Brain Blood Supply, Traumatic Brain Injuries and CVA

Question 1

Arterial Supply:

Answer 1

Supplied by two pairs of arteries:
- Internal carotid arteries → anterior and middle cerebral arteries.
- Vertebral arteries → form the basilar artery, giving rise to the posterior cerebral arteries.

Question 2

Venous Drainage:

Answer 2

Drained via dural venous sinuses, which converge into the sigmoid sinuses, then drain into the internal jugular veins.

Question 3

Anterior cerebral artery (ACA)

Answer 3

Supplies medial frontal and parietal lobes — involved in motor/sensory control of the lower limbs.

Question 4

Middle cerebral artery (MCA)

Answer 4

Supplies lateral frontal, parietal, and temporal lobes — speech, face and upper limb function, hearing.

Question 5

Posterior cerebral artery (PCA)

Answer 5

Supplies occipital lobe and inferior temporal lobe — visual processing.

Question 6

Blood-Brain Barrier (BBB)

Answer 6

• Formed by tight junctions between capillary endothelial cells and astrocyte end-feet.
• Regulates passage of substances; allows gases, water, alcohol; restricts proteins, drugs, and toxins.
• Function: Protects the brain’s microenvironment; compromised in inflammation or trauma.

Question 7

Adequate Blood Supply

Answer 7

Brain uses 20% of the body’s oxygen and 70% of glucose, has no fuel reserves, and cannot survive long without supply.

Question 8

Circle of Willis

Answer 8

equalises pressure and redistributes blood if one artery is blocked, helping maintain perfusion during vascular compromise.

Question 9

Stroke (CVA) Definition

Answer 9

“A sudden onset of focal or global neurological deficit lasting >24 hours or causing death, of presumed vascular origin”

Question 10

Major Stroke Risk Factors

Answer 10

• Modifiable: Hypertension (most important), diabetes, smoking, high cholesterol, atrial fibrillation, obesity, alcohol, contraceptives, cocaine.
• Non-modifiable: Age, family history, previous TIA or stroke.

Question 11

Infarct

Answer 11

Permanent brain tissue death due to prolonged ischemia; leads to irreversible neurological deficits.

Question 12

Transient Ischemic Attack (TIA)

Answer 12

Temporary blockage of blood flow; symptoms resolve in <24 hours without permanent damage but warning of stroke.

Question 13

Ischaemic Stroke Mechanism

Answer 13

• Thrombosis (local clot from atherosclerosis).
• Embolism (clot from elsewhere, often heart).
• Hypoperfusion (shock).

Question 14

Ischaemic Stroke Affected Areas

Answer 14

Based on vessels involved — MCA most commonly affected, especially at arterial branch points.

Question 15

What Happens in Ischaemic Tissue

Answer 15

• Deprivation of O₂ and glucose → ATP depletion → ion pump failure → cell swelling (cytotoxic oedema) → necrosis.
• Reperfusion may cause petechial haemorrhage, not the same as haemorrhagic stroke.

Question 16

Ischaemic Penumbra

Answer 16

Area of hypoperfused but viable tissue surrounding core infarct.
Significance: Target for treatment; timely reperfusion can prevent permanent damage. Dependent on collateral circulation

Question 17

Liquefaction Necrosis

Answer 17

• Neurons and glia die and disintegrate; enzymes liquefy tissue.
• Astrocytes line the cavity; replaced with CSF over time.

Question 18

Cytotoxic

Answer 18

Early (minutes); cell swelling due to ATP failure and ion imbalance.

Question 19

Vasogenic

Answer 19

Later (hours–days); leaky vessels from inflammation → fluid accumulates in extracellular space.

Question 20

Oedema & Intracranial Pressure (ICP)

Answer 20

• Skull is rigid → oedema increases pressure (normal ICP: 5–13 mmHg).
• CSF and blood displaced first; if pressure exceeds capacity → brain herniation.
• Consequences: Compression of brainstem, respiratory centres, potentially fatal.

Question 21

Brain Herniation

Answer 21

Types:
- Subfalcine
- Uncal
- Transtentorial
- Tonsillar
Effect: Brain tissue displaced; cuts off blood supply, compresses vital centres.

Question 22

Stroke in Evolution

Answer 22

• Thrombus develops over time → progressive worsening of symptoms.
• Warning signs include TIAs; reflects unstable occlusion that may fully block supply.

Question 23

Haemorrhagic Stroke

Answer 23

• Less common (10–15%) but higher mortality.
  Types:
• Intracerebral: Bleeding into brain tissue.
• Subarachnoid: Bleeding into subarachnoid space.
• Symptoms: Headache, vomiting, decreased consciousness, seizures more common than in ischaemic strokes.

Question 24

Intracerebral Haemorrhage (ICH)

Answer 24

• Causes: Hypertension (most common), aneurysm rupture, AV malformations, tumour, infection.
• Sites: Basal ganglia, thalamus, cerebellum, pons.
• Mechanism: Compression from haematoma, increased ICP, tissue damage.

Question 25

Subarachnoid Haemorrhage & Aneurysms

Answer 25

- Caused by rupture of berry aneurysm. - Blood irritates meninges → severe headache, neck stiffness, photophobia. - Vasospasm may occur days later, worsening outcomes.

Question 26

Acute Stroke Sudden focal deficits:

Answer 26

- Left hemisphere: Aphasia, right hemiparesis. - Right hemisphere: Left neglect, spatial disorientation. - Brainstem/cerebellum: Bilateral signs, ataxia, nystagmus.

Question 27

Acute care stroke management

Answer 27

- Imaging (CT/MRI) - Clot-busting drugs (e.g., tPA for ischaemic stroke within 4.5 hours) - Antiplatelets/anticoagulants - Manage BP, glucose, ICP - Rehab: physical, occupational, and speech therapy

Question 28

Post-Traumatic Amnesia (PTA)

Answer 28

Temporary memory loss following head trauma; includes confusion, agitation, reduced attention. Associated with vascular and cellular disruption

Question 29

Post-Traumatic Amnesia (PTA). duration

Answer 29

indicates severity: <5 min = very mild 5–60 min = mild 1–24 hr = moderate 1–7 days = severe 7 days = very severe