Stroke Flashcards

1
Q

What is a stroke?

A

Sudden onset of impairment in neurological functioning due to severe decrease of blood supply to the brain.

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2
Q

What causes stroke?

A

Ischemia, or insufficient blood supply to an organ, usually due to a blocked artery.

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3
Q

What do strokes produce?

A

Infarcts, or area of necrotic tissue resulting from obstruction of local blood supply or ischemia

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4
Q

Which is more common, thromboembolic ischemic stroke or hemorrhagic stroke?

A

Thromboembolic or ischemic stroke is most common in adults (about 88% of all stroke).

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5
Q

What is thromboembolic ischemic stroke?

A

Produces neuronal damage related to decreased cerebral blood flow due to an obstruction (like a plaque or blood clot), which can originate at the site of the occlusion (thrombus) or at a distance from the occlusion (embolus).

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6
Q

Which circulation system is most frequently affected by thromboembolic ischemic stroke?

A

Anterior circulation (WHICH IS: anterior cerebral territory, middle cerebral territory, and anterior choroidal arteries). The anterior circulation is affected in 80% of cases. The vertebrovasilar or posterior circulation (including posterior cerebral artery) is affected in 20% of cases. The MCA territory encompasses about 60% of the brain.

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7
Q

Which has higher mortality, thromboembolic ischemic stroke, or hemorrhagic stroke?

A

Hemorrhagic stroke - particularly subarachnoid hemorrhage, which has 50% mortality in the first 6 months after stroke.
Aneurysm of the anterior communicating artery is the most common cause of subarachnoid hemorrhage.

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8
Q

What are intracerebral hemorrhages?

A

Hemorrhages that tend to occur deep in the brain, as they primarily affect small penetrating arteries. Etiology, especially for deep intracerebral hemorrhage, is usually hypertension.

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9
Q

What are common causes of stroke in younger people?

A

Aneurysms and arteriovenous malformation (AVM)

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10
Q

What are the direct and indirect causes of thromboembolic stroke?

A

Direct causes are embolism, thrombotic, and vasospasm. Indirect causes or mechanisms are atherosclerosis, HTN, atrial fib, vasculitis, or coagulopathy.

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11
Q

What are the direct and indirect causes of hemorrhagic stroke?

A

Direct causes are intracerebral hemorrhage and subarachnoid hemorrhage.

Indirect causes or mechanisms are hypertensive hemorrhage (50% of cases), amyloid angiopathy hemorrhage, aneurysm, arteriovenous malformation, hypertension, cocaine use)

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12
Q

What is the time window for tissue plasminogen activator (TPA treatment)?

A

3 hours.

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13
Q

What is the primary injury from stroke?

A

In the case of ischemia, lack of oxygen and nutrients can produce neuronal damage and cell death within minutes. Typically a center zone of ischemic damage or infarct does not recover with a surrounding ischemic pneumbra that contains neurons that may recover.

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14
Q

What is the secondary injury from stroke?

A

Brain herniation and death can occur if intracranial pressure is not managed properly following hemorrhagic stroke.
Other examples of secondary injury include vasospasm, which may result in additional infarction, swelling/edema which can lead to mass effect (pressure on areas of the brain not directly involved in stroke), and decreased blood flow to distant regions.
Other secondary problems include seizures or infection from surgical intervention to reduce ICP.

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15
Q

What are risk factors for stroke?

A

Age ( risk doubles every decade after age 55)
HTN
Afib
Family history (3x risk if parent had ischemic stroke)
Prior TIA (4x risk of age matched sample)
Cocaine
Diabetes
Smoking
Sleep apnea
Serum lipid abnormalities
Obesity

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16
Q

Beyond age, what other demographic factors are relevant to stroke?

A

African Americans have higher stroke incidence and mortality than Caucasians, even after excluding sickle cell disease.

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17
Q

What determines severity of stroke?

A

Age of person
Size and location of infarct or hemorrhage
If acute treatment is in place (e.g., TPA)
Medical comorbidities (e.g., prior stroke)
Secondary medical events such as recurrent stroke, coma, infection, and cardiovascular risk factors (are they treated to prevent additional events)

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18
Q

When someone is having a stroke and they are nauseous or vomitting, what are these symptoms correlated with?

A

High ICP.

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19
Q

What are common symptoms of anterior circulation strokes?

A

Hemiparesis, hemianesthesia (loss of sensation on 1 side of body), aphasia, visuospatial deficits, as well as visual field cuts if the visual pathway is affected.
Hemiparesis is more common with involvement of the superior branch of the MCA.
Visual field cuts are more common with involvement of the inferior branch of the MCA as well as damage in the PCA.

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20
Q

What medical sequelae can complicate recovery from stroke?

A
Dysphagia
Incontinence
Mechanical ventilation 
Arrhythmia or other metabolic abnormalities such as diabetes
Deep vein thrombosis of paretic limb
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21
Q

What are head CTs helpful for?

A

To detect acute intracerebral hemorrhage.
They are not as sensitive to ischemic damage, particularly during the first 24 hours post insult.
A normal head CT during the first 24 hours is not a good indicator of whether the stroke produced damage or not.

22
Q

How are MRIs helpful?

A

Standard MRI can be normal a few hours after stroke, but diffusion-weighted MRI can detect infarcts within minutes of onset. MRI beats CT in detecting ischemic insults, big time. MRIs are also more sensitive to detecting lacunar infarcts which are usually silent or covert clinically - but if strategically placed can produce neurocognitive deficits.

23
Q

How are neuropsychological assessments helpful in the acute phase post stroke?

A

To create a baseline from which to track change
To inform cog rehab
To help manage behavioral problems and psych distress, such as depression

24
Q

What is the value of neuropsych assessment for left sided hemisphere stroke?

A

If auditory comprehension deficits are significant, the value of assessment might be limited. If auditory comprehension deficits are not significant, the assessment should still be brief, as cognitive status often improves over the first 6 months.

25
Q

What is TPA?

A

A powerful thrombolytic agent considered for adult patients within 3 hours of ISCHEMIC stroke. To receive TPA, the patient cannot have hemorrhage on head CT. There are other therapies that might be considered beyond the 3 hours window, including clot retrieval mechanical devices.

26
Q

How is hemorrhagic stroke treated?

A

First anticoagulant medications are discontinued. Hemorrhage size is monitored as this may influence ICP. Treatments to reduce ICP include medications as well as invasive procedures such as shunt placement for hydrocephalus or surgical evacuation of the hemorrhage.
If the cause of the stroke is an aneurysm, the aneurysm may be clipped at the neck or removed from the circulation by endovascular coil insertion into the aneurysm to cause clotting.
AVMs can be treated surgically by directly removing it or using radiation to destroy it over time, or with endovascular embolization which entails threading a catheter to the malformations feeder artery to block its blood flow with a glue like substance.

27
Q

What is the recovery timeline post stroke?

A

Most of recovery is done by 1 year, although there is variability. Most gains are observed 1 to 3 months afterwards. Most patients do not fully recover.

28
Q

What can complicate recovery post stroke?

A

Aphasia after left hemisphere stroke and lack of awareness of deficits/attention deficits - both observed more after right hem stroke.
Depression can also interfere and is more common after left frontal damage. antidepressant medication can be helpful.
Dystonia, weakness, spasticity, dysphagia, and dysarthria can occur.

29
Q

What are the neural mechanisms for recovery post stroke?

A

1) functional recovery of the infarcted penumbra (neurons return to normal or near normal functioning).
2) New synaptic connections or rerouting of connections to other areas; take over of the affected region’s functioning by normal tissue or homologous tissue in the opposite hemisphere.
3) compensation strategies

30
Q

What are the implications for NP asst for stroke? (think of recommendations)

A

1) Capacity to live independently, make important decisions regarding healthcare and finances
2) Return to driving
3) Disability status / vocational recs
4) Referral to ST, PT, OT, cog rehab
Important to note that it will be difficult to make long-term recs if the stroke occurred less than a year ago, as recovery may still be taking place

31
Q

Strokes in which area are associated with anosognosia?

A

Anterior communicating aneurysm rupture with damage to the frontal lobe;
Patients with Wernicke’s aphasia lack awareness of their comprehension deficits;
Patients with hemispatial inattention associated with right parietal damage

32
Q

In considering planning for NP evaluation, what should you consider first?

A

If aphasia or hemispatial inattention is present as these can affect performance in other domains.

Aphasia will likely confound tests of premorbid functions, and as such, demographic predictors would be more predictive.

33
Q

Discuss how language is affected when a stroke occurs in left hemisphere by right and left handers

A

Left hem damage produces language deficits or aphasia in 99% of right handers and 60-70% of left handers.

34
Q

How do you assess for hemispatial inattention?

A

Line bisection, letter cancellation, or double simultaneous visual stimulation.

35
Q

What aspects of language should you assess?

A

Auditory comprehension for 1-step to complex commands, confrontation naming to assess for dysnomia, and watch for qualitative speech defects, such as hesitations, neologisms, or paraphasic errors.

36
Q

What is the common triad of symptoms seen after anterior communicating artery hemorrhage?

A

Impaired memory (Korsakoff like), confabulation, and personality change. This is the most common location for subarachnoid hemorrhage.

37
Q

What is amyloid angiopathy hemorrhage?

A

Intracranial hemorrhage due to cerebral amyloid angiopathy, which refers to the deposition of beta amyloid in small and mid-sized arteries of the brain.

38
Q

What is cerebral vasospasm?

A

Acute narrowing of a cerebral blood vessel that reduces the blood flow and therefore increases risk for stroke.

39
Q

What is dysarthria?

A

Speech articulation disorder caused by impaired muscular control due to damage to the central or peripheral nervous system. Due to CNS damage and characterized by impaired sequencing of the muscles used in speech (tongue, lips, jaw muscles, vocal cords).

40
Q

What is lacunar infarct?

A

Small subcortical cerebral infarcts related to occlusion or stenosis of small penetrating branches of the MCA, PCA, or basilar artery. Typically associated with chronic hypertension.

41
Q

What is vasculitis?

A

Inflammation of blood vessels, which can lead to narrowing of the vessel, blood clot formation, or aneurysm formation due to the weakening of the vessel wall, all increase the probability of stroke.

42
Q

What deficits are apparent after left MCA superior division infarct?

A

Nonfluent, or Broca’s aphasia and right face and arm weakness, impaired working memory and executive function deficits.

43
Q

What deficits are apparent after left MCA inferior div infarct?

A

Fluent or Wernicke’s aphasia, and a right visual field deficit. There may be right face and arm sensory loss, and parts of Gerstmann syndrome (agraphia, acaculia, right-left disorientation, finger agnosia). Motor findings are usually absent.

44
Q

Deficits after left MCA stem infarct?

A

Combination of deficits after superior and inferior MCA infarct, with right hemiplegia, right homonymous hemianopia, and global aphasia. Often a left gaze preference due to damage of cortical areas important for moving the eyes to the right.

45
Q

Deficits after right MCA superior div infarct?

A

Left face and arm weakness, impaired working memory and executive functions. Left hemineglect may be present.

46
Q

Deficits after right MCA inferior div infarct?

A

Profound left hemineglect. Decreased voluntary or spontaneous initiation of movements on left side. There may be anosognosia and visuospatial deficits, characterized by constructional apraxia, dressing apraxia, and writing, reading, math px due to neglect and spatial difficulties. Patients may appear confused!

47
Q

Deficits after right MCA stem div infarct?

A

Combination of all right MCA deficits, with left hemiplegia, left homonymous hemianopia, profound left hemineglect, visuospatial px, and anosognosia. There is usually a right gaze preference.

48
Q

Deficits after left ACA infarct?

A

Right leg weakness and sensory loss. Exec function px, and transcortical aphasia can be seen.

49
Q

Deficits after right ACA infarct?

A

Left leg weakness and sensory loss. Exec function px and left heminegelect.

50
Q

Deficits after left PCA infarct?

A

Right homonymous hemianopia. Extension to the splenium of the corpus callosum can cause alexia without agraphia. Larger infarcts that extend to thalamus and internal capsule may cause aphasia, right hemisensory loss, and right hemiparesis. Verbal memory px can be seen if extends to left temp lobe.

51
Q

Deficits after right PCA infarct?

A

Left homonymous hemianopia. Larger infarcts including the thalamus and internal capsule may cause left hemisensory loss and left hemiparesis. Spatial memory deficits may be present if lesion extends to the right medial temp lobe.