Part II · Chapter 6 · Lectures 5 & 6

Stroke, aphasia & head trauma

Why the brain's blood supply is its weak point, the three arteries and what they feed, how vessels fail, what aphasia taught us about language, and the two ways a blow to the head injures the brain.

1. Blood supply: the brain's single point of failure

The brain is about 2% of body weight but takes ~20% of the body's blood flow, through roughly 500 miles of blood vessels. It has almost no energy reserve: it cannot function with prolonged oxygen deprivation, and 10 seconds of blocked blood supply means unconsciousness. That's why vascular problems are the first category of brain dysfunction the course covers.

The three cerebral arteries

Arterial territories (as given in lecture) — click an artery
Schematic by lobe, following the study guide. Real territories follow the vessels rather than lobe borders.
ArterySuppliesHook
Anterior cerebral arteryFrontal + parietalAnterior = front → starts at frontal
Middle cerebral arteryTemporal + parietalMiddle = the side of the head (temporal)
Posterior cerebral arteryOccipital + temporalPosterior = back → occipital (vision)
Intuition Each artery is named for where it starts its territory, and the neighbouring lobe is shared. Frontal, occipital are each owned by one artery; parietal (ACA + MCA) and temporal (MCA + PCA) are each shared by two. going deeper Clinically, a PCA stroke often shows up as a visual-field loss because it feeds occipital cortex (Ch. 9).

2. How vessels fail — and the two kinds of stroke

Three vessel vulnerabilities
Atherosclerosis build-up of plaques arteryvein Arteriovenous malformation abnormal tangle: artery → vein directly Aneurysm bulging, weak vessel wall
What to notice: the first narrows the pipe (→ blockage); the other two are weak spots that can burst. Two ways to stop an aneurysm bursting: clipping (a clip across its neck) and coiling (filling it with a coil so it clots off). The lecture's case: actor Emilia Clarke's ruptured aneurysm.
Ischemic strokeBlood flow to part of the brain is blocked or reduced — usually a blood clot or atherosclerosis. (Ischemia = not enough blood.)
Hemorrhagic strokeA blood vessel in the brain bursts. (Hemorrhage = bleeding — think aneurysm or AVM rupturing.)
Practical relevance — act F.A.S.T. Face drooping · Arm weakness · Speech difficulty · Time to call 911. Minutes matter because of that 10-second, no-reserve fact above.

3. What stroke taught us about language

Definition Aphasia — a language disorder resulting from damage to brain regions responsible for language.
ProductionComprehensionWhat it sounds like
Broca's aphasia✗ Impaired✓ IntactEffortful, halting, few words — but understands you
Wernicke's aphasia✓ Intact✗ ImpairedFluent, flowing speech that doesn't make sense; doesn't understand you
Key idea Broca's + Wernicke's = a double dissociation between language production and comprehension (Ch. 5) → they rely on distinct processes and regions.
Common mistake Swapping them. Hook: Broca = Broken speech (production). Wernicke = Wordy but Weird (fluent, can't comprehend). And "fluent" ≠ "intact meaning" — Wernicke's patients produce fluent but often meaningless speech; the study guide's "intact production" means fluent output.

Singing is intact in Broca's aphasia patients — and not just for over-learned songs. A patient who can't speak a sentence can sing its words. That's another dissociation: speech production vs singing, suggesting music draws on partly different machinery (recall the RH-melody result in Ch. 5).

4. Traumatic brain injury: two mechanisms

Coup–contrecoup vs rotational shear
What to notice: the brain floats in fluid, so on impact it keeps moving and hits the skull — first where the blow landed, then on the opposite side.
MechanismWhat happensResult
1. Direct force (coup–contrecoup)Brain hits the skull and shears against bony ridges — at the impact site (coup) and the opposite side (contrecoup)Contusions: bruises in the brain — injured tissue where capillaries rupture. Orbitofrontal damage → social regulation problems (the orbital frontal cortex sits on bony ridges above the eyes).
2. Diffuse axonal injuryRotational components put major shear stress on axons connecting brain cellsAxon tearing, cognitive changes; can cause immediate coma

Chronic traumatic encephalopathy (CTE): trauma meets degeneration

CTE — repeated head trauma, with or without loss of consciousness. Leads to a build-up of tau in the frontal cortex (tau also appears in Alzheimer's — Ch. 7). Ranked by football position, the players who take the most repeated hits carry the most risk.

CTE symptom progression
What to notice: attention and mood come first; memory, executive function and dementia come later — tracking tau spreading from frontal cortex outward.
Someone you like hits their head and loses consciousness at a party. You should…
Why: The lecture's answer is options 1 and 4 together: medical attention immediately (concussion or internal bleeding — e.g. a hemorrhage — can be serious), and keeping them awake and talking so you can monitor for confusion or disorientation.

5. Check yourself

A clot blocks the posterior cerebral artery. Which lobes are most at risk?
Why: PCA → occipital + temporal. Frontal + parietal is ACA; temporal + parietal is MCA. This is an ischemic stroke.
A patient speaks fluently in long sentences that make little sense and can't follow simple instructions. Diagnosis?
Why: Fluent production + impaired comprehension. Broca's is the reverse: halting speech, good comprehension.
An aneurysm ruptures. This is a…
Why: A burst vessel = hemorrhage. Ischemic is a blockage (clot or plaque).
After a car crash with a lot of head rotation, a patient is in an immediate coma but scans show few bruises. Most likely mechanism?
Why: Rotation shears axons throughout the brain — "diffuse", not a localized bruise. CTE needs repeated trauma over time.