Charcot-Bouchard

Intraparenchymal hemorrhage · Hypertensive microaneurysm · Deep brain vessels

Board Challenge

Can you crack the CT?

Read the case. Choose before you scroll. The clues are already there.

Clinical Encounter

A 72-year-old woman is brought to the emergency department by her daughter because of sudden-onset weakness and numbness on the left side of her body. Her daughter reports that she collapsed at home about two hours ago. The patient has not seen a physician in over 20 years and takes no medications. On examination, she is obtunded but responsive to voice. Blood pressure 195/100 mmHg. Heart rate 88. Temperature 37.1°C. Pupils are equal and reactive bilaterally. Motor examination reveals strength 1/5 in the left upper and lower extremities. Sensation is diminished throughout the left side. There is no facial droop. A non-contrast head CT is obtained showing a large hyperdense lesion in the right basal ganglia with surrounding edema. There is no midline shift. Which of the following best describes the underlying vascular lesion responsible for this presentation?

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The Mechanism

Vessel Siege

Watch hypertension destroy a deep penetrating artery one stage at a time. Advance through the chain.

Stage 1 of 5 — The Healthy Vessel

Lenticulostriate arteries are small, deep-penetrating branches of the MCA that supply the basal ganglia, internal capsule, and thalamus. They are end arteries with no collateral flow. In a healthy state, the muscular wall withstands normal pulsatile pressure. No weakness, no outpouching.

Years of uncontrolled hypertension force the vessel wall into lipohyalinosis. Smooth muscle cells die. The wall is replaced by hyaline fibrous tissue: stiff, brittle, unable to vasoconstrict. Lipid deposits accumulate. The wall loses its structural integrity. This is the setup for what comes next.

The weakened wall cannot resist pulsatile pressure. It balloons outward, forming a Charcot-Bouchard microaneurysm. These are microscopic, 50-200 microns. Too small to see on angiography. This is the key discriminator from berry aneurysms. The aneurysm pulsates with every heartbeat, wall thinning with each cycle.

The wall fails. Blood erupts into the brain parenchyma under arterial pressure. The blood is trapped inside the brain tissue. Right basal ganglia bleed produces contralateral weakness and sensory loss. The CT shows a hyperdense (bright white) lesion immediately, the key board discriminator from ischemic stroke (which is hypodense or invisible acutely).

The full chain, locked in: Chronic hypertension damages small penetrating arteries via lipohyalinosis. The weakened wall forms a microaneurysm. That aneurysm ruptures. Blood fills the deep brain parenchyma. Location: deep structures only. Never cortex. CT: hyperdense immediately.

RouteHTN → lipohyalinosis → microaneurysm → rupture → deep parenchymal bleed

PatternHyperdense CT + deep location + chronic HTN history

PearlAngiography negative: too small (50-200 microns) to visualize. That is the board clue.

LocationPutamen/GP > thalamus > pons > cerebellum. NOT cortex.

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Differential Discriminator

The Four Bleeds

Every hemorrhage has a signature. Lock in the discriminators.

Charcot-Bouchard Microaneurysm

Lenticulostriate · Thalamoperforating arteries · Deep penetrating branches

Mechanism

Chronic HTN → lipohyalinosis → microaneurysm rupture

Classic Patient

Elderly, chronic uncontrolled HTN, often no recent medical care

Location

Deep: putamen/GP, thalamus, pons, cerebellum. NOT cortex.

CT Finding

Hyperdense lesion immediately. Intraparenchymal. No subarachnoid component.

Angiography

Negative. Too small (50-200 microns) to visualize.

Board Clue

Elderly + HTN + hyperdense deep lesion + angio negative = this diagnosis.

Berry (Saccular) Aneurysm

Circle of Willis · Anterior communicating, Posterior communicating, MCA bifurcation, basilar tip

Mechanism

Congenital media defect + HTN + age → saccular outpouching at vessel branch points

Classic Patient

Adult, ADPKD or Ehlers-Danlos association; HTN is a risk factor

Location

Subarachnoid space. Rupture fills cisterns, not parenchyma.

CT Finding

Subarachnoid hyperdensity in cisterns. Star-shaped pattern.

Angiography

Positive. Visible saccular outpouching on CTA/DSA.

Board Clue

"Worst headache of my life" + subarachnoid cistern blood + CN III palsy (posterior communicating artery). Not deep basal ganglia.

Arteriovenous Malformation (AVM)

Congenital vessel tangle · Often lobar/cortical location

Mechanism

Congenital arteriovenous shunting, no capillary bed → high-pressure venous bleeding

Classic Patient

Young adult, often no HTN. May present with seizure before hemorrhage.

Location

Often lobar/cortical. Sturge-Weber association with port-wine stain.

CT Finding

Intraparenchymal or subarachnoid. Tangled vascular nidus on CTA.

Angiography

Positive. Classic "bag of worms" feeding vessels.

Board Clue

Young + no HTN + seizure history + lobar bleed + positive angio.

Cerebral Amyloid Angiopathy

Cortical & leptomeningeal vessels · Beta-amyloid deposition

Mechanism

Beta-amyloid in cortical vessel walls → fragile vessels → spontaneous cortical rupture

Classic Patient

Very elderly (>65), Alzheimer disease, ApoE4 genotype. Recurrent bleeds.

Location

LOBAR / CORTICAL only. NOT basal ganglia, thalamus, or pons.

CT Finding

Lobar hyperdense hematoma. Multiple prior bleeds. MRI gradient echo shows hemosiderin deposits.

Angiography

Usually negative. Congo red staining on biopsy is gold standard.

Board Clue

Elderly + Alzheimer + LOBAR recurrent bleed. Location is cortical. Basal ganglia = Charcot-Bouchard.

CT Decision Challenge

Diagnostic Tree

Work through the CT findings step by step. Choose at each node before the feedback appears.

NODE 1 A non-contrast head CT shows a bright white (hyperdense) lesion. What does this tell you about the type of stroke before you even look at the location?

Acute blood on non-contrast CT is hyperdense because of hemoglobin protein density. Ischemic strokes are hypodense or invisible for the first 24-48 hours. Hyperdense lesion = hemorrhagic stroke. The next question is where the blood is.

NODE 2 The hyperdense lesion is in the right basal ganglia. The patient is 72 with BP 195/100 and no medical care for 20 years. Which single feature most strongly points to Charcot-Bouchard over all other causes?

Age alone doesn't discriminate (amyloid angiopathy also affects the elderly). Size doesn't discriminate. The discriminator is the combination: deep location plus a long history of uncontrolled hypertension. Amyloid angiopathy causes lobar/cortical bleeds. AVM bleeds affect the young without HTN. Berry ruptures cause subarachnoid blood.

NODE 3 A cerebral angiogram is ordered. What do you predict, and why does it support Charcot-Bouchard?

Charcot-Bouchard microaneurysms are 50-200 microns, far below angiography resolution. A negative angiogram in the setting of deep hemorrhage plus chronic HTN is not a failed study. It is confirmatory evidence for the diagnosis. The absence of a visible aneurysm IS the positive finding.

Diagnosis Locked

Charcot-Bouchard Hemorrhage: Hyperdense lesion on non-contrast CT + deep brain location + chronic uncontrolled HTN + negative angiography. Chain: HTN → lipohyalinosis → microaneurysm → rupture → contralateral motor and sensory loss.

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Memory Hooks

Lock it in

Tap each card to reveal the hook.

Where does Charcot-Bouchard bleed? Deep or surface?

HTN is a wrecking ball that only reaches the basement. Lenticulostriate arteries are the deep-basement pipes. HTN pressure tunnels down into the brain's core: putamen, thalamus, pons, cerebellum. The cortex is upstairs, safe. Amyloid angiopathy is the upstairs tenant. If the bleed is in the cortex, HTN is not your answer.

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Why is CT bright white (hyperdense) for hemorrhage but dark for ischemic stroke?

Blood clot = dense protein (hemoglobin) = stops X-rays = white on CT. Think of it like a lead apron on the beam. Ischemic stroke = water-swollen tissue = low density = dark. Hyperdense is your red flag for bleeding. You never need contrast to spot fresh blood. Hyperdense = it just happened.

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Why is angiography always negative for Charcot-Bouchard?

These microaneurysms are 50-200 microns wide. A human hair is 70 microns. Angiography resolves down to about 1-2 millimeters. You are trying to see a single hair strand with a camera designed for ropes. A negative angiogram in an elderly hypertensive with a deep bleed is NOT reassuring. It confirms the diagnosis. The absence of a visible aneurysm IS the finding.

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What is lipohyalinosis and why does it matter?

Lipohyalinosis is what chronic HTN does to small arteries: smooth muscle dies and is replaced by hyaline fibrous material. The wall goes from elastic rubber to brittle glass. A rubber pipe stretches under pressure. A glass pipe cracks. Same pathology causes both lacunar infarcts (vessel occludes) and Charcot-Bouchard hemorrhage (vessel ruptures). Same cause, two endings.

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Berry aneurysm vs Charcot-Bouchard: one sentence each

Berry = saccular, circle of Willis, subarachnoid blood, worst headache of life, angiography positive. Charcot-Bouchard = microaneurysm, deep penetrating arteries, parenchymal blood, chronic HTN, angiography negative. Big junction vessels = big, visible aneurysm = subarachnoid. End arteries = small, deep, invisible microaneurysm = parenchymal. Opposite ends of the vascular tree.

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Clinical Images