Stroke Flashcards

1
Q

What proportion of patients diagnosed with a ischemic stroke will statistically be alive in 5 years?

A

Approximately 50%

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2
Q

What proportion of patients diagnosed with a TIA will go on to:
a) have a ischemic infarct within 3 months,
b) have another TIA,
c) have passed away, had an ischemic infarct or another TIA?

A

a) Approx 15%
b) Approx 9%
c) Approx 25%

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3
Q

What is the most commonly used scale to rank disability from stroke?
Which categories are considered a good outcome from stroke? (0-6 scale).

A
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4
Q

Total Anterior cerebral strokes include which main vessel?

A

Middle cerebral a.

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5
Q

Embolic causes consitute approx 80% of all Total anterior cerebral strokes (TACS) and Partial anterior cerebral stroks (PACS) what are the two most common causes of the emboli?

A
  1. Carotid stenosis / atherosclerosis.
  2. Cardiac causes…. most commonly atrial fibrilation
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6
Q

What is a tell tale sign of a posterior cerbral arterial stroke?

A

Mixed side involvement ie. CN involvement of the Left and motor / sensory deficit on the other side or other mixed side combinations ie cerebella dysfunction on one side without controlateral accompanying sensory / motor deficit (remember cerebella input is ipsilateral).

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7
Q

What scale is more commonly used for measuring stroke nowdays? What consitutes a moderate stroke?

A

NIH Stroke Scale - a score 11 or above is considered a moderate stroke

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8
Q

How do you divide stroke presentations into acute treatment groups were:
Group 1 may receive tPA +/- endovascular clot retrieval and
Group 2 receives only 300mg of Asprin.

A

Large vessel anterior strokes would be assessed for appropriateness for Group 1 acute treatment options.

Small vessel / posterior strokes would be provided with Group 2 treatment.

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9
Q

Is a loss of consciousness (ALOC) common in stroke & TIA?

A

No - a significant occlusion is required to cause ALOC therefore a patient reporting ‘funny turn’ including ALOC is not a TIA.

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10
Q

What are the TIA Commandments / what constitutes a TIA?

A

See image

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11
Q

It is important to be able to localise / determine which vessel is implicated in stroke, why?
(2 reasons)

A

Large v small vessel - effects treatment (rapid intervention + secondary prevention vs only secondary prevention).
It is also important because if a vascular territory cannot be determined and deficits are more generalised / over many vascular territories then diagnositic mimics are more likely.

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12
Q

What are Lucuna Strokes?

A

Small vessel strokes located deep within the cerebral hemispheres.
Signs of Lucuna strokes include at least 2/3 of:
1. Face, arm or leg without cortical or brainstem signs
2. RV in literature lecture provided minimal information

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13
Q

What is Capsular Warning Syndrome?

A
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14
Q

Pronator drift is a sign of Upper or Lower motor neuron damage?

A

Upper motor neuron damage causes pronator drift of the UL and extension of the LL - which over time sits in spastic contraction. Think evolution - paralyised arm gets tucked up across the chest & leg extends so it can still be walked on.

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15
Q

How do you differentiate between central and peripheral vertigo? in an acute presentation and non-fluctuating and non-positional.

A

HINTS
1. Head impulse test (assesses occulomotor reflex) - over correction observed when patient is asked to keep focus on your nose and then you rapidly move their head to one side. The overcorrection is observed when the head is moved to the side of the lesion.
*Negative test - central nastagmus. Positive test - peripheral nastagmus.

  1. Nastagmus
    *Nastagmus with changing directions (central vertigo).
    Peripheral nastagmus has fast beating (thats the side it is named after L / R) that continues to only have its fast beating face for either the L or Right only.
  2. Skew deviation (vertical realignment of the eyes when one is covered and the other is fixated on an object when you uncover the covered eye to test the other eye you notice the covered eye realign vertically with the tested eye - central vertigo / central lesion).
    *Positive test - central vertigo.
    *Negative test - periperal vertigo.
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16
Q

30% of stroke presentations are mimics. What are possible mimics of stroke?

A
17
Q

What are the most common stroke mimics (approximately 2/3rds of all mimics)?

A

Seizure
Sepsis
Toxic / metabolic (medication / drugs / electrolyte imbalances / glucose).
Space occupying lesion
Syncope / presyncope
Acute confusional state

18
Q

Signs that a stroke mimic may be more likely than a stroke include:

A
  1. Unable to identify an onset,
  2. Symptoms are not localisable to a vascular region,
  3. Cognitive impairement,
  4. Another system (ie resp) abnormalities observed,
  5. Normal vascular exam ie. no AF, no hypertension, normal puses, no vascular disease).
19
Q

Acute treatment of Stroke includes (large vessel vs small vessel):

A
  1. Large vessel (ie Anterior strokes TACS or PACS) Thrombolysis tPA or
    Clot retrieval.
  2. Small vessel (ie Posterior stroke POCS)
    Asprin 300mg.
20
Q

What important non-pharmacological treatment requirements for acute stroke?
(5)

A
  • Panadol for fever
  • Manage blood glucose levels
  • Manage hypertension gently - witholding antihypertensives or agressive antihypertensive managment is associated with poorer outcomes
  • Avoid IDC unless absolutely necessary
  • Continue normal medications.
21
Q

Secondary prevention in stroke includes (4 medication classes):

A
  1. Antiplatelets - Asprin being first line; combined with Clopridogrel in the first 3 weeks post stroke only.
  2. Anticoagulate if AF is a cause - after haemorrhage risk has past
  3. Statins (highest dose tolerated).
  4. Antihypertensives even if the patient is normally normo-tensive. ie Perindorpril
22
Q

What investigations should you use in suspected Anterior Stroke?

A
  1. CTA - CT angiography from aortic arch to head increasingly used for acute presentations.
  2. US - Carotids ok to ascertain surgical / further imaging candidates.
  3. Ecocardiogram - Dilated L atrium may indicated AF even if holter is normal; PFO (patent foramen ovale) - closure can prevent further strokes esp in young candidates.
  4. Holter monitoring very low yield - however provides documented evidence to justify anticoagulation. Required prior to anticoag therapy commencement.
  5. MRI - can confirm diagnosis; can add information about mechanism of stroke; clarify stroke v’s mimic ie. multiple mini strokes v’s amyloid angiopathy.
23
Q

What investigations should you use in suspected posterior Stroke?

A
  1. CTA - CT angiography from aortic arch to head increasingly used for acute presentations - required for small vessel imaging.
  2. Cardioembolic work up is still important as constitutes the cause for approx 20% of POCS (echo & holter).
  3. Rare anatomical varients can be cause.
24
Q

If a patient presents withsymptoms and has a stenosis of greater than 70% in a carotid a what is required?

A

Urgent operation -endarterectomy with the greatest benifit in the first 2 weeks. Not useful post 3 months.

25
Q

In terms of stroke, what does the Penumbra mean?

A

The salvagable tissue following a stroke - not the infarcted region.

26
Q

What is this image an example of?

A

This is a CTP (CT perfustion scan) it shows areas of the brain that are infarcted and areas at risk (the penumbra).

27
Q

How is a CTP scan useful in guiding treatment.

A

If a patient has a large penumbra / salvagable brain area tPA (thrombolysis) or clot retrieval is more likely to be performed = increased benifit vs risk.

28
Q

What are two common examples of tPA (thrombolysis medications) used in the acute treatment of anterior strokes?

A

Alteplase
Tenectaplase

29
Q

What is the role of tPA medications in the treatment of acute anterior strokes.

A

Treatment does not alter death rates following large strokes (not better or worse); it does however reduce the Modfied Rankin scale of disability. Therefore it increases the survival of penumbra (salvagable tissue) thus reducing the affected tissue = functional deficits associated with the stroke.

30
Q

What is the number to treat for endovascular clot retrieval

A

4-6 individuals within 6 hours

31
Q

Does the performance of endovascular clot retrieval prevent the use of tPA?

A

No, currently thrombolysis is still used prior to the performance of endovascular clot retrieval.

32
Q

Which UL muscle groups are weak in upper motor neuron lesions?

A

Think: what happens to the UL with upper motor neuron lesions (arm pronates and sits across the chest)… therefore all the muscles that are weak in the UL with upper motor neuron lesions are those that fail to oppose this action… the extensors and abductors.

Typical progression of muscle weakness:
Finger extension > shoulder abduction (distal first then proximal) > elbow extensors / distal > proximal > middle.
+ strong flexors
+ Pronator drift
= likely upper motor neuron

33
Q

Which LL muscle groups are weak in upper motor neuron lesions?

A

Flexor muscle weakenss of the lower limb with a pattern of proximal > distal > middle muscle groups.