Medicine – Cerebrovascular Disease

Cerebrovascular disease refers to disorders affecting the blood vessels supplying the brain. The two major clinical syndromes are transient ischaemic attack (TIA) and stroke.

A stroke may be caused by ischaemia from arterial occlusion or by intracranial haemorrhage. Rapid recognition is essential because some treatments are highly time-dependent.

1. Transient Ischaemic Attack

A transient ischaemic attack (TIA) is a temporary episode of focal neurological dysfunction caused by cerebral, spinal cord, or retinal ischaemia without acute infarction.

The older definition used:

Complete recovery within 24 hours.

Modern practice is more tissue-based rather than purely time-based.

Most TIAs actually resolve within:

Minutes to less than 1 hour.

2. Mechanism of TIA

TIAs are usually caused by transient interruption of blood flow.

Mechanisms include:

Artery-to-artery embolism.

Cardioembolism.

Small-vessel disease.

Critical arterial stenosis with transient hypoperfusion.

Therefore, embolism is important but is not the only mechanism.

3. Clinical Importance of TIA

A TIA is a major warning sign for future stroke.

The risk is particularly high:

In the first hours and days after the event.

Therefore, a patient with suspected TIA requires urgent assessment and secondary prevention.

4. Stroke

A stroke, traditionally called cerebrovascular accident or CVA, is an acute neurological deficit caused by:

Cerebral infarction.

or

Intracranial haemorrhage.

Unlike a TIA, stroke produces persistent neurological dysfunction and/or demonstrable brain tissue injury.

5. Main Types of Stroke

Stroke can be divided into:

Ischaemic stroke.

and

Haemorrhagic stroke.

Ischaemic stroke is more common.

6. Ischaemic Stroke

Ischaemic stroke occurs when an artery supplying the brain becomes occluded.

Important mechanisms include:

Cardioembolism.

Large-artery atherosclerotic thrombosis or embolism.

Small-vessel occlusion.

Other less common causes such as dissection or vasculitis.

7. Cardioembolic Stroke

Important cardiac sources include:

Atrial fibrillation.

Recent myocardial infarction with ventricular thrombus.

Mechanical heart valves.

Mitral stenosis with atrial thrombus.

Infective endocarditis.

Atrial fibrillation is one of the most important causes.

8. Large-Artery Atherosclerotic Stroke

Atherosclerosis of major arteries can cause:

Local thrombosis.

or

Artery-to-artery embolism.

The carotid arteries are particularly important in anterior-circulation stroke.

9. Haemorrhagic Stroke

Haemorrhagic stroke includes:

Intracerebral haemorrhage.

and, in broader cerebrovascular disease discussions,

Subarachnoid haemorrhage.

Common causes of intracerebral haemorrhage include:

Hypertension.

Cerebral amyloid angiopathy.

Anticoagulation.

Vascular malformations.

Tumours.

10. Clinical Presentation of Stroke

Stroke classically causes:

Sudden-onset focal neurological deficit.

Possible symptoms include:

Weakness.

Sensory loss.

Speech disturbance.

Visual loss.

Diplopia.

Ataxia.

Vertigo.

Dysphagia.

The exact pattern depends on the vascular territory involved.

11. Anterior Circulation Stroke

Anterior circulation strokes involve the:

Internal carotid artery system.

This includes the:

Middle cerebral artery.

and

Anterior cerebral artery.

12. Contralateral Weakness and Sensory Loss

Anterior circulation stroke commonly produces:

Contralateral motor weakness.

and/or

Contralateral sensory loss.

The face, arm, and leg may be involved to different degrees depending on the vessel.

13. Middle Cerebral Artery Pattern

A typical middle cerebral artery stroke may cause:

Contralateral face and arm weakness greater than leg weakness.

Contralateral sensory loss.

Aphasia if the dominant hemisphere is affected.

Neglect if the non-dominant hemisphere is affected.

Homonymous hemianopia.

14. Anterior Cerebral Artery Pattern

Anterior cerebral artery stroke more often causes:

Contralateral leg weakness greater than arm weakness.

It may also produce:

Behavioural change.

Abulia.

Urinary incontinence.

because medial frontal structures may be involved.

15. Amaurosis Fugax

Amaurosis fugax is transient monocular visual loss caused by retinal ischaemia.

It is often described as:

A curtain descending over one eye.

It usually reflects embolic disease from the ipsilateral carotid circulation.

16. Homonymous Hemianopia

A homonymous hemianopia affects the same side of the visual field in both eyes.

For example:

Right homonymous hemianopia → left retrochiasmal lesion.

It may occur with lesions of:

Optic tract.

Optic radiations.

Occipital cortex.

17. Aphasia

Aphasia indicates dysfunction of the dominant cerebral hemisphere, usually the left hemisphere.

Possible forms include:

Expressive aphasia.

Receptive aphasia.

Global aphasia.

Aphasia is particularly associated with dominant middle cerebral artery stroke.

18. Dysarthria

Dysarthria is impaired articulation of speech due to motor dysfunction.

Unlike aphasia:

Language formulation and comprehension may remain intact.

Dysarthria can occur with cortical, subcortical, brainstem, or cerebellar stroke.

19. Posterior Circulation Stroke

Posterior circulation stroke involves the:

Vertebral arteries.

Basilar artery.

Posterior cerebral arteries.

It supplies the:

Brainstem.

Cerebellum.

Occipital lobes.

20. Crossed Neurological Signs

Brainstem stroke may produce:

Ipsilateral cranial nerve deficits

with

Contralateral limb weakness or sensory loss.

This is a classic “crossed” pattern.

For example:

Ipsilateral facial sensory abnormality + contralateral limb sensory abnormality.

21. Posterior Circulation Symptoms

Important symptoms include:

Vertigo.

Diplopia.

Dysarthria.

Dysphagia.

Ataxia.

Nystagmus.

Visual field loss.

Limb weakness or sensory loss.

22. Visual Loss in Posterior Circulation Stroke

Posterior cerebral artery infarction may produce:

Contralateral homonymous hemianopia.

Bilateral occipital involvement can produce profound visual loss.

23. Cerebellar Stroke

Cerebellar stroke may cause:

Severe vertigo.

Vomiting.

Gait or truncal ataxia.

Limb incoordination.

Nystagmus.

A patient may have severe inability to stand or walk even without major limb weakness.

24. Basilar Artery Occlusion

Basilar artery occlusion is a neurological emergency.

Possible features include:

Quadriparesis.

Cranial nerve abnormalities.

Reduced consciousness.

Dysarthria.

Dysphagia.

Locked-in syndrome.

25. Lacunar Infarctions

Lacunar infarcts are small subcortical infarctions caused by occlusion of small penetrating arteries.

They are strongly associated with:

Chronic hypertension.

Diabetes mellitus.

Small-vessel lipohyalinosis.

26. Pure Motor Stroke

A classic lacunar syndrome is:

Pure motor hemiparesis.

A common lesion site is:

Posterior limb of the internal capsule.

Other sites can include the:

Pons.

Corona radiata.

27. Pure Sensory Stroke

Another classic lacunar syndrome is:

Pure sensory stroke.

The typical site is the:

Thalamus.

This may produce numbness or altered sensation affecting one side of the body.

28. Other Lacunar Syndromes

Other important lacunar syndromes include:

Ataxic hemiparesis.

Dysarthria–clumsy hand syndrome.

These can help localise small-vessel subcortical infarction.

29. Diagnosis

Stroke diagnosis begins with:

Clinical assessment.

The first goals are to determine:

Is this a stroke?

Is it ischaemic or haemorrhagic?

When was the patient last known well?

Is reperfusion therapy possible?

30. Immediate Brain Imaging

Urgent brain imaging is essential.

The initial study is commonly:

Non-contrast CT brain.

Its main immediate purpose is to identify:

Intracranial haemorrhage.

It may also show early signs of ischaemia.

31. MRI Brain

MRI, particularly diffusion-weighted imaging, is highly sensitive for:

Acute cerebral infarction.

It can be especially useful in:

Posterior circulation stroke.

Small infarcts.

Diagnostic uncertainty.

32. CT Angiography

Modern acute stroke assessment often includes:

CT angiography.

This can identify:

Large-vessel occlusion.

Carotid disease.

Intracranial arterial stenosis or occlusion.

This is particularly important when considering mechanical thrombectomy.

33. Blood Pressure Assessment

Blood pressure should be measured because hypertension is:

A major stroke risk factor.

and

An important consideration in acute treatment decisions.

Acute blood pressure management depends on whether the stroke is ischaemic or haemorrhagic and whether thrombolysis is planned.

34. ECG

ECG is performed to look for:

Atrial fibrillation.

Other cardiac abnormalities may also suggest an embolic source.

Because paroxysmal AF may be missed on a single ECG, longer cardiac rhythm monitoring may be required.

35. Lipids

A lipid profile helps identify:

Dyslipidaemia.

This supports vascular risk assessment and guides lipid-lowering therapy.

36. Glucose

Blood glucose is checked because:

Hypoglycaemia can mimic stroke.

Hyperglycaemia is also associated with poorer outcomes in acute stroke.

Therefore:

Always check glucose early.

37. ESR and CRP

Inflammatory markers such as:

ESR.

CRP.

may be useful when there is suspicion of:

Giant cell arteritis.

Vasculitis.

Inflammatory or infectious disease.

They are not routine diagnostic markers for every stroke.

38. Thrombophilia Testing

The older note suggests thrombophilia screening in everyone under 45.

Modern practice is more selective.

Testing may be considered in:

Young patients with unexplained stroke.

especially when there is:

Venous thrombosis.

Pregnancy-related thrombosis.

Recurrent thrombosis.

Strong family history.

Suspected antiphospholipid syndrome.

Routine broad thrombophilia screening is not necessary for every young stroke patient.

39. Carotid Imaging

Carotid imaging is important after:

Anterior circulation TIA or ischaemic stroke.

It may be performed with:

Carotid Doppler ultrasound.

CT angiography.

MR angiography.

The purpose is to identify significant carotid stenosis.

40. Echocardiography

Echocardiography may be used to identify a cardiac embolic source.

Possible abnormalities include:

Mural thrombus.

Valvular disease.

Intracardiac tumour.

Patent foramen ovale in selected patients.

41. Transoesophageal Echocardiography

TOE gives improved visualisation of structures such as:

Left atrium and atrial appendage.

Aortic arch.

Interatrial septum.

It can be useful when the embolic source remains uncertain.

42. Acute Stroke Unit Care

Patients with acute stroke should ideally be managed in a:

Dedicated stroke unit.

Stroke-unit care improves outcomes through organised multidisciplinary management.

43. Hydration

Adequate hydration is important.

However, fluid therapy should be:

Carefully controlled.

Excess free water should be avoided, and hypotonic fluids are generally not preferred.

44. Swallow Assessment

Every acute stroke patient should have:

Swallow screening before oral food, fluids, or medication.

If swallowing is unsafe:

Keep nil by mouth initially.

This reduces the risk of:

Aspiration pneumonia.

45. Hyperglycaemia

Marked hyperglycaemia should be treated appropriately.

However, overly aggressive glucose lowering can cause hypoglycaemia.

The goal is generally:

Avoid severe hyperglycaemia and avoid hypoglycaemia.

Routine insulin for every patient is not required.

46. Fever

Fever should be investigated and treated because it may worsen neurological injury.

Paracetamol can be used for:

Pyrexia.

The underlying cause, such as infection, should also be sought.

47. DVT Prophylaxis

Immobile stroke patients are at increased risk of:

Deep vein thrombosis.

Pulmonary embolism.

Mechanical prophylaxis, particularly:

Intermittent pneumatic compression, may be used.

Pharmacological prophylaxis depends on bleeding risk and stroke type.

48. Rehabilitation

Early rehabilitation is important.

This may involve:

Physiotherapy.

Occupational therapy.

Speech and language therapy.

Swallowing therapy.

Neuropsychology.

Social support.

49. Aspirin in Ischaemic Stroke

Once intracranial haemorrhage has been excluded, aspirin is commonly given in acute ischaemic stroke when thrombolysis-related timing and contraindications permit.

It reduces the risk of:

Early recurrent ischaemic events.

50. Modern Antiplatelet Therapy

The older sequence of aspirin, then dipyridamole, then clopidogrel is outdated.

For long-term secondary prevention of non-cardioembolic stroke, common options include:

Clopidogrel monotherapy.

or

Aspirin-based therapy depending on local guidance and patient factors.

51. Dual Antiplatelet Therapy

For selected patients with:

High-risk TIA

or

Minor ischaemic stroke,

short-term dual antiplatelet therapy with:

Aspirin + clopidogrel

may be used for a limited period, followed by single antiplatelet therapy.

It is not used indefinitely because bleeding risk rises.

52. Intravenous Thrombolysis

The older note states thrombolysis within:

3 hours.

Modern treatment windows are broader in selected patients.

Intravenous thrombolysis may be considered up to approximately:

4.5 hours from symptom onset

in eligible patients, with some imaging-selected exceptions beyond this in specialist protocols.

53. Thrombolytic Drugs

A commonly used thrombolytic is:

Alteplase.

In some systems:

Tenecteplase

is also used.

The goal is to dissolve the clot and restore blood flow.

54. Mechanical Thrombectomy

A major modern addition is:

Mechanical thrombectomy.

This is used for selected patients with:

Large-vessel occlusion.

A catheter device is used to physically remove the clot.

55. Thrombectomy Time Window

Mechanical thrombectomy is most effective when performed early.

However, selected patients may benefit:

Up to 24 hours from last known well

when advanced imaging demonstrates salvageable brain tissue and appropriate vessel occlusion.

56. Blood Pressure in Acute Ischaemic Stroke

The older note says to treat hypertension 2 weeks after CVA.

This is too simplistic.

In acute ischaemic stroke:

Blood pressure is often allowed to remain moderately elevated initially because aggressive lowering can reduce cerebral perfusion.

However, blood pressure may need urgent treatment if:

Thrombolysis is planned.

There is severe hypertension.

There is another hypertensive emergency.

Long-term BP control should begin once clinically appropriate.

57. Smoking Cessation

Smoking substantially increases vascular risk.

Therefore:

Smoking cessation is an important component of secondary prevention.

58. Statins

Statin therapy is commonly used after ischaemic stroke or TIA of atherosclerotic origin.

Statins reduce:

LDL cholesterol.

Future stroke risk.

Other cardiovascular events.

59. Anticoagulation in Atrial Fibrillation

If stroke or TIA is caused by atrial fibrillation, long-term prevention usually requires:

Oral anticoagulation.

Modern treatment commonly uses:

Direct oral anticoagulants, DOACs

for non-valvular AF when appropriate.

60. Timing of Anticoagulation

The older rule of “2 weeks after infarct” is too rigid.

The timing depends on:

Infarct size.

Stroke severity.

Haemorrhagic transformation.

Bleeding risk.

Cardioembolic risk.

Smaller strokes may permit earlier anticoagulation, while large infarcts often require a longer delay.

61. TIA and Anticoagulation

After a TIA caused by atrial fibrillation, anticoagulation may often be started:

Early, once intracranial bleeding has been excluded and no contraindication exists.

62. Mitral Stenosis and Mural Thrombus

Anticoagulation may also be indicated with:

Mitral stenosis and atrial fibrillation.

Intracardiac mural thrombus.

Mechanical heart valves.

The precise anticoagulant depends on the cardiac condition.

63. Carotid Endarterectomy

Carotid endarterectomy can reduce recurrent stroke risk in selected patients with:

Symptomatic carotid stenosis.

The older threshold of >80% is too restrictive.

Benefit is strongest in:

Severe symptomatic stenosis, especially 70–99%.

Selected patients with:

50–69% stenosis

may also benefit depending on age, sex, surgical risk, and timing.

64. Timing of Carotid Surgery

When indicated, carotid endarterectomy is generally most beneficial when performed:

Soon after the TIA or non-disabling stroke, once the patient is medically stable.

Early treatment reduces the period of highest recurrent stroke risk.

65. Haemorrhagic Stroke Management

Management of intracerebral haemorrhage focuses on:

Blood pressure control.

Reversal of anticoagulation if appropriate.

Management of raised intracranial pressure.

Neurosurgical assessment when indicated.

Treatment of complications.

66. Neurosurgery in Haemorrhagic Stroke

Neurosurgery may be considered in selected cases such as:

Cerebellar haemorrhage with compression.

Hydrocephalus.

Certain superficial lobar haemorrhages.

Deteriorating neurological state.

Not every intracerebral haemorrhage requires surgery.

67. Blood Pressure in Intracerebral Haemorrhage

Unlike many acute ischaemic strokes, intracerebral haemorrhage often requires:

Earlier controlled blood-pressure reduction.

The goal is to reduce haematoma expansion while avoiding cerebral hypoperfusion.

68. Prognosis

Stroke remains a major cause of:

Death.

Long-term disability.

Cognitive impairment.

Epilepsy.

Depression.

Loss of independence.

Outcome depends greatly on stroke type, size, location, age, initial severity, and treatment speed.

69. Mortality

The older estimate of:

20–30% mortality

is too broad to apply universally.

Mortality varies substantially between:

Minor ischaemic stroke.

Large-vessel ischaemic stroke.

Intracerebral haemorrhage.

Subarachnoid haemorrhage.

Haemorrhagic strokes generally have higher early mortality.

70. Long-Term Disability

A substantial proportion of stroke survivors remain functionally impaired.

Possible residual deficits include:

Weakness.

Aphasia.

Dysphagia.

Visual field loss.

Cognitive impairment.

Gait problems.

Depression.

Loss of independence.

Early rehabilitation can significantly improve outcome.

71. TIA – Note Form

Definition:

Transient focal neurological dysfunction caused by ischaemia without acute infarction.

Old rule:

Symptoms resolve within 24 hours.

Modern reality:

Most resolve within minutes to less than 1 hour.

Importance:

Strong warning sign for subsequent stroke.

72. Stroke – Note Form

Ischaemic stroke:

Arterial occlusion → cerebral infarction.

Haemorrhagic stroke:

Intracranial bleeding.

Main ischaemic mechanisms:

Cardioembolism.

Large-artery atherosclerosis.

Small-vessel disease.

Other causes such as dissection or vasculitis.

73. Anterior Circulation – Note Form

Contralateral face/arm/leg weakness or sensory loss.

Ipsilateral monocular visual loss.

Homonymous hemianopia.

Aphasia if dominant hemisphere.

Neglect if non-dominant hemisphere.

Dysarthria may occur.

74. Posterior Circulation – Note Form

Vertigo.

Diplopia.

Dysarthria.

Dysphagia.

Ataxia.

Nystagmus.

Homonymous visual field loss.

Ipsilateral cranial nerve signs with contralateral limb signs may occur.

75. Lacunar Stroke – Note Form

Cause:

Occlusion of small penetrating arteries.

Risk factors:

Hypertension.

Diabetes.

Pure motor hemiparesis:

Posterior limb of internal capsule.

Pure sensory stroke:

Thalamus.

76. Acute Investigation – Note Form

Check glucose immediately.

Urgent non-contrast CT brain.

MRI if needed.

CT angiography for large-vessel occlusion.

ECG for AF.

BP.

Lipids.

Glucose/HbA1c.

Carotid imaging when appropriate.

Echocardiography for suspected cardiac embolic source.

77. Acute Ischaemic Stroke Treatment – Note Form

Stroke unit care.

Swallow assessment before oral intake.

Hydration.

Treat fever and major glucose disturbance.

DVT prevention.

Early rehabilitation.

Antiplatelet therapy after haemorrhage excluded.

IV thrombolysis in eligible patients, generally up to about 4.5 hours.

Mechanical thrombectomy for selected large-vessel occlusion, sometimes up to 24 hours with imaging selection.

78. Secondary Prevention – Note Form

Stop smoking.

Control blood pressure.

Treat diabetes.

Statin therapy when appropriate.

Antiplatelet therapy for non-cardioembolic disease.

Anticoagulation for AF or other cardioembolic indications.

Carotid endarterectomy for appropriate symptomatic carotid stenosis.

79. Haemorrhagic Stroke – Note Form

Control blood pressure.

Reverse anticoagulation when indicated.

Manage raised intracranial pressure.

Neurosurgical assessment if appropriate.

80. Important Corrections to the Original Notes

TIA = not simply “<24 hours.” Modern definition is tissue-based and requires no acute infarction.

TIA is not caused only by emboli. It can also result from small-vessel disease or transient hypoperfusion.

Thrombolysis is not limited to 3 hours. Standard IV treatment may extend to about 4.5 hours in eligible patients.

Mechanical thrombectomy is a major modern treatment for large-vessel occlusion and may be possible in selected patients up to 24 hours.

Dipyridamole as “second line after aspirin failure” is outdated. Modern antiplatelet choice is more individualised, with clopidogrel commonly used.

Anticoagulation timing after stroke is not always 2 weeks. It depends on infarct size and bleeding risk.

Carotid endarterectomy is not restricted to >80% stenosis. Greatest benefit is in symptomatic 70–99%, with selected benefit in 50–69%.

Treating hypertension after stroke is more nuanced than waiting 2 weeks. Acute management depends on stroke type, blood pressure level, and reperfusion treatment.

Key Clinical Pattern

Think of cerebrovascular disease as:

TIA = TEMPORARY FOCAL ISCHAEMIC DEFICIT WITHOUT INFARCTION.

STROKE = PERSISTENT DEFICIT FROM INFARCTION OR HAEMORRHAGE.

For localisation:

ANTERIOR CIRCULATION → CONTRALATERAL WEAKNESS/SENSORY LOSS ± APHASIA ± MONOCULAR VISUAL LOSS.

POSTERIOR CIRCULATION → VERTIGO + DIPLOPIA + DYSPHAGIA + DYSARTHRIA + ATAXIA ± CROSSED SIGNS.

For lacunar stroke:

PURE MOTOR → INTERNAL CAPSULE.

PURE SENSORY → THALAMUS.

For acute management:

CT FIRST → ISCHAEMIC OR HAEMORRHAGIC?

Then consider:

THROMBOLYSIS ± THROMBECTOMY for eligible ischaemic stroke.

And for prevention:

ANTIPLATELET or ANTICOAGULATION + STATIN + BP CONTROL + SMOKING CESSATION + CAROTID TREATMENT WHEN INDICATED.