Which part of the homunculus does the anterior cerebral artery supply?

The ACA supplies the medial part of the motor and sensory strips, where the foot, leg and thigh are represented; on the sensory map the genitals sit there too. That medial region, which includes the paracentral lobule, is why an ACA stroke weakens and numbs the opposite leg. The arm, hand and face are mapped on the lateral convexity, which the middle cerebral artery supplies, so they are largely spared.

Why does an ACA stroke cause urinary incontinence?

The medial frontal lobe sends inhibitory input to the pontine micturition center, the brainstem relay that triggers voiding. An ACA infarct damages this frontal region and removes the brake, leaving an uninhibited bladder that empties without voluntary control. New incontinence together with leg-predominant weakness is a classic clue to ACA territory. A spinal cord lesion between the pons and sacral cord causes a different pattern, a spastic bladder or detrusor-sphincter dyssynergia.

What happens if both anterior cerebral arteries are blocked?

Bilateral ACA infarction weakens both legs and can cause akinetic mutism, in which the patient is awake but barely moves or speaks, along with frontal release signs such as forced grasping. It is rare and is linked to an azygos (unpaired) ACA, a hypoplastic or absent A1 segment, or vasospasm after a ruptured anterior communicating artery aneurysm. Because both legs are weak, it can be mistaken for a spinal cord lesion, and one azygos case mimicked basilar artery occlusion.

How do you tell an ACA stroke from an MCA stroke?

Compare which body part is weakest, then look at the cortical signs. An ACA stroke causes leg-predominant weakness and sensory loss with frontal signs: incontinence, abulia, a grasp reflex and, on the left, transcortical motor aphasia with normal repetition. An MCA stroke weakens the face and arm more than the leg and often causes a homonymous hemianopia, plus aphasia when the dominant hemisphere is hit or neglect and apraxia when the nondominant side is hit.

How is an acute ACA stroke treated?

Treatment follows the 2026 AHA/ASA acute ischemic stroke guideline. Once CT excludes hemorrhage, a patient with a disabling deficit within 4.5 hours gets IV tenecteplase (0.25 mg/kg, maximum 25 mg) or alteplase (0.9 mg/kg, maximum 90 mg), whatever the NIHSS score, with blood pressure below 185/110 mm Hg. Non-disabling deficits get dual antiplatelet therapy instead. Thrombectomy is not routinely recommended for medium or small artery occlusions, which include ACA branch occlusions.

Anterior Cerebral Artery Syndrome: Signs & USMLE Case

Q: What is anterior cerebral artery syndrome?

Anterior cerebral artery (ACA) syndrome is the set of deficits caused by a stroke in ACA territory: the medial frontal and parietal lobes and the corpus callosum. The hallmark is contralateral weakness and sensory loss of the leg and foot, worse than in the arm, with the face spared. Frontal signs complete the picture: urinary incontinence, abulia, a grasp reflex and gait apraxia. A left-sided stroke can add transcortical motor aphasia, and bilateral infarcts can cause akinetic mutism.

Anterior cerebral artery (ACA) syndrome is a stroke of the medial frontal and parietal lobes that causes contralateral weakness and sensory loss of the leg and foot, worse than in the arm, with the face spared, plus frontal-lobe signs: urinary incontinence, abulia, a grasp reflex and gait apraxia. The leg takes the hit because its motor and sensory maps lie on the medial surface, in ACA territory; the hand and face lie on the lateral convexity, supplied by the middle cerebral artery (MCA). A left (dominant) ACA stroke can add transcortical motor aphasia, callosal or medial frontal damage can produce an alien hand, and bilateral ACA infarction (from an azygos ACA, one A1 segment feeding both ACAs, or vasospasm after a ruptured anterior communicating artery aneurysm) can weaken both legs and cause akinetic mutism. ACA infarcts are uncommon, 0.3% to 4.4% of strokes.

ACA syndrome at a glance

Feature	What to know
Territory	Medial frontal and parietal lobes and the corpus callosum; through the recurrent artery of Heubner, the caudate head and part of the anterior limb of the internal capsule
How common	0.3% to 4.4% of strokes in published series; men and the left hemisphere are affected more often
Signature sign	Contralateral leg-predominant weakness (86% to 96% of patients across series), sometimes with leg sensory loss; the arm is mildly weak or spared, the face spared
Frontal signs	Urinary incontinence, abulia and apathy, confusion, poor judgment, mutism, grasp reflex, gait apraxia
Left (dominant) ACA	Transcortical motor aphasia: nonfluent like Broca aphasia, but repetition is normal
Main causes	ACA atherosclerosis, cardioembolism (atrial fibrillation), dissection, vasospasm
Acute treatment (2026 AHA/ASA)	IV tenecteplase or alteplase within 4.5 hours for a disabling deficit; thrombectomy not routinely recommended for medium or small artery occlusions outside a trial

ACA anatomy: segments, branches and territory

The ACA is a terminal branch of the internal carotid artery. Its A1 (horizontal, precommunicating) segment runs from the carotid bifurcation toward the longitudinal fissure, where the anterior communicating artery (ACom) links it to the opposite ACA. The A2 (postcommunicating) segment starts at the ACom and rises in front of the corpus callosum; A3 to A5 form the pericallosal artery.

Branch	Course or territory	Stroke clue
Recurrent artery of Heubner	Largest artery from A1 or proximal A2; supplies the caudate head, anterior third of the putamen and anteroinferior part of the anterior limb of the internal capsule	Contralateral face and arm weakness: the exception to "ACA spares the arm"
Cortical branches (orbitofrontal, frontopolar, internal frontal, paracentral, parietal)	Basal frontal lobe, superior frontal gyrus and the anterior two-thirds of the medial hemisphere, including the medial ends of the precentral and postcentral gyri (the paracentral lobule)	Leg weakness and sensory loss; frontal signs
Pericallosal artery (A3–A5)	Wraps around the corpus callosum	Callosal signs such as an alien hand

The ACA's robust anastomotic network may account for the low rate of ACA infarcts, and some distal ACA branches supply part of the opposite hemisphere. Picture the ring with the circle of Willis memory palace.

The ACA homunculus: why the leg

On the motor and sensory homunculus, the ACA supplies the medial part of the strip, where the foot, leg and thigh are mapped (with the genitals on the sensory side); the MCA supplies the lateral convexity, where the arm, hand and face are mapped. The medial paracentral lobule controls the foot, leg and thigh; moving laterally come the trunk, the arm and hand, and the face and head just above the lateral fissure, with the hand and face areas disproportionately large. The sensory map on the postcentral gyrus follows the same plan: genitals and lower limb medially, face inferolaterally.

Homunculus area	Body part	Artery	Infarct
Medial surface (paracentral lobule); medial and superior postcentral gyrus	Foot, leg, thigh; genitals on the sensory map	ACA	Contralateral leg weakness and numbness
Lateral convexity	Arm and hand	MCA (superior division for the motor strip)	Contralateral arm weakness and numbness
Inferolateral strip, above the lateral fissure	Face and head	MCA	Contralateral face weakness and numbness

The precentral gyrus lies above the pyramidal decussation, so the weakness is contralateral with upper motor neuron signs. Hence the board rule: leg > arm is ACA; face and arm > leg is MCA. Lobe-by-lobe localization is drilled in cerebral cortex localization.

Signs of ACA syndrome: lesion-to-deficit map

ACA territory	Deficit	Vignette clue
Paracentral lobule (medial motor and sensory cortex)	Contralateral leg > arm weakness with upper motor neuron signs and sensory loss; face spared	"Her foot drags," arm nearly normal
Medial frontal cortex	Urinary incontinence	New incontinence alongside leg weakness
Anterior cingulate and medial prefrontal cortex	Abulia, apathy, slowed responses; bilateral lesions → akinetic mutism	Awake but won't start moving or talking
Supplementary motor area, left side	Transcortical motor aphasia, sometimes after a period of muteness	Says little but repeats sentences well
Medial frontal lobe	Grasp reflex, gait apraxia, motor perseveration	Grips the examiner's hand; can't get walking started
Corpus callosum and medial frontal cortex	Alien hand	One hand acts on its own
Recurrent artery of Heubner	Contralateral face and arm weakness	Proximal ACA stroke that doesn't spare the arm

Sensory loss is less common than weakness (29% of patients in one registry) and usually accompanies the weak leg; a purely sensory ACA infarct is a case-report rarity.

The frontal signs, explained

Urinary incontinence. The pontine micturition center triggers voiding by driving the bladder's sacral motor neurons and relaxing the external urethral sphincter. Inhibitory input from the medial frontal lobe holds it in check, so a lesion above the pons leaves an uninhibited bladder; a lesion between the pons and the sacral cord gives a spastic bladder or detrusor-sphincter dyssynergia instead.

Abulia and akinetic mutism. Abulia is a lack of will, drive or initiative for action, speech and thought. Abulia minor is apathy; abulia major is akinetic mutism, limited verbal and motor responsiveness in a patient who is neither paralyzed nor comatose. Anterior cingulate damage, typically from an ACA infarct, is the most common lesion and produces abulia minor; bilateral medial frontal lesions cause persistent abulia. Antidepressants are not effective, so don't mistake it for depression; carbidopa-levodopa, amantadine and bromocriptine are used.

Transcortical motor aphasia. A left ACA infarct that damages the supplementary motor area can cause transcortical motor aphasia, sometimes after a period of muteness. Speech is nonfluent as in Broca aphasia, but repetition is normal (Broca aphasia impairs it) and articulation is often unaffected; the lesion lies in the left frontal lobe outside Broca and Wernicke areas. Aphasia from ACA infarcts tends to improve within a short time, unlike aphasia from MCA lesions.

Alien hand (alien limb). One hand makes involuntary yet purposeful movements that the patient cannot control and may feel are foreign; the leg is sometimes involved (alien limb). ACA strokes are among the common causes, and both anterior variants fit ACA territory:

Frontal variant: groping, grasping or compulsive use of tools, from lesions of the supplementary motor area, cingulate cortex, dominant medial prefrontal cortex or corpus callosum.
Callosal variant: intermanual conflict, the two hands working against each other, mostly from callosal damage.

Bilateral ACA infarction: azygos ACA, single A1 and vasospasm

Bilateral ACA infarction is rare. Three classic settings:

Azygos ACA: an unpaired ACA trunk (azygos means unpaired) serves both hemispheres, so its occlusion can infarct both sides at once. One reported case mimicked basilar artery occlusion and was fatal.
Hypoplastic or absent A1: one A1 carries the flow for both ACAs, which favors embolism.
Vasospasm after a ruptured ACom aneurysm (next section).

Expect weakness of both legs (paraparesis), akinetic mutism and frontal disinhibition signs such as an enhanced glabellar tap, utilization behavior and forced grasping. With both legs weak, it can be mistaken for a spinal cord lesion:

Clue	Bilateral ACA infarction	Anterior spinal artery infarction
Onset	Sudden	Sudden back pain radiating around the trunk, then weakness within minutes
Legs	Weak with upper motor neuron signs	Sudden bilateral flaccid weakness
Sensation	No sensory level	Pain and temperature lost below a level; position and vibration relatively spared
Mind and speech	Abulia or akinetic mutism; grasp reflexes	Normal
Imaging	Diffusion-weighted MRI of the brain	MRI of the spine

The cord's anatomy is laid out in spinal cord tracts.

The ACom aneurysm link

The junction of the ACA with the ACom is one of the most common sites of saccular (berry) aneurysms, and about 85% of cerebral aneurysms lie in the anterior circulation. Rupture causes subarachnoid hemorrhage, whose most common symptom is "the worst headache of my life." The aneurysm itself is not an ACA stroke: ACA ischemia comes later, mainly from vasospasm, which starts around day 3 to 5 and peaks at day 7, or from inadvertent clipping of ACA branches during surgery. Vasospasm is a recognized cause of ACA infarction, and ruptured ACom aneurysms are a listed cause of abulia. Oral nimodipine 60 mg every 4 hours for 21 days is given to improve outcomes; the bleed itself is covered in hemorrhagic stroke (ICH and SAH).

Causes of ACA stroke

Atherosclerosis of the ACA itself, which blocks the artery by in situ thrombosis, branch occlusion or artery-to-artery embolism; it is a primary cause particularly in Asian populations (risk factors: hypertension, hypercholesterolemia, diabetes, smoking).
Cardioembolism from atrial fibrillation, intracardiac thrombus, valve disease or tumors, the leading cause (45%) in a Spanish registry of 51 patients; a hypoplastic or absent A1 is thought to favor embolic strokes.
Arterial dissection and vasospasm, classically after subarachnoid hemorrhage.
Thrombectomy for an MCA occlusion: ACA infarcts appeared on follow-up imaging in 5.7% of 105 patients treated for M1 occlusion.

Imaging and workup

Noncontrast head CT excludes hemorrhage, alongside a glucose check, an NIH Stroke Scale (NIHSS) score and the time last known well; the AHA target is an initial brain scan within 25 minutes of arrival. CT can miss ACA infarcts: in one series, 37.5% (6 of 16) were visible only after contrast injection or angiography. A hyperdense ACA on CT can aid diagnosis in the acute phase.
CT angiography of the head and neck should follow promptly.
Diffusion-weighted MRI demarcates the ischemic boundaries.

Acute management under the 2026 AHA/ASA guideline

The AHA/ASA 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke (published online 26 January 2026) applies to ACA strokes as to any other:

IV thrombolysis within 4.5 hours for a disabling deficit, regardless of NIHSS score and without advanced imaging selection: tenecteplase 0.25 mg/kg (maximum 25 mg) as a single IV bolus or alteplase 0.9 mg/kg (maximum 90 mg). IV thrombolysis alone has low recanalization rates in proximal ACA occlusions.
Non-disabling deficits: thrombolysis has shown no benefit; dual antiplatelet therapy (aspirin plus clopidogrel, started within 24 hours, for 21 days) is preferred.
Extended window: thrombolysis for selected patients with unknown onset or 4.5 to 9 hours from onset who show DWI–FLAIR or perfusion mismatch.
Thrombectomy: standard for large vessel occlusion and strongly recommended for basilar artery occlusion within 24 hours with NIHSS ≥10. For blockages in medium or small arteries it is not routinely recommended and may be considered in a clinical trial. In the 2025 DISTAL trial, whose eligibility covered A1–A3 ACA occlusions and MCA and PCA branches, thrombectomy did not reduce disability or death compared with best medical treatment. Treated ACA occlusions also tend to have fewer good outcomes and more symptomatic hemorrhage than MCA or ICA occlusions.
Blood pressure: the standard thresholds are below 185/110 mm Hg before thrombolysis and below 180/105 mm Hg for the first 24 hours after. Without thrombolysis or thrombectomy, the classic rule is to treat only above 220/120 mm Hg; current guidance says lowering pressures below that in the first 48 to 72 hours does not improve outcomes, and calls the benefit of treating higher pressures uncertain. The 2026 guideline advises against intensive systolic lowering to below 140 mm Hg after thrombolysis or thrombectomy, even with complete reperfusion, and against intensive glucose control to 80–130 mg/dL.
Antithrombotics: none within 24 hours of thrombolysis; secondary prevention includes anticoagulants where indicated.

Practice the decisions with tPA and thrombectomy questions.

ACA vs MCA vs PCA vs basilar vs lacunar stroke

Feature	ACA	MCA	PCA	Basilar (vertebrobasilar)	Lacunar
Weakness	Contralateral, leg > arm, face spared	Contralateral, face and arm > leg	Usually none	Spastic paresis; crossed sensory and motor deficits	Pure motor hemiparesis or ataxic hemiparesis
Vision	Spared	Contralateral homonymous hemianopia	Contralateral homonymous hemianopia, often with macular sparing	Diplopia, nystagmus, sometimes blindness	Spared
Higher function	Abulia, mutism, poor judgment; left: transcortical motor aphasia	Left: aphasia; right: apraxia and sensory neglect	Memory loss	Impaired consciousness, coma	No cortical deficits
Other clues	Incontinence, grasp reflex, gait apraxia	Dysarthria, hemianesthesia	CN III palsy, hemiballismus	Vertigo, dysphagia, ataxia, labile blood pressure	Pure sensory stroke, dysarthria–clumsy hand

The anterior inferior cerebellar artery (AICA) branches from the basilar artery, so an AICA stroke brings vertebrobasilar signs (vertigo, nystagmus, ataxia, cranial nerve deficits), not leg-predominant weakness with frontal signs. Field cuts are worked through in posterior cerebral artery syndrome, small-vessel strokes in lacunar infarcts, and every territory in stroke localization by artery.

How USMLE tests it: traps and look-alikes

Trap	What's actually true
Both legs weak means a spinal cord lesion	Bilateral ACA infarction weakens both legs; abulia, akinetic mutism and grasp reflexes mean brain, a sensory level means cord
Nonfluent speech means Broca aphasia	Normal repetition makes it transcortical motor aphasia (left ACA, supplementary motor area)
A mute, apathetic patient is depressed	Abulia or akinetic mutism; antidepressants are not effective
An ACA stroke always spares the arm	The recurrent artery of Heubner causes face and arm weakness
A ruptured ACom aneurysm is an ACA stroke	Rupture causes subarachnoid hemorrhage; ACA ischemia comes later, mainly from vasospasm (from about day 3) or from surgical clipping of ACA branches
Every occlusion on CTA gets thrombectomy	Not routinely for medium or small arteries; DISTAL, whose criteria included A1–A3 occlusions, showed no benefit

More walkthroughs are collected on the Neurology hub.

Practice question: why every answer choice matters

A 66-year-old man with atrial fibrillation is brought in by his wife, who found him sitting silently on the edge of the bed, incontinent of urine. He answers questions with one or two words after long pauses but repeats sentences accurately. Right leg strength is 2/5 and right arm strength is 4+/5; his face is symmetric. Pinprick is reduced over the right foot, he has a right Babinski sign, and he has a grasp reflex in the right hand. Which artery is most likely occluded?

A. Left anterior cerebral artery
B. Left middle cerebral artery, superior division
C. Lenticulostriate branch to the left internal capsule
D. Right anterior cerebral artery
E. Anterior spinal artery

Answer: A, left ACA. Right leg weakness far worse than arm weakness, with a spared face and a numb right foot, localizes to the left paracentral lobule. Incontinence, abulia, the grasp reflex and sparse speech with preserved repetition (transcortical motor aphasia) are left medial frontal signs, and atrial fibrillation supplies the embolus.

B: a left MCA superior-division stroke weakens the right face and arm more than the leg, and a left frontal lesion that includes Broca area causes Broca aphasia, in which repetition is impaired.
C: a lacunar infarct in the internal capsule causes pure motor hemiparesis without cortical deficits, so it cannot explain abulia, aphasia or a grasp reflex.
D: a right ACA stroke weakens the left leg.
E: an anterior spinal artery infarct causes sudden back pain and bilateral flaccid leg weakness with pain and temperature loss below a spinal level, and no abulia or aphasia.

What happens next: the time last known well decides eligibility. Within 4.5 hours, a disabling deficit calls for IV tenecteplase or alteplase once CT excludes hemorrhage and recent anticoagulant use is ruled out; with unknown onset, thrombolysis needs a DWI–FLAIR or perfusion mismatch. Anticoagulation for atrial fibrillation follows.

More worked vignettes

Vignette 2: the posterior circulation distractors. A 74-year-old right-handed woman with atrial fibrillation, on no anticoagulant, arrives 2 hours after she suddenly could not stand up from her chair. She is alert but apathetic; speech is normal. Her left leg is 1/5, left arm 4/5 and face symmetric; pinprick is reduced over the left foot, she has a left grasp reflex, and she has been incontinent of urine. Visual fields and eye movements are full, with no vertigo, nystagmus, dysarthria or ataxia. Which artery is occluded: basilar, right AICA, right PCA, right MCA superior division or right ACA?

Answer: Right ACA.

Reasoning: Leg-predominant weakness and numbness with a spared face, apathy, a grasp reflex and incontinence localize to the right medial frontal and parietal cortex. Basilar occlusion brings crossed deficits, cranial nerve signs and impaired consciousness; AICA brings vertigo, nystagmus and ataxia. A right PCA stroke causes a left homonymous hemianopia, and a right MCA superior-division stroke weakens the face and arm more than the leg. If CT shows no hemorrhage, she is a candidate for IV thrombolysis.

Vignette 3: bilateral ACA infarction. A 52-year-old woman had a ruptured ACom aneurysm secured after a subarachnoid hemorrhage. On day 7 she lies awake with her eyes open but barely moves or speaks. She is newly incontinent, both legs are weak with bilateral Babinski signs, and she grasps the examiner's hands. Arm strength is nearly normal, and there is no sensory level. What is the most likely cause, and which drug is given after the bleed to improve outcomes?

Answer: Bilateral ACA infarction from vasospasm; oral nimodipine 60 mg every 4 hours for 21 days.

Reasoning: Vasospasm starts around day 3 to 5 and peaks at day 7, and the aneurysm sits where the two ACAs are joined. Paraparesis, akinetic mutism, incontinence and forced grasping are bilateral medial frontal signs. An anterior spinal artery infarct would cause back pain, flaccid weakness and a sensory level without mutism; basilar occlusion would cause cranial nerve signs and impaired consciousness. A head CT should still exclude hydrocephalus or rebleeding.

Vignette 4: acute management. A 68-year-old man arrives 90 minutes after sudden right leg weakness that keeps him from walking, with mild right arm weakness and new urinary incontinence. Glucose is normal, blood pressure is 172/94 mm Hg, NIHSS is 4 and noncontrast CT shows no hemorrhage. CT angiography shows a left A2 occlusion. He takes no anticoagulant. What is the best next step?

Answer: IV tenecteplase 0.25 mg/kg (maximum 25 mg) as a single bolus, or alteplase 0.9 mg/kg (maximum 90 mg).

Reasoning: He is within 4.5 hours with a disabling deficit, so an NIHSS of 4 does not exclude him, and his blood pressure is already below 185/110 mm Hg. Dual antiplatelet therapy is for non-disabling deficits. An A2 occlusion counts as a medium or distal vessel occlusion, for which thrombectomy is not routine outside a trial.

Key takeaways

ACA syndrome = medial frontal and parietal cortex: contralateral leg > arm weakness and sensory loss, face spared.
On the homunculus the ACA owns the medial strip (foot, leg, thigh; genitals on the sensory map); the MCA owns the arm, hand and face.
Frontal signs: incontinence, abulia, grasp reflex, gait apraxia; the left side adds transcortical motor aphasia, callosal damage an alien hand, Heubner's artery face and arm weakness.
Bilateral ACA infarction (azygos ACA, single A1, vasospasm after ACom aneurysm rupture) causes paraparesis and akinetic mutism; don't call it a cord lesion.
2026 AHA/ASA: tenecteplase or alteplase within 4.5 hours for a disabling deficit regardless of NIHSS; thrombectomy is not routine for medium or small artery occlusions.