Cerebral cortex localization means matching a deficit to the lobe, and then the artery, that explains it. Frontal lesions affect movement, speech output (Broca area), gaze and executive behavior; parietal lesions affect sensation, with Gerstmann syndrome on the dominant side and hemineglect on the nondominant side; temporal lesions affect language comprehension (Wernicke area), memory and the upper visual field; occipital lesions cause a contralateral homonymous hemianopia, often with macular sparing. Then add the homunculus: face and arm weakness points to the lateral convexity (middle cerebral artery, MCA), leg weakness to the medial surface (anterior cerebral artery, ACA). Language sits in the left hemisphere in almost all right-handed people and in about two-thirds of left-handed people.
The Q-bank vignette
A 67-year-old right-handed man is brought to the emergency department 1 hour after he suddenly had trouble speaking. He is alert and follows three-step commands correctly. Asked why he came in, he says, "Uh... the... um... arm... bad," in slow, effortful bursts, and he cannot repeat "no ifs, ands, or buts." He is visibly frustrated. His eyes rest deviated to the left, and he has weakness of the right lower face and right arm, with milder weakness of the right leg. Sensation and visual fields are normal.
Which cortical region is most likely affected?
A. Wernicke area (posterior superior temporal gyrus, dominant hemisphere) B. Broca area (inferior frontal gyrus, dominant hemisphere) C. Paracentral lobule (medial primary motor cortex) D. Primary visual cortex (calcarine cortex) E. Primary auditory cortex (Heschl gyri) F. Angular gyrus (dominant inferior parietal lobule) G. Nondominant (right) parietal lobe H. Bilateral amygdalae (anterior temporal lobes)
Step 1: Classify the aphasia
Three bedside tests sort every aphasia: fluency, comprehension and repetition. This patient is nonfluent, understands commands, cannot repeat, and knows his speech is wrong. That is Broca (expressive) aphasia.
Step 2: Let the neighbors confirm it
- Right face and arm worse than leg: the face and arm areas sit on the lateral precentral gyrus, just behind Broca area; the leg area sits medially. Lateral cortex = MCA territory.
- Eyes deviated to the left: a destructive hemispheric lesion leaves the eyes looking toward the lesion (away from the weak side), because the damaged left frontal eye field can no longer drive gaze to the right.
- Normal sensation and visual fields: the parietal and temporal lobes, and the optic radiations, are spared.
Together this is an infarct of the left MCA superior division, which supplies the lateral inferior frontal lobe, including Broca area.
Answer: B. Broca area
Broca area is the posterior inferior frontal gyrus of the dominant hemisphere, just in front of the motor cortex for the face. Damage causes slow, effortful speech in short phrases that drop small words such as "is" and "the," with impaired repetition and writing but relatively preserved comprehension. Patients are usually aware of the problem and frustrated by it, and right arm and face weakness often comes with it.
Why every other choice is wrong
- A. Wernicke area: speech would be fluent but empty (paraphasias, "word salad"), with poor comprehension and impaired repetition, and the patient would typically be unaware of the errors. A right visual field cut often accompanies it because the optic radiations run nearby. It lies in the MCA inferior division territory.
- C. Paracentral lobule: the medial motor strip controls the leg. An ACA-territory lesion here gives contralateral weakness maximal in the leg, often with urinary incontinence, apathy and a grasp reflex, but not this aphasia: ACA strokes can cause mutism, whereas nonfluent speech with impaired repetition points to the lateral frontal lobe. See anterior cerebral artery syndrome.
- D. Primary visual cortex: a calcarine lesion, usually a posterior cerebral artery (PCA) infarct, causes a contralateral homonymous hemianopia, often with macular sparing, because the occipital tip gets blood from both the MCA and the PCA. It causes no aphasia or weakness.
- E. Primary auditory cortex: each ear projects to both hemispheres, so a unilateral Heschl gyrus lesion does not cause deafness; bilateral temporal lesions can cause auditory agnosia. Failing to understand speech points to Wernicke area, and this patient understands.
- F. Angular gyrus: a dominant inferior parietal lesion causes Gerstmann syndrome: agraphia, acalculia, finger agnosia and left-right disorientation, not effortful speech with face and arm weakness.
- G. Nondominant parietal lobe: a right parietal lesion causes left hemineglect and anosognosia (unawareness or denial of the deficit), sometimes with dressing apraxia. This patient's deficits are right-sided and include aphasia, so the lesion is in the left hemisphere.
- H. Bilateral amygdalae: Klüver-Bucy syndrome follows bilateral temporal lobe damage (NORD); review books frame it as bilateral amygdala, or anterior temporal, lesions. It causes hyperorality, hypersexuality, docility, loss of fear and visual agnosia, and herpes simplex encephalitis is the classic cause. It is bilateral and behavioral, not a sudden aphasia. More in the limbic system review.
Lobe-by-lobe localization
| Lobe | Area | Lesion causes | Classic clue |
|---|---|---|---|
| Frontal | Primary motor cortex (precentral gyrus) | Contralateral weakness: face and arm laterally, leg medially | Upper motor neuron signs |
| Frontal | Broca area (dominant inferior frontal gyrus) | Nonfluent (expressive) aphasia | Effortful speech, aware and frustrated |
| Frontal | Frontal eye fields | Eyes deviate toward a destructive lesion, away from a seizure focus | Gaze preference in a stroke or seizure |
| Frontal | Prefrontal cortex | Dorsolateral: poor working memory and planning. Orbitofrontal: disinhibition, lability. Medial: abulia (apathy, slowness) | Personality change, as in a frontal tumor or frontotemporal dementia |
| Parietal | Primary somatosensory cortex (postcentral gyrus) | Contralateral cortical sensory loss, astereognosis | Cannot identify a key by touch |
| Parietal | Dominant angular gyrus | Gerstmann syndrome: agraphia, acalculia, finger agnosia, left-right disorientation | Cannot write, calculate or name fingers |
| Parietal | Nondominant parietal lobe | Hemineglect (usually left-sided), anosognosia, dressing apraxia | Ignores the left side, denies weakness |
| Parietal | Superior optic radiations | Contralateral inferior homonymous quadrantanopia ("pie on the floor") | Field cut with a parietal tumor or stroke |
| Temporal | Wernicke area (dominant posterior superior temporal gyrus) | Fluent (receptive) aphasia | Word salad, unaware of errors |
| Temporal | Meyer loop (inferior optic radiations) | Contralateral superior homonymous quadrantanopia ("pie in the sky") | Field cut with a temporal lesion |
| Temporal | Both temporal lobes (classic framing: bilateral amygdalae) | Klüver-Bucy syndrome | Hyperorality, hypersexuality, docility |
| Temporal | Medial temporal lobe (hippocampus) | Memory loss; bilateral lesions cause anterograde amnesia | PCA stroke, herpes simplex encephalitis |
| Temporal | Inferotemporal (fusiform) cortex, often bilateral | Prosopagnosia | Cannot recognize familiar faces |
| Occipital | Primary visual cortex (calcarine) | Contralateral homonymous hemianopia with macular sparing | PCA stroke |
| Occipital | Both occipital lobes | Cortical blindness; Anton syndrome (unaware of blindness, confabulates) | Bilateral PCA infarcts |
| Occipital | Left occipital cortex plus splenium of the corpus callosum | Alexia without agraphia | Can write but cannot read it back |
Bilateral parieto-occipital damage causes Balint syndrome: simultanagnosia (sees one object at a time), optic ataxia (misreaches) and ocular apraxia.
Aphasias: fluency, comprehension, repetition
| Aphasia | Fluency | Comprehension | Repetition | Lesion (dominant hemisphere) |
|---|---|---|---|---|
| Broca | Nonfluent | Relatively intact | Impaired | Inferior frontal gyrus (frontal or frontoparietal) |
| Wernicke | Fluent, paraphasic | Impaired | Impaired | Posterior superior temporal gyrus (temporoparietal) |
| Conduction | Fluent, many paraphasias | Intact | Severely impaired | Subcortical, often under the superior temporal gyrus or inferior parietal lobe (classically the arcuate fasciculus) |
| Global | Nonfluent, sparse | Impaired | Impaired | Large frontotemporoparietal lesion covering Broca and Wernicke areas |
| Transcortical motor | Nonfluent | Intact | Intact | Frontal lobe around but sparing Broca area (often an ACA-MCA watershed infarct) |
| Transcortical sensory | Fluent | Impaired | Intact | Temporoparietal cortex around but sparing Wernicke area (often an MCA-PCA watershed infarct) |
| Mixed transcortical | Nonfluent | Impaired | Intact (echolalia) | Often watershed infarcts, with Broca and Wernicke areas spared |
| Anomic | Fluent, word-finding pauses | Intact | Intact | Small lesion anywhere in the language areas |
- Repetition is the tiebreaker: if repetition is intact, think transcortical or anomic aphasia.
- Broca patients are aware; Wernicke patients usually are not. Wernicke aphasia can be mistaken for delirium, but there is no fluctuating consciousness, inattention or hallucination.
- Aphasia is not dysarthria. Dysarthria is a motor speech problem with normal language; aphasia is a language problem.
- Stroke is the leading cause of aphasia; about one-third of stroke survivors have it (National Aphasia Association, cited by NIDCD).
Vascular territories: ACA vs MCA vs PCA
| Artery | Cortex supplied | Typical deficits |
|---|---|---|
| ACA | Medial frontal and parietal lobes, corpus callosum | Contralateral weakness maximal in the leg, urinary incontinence, apathy, poor judgment, grasp reflex, gait apraxia |
| MCA | Most of the lateral frontal, parietal and temporal lobes | Contralateral face and arm more than leg weakness, hemisensory loss, homonymous hemianopia; aphasia if dominant, neglect and apraxia if nondominant |
| MCA superior division | Lateral inferior frontal lobe, including Broca area (supply of the face and arm motor and sensory cortex varies between divisions) | Broca aphasia with face and arm weakness (this vignette) |
| MCA inferior division | Lateral superior temporal lobe, including Heschl gyrus and Wernicke area | Wernicke aphasia, often with a visual field cut |
| PCA | Occipital lobe, medial temporal lobe (hippocampus), thalamus | Contralateral homonymous hemianopia with macular sparing, memory loss; alexia without agraphia (left PCA) |
Drill these with stroke localization by artery, the MCA syndrome breakdown and the PCA syndrome breakdown.
Gaze deviation rules
| Lesion | Eyes look | Why |
|---|---|---|
| Destructive hemispheric lesion (e.g., MCA stroke) | Toward the lesion, away from the hemiparesis | The intact frontal eye field pushes gaze unopposed toward the damaged side |
| Seizure focus in one hemisphere | Away from the focus (usually) | The irritated frontal eye field over-drives gaze to the opposite side |
| Pontine lesion (horizontal gaze center) | Away from the lesion, toward the hemiparesis | Ipsilateral horizontal gaze palsy |
How USMLE tests it
- Language deficit = dominant (usually left) hemisphere; neglect = nondominant (usually right) parietal lobe.
- Leg weakness more than arm = ACA; face and arm more than leg = MCA. A paracentral lobule lesion is the "leg" answer.
- Field cuts: "pie in the sky" = temporal lobe (Meyer loop); "pie on the floor" = parietal lobe; hemianopia with macular sparing = occipital lobe (PCA).
- Gerstmann vs alexia without agraphia: the dominant angular gyrus gives agraphia with acalculia and finger agnosia; a left PCA infarct involving the splenium spares writing.
- Bilateral lesions make the syndromes: Klüver-Bucy (temporal lobes, classically the amygdalae), Balint (parieto-occipital), Anton syndrome (occipital) and prosopagnosia (often bilateral fusiform gyri).
Key takeaways
- Classify aphasia by fluency, comprehension and repetition; intact repetition means transcortical or anomic.
- Broca: nonfluent, understands, frustrated, right face and arm weakness, MCA superior division.
- Wernicke: fluent nonsense, poor comprehension, unaware, often a right visual field cut, MCA inferior division.
- Dominant parietal = Gerstmann; nondominant parietal = hemineglect and anosognosia.
- Temporal = superior quadrantanopia and Klüver-Bucy (bilateral temporal lobes, classically the amygdalae); occipital = homonymous hemianopia with macular sparing.
- Eyes look toward a destructive hemispheric lesion and away from a seizure focus or a pontine lesion.
Sources
- Overview of Cerebral Function — Merck Manual Professional Edition (2026)
- Aphasia — Merck Manual Professional Edition (2025)
- Agnosia — Merck Manual Professional Edition (2025)
- Overview of Stroke — Merck Manual Professional Edition (2026)
- Overview of Coma and Impaired Consciousness — Merck Manual Professional Edition (2026)
- Seizure Disorders — Merck Manual Professional Edition (2026)
- Aphasia — StatPearls, NCBI Bookshelf (2024)
- Aphasia — National Institute on Deafness and Other Communication Disorders (NIH)
- Compressive Visual Field Defects — EyeWiki, American Academy of Ophthalmology (2026)
- Alexia without Agraphia — EyeWiki, American Academy of Ophthalmology (2026)
- Kluver-Bucy Syndrome — National Organization for Rare Disorders (2023)
- Middle Cerebral Artery — Radiopaedia (2025)
Frequently Asked Questions
How do you localize a lesion in the cerebral cortex?
Match the deficit to a lobe, then to an artery. Frontal lesions cause contralateral weakness, nonfluent Broca aphasia, gaze deviation and personality or executive changes. Parietal lesions cause cortical sensory loss, Gerstmann syndrome on the dominant side and hemineglect on the nondominant side. Temporal lesions cause Wernicke aphasia, memory problems and a superior quadrantanopia. Occipital lesions cause a contralateral homonymous hemianopia, often with macular sparing. Face and arm weakness suggests the MCA; leg weakness suggests the ACA.
What is the difference between Broca and Wernicke aphasia?
Broca aphasia comes from a lesion of the dominant inferior frontal gyrus: speech is slow, effortful and nonfluent, comprehension is relatively preserved, repetition is impaired, and patients are aware and frustrated, often with right face and arm weakness. Wernicke aphasia comes from a lesion of the dominant posterior superior temporal gyrus: speech is fluent but meaningless, comprehension and repetition are impaired, and patients are usually unaware of their errors, often with a right visual field cut.
What is Gerstmann syndrome and where is the lesion?
Gerstmann syndrome is the combination of agraphia (inability to write), acalculia (inability to calculate), finger agnosia (inability to name or identify fingers) and left-right disorientation. It localizes to the angular gyrus of the dominant parietal lobe, which is the left parietal lobe in most people. Nondominant parietal lesions are different: they cause hemineglect and anosognosia rather than problems with writing and calculation.
Which brain lesion causes hemineglect?
Hemineglect usually follows an acute lesion of the nondominant parietal lobe, which is the right parietal lobe in most people, often from a right middle cerebral artery stroke. Patients ignore the left side of their body and surroundings and may have anosognosia, denying that a paralyzed left arm is weak or even theirs. Smaller lesions can cause apraxia, such as difficulty dressing. Dominant (left) parietal lesions instead cause Gerstmann syndrome.
What does pie in the sky mean in neurology?
Pie in the sky is a contralateral superior homonymous quadrantanopia: loss of the upper quarter of the visual field on the side opposite the lesion, in both eyes. It comes from damage to Meyer loop, the inferior fibers of the optic radiation that sweep through the temporal lobe. A parietal lesion affecting the superior optic radiation fibers causes the opposite pattern, an inferior quadrantanopia called pie on the floor.
Which way do the eyes deviate in a stroke or a seizure?
With a destructive cerebral hemisphere lesion, such as a large middle cerebral artery stroke, the eyes deviate toward the side of the lesion and away from the paralyzed limbs, because the intact frontal eye field drives gaze unopposed. During a focal seizure, the head and eyes usually turn away from the seizure focus. With a pontine lesion involving the horizontal gaze center, the eyes deviate away from the lesion, toward the weak side.