# Stroke Localization Chart for USMLE by Artery

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

One chart for every stroke territory, the five lacunar syndromes, brainstem crossed findings and the 2026 AHA/ASA treatment windows, tuned to how USMLE stems hide the clue.

Localize a stroke in two steps. First, cortical signs (aphasia, neglect, gaze deviation or a homonymous field cut) mean a cortical branch; pure motor or pure sensory loss means a lacune in the internal capsule, pons or thalamus. Then map the deficit: face and arm to MCA, leg to ACA, vision to PCA, crossed face-body findings to brainstem.

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

Start with the question that removes the most answer choices: is the cortex involved? Language, attention, voluntary gaze and conscious vision are cortical functions, so aphasia, hemineglect, a gaze preference toward the lesion or a homonymous hemianopia implicates a cortical branch of the MCA, ACA or PCA. A field cut can also arise deeper, in the optic tract or lateral geniculate body, as in the anterior choroidal artery syndrome.

Weakness alone or numbness alone, with those four functions intact, points to a small penetrating artery. The body map then narrows the territory: the leg area of the motor and sensory cortex lies on the medial surface of the hemisphere, fed by the ACA, and the face and arm areas sit on the lateral convexity, fed by the MCA.

Finally, apply the crossed-findings rule: a cranial nerve deficit on one side with body weakness or sensory loss on the other places the lesion in the brainstem, on the side of the cranial nerve finding. More neurology guides are collected on the [Neurology](/topics/neurology) hub.

## Stroke localization chart: artery, territory, deficits and exam clue

The chart lists each artery with the tissue it feeds, the deficit its occlusion causes and the clue a vignette usually plants. Body findings are contralateral to the lesion unless marked ipsilateral.

| Artery | Territory | Deficits | Classic exam clue |
| --- | --- | --- | --- |
| ACA | Medial frontal and parietal lobes | Leg-predominant weakness and sensory loss; apathy, urinary incontinence, grasp reflex | Leg weaker than arm, plus apathy or incontinence |
| MCA superior division | Lateral frontal and anterior parietal lobes, Broca area | Face and arm weakness and sensory loss; Broca aphasia if dominant; gaze toward the lesion | Effortful, halting speech with good comprehension |
| MCA inferior division | Lateral temporal and inferior parietal lobes, Wernicke area | Wernicke aphasia if dominant, visuospatial deficits if nondominant; superior quadrantanopia or hemianopia; strength often spared | Fluent, meaningless speech with near-normal strength |
| MCA stem (M1) | Whole MCA territory, cortical and deep | Hemiplegia, hemisensory loss, homonymous hemianopia, gaze deviation; global aphasia if dominant, neglect if nondominant | Whole-side deficit: large-vessel occlusion |
| Lenticulostriate arteries | Putamen, globus pallidus, internal capsule | Pure motor hemiparesis; hypertensive putaminal hemorrhage | Hypertension or diabetes with no cortical signs |
| Anterior choroidal (from ICA) | Posterior limb of internal capsule, optic tract, lateral geniculate body, medial temporal lobe | Hemiparesis, hemisensory loss and homonymous hemianopia | Motor, sensory and field loss from one deep infarct |
| PCA | Occipital lobe, inferomedial temporal lobe, thalamus, midbrain | Homonymous hemianopia with macular sparing; alexia without agraphia (left PCA); memory loss; deep branches: thalamic sensory loss, CN III palsy | Isolated field cut with full strength |
| Basilar | Pons on both sides, midbrain, cerebellum, occipital lobes | Quadriplegia and loss of speech with intact awareness, blinking and vertical gaze (locked-in); coma or death with extensive infarction | Awake patient who answers only by blinking or looking up |
| AICA | Lateral pons, middle cerebellar peduncle, inner ear | Ipsilateral facial paralysis, hearing loss, vertigo, nystagmus, ataxia; body pain and temperature loss | Sudden one-sided deafness with facial droop |
| PICA or vertebral | Lateral medulla, inferior cerebellum | Ipsilateral facial pain and temperature loss, Horner syndrome, dysphagia, hoarseness, ataxia; vertigo, vomiting, hiccups; body pain and temperature loss | Crossed sensory loss with hoarseness and dysphagia |
| Anterior spinal (vertebral branches) | Medial medulla: pyramid, medial lemniscus, hypoglossal fibers | Arm and leg weakness, loss of vibration and position sense; ipsilateral tongue weakness | Tongue deviates toward the lesion, away from the weak limbs |
| Watershed (border zones) | Strips between ACA, MCA and PCA territories | Proximal arm weakness sparing the face (ACA-MCA zone); after global hypoperfusion, weakness of both arms with strong legs ("man in a barrel"); transcortical aphasias | After cardiac arrest, profound hypotension or severe carotid stenosis |

## Why each deficit points to one artery

Emboli from atrial fibrillation or a carotid plaque most often reach the MCA, the territory most commonly affected, and embolic deficits are usually maximal within minutes, whereas atherothrombotic strokes can evolve over 24 to 48 hours. Lacunes arise when lipohyalinosis closes a single penetrating artery, so they cluster in patients with hypertension and diabetes. Watershed infarcts form where two territories meet and perfusion is lowest, after hypotension or behind a tight stenosis.

The brainstem follows a medial-lateral rule. Near the midline run the corticospinal tract, the medial lemniscus and the motor nuclei of cranial nerves III, IV, VI and XII; laterally run the spinothalamic tract, spinal trigeminal nucleus, descending sympathetic fibers, vestibular nuclei and cerebellar peduncles. The cranial nerve gives the level: III and IV for the midbrain, V through VIII for the pons, IX, X and XII for the medulla.

## Cortical signs that rule out a lacune

Aphasia, neglect and higher visual deficits each have a fixed address. Language sits in the dominant hemisphere, the left in most people, and spatial attention in the nondominant parietal lobe.

| Sign | Lesion | Usual artery |
| --- | --- | --- |
| Nonfluent (Broca) aphasia: comprehension good, repetition impaired | Dominant frontal cortex including Broca area | MCA superior division |
| Fluent (Wernicke) aphasia: comprehension and repetition impaired | Dominant temporoparietal cortex including Wernicke area | MCA inferior division |
| Conduction aphasia: repetition impaired, comprehension good | Dominant white matter under the superior temporal gyrus or inferior parietal lobe | MCA |
| Gerstmann syndrome: agraphia, acalculia, finger agnosia, left-right disorientation | Dominant angular gyrus | MCA |
| Hemineglect, anosognosia, dressing apraxia | Nondominant parietal lobe | Nondominant MCA |
| Alexia without agraphia | Left occipital lobe plus splenium of the corpus callosum | Left PCA |
| Cortical blindness, sometimes unrecognized by the patient (Anton syndrome) | Both occipital lobes | Both PCAs |

Preserved repetition marks the transcortical aphasias, whose lesions spare the Broca and Wernicke areas. In alexia without agraphia the patient writes from dictation but cannot read it back, usually with a right homonymous hemianopia.

Gaze deviation needs a direction check. A destructive hemispheric lesion pulls the eyes toward the lesion, away from the weak side, whereas a pontine lesion abolishes horizontal gaze toward its own side, so the eyes rest toward the weak limbs.

## Pure motor stroke localization and the five lacunar syndromes

A pure motor stroke localizes to a lacune in the posterior limb of the internal capsule, the basis pontis or the corona radiata, and pure motor hemiparesis accounts for roughly 45% of lacunar strokes. Lacunes are deep infarcts of 1.5 cm or less in the basal ganglia, internal capsule, thalamus and pons, defined by what is missing: no aphasia, neglect, gaze preference or field cut.

| Lacunar syndrome | Usual lesion site | Contralateral findings | What is absent |
| --- | --- | --- | --- |
| Pure motor hemiparesis (most common) | Posterior limb of internal capsule, basis pontis, corona radiata | Weakness of face, arm and leg | Sensory loss and cortical signs |
| Pure sensory stroke | Thalamus: VPL for the body, VPM for the face | Numbness of face, arm and leg | Weakness |
| Ataxic hemiparesis | Posterior limb of internal capsule, basis pontis, corona radiata | Weakness with same-side limb ataxia out of proportion to it | Cortical signs |
| Dysarthria-clumsy hand | Basis pontis, genu or anterior limb of internal capsule, corona radiata | Dysarthria, facial weakness, a clumsy hand | Aphasia; language is intact |
| Sensorimotor stroke | Thalamus plus the adjacent internal capsule | Weakness and numbness together | Cortical signs |

Corticospinal fibers converge in the posterior limb, so an infarct a few millimeters wide can cause dense hemiplegia, and the size of the deficit tempts students toward an MCA occlusion. Early CT often looks normal; diffusion-weighted MRI shows the infarct.

## Brainstem syndromes and the crossed-findings rule

Classic brainstem syndromes pair an ipsilateral cranial nerve sign, which gives the level and side, with a contralateral long-tract sign; locked-in syndrome is the bilateral exception.

| Syndrome and level | Artery | Ipsilateral findings | Contralateral findings |
| --- | --- | --- | --- |
| Weber (medial midbrain) | PCA paramedian branches | CN III palsy: ptosis, eye down and out | Hemiparesis |
| Benedikt (midbrain tegmentum) | PCA or basilar paramedian branches | CN III palsy | Tremor or ataxia from red nucleus damage |
| Medial pontine | Basilar paramedian branches | Abducens or horizontal gaze palsy | Hemiparesis |
| Lateral pontine | AICA | Facial paralysis, hearing loss, vertigo, nystagmus, ataxia | Body pain and temperature loss |
| Locked-in (ventral pons, both sides) | Basilar | Facial, bulbar and horizontal gaze paralysis on both sides | Quadriplegia; vertical gaze and blinking spared |
| Medial medullary | Anterior spinal or vertebral | Tongue weakness; tongue deviates toward the lesion | Hemiparesis; loss of vibration and position sense |
| Lateral medullary (Wallenberg) | Vertebral or PICA | Facial pain and temperature loss, Horner syndrome, hoarseness, dysphagia, ataxia | Body pain and temperature loss |

NINDS lists vertebral artery as well as PICA blockage as causes of lateral medullary syndrome, so "vertebral artery" can be the right answer. Its hoarseness and dysphagia come from the nucleus ambiguus.

## Ischemic or hemorrhagic: imaging decides

No bedside sign reliably separates ischemia from hemorrhage, so every suspected stroke gets immediate imaging, usually a non-contrast CT to exclude blood, plus a fingerstick glucose. Sudden headache, vomiting, early loss of consciousness and seizures favor hemorrhage, but small bleeds can mimic ischemia. Early ischemic changes on CT are subtle, whereas diffusion-weighted MRI detects ischemia earlier and more accurately. CT or MR angiography looks for a large-vessel occlusion, and ECG monitoring, echocardiography and carotid imaging look for the source.

## Acute ischemic stroke treatment windows under the 2026 AHA/ASA guideline

The 2026 AHA/ASA acute ischemic stroke guideline, published on 26 January 2026, replaced the 2018 guideline and its 2019 update.

- **Thrombolysis up to 4.5 hours:** alteplase 0.9 mg/kg (maximum 90 mg) or tenecteplase 0.25 mg/kg (maximum 25 mg) within 4.5 hours of onset or last known well for a disabling deficit, without waiting for advanced imaging. Both US drug labels still specify 3 hours, and older teaching framed the window as 3 hours, extended to 4.5 in selected patients.
- **Later or unknown onset:** thrombolysis may be reasonable at 4.5 to 9 hours from last known well, or on waking within 9 hours of the midpoint of sleep, when automated perfusion imaging shows salvageable penumbra; with unknown onset, an MRI DWI-FLAIR mismatch can select patients for treatment within 4.5 hours of symptom recognition.
- **Non-disabling deficits:** dual antiplatelet therapy (aspirin plus clopidogrel, 21 days in minor noncardioembolic stroke) is preferred over thrombolysis.
- **Thrombectomy:** standard for ICA or M1 occlusion within 6 hours; selected patients qualify up to 24 hours on imaging, including some large core infarcts, as does basilar occlusion within 24 hours with an NIHSS score of 10 or more. Thrombectomy is not recommended for medium or distal branch occlusions (nondominant M2, distal MCA, ACA or PCA).
- **Blood pressure:** under 185/110 before thrombolysis and under 180/105 for 24 hours after; a systolic target under 140 after thrombolysis or successful thrombectomy is not recommended. Without reperfusion therapy, lowering pressure that is below 220/120 in the first 48 to 72 hours does not improve outcomes.
- **Glucose and aspirin:** treat glucose below 60 mg/dL, avoid intensive insulin aimed at 80 to 130 mg/dL, and start aspirin within 48 hours of onset; the safety of antiplatelet drugs in the first 24 hours after thrombolysis is uncertain.

## Where hemorrhages sit: hypertensive bleeds, amyloid and aneurysms

Hypertensive intracerebral hemorrhage comes from rupture of Charcot-Bouchard microaneurysms on the small perforating arteries that also cause lacunes. The putamen is the most common site; the thalamus, pons and cerebellum are the other classic ones. Pontine bleeds cause coma with pinpoint pupils, and a cerebellar hematoma over 3 cm can compress the brainstem, so surgical evacuation is often lifesaving. A lobar bleed in an older adult suggests cerebral amyloid angiopathy. Systolic pressure between 150 and 220 is lowered toward 140, and anticoagulants are reversed.

A thunderclap "worst headache of life" peaking within seconds is subarachnoid hemorrhage until proven otherwise; about 85% of nontraumatic cases come from a ruptured saccular (berry) aneurysm, and polycystic kidney disease raises aneurysm risk. CT is very sensitive within 6 hours; if it is negative and suspicion persists, lumbar puncture looks for xanthochromia. Nimodipine is given to prevent vasospasm, whose risk peaks between about 72 hours and 10 days. Neck stiffness overlaps with [bacterial, viral and fungal meningitis](/blog/meningitis-bacterial-viral-fungal-usmle), but the seconds-to-peak onset separates them.

## Stroke mimics to exclude

Hypoglycemia can reproduce a focal deficit, which is why bedside glucose is mandatory in every stroke evaluation. The other common mimics are postictal (Todd) weakness after a seizure, covered in [seizure classification and antiepileptic drugs](/blog/seizure-classification-antiepileptic-drugs-usmle), hemiplegic migraine, CNS infection and functional neurologic disorder, a diagnosis of exclusion.

> **10-second localization check:** 1) Aphasia, neglect or gaze toward the lesion: cortical MCA. 2) Leg worse than arm: ACA. 3) Field cut with full strength: PCA. 4) Cranial nerve on one side, body on the other: brainstem. 5) Hoarseness and dysphagia: PICA or vertebral; deafness and facial palsy: AICA; tongue toward the lesion: medial medulla. 6) Pure motor or pure sensory, nothing cortical: lacune. 7) Thunderclap headache or early coma: image for blood first.

## How USMLE tests stroke localization

Most stems hide one discriminating clause and ask for the artery, the syndrome or the next step.

- **Atrial fibrillation, right face and arm weakness, effortful speech with good comprehension:** embolus to the left MCA superior division.
- **Leg weakness, urinary incontinence and apathy:** contralateral ACA.
- **Left ptosis with the left eye down and out, right hemiparesis:** left Weber syndrome in the midbrain.
- **Weakness of both proximal arms, with a normal face and legs, after cardiac arrest:** bilateral ACA-MCA watershed infarction ("man in a barrel").

## Worked vignette: pure motor stroke

A 70-year-old woman with long-standing hypertension and type 2 diabetes wakes with weakness of her left face, arm and leg. She names objects, repeats phrases and follows commands normally, attends to both sides of space, and has normal sensation, visual fields and eye movements. Non-contrast CT shows no hemorrhage. Where is the lesion most likely located?

- A. Right MCA superior division cortex
- B. Right posterior limb of the internal capsule
- C. Right ventral posterolateral (VPL) thalamus
- D. Left basis pontis
- E. Right lateral medulla

**Answer: B.** A face-arm-leg hemiparesis with no aphasia, neglect, gaze preference, sensory loss or field cut is pure motor hemiparesis, the most common lacunar syndrome, and her hypertension and diabetes fit lipohyalinosis of a lenticulostriate branch. A right superior division MCA stroke (A) would usually add face and arm sensory loss or a gaze preference toward the lesion, and would weaken the face and arm more than the leg. A VPL lacune (C) causes pure sensory loss. A basis pontis lacune can cause pure motor hemiparesis, but a left-sided one (D) would weaken the right side. The lateral medulla (E) produces crossed pain and temperature loss, not isolated hemiparesis.

Because she woke with the deficit, her last known well time is bedtime; if that was more than 4.5 hours ago, thrombolysis would need advanced imaging selection, such as an MRI DWI-FLAIR mismatch.

## Common wrong-answer traps

- **Calling every hemiparesis an MCA stroke.** Without aphasia, neglect, gaze preference or a field cut, a face-arm-leg deficit is a capsular or pontine lacune.
- **Reading gaze deviation backward.** Hemispheric lesions drive the eyes toward the lesion; pontine lesions leave them looking toward the weak side.
- **Sending the tongue the wrong way.** In medial medullary syndrome the tongue deviates toward the lesion, opposite the weak limbs.
- **Naming PICA when the stem gives deafness and facial paralysis.** That is AICA; hoarseness and dysphagia mark PICA or the vertebral artery.
- **Stopping thrombolysis at 3 hours.** Current guidance treats disabling deficits up to 4.5 hours, and imaging can select some later patients.
- **Lowering blood pressure in every ischemic stroke.** Without reperfusion therapy, pressure below 220/120 is left alone early; after thrombolysis it is held under 180/105.

## Sources

- AHA/ASA: [2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke](https://professional.heart.org/en/science-news/2026-guideline-for-the-early-management-of-patients-with-acute-ischemic-stroke), [top things to know](https://professional.heart.org/en/science-news/2026-guideline-for-the-early-management-of-patients-with-acute-ischemic-stroke/top-things-to-know), [guideline record (PubMed)](https://pubmed.ncbi.nlm.nih.gov/41582814/)
- StatPearls (NCBI Bookshelf): [Ischemic stroke](https://www.ncbi.nlm.nih.gov/books/NBK499997/), [Acute stroke](https://www.ncbi.nlm.nih.gov/books/NBK535369/), [Lacunar stroke](https://www.ncbi.nlm.nih.gov/books/NBK563216/), [Brainstem stroke](https://www.ncbi.nlm.nih.gov/books/NBK560896/), [Man in a barrel syndrome](https://www.ncbi.nlm.nih.gov/books/NBK559186/)
- NINDS: [stroke assessment and treatment](https://www.ninds.nih.gov/health-information/stroke/assess-and-treat), [lateral medullary syndrome](https://www.ninds.nih.gov/health-information/disorders/wallenbergs-syndrome), [locked-in syndrome](https://www.ninds.nih.gov/health-information/disorders/locked-syndrome)

Make territory, syndrome and next step arrive together on test day: [Practice stroke localization questions on StepGenie](https://dashboard.stepgenie.app/sign-up).

## Frequently asked questions

### Where is the lesion in a pure motor stroke?

A pure motor stroke is usually a lacunar infarct in the posterior limb of the internal capsule, the basis pontis or the corona radiata. It weakens the face, arm and leg on the opposite side without sensory loss, aphasia, neglect or a visual field cut. Pure motor hemiparesis is the most common lacunar syndrome, roughly 45% of lacunar strokes, and reflects lipohyalinosis of a small penetrating artery in patients with hypertension or diabetes.

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

Stem and superior-division MCA strokes weaken and numb the opposite face and arm more than the leg and push the eyes toward the side of the lesion. A dominant-hemisphere stroke adds aphasia: nonfluent Broca aphasia with superior-division occlusion, fluent Wernicke aphasia with inferior-division occlusion and global aphasia when the stem is blocked. A nondominant stroke adds hemineglect and anosognosia, and inferior-division strokes, which often spare strength, add a superior quadrantanopia or hemianopia.

### How do PICA and AICA strokes differ?

Both cause vertigo, nystagmus, ipsilateral limb ataxia and loss of pain and temperature sensation on the opposite side of the body. PICA or vertebral occlusion infarcts the lateral medulla, so hoarseness, dysphagia and a weak gag from the nucleus ambiguus set it apart, usually with an ipsilateral Horner syndrome. AICA infarcts the lateral pons and inner ear, so ipsilateral facial paralysis and sudden one-sided hearing loss set it apart.

### How do you tell a medial from a lateral brainstem stroke?

Medial brainstem strokes damage midline structures, so they cause contralateral hemiparesis plus an ipsilateral motor cranial nerve palsy: CN III in Weber syndrome, CN VI or horizontal gaze in medial pontine syndrome and CN XII in medial medullary syndrome, where the tongue deviates toward the lesion. Lateral strokes damage sensory, sympathetic, vestibular and cerebellar pathways, giving contralateral body pain and temperature loss, vertigo and ataxia, with Horner syndrome in the lateral medullary syndrome.

### What are the current time windows for stroke thrombolysis and thrombectomy?

Under the 2026 AHA/ASA guideline, alteplase or tenecteplase is recommended within 4.5 hours of onset or last known well for a disabling deficit, and selected patients at 4.5 to 9 hours or with unknown onset may be treated when advanced imaging, such as a perfusion or MRI DWI-FLAIR mismatch, supports it. Thrombectomy is standard for ICA or M1 occlusion within 6 hours and extends to 24 hours in selected patients, including basilar occlusion with an NIHSS score of 10 or more.

---

Canonical page: [Stroke Localization Chart for USMLE by Artery](https://www.stepgenie.app/blog/stroke-localization-usmle)
Topic hub: [Neurology](https://www.stepgenie.app/topics/neurology)