Middle cerebral artery (MCA) syndrome is an infarct of the lateral surface of one hemisphere: contralateral weakness and sensory loss of the face and arm, worse than the leg, a contralateral homonymous visual field defect and, early on, eyes deviated toward the side of the lesion. The hemisphere decides the cortical sign: a dominant (usually left) MCA stroke causes aphasia, and a nondominant (usually right) MCA stroke causes hemineglect and anosognosia. The superior division carries the weakness and Broca aphasia; the inferior division carries Wernicke aphasia or neglect with a field cut and little weakness.
MCA anatomy behind every finding
- Stem and divisions: the MCA is a terminal branch of the internal carotid artery. Its first segment (M1) gives off the lenticulostriate arteries to the basal ganglia and internal capsule, then splits into superior and inferior divisions.
- Cortical territory: almost the entire lateral convexity of the frontal, parietal and temporal lobes, plus the insula. The medial frontal and parietal cortex belongs to the ACA; most of the occipital lobe belongs to the PCA.
- Homunculus: the face, arm and hand areas sit on the lateral convexity, so they take the hit. The leg area sits on the medial surface (ACA territory) and is relatively spared.
- What else lives there: Broca area (posterior inferior frontal lobe), Wernicke area (posterior superior temporal lobe), the frontal eye field and the optic radiations.
- How common: MCA occlusion is the most common anterior circulation stroke. Exam stems usually hand you the embolic source: atrial fibrillation or carotid atherosclerosis.
- Textbook vs real anatomy: the classic teaching sends the superior division to the frontal lobe and the inferior division to the temporal lobe, with the parietal lobe going to either. Real branching varies, so stems describe a deficit pattern rather than a named branch.
Superior vs inferior division vs M1
| Feature | Superior division | Inferior division | M1 stem (whole MCA) |
|---|---|---|---|
| Cortex lost | Lateral frontal lobe and adjacent anterior parietal lobe: face and arm motor and sensory cortex, frontal eye field, Broca area | Temporal and inferior parietal lobe: Wernicke area, angular gyrus, Meyer loop | Entire convexity plus the deep lenticulostriate territory |
| Weakness | Contralateral face and arm > leg | Little or none | Dense hemiplegia; capsular infarction adds the leg |
| Dominant side | Broca aphasia: nonfluent and effortful, comprehension relatively spared, patient aware and frustrated | Wernicke aphasia: fluent but empty speech, poor comprehension, patient unaware of errors | Global aphasia |
| Nondominant side | Face and arm weakness, dysarthria | Hemineglect, anosognosia, apraxia for tasks like dressing | Hemiplegia with neglect and anosognosia |
| Vision | Usually spared | Contralateral superior quadrantanopia (Meyer loop) or hemianopia | Contralateral homonymous hemianopia |
| Stem giveaway | "Her right arm won't work and she can't get the words out" | "Talks nonstop in nonsense, strength normal" | "Can't speak, understand or move the right side" |
A strength-sparing inferior-division stroke is the one students miss: a fluent, confused-sounding patient with normal power still has a stroke, and the right upper quadrant field cut is the tell.
Dominant vs nondominant: aphasia or neglect
Language sits in the left hemisphere in right-handed people and in about two-thirds of left-handed people, so "dominant" nearly always means left.
| Finding | Dominant (usually left) MCA | Nondominant (usually right) MCA |
|---|---|---|
| Weakness and numbness | Right face and arm > leg | Left face and arm > leg |
| Signature cortical sign | Aphasia: Broca, Wernicke or global | Left hemineglect: ignores people, food and text on the left |
| Insight | Broca: aware and frustrated; Wernicke: unaware | Anosognosia: may deny the left-sided paralysis |
| Parietal extras | Gerstmann syndrome (angular gyrus): agraphia, acalculia, finger agnosia, left-right disorientation; alexia | Apraxia for well-learned tasks such as dressing; poor drawing |
| Visual field | Right homonymous hemianopia or quadrantanopia | Left homonymous hemianopia or quadrantanopia |
| Eyes, acutely | Deviated to the left | Deviated to the right |
Why the eyes look toward the lesion
- The frontal eye field launches voluntary horizontal saccades to the opposite side. When an MCA stroke knocks it out, the patient cannot look away from the lesion, and the eyes rest toward the lesion, away from the weak limbs.
- It is an early sign: a deficit confined to the frontal eye field recovers with time.
- The pons flips the rule. A pontine stroke abolishes horizontal gaze toward the side of the lesion, so the eyes rest away from the lesion, toward the weak side, usually with crossed cranial nerve findings (review them with the brainstem syndromes mnemonic).
- Memory line: hemisphere, the eyes look at the lesion; pons, the eyes look at the weakness.
MCA vs ACA vs PCA vs lacunar stroke
| Feature | MCA | ACA | PCA | Lacunar infarct |
|---|---|---|---|---|
| Weakness | Face and arm > leg | Leg > arm, face spared | Usually none | Face = arm = leg (pure motor) |
| Cortical signs | Aphasia or neglect, gaze toward the lesion | Apathy, urinary incontinence, grasp reflex, gait apraxia | Memory loss | None: no aphasia, neglect or field cut |
| Vision | Hemianopia or quadrantanopia | Spared | Contralateral homonymous hemianopia, often with macular sparing | Spared |
| Extra clues | Embolic source such as atrial fibrillation | Confusion, poor judgment, mutism | Third nerve palsy or hemiballismus from deep branches | Hypertension or diabetes; lipohyalinosis; infarct 1.5 cm or smaller |
The leg-predominant pattern is dissected in the anterior cerebral artery syndrome breakdown, the isolated field cut in the posterior cerebral artery syndrome breakdown, and every territory side by side in stroke localization by artery.
Practice question
A 72-year-old woman with hypertension and atrial fibrillation, who stopped taking her anticoagulant 2 months ago, is brought to the emergency department after her daughter found her unable to use her left hand at breakfast; she was normal 1 hour earlier. She speaks fluently and follows commands. Her eyes rest deviated to the right, and she does not turn toward her daughter, who is standing on her left. She has a left lower facial droop, 1/5 strength in the left arm and 4/5 in the left leg, and reduced pinprick over the left face and arm. She insists her left arm is fine. Confrontation testing shows a left homonymous hemianopia. Noncontrast head CT shows no hemorrhage. Which artery is most likely occluded?
- A. Left middle cerebral artery
- B. Right anterior cerebral artery
- C. Right middle cerebral artery
- D. Right posterior cerebral artery
- E. Lenticulostriate branch to the right internal capsule
- F. Basilar artery perforators to the right pons
Answer: C, right MCA. Left face and arm weakness far worse than leg weakness, left face and arm numbness, left hemineglect, anosognosia, a left field cut and eyes deviated toward the right hemisphere all localize to the right lateral convexity. Atrial fibrillation without anticoagulation is the embolic source.
- A, left MCA: right-sided weakness, aphasia and eyes deviated to the left. Right territory, wrong side.
- B, right ACA: left leg weaker than arm with the face spared, plus incontinence and apathy. Her arm is far weaker than her leg and her face is involved.
- D, right PCA: explains the left hemianopia, but not the face and arm weakness, the neglect or the denial of weakness.
- E, lenticulostriate lacune: pure motor hemiparesis with face, arm and leg equally weak and no cortical signs. Neglect, anosognosia, a field cut and gaze deviation all mean cortex.
- F, right pontine perforators: left hemiparesis, but the eyes would rest to the left, toward the weak side, and the stem would usually carry crossed cranial nerve signs instead of neglect or a field cut.
Next step in the same patient: she is within 4.5 hours of last known well with no hemorrhage, so give IV thrombolysis if she has no contraindications, and get CT angiography to look for a large-vessel occlusion that qualifies for thrombectomy.
Change one detail
| If the stem shows instead... | Localize to |
|---|---|
| Right face and arm weakness, halting nonfluent speech, good comprehension, eyes to the left | Left MCA, superior division |
| Fluent but meaningless speech, poor comprehension, unaware of errors, right upper quadrant field loss, normal strength | Left MCA, inferior division |
| Global aphasia, dense right hemiplegia including the leg, right hemianopia, eyes to the left | Left MCA stem (M1) |
| Left neglect and left hemianopia with little or no weakness | Right MCA, inferior division |
| Agraphia, acalculia, finger agnosia and left-right confusion | Left angular gyrus (dominant parietal lobe) |
| Left leg weaker than arm, urinary incontinence, apathy | Right ACA |
| Left hemianopia with macular sparing and normal strength | Right PCA |
| Equal face, arm and leg weakness with no cortical signs in a patient with long-standing hypertension | Lacunar infarct |
Management clues that come with MCA stems
- Noncontrast CT first to exclude hemorrhage. Even a large MCA infarct can look subtle in the first hours; early signs include a dense MCA sign, loss of the insular ribbon and loss of the gray-white junction. Diffusion-weighted MRI is highly sensitive for early ischemia.
- IV thrombolysis with alteplase (tenecteplase is a reasonable alternative) within 4.5 hours of last known well if there are no contraindications.
- Mechanical thrombectomy for anterior circulation large-vessel occlusion within 6 hours, and in selected patients up to 16 hours (DEFUSE 3) or 24 hours (DAWN) when imaging shows a small infarct with salvageable brain or a large mismatch between infarct size and deficit. Give IV thrombolysis first if the patient qualifies. CT or MR angiography finds the occlusion.
- Malignant MCA infarction: severe edema raises intracranial pressure, and worsening consciousness in the first 48 to 72 hours is more often from edema than from infarct extension. Some centers perform emergency decompressive craniectomy.
- Secondary prevention for atrial fibrillation: anticoagulation, with a direct oral anticoagulant or warfarin (INR 2 to 3).
Key takeaways
- MCA = lateral convexity: contralateral face and arm > leg weakness and sensory loss, a homonymous field defect and eyes toward the lesion.
- A dominant (left) MCA stroke adds aphasia; a nondominant (right) MCA stroke adds hemineglect and anosognosia.
- Superior division: weakness plus Broca aphasia. Inferior division: Wernicke aphasia or neglect plus a field cut, often with little weakness. M1: all of it, including the leg.
- The eyes look toward a hemispheric lesion and away from a pontine one.
- Leg > arm is ACA, an isolated field cut is PCA, and face = arm = leg without cortical signs is a lacune.
- CT rules out hemorrhage; thrombolysis within 4.5 hours of last known well; vessel imaging and thrombectomy for large-vessel occlusion.
Sources
- Overview of Stroke — Merck Manual Professional Edition
- Ischemic Stroke — Merck Manual Professional Edition
- Aphasia — Merck Manual Professional Edition
- Overview of Cerebral Function — Merck Manual Professional Edition
- Conjugate Gaze Palsies — Merck Manual Professional Edition
- Aphasia — National Institute on Deafness and Other Communication Disorders (NIH)
- Anterior Circulation Stroke — Medscape Reference (2019)
- Ocular Motor Control — Neuroscience Online, McGovern Medical School at UTHealth
- Visual Processing: Cortical Pathways — Neuroscience Online, McGovern Medical School at UTHealth
- Middle Cerebral Artery — neuroangio.org
Frequently Asked Questions
What are the symptoms of a middle cerebral artery stroke?
An MCA stroke causes sudden weakness and numbness of the opposite face and arm, worse than the leg, often with a homonymous visual field defect, slurred speech and the eyes deviated toward the side of the lesion. A left (dominant) MCA stroke adds aphasia, while a right (nondominant) MCA stroke adds neglect of the left side and denial of the deficit.
What is the difference between a left and a right MCA stroke?
Both cause weakness and sensory loss of the opposite face and arm. A left MCA stroke hits the language-dominant hemisphere in most people, so it causes aphasia and sometimes Gerstmann syndrome (agraphia, acalculia, finger agnosia and left-right disorientation). A right MCA stroke causes left hemineglect, anosognosia and trouble with tasks such as dressing and drawing.
What is the difference between superior and inferior division MCA strokes?
In the classic teaching the superior division supplies the lateral frontal lobe and the adjacent sensorimotor cortex, so its occlusion causes contralateral face and arm weakness and sensory loss and, on the dominant side, nonfluent Broca aphasia. The inferior division supplies the temporal and inferior parietal lobe, so its occlusion causes fluent Wernicke aphasia (dominant side) or neglect (nondominant side) with a field cut and little or no weakness. Occlusion of the M1 stem produces both patterns, and infarction of the internal capsule weakens the leg as well.
Why do the eyes deviate toward the lesion in an MCA stroke?
The frontal eye field drives voluntary horizontal gaze toward the opposite side. When an MCA stroke destroys it, the patient cannot look away from the lesion, so the eyes rest toward the damaged hemisphere and away from the weak limbs. A pontine stroke does the opposite: it abolishes gaze toward the side of the lesion, so the eyes rest toward the weak side.
Why does an MCA stroke affect the face and arm more than the leg?
The face, arm and hand areas of the motor and sensory cortex lie on the lateral convexity of the hemisphere, which the MCA supplies. The leg area lies on the medial surface, which the anterior cerebral artery supplies. An MCA occlusion therefore relatively spares the leg, unless the M1 stem is blocked and the internal capsule is infarcted too.
How do you tell an MCA stroke from a lacunar stroke?
Look for cortical signs. An MCA stroke produces aphasia, neglect, a visual field cut or gaze deviation, with weakness of the face and arm more than the leg. A lacunar infarct is a small deep infarct, usually from lipohyalinosis in a patient with hypertension or diabetes, and causes a pure motor, pure sensory or other lacunar syndrome with no cortical signs.