HoyaDocs · Block 5 HNSS · Neuro · Updated Oct 1, 2026 · Revision 1.2

HNSS17 · 7 learning objectives

Vascular & Ventricular Systems of the CNS

LO 1

Know the components of the blood brain barrier and how compounds enter the CNS from the vasculature

Key questions

  1. Q1What makes up the blood–brain barrier, and what does it block?
    Brain endothelial cells joined by tight junction proteins that mostly lack fenestrations. It blocks high-molecular-weight and charged substances.
  2. Q2What gets through the BBB?
    Small or lipophilic substances (e.g., L-dopa, estrogen) and molecules moved by specific transporters.
  3. Q3How do hydrophilic molecules like glucose cross the BBB?
    By facilitated transport through endothelial transporters (e.g., GLUT1); the barrier itself blocks hydrophilic molecules.
  4. Q4What must a CNS drug be, and where can it act despite the BBB?
    Lipophilic or attached to a sequence that is actively transported. Drugs can also reach areas where the BBB is disrupted, such as sites of trauma.
  5. Q5How can the BBB be useful for drug design?
    Drugs made not to cross it avoid CNS side effects — e.g., the non-drowsy antihistamine Allegra (fexofenadine); many chemotherapy drugs are also designed to stay out.
  6. Q6How can a large biologic drug be delivered past the BBB?
    By engaging the transferrin receptor for transport by endocytosis — used for a drug for Hunter syndrome (a lysosomal storage disease of complex polysaccharides, mostly in young boys).
  7. Q7What are circumventricular organs, and which ones sense blood directly?
    Areas with an incomplete barrier. Sensing: area postrema (vomiting in response to toxins); subfornical organ and organum vasculosum (water and ion balance; immune signals → fever, warmth-seeking, loss of appetite).
  8. Q8Which circumventricular organs release substances into blood?
    Hypothalamus–pituitary (growth, homeostasis, reproduction) and the pineal gland (melatonin, circadian rhythm).

The BBB = endothelial tight junctions without fenestrations: big or charged molecules stay out; small or lipophilic ones get in. Circumventricular organs (area postrema, subfornical organ, OVLT, pituitary, pineal) are deliberate gaps for sensing blood or secreting into it.

Crosses the BBB

  • Small, lipophilic molecules (O₂, CO₂, L-dopa, estrogen)
  • Substances with transporters (glucose via GLUT1)
  • Receptor-mediated endocytosis (transferrin receptor → biologics)

Blocked

  • Large molecules (proteins)
  • Charged molecules
  • Drugs designed to stay peripheral (fexofenadine)
Circumventricular organRole
Area postremaSenses toxins → vomiting
Subfornical organ, OVLTSense osmolality/ions and cytokines → thirst, fever, sickness behavior
Hypothalamus–pituitaryRelease hormones (growth, homeostasis, reproduction)
Pineal glandReleases melatonin (circadian rhythm)
HY · Step 1
  • BBB = endothelial tight junctions + basement membrane + astrocyte foot processes.
  • Parkinson therapy: give L-dopa (crosses) with carbidopa (doesn't cross; blocks peripheral conversion).
  • Area postrema is the chemoreceptor trigger zone (targeted by ondansetron/D2 blockers).
  • Hyperosmolar mannitol shrinks the brain across the intact BBB; infarct, tumor and infection break it (vasogenic edema).
LO 2

Describe the mechanisms for delivery of nutrients and oxygen to the CNS

Key questions

  1. Q9How much energy does the brain use?
    20% of the body's oxygen and calories, while being only 2% of body weight.
  2. Q10How fast does lack of blood harm the brain?
    Consciousness is lost in ~10 seconds; after ~6 minutes damage is irreversible or death follows. With mild hypothermia, patients can survive 10–20 minutes with little damage.
  3. Q11How is oxygen released to active brain tissue?
    Hemoglobin releases O₂ in regions of low pH.
  4. Q12What is the brain's fuel?
    Glucose is the main ATP source; lactate and ketone bodies can supplement it.
  5. Q13How does blood flow match demand?
    Vasodilation where ATP is low (high neural activity or hypoxia); overall flow is held constant by autoregulation across a range of arterial pressures.
  6. Q14What does chronic high blood pressure do?
    Alters vessel structure → higher risk of stroke and dementia.

Brain = 2% of weight, 20% of O₂ and calories. O₂ comes off hemoglobin in low-pH tissue; glucose is the fuel (lactate, ketones backup); flow is autoregulated overall and vasodilates where activity is high.

↑ Neural activity→↓ ATP, ↓ pH, hypoxia→Local vasodilation + O₂ unloading→↑ Flow to active region
FactNumber
Share of body O₂ and calories20%
Share of body weight2%
No blood → unconscious~10 seconds
No blood → irreversible damage~6 minutes (10–20 min with mild hypothermia)
Share of intracranial deficits that are vascular50%
HY · Step 1
  • Autoregulation holds flow steady at MAP ~60–150 mmHg.
  • PaCO₂ is the strongest regulator: ↑ CO₂ → vasodilation → ↑ ICP; hyperventilation (↓ CO₂) → vasoconstriction → quick ↓ ICP.
  • Cushing reflex (↑ ICP): hypertension + bradycardia + irregular breathing.
  • In prolonged fasting the brain shifts to ketone bodies.
LO 3

Know the major arteries of the CNS and the structures that they perfuse

Key questions

  1. Q15Where do the internal and external carotids go?
    Common carotid → internal carotid (through the carotid canal to the Circle of Willis) and external carotid (neck, face, scalp).
  2. Q16Trace the posterior circulation.
    Vertebral arteries (branches of the subclavians) run through the transverse foramina of the cervical vertebrae, enter via the foramen magnum and join to form the basilar artery.
  3. Q17What feeds the anterior vs posterior parts of the Circle of Willis?
    Anterior: internal carotids. Posterior: vertebral (basilar) arteries.
  4. Q18Besides the cerebral arteries, which branches of the internal carotid did the lecture name?
    Ophthalmic artery (eye) and anterior choroidal artery (deeper brain structures and choroid plexus).
  5. Q19Which deep structures do the MCA and PCA also feed?
    MCA: the striatum (lenticulostriate branches). PCA: the thalamus.
  6. Q20Name the cerebral and cerebellar arteries.
    Cerebral: anterior (ACA), middle (MCA), posterior (PCA). Cerebellar: superior (SCA), anterior inferior (AICA), posterior inferior (PICA).
  7. Q21What supplies the pons?
    Short circumferential branches of the basilar artery — the source of pontine infarctions.
  8. Q22How is the spinal cord supplied?
    Anterior spinal artery and posterior spinal arteries branch from the vertebrals (or PICA) and run down the cord, reinforced by radicular arteries.
  9. Q23What are watershed areas?
    Border zones between the territories of two cerebral arteries, most vulnerable to low perfusion.
  10. Q24How can the vertebral arteries be damaged?
    Vertebrobasilar occlusion (atherosclerosis) or vertebral artery dissection (trauma, neck distortion).

Anterior circulation = internal carotids → ACA + MCA. Posterior circulation = vertebrals → basilar → PCA, with SCA, AICA, PICA to the cerebellum and short circumferential branches to the pons. Spinal cord = anterior + posterior spinal arteries.

Aorta→Common carotid→Internal carotid→Circle of Willis → ACA, MCA
Subclavian→Vertebral (transverse foramina, foramen magnum)→Basilar→PCA; SCA, AICA; pontine branches
ArterySourceSupplies
ACAICAMedial frontal + parietal lobes (leg/foot cortex)
MCAICALateral cortex (face, arm, language areas) + striatum (lenticulostriates)
PCABasilarOccipital lobe (vision), inferior temporal + thalamus
SCABasilarUpper cerebellum
AICABasilarLower cerebellum, lateral pons/brainstem, inner ear (labyrinthine a.)
PICAVertebralPosteroinferior cerebellum, lateral medulla
OphthalmicICAEye
Anterior choroidalICADeep structures, choroid plexus
Pontine (short circumferential)BasilarPons
Anterior spinalVertebralsAnterior 2/3 of cord
Posterior spinalVertebral or PICAPosterior cord (dorsal columns)
HY · Step 1 (stroke syndromes)
  • MCA: contralateral face + arm weakness/sensory loss; aphasia (dominant) or neglect (nondominant). ACA: contralateral leg. PCA: contralateral homonymous hemianopia with macular sparing.
  • PICA (lateral medullary, Wallenberg): vertigo, hoarseness/dysphagia (nucleus ambiguus), ipsilateral face + contralateral body pain/temp loss, ipsilateral Horner. AICA (lateral pons): facial paralysis, ipsilateral deafness.
  • Basilar occlusion → locked-in syndrome. Anterior spinal artery occlusion → loss of motor + pain/temp below lesion, dorsal columns spared.
  • Most common aneurysm site: ACom (bitemporal field loss); PCom → CN III palsy.
LO 4

Understand the various types of CNS vascular compromise

Key questions

  1. Q25Embolism vs thrombosis?
    Embolism: a traveling clot obstructs a cerebral vessel → ischemia (ischemic stroke). Thrombosis: clot forms in place, in large or small brain vessels.
  2. Q26What is an aneurysm, where does it form, and how is it treated?
    A dilation of the vessel wall, often at branch points; usually asymptomatic until it ruptures. Treated by clipping its stalk.
  3. Q27What is a hemorrhagic stroke?
    Breakage of a blood vessel with bleeding into or around the brain.
  4. Q28What is an arteriovenous malformation (AVM)?
    A tangle of abnormal vessels connecting arteries directly to veins, most common in the CNS. It reduces tissue oxygen and puts arterial pressure on weak veins/sinuses → hemorrhage. Early signs: seizures, headaches, weakness; sometimes only a pulsatile "whooshing" bruit. Treated by surgical removal.
  5. Q29What is a dural fistula?
    An AVM in which meningeal arteries connect directly to a dural sinus; years of arterial pressure raise hemorrhage risk. Treated by neuroradiology and surgery.
  6. Q30Name the five types of intracranial hemorrhage.
    Intraparenchymal, intraventricular, subarachnoid, subdural and epidural.
  7. Q31How is an intracranial hemorrhage managed?
    Control blood pressure, reduce intracranial pressure, and surgically evacuate the hematoma.
  8. Q32Which imaging is used for vascular problems?
    CT identifies hemorrhage types; MRI rules out tumors; MRA and angiography show the vertebrals, basilar, internal and external carotids, Circle of Willis and cerebral arteries (angiography diagnosed the lecture's dural fistula).

Two big groups: ischemic (embolism, thrombosis) and hemorrhagic (vessel rupture — from aneurysm, AVM or dural fistula). Aneurysms get clipped; AVMs get removed; bleeds get BP + ICP control ± evacuation.

TypeMechanismClueTreatment
EmbolismTraveling clot blocks vessel → ischemiaSudden deficit; AFib, carotid plaqueReperfusion
ThrombosisClot forms in place (large or small vessels)Stepwise; atherosclerosisReperfusion, prevention
AneurysmWall dilation at branch pointsSilent until ruptureClip the stalk
Hemorrhagic strokeVessel breaksHeadache, ↓ consciousnessBP + ICP control, evacuate
AVMArteries connect directly to veins → flow too fast or too sluggish → ↓ tissue O₂; arterial pressure on weak veinsSeizures, headache, weakness, bruit, bleedSurgical removal
Dural fistulaMeningeal arteries → dural sinusPulsatile tinnitusNeuroradiology / surgery

Intracranial hemorrhage types: intraparenchymal, intraventricular, subarachnoid, subdural, epidural. Imaging: CT (bleed), MRI (rule out tumor), MRA/angiogram (vessels).

HY · Step 1
  • Berry aneurysm rupture → subarachnoid hemorrhage ("worst headache of my life"); risks: ADPKD, Ehlers-Danlos, Marfan, HTN, smoking. Complication: vasospasm days 3–10 (nimodipine).
  • Charcot-Bouchard microaneurysms (chronic HTN) → intraparenchymal bleed in basal ganglia/thalamus.
  • Ischemic stroke: tPA within 4.5 h (after CT rules out bleed); thrombectomy for large vessel occlusion.
  • Neurons die first ~12–24 h (red neurons), then neutrophils, microglia, and a cystic cavity with gliosis.
LO 5

Know the major veins and sinuses of the CNS

Key questions

  1. Q33Name the external (superficial) veins.
    Superficial cerebral veins (superior, middle, inferior) and superficial cerebellar veins (superior, inferior).
  2. Q34Where do the internal veins drain?
    Veins of the striatum, thalamus, choroid plexus and hippocampus → internal cerebral veins → great cerebral vein (of Galen) → straight sinus.
  3. Q35What are dural venous sinuses, and how do they differ from veins?
    Spaces between the outer and inner layers of dura. No endothelial lining, no valves, so flow is not strictly one-way.
  4. Q36Name the major sinuses.
    Superior sagittal, inferior sagittal, straight, occipital, transverse, superior petrosal, inferior petrosal, sigmoid.
  5. Q37Where does all this blood end up?
    Sinuses → sigmoid sinus → internal jugular vein. Emissary veins also connect scalp veins to the sinuses.

Superficial and deep veins drain into dural venous sinuses (between the dura layers, no valves), which flow to the sigmoid sinus → internal jugular vein. Deep veins go through the great cerebral vein of Galen → straight sinus.

Superior sagittal→Confluence of sinuses→Transverse→Sigmoid→Internal jugular
Internal cerebral veins→Great cerebral v. (Galen)+Inferior sagittal→Straight sinus→Confluence
Cavernous sinus→Superior petrosal → transverse/sigmoid; inferior petrosal → IJV

External veins

  • Superficial cerebral: superior, middle, inferior
  • Superficial cerebellar: superior, inferior

Internal veins

  • From striatum, thalamus, choroid plexus, hippocampus
  • → internal cerebral veins → vein of Galen
HY · Step 1
  • Valveless sinuses + emissary veins let scalp/face infections spread inward (danger triangle → cavernous sinus thrombosis: CN III, IV, V1, V2, VI palsies).
  • Dural venous sinus thrombosis: hypercoagulable states (pregnancy, OCPs) → headache, ↑ ICP, venous infarcts.
  • Arachnoid granulations drain CSF into the superior sagittal sinus.
LO 6

Describe the production, composition, distribution, and clearance of cerebrospinal fluid (CSF)

Key questions

  1. Q38What does CSF do?
    Often called the brain's lymphatic system: it cushions the brain and gives buoyancy (including to the ventral arteries), removes waste, and transports hormones and ions.
  2. Q39What are the normal CSF volume, production and pressure?
    About 150 mL total; 400–500 mL made per day; normal pressure 70–180 mm H₂O.
  3. Q40Where and how is CSF made?
    By the choroid plexus — tufts of specialized ependymal cells folded into villi in the lateral, third and fourth ventricles — which filters arterial blood and actively transports some molecules (choroidal artery and vein).
  4. Q41Compare CSF with plasma.
    CSF: K⁺ 2.8 mM (plasma 4.5), Ca²⁺ 1.0 mM (2.4), protein 34 mg/dL (6500), 0–5 WBCs and no RBCs.
  5. Q42How does CSF flow and leave?
    Choroid plexus → through the ventricles → into the subarachnoid space around brain and cord → through arachnoid granulations into the superior sagittal sinus.
  6. Q43What are arachnoid granulations, and why is flow one-way?
    Protrusions of arachnoid through the dura, only in the superior sagittal sinus. CSF pressure exceeds venous pressure, so CSF flows one way into the sinus.
  7. Q44What CSF findings point to which disease?
    Neutrophils + cloudy: bacterial meningitis. Lymphocytes (IgG): active multiple sclerosis. RBCs: subarachnoid hemorrhage. Malignant cells: metastatic cancer.
  8. Q45When is a lumbar puncture justified?
    Signs such as severe headache, stiff neck, confusion, seizures, persistent flu-like symptoms, fatigue, altered consciousness, severe nausea, fever or rash, light sensitivity, poor coordination.

Choroid plexus makes ~500 mL/day; ~150 mL circulates through ventricles → subarachnoid space → arachnoid granulations → superior sagittal sinus. CSF has less K⁺, Ca²⁺ and far less protein than plasma, and almost no cells.

Choroid plexus (lateral ventricles)→ interventricular foramen →3rd ventricle→ cerebral aqueduct →4th ventricle→ foramina →Subarachnoid space→Arachnoid granulations→Superior sagittal sinus
CSFPlasmaWhy it matters if the BBB breaks
K⁺2.8 mM4.5 mMAlters neuron excitability
Ca²⁺1.0 mM2.4 mMAlters signaling
Protein34 mg/dL6500 mg/dL—
WBCs0–5PresentInflammation
RBCs0PresentIron deposition

Numbers

  • Volume ~150 mL
  • Production 400–500 mL/day (turns over ~3×)
  • Pressure 70–180 mm H₂O

CSF in disease

  • Neutrophils, cloudy → bacterial meningitis
  • Lymphocytes, IgG → active MS
  • RBCs → subarachnoid hemorrhage
  • Malignant cells → metastasis
HY · Step 1
  • Meningitis CSF: bacterial ↑ PMNs, ↑ protein, ↓ glucose; viral ↑ lymphocytes, normal glucose; fungal/TB ↑ lymphocytes, ↓ glucose, ↑↑ protein.
  • MS: oligoclonal IgG bands. SAH: xanthochromia (yellow) after hours.
  • LP is done at L3–L4 or L4–L5 (below the conus at L1–L2); rule out mass effect first to avoid herniation.
LO 7

Understand the symptoms and treatment of the different types of hydrocephalus

Key questions

  1. Q46What is hydrocephalus, and what causes it?
    Increased CSF volume and pressure with enlarged ventricles, from blocked CSF movement or failed absorption.
  2. Q47What is obstructive (non-communicating) hydrocephalus?
    A block inside the ventricular system — e.g., at the interventricular foramen or cerebral aqueduct.
  3. Q48What is communicating hydrocephalus, and what causes it?
    CSF flows freely through the ventricles and subarachnoid space, but can't get into the venous system: congenital absence of arachnoid villi, or villi blocked by RBCs after hemorrhage or protein after infection.
  4. Q49What is normal pressure hydrocephalus?
    A misnomer — CSF pressure is elevated across repeated measurements. Usually elderly. Triad: urinary problems, dementia, impaired gait ("wet, wacky and wobbly").
  5. Q50How is hydrocephalus treated?
    Shunting, removing the blockage, or supportive care.
  6. Q51How does a CSF shunt work?
    An inflow catheter in a ventricle, a one-way valve and an outflow catheter; it drains CSF when pressure rises, through subcutaneous tubing, usually to the peritoneum. About a 1-hour surgery, adjustable to CSF pressure, 50–80% success.

Obstructive = block inside the ventricles (foramen, aqueduct). Communicating = flow OK but absorption at arachnoid villi fails (hemorrhage, infection, absent villi). NPH = elderly, wet, wacky, wobbly. Treat with shunt (ventriculoperitoneal), removal of the block, or support.

TypeProblemCausesClues
Obstructive (non-communicating)Block inside ventriclesAqueductal stenosis, tumor (e.g., medulloblastoma at 4th ventricle), colloid cystVentricles above the block enlarge
CommunicatingCan't absorb into venous bloodAbsent arachnoid villi; villi clogged by RBCs (hemorrhage) or protein (infection)All ventricles enlarge
Normal pressureElevated pressure (misnomer), elderlyOften idiopathicWet, wacky, wobbly

Symptoms of raised pressure

  • Headache, vomiting, sleepiness
  • Infants: enlarging head, bulging fontanelle
  • NPH: incontinence, dementia, magnetic gait

Treatment

  • Ventriculoperitoneal shunt (adjustable; 50–80% success)
  • Remove the blockage
  • Supportive care
Memory hook

NPH = wet (urinary incontinence), wacky (dementia), wobbly (gait) — and it's reversible with a shunt, unlike Alzheimer's.

HY · Step 1
  • NPH: gait improves after large-volume lumbar tap → predicts shunt response. Stretching of periventricular corona radiata fibers causes the triad.
  • Hydrocephalus ex vacuo: ventricles look big because brain has atrophied (Alzheimer, HIV) — pressure normal, not true hydrocephalus.
  • Congenital obstructive causes: aqueductal stenosis, Dandy-Walker (4th ventricle cyst), Chiari II.
  • Shunt complications: infection, obstruction, over-drainage.

Application questions

1. A 72-year-old has a shuffling, "magnetic" gait, urinary incontinence and forgetfulness. MRI shows enlarged ventricles out of proportion to sulci. What is the diagnosis, and what treatment may reverse it?

  1. Alzheimer disease — cholinesterase inhibitor
  2. Normal pressure hydrocephalus — ventriculoperitoneal shunt
  3. Parkinson disease — levodopa
  4. Hydrocephalus ex vacuo — none
  5. Communicating hydrocephalus from meningitis — antibiotics
Answer
B. Wet, wacky and wobbly with ventriculomegaly = NPH; a shunt can reverse it.

2. A patient has vertigo, hoarseness, trouble swallowing, loss of pain and temperature on the left face and right body, and a left Horner syndrome. Which artery is occluded?

  1. Left MCA
  2. Left PICA
  3. Basilar artery
  4. Right ACA
  5. Anterior spinal artery
Answer
B. Lateral medullary (Wallenberg) syndrome from PICA (or vertebral) occlusion; ipsilateral signs are on the left.

3. CSF from a febrile patient with neck stiffness is cloudy with many neutrophils. What is the diagnosis?

  1. Multiple sclerosis
  2. Subarachnoid hemorrhage
  3. Bacterial meningitis
  4. Metastatic cancer
  5. Normal CSF
Answer
C. Neutrophil-predominant, cloudy CSF indicates bacterial meningitis; lymphocytes/IgG suggest MS; RBCs suggest SAH.

4. A new antihistamine is designed so it does not cause drowsiness. Which property keeps it out of the brain?

  1. Small size
  2. High lipophilicity
  3. Large or charged structure that can't cross endothelial tight junctions
  4. Transport by GLUT1
  5. Entry via the transferrin receptor
Answer
C. The BBB blocks large and charged molecules; non-sedating antihistamines like fexofenadine are designed to stay peripheral.

5. After a subarachnoid hemorrhage, a patient develops ventricular enlargement with open ventricular pathways. What is the mechanism?

  1. Aqueductal stenosis
  2. Blood cells clogging the arachnoid granulations
  3. Overproduction by a choroid plexus tumor
  4. Brain atrophy
  5. Absent choroid plexus
Answer
B. Communicating hydrocephalus: RBCs block absorption at the arachnoid villi even though flow through the ventricles is open.

Each objective opens with the one-line answer. Yellow boxes are high-yield Step 1 add-ons and may go beyond the lecture.