W3 - Cerebrovascular disease - condensed Flashcards
Define the term “cerebrovascular disease” and list 5 predisposing factors.
Definition: Any condition affecting the blood vessels of the brain.
Predisposing factors (any 5 of the following):
Non-modifiable
- Age (increasing age)
- Gender (males more common)
- Genetic/Family Hx (increased likelihood)
Modifiable
- Overweight/obesity
- Smoking
- Diabetes
- Sedentary lifestyle
- Hypertension (high BP)
Briefly discuss the meaning of the terms: “Stroke” and “cerebrovascular accident”. In your discussion indicate the preferred terminology for these processes.
Stroke and CVA are commonly used terms that are reasonably unidentifiable/non-specific. Ischaemic/occlusive stroke and haemorrhagic stroke are the preferred terms, as they indicate the cause and pathophysiology.
List the key processes which commonly result in cerebral ischaemia.
- Atherosclerosis
- Thrombosis (may result in vascular occlusion)
- Embolism
Less common processes:
- Dissecting aortic aneurysm
- Vasculitis
- Cerebral vein occlusion
- Vascular trauma
- Hypoxia (respiratory arrest)
- Cardiac arrest/arrhythmia
Define the term “atherosclerosis” and list and discuss the vascular consequences
A disease of the arteries characterised by the build-up of fatty tissue/cholesterol (“plaques”) on their inner walls.
Vascular consequences:
- Narrowing of blood vessels
- Thrombosis - May result in vascular occlusion
- Ulceration - Resulting in release of emboli into circulation
List and briefly discuss the main processes which result in the production of cerebral emboli
- 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.
Write notes on “Transient Ischaemic Attacks (TIAs)”.
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
List the main clinical manifestations of cerebral infarction.
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, aprosodia
- Optic radiation - Contralateral hemianopsia
Posterior cerebral artery occlusion:
- Occipital lobe - Cortical-type vision loss
Vertebrobasilar artery occlusion:
- Cerebellum - Intention tremor, incoordination, hypotonia
Discuss the relative speed of onset of the clinical manifestations of cerebral infarction
Speed with which Ssx appear may indicate underlying aetiology.
- Instantaneous/explosive = haemorrhagic
- Medium = Embolism (slowly pushed deeper)
- Slow = Thrombosis
Briefly outline the treatment of patients suffering from cerebral infarction.
Acute phase - Reducing cerebral oedema and raised ICP. Treatment includes thrombolysis, corticosteroids and diuretics.
Post-acute phase - Supportive treatment to maintain vital functions.
Chronic stage - Early and intense specialised physical and functional rehabilitation
Discuss the prognosis of cerebral infarction
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
- May get complete neurological recovery
List the main causes of intracranial haemorrhage.
- Hypertension
- Berry aneurysms
- Venous occlusion
Define the term “intra-cerebral haemorrhage”
A non-traumatic haemorrhage from small arteries deep in the brain substance
Discuss the following for intra-cranial haemorrhage:
a) Aetiology
b) Pathology and pathogenesis
c) Prognosis
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
Discuss the events which occur during intra-cerebral haemorrhage
- Sudden increase in BP
- Rupture of aneurism (Charcot-Bouchard)
- Growing blood clot dissects and destroys brain tissue
- Haematoma, resulting in increased ICP
- Death (via tentorial hermiation) or recovery (breakdown of blood/breakdown of necrotic tissue/cystic area with reactive gliosis)
Define the term “sub-arachnoid haemorrhage”. What is it’s main cause?
Non-traumatic haemorrhage resulting from larger arteries, passing through subarachnoid space.
Main cause: Rupture of a berry aneurism (95% of cases)
