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Phase 3a - Neurology > Cerebrovascular Disorders > Flashcards

Cerebrovascular Disorders Flashcards

1
Q

Define stroke.

A

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

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2
Q

What are the main types of stroke?

A

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

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3
Q

List the subtypes of haemorrhagic stroke.

A

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

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4
Q

What are the modifiable risk factors for stroke?

A

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

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5
Q

Name some non-modifiable risk factors for stroke.

A

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

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6
Q

What are the main mechanisms of ischaemic stroke?

A

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

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7
Q

What classification system is used for ischaemic strokes?

A

The Bamford Classification, which categorizes strokes into:

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

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8
Q

What are the common symptoms of stroke?

A

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

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9
Q

What type of headache is associated with subarachnoid haemorrhage?

A

A “thunderclap” headache with sudden onset.

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10
Q

What is the first-line investigation for suspected stroke?

A

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

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11
Q

Outline the acute management of ischaemic stroke.

A

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

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12
Q

What is the immediate management of haemorrhagic stroke?

A

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

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13
Q

What are key strategies for secondary prevention of stroke?

A

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

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14
Q

List complications of stroke.

A

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

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15
Q

What is a Transient Ischaemic Attack (TIA)?

A

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.

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16
Q

Why is a TIA considered a medical emergency?

A

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

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17
Q

What are the main causes of a TIA?

A

Atherosclerosis

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

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18
Q

List common risk factors for a TIA.

A

Hypertension

Diabetes mellitus
Hyperlipidemia
Smoking
Atrial fibrillation
Carotid artery stenosis

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19
Q

What symptoms might indicate a TIA?

A

Sudden unilateral weakness or numbness

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

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20
Q

How is a TIA diagnosed?

A

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

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21
Q

What scoring system is used to assess TIA risk?

A

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

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22
Q

What is the immediate management of a suspected TIA?

A

Initiate antiplatelet therapy (aspirin 300 mg daily).

Admit high-risk cases for urgent imaging and evaluation.

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23
Q

What long-term management strategies are used?

A

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).

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24
Q

What is the prognosis after a TIA?

A

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

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25
Q

What is the role of carotid endarterectomy in TIA management?

A

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

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26
Q

What is a Subarachnoid Haemorrhage (SAH)?

A

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.

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27
Q

What are common causes of Subarachnoid Haemorrhage?

A

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

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28
Q

What is the classical presentation of SAH?

A

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.

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29
Q

What are risk factors for SAH?

A

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

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30
Q

How is SAH diagnosed?

A

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 confirms SAH even with a negative CT.
Angiography: Identifies the source of bleeding.

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31
Q

What is xanthochromia, and how is it detected?

A

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

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32
Q

What are key findings on cerebrospinal fluid (CSF) analysis in SAH?

A

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.

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33
Q

What imaging features are seen in SAH?

A

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

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34
Q

How is SAH managed in acute settings?

A

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

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35
Q

What complications are associated with SAH?

A

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.

36
Q

What is the prognosis for SAH?

A

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

37
Q

What is subdural Haemorrhage?

A

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

38
Q

Risk Factors for Subdural Haemorrhage?

A

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

39
Q

CT appearance of Subdural Haemorrhage?

A

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

40
Q

Acute Subdural Haemorrhage?

A

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

41
Q

Subacute Subdural Haemorrhage?

A

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

42
Q

Chronic Subdural Haemorrhage?

A

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

43
Q

Symptoms of Subdural Haemorrhage?

A

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

44
Q

Signs of Subdural Haemorrhage?

A

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

45
Q

Ix for Subdural Haemorrhage?

A

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

46
Q

Management of acute Subdural Haemorrhage?

A

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

47
Q

Managament of chronic Subdural Haemorrhage?

A

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

48
Q

Complications of Subdural Haemorrhage?

A

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

49
Q

Prognosis of Subdural Haemorrhage?

A

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

50
Q

What is an extradural haemorrhage?

A

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.

51
Q

What is the primary cause of EDH?

A

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

52
Q

Which group is most at risk of developing EDH?

A

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

53
Q

Describe the pathophysiology of EDH.

A

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.

54
Q

What are the hallmark symptoms of EDH?

A

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).

55
Q

What imaging modality is used to diagnose EDH?

A

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

56
Q

Why does EDH not cross suture lines?

A

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

57
Q

How does EDH differ from subdural haemorrhage (SDH)?

A

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

58
Q

What are the potential complications of untreated EDH?

A

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

59
Q

What is the initial management of EDH?

A

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

60
Q

What is the definitive treatment for EDH?

A

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

61
Q

What is the prognosis for EDH?

A

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

62
Q

What is the classic presentation of an EDH?

A

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

63
Q

What is Giant Cell Arteritis?

A

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

64
Q

Who is most at risk for GCA?

A

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

65
Q

What are the key symptoms of GCA?

A

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

66
Q

What symptoms are considered ophthalmic emergencies in GCA?

A

Sudden painless vision loss, potentially progressing to permanent blindness.

67
Q

What causes the symptoms in GCA?

A

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

68
Q

What diagnostic criteria and tests are used for GCA?

A

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.

69
Q

What conditions mimic GCA?

A

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

70
Q

What is the mainstay of treatment for GCA?

A

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

71
Q

What additional steps are taken after initiating treatment?

A

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

72
Q

What are the major complications of untreated GCA?

A

Permanent blindness
Stroke
Aortic aneurysm or dissection.

73
Q

What is the prognosis with timely treatment?

A

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

74
Q

What is the relationship between GCA and PMR?

A

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

75
Q

What is cerebral palsy?

A

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.

76
Q

Causes of cerebral palsy?

A

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.

77
Q

Clinical features of cerebral palsy?

A

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

78
Q

Ix for cerebral palsy?

A

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

79
Q

Management of cerebral palsy?

A

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.

80
Q

What is Hypoxic-Ischaemic Encephalopathy (HIE)?

A

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

81
Q

Causes of Hypoxic-Ischaemic Encephalopathy

A

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

82
Q

Clinical Features of Hypoxic-Ischaemic Encephalopathy

A

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

83
Q

Stages of Severity for Hypoxic-Ischaemic Encephalopathy

A

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

84
Q

Dx for Hypoxic-Ischaemic Encephalopathy

A

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

85
Q

Management of Hypoxic-Ischaemic Encephalopathy

A

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

86
Q

Prognosis of Hypoxic-Ischaemic Encephalopathy

A

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

Phase 3a - Neurology (18 decks)

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