an anterior circulation stroke? (ACA and MCA)?

A
  • may have one or all of the following sxs:
    face-hand-arm-leg contralateral hemiparesis
    aphasia
    dysarthria
51
Q

ACA occlusion may cause what sxs?

A
  • leg weakness and sensory loss (contralateral side affected)
  • arm (esp proximal) weakness and sensory loss: contralateral side - pronator drift
  • urinary incontinence
52
Q

MCA occlusion may cause what sxs?

A
  • contralateral hemiplegia in the face-arm-leg
  • homonymous hemianopsia
  • if on L and it is dominant hemisphere = aphasia:
    wernickes (receptive)
    brocas (expressive)
  • nondominant right hemisphere: confusion, spatial disorientation, sensory and emotional neglect of other side of body
  • apraxia
53
Q

Structures that rely on posterior circulation blood supply?

A 
- structures that rely on posterior circulation blood supply:
brainstem
thalamus
hippocampus
cerebellum
visual cortex
temporal lobes
occipital lobe
54
Q

What CNs are housed in midbrain?

A
  • III and IV
55
Q

What CNs are housed in pons?

A
  • V, VI, VII, VIII
56
Q

What CNs are housed in medulla?

A
  • IX, X, XI, XII
57
Q

What cranial nerves can be affected by a stroke affecting the brainstem?

A
  • CNs III-XII
58
Q

Sxs of posterior circulation stroke?

A
  • vertigo
  • diplopia, dysconjugate gaze, ocular palsy, homonymous hemianopsia
  • sensorimotor deficits - ipsilateral face and contralateral limbs (crossed findings), drop attack
  • dysarthria
  • ataxia
59
Q

What do you have to rule out if a pt presents with vertigo?

A
  • posterior circulation stroke!
60
Q

What are the 5 D’s of posterior stroke sxs?

A
  1. dizziness
  2. diplopia
  3. dysarthria: difficulty speaking (loss of motor control for speech)
  4. dysphagia: diff swallowing
  5. dystaxia: difficulty controlling voluntary movement
61
Q

Sxs of lacunar stroke?

A
  • pure motor loss (weakness): most common presentation in up to 2/3 of cases
  • or pure sensory
  • many other lacunar snydromes including:
    senorimotor stroke (2nd most common)
    ataxic hemiparesis
62
Q

NIH stroke scale?

A
  • use in both clinical trial and as part of clinical care in US
  • 0 = no stroke
  • 1-4 = minor
  • 5-15 = mod
  • 16-20 = mod to severe
  • 21-42 = severe
63
Q

Acute eval? what is criticual to know?

A
  • timing of onset of sxs is critical
  • assessment of stroke risk factors
  • physical exam looking for stroke sources
64
Q

Blood work for suspected CVA?

A
  • lipid profile
  • blood sugar
  • CBC
  • CMP
  • PT/PTT
  • cardiac biomarkers to R/O cardiac ischemia
65
Q

Dx workup of CVA?

A
  • acute workup = noncontrast CT of head (rule out/in hemorrhagic stroke)
  • later = MRI +/- MRA of brain
  • EKG
  • US of carotids
  • echo
66
Q

Window of opportunity to tx a CVA?

A
  • time is very impt in order to receive medication
  • window of opportunity to start tx stroke pts is 3 hrs, but to be eval and receive tx, pts need to get to hospital w/in 60 min
67
Q

What is in your medical tool bag for CVA tx?

A
  • ASA
  • heparin or lovenox
  • fibrinolytics
  • percutaneous intracerebral intervention in selected cases
68
Q

Tx of ischemic stroke?

A
  • clot-busters

- must give w/in 3-4.5 hrs and within an hour of arrival to hospital

69
Q

Tx of hemorrhagic stroke?

A
  • correct cause of hemorrhage
70
Q

What should be continuously monitored in stroke pts?

A
  • vital signs, neuro status, cardiac and respiratory status
  • medical support as needed:
    if they can’t protect airway: support airway - intubate
71
Q

What is tPA?

A
  • tissue plasminogen activator
  • clot busting drug aka fibrinolytic aka thrombolytic
  • dissolve clot in ischemic strokes and neuro deficits are more likely to improve
  • if mistakenly given to hemorrhagic stroke pts = death
72
Q

Inclusion criteria for thrombolytics?

A
  • clinical dx of ischemic stroke causing measurable neuro deficit
  • onset of sxs less than 4.5 hrs before beginning tx
  • 18 or older
73
Q

Exclusion criteria for thrombolytics (hx)?

A
  • sig stroke or head trauma in previous 3 months
  • previous ICH
  • intracranial neoplasm, AVM, or aneurysm
  • recent intracranial or intraspinal surgery
  • arterial puncture at a noncompressible site in previous 7 days
74
Q

Exclusion criteria for thrombolytics (clinical)?

A
  • sxs suggestive of SAH
  • persistent BP elevation (SBP 185 or greater or DBP 110 or greater)
  • serum glucose less than 50 mg/dl
  • active internal bleeding
  • acute bleeding diathesis, including but not limited to conditions defined in hematologic
  • Head CT scan:
    evidence of hemorrhage
    evidence of multilobar infarction with hypodensity involved more than 33% of cerebral hemisphere
75
Q

Exclusion criteria for thrombolytics (hematologic)?

A
  • platelet count below 100,000 mm3
  • current anticoag use with INR greater than 1.7, or PT greater than 15 sec
  • Heparin use within 48 hrs and abnorm elevated aPTT
  • current use of direct thrombin inhibitor or direct factor Xa inhibitor with evidence of anticoag efect by lab tests
76
Q

Relative exclusion criteria for thrombolytics?

A
  • only minor and isolated neuro signs
  • spontaneously clearing stroke sxs
  • major surgery or serious trauma in last 14 days
  • GI or urinary tract bleedin in previous 21 days
  • MI in previous 3 months
  • seizure at onset of stroke with postictal neuro impairments
  • pregnancy
77
Q

Relative exclusion criteria for tx from 3-4.5 hrs from sx onset?

A
  • age: older than 80
  • oral anticoag use regardless of INR
  • very severe stroke (NIHSS score above 25)
  • combo of both previous ischemic stroke and DM
78
Q

Medical management for stroke pts?

A
  • dietary
  • neuro
  • PT and OT
  • ST: swallowing eval, and speech retraining
  • nursing
  • physical med and rehab Dr. consultation
79
Q

D/C meds for stroke pts?

A
  • ASA
  • statin
  • maybe anticoag (for sure if A fib)
  • plavix?
  • antiHTNs
  • assess adequacy of blood sugar control if DM
  • don’t give anticoag initially after stroke - bleed again, also don’t want to give antiHTNs because need high BP for better perfusion to the brain
  • d/c pts on these meds though
80
Q

Recovery from aphasia?

A
  • after stroke - if sxs last longer than 2 or 3 months, complete recovery is unlikely:
    people continue to improve over period of time
  • slow process
  • need to learn compensatory strategies for communicating
81
Q

Residual effects of strokes?

A
  • emotional lability (mood swings, depression)
  • perceptual effects: difficulty recognizing, understanding familiar objects
  • difficulty planning and carrying out simple tasks
  • loss of awareness (one sided neglect)
  • dysphagia (diff swallowing) and aspiration
82
Q

Medical complications of a stroke?

A
  • bladder dysfxn
  • bowel dysfxn
  • pressure ulcers
  • malnutrition
  • dehydration
  • falls and injuries
  • recurrent strokes
  • DVT
  • dysphagia
  • aspiration pneumonia
  • seizures
  • spasticity
83
Q

What is a TIA?

A
  • stroke like event lasting less than 24 hrs (usually 20 min) that occurs secondary to cerebral ischemia
  • sxs resolve completely
  • all TIAs are ischemic
84
Q

Likelihood of having a stroke after having a TIA?

A
  • more than 1/3 of people will go on to have a stroke
  • 5% of strokes will occur within 1 month of TIA or first stroke
  • 12% will occur w/in 1 year
  • 20% will occur w/in 2 years
  • 25% will occur w/in 3 years
85
Q

Etiology and RFs of TIA?

A
  • same as ischemic sources
  • etiologies:
    from cardiac source: A fib. ASD/AVD, recent MI, endocarditis, cardiac tumor, valvular disorder
    other sources: atherosclerotic plaques: emboli from rupture or lack of perfusion from stenosis, vasculitis, prothrombotic state, cerebral hemorrhage

RFs:
HTN, DM, hyperlipidemia, cig smoking, cardiac disease, elev blood homocysteine levels, AIDS, recreational drug abuse, heavy ETOH consumption, family hx of stroke, overweight, ischemic heart disease, PVD, sedentary lifestyle, men older than 45 and women older than 55, OCPs with smoking, hypercoagulopathy, polycythemia, prior stroke, sleep apnea,and bleeding disorders

86
Q

Types of TIA?

A
  • amarosis fugax (transient monocular blindness)
  • low flow (severe episode of hypotension)
  • embolic
  • thrombotic
87
Q

Workup of TIA?

A
  • CT or MRI
  • carotid US
  • eval for soruce of emboli or thrombus
88
Q

Tx of TIA?

A
  • consider admission to hosp if seen within 72 hrs of sxs
  • RF management is same as if pt has had a stroke
  • be d/c on ASA, statin
  • maybe anticoag?
89
Q

Why do you want to avoid aggressive BP control in ischemic strokes?

A
  • want to increase cerebral perfusion

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