Cortical Localization, Aphasias & Neglect

Frontal lobe

Prefrontal cortex. The prefrontal cortex plans, inhibits and judges. Lesions from trauma, tumors, anterior cerebral artery (ACA) infarcts or frontotemporal dementia spare strength but change behavior. Orbitofrontal damage produces disinhibition, impulsivity and poor judgment; dorsolateral damage produces poor planning and perseveration; medial frontal damage produces abulia (loss of drive). Phineas Gage, whose 1848 tamping-iron injury destroyed much of his left frontal lobe, is the classic case of personality change with preserved strength and intellect.

Release signs and incontinence. Frontal damage unmasks primitive reflexes suppressed since infancy: grasp, rooting, sucking, snout and palmomental reflexes. The medial frontal lobe also provides voluntary control of micturition, so medial (ACA-territory) lesions cause urinary incontinence.

Frontal eye fields. Each frontal eye field (Brodmann area 8) drives conjugate saccades toward the opposite side. After a destructive lesion such as an MCA infarct, the unopposed healthy side pushes the eyes toward the lesion, so the patient looks at the lesion and away from the hemiparesis. A seizure focus in the frontal eye field does the opposite, driving the eyes away from the focus. Pontine gaze center (PPRF) lesions cause deviation away from the lesion, toward the hemiparesis.

Parietal lobe

Dominant parietal lobe. A lesion of the dominant (usually left) inferior parietal lobule at the angular gyrus produces Gerstmann syndrome: agraphia, acalculia, finger agnosia and left-right disorientation. Alexia and ideomotor apraxia (inability to perform learned movements on command despite normal strength) often accompany it.

Nondominant parietal lobe. The right hemisphere attends to both halves of space, while the left attends mainly to the right. Right parietal lesions therefore cause striking left hemispatial neglect: patients eat from one side of the plate, draw half a clock, shave half the face and extinguish the left stimulus when both sides are touched at once. Anosognosia (unawareness or denial of the deficit, even a paralyzed arm), dressing apraxia and constructional apraxia (inability to copy or assemble figures) complete the syndrome. Neglect after left-sided lesions is rare and mild.

Parietal optic radiations. The dorsal optic radiations carry the lower visual field, so parietal lesions cause a contralateral inferior homonymous quadrantanopia ("pie on the floor").

Temporal lobe and limbic structures

Meyer loop. The inferior optic radiation fibers, carrying the upper visual field from the inferior retina, loop forward through the temporal lobe. Temporal tumors, temporal lobectomy or an inferior-division MCA infarct therefore cause a contralateral superior homonymous quadrantanopia ("pie in the sky").

Hippocampus and amygdala. Bilateral hippocampal damage (hypoxia, HSV-1 encephalitis, surgical removal) causes anterograde amnesia. Bilateral amygdala damage in the anterior temporal lobes, classically from HSV-1 encephalitis, trauma or frontotemporal dementia, produces Klüver-Bucy syndrome: hyperorality, hypersexuality, placidity with loss of fear, and visual agnosia.

Mammillary bodies. Thiamine deficiency from alcohol use disorder, malnutrition or hyperemesis damages the mammillary bodies and dorsomedial thalamus. Acute Wernicke encephalopathy (confusion, ophthalmoplegia, ataxia) can progress to Korsakoff syndrome, with anterograde and retrograde amnesia and confabulation; mammillary body atrophy is characteristic. Cerebellar vermis atrophy in alcohol use disorder causes gait ataxia, not amnesia.

Give IV thiamine before glucose to at-risk patients; glucose without thiamine can precipitate or worsen Wernicke encephalopathy.

Occipital lobe

Unilateral lesions. The primary visual cortex lines the calcarine sulcus. A posterior cerebral artery (PCA) infarct causes a contralateral homonymous hemianopia with macular sparing, because the occipital pole, where central vision is represented, also receives collateral MCA supply.

Bilateral lesions. Bilateral occipital infarcts, for example from an embolus to the top of the basilar artery, cause cortical blindness. Pupillary light reflexes stay normal because the reflex runs from the optic tract to the pretectal nucleus, bypassing the lateral geniculate body and cortex. In Anton syndrome the patient denies being blind and confabulates descriptions of the room.

Alexia without agraphia. A left PCA infarct that destroys the left visual cortex and the splenium of the corpus callosum disconnects the intact right visual cortex from left-hemisphere language areas. The patient writes normally but cannot read, even what he has just written, and has a right homonymous hemianopia.

Aphasias

Aphasia versus dysarthria. Aphasia is a disorder of language itself (comprehension, word choice, grammar, reading and writing) from dominant-hemisphere cortex, which is left-sided in about 95% of right-handers and in most left-handers. Dysarthria is poor articulation with normal language, from brainstem, cerebellar or corticobulbar lesions; a dysarthric patient writes normally. In the classic model, a heard word travels from the primary auditory cortex (Heschl gyrus) to Wernicke area, then through the arcuate fasciculus to Broca area and the face and larynx motor cortex. Aphasias are classified by fluency, comprehension and repetition.

Broca aphasia. Damage to the posterior inferior frontal gyrus (Brodmann areas 44 and 45), usually from occlusion of the superior division of the left MCA, produces effortful, telegraphic, agrammatic speech with poor repetition but good comprehension. Patients recognize their errors and are frustrated, and involvement of the neighboring motor cortex often adds right face and arm weakness.

Wernicke aphasia. Damage to the posterior superior temporal gyrus (area 22), usually from the inferior division of the left MCA, produces fluent speech with normal rhythm but paraphasias, neologisms and little meaning ("word salad"), with poor comprehension and repetition. Patients are often unaware of the problem and may be mistaken for psychotic; hemiparesis is usually absent, though a right superior quadrantanopia can accompany it.

Conduction and global aphasia. An arcuate fasciculus or supramarginal gyrus lesion leaves speech fluent and comprehension good but makes repetition strikingly poor, with phonemic paraphasias the patient tries to correct. A large left MCA stem infarct destroys the whole perisylvian region, causing global aphasia with right hemiplegia and hemianopia.

Transcortical aphasias. Watershed infarcts after prolonged hypotension or with carotid stenosis spare the perisylvian loop but isolate it from surrounding cortex, so repetition is preserved, sometimes as echolalia. Transcortical motor aphasia (ACA–MCA border zone, anterior to Broca) resembles Broca aphasia with intact repetition; transcortical sensory aphasia (MCA–PCA border zone, posterior to Wernicke) resembles Wernicke aphasia with intact repetition.

If the patient can repeat, the perisylvian loop is intact: think transcortical (watershed) or anomic aphasia.

Vascular territories and the homunculus

Reading the homunculus. On the motor and sensory strips, the face and hand lie on the lateral convexity (MCA territory), while the leg and foot hang over the medial surface in the paracentral lobule (ACA territory). The weakest body part therefore points to the vessel.

Aphasia, neglect or a field cut places the lesion in the cortex; equal face, arm and leg weakness without cortical signs suggests a lacune in the internal capsule.