Stroke Flashcards

1
Q

What is a stroke?

A

An acute, rapidly-developing focal neurological dysfunction due to an abnormal perfusion of brain tissue, resulting in cellular death (infarction).
In other words, stroke is all about interruption of the normal blood supply to the brain (ischemia), resulting in neuro dysfunction and the death of brain cells. emphasis on imaging and neurological deficits and de-emphasis of temporal aspects for former definitions (i.e., ≥ 24 hours). Included in the definition of stroke, in addition to cerebral infarctions, are spinal and retinal infarctions.
Clinically, “stroke” continues to typically be used to refer to cerebral infarctions.

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2
Q

Define ischemic stroke and prevalence

A

Ischemic: due to thrombosis, embolism, or systemic hypoperfusion. About 87% of all strokes are ischemic.
Most common site is the middle cerebral artery (MCA)
Transient ischemic attacks (TIA) are an important warning sign.
“Cardioembolic”: includes A-Fib, ventricular thrombus, prosthetic valves, rheumatic heart disease, other cardiac sources.

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3
Q

Define the two types of hemorrhagic strokes, prevalence, and what to call them

A

Subarachnoid hemorrhage (SAH), about 3%
Bleeding in the subarachnoid space
Intracerebral hemorrhage (ICH), about 10%
Bleeding inside the brain
AHA/ASA discourages use of the term “hemorrhagic stroke” for its lack of specificity

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4
Q

Who has a stroke?

A

Females have a higher lifetime incidence than males – approximately 1 in 5 for females 55 to 75 years old and 1 in 6 for males in the same age group.
At younger ages, this is reversed, with males having a higher incidence of stroke.
Age-adjusted incidence of first ischemic stroke per 1,000 population is 0.88 in non-Hispanic whites, 1.91 in blacks, and 1.49 in Hispanics.
Age itself is a major risk factor for stroke, with nearly 3/4 of all strokes occurring in in people over age 65. 17% of all strokes occur in people over age 85.

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5
Q

Who dies from a stroke?

A

The age-adjusted death rate for non-Hispanic black Americans in 2015 was 52.2 per 100,000, and for non-Hispanic white Americans it was 36.4 /100,000; the ratio is approximately 1.4:1).
People living in the southern state “stroke belt” (NC, SC, GA, TN, MS, AL, LA and AR) have a stroke mortality about 20% higher than the rest of the US. The “stroke belt buckle” of coastal NC, SC and GA has a stroke mortality rate 40% higher than the rest of the US.
Mortality increases with age: about 10% < 65, 20% between 65-74, 30% between 75-84 and 40% ≥ 85
Roughly 25% of people over age 65 will die within a year of their first stroke.
Roughly 50% of people over age 65 will die within 5 years of their first stroke.

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6
Q

What is happening to the stroke rate and why?

A

The decline is due to a decrease in both stroke incidence and stroke mortality.
AHA/ASA attributes the decline to improved BP control, as well as reduced smoking, improved DM control and improved lipid control (Lackland et al., 2014).

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7
Q

What are causes of stroke?

A

Thrombus within cerebral vasculature
Usually starts when atherosclerotic plaque becomes unstable, similar to MI.
Embolus, usually of cardiac or carotid origin
Large cerebral artery occlusion is typically embolic
Atrial Fibrillation
Valvular thrombi: mitral stenosis, endocarditis or prosthetic valve
http://watchlearnlive.heart.org/CVML_Player.php?moduleSelect=iscstr
Small vessel disease (e.g., lacunar infarct)
Hypoperfusion (low BP state, ↓ cerebral perfusion pressure)
Hyperviscous blood
Sickle Cell Disease
Polycythemia Vera
Cryptogenic

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8
Q

Define and explain cryptogenic stroke

A

= ischemic stroke for which no probable cause is identified after adequate diagnostic evaluation.
Is a Dx of exclusion
20-30% of all ischemic strokes designated cryptogenic after standard work up:
MRI or CT of brain
CTA or MRA of brain, neck and thoracic arteries; ultrasound if CTA and MRA contraindicated or unavailable
TTE, TEE
ECG, Holtor monitor, 30-day event monitor, loop recorder
Hematologic testing for hypercoagulable states
Occult “low burden” paroxysmal AF may be found: significance unclear
Patent foramen ovale (PFO) may be found

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9
Q

What are “nonmodifiable” risk factors for stroke?

A

Age – single most important non-modifiable factor
Sex (higher lifetime incidence older females > older males)
Race and ethnicity (AA, Latino, Native Americans > non-Latino white, Asian)
Sickle cell disease
Family history
An ischemic stroke in either parent by the age of 65 is associated with a 3-fold increase in the risk of ischemic stroke in offspring. Importance of taking a good family history!
A prior stroke or TIA puts you at increased risk for a subsequent stroke.
Cumulative risk of a stroke in the 5 years after an initial stroke is roughly 25%.
Cumulative risk of a stroke, ACS, or CVD death in the 5 years after a TIA is roughly 13%. (Amarenco et al., 2018)

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10
Q

What are modifiable risk factors for stroke?

A

General rule: The things that keep our patients’ hearts healthy will also keep their brains healthy.*

  • Evidence regarding cholesterol is not as clear in stroke prevention as it is in MI prevention.
    1. Hypertension
    2. Diabetes
    3. Atrial fibrillation
    4. Other cardiac morbidities including HF
    5. Carotid Artery Stenosis
    6. HLD (?)
    7. smoking
    8. Heavy ETOH use
    9. physical inactivity
    10. CKD
    11. “Obesity” (?)
    12. Sleep apnea
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11
Q

Discuss HTN and stroke

A

About 3/4 of those who have a first stroke have BP > 140/90. Diabetics with BP < 120/80 have half the lifetime risk of stroke compared with people with HTN (not just just diabetics with HTN)

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12
Q

Discuss DM and stroke

A

DM more than doubles the risk for ischemic stroke
DM particularly increases the risk of a stroke at a younger age: < 55 y.o. for blacks and < 65 y.o. for whites.
Duration of DM matters, esp. in pts. with AF. Longer duration  greater risk of ischemic stroke.

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13
Q

Discuss afib and stroke

A

AF independently increases the risk of stroke about 5-fold at all ages. AF causes about 1.5% of strokes in age 50 to 59, but about 23.5% at 80 to 89. It is likely these are underestimates, because AF is often asymptomatic and undetected. note that the incidence of AF itself increases with age, so this plays a significant role in the age-related increase in AF-induced stroke.
Females with AF have approx. double the relative risk of having a stroke as males. Reasons for this are unclear.
Other cardiac morbidities increase the risk of stroke. In older adults, HF is associated with a 4-fold increase in stroke risk.

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14
Q

What is the left atrial appendage and why is it key?

A

In non-valvular afib, over 90% of stroke is caused by blood clots that form in the LAA

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15
Q

Discuss Carotid Artery Stenosis and Stroke risk

A

Greater degrees of stenosis are associated with greater stroke risk. In general, CAS doubles the risk of a stroke.

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16
Q

Discuss HLD and stroke risk

A

Data is not completely settled; the effect of total cholesterol seems to wane with age. Most studies have found high total cholesterol to be a risk factor for ischemic stroke, but the relationship is not strong – especially in people over age 75 – and other studies contradict. Effect of HDL-C on stroke risk is not clear.

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17
Q

Discuss smoking and stroke risk

A

Current smokers have a risk for stroke 2 to 4 times greater than nonsmokers and those who quit > 10 years ago.
Is the most important modifiable risk factor in preventing SAH

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18
Q

Discuss ETOH use and stroke risk

A

Key is “heavy,” because low and moderate use of alcohol is associated with decreased risk of stroke.
The National Institute on Alcohol Abuse and Alcoholism defines heavy drinking for a man as >4 drinks in any single day or >14 drinks per week and defines heavy drinking for a woman as >3 drinks any single day and >7 drinks per week. A standard drink is defined as 12 fl oz of regular beer, 5 fl oz of table wine, or a 1.5–fl oz shot of 80-proof spirits.

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19
Q

Discuss physical inactivity and stroke risk

A

Moderate to vigorous physical activity is associated with a 35% reduction in the risk of ischemic stroke.

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20
Q

Discuss CKD and stroke risk

A

Creatinine ≥ 1.5 mg/dL or GFR < 60 are both associated with greater stroke risk.
Proteinuria and albuminuria are better predictors of stroke risks than eGFR in patients with existing kidney disease.

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21
Q

Discuss the role of “obesity” and stroke risk

A

In BMI range of 25 to 50 kg/m2 there is a 40% increased stroke mortality with each 5-kg/m2 increase in BMI.
However, “There is no clear and compelling evidence that weight loss in isolation reduces the risk of stroke because of the difficulty in isolating the effects of weight loss as a single contributing factor rather than as a component contributing to better control of hypertension, diabetes mellitus, metabolic syndrome, and other stroke risk factors.” Meschia et al. (2014).

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22
Q

Discuss the role of sleep apnea and stroke risk

A

Increases the risk of stroke 2-fold. The risk increases with the severity of the apnea.
Relationship is bi-directional: Sleep apnea is common after stroke and CPAP reduces the risk of recurrent vascular events.

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23
Q

What are some modifiable risks specifically related to people able to get pregnant or with estrogen as dominant hormone?

A

Migraine with aura (> common in females than males), doubles risk for ischemic stroke, esp. in younger females.
Use of oral contraceptives, estrogen plus progestin or estrogen alone
Use of hormone replacement therapy (estrogen alone or progestin/estrogen in combo) in post-menopausal females associated w/increased stroke risk
FYI, pregnancy and the first six weeks post-partum raise the risk of ischemic stroke or ICH to a rate 2.4 times greater than for pregnant females of similar age and race.

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24
Q

What primary care interventions should be done for modifiable risk factors?

A

Hypertension – screen and treat!
Diabetes – screen and treat!
Atrial fibrillation – screen and probably refer (but anticoagulate meanwhile)!
Carotid stenosis – screen! U/S, depending!
Smoking – keep bringing it up! Assist w/cessation!
Sleep Apnea – Ask! Epworth Sleepiness Scale! Sleep study!
CKD – track that albuminuria!
Alcohol use disorder – Screen! Refer!

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25
Q

What are general guidelines for primary prevention of stroke according to 2014 American Heart Association/American Stroke Association Guidelines for the Primary Prevention of Stroke?

A

Obtain a complete family history
Screen everyone for their stroke risk with a validated tool such as the Modified Framingham Stroke Risk Profile, or ACC/AHA ASCVD Risk Estimator https://tools.acc.org/ascvd-risk-estimator-plus/#!/calculate/estimate/
Treat HTN to keep BP < 140/90 (*but individualize to pt. )
Encourage pts. who do not smoke to never start, and help pts. who do smoke to stop smoking with a combo of counseling and medication.

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26
Q

What are stroke-prevention DM recommendations?

A

BP control as above. Use of an ACEI or an ARB.
Statin is recommended. However, adding a fibrate to a statin has not been shown to decrease stroke risk and is “not useful”.
AHA/ASA guideline is silent on specific glycemic targets, noting that there is a “lack of convincing support from any individual clinical trial for intensified glycemic control to reduce stroke incidence in patients with diabetes mellitus”
Some evidence that getting BG under control in Type 2 DM patients with BMI > 30 has a protective effect.
ADA Standards of Medical Care in Diabetes (2019) also do not make a strong link between specific glycemic targets and stroke.

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27
Q

Primary prevention with HLD?

A

Lifestyle changes + treatment with a statin recommended for patients with a high 10-year ASCVD risk.
No good evidence that fibrates, nor niacin nor other lipid-lowering therapies decrease the risk of stroke.

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28
Q

Afib and primary prevention?

A

Screen everyone > 65 for AF (pulse plus ECG if indicated)
In non-valvular AF, anticoagulation for all pts. at high risk:
For most patients a DOAC/NOAC (Direct-acting Oral Anticoagulant/ Non-Vitamin K Antagonist Oral Anticoagulant), including dabigatran (Pradaxa) or apixaban (Eliquis), rivaroxaban (Xarelto) or edoxaban (Savaysa) is preferred over warfarin.
For those w/non-valvular* AF at moderate risk, any of: no antithrombotic** therapy, anticoagulation, or aspirin “may be considered”.
For those at low risk, aspirin is no longer recommended.

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29
Q

What is the Watchman?

A

Approved by FDA in 2015 for nonvalvular A-Fib in patients who “have an appropriate rationale to seek a non-pharmacologic alternative to warfarin. “
“Noninferior” or “comparable” to warfarin in 5-year follow-ups.
Not part of any guideline recommendations.
CMS covers the device as of February 2016, with strict criteria.

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30
Q

How can you determine risk level with AF patients?

A

CHA2DS2-VASc criteria:

Congestive heart failure: 1 point
Hypertension: 1 point
Age 65 to 74: 1 point
Age ≥ 75: 2 points
Diabetes: 1 point
Stroke or TIA: 2 points
Sex (female): 1 point
Vascular disease (MI, PAD or aortic plaque): 1 point

Low risk: 0 points if male, 1 point if female
Moderate risk: 1 point if male, 2 points if female
High risk: ≥ 2 points if male, ≥ 3 points if female.
Most of our older adult patients with AF will be HIGH RISK!

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31
Q

Primary prevention, carotid artery stenosis

A

Asymptomatic patients should be treated with aspirin + statin
Selection of patients for revascularization is dependent on comorbidities, life expectancy and other individual factors
Reasonable to consider performing carotid endarterectomy (CEA) in asymptomatic patients who have >70% stenosis of the internal carotid artery if the risk of perioperative stroke, MI, and death is low (<3%). However, its effectiveness compared with medical management alone is not well established.
Prophylactic CEA may be performed in highly selected patients (minimum 60% stenosis on angiography, 70% on Doppler ultrasound), but its effectiveness compared with medical therapy alone in this situation is not well established.
In asymptomatic patients at high risk of complications for carotid revascularization by either CEA or CAS, the effectiveness of revascularization versus medical therapy alone is not well established.

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32
Q

Primary stroke prevention, migraine with aura

A

Smoking cessation

Tx to reduce migraine frequency “might be reasonable”

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33
Q

Rec for diet/nutrition

A

A Mediterranean diet supplemented with nuts “may be considered”

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34
Q

Recs for physical activity

A

moderate- to vigorous-intensity aerobic physical activity at least 40 min/day, 3 to 4 days/week

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35
Q

Recs for “obesity”

A

Among overweight and obese, weight reduction is recommended to lower BP and reduce risk of stroke

36
Q

Recs for ETOH

A

Reduction or cessation of alcohol use by heavy drinkers

1 to 2 drinks/day for males and 1 drink/day for females “might be reasonable”

37
Q

Recs for sleep apnea

A

Because of its association with stroke risk, screening for sleep apnea through a detailed history, including structured questionnaires (e.g., Epworth Sleepiness Scale) physical examination, and, if indicated, polysomnography may be considered
Treatment of sleep apnea to reduce the risk of stroke may be reasonable, although its effectiveness for primary prevention of stroke is unknown

38
Q

How should you approach use of aspirin for primary stroke prevention?

A

Talk to your patients.
Tell them the risk versus the benefits.
Listen to their concerns. (Family Hx of MI or stroke? Worried about a bleed?)
Make a decision together that works for that individual patient.
Revisit the decision in the future.
Once on the med list, aspirin tends to stay “stuck” there!

39
Q

What is the NIH stroke Scale?

A

Widely used to determine stroke severity
11 items, maximum possible score is 42.
Level of consciousness, best gaze, visual fields, facial palsy, motor arm, motor limb, limb ataxia, sensory, best language, dysarthria, extinction and inattention (formerly neglect)
Scores > 20 are considered severe

40
Q

What happens during an ischemic stroke?

A

In the core area of cerebral occlusion, CBF is so low that the area will infarct.
Surrounding the core area is another area called the penumbra that has slightly higher CBF. Cells in this area lose electrical function but maintain structural integrity.
The penumbra represents an area of brain tissue that may be saved if perfusion is restored quickly.
Cerebral hypoxia sets into motion a series of events called the “ischemic cascade”.
Neurons cannot maintain aerobic respiration  anaerobic respiration and the accumulation of lactic acid
Neurons cannot maintain ionic balance (Na+/K+ pump cannot function with insufficient oxygen, due to lack of ATP production)
Glutamate, the chief excitatory neurotransmitter excessively stimulates the neurons and depolarizes the cellular membrane
Sodium, chloride and water flow into the cell  cytotoxic edema.
Calcium also flows into the cell  neuronal death
The above scenario takes some time to play out, so a stroke is not just an event, it is a process that evolves over time.

41
Q

What is the penumbra?

A

Surrounding the core area is another area called the penumbra that has slightly higher CBF. Cells in this area lose electrical function but maintain structural integrity.
The penumbra represents an area of brain tissue that may be saved if perfusion is restored quickly.

42
Q

What happens to neurons during the ischemic cascade?

A

Neurons cannot maintain aerobic respiration  anaerobic respiration and the accumulation of lactic acid
Neurons cannot maintain ionic balance (Na+/K+ pump cannot function with insufficient oxygen, due to lack of ATP production)
Glutamate, the chief excitatory neurotransmitter excessively stimulates the neurons and depolarizes the cellular membrane
Sodium, chloride and water flow into the cell  cytotoxic edema.
Calcium also flows into the cell  neuronal death

43
Q

Discuss mechanical thrombectomy

A

Mechanical Thrombectomy Can Extend the Time for reperfusion beyond tPA’s 3-4.5 Hour Window to 16 to 24 hours
-DAWN trial, functional independence within 90 days was 49%, DEFUSE trial, was 45%
Patients selected for thrombectomy had:
Large vessel occlusion (internal carotid or proximal middle cerebral artery)
An area of infarct that was relatively small, compared to the penumbra/hypoperfused/ischemic tissue.

44
Q

How might older adults differ from younger adults in ability to recover from stroke?

A

Experiments with animals indicate that older brains may
Be less resistant to ischemia. This is in part due to age-related atrophy and loss of brain volume.
Be less able to neutralize free radicals and extrude calcium from cells
Be less able to synthesize proteins needed in the recovery period
Be more likely to allow toxins through the blood-brain barrier
Be less likely to have intact collateral circulation that can mitigate ischemic effects of artery occlusion
Have less elastic blood vessels, reducing the effectiveness of any compensatory response to ischemia and acidosis
However:
DEFUSE 3 trial: Median age 70 (range: 59-79)
DAWN trial: 23% of thrombectomy patients were ≥ 80 yrs.

45
Q

What is the most common vessel to be occluded in ischemic stroke?

A

Middle cerebral artery

46
Q

What does the frontal love do?

A

controls skeletal muscle movement, behavioral expression and Broca’s area.

47
Q

What does the parietal lobe do?

A

Houses sensory cortex; damage can affect superior contralateral vision.

48
Q

What does the temporal lobe do?

A

controls smell and hearing; damage can affect inferior contralateral vision and Wernicke’s area.

49
Q

What does the occipital lobe do?

A

primarily controls vision.

50
Q

What is the difference between Broca’s aphasia and Wernicke’s aphasia?

A
  1. Broca’s area is located on the frontal lobe of the left hemisphere.
    -nonfluent or expressive aphasia.
    Patient may comprehend speech and know what he or she wants to say
    But not able to find and speak the words needed to form complete sentences. Words like “is” and “the” are often omitted.
    Both vocal and written language severely reduced.
    Very frustrating for the patient!
  2. Wernicke’s area is located on the temporal lobe of the left hemisphere (fluent/receptive aphasia, less distress)
    Patient will have comprehension difficulties, be unable to grasp the meaning of spoken words.
    Will produce fluent, connected speech that is primarily a series of meaningless words that sound like sentences.
    Patient may not even realize that his/her speech is incorrect.
    Both reading and writing will be impaired.
51
Q

What is the basal ganglia?

A

Basal ganglia are composed of the caudate, putamen and globus pallidus.
Primary role is the coordination of movement

52
Q

What is the limbic system?

A

The limbic system is composed of the amygdala, cingulate gyrus and the hippocamus.
Amygdala and cingulate gyrus are important for memory and emotion.
Hippocamus important for memory (esp. for converting short-term to long-term memory) and learning.

53
Q

What is the diencephalon?

A

The diancephalon is located between the brainstem and the cerebrum and is composed of the thalamus, hypothalamus and pituitary and pineal glands.
Thalamus is crucial to sensory function and is connected all the major areas of the brain.
Hypothalamus is critical for autonomic and endocrine functions.
Pineal gland is important in sleep/wake cycles
Pituitary gland controls many hormonal functions.

54
Q

What is the cerebellum?

A

The cerebellum is adjacent to the brain stem
Crucial for motor function, especially coordination, balance and position sense.
Also affects speech and ocular movement.

55
Q

What is the medulla, pons, and midbrain?

A

Brain stem is the most primitive part of the brain
Crucial in controlling breathing, blood pressure and alertness.
10 of the cranial nerves arise in the brain stem.
In the medulla, the corticospinal tracts traverse the midline, decussate and send impulses to the opposite side of the body.

56
Q

What do the middle cerebral arteries supply?

A

Surface branches supply all 4 lobes of the cortex
Penetrating branches supply:
deep white matter
Part of the diencephalon
* supplies a large area of the brain and is most common vessel to be occluded during infarct

57
Q

Occlusion of the MCA Predominantly Affects ?

A

Face and Upper Limb Sensory & Motor Function

58
Q

What are symptoms of MCA stroke

A

global aphasia (dominant), neglect (non dominant), contralateral homonymous hemianopsia, contralateral motor/sensory loss of face, arm, and leg,

  • if inferior MCA, Wernicke’s aphasia
  • is superior, Brocas
59
Q

What is homonymous hemianopsia?

A

visual field loss on the same side of both eyes.

60
Q

What is the most frequent site for cerebellar stroke?

A

Posterior inferior cerebellar artery

61
Q

Why should you hope it’s not vertebrobasilar artery stroke?

A

Devastating, approx 85% mortality rate, supplies the brainstem

62
Q

What is a lacunar stroke?

A

The occlusion of a deep penetrating artery branching off a larger artery, such as the MCA, also known as “small vessel occlusions” or “small vessel disease”.
Account for 25% of all ischemic strokes
HTN is a major contributing factor; smoking, diabetes contribute as well.
Dyslipidemia not considered to be a major factor, as these vessels typically do not have atherosclerotic lesions, although the parent vessel may.
Typically will not present with aphasia, agnosia, neglect, apraxia, or hemianopsia (“cortical” signs).
Coma, loss of consciousness, and seizures also are typically absent.

63
Q

What are cortical signs?

A

aphasia - loss of ability to understand or express speech
agnosia - inability to interpret sensations and hence to recognize things
neglect - failure to attend to the side opposite a brain lesion
apraxia - difficulty with the motor planning to perform tasks or movements when asked
hemianopsia -less vision or blindness (anopsia) in half the visual field, usually on one side of the vertical midline

64
Q

How does a lacunar stroke typically present?

A

Most common, approx. 50% of lacunar infarcts: Pure motor hemiparesis (weakness) of face, arm and leg without sensory deficits or cortical signs, such as aphasia; or
ataxic hemiparesis (ataxia & weakness of one leg); or
facial weakness, dysarthria, dysphagia, and slight weakness and clumsiness of one hand; or
decreased sensation/numbness of unilateral face, arm, and leg, without motor deficits or cortical signs; or
weakness and numbness of the face, arm, and leg on one side of the body
Often is clinically silent and discovered incidentally on brain imaging, particularly in older adults.

65
Q

DDX Stroke

A
Seizure
Hypoglycemia
Migraine
Hyponatremia
Brain tumor
Meningitis/encephalitis
DKA/HHS
Drug Toxicity
Meniere's, labrynthitis
Bell's Palsy
Hypotension
66
Q

What are potential sequelae following stroke in older adult?

A

In the Framingham Heart Study, among ischemic stroke survivors ≥ 65, the following disabilities were seen at 6 months post-stroke:
50% had some hemiparesis
30% were unable to walk without some assistance
46% had cognitive deficits
35% had depressive symptoms
19% had aphasia
26% were dependent in some or all ADLs
26% were in a nursing home
Seizures
Pneumonia
Dysphagia
Immobility
Incontinence
UTI
Spasticity or contracture
Shoulder displacement and/or shoulder pain
Post-stroke pain more generally, esp. central pain
Pressure wounds, depending on the level of disability
Females are half as likely as males to be independent in ADLs, even after controlling for age, race, education and marital status
The good news is that about 14% of older adults can be expected to make a full recovery.

67
Q

Describe mood as it related to stroke?

A

About 1/3 of all stroke survivors experience post-stroke depression. Many also have anxiety.
Screen for depression!
Depression correlates with stroke severity, physical disability, cognitive impairment and lack of social support.
Language impairment particularly appears to be linked to depression.
Patients with post-stroke depression have higher mortality rates in the first few years after a stroke.
Post-stroke cognitive impairment plus depression may appear to be dementia.

68
Q

How do stroke and frailty relate?

A
Stroke may precipitate or potentiate frailty
Immobility
Deconditioning
Osteoporosis
Muscle atrophy
Risk for pressure ulcers
Risk for DVT
69
Q

Where Do Older Adults Go After a Stroke?

A

About 45% return home and 32% of those people use home healthcare services.
24% are sent to inpatient rehabilitation facilities
31% are sent to skilled nursing facilities.
Patients > 85 have longer hospitalizations, are less likely to be discharged home and are less likely to receive evidence-based care.

70
Q

Describe an acute inpatient rehab

A

Known as IRFs (Inpatient Rehabilitation Facilities)
Includes PT, OT, ST and recreational therapy
Nursing and medical care, including a physician always available
Social worker
Dietician
Often a neuropsychologist
Greater intensity of physical therapy and occupational therapy result in improved functional outcomes
Patient must be able to tolerate therapy 3 hours per day; does not need to see all types of therapists every day
2016 stroke rehab guidelines from AHA/ASA recommend that “stroke survivors who qualify for and have access to IRF care receive treatment in an IRF in preference to a SNF”

71
Q

Describe post stroke recovery including risks

A

Neurological recovery peaks within the first 3 months, but some improvement may be seen for up to 3 years. Important message for our patients and their caregivers!
Recovery is dependent on the plasticity of the adjacent brain.
Axonal sprouting of undamaged neurons and new cortical connections can occur post-stroke
Early rehabilitation is associated with better outcomes.
Falls typically occur in the first 6 months of recovery, with the largest percentage in the first month. They typically occur during transfer and during ambulation. They can occur in any setting: hospital, rehab or home.

72
Q

What is a TIA?

A

TIA = Transient Ischemic Attack
TIA is a “transient episode of neurological dysfunction resulting from focal brain, spinal cord or retinal ischemia, without acute infarction”.
No longer defined simply as an event lasting < 24 hours, because this definition was too broad; 30-50% of these “TIAs” actually showed permanent brain injury on diffusion-weighted MRI
An important warning sign!
10-15% of pts. w/TIA will have a stroke in 3 months. Half of those strokes will occur within 48 hours.
Widely believed to be underrecognized by patients and underdiagnosed by healthcare providers. Best estimates are about 200,000 to 500,000 TIAs occur each year in the US.
Is a major risk factor for subsequent cardiac events, including MI and sudden cardiac death.
Diffusion-weighted MRI is the recommended imaging modality, but it is recommended within 24 hours of symptom onset.
Patients should be evaluated ASAP after symptoms
Ultrasound, MRA or CTA should be performed as the initial screen of extracranial vasculature.
Transcranial Doppler can be performed to evaluate for intracranial stenosis, but the “gold standard” is still angiography.
ECG should be performed ASAP.
Telemetry or Holter may be required if the source of the TIA cannot be determined.
Echocardiogram (at least TTE) “is reasonable” as is CBC, CMP, PT/PTT, Lipid panel

73
Q

What is an ABCD score and what does the score mean?

A

“It is reasonable” to hospitalize if the pt. presents within 72 hours of TIA and:
ABCD2 score ≥ 3
ABCD2 score 0 – 2 and uncertainty that diagnostic workup can be accomplished in 2 days as an outpatient
ABCD2 score 0-2 and other evidence that the TIA was caused by focal ischemia

Age: 1 point for age ≥ 60 years,
Blood pressure ≥ 140/90: 1 point for hypertension at the acute evaluation
Clinical features: 2 points for unilateral weakness, 1 for speech disturbance without weakness
Duration of symptoms: 1 point for 10–59 minutes, 2 points for ≥ 60 minutes.
Diabetes: 1 point

Total score ranges from 0 to 7. Risk for stroke in next 2 days:

0-3: low risk
4-5: moderate risk
6-7: high risk

74
Q

Secondary stroke prevention, HTN, discuss

A

Hypertension: “Treatment of hypertension is possibly the most important intervention for secondary prevention of ischemic stroke.”
Initiate therapy for previously untreated patients with ischemic stroke or TIA who, after the first several days, have an established SBP ≥140 mm Hg or DBP ≥90 mm Hg.**
For patients with a recent lacunar stroke, it “might be reasonable” to target a SBP of <130 mm Hg
Salt restriction; weight loss; consumption of a diet rich in fruits, vegetables, and low-fat dairy products; regular aerobic physical activity; and limited alcohol consumption is “reasonable”
Optimal drug regimen is uncertain, but diuretics and an ACEI may be useful, based on available data.
**Recommendation will likely change w/new AHA BP target.

75
Q

Secondary prevention diabetes

A

Use existing guidelines for glycemic control and management of cardiovascular risk factors for patients with DM or pre-DM
Screen all patients who have had a stroke or TIA for DM if not previously diagnosed

76
Q

Secondary prevention HLD

A

In patients with stroke or TIA presumed to be of atherosclerotic origin, statin therapy with “intensive lipid-lowering effects”, even in patients with LDL < 100 and no evidence of other clinical ASCVD
Manage other risk factors in accordance with 2013 AHA/ACC cholesterol guidelines.
No stroke guideline yet calls for PCSK9 inhibitor therapy to lower LDL, but ACC focused update of cholesterol guidelines discusses when consideration of PCSK9 inhibitor is appropriate (Lloyd-Jones et al., 2017).

77
Q

Secondary prevention, smoking, ETOH, activity, discuss

A

Smoking, alcohol consumption, physical activity
Smoking: Same as for primary prevention, with additional recommendation to avoid passive/secondary smoke.
Data for smoking and primary prevention are actually stronger than data for secondary prevention.
Alcohol: Same as primary prevention
Physical activity:
If capable, at least 3 to 4 sessions per week of moderate- to vigorous-intensity aerobic physical activity.
For those disabled, have supervised physical activity with a PT or cardiac rehab professional, at least on initiation.

78
Q

Secondary prevention, carotid stenosis

A

Carotid stenosis: Primary care NPs will not usually be making these treatment decisions, but our patients may ask us our opinion.
For ipsilateral severe stenosis (70-99%), CEA recommended if perioperative morbidity and mortality risk < 6%
If ipsilateral stenosis is moderate (50-69%), CEA recommended depending on age, sex, comorbidities and same m/m risk as above
If stenosis is < 50%, there is no indication for carotid revascularization by either CEA or CAS
If CEA is indicated, surgery should be within 2 weeks of the stroke or TIA, if there are no contraindications
Stenting (CAS) is an alternative to CEA for pts. at average or low risk of complications if the internal carotid artery lumen is reduced by > 70% (noninvasive imaging) or > 50% by angiography, if the risk of death or stroke is < 6%.
Choosing between CAS and CEA: For patients > 70 years, CEA may be associated with improved outcome compared with CAS. For younger patients, CAS is equivalent to CEA in terms of risk for periprocedural complications.
All pts. with carotid stenosis should have antiplatelet therapy, statin therapy and risk factor modification (“optimal medical therapy”).

79
Q

What is optimal medical therapy for pts with carotid stenosis?

A

All pts. with carotid stenosis should have antiplatelet therapy, statin therapy and risk factor modification (“optimal medical therapy”).

80
Q

Secondary Prevention, atherosclerosis of a major intracranial artery

A

Aspirin 325 mg is recommended over warfarin. Adding clopidogrel x 90 days “may be reasonable”
Maintain SBP < 140 and initiate high-intensity statin
Usefulness of angioplasty or stent is unknown

81
Q

Secondary prevention, Afib

A

For cryptogenic stroke or TIA with no other apparent cause, prolonged rhythm monitoring (≈30 days) for detection of AF “is reasonable”
If AF, anticoagulant (DOAC/NOAC) used in Primary Prevention; initiate within 14 days
An antiplatelet can be added to anticoagulant for pts. with CAD
If unable to take anticoagulants, aspirin should be initiated and clopidigrel is “reasonable” to add to aspirin
As always, must assess bleeding risk!
As always, the cognitive status of the patient and the availability of caregivers must be taken into consideration.
If anticoagulant therapy must be interrupted (e.g., for medical procedure), bridge with LMWH

82
Q

Discuss antithrombotic therapy for noncardioembolic stroke

A

The use of antiplatelet agents rather than oral anticoagulation is recommended.
Aspirin 50 mg to 325 mg, or aspirin 25 mg + dipyridamole 200 mg, or clopidogrel monotherapy are all acceptable.
Aspirin plus clopidogrel is not recommended for routine secondary prevention after stroke or TIA and if initiated, should only continue for 21 days or less (too high a risk of bleeding) [recent studies may change this recommendation]
If aspirin allergy  clopidogrel monotherapy is “reasonable”
For pts. who had an ischemic stroke while taking aspirin, there is no evidence that increasing the dose of aspirin provides additional benefit, nor is there sufficient evidence to choose any other single agent or combo.

83
Q

Discuss anticoagulation following SAH or ICH

A

Discontinue all anticoagulants for at least 1 week
The decision to restart anticoagulation depends on the risk of subsequent thromboembolism, risk of recurrent cerebral bleed and overall status of the patient.

84
Q

Discuss post-stroke assessment

A
Assess bowel and bladder function
Assess cognitive status
Assess chronic comorbid conditions
Assess ability to communicate
Assess risk for DVT
Assess risk for depression
Assess risk for dysphagia and aspiration
Assess limbs for range of motion, motor/sensory deficits and painful conditions
Assess for spasticity
Assess shoulder dysfunction
Assess nutrition and hydration status
Assess skin integrity and risk for pressure ulcers
Assess risk for falls and fractures

Treat all of the above if they are present!
Develop a rehab plan to maximize function
Develop a plan to prevent recurrent strokes. The guidelines are more cautious about anticoagulation therapy in older adults.

85
Q

Discuss caregiver role strain following a stroke

A

Stroke caregivers suffer considerable role strain:
Depression
Exhaustion
They may be older themselves, with their own health issues
They may feel like they are losing their sense of who they are
Worry about what will happen to their loved one if they get sick
Get tired of being “on alert” all the time
May mourn what they have lost
Stress about incontinence, impaired mobility, lack of safety awareness of their loved one.
More disability of the stroke survivor  more physical and mental health issues of the caregiver