# Stroke Localization by Artery (USMLE)

> How do you identify the affected artery from stroke symptoms?

A two-step method for stroke vignettes: separate cortical from lacunar findings, then match the deficit to its vascular territory.

Localize a stroke in two steps. First ask whether cortical signs are present: aphasia, neglect, gaze preference or a homonymous field cut means a cortical branch, while a pure motor or pure sensory deficit means a small deep vessel. Then match the pattern to a territory: face and arm for MCA, leg for ACA, vision for PCA.

## How do you identify the affected artery from stroke symptoms?

**Cortical versus subcortical comes first because it halves the answer choices.** Cortex generates language, attention, gaze and vision, so any of those findings means a cortical branch. A purely motor or purely sensory deficit sparing all four means a deep perforator.

**The territory then follows the homunculus.** The medial hemisphere carries the leg, so ACA occlusion gives leg-predominant weakness; the lateral convexity carries face and arm. **Crossed findings localize to the brainstem and nothing else does:** ipsilateral cranial nerve findings with contralateral body findings put you in the midbrain, pons or medulla. [Neurology](/topics/neurology) rewards the same anatomy-first order.

## The artery-to-deficit map

| Artery | Brain Region | Classic Deficits | Board-Tested Clue |
| --- | --- | --- | --- |
| **MCA, dominant (left)** | Lateral frontoparietal cortex | Contralateral face and arm weakness, aphasia, gaze toward lesion | Face and arm worse than leg, plus aphasia |
| **MCA, non-dominant** | Right parietal cortex | Hemineglect, anosognosia, apraxia, same motor pattern | Patient ignores and denies the left side |
| **ACA** | Medial frontal cortex | Contralateral leg weakness, abulia, incontinence | Leg worse than arm, plus personality change |
| **PCA** | Occipital cortex, splenium, thalamus | Homonymous hemianopia with macular sparing, alexia without agraphia | Isolated field cut with full strength |
| **Basilar** | Ventral pons, corticospinal tracts | Quadriplegia, bulbar palsy, preserved awareness and vertical gaze | Locked-in: blinking and upgaze only |
| **PICA (lateral medullary)** | Lateral medulla | Ipsilateral facial pain/temperature loss, Horner, dysphagia, hoarseness, ataxia; contralateral body loss | Crossed sensory loss with a hoarse voice |
| **AICA (lateral pontine)** | Lateral pons, inner ear | Ipsilateral facial palsy, deafness, vertigo, Horner, ataxia; contralateral body loss | Sudden deafness with facial droop |
| **Lenticulostriate** | Putamen, internal capsule | Pure motor hemiparesis of face, arm and leg | Long-standing hypertension, normal CT |
| **Anterior choroidal** | Internal capsule posterior limb, optic tract | Hemiplegia, hemianesthesia and hemianopia together | Three deficits, no aphasia or neglect |

## Cortical signs versus a deep, silent capsule

**Four findings prove cortical involvement:** aphasia from dominant perisylvian cortex, hemineglect from the non-dominant parietal lobe, gaze preference toward the lesion from the frontal eye field, and hemianopia from the optic radiations. Any one excludes a lacune, except an anterior choroidal field cut.

**The internal capsule and thalamus have no cortex to lose.** Corticospinal fibers pack into the posterior limb, so a millimeter-wide lesion gives dense hemiplegia with normal language, attention and vision. A VPL thalamic lesion mirrors it: dense numbness, full strength.

## The five lacunar syndromes

| Lacunar Syndrome | Lesion Site | Findings | Absent Findings |
| --- | --- | --- | --- |
| **Pure motor hemiparesis** (most common) | Posterior limb or basis pontis | Face, arm and leg weakness in equal proportion | No sensory or cortical signs |
| **Pure sensory stroke** | VPL thalamus | Contralateral numbness of face, arm and leg | No weakness |
| **Ataxic hemiparesis** | Posterior limb, corona radiata or basis pontis | Leg-predominant weakness with ataxia out of proportion to it | No vertigo or sensory loss |
| **Dysarthria-clumsy hand** | Basis pontis or capsular genu | Slurred speech, facial weakness, clumsy fine motor control of one hand | No aphasia |
| **Sensorimotor stroke** | Thalamus plus posterior limb | Contralateral weakness and numbness together | No cortical signs |

**Lacunes come from lipohyalinosis of penetrating arteries**, so the stem carries a small-vessel profile: poorly controlled hypertension, plus diabetes, smoking and hyperlipidemia. Expect a normal early CT and a punctate infarct on diffusion-weighted MRI.

## Ischemic or hemorrhagic, and the first hour

**Headache, vomiting, depressed consciousness, seizure at onset and very high blood pressure favor hemorrhage**, while a deficit maximal at onset and confined to one territory favors ischemia. Neither is reliable enough to act on, so **non-contrast head CT is the first imaging step in every suspected stroke**, excluding blood before thrombolysis.

Thrombolysis is given within **4.5 hours of last known well**, and thrombectomy for large-vessel occlusion within **6 hours**, extended to **24 hours** in selected patients with favorable perfusion imaging. Pressure must be under 185/110 before thrombolysis and under 180/105 for 24 hours after. Otherwise permissive hypertension rules: leave pressure alone below 220/120. Intracerebral hemorrhage reverses the target, lowering systolic pressure toward 140 and reversing anticoagulation.

## Where hypertensive bleeds and aneurysms sit

**Hypertensive bleeds rupture Charcot-Bouchard microaneurysms on the same lenticulostriate vessels that cause lacunes.** The putamen is the most common site, then thalamus, pons and cerebellum. Putaminal bleeds give hemiplegia with eyes toward the lesion; thalamic bleeds hemisensory loss with eyes down and inward; pontine bleeds coma with pinpoint reactive pupils; cerebellar bleeds occipital headache, vomiting and inability to walk without hemiparesis, a surgical emergency from brainstem compression. A lobar bleed in an elderly normotensive is amyloid angiopathy.

**Thunderclap "worst headache of life" with nuchal rigidity is subarachnoid hemorrhage from a ruptured berry aneurysm**, most often at the anterior communicating artery and linked to polycystic kidney disease. A negative CT is followed by lumbar puncture showing xanthochromia, and nimodipine prevents vasospasm peaking days 7 to 10. The neck stiffness overlaps with [bacterial, viral and fungal meningitis](/blog/meningitis-bacterial-viral-fungal-usmle), separated by the abrupt onset.

## Stroke mimics you must exclude

**Fingerstick glucose is mandatory in every stroke code because hypoglycemia reproduces focal deficits** and reverses with dextrose. **Todd paralysis** is focal weakness after a convulsion, clearing over hours, so a witnessed seizure changes the differential, as in [seizure classification and antiepileptic drugs](/blog/seizure-classification-antiepileptic-drugs-usmle). **Complex or hemiplegic migraine** builds over minutes with positive visual phenomena in a young patient with prior attacks. **Conversion disorder** gives non-anatomic weakness with a positive Hoover sign.

## The 10-second localization decision tree

> **Exam-day cheat sheet.** 1) Aphasia or neglect -> cortical MCA. 2) Leg worse than arm -> ACA. 3) Isolated field cut -> PCA. 4) Crossed face-versus-body findings -> brainstem: hoarseness and dysphagia = PICA, deafness and facial palsy = AICA. 5) Pure motor or pure sensory with normal cortex -> lacune. 6) Thunderclap headache or coma with vomiting -> CT for blood.

## How stroke localization is tested in vignettes

**A 68-year-old in atrial fibrillation has right face and arm weakness and cannot name objects.** Answer a cardioembolic left MCA occlusion.

**A hypertensive man has vertigo, hoarseness, right facial numbness, left body numbness and a right Horner syndrome.** Answer right PICA occlusion: lateral medullary syndrome.

**A 72-year-old hypertensive has dense left face, arm and leg weakness with normal speech, sensation and fields.** Answer a lacunar infarct of the internal capsule's posterior limb.

## Common wrong-answer traps

**Trap: calling any hemiparesis an MCA stroke.** Without aphasia, neglect, gaze preference or a field cut, a proportionate face-arm-leg deficit is a capsular lacune.

**Trap: reading gaze deviation backward.** Cortical frontal eye field strokes drive the eyes toward the lesion, away from the weak side; a pontine lesion reverses this.

**Trap: lowering blood pressure in every stroke.** Without thrombolysis, ischemic pressure is left alone below 220/120 to preserve penumbral perfusion; hemorrhage is actively lowered.

## Sources

- [NINDS stroke information](https://www.ninds.nih.gov/health-information/disorders/stroke)
- [AAN clinical practice guidelines](https://www.aan.com/practice/guidelines)
- [USMLE Step 2 CK outline](https://www.usmle.org/step-exams/step-2-ck)

Localization is built by repetition against stems that hide the clue in one clause. [Practice stroke localization questions on StepGenie](https://dashboard.stepgenie.app/sign-up) until territory, syndrome and next step arrive together.

## Frequently asked questions

### How do you tell a cortical stroke from a lacunar stroke?

Cortical strokes produce at least one of four findings: aphasia, hemineglect, conjugate gaze preference toward the lesion, or a homonymous visual field cut. Lacunar strokes spare all four because the infarct sits in the internal capsule, thalamus or pons, well below cortex. A dense hemiparesis with completely normal language, attention and vision is therefore a lacune, not a middle cerebral artery occlusion.

### What are the classic signs of a middle cerebral artery stroke?

MCA occlusion causes contralateral weakness and sensory loss in which the face and arm are affected more than the leg, plus conjugate gaze preference toward the side of the lesion and a contralateral homonymous hemianopia. A dominant, usually left, hemisphere lesion adds aphasia; a non-dominant lesion adds hemineglect and anosognosia, with the patient ignoring or denying the affected left side.

### How do PICA and AICA strokes differ?

Both produce crossed sensory loss, meaning ipsilateral facial and contralateral body loss of pain and temperature, along with vertigo, ataxia and Horner syndrome. PICA infarcts the lateral medulla, so the distinguishing features are dysphagia and hoarseness from the nucleus ambiguus. AICA infarcts the lateral pons and the inner ear, so the distinguishing features are ipsilateral facial paralysis and sudden ipsilateral deafness.

### What is the time window for thrombolysis and thrombectomy in stroke?

Intravenous thrombolysis is given within 4.5 hours of the time the patient was last known well, after a non-contrast head CT excludes hemorrhage and blood pressure is brought under 185/110. Mechanical thrombectomy for a large-vessel occlusion is performed within 6 hours, and can extend to 24 hours in selected patients whose perfusion imaging shows salvageable tissue.

### Where do hypertensive intracerebral hemorrhages occur most often?

Hypertensive bleeds rupture Charcot-Bouchard microaneurysms on the deep penetrating arteries. The putamen is the most common site, followed by the thalamus, pons and cerebellum. Putaminal bleeds cause hemiplegia with the eyes deviated toward the lesion, pontine bleeds cause coma with pinpoint reactive pupils, and cerebellar bleeds cause headache, vomiting and inability to walk, requiring urgent surgical evaluation.

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