Ischemic Stroke, Intro (1) Flashcards

0
Q

What is the difference between stroke and Transient ischemic attack (TIA)?

A

A stroke causes focal neurological deficits that are permanent, while a TIA is defined as the abrupt onset of focal neurological deficits that fully resolve within 1 hour

*main difference is whether or not the deficits are reversible

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1
Q

What is a stroke?

A

Brain injury due to interruption of blood flow to the brain, whether ischemic or hemorrhagic

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2
Q

What is a Resolving Ischemic Neurologic Deficit (RIND)?

A

Acute focal neurological deficits that resolve completely, but take longer than 1 hour to do so; these have detectable injury on MRI brain scans, although no functional deficits are seen, so are referred to as “silent strokes”

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3
Q

What is the most common type of stroke (among the main two types)?

A

Ischemic –> due to interruption of blood flow to brain

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4
Q

What is MC type of ischemic stroke?

A

Cryptogenic–> etiology unknown

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5
Q

Stroke due to disease of the lumen of small arterioles

A

Lacunar infarct–> 25% of ischemic strokes, most common after the cryptogenic variety

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6
Q

Other than lacunar or cryptogenic, what are the two main causes of a ischemic stroke?

A
  1. Atherosclerotic cerebrovascular disease
  2. Embolism
  • both represent ~20% of ischemic strokes
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7
Q

What two types of hemorrhagic strokes are there? What % of strokes do hemorrhagic strokes represent?

A
  1. Intracerebral –> bleeding into parenchyma of brain
  2. Subarachnoid–> bleeding around surface of brain
  • around 20% of strokes; these two types are roughly equal, so each independently represent ~10% of strokes
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8
Q

Stroke is the _____ leading cause of death in the U.S.

A

Third leading cause of death

*is leading cause of adult disability

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9
Q

Which three states have the highest incidence of strokes in the U.S?

A

South Carolina, Arkansas, and TN–> southeast known as the “Stroke Belt”
Esp prominent in east Appalachia and in the mid-south

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10
Q

What are the four general non-modifiable risk factors for stroke?

A
  1. Age
  2. Gender
  3. Race
  4. Family Hx
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12
Q

How does stroke risk increase with age?

A

Incidence doubles for each decade above 55

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13
Q

What are 8 modifiable risk factors for stroke?

A
  1. HTN
  2. DM
  3. Hyperlipidemia
  4. Smoking
  5. Carotid artery stenosis
  6. Atrial fibrillation
  7. Obesity
  8. Physical inactivity
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14
Q

What is the number one risk factor for stroke?

A

Hypertension!

  • A-fib actually has the highest incidence of stroke, but it’s prevalence is way less, so when taking into account both prevalence and relative risk for stroke, HTN is #1, followed by Hyperlipidemia, smoking, and inactivity (these three all add the same risk)
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15
Q

What is the difference between cerebral infarction and selective ischemic necrosis? When is selective ischemic necrosis more often seen?

A

Cerebral infarction is necrosis of all cellular elements in the brain(neurons, glial cells, etc.); selective ischemic necrosis effects neurons alone
*selective ischemic necrosis is more commonly encountered due to transient global brain ischemia from cardiac arrest and successful cardiac resuscitation

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16
Q

What two neuron types are especially vulnerable to ischemic insult?

A
  1. CA1 pyramidal neurons of the hippocampus

2. Cerebellar Purkinje cells of the cerebellum

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17
Q

How long can the brain survive on its energy stores in the absence of blood flow? What happens when these stores are depleted?

A

2 1/2 minutes–> each 100 gm of brain stores this, so focal injury doesn’t take long

  • in ischemia, lactic acid levels build up due to increased glycolytic metabolism–> triggers catabolic mechanisms that lead to cell death
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18
Q

What two conditions can accurate the catabolic processes that are initiated by ischemia/ depletion of brain energy stores?

A
  1. Hyperthermia
  2. Hyperglycemia

*therefore normalizing body temp and glucose levels are goals for acute stroke intervention

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19
Q

What is the term for the central area around an infarct with the most severe blood flow reduction? How long does it take to get irreversible damage to such an area?

A

Ischemic core–> irreversible damage in 1 hour or less

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20
Q

What is the term for the parts of the brain damaged by infarct more distal to the occlusion that may have some collateral blood flow and therefore slightly less ischemia? How long can these areas go until irreversible damage may be seen?

A

Ischemic penumbra–> these areas may survive for a few hours

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21
Q

Acute stoke intervention has a therapeutic window of __-__ hours.

A

4-6 hours to restore blood flow and salvage brain tissue otherwise destined to die

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22
Q

How is MAP calculated?

A

MAP = CO x SVR

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23
Q

Which gender and which race are non-modifiable risk factors for stroke, along with age?

A
  1. Male gender (1.5x risk for females)
  2. African-American (2x risk of Caucasians)

*Family Hx is also a non-modifiable risk factor

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24
Q

What is the relationship of mean arterial pressure to cerebral blood flow and cerebral vascular resistance?

A

CBF = MAP/CVR

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25
Q

What is the normal range of MAP? How does CBF fluctuate in this range?

A

55 mmHg - 155 mmHg

  • CBF is constant in this range, so is independent of MAP; however when it is above or below this range, CBF is directly proportional to MAP
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26
Q

What does MAP below 55 do to CBF? Result?

A

CBF drops in a linear relationship along with MAP, resulting in syncope

  • due to a loss of auto regulatory control; capacity to protect against MAP changes has been overwhelmed
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27
Q

Above 155 mmHg, what happens to CBF? What results?

A

It increases in a linear relationship with MAP, leading to hypertensive encephalopathy

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28
Q

In chronic HTN, what value does CBF start falling in proportion to MAP?

A

At 75 mmHg–> the chronic HTN means the cerebral vasculature is more dilated, as a compensatory mechanism to protect against damage. So a less marked drop in MAP will cause the CBF to also begin decreasing

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29
Q

What guidelines are recommended for the treatment of acute stroke in people with chronic HTN?

A

DONT lower BP unless the systolic is over 220 or if diastolic is over 120; also lower only by 10-15% in the first 24 hrs

*lowering any quicker will result in poor perfusion to ischemic penumbral areas and more ischemia/necrosis will result than would have normally

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30
Q

What are 6 neurologic signs/symptoms commonly seen with stroke?

A
  1. Weakness or paralysis
  2. Loss of sensation
  3. Loss of vision in one eye or field
  4. Difficulty with language comprehension
  5. Difficulty with organization or perception
  6. Clumsiness or lack of balance
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31
Q

What are 4 arteries involved in Anterior Circulation strokes?

A
  1. Internal carotid
  2. Middle Cerebral Artery (MCA)
  3. Anterior Cerebral Artery (ACA)
  4. Lateral striate artery
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32
Q

What are 5 arteries involved in posterior circulation strokes?

A
  1. Vertebral artery (VA)
  2. Posterior Cerebral artery (PCA)
  3. Superior cerebellar artery (SCA)
  4. Anterior inferior cerebellar artery (AICA)
  5. Posterior inferior cerebellar artery (PICA)
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33
Q

Occlusion of the middle cerebral artery would affect what 4 functional areas of the brain?

A
  1. Motor cortex - upper limbs and face
  2. Sensory cortex - upper limbs and face
  3. Wernicke’s area (temporal lobe)
  4. Broca’s area (frontal lobe)
34
Q

What 3 symptoms would be expected in anterior circulation stroke involving the middle cerebral artery?

A
  1. Contralateral paralysis - upper limb and face
  2. Contralateral loss of sensation - upper limb and face
  3. Aphasia (if on dominant hemisphere) OR sensory hemineglect (if on non-dominant hemisphere)
35
Q

What two functional areas of brain would be affected by occlusion of the anterior cerebral artery in an anterior circulation stroke?

A
  1. Motor cortex - lower limbs
  2. Sensory cortex - lower limbs

*think about the area of brain served by the arteries and the homunculus –> anterior serves the interior surface of hemispheres! this is the part serving the lower limbs, etc

36
Q

What neurological symptoms would be expected in someone with occlusion of the anterior cerebral artery? (2)

A

Contralateral paralysis and sensory loss of lower limbs

37
Q

What functional areas (2) of the brain would be affected by occlusion of the posterior cerebral artery in a posterior circulation stroke?

A
  1. Occipital cortex

2. Visual cortex

38
Q

What symptom would be expected if the posterior cerebral artery were occluded?

A

Contralateral hemianopia

39
Q

Occlusion to the posterior inferior cerebellar artery affects what area of the brain?

A

Lateral medulla –> vestibular nuclei! lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguus, sympathetic fibers, inferior cerebellar peduncle

  • Lareral Medullary (Wallenberg’s) Syndrome
40
Q

What two clinical symptoms seen in PICA occlusion indicate damage to the nucleus ambiguus (damage to nucleus ambiguus is specific to PICA occlusion)?

A
  1. Hoarseness
  2. Dysphagia
  • “Don’t PICA horse (hoarseness) that can’t eat (dysphagia)
41
Q

Other than vomiting, vertigo, and nystagmus, what are 5 symptoms of a Posterior inferior cerebellar artery occlusion? (1st two give the ones more specific to a PICA occlusion; other 3 also seen with AICA occlusions)

A
  1. Decreased protopathic (pain/temp) sensation to limbs/face
  2. Decreased gag reflex (CN IX, X involvement)
  3. Ipsilateral Horner’s syndrome
  4. Ataxia
  5. Dysmetria (due to inferior cerebellar peduncle involvement)
42
Q

What regional area of brain is effected by anterior inferior cerebellar artery occlusion in posterior circulation strokes?

A

Lateral pons - cranial nerve nuclei, vestibular nuclei, spinal trigeminal nucleus, cochlear nuclei, sympathetic fibers, middle andi inferior cerebral peduncle

  • Lateral pontine syndrome
43
Q

What is a main feature of AICA occlusion that indicates damage to the facial nucleus, damage to which is specific for AICA occlusion?

A
  1. Paralysis of face

* “Facial droop means PICA’s pooped”

44
Q

Other than vomiting, vertigo, nystagmus, what are 4 symptoms of AICA occlusion that are fairly specific for it?

A
  1. Decreased lacrimation and salivation
  2. Decreased taste sensation from anterior 2/3 of tongue
  3. Decreased corneal reflex
  4. Decreased hearing, ipsilateral side
  • (lateral pontine stroke syndrome)
  • also ataxia, dysmetria, and ipsilateral Horner’s, and decreased pain and temperature sensation to face
45
Q

What portion of the brain would be expected to be damaged by occlusion of the posterior cerebral artery (central and/or paramedian branches)?

A

Central midbrain

*(Benedikt’s syndrome)

46
Q

What three symptoms would be seen in a posterior cerebral artery occlusion that damaged the central midbrain?

A
  1. Ipsilateral CN III palsy and loss of pupillary constriction–> (eye abducted and rotated down)
  2. Contralateral ataxia and tremor (due to lesion of ipsilateral red nucleus, involved in cerebellar function)
  3. Contralateral discriminative (epicritic) touch loss (due to damage to the medial leminiscus)
47
Q

What are four signs/symptoms that would be indicative of an Anterior circulation stroke?

A
  1. Ipsilateral blindness or contralateral inferior quadrantanopsia
  2. Contralateral gaze paresis
  3. Contralateral mono/ hemiparesis and/or mono/hemisensory neglect
  4. Aphasia (if dominant hemisphere) or neglect in nondominant hemisphere
48
Q

Want causes the ipsilateral blindness or contralateral inferior quadrantanopsia in anterior circulation strokes?

A

Occlusion of the opthalmic artery, branch of internal carotid. Also, the anterior cerebral artery serves the part of brain that contains the optic nerves

49
Q

What causes the hemiparesis and/ or sensory issue in an anterior circulation stroke?

A

Together, the anterior and middle cerebral arteries serve the motor and sensory cortices, so occlusion affects function in those areas

50
Q

What is the cause of the aphasia or hemisensory neglect seen with anterior circulation strokes?

A

The middle cerebral artery serves the lateral part of the cortex containing Broca’s and Wernickes areas, so language is affected if dominant hemisphere affected (usually left) or sensory neglect if non-dominant (usually right)

51
Q

What is different about the motor and sensory deficits seen Ina posterior circulation stroke compared to anterior circulation?

A

The deficits may be bilateral, unilateral, or crossed (weakness of right body and left face)

52
Q

What is different about the visual deficits seen in posterior circulation strokes vs. anterior circulation?

A

Posterior–>

  1. Contralateral homonymous hemaniopsia (loss of half of field of vision, on same side in each eye, loss is contralateral to side of lesion)
  2. Contralateral superior quadrantopsia (vs, inferior in anterior stroke)
53
Q

What are two behavioral type symptoms that are more specific to posterior circulation strokes?

A
  1. Altered consciousness

2. Amnesia

54
Q

What are 6 other symptoms that are more specific to posterior circulation strokes?

A
  1. Vertigo
  2. Nausea/vomiting
  3. Gait ataxia
  4. Diplopia
  5. Dysphagia
  6. Horner’s syndrome
55
Q

What four syndromes may be caused by lacunar infarcts?

A
  1. Pure motor hemiparesis
  2. Ataxic hemiparesis
  3. Dysarthria-clumsy hand syndrome
  4. Pure hemisensory deficit
56
Q

Which of the lacunar syndromes is most common? What two parts of the brain are frequently involved?

A

Pure motor hemiparesis (33-50%) –> posterior limb of internal capsule and anterior pons (basilar pontis)

57
Q

Which of the lacunar syndromes is 2nd most common? What symptoms are seen?

A

Ataxic hemiparesis–> post limb of internal capsule anterior pons! or red nucleus= weakness and clumsiness are seen on side of body contralateral to lesion (affects the lower limbs more so than arms)

*SCA or ACA infarcts

58
Q

What is dysarthria-clumsy hand syndrome?

A

Just what it seems like –> trouble speaking due to muscle dysfunction and clumsiness of hand, usually manifested as troubles esp when writing

*anterior limb of internal capsule, basal ganglia, thalamus, or cerebral peduncle lesions

59
Q

Why are lacunar strokes called lacunar?

A

Small areas of ischemic necrosis due to occlusion of small arteries create small “caves” in the brain (look like ventricles but are due to liquefactive necrosis in infartec tend areas of the brain)

60
Q

What are nine other possible causes of acute-onset focal neurologic lesions that should be included in the differential for work up of such symptoms?

A
  1. Subdural hematoma
  2. Radiculopathy
  3. Bell’s palsy
  4. Multiple Sclerosis
  5. Migraine
  6. Seizure
  7. Hypo/hyperglycemia
  8. Hypoxia
  9. Syncope
61
Q

What are 6 common causes of ischemic stroke?

A
  1. Atherothrombosis/ atheroemboli
  2. Lipohyalinosis and fibrinoid necrosis
  3. Cardiogenic emboli
  4. Vasculitis
  5. Hematologic disorders
  6. Drug-related
62
Q

What are six common sites for formation of atherothrombotic plaques?

A
  1. Origins of carotid and vertebral arteries
  2. Bifurcation of common carotid artery*
  3. Internal carotid artery at carotid siphon (where it bends in carotid canal)
  4. Branch points of middle and anterior cerebral arteries
  5. M1 segment of MCA
  6. Vertebrobasilar artery
    * basically anywhere the arteries branch or bend = causes turbulence
63
Q

What is a common cause of lipohyalinosis and fibrinoid necrosis that contribute to lacunar strokes?

A

Chronic hypertension–> these processes occur in the smooth muscle and intima of small penetrating cerebral vessels

  • may also be caused by microemboli from more proximal vessels or the heart
64
Q

What are 5 common causes of Cardiogenic emboli?

A
  1. Atrial fibrillation
  2. Mitral stenosis
  3. Bacterial endocarditis
  4. Prosthetic heart valves
  5. Mural thrombosis (due to MI)
65
Q

What are 3 uncommon causes of Cardiogenic emboli?

A
  1. Atrial myxoma
  2. Mitral valve prolapse
  3. Paradoxical embolus (embolus coming from lower extremity, bypasses lungs due to right-left shunt)
66
Q

What is a Libman-sacks embolus?

A

Embolus caused by nonbacterial (marantic) endocarditis, usually die to CA or SLE

67
Q

What is a rare cause of a mural thrombus?

A

Cardiomyopathy

68
Q

How do strokes from CNS vasculitis present different from normal strokes?

A

They present with multifocal neurological signs, due to the possible involvement of multiple different blood vessels,a s opposed to most strokes, which are due to occlusion of a single artery

  • vasculititudes affect multiple small and medium size arteries
69
Q

What is the most common cause of a CNS vasculitis?

A

Lupus erythematosus

70
Q

What is a common cause of CNS vasculitis in patients over 55? Why is important to catch?

A

Giant cell (temporal) arteritis–> responds well to steroids and can cause blindness overnight if untreated

71
Q

What are two hyperviscosity syndromes that may cause ischemic strokes?

A
  1. Polycythemia

2. Multiple myeloma

72
Q

What are 6 conditions that can lead to a hypercoagulable state?

A
  1. Antiphospholipid syndrome
  2. Protein C or S deficiencies
  3. Leiden factor V deficiency
  4. Thrombocytosis
  5. Pregnancy
  6. Cancer
73
Q

What hemoglobinopathy can cause an ischemic stroke?

A

Sickle cell

74
Q

What is the most common drug of abuse that can cause stroke?

A

Cocaine

  • also amphetamines, LSD, or sympathomimetics
75
Q

What type of prescription drugs are notorious for causing clots?

A

Oral contraceptives

76
Q

How can excess Etoh cause clots?

A

Dehydration–> so can cause a hyperviscous state

77
Q

What is fibromuscular dysplasia and how can it cause strokes?

A

Abnormal proliferation of muscle tissue within vessels walls–> occluded vessels via growth

78
Q

How can subarachnoid hemorrhage cause stroke?

A

Blood in subarachnoid space may cause vasospasm

79
Q

Elevated serum levels of what may lead to stroke?

A

Homocysteine

80
Q

What type of headache is linked with increased risk of stroke?

A

Migraine –> particularly in women who smoke and/or are on oral contraceptives

81
Q

What structural arterial mishap may lead to stroke?

A

Dissection of carotid or vertebral arteries –> esp in younger patients! these don’t take much trauma to occur at times