S9) The Anatomy and Physiology of Stroke Flashcards

1
Q

What is a stroke?

A

A stroke is the damaging/killing of brain cells starved of O2 as a result of blood supply to part of the brain being cut off

Stroke, AKA a ‘cerebrovascular accident’, is a ‘serious life threatening condition that occurs when the blood supply to part of the brain is cut off’. The symptoms and signs persist for more than 24 hours

“a neurological deficit attributed to an acute focal injury of the central nervous system (CNS) by a vascular cause, including cerebral infarction, intracerebral hemorrage (ICH), and subarachnoid hemorrhage (SAH)”[1]

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2
Q

What is a TIA?

A

A transient ischaemic attack is a stroke that recovers within 24 hours from the onset of symptoms

Transient ischaemic attacks (TIAs), sometimes colloquially called ‘mini strokes’, have similar clinical features of a stroke but completely resolve within 24 hours

“a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.”[2]

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3
Q

What is stroke syndrome?

A

Stroke syndrome is the constellation of signs and symptoms produced due to occlusion or damage of an artery supplying part of the brain

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4
Q

What are the two main types of stroke?

A
  • Ischaemic (85%)
  • thromboembolic
  • Haemorrhagic (10%)
  • intracerebral (rupture of a vessel in brain parenchyma)
  • subarachnoid
  • Other – dissection (separation of walls of artery, can occlude branches), venous sinus thrombosis ((occlusion of veins causes back pressure and ischaemia due to reduced blood flow), hypoxic brain injury (e.g. post cardiac arrest) (5%)
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5
Q

Identify the causes of stroke in young people vs old people

A
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6
Q

Identify risk factors for stroke

A
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7
Q

What does the emergency management of stroke include?

A

o Two main principles
→ Are they within the window for thrombolysis (<4 hours)?
→ Do a CT head to determine if it is a bleed (if bleed cannot proceed with thrombolysis)

o Acute imaging of stroke
→ CT
• Ischaemic area of brain not visible early on (as infarct becomes more established the ischaemic area will become hypodense)

• A bleed will show up as a bright white area, maybe with mass effect

→ MRI
• Sometimes performed

• Ischaemia shows up as a high signal area

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8
Q

What is MMSE?

A

The Mini–Mental State Examination or Folstein test is a 30-point questionnaire that is used extensively in clinical and research settings to measure cognitive impairment. It is commonly used in medicine and allied health to screen for dementia.

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9
Q

What is phq 9?

A

The 9-question Patient Health Questionnaire is a diagnostic tool introduced in 2001 to screen adult patients in a primary care setting for the presence and severity of depression. It rates depression based on the self-administered Patient Health Questionnaire.

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10
Q

In a stroke, what are the possible locations where the clot could have come from?

A
  • Brain
  • Carotid arteries
  • The vertebral / basilar arteries
  • Aorta
  • Heart
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11
Q

Provide four possible conditions which could lead to blood clots arising from the heart and causing a stroke

A
  • Atrial Fibrillation
  • Valvular disease / prosthetic valves
  • Septic emboli (endocarditis)
  • Intra-cardiac thrombus
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12
Q

Identify three unusual conditions which could lead to a stroke

A
  • Vasculitis
  • Sickle cell anaemia
  • Cocaine (coke stroke)
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13
Q

Blood supply to the brain

A
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14
Q

Which part of the brain does the anterior cerebral artery supply?

A

The anterior cerebral artery supplies the medial aspects of the frontal and parietal lobe and the anterior part of corpus callosum

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15
Q

What does the part of the brain supplied by the ACA do?

A
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16
Q

What occurs in an anterior cerebral artery (ACA) infarct? (ACA stroke)

A

Contralateral weakness in lower limb

– Lower limb affected much worse than upper limb and face (as ACA supplies the medial areas of the sensory and motor homunculus)

Contralateral sensory changes in same pattern as motor deficits
(sensory homunculus in similar arrangement as motor homunculus)

Urinary incontinence due to paracentral lobules being affected

  • Paracentral lobules are essentially the most medial part of the motor/sensory cortices and supply the perineal area

Apraxia

  • Inability to complete motor planning (e.g. difficulty dressing oneself even when power is normal)
  • Often caused by damage to left frontal lobe

Dysarthria / aphasia

  • A very unusual sign in ACA infarcts compared with MCA infarcts
  • May be related to frontal lobe damage

Split brain syndrome / alien hand syndrome (both rare)

  • Caused by involvement of corpus callosum which is normally supplied by the ACA
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17
Q

How could an anterior cerebral artery stroke affect the parietal lobe and corpus callosum?

A
  • Corpus callosum – split brain syndrome, alien hand syndrome
  • Parietal lobes – loss of voluntary control of micturition - as paracentral lobules are affected
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18
Q

How would a patient present with a left ACA stroke?

A
  • Sensory – contralateral loss of all sensory modalities in the lower limb
  • Motor –contralateral paralysis in lower limb more so than upper limb (initially flaccid paralysis then spasticity, UMN signs)
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19
Q

Which part of the brain does the middle cerebral artery supply?

A

Majority of the hemisphere:

  • Basal ganglia
  • Internal capsule
  • Macular cortex
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20
Q

What is the significance of the middle cerebral artery?

A

– As MCA supplies a large area of brain these stroke can have very widespread effects and are associated with an 80% mortality if the main trunk of the MCA is affected due to resulting cerebral oedema

– Haemorrhagic transformation can occur if the vessels in the infarcted area break down

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21
Q

What would be the result of a main trunk occlusion in the middle cerebral artery?

A

Considerable cerebral oedema:

  • May lead to coma/death
  • Malignant MCA
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22
Q

What does the part of the brain supplied by the middle cerebral artery do?

A
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23
Q

The MCA can be occluded at 3 main points. What are they?

A

Proximal MCA (main stem, before the lenticulostriate arteries come off)

Lenticulostriate arteries

Distal branches i.e. where the MCA splits into superior and inferior division

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24
Q

How does a patient present with a left MCA stroke?

A
  • Sensory – contralateral loss of all sensory modalities in the upper limb and face
  • Motor – contralateral upper limb and face affected more than lower limb (initially flaccid paralysis then spasticity UMN signs)
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25
What will be affected by an occlusion at arrow 1?
**Occlusion at this point will affect:** - **Lateral motor cortex** – responsible for the face and arm - **Internal capsule** – carries descending motor fibres from the entirety of the motor cortex (face, arm and leg may be affected)
26
What will be seen in a Proximal MCA occlusion? Explain motor, sensory, visual fields, aphasia and any other features
In this case, **all branches of MCA will be affected** including lenticulostriates and distal branches to cortical areas. – **Contralateral full hemiparesis** (face, arm and leg affected) because the **internal capsule** has been affected which carries fibres to face, arm and leg so even though the MCA supplies the face and arm area (lateral aspect) of the motor homunculus, this is irrelevant – **Contralateral sensory loss** → Probably in the distribution of primary sensory cortex supplied by MCA (i.e. often solely the face and arms), but could involve larger areas if sensory fibres in internal capsule affected - however we find the motor fibres anteriorly and the sensory fibres more posteriorly - sensory fibres said to be more likely supplied by the PCA. – **Visual field defects** → Usually **contralateral homonymous hemianopia _without_ macular sparing** → Due to destruction of both superior and inferior optic radiations as they run through (superior) temporal and parietal lobes → More distal occlusions may affect one radiation alone causing quadrantanopias – **Aphasia** - if left sided → Global if dominant (usually left) hemisphere affected - as both Broca's and Wernicke's area can be affected - so we get Broca's and Wernicke's aphasia .: Global aphasia → Therefore, cannot understand or articulate words – **Contralateral neglect** - more commonly right sided → Usually in lesions of right parietal lobe (can be caused by occlusions of more distal branches as well) - not see in left parietal lobe as LHS is said to have bilateral supply → Essentially an issue with not ‘acknowledging’ that the usually left side of space or even your own body exists. Visual fields normal – **Other features** → **Tactile extinction** (if touch each side simultaneously doesn’t feel the affected side) → **Visual extinction** (as with half clock face etc.) → **Anosognosia** (literally does not acknowledge that they have had a stroke, so will confabulate to explain disability)
27
What will be affected by an occlusion at arrow 2?
Occlusion at this point spares the **internal capsule** but still damages the **lateral motor cortex,** thus only the face and arm are affected
28
What are the visual effects of proximal and distal occlusions of the middle cerebral artery respectively?
- **Proximal occlusion of MCA** leads to contralateral homonymous hemianopia - **Distal occlusion of the MCA** may lead to contralateral homonymous superior or inferior quadrantanopia (rare)
29
How does a middle cerebral artery occlusion affect speech?
**Symptoms depend on:** - Dominant hemisphere - Which branch of MCA is occluded
30
What happens if the dominant hemisphere (most likely left) is affected by a middle cerebral artery occlusion?
- Global aphasia caused by main trunk occlusion - Broca’s (expressive) aphasia - Wernicke’s (receptive) aphasia
31
What happens if the non-dominant hemisphere (most likely right) is affected by a middle cerebral artery occlusion?
- Hemispatial neglect - Tactile extinction - Visual extinction - Anosognosia
32
What occurs in a lenticulostriate artery occlusion AKA lacunar stroke?
→ Cause **destruction** of **small areas of internal capsule and basal ganglia** **–** Essential distinguishing feature from, say, a proximal MCA infarct is that they **do not cause cortical** **features** (e.g. neglect or aphasia) Types that we can get: – Pure motor (face, arm and leg affected equally, caused by damage to motor fibres travelling through internal capsule due to occlusion of lenticulostriate arteries) – Pure sensory (face, arm and leg affected equally, caused by damage to sensory fibres travelling through internal capsule probably due to occlusion of thalamoperforator arteries and maybe also lenticulostriate) – Sensorimotor (mixed, caused by infarct occurring somewhere at boundary between motor and sensory fibres)
33
MCA splits into a superior and inferior division. What does the superior division and inferior division supply?
* *Superior division** essentially supplies **lateral frontal lobe** including **primary motor cortex** and * *Broca’s area** **Inferior division** essentially supplies **lateral parietal lobe** and **superior temporal lobe** including **primary sensory cortex, Wernicke’s area** and **both optic radiations**
34
What occurs when the MCA distal branch - superior division is occluded?
Occlusion will cause **contralateral face and arm weakness** and **expressive aphasia (Broca's area affected)** if **left hemisphere affected**
35
What occurs when the MCA distal branch - inferior division is occluded?
Occlusion will cause **contralateral sensory change in face and arm**, **receptive aphasia (Wernicke's area affected)** if **left hemisphere** and **contralateral visual field defect without macular sparing** (often homonymous hemianopia as both radiations damaged)
36
What will we see if there was an occlusion of the distal branches of the MCA past the superior and inferior divisions point?
Occlusion of branches distal to superior/inferior division may produce even more specific effects, e.g. taking out Broca’s areas specifically with no motor deficit
37
Which part of the brain is supplied by the posterior cerebral artery?
- Occipital lobe - Inferior temporal lobe - Also supplies the thalamus and part of the brainstem
38
How does a patient present with a PCA stroke?
Somatosensory and visual dysfunction typical: **– Contralateral homonymous hemianopia with macular sparing** due to collateral supply from MCA) – **Contralateral sensory loss** due to **damage to thalamus** (the sensory pathways running through the thalamus and internal capsule - found more posteriorly - supplied by PCA)
39
Which part of the brain do the cerebellar arteries supply?
- Cerebellum - Brain stem
40
What does the part of the brain supplied by the cerebellar arteries do?
**Cerebellum** – plays a role in the coordination, precision and timing of purposeful movement
41
What are the symptoms seen in a patient with cerebellar infarct?
– Nausea – Vomiting – Headache – Vertigo / dizziness
42
What are the signs seen in a patient with cerebellar arteries occlusions?
– **Ipsilateral cerebellar signs** (remember DANISH) – **Possible ipsilateral brainstem signs** since cerebellar arteries supply brainstem as they loop round to the cerebellum – **Possible contralateral sensory deficit** – **Possible ipsilateral Horner’s** (once again due to brainstem involvement as the sympathetics runs on the lateral side of the brainstem)
43
How will a patient present with a cerebellar artery stroke (cerebellar signs)?
- **D**ysdiadochokinesia - **A**taxia - **N**ystagmus - **I**ntention tremor - **S**lurred speech - **H**ypotonia
44
Account for the variation in presentation of a patient with a cerebellar artery stroke
**Cerebellar arteries also supply the brainstem:** - **Proximal occlusion** may cause brainstem and cerebellar signs - **Distal occlusion** may cause cerebellar signs alone
45
Cranial nerve nuclei reside in brainstem. In light of this, explain the possible brainstem signs that a patient could present with a cerebellar artery stroke
- Damage to ascending / descending tracts affects **contralateral side of body** - Damage to cranial nerves or their nuclei gives **ipsilateral signs**
46
The severity of a basilar artery stroke depends on location of occlusion. What is the presentation for a distal and proximal occlusion respectively?
- **Distal occlusion** I. Bilateral occipital lobe infarction II. Bilateral thalamic infarction III. Bilateral midbrain infarction - **Proximal occlusion** – ’locked-in-syndrome’ (body + facial muscles paralysed)
47
What part of the brain does the lenticulostriate artery (small branch of the MCA) supply?
Internal capsule (amongst other things)
48
What does the internal capsule do?
Posterior limb – carries descending motor fibres
49
How does a left lenticulostriate artery stroke present?
**Pure motor hemiparesis:** - Isolated contralateral paralysis (initially flaccid followed by spasticity) - Involving face, upper limb and lower limb
50
What part of the brain does the thalamoperforator artery (small branch of PCA) supply?
Part of the thalamus
51
What does the part of the brain supplied by the thalamoperforator artery do?
**Thalamus** – relays sensory information to the left post-central gyrus (somatosensory cortex)
52
How does a left thalamoperforator artery stroke present?
**Pure sensory stroke:** - Isolated contralateral sensory loss of all modalities - Involving face, upper limb and lower limb
53
Not every case of dysphasia and/or weakness is a stroke. Identify four other conditions that mimic the presentation of a stroke
- **H**ypoglycaemia - **E**pilepsy - **M**igraine (hemiplegic) - **I**ntracranial tumours/infections
54
Describe the findings in the following CT scan of the brain
Direct visualisation of the clot (hyperdense artery)
55
Describe the findings in the following CT scan of the brain:
- Early parenchymal changes - Grey matter becomes hypodense (dark) - Loss of grey/white matter differentiation
56
What does the basilar artery supply?
The basilar artery (BA) serves as the main conduit for blood flow through the posterior circulation. It directly supplies **the brainstem and cerebellum** and provides distal blood flow to the thalami and medial temporal and parietal lobes.
57
What can occurs in a distal basilar artery occlusion?
As this vessel supplies the brainstem (which contains many vital centres), occlusion can sometimes cause **sudden death** **Occlusion of distal (superior) basilar artery** – Visual and oculomotor deficits (as basilar sends some branches to midbrain which contains oculomotor nuclei. – Also, occlusion at this site can prevent blood flowing into PCAs affecting occipital lobes – Behavioural abnormalities – Somnolence, hallucinations and dreamlike behaviour (as brainstem contains important centres for sleep regulation – reticular activating system etc – Motor dysfunction often absent (if the cerebral peduncles can get blood from the PCAs which in turn are being filled by the posterior communicating arteries)
58
What occurs in a proximal basilar artery occlusion?
As this vessel supplies the brainstem (which contains many vital centres), occlusion can sometimes cause **sudden death** **Proximal basilar occlusion** (at level of pontine branches. Embolus in basilar artery can occlude pontine branches on each side) – Can cause locked in syndrome – Complete loss of movement of limbs however preserved ocular movement due to lesion below the oculomotor nuclei in midbrain. Eyes still move because midbrain is getting supply from PCAs via posterior communicating arteries – Preserved consciousness (maybe because midbrain reticular formation is still intact)
59
The rule of 4s for brainstem strokes - look at both sides
60
How can brainstem strokes present?
– A huge number of named syndromes (not important to know specifics) – A typical feature is that **contralateral limb weakness** is seen with **ipsilateral cranial nerve signs** • This can be explained by **damage to corticospinal tracts** (above decussation of pyramids) and **damage to cranial nerve nuclei on same side** **Ipsilateral cranial nerve signs + Contralateral sensory and motor tract deficits = Brainstem pathology**
61
What is Bamford/ Oxford classification system?
– This is a **clinical tool** to **quickly diagnose strokes**
62
How do we classify TACs?
63
How do we classify PACs?
64
How do we classify POCS?
65
How do we classify LACs?