Circulatory system and stroke Flashcards

1
Q

Circle of Willis

A

the joining area of several arteries at the bottom (inferior) side of the brain - the internal carotid arteries branch into smaller arteries that supply oxygenated blood to over 80% of the cerebrum

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2
Q

Anastome

A

connections b/w different cerebral arteries on cerebral surface - helps limit extent of cortical damage in stroke BUT creates vulnerability in “border zones/watershed areas” between arteries as they are the most distant portions of blood supply

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3
Q

Two kinds of Cerebrovascular accident (CVA) (a.k.a. stroke)

A

Ischemic stroke - when a blood vessel supplying the brain becomes blocked by blood clot, resulting in reduced oxygen

  • Thrombotic strokes - caused when a blood clot forms in an artery leading to the brain
  • Embolic strokes begin with a clot forming elsewhere in the body that breaks loose and travels to the brain.

Hemorrhagic stroke - when a blood vessel bursts, leaking blood into the brain.

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4
Q

Cerebrovascular accident (CVA) (a.k.a. stroke)

A
  • can cause seizures d/t scar tissue
  • can cause depression in 30% more left-sided CVAs
  • function usually improves but can show worsening deficits d/t cerebral edema (swelling)
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5
Q

Ischemia vs. infarct

A

Ischemia - blood flow to tissue has been decreased, resulting in hypoxia

Infarction - goes one step further, means blood flow has been completely cut off resulting in necrosis/cellular death

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6
Q

3 main cerebral arteries

A

Anterior cerebral artery
Middle cerebral artery
Posterior cerebral artery

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7
Q

Anterior cerebral artery (ACA)

A

Supplies:
Surface - cortex on the anterior medial surface, from the frontal to the anterior parietal lobes including medial sensorimotor cortex (sensory for lower extremity)
Deep - head of caudate, anterior putamen, globus pallidus, internal capsule

Clinical syndromes (infarcts/blockages are uncommon)
1. Usually produce contralateral lower extremity cortical sensory loss and weakness of the upper motor neuron
2. Alien hand syndrome = damage to supplementary area, semiautomatic movements of contralateral arm not under control
3. Frontal lobe dysfunction - impaired judgement, indecisiveness, flat affect, pseudobulbar palsy (inability to control face movements)
4. Bilateral occlusion = apathy, confusion, and mutism

Grasp reflex

can also produce diencephalic amnesia (resulting in confabulation)

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8
Q

Middle cerebral artery (MCA)

A

most common infarcts and ischemic events

Supplies:
Surface - most of the dorsolateral cortex (involving frontal, parietal, and temporal lobes)
Deep: basal ganglia, internal capsule

Clinical syndromes (infarcts/ischemic events more common than ACA and PCA because of larger territory)
1. Left hemisphere lesions - contralateral hemiparesis, hemi-sensory loss, homonymous hemianopia, aphasia, apraxia
2. Right hemisphere lesions - hemi-attention, anosagnosia, dysprosody, possible apraxia
3. MCA watershed area affected: transcortical aphasia or global aphasia

Anterior: Broca’s aphasia
Posterior: fluent aphasia
Angular gyrus syndrome - fluent aphasia, Alexia with agraphia, Gerstmann’s syndrome

Infarcts occur in three areas:
- Superior division - supplies cortex above Sylvia fissure/lateral sulcus
- Inferior division - supplies cortex of lateral temporal and occipital lobes lobes below Sylvian fissure and part of lateral cortex
- Deep territory - includes internal capsule and much of the BG

MCA = gaze preference TOWARD lesion

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9
Q

Posterior cerebral artery (PCA)

A

Supplies:
Surface - inferior and medial temporal cortex, occipital cortex (including visual cortex)
Deep - thalamus

Clinical syndromes:
1. Typically causes contralateral homonymous hemianopia
2. Smaller vessels may lead to infarct of thalamus/posterior limb of internal capsule:
- contralateral sensory loss, hemiparesis, and/or homonymous hemianopia
- Thalamic aphasia (if in language dom hemisphere) - lexical-semantic deficits and intact word repetition
- Alexia without agraphia if involve left occipital cortex

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10
Q

What is a watershed infarct?

A

stroke caused by a drop in circulating pressure and or volume that results in critical ischemia or infarction between territories

Constitute approximately 10% of all cerebral infarcts

Locations:
- Between ACA and MCA: in frontal cortex extending from anterior horn to the cortex
- Between MCA and PCA: in parieto-occipital region extending from posterior horn to the cortex
- Parallel parafalcine stripes in subcortical white matter at the vertex suggests profound hypoperfusion (reduced blood flow)

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11
Q

Left MCA superior division infarct

A
  • Broca’s aphasia
  • Right face and arm weakness of the upper motor neuron type (sometimes sensory loss may be present)
  • Impaired working memory and executive function deficits.

Visual field cut is usually absent.

Limb apraxia may be seen in the right arm after resolution of paresis, and/or in the left arm.

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12
Q

Left MCA inferior division infarct

A
  • Wernicke’s aphasia
  • Right visual field deficit

There may also be right face and arm cortical-type sensory loss, limb apraxia, and parts of Gerstmann’s syndrome (agraphia, acalculia due to conceptual difficulty, right-left disorientation, finger agnosia).

Motor findings are usually absent but mild right-sided weakness may be present, especially at onset.

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13
Q

Left MCA deep territory infarct

A

Right pure motor hemiparesis (weakness) of the upper motor neuron type.
…effect internal capsule

Larger infarcts may produce “cortical” deficits, such as aphasia.

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14
Q

Left MCA stem (initial part of the MCA is a single vessel called the stem)

A

Combination of left MCA infarcts +
- right hemiplegia
- right hemianesthesia (loss of tactile sensation)
- right homonymous hemianopia
- global aphasia

Left gaze preference

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15
Q

Right MCA superior division infarct

A
  • Left face and arm weakness of the upper motor neuron type
  • Impaired working memory and executive functions.
  • Left hemineglect is present to a variable extent.
  • May also be some left face and arm cortical-type sensory loss.
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16
Q

Right MCA inferior division infarct

A
  • Profound left hemineglect.
  • Left visual field and somatosensory deficits are often present
  • Motor neglect with decreased voluntary or spontaneous initiation of movements on the left side can also occur.
  • Some mild, left-sided weakness and right gaze preference may be present especially at stroke onset.
  • There may also be anosognosia and visuospatial deficits characterized by Impaired visuospatial skills and writing, reading and arithmetic problems due to neglect and spatial difficulties
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17
Q

Right MCA deep territory infarct

A
  • Left pure motor hemiparesis of the upper motor neuron type.
    …because of internal capsule
  • Larger infarcts may produce “cortical” deficits, such as left hemineglect and visuospatial deficits as well, emphasizing the importance of larger circuits.
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18
Q

Deep territory infarcts produce…

A

contralateral motor hemiparesis
…because of internal capsule

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19
Q

Right MCA stem infarct

A

Combination of Right MCA infarcts+

  • left hemiplegia,
  • left hemianesthesia
  • left homonymous hemianopia
  • profound left hemineglect,
  • visuospatial deficits
  • anosognosia.

Right gaze preference

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20
Q

Left ACA infarct

A
  • Right leg weakness of the upper motor neuron type
  • Right leg cortical-type sensory loss.

Grasp reflex, executive function deficits, and transcortical motor aphasia can also be seen.

Larger infarcts may cause right hemiplegia.

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21
Q

Right ACA infarct

A
  • Left leg weakness of the upper motor neuron type
  • left leg cortical-type sensory loss.

Grasp reflex, executive function deficits, and left hemineglect can also be seen.

Larger infarcts may cause left hemiplegia.

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22
Q

Left PCA infarct

A
  • Right homonymous hemianopia
  • alexia without agraphia if extends to splenium (tail end) of corpus callous

Larger infarcts may cause:
- transcortical sensory aphasia
- right hemisensory loss
- right hemiparesis.

Verbal memory deficits may be present if the lesion extends to the left medial temporal lobe, especially the hippocampus.

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23
Q

Right PCA infarct

A

Left homonymous hemianopia.

Larger infarcts may cause:
- left hemisensory loss
- left hemiparesis.

Spatial memory deficits may be present if lesion extends to the right medial temporal lobe, especially the hippocampus.

24
Q

Aneurysm

A

bulge in blood vessel caused by weakness in blood vessel wall

usually where the blood vessel branches

Most common locations for aneurysms are the:
- origin of ACA
-origin of PCA
- bifurcation points on MCA

25
Q

Hypoperfusion

A

reduced blood flow

  • leads to watershed (border zone) infarcts

Regions particularly vulnerable to ischemic-anoxic insults (reduced blood flow leading to reduced oxygenation):
Hippocampus
cerebellum
cerebral cortex

26
Q

Cerebellar hemorrhage symptoms

A

occipital headaches (throbbing pain in upper neck or back of head) nuchal rigidity
gait ataxia
dysarthria (slurred speech)
lethargy (diminished energy)

27
Q

Transient ischemic attack (TIA)

A

“Mini stroke”

Symptoms are the same for stroke just limited in time

Temporary neurological deficit (<24 hrs, usually ~10 minutes) brain ischemia (inadequate blood flow)

May be caused by:
- embolism that dissolves
- thrombus (blood clot)
- vasospasm leading to temporary narrowing of vessel

Indicative of underlying atherosclerotic cerebrovascular disease (plaque) and increased risk of sustaining stroke

Slightly more common in PCA than MCA/ACA

28
Q

Sensorimotor deficit profile in each kind of cerebral artery infarct

A

ACAs - lower extremity

MCA - face and arm (think stroke signs)

PCA - present in large infarcts

29
Q

Visual field cut (anopia) profile in each kind of cerebral artery infarct

A

ACA: none

MCA: yes
inferior division > superior

PCA: yes (definitely)

30
Q

Clinical features of watershed infarcts

A

Bilateral ACA/MCA: “man in a barrel” - weakness of arms and legs BUT with preservation of hand and feet strength

Left ACA/MCA: transcortical motor aphasia

Left MCA/PCA: transcortical sensory aphasia
- Alexia without agraphia if lesion extends to splenium of corpus callosum

Right MCA/PCA: Balint’s syndrome (optic ataxia, oculomotor apraxia, simultanagnosia)

31
Q

Perinatal stroke

A

typically refers to strokes occurring between approximately 20 weeks gestation and the first 28 days of life.

32
Q

Which stroke is more common in adults?

Thromboembolic ischemic stroke or Hemorrhagic stroke?

A

Thromboembolic ischemic stroke (88%)

Hemorrhagic stroke (12%) -
intracerebral hemorrhages - 9% subarachnoid hemorrhages - 3%
associated with higher mortality, particularly subarachnoid

Equal occurrence in childhood

33
Q

Stroke risk factors

A
  • older age
  • hypertension/HBP
  • family history
  • prior TIA
  • cocaine
  • smoking
  • diabetes
  • obesity
34
Q

Anterior vs posterior circulation system

A

Anterior circulation (anterior cerebral, middle cerebral) - 80%
- may include hemiparesis, hemianesthesia, aphasia, and visuospatial deficits, as well as visual field cuts if the visual pathway is affected. Visuospatial deficits are less commonly noticed by patients.

Posterior circulation (posterior cerebral artery) - 20%

35
Q

The two major forms of infarction in children

A

arterial ischemic stroke (AIS) - Seizures are the most common presentation

cerebral sinovenous thrombosis (CSVT).

36
Q

Neuroimaging for stroke

A

Brain CT common to detect hemorrhage, but not as sensitive to ischemic damage (particularly acutely)

37
Q

Chronic dystonia is most likely to occur following a stroke in…?

A

the basal ganglia

38
Q

long-term definitive prognostic statements are unrealistic unless the stroke occurred at least…

A

6 months and more ideally at least 1 year prior to evaluation because of the likelihood of some continued recovery

39
Q

Crowding effect

A

language skills may be lateralized to the right hemisphere after an early focal left-hemisphere lesion, leading to reduced visuospatial skills.

motor dominance does NOT reorganize

left side stroke = visuospatial deficits + right side weakness

In the majority of cases, sensory and motor functions retain their usual lateralization, although “pathological” left-handedness can occur.

40
Q

Lacunar infarct

A

Small subcortical cerebral infarct related to occlusion or stenosis (narrowing) of small penetrating branches of the MCA, PCA, or basilar artery.

Lacunes are frequently associated with chronic hypertension.

41
Q

Vasculitis

A

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

42
Q

Ischemic strokes in adults are most common in what vascular distribution

A

MCA

43
Q

endovascular embolization

A

treatment for aneurysm - fills or closes blood vessels to prevent bleeding and rupturing

44
Q

What treatment has the greatest empirical support in clinical trials for depression following a stroke?

A

pharmacological treatment

45
Q

Cortical-subcortical lesions lead to better or worse cognitive outcomes in stroke?

A

Several studies have shown that combined cortical-subcortical lesions are associated with worse cognitive outcomes than cortical or subcortical lesions alone.

46
Q

What accounts for the majority of ischemic childhood stroke?

A

ICA

cerebral arteriopathy (e.g., vasculitis – blood vessel inflammation which can lead to stenosis/narrowing)

47
Q

What accounts for the majority of hemorrhagic childhood stroke?

A

HAM

Arteriovenous malformation – which is an abnormal tangle of blood vessels connecting arteries and veins, which disrupts normal blood flow and oxygen circulation and can lead to uncontrollable bleeding or hemorrhaging

48
Q

Risk factors for strokes in adults vs. children:

A

Traditional adult stroke risk factors such as hypertension, diabetes, smoking, and hypercholesterolemia are uncommon in children. Instead, pediatric stroke risk factors include arteriopathy and vascular malformations, congenital heart disease, sickle cell disease, and hematologic abnormalities among others.

49
Q

The etiology of amnesia most likely to result in confabulation is an

A

anterior communicating artery (ACoA) aneurysm.

An aneurysm of the ACoA would be an example of a pathology producing diencephalic amnesia with resultant confabulation typically involves frontal systems

50
Q

Hemorrhagic stroke or ischemic stroke has higher mortality rate?

A

Hemorrhagic

51
Q

What is the most likely cause for transient global amnesia?

A

basilar artery transient ischemic attack (TIA)

52
Q

What is a transient global amnesia?

A

episode of confusion that comes on suddenly in a person who is otherwise alert

person is unable to create new memory, so the memory of recent events disappears. You can’t remember where you are or how you got there. You may not remember anything about what’s happening right now. You may keep repeating the same questions because you don’t remember the answers you’ve just been given. You may also draw a blank when asked to remember things that happened a day, a month or even a year ago.

You do remember who you are & address, and you recognize the people you know well. Episodes of transient global amnesia always get better slowly over a few hours.

53
Q

Standard therapy for transient ischemic attack

A

Aspirin - because it interferes with platelet adhesion

54
Q

Which kind of stroke most often appears as patients awake in the morning?

A

Cerebral thrombosis

55
Q

Which kind of stroke most often develops during sex?

A

Subarachnoid hemorrhage