Cerebrovascular Disorders

Question 1

Define stroke.

Answer 1

A cerebrovascular event causing disrupted blood supply to the brain, characterized by sudden focal/global cerebral dysfunction lasting >24 hours or causing death.

Question 2

What are the main types of stroke?

Answer 2

Ischaemic Stroke (87%)
Haemorrhagic Stroke (13%)

Question 3

List the subtypes of haemorrhagic stroke.

Answer 3

Intracerebral Haemorrhage (e.g., intraparenchymal or intraventricular bleeding).
Subarachnoid Haemorrhage (bleeding between the pia and arachnoid mater).

Question 4

What are the modifiable risk factors for stroke?

Answer 4

Hypertension, diabetes, smoking, hyperlipidemia, atrial fibrillation, obesity, physical inactivity, and alcohol misuse.

Question 5

Name some non-modifiable risk factors for stroke.

Answer 5

Age, male sex, family history, and genetic predisposition.

Question 6

What are the main mechanisms of ischaemic stroke?

Answer 6

Embolism (e.g., from atrial fibrillation).
Thrombosis (local clot formation due to atherosclerosis).
Systemic hypoperfusion (e.g., cardiac arrest).
Cerebral venous sinus thrombosis.

Question 7

What classification system is used for ischaemic strokes?

Answer 7

The Bamford Classification, which categorizes strokes into:

Total Anterior Circulation Stroke (TACS).
Partial Anterior Circulation Stroke (PACS).
Lacunar Stroke (LACS).
Posterior Circulation Stroke (POCS).

Question 8

What are the common symptoms of stroke?

Answer 8

Weakness, sensory disturbances, visual disturbances, speech disturbances, ataxia, dysphagia, reduced consciousness, and pain.

Question 9

What type of headache is associated with subarachnoid haemorrhage?

Answer 9

A “thunderclap” headache with sudden onset.

Question 10

What is the first-line investigation for suspected stroke?

Answer 10

Non-contrast CT of the brain to differentiate between ischaemic and haemorrhagic strokes

Question 11

Outline the acute management of ischaemic stroke.

Answer 11

IV thrombolysis with alteplase (if <4.5 hours since onset).
Mechanical thrombectomy (for large vessel occlusions).
Antiplatelet therapy (e.g., aspirin).

Question 12

What is the immediate management of haemorrhagic stroke?

Answer 12

Blood pressure control, neurosurgical intervention (if indicated), and monitoring for increased intracranial pressure.

Question 13

What are key strategies for secondary prevention of stroke?

Answer 13

Antiplatelets (e.g., aspirin, clopidogrel).
Anticoagulation for atrial fibrillation.
Statin therapy for lipid management.
Lifestyle modifications (e.g., diet, smoking cessation, exercise).

Question 14

List complications of stroke.

Answer 14

Long-term disability (e.g., hemiparesis).
Speech difficulties (aphasia, dysarthria).
Swallowing difficulties (dysphagia).
Post-stroke depression and fatigue.
Recurrent strokes.

Question 15

What is a Transient Ischaemic Attack (TIA)?

Answer 15

A TIA is a temporary interruption of blood flow to the brain, resulting in stroke-like symptoms that resolve completely within 24 hours without causing permanent damage.

Question 16

Why is a TIA considered a medical emergency?

Answer 16

It is a warning sign for potential future strokes, with a significant risk in the following hours to days.

Question 17

What are the main causes of a TIA?

Answer 17

Atherosclerosis

Thromboembolic events
Cardioembolic sources (e.g., atrial fibrillation)

Question 18

List common risk factors for a TIA.

Answer 18

Hypertension

Diabetes mellitus
Hyperlipidemia
Smoking
Atrial fibrillation
Carotid artery stenosis

Question 19

What symptoms might indicate a TIA?

Answer 19

Sudden unilateral weakness or numbness

Dysphasia or aphasia
Amaurosis fugax (temporary vision loss in one eye)
Vertigo or ataxia
Diplopia

Question 20

How is a TIA diagnosed?

Answer 20

Primarily clinical history supported by investigations:

Brain imaging: MRI with DWI preferred.
Vascular imaging: Carotid Doppler, CT/MR angiography.
Cardiac assessment: ECG and echocardiogram to rule out embolic sources.
Blood tests: FBC, glucose, cholesterol, and clotting studies

Question 21

What scoring system is used to assess TIA risk?

Answer 21

The ABCD2 score evaluates the risk of stroke following a TIA.

Question 22

What is the immediate management of a suspected TIA?

Answer 22

Initiate antiplatelet therapy (aspirin 300 mg daily).

Admit high-risk cases for urgent imaging and evaluation.

Question 23

What long-term management strategies are used for TIA management ?

Answer 23

Antiplatelets: Clopidogrel or aspirin with dipyridamole.

Statin therapy: For cholesterol control.
Blood pressure control: Using ACE inhibitors or other antihypertensives.
Anticoagulation: In cases with atrial fibrillation.
Lifestyle modifications (e.g., smoking cessation, healthy diet).

Question 24

What is the prognosis after a TIA?

Answer 24

Without intervention, the risk of a stroke within 90 days is approximately 10-20%, most within the first 48 hours.

Question 25

What is the role of carotid endarterectomy in TIA management?

Answer 25

Indicated for patients with symptomatic carotid artery stenosis (>70%) to prevent further events.

Question 26

What is a Subarachnoid Haemorrhage (SAH)?

Answer 26

SAH is bleeding into the subarachnoid space, typically caused by the rupture of a cerebral aneurysm, often at the Circle of Willis. It accounts for 5% of strokes.

Question 27

What are common causes of Subarachnoid Haemorrhage?

Answer 27

Berry aneurysms: Most common, often linked to hypertension or genetic conditions like autosomal dominant polycystic kidney disease (ADPKD). Arteriovenous malformations (AVMs). Trauma.

Question 28

What is the classical presentation of SAH?

Answer 28

Thunderclap headache: Sudden, severe headache reaching peak intensity within seconds. Often described as the worst headache ever experienced. Associated symptoms: vomiting, confusion, neck stiffness, reduced consciousness, or focal neurological signs.

Question 29

What are risk factors for SAH?

Answer 29

Smoking. Hypertension. Heavy alcohol use. Family history of aneurysms. Genetic conditions (e.g., Ehlers-Danlos syndrome, ADPKD).

Question 30

How is SAH diagnosed?

Answer 30

CT Head: Detects >95% of SAHs within 6 hours of symptom onset. Lumbar Puncture (if CT is inconclusive): Performed >12 hours post-onset to check for xanthochromia (CSF discoloration due to RBC breakdown). Xanthochromia ( a breakdown product of blood) confirms SAH even with a negative CT. Angiography: Identifies the source of bleeding.

Question 31

What is xanthochromia, and how is it detected?

Answer 31

Yellow discoloration of CSF caused by bilirubin from RBC breakdown. Detected via spectrophotometry after a lumbar puncture performed >12 hours after symptom onset.

Question 32

What are key findings on cerebrospinal fluid (CSF) analysis in SAH? Appearance: Opening pressure: RBC count: WBC count: Glucose: Protein:

Answer 32

Appearance: Initially blood-stained, later xanthochromic (>12 hours). Opening pressure: Elevated. RBC count: Elevated. WBC count: Elevated (WBC-to-RBC ratio ~1:1000). Glucose: Normal. Protein: Elevated.

Question 33

What imaging features are seen in SAH?

Answer 33

CT scan: Hyperdensity around sulci/gyri or basal cisterns. Often located near the Circle of Willis.

Question 34

How is SAH managed in acute settings?

Answer 34

Initial stabilization: Airway, breathing, circulation (ABC). Blood pressure control: Maintain systolic BP <160 mmHg to prevent rebleeding. Definitive management: Endovascular coiling or surgical clipping of the aneurysm. Early treatment (<72 hours) reduces rebleeding risk. Nimodipine: Reduces risk of delayed ischemia from cerebral vasospasm

Question 35

What complications are associated with SAH?

Answer 35

Rebleeding: High risk within 24-48 hours. Cerebral vasospasm: Causes delayed ischemia (treated with nimodipine). Hydrocephalus: Treated with ventricular shunting. Seizures: Common; managed with antiepileptics. Hyponatremia: Due to SIADH or cerebral salt-wasting syndrome.

Question 36

What is the prognosis for SAH?

Answer 36

Mortality rate: ~40-50% within the first 30 days. Long-term disability is common in survivors.

Question 37

What is subdural Haemorrhage?

Answer 37

Bleeding into the space between the dura and arachnoid mater due to tearing of bridging veins.

Question 38

Risk Factors for Subdural Haemorrhage?

Answer 38

Brain atrophy (elderly, chronic alcohol use). Head trauma, even minor. Anticoagulant use increases risk of bleeding.

Question 39

CT appearance of Subdural Haemorrhage?

Answer 39

Crescent-shaped (banana-like) bleed, as the blood can flow freely beneath the dura.

Question 40

Acute Subdural Haemorrhage causes and progression ?

Answer 40

Occurs shortly after a severe head injury. Rapid progression of symptoms.

Question 41

Subacute Subdural Haemorrhage?

Answer 41

Develops days to weeks post-injury. Slower symptom progression.

Question 42

Chronic Subdural Haemorrhage?

Answer 42

Seen weeks after minor trauma. Common in elderly and alcoholics.

Question 43

Symptoms of Subdural Haemorrhage?

Answer 43

Altered consciousness. Headache. Neurological deficits (e.g., hemiparesis, seizures). Confusion, drowsiness, or coma in severe cases.

Question 44

Signs of Subdural Haemorrhage?

Answer 44

Fluctuating Glasgow Coma Scale (GCS). Focal neurological signs, e.g., weakness. Rarely, isolated parkinsonism or cranial nerve palsy.

Question 45

Ix for Subdural Haemorrhage?

Answer 45

CT Head: Crescent-shaped hematoma crossing suture lines. Differentiates from epidural hematoma (lens-shaped). MRI for subacute/chronic presentations.

Question 46

Management of acute Subdural Haemorrhage?

Answer 46

Emergency craniotomy if large or causing significant mass effect. Supportive care in ICU: monitoring ICP, correcting coagulopathies.

Question 47

Managament of chronic Subdural Haemorrhage?

Answer 47

Burr hole drainage for symptomatic cases. Conservative management for small, asymptomatic bleeds

Question 48

Complications of Subdural Haemorrhage?

Answer 48

Brain herniation (uncal or transtentorial). Chronic neurological deficits. Risk of rebleeding.

Question 49

Prognosis of Subdural Haemorrhage?

Answer 49

Worse in acute cases with severe brain injury. Good outcomes in chronic cases with appropriate treatment.

Question 50

What is an extradural haemorrhage?

Answer 50

An extradural haemorrhage (EDH) is a collection of blood between the dura mater and the inner surface of the skull, typically due to arterial bleeding, most commonly from the middle meningeal artery.

Question 51

What is the primary cause of EDH?

Answer 51

EDH is primarily caused by head trauma, often involving fractures of the temporal bone that damage the middle meningeal artery

Question 52

Which group is most at risk of developing EDH?

Answer 52

Younger individuals, as the dura mater is less adherent to the skull compared to older adults.

Question 53

Describe the pathophysiology of EDH.

Answer 53

Trauma causes arterial bleeding into the extradural space. The blood accumulates rapidly, compressing brain tissue. This creates a biconvex (lens-shaped) haematoma visible on imaging.

Question 54

What are the hallmark symptoms of EDH?

Answer 54

Lucid interval: Temporary recovery of consciousness before rapid deterioration. Severe headache. Nausea and vomiting. Focal neurological deficits (e.g., weakness, cranial nerve abnormalities). Reduced Glasgow Coma Scale (GCS) score. Fixed, dilated pupil on the side of the haematoma (indicating herniation).

Question 55

What imaging modality is used to diagnose EDH?

Answer 55

A CT head scan showing a biconvex, hyperdense lesion that does not cross suture lines.

Question 56

Why does EDH not cross suture lines?

Answer 56

The dura mater is tightly adhered to the sutures, preventing blood from spreading beyond these boundaries.

Question 57

How does EDH differ from subdural haemorrhage (SDH)?

Answer 57

EDH: Biconvex shape, arterial bleeding, does not cross sutures. SDH: Crescentic shape, venous bleeding, crosses sutures.

Question 58

What are the potential complications of untreated EDH?

Answer 58

Raised intracranial pressure (ICP). Brain herniation (e.g., uncal herniation). Permanent neurological deficits. Death.

Question 59

What is the initial management of EDH?

Answer 59

Airway management (ABC approach). Stabilize circulation and oxygenation. Monitor neurological status closely.

Question 60

What is the definitive treatment for EDH?

Answer 60

Surgical evacuation of the haematoma via craniotomy. Temporary medical measures (e.g., mannitol or hypertonic saline) to reduce ICP

Question 61

What is the prognosis for EDH?

Answer 61

If treated promptly, EDH has a good prognosis. Delayed treatment increases the risk of permanent damage or death due to herniation.

Question 62

What is the classic presentation of an EDH?

Answer 62

Traumatic head injury. Initial loss of consciousness, followed by a lucid interval. Rapid neurological deterioration, indicating raised ICP or herniation.

Question 63

What is Giant Cell Arteritis?

Answer 63

GCA, also known as temporal arteritis, is a systemic vasculitis primarily affecting medium and large arteries, particularly the temporal artery.

Question 64

Who is most at risk for GCA?

Answer 64

It predominantly affects individuals over 50 years of age, with women being at higher risk.

Question 65

What are the key symptoms of GCA?

Answer 65

Headache (usually temporal) Scalp tenderness Jaw claudication (pain while chewing) Vision changes, including transient or permanent loss Systemic symptoms: fatigue, fever, and weight loss.

Question 66

What symptoms are considered ophthalmic emergencies in GCA?

Answer 66

Sudden painless vision loss, potentially progressing to permanent blindness.

Question 67

What causes the symptoms in GCA?

Answer 67

Inflammation of arterial walls leads to narrowing or occlusion, causing ischemia to affected tissues, including the optic nerve and retina.

Question 68

What diagnostic criteria and tests are used for GCA?

Answer 68

History: Headache, jaw claudication, and vision changes in a patient over 50. Physical Examination: Palpable, tender temporal arteries, sometimes with a diminished pulse. Investigations: Elevated inflammatory markers: ESR and CRP. Temporal artery biopsy: Gold standard showing granulomatous inflammation with multinucleated giant cells.

Question 69

What conditions mimic GCA?

Answer 69

Migraine Polymyalgia Rheumatica (closely associated with GCA) Tension headache Non-arteritic anterior ischemic optic neuropathy (NAION)

Question 70

What is the mainstay of treatment for GCA?

Answer 70

High-dose corticosteroids (e.g., prednisolone). Immediate treatment is crucial to prevent vision loss.

Question 71

What additional steps are taken after initiating treatment?

Answer 71

Referral to ophthalmology or rheumatology for further evaluation. Consideration of bone protection (e.g., bisphosphonates) due to prolonged steroid use.

Question 72

What are the major complications of untreated GCA?

Answer 72

Permanent blindness Stroke Aortic aneurysm or dissection.

Question 73

What is the prognosis with timely treatment?

Answer 73

Vision loss can be prevented in the majority of cases, and systemic symptoms typically resolve.

Question 74

What is the relationship between GCA and PMR?

Answer 74

About 50% of patients with GCA also have PMR, presenting with symmetrical pain and stiffness in the shoulders and hips.

Question 75

What is cerebral palsy?

Answer 75

Cerebral palsy is a group of permanent movement disorders resulting from a non-progressive brain injury or malformation occurring in the developing brain, often before birth.

Question 76

Causes of cerebral palsy?

Answer 76

Prenatal: Brain malformations, infections (e.g., TORCH infections), maternal trauma. Perinatal: Birth asphyxia, hypoxic-ischaemic encephalopathy, preterm birth, intracranial hemorrhage. Postnatal: Trauma, infections (e.g., meningitis), or hypoglycemia.

Question 77

Clinical features of cerebral palsy?

Answer 77

Motor symptoms: Spasticity, dyskinesia, or ataxia. Delayed developmental milestones. Feeding difficulties due to poor oral motor control. Seizures and intellectual disabilities may co-occur.

Question 78

Ix for cerebral palsy?

Answer 78

History and clinical examination. Imaging: MRI or CT to identify structural brain abnormalities. Exclusion of progressive disorders.

Question 79

Management of cerebral palsy?

Answer 79

Multidisciplinary approach: physiotherapy, speech therapy, and occupational therapy. Medications: Antispastic agents like baclofen or botulinum toxin. Orthopedic interventions for contractures. Nutritional support for feeding difficulties.

Question 80

What is Hypoxic-Ischaemic Encephalopathy (HIE)?

Answer 80

HIE refers to brain dysfunction caused by insufficient oxygen (hypoxia) and blood flow (ischaemia) around the time of birth.

Question 81

Causes of Hypoxic-Ischaemic Encephalopathy

Answer 81

Perinatal events: Umbilical cord prolapse, placental abruption, uterine rupture. Neonatal conditions: Severe prematurity or respiratory distress.

Question 82

Clinical Features of Hypoxic-Ischaemic Encephalopathy

Answer 82

Neurological signs: Hypotonia, altered consciousness, poor feeding, seizures. Multi-organ involvement: Renal, cardiac, and hepatic dysfunction.

Question 83

Stages of Severity for Hypoxic-Ischaemic Encephalopathy

Answer 83

Mild: Irritability, hyperalertness, minimal muscle tone changes. Moderate: Lethargy, hypotonia, seizures. Severe: Coma, absent reflexes, respiratory failure.

Question 84

Dx for Hypoxic-Ischaemic Encephalopathy

Answer 84

Clinical assessment and Apgar scores. Blood gases (acidosis) and imaging (MRI).

Question 85

Management of Hypoxic-Ischaemic Encephalopathy

Answer 85

Neonatal resuscitation. Therapeutic hypothermia within six hours of birth to reduce brain injury. Supportive care for organ dysfunction.

Question 86

Prognosis of Hypoxic-Ischaemic Encephalopathy

Answer 86

Mild HIE: Likely full recovery. Moderate to severe HIE: Risk of CP, intellectual disabilities, or death.