W3 - Cerebrovascular disease Flashcards

1
Q

Define the term “cerebrovascular disease” and list 5 predisposing factors.

A

Definition: Any condition affecting the blood vessels of the brain.

Predisposing factors:
Non-modifiable
- Age (increasing age)
- Gender (males more common)
- Genetic/Family Hx (increased likelihood)
Modifiable
- Overweight/obesity
- Smoking
- Diabetes
- Sedentary lifestyle
- Hypertension (high BP)
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2
Q

Briefly discuss the meaning of the terms: “Stroke” and “cerebrovascular accident”. In your discussion indicate the preferred terminology for these processes.

A

Stroke and CVA are commonly used terms that are reasonably unidentifiable/non-specific (provide no information about underlying nature of condition causing neurological deficit). Ischaemic/occlusive stroke and haemorrhagic stroke are the preferred terms, as they indicate the cause and pathophysiology (from which you can derive an appropriate treatment and prognosis etc)..

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3
Q

List the key processes which commonly result in cerebral ischaemia.

A
  • Atherosclerosis (larger arteries, sites of arterial branching or curvature) - causes narrowing of blood vessels
  • Thrombosis (commonly carotid sinus/carotid bifurcation) - May result in vascular occlusion
  • Embolism - Lodge in cerebral circulation, potentially resulting in cerebral ischaemia and infarction (main causes: myocardial infarction, infective endocarditis, prosthetic cardiac valves, mitral stenosis & associated atrial fibrillation, advanced atherosclerosis)

Less common processes:

  • Dissecting aortic aneurysm
  • Vasculitis
  • Cerebral vein occlusion
  • Vascular trauma
  • Hypoxia (respiratory arrest)
  • Cardiac arrest/arrhythmia
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4
Q

Define the term “atherosclerosis” and list and discuss the vascular consequences

A

A disease of the arteries characterised by the build-up of fatty tissue/cholesterol (“plaques”) on their inner walls that may cause occlusion and/or lead to a thrombus/embolus.

Vascular consequences:

  • Narrowing of blood vessels
  • Thrombosis - May result in vascular occlusion (common in carotid sinus/bifurcation)
  • Ulceration - Resulting in release of emboli into circulation
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5
Q

List and briefly discuss the main processes which result in the production of cerebral emboli

A
  • Infective endocarditis - Vegetation of valves of the heart, where friable material may break off to form emboli
  • Prosthetic cardiac valves - Mechanical trauma may displace, causing embolism
  • Mitral stenosis (causing atrial fibrillation) - Lack of contraction causes blood to pool –> increases risk of coagulation and consequently embolism
  • Advanced atherosclerosis - Breaking off of atherosclerotic plaques causing emboli. Commonly from aortic arch, carotids, Circle of Willis.
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6
Q

Write notes on “Transient Ischaemic Attacks (TIAs)”.

A

Definition: Transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia without acute infarction.

Causes:

  • Conditions resulting in decreased cerebral blood flow in patients with severe atherosclerotic narrowing of cerebral arteries
  • Small platelet/cholesterol emboli originating from ulcerated atheroma in cerebral vessels/carotid/aorta
  • Small emboli or thrombi from other sources

Mechanisms:
- Decreased blood flow caused by thrombi/emboli results in ischaemic neurological deficit that reverses as thrombus/embolus is rapidly dissolved and blood flow is returned to normal.

Significance:

  • Indicate severe atherosclerosis in cerebral vasculature
  • “Warning sign” - 30% of pt’s will suffer cerebral infarction within 5 years.

Treatment:

  • Depends on cause
  • Includes surgery and anticoagulant medication
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7
Q

List the main clinical manifestations of cerebral infarction.

A

Signs of increased ICP:

- Headache (diffuse and instant), seizures, vomiting, loss of consciousness

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8
Q

Give four (4) examples of focal (localising) manifestations due to cerebral infarction. In each case name the blood vessel which is involved.

A

Anterior cerebral artery occlusion:

  • Frontal lobe - Personality changes, loss of pupil conjugate gaze, confusion and disorientation
  • Motor & sensory cortex - Contralateral weakness (hemiparesis) and sensory loss in the lower limb

Middle cerebral artery occlusion:

  • Lateral surface of cerebrum - Hearing loss, balance changes, contralateral hemiparesis and sensory loss (head & upper limb), extinction
  • Speech area (dominant hemisphere) - Expressive aphasia (loss of ability to produce speech), aprosodia
  • Optic radiation - Contralateral hemianopsia (visual field loss on L or R side of vertical midline)

Posterior cerebral artery occlusion:
- Occipital lobe - Cortical-type vision loss

Vertebrobasilar artery occlusion:
- Cerebellum - Intention tremor, incoordination, hypotonia

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9
Q

Discuss the relative speed of onset of the clinical manifestations of cerebral infarction

A

Speed with which Ssx appear may indicate underlying aetiology.

  • Instantaneous/explosive = haemorrhagic
  • Medium = Embolism (slowly pushed deeper)
  • Slow = Thrombosis
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10
Q

Briefly outline the treatment of patients suffering from cerebral infarction.

A

Acute phase - Reducing cerebral oedema and raised ICP. Treatment includes thrombolysis (should be initiated ASAP after onset of Ssx), corticosteroids (reduce inflammation) and diuretics (removal of fluid).

Post-acute phase - Supportive treatment to maintain vital functions.

Chronic stage - Early and intense specialised physical and functional rehabilitation

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11
Q

Discuss the prognosis of cerebral infarction

A

Haemorrhagic - Likely death

Ischaemic - Better prognosis

  • Improvement for ischaemic cells (as blood supply is returned) –> improvement in neurological function
  • Necrotic cells will not recover.
  • Opportunity for neuroplasticity (neighbouring areas pick up function of infarcted areas)
  • May get complete neurological recovery
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12
Q

List the main causes of intracranial haemorrhage.

A
  • Hypertension - Causes spontaneous intracerebral haemorrhage
  • Berry aneurysms - Causes spontaneous subarachnoid haemorrhage
  • Venous occlusion - Associated with vascular malformation, neoplasms or with bleeding diathesis
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13
Q

Define the term “intra-cerebral haemorrhage”

A

A non-traumatic haemorrhage from small arteries deep in the brain substance

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14
Q

Discuss the following for intra-cranial haemorrhage:

a) Aetiology
b) Pathology and pathogenesis
c) Prognosis

A

a) Aetiology
- 80% occur secondary to hypertension
- 10% of all stroke cases
- Most occur >40 years old
- Common sites: Basal ganglia or internal capsule (rupture of lenticulo-striate arteries)
- Very high death rate

b) Pathology and pathogenesis
- Rupture of a microaneurism (Charcot-Bouchard) in the lenticulostriate arteries

c) Prognosis
- Most devastating type of stroke with greatest mortality rate.
- No clinically proven therapies
- Treatment typically supportive
- FAST - Facial drooping, inability to lift both arms, slurred speech, timing critical

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15
Q

Discuss the events which occur during intra-cerebral haemorrhage

A
  1. Sudden increase in BP
  2. Rupture of aneurism (Charcot-Bouchard)
  3. Growing blood clot dissects and destroys brain tissue
  4. Haematoma, resulting in increased ICP
  5. Death (via tentorial hermiation) or recovery (breakdown of blood/breakdown of necrotic tissue/cystic area with reactive gliosis)
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16
Q

Define the term “sub-arachnoid haemorrhage”. What is it’s main cause?

A

Non-traumatic haemorrhage resulting from larger arteries, passing through subarachnoid space.

Main cause: Rupture of a berry aneurism (95% of cases)

17
Q

Write brief notes on “berry aneurisms”.

A

Definition: Saccular aneurisms that arise from congenital defects in the media of cerebral arteries (commonly the Circle of Willis).

Sites:

  • Anterior communicating artery (30%)
  • Join between posterior communicating and ICA (30%)
  • Middle cerebral artery (10%)
  • Basilar artery (10%)
18
Q

Discuss the events occurring during sub-arachnoid haemorrhage. What is it’s prognosis?

A

Events:

  1. Rupture of berry aneurism and bleeding into subarachnoid space
    - Often leaks before rupture - If this happens, clotting occurs and fusing of berry aneurism to surface of brain –> intra-cerebral haemorrhage
  2. Arterial spasm in distal arteries –> cerebral ischaemia and oedema

Prognosis:

  • Death occurs rapidly (15% of cases) and death risk of recurrence in survivors
  • Surgical correction is urgent
  • 1/3 of pt’s left permanently disabled.
19
Q

Discuss the clinical manifestations of sub-arachnoid haemorrhage.

A
  • Headache (sudden, severe, bursting)
  • Vomiting
  • Neck pain
  • Rapid loss of consciousness
  • Marked neck stiffness (meningeal irritation)
    If more severe: Ssx of increased ICP, papilloedema