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The hemispheresHemispheresintermediate · 50 min

09 The hemispheres: lobes, proportions and the visual pathway

The cortex is where localization becomes least precise and also most interesting, because a lesion there can take away abilities that no lower level of the nervous system can touch.

The cortex is where localization becomes least precise and most interesting. A lesion there can take away a word, half of the visual world, or a person's awareness that anything is missing at all.

From the history

In 1865 Paul Broca (1824–1880) wrote that we speak with the left hemisphere, and noticed that a small lesion could abolish speech while a much larger one only impaired it. Nine years later Carl Wernicke (1848–1905) placed the understanding of words in the temporal lobe. (Brazis 2011, pp. 1-2)

By the end of this module you can

  • Recognize the signs that only a cortical lesion can produce, and use them to lift a hemiparesis to the hemisphere.
  • Use the proportion of face, arm and leg weakness to separate lateral cortex, medial cortex and internal capsule.
  • Map a visual field defect to its site, and test the fields in a child.
  • Separate acquired from developmental language problems, and recognize the exam patterns of perinatal brain injury.
01

Signs of a cortical lesion

In the cord and the brainstem you localize by wiring, because tracts cross at known levels and nuclei sit beside them. The hemispheres call for different reasoning. Much of what we know about where functions live there was first learned from strokes and other lesions, true "experiments of Nature" (Brazis 2011, p. 493). At the bedside you read the map by noticing which abilities have gone missing.

Signs that point to the cortex

A cord or brainstem lesion can weaken a hand, but only a hemisphere lesion can take away the ability to name that hand, to notice it, or to recognize a coin placed in it. Cortical signs include these (Pearl 2014, p. 108).

  • Aphasia, from a lesion of the language-dominant hemisphere, which is the left in almost all right-handers.
  • Homonymous visual field cuts.
  • Cortical sensory loss, in which touch is felt but an object goes unrecognized, two points cannot be told apart, and a number drawn on the palm cannot be read.
  • Agnosia and neglect, classically of the left side of space after a right parietal lesion.
  • Apraxia, in which a strong limb with normal sensation cannot carry out a complex task.
  • A dissociated weakness, with the face and arm affected differently from the leg (next section).

Seizures and gaze preference also belong here. A seizure arises in the cortex, and a focal seizure is often the most precise localizing sign a child gives. A gaze preference comes from the frontal eye fields, each of which drives the eyes toward the opposite side. A destructive lesion lets the eyes drift toward the lesion, and a seizure drives them away (Pearl 2014, pp. 9-10).

Hemiparesis and its neighboring signs

When you find a hemiparesis, look for aphasia, hemisensory loss, homonymous hemianopia, unawareness of the deficit and a history of focal seizures (Brazis 2011, p. 11). Any one of them places the lesion above the brainstem, usually in the cortex or the white matter beneath it. A pure motor hemiparesis with none of them points deeper, to the internal capsule or the brainstem (Brazis 2011, p. 12).

In a child

Young children cannot report most of these signs, so watch for them. In a toddler neglect looks like ignoring the toys on one side, apraxia like failing to copy a simple gesture, and aphasia like losing words that were there last month.

Key points

  • Much of cortical localization was first learned from strokes and other lesions, the "experiments of Nature" (Brazis 2011, p. 493).
  • The signatures of a cortical lesion include aphasia, homonymous field cuts, cortical sensory loss, neglect, apraxia and a dissociated weakness (Pearl 2014, p. 108).
  • A destructive frontal lesion lets the eyes drift toward the lesion, and a seizure drives them away from it (Pearl 2014, pp. 9-10).
  • A hemiparesis with cortical signs beside it lies in the hemisphere, while a pure motor hemiparesis points deeper (Brazis 2011, pp. 11-12).

Check your understanding

A 10-year-old wakes with weakness of his left arm and the lower half of his face. His eyes rest looking to the right, he ignores you when you stand on his left, and he does not seem troubled by the weakness. Where is the lesion?

Select an answer to reveal the explanation


02

Reading the proportions of a weakness

The motor strip lies like a figure upside down over the surface of the hemisphere. The face sits low on the lateral convexity, with the arm and hand above it, and the leg folds over the top onto the medial surface between the two hemispheres. The blood supply matches, with the middle cerebral artery feeding the lateral convexity, which holds the face, arm and tongue, and the anterior cerebral artery feeding the medial surface, which holds the leg (Pearl 2014, p. 7).

Comparing face, arm and leg

The proportions of a weakness therefore tell you where the lesion is. Grade the face, arm and leg separately and compare them with the table (Pearl 2014, pp. 7, 9-10, 108-109; Brazis 2011, p. 11).

PatternWhere
Face and arm more than legLateral cortex and the white matter under it: middle cerebral territory
Leg more than arm, face sparedMedial cortex near the top of the hemisphere: anterior cerebral territory
Face, arm and leg equalInternal capsule, where the fibers are packed tightly together

In the cortex the fibers for face, arm and leg spread over a large surface, so a lesion usually catches one part more than another. In the internal capsule the same fibers are bundled into a small space, so one small lesion can take all of them equally (Pearl 2014, p. 7).

The face tells you the level

Upper motor neuron facial weakness usually spares the forehead, because the upper face receives cortical input from both sides. When a lower facial droop is on the side of a hemiparesis, the lesion is generally above the upper pons, most often in the cortex, the corona radiata or the internal capsule (Brazis 2011, p. 11). If the lower face is spared and the tongue deviates toward the strong side, consider a functional weakness (Brazis 2011, p. 12).

Tumors, seizures and children

Tumors do not respect vascular territories, so their deficits are less tidy and build up over time (Pearl 2014, p. 10). Most childhood hemispheric lesions are not strokes, so check the proportions against the rest of the story. A focal motor seizure can show the same map in motion. Twitching that spreads from the face to the hand and then to the leg is following the order of the motor strip (Pearl 2014, p. 10).

Watch it at the bedside
Hemiplegic gait

Circumduction of the leg, with the arm flexed and the thumb tucked into the fist on the same side.

NeuroLogic Exam, Larsen & Stensaas. CC BY-NC-SA. Source · Credits

Central facial weakness

Weakness of the lower face with the forehead relatively spared, the pattern of an upper motor neuron lesion.

NeuroLogic Exam, Larsen & Stensaas; courtesy of Alejandro Stern, Stern Foundation. CC BY-NC-SA. Source · Credits

Key points

  • The middle cerebral artery serves the face, arm and tongue, and the anterior cerebral artery serves the leg (Pearl 2014, p. 7).
  • Face and arm weaker than leg suggests the lateral cortex, leg weaker than arm suggests the medial cortex, and equal weakness of all three suggests the internal capsule.
  • Upper motor neuron facial weakness spares the forehead, and a lower facial droop on the side of a hemiparesis generally places the lesion above the upper pons (Brazis 2011, p. 11).
  • Tumors do not respect vascular territories, so in children proportion is a guide that needs checking (Pearl 2014, p. 10).

Check your understanding

A 14-year-old has a weak right leg, slight clumsiness of the right hand, a normal face and normal speech. The right knee and ankle reflexes are brisk. Where is the lesion most likely to be?

Select an answer to reveal the explanation


03

The visual pathway

Visual pathwayTap a point on the pathway. Each eye's field is calculated by following its fibers, and only the nasal fibers cross at the chiasm.
left eyeright eyeMeyer'sloopoccipital cortex

Seen from above, patient's left on the left.

Left eye
Right eye

Optic chiasm: Bitemporal hemianopia.

Fields are drawn as the patient sees them, left field on the left. Black is lost. Real tract and radiation defects are often incongruous (unequal in the two eyes), and they become more congruous closer to the occipital lobe; macular sparing reflects the occipital pole's dual blood supply (Pearl 2014, pp. 27-28).

The visual pathway localizes better than any other system in the hemispheres. It runs from the front of the brain to the back, and damage to each segment leaves its own pattern in the visual field, and three anatomical facts explain most of those patterns.

Three anatomical facts

  • The image is reversed and inverted. The nasal retina sees the temporal field and the lower retina sees the upper field, and that inversion persists all the way back (Pearl 2014, pp. 26-27).
  • Nasal fibers cross at the chiasm. Behind the chiasm, each hemisphere carries the opposite half of space from both eyes.
  • Behind the thalamus the fibers fan out. Those carrying the upper field loop forward through the temporal lobe in Meyer's loop, and those carrying the lower field run through the parietal lobe (Pearl 2014, p. 27).

Defects by site

  • Optic nerve: one eye, often with a central scotoma.
  • Chiasm: both temporal fields, a bitemporal hemianopia.
  • Optic tract: the opposite half-field of both eyes, a homonymous hemianopia.
  • Temporal lobe: the opposite upper quadrant.
  • Parietal lobe: the opposite lower quadrant.
  • Occipital lobe: an opposite homonymous hemianopia, often sparing central vision (Pearl 2014, pp. 27-28).

Try each site in the figure above and watch which quadrants go dark.

Occipital lesions

Near the calcarine cortex the fibers from the two eyes gather into tight bundles, so a lesion there affects both eyes alike, a congruous defect. The macular area also has a dual blood supply, from the posterior and middle cerebral arteries, so a posterior cerebral infarct often spares central vision. The more congruous and the more macula-sparing the defect, the more confidently you can place the lesion in the occipital lobe (Pearl 2014, pp. 27-28).

Testing a child

Test each eye separately, and make sure the child's eyes stay on your face. Counting fingers in each quadrant is the best bedside method. Wiggling fingers is easier for children but less sensitive (Pearl 2014, p. 26). In younger children a small toy brought in from the side, or a blink to a threatening hand, can stand in. Presenting stimuli on both sides at once looks for extinction, a sign of neglect (Pearl 2014, p. 26). Children rarely report a field defect themselves. The first hint is often bumping into door frames on one side, or missing the start of each line when reading.

Watch it at the bedside
Homonymous hemianopia on confrontation

Loss of the right half of the visual field in both eyes, from a lesion behind the chiasm on the left.

NeuroLogic Exam, Larsen & Stensaas. CC BY-NC-SA. Source · Credits

Key points

  • The retinal image is inverted and the nasal fibers cross, so behind the chiasm each hemisphere sees the opposite half of space (Pearl 2014, pp. 26-27).
  • A chiasmal lesion gives a bitemporal defect, a tract lesion a homonymous one, a temporal lesion the opposite upper quadrant and a parietal lesion the opposite lower quadrant.
  • The more congruous and macula-sparing the defect, the more likely the lesion is occipital (Pearl 2014, pp. 27-28).
  • Test each eye separately, prefer finger counting to finger wiggling, and present stimuli on both sides at once to look for extinction (Pearl 2014, p. 26).

Check your understanding

A 12-year-old with headaches is found on confrontation to miss your fingers in the upper left quadrant of both eyes. The defect is roughly similar in each eye but not identical. Where is the lesion most likely to be?

Select an answer to reveal the explanation


04

Language and the developing brain

In the 1860s Paul Broca argued that language belongs to the left hemisphere. That overturned the old assumption that paired organs do identical work, and aphasia has stayed at the center of debates about localization ever since (Brazis 2011, p. 1). His central claim still holds in the clinic, since the left hemisphere is dominant for language in almost all right-handed people (Pearl 2014, p. 10).

Go deeper: Broca's caution about lesion size

In Broca's patients, the size of the lesion in the left inferior frontal gyrus did not reliably predict how much speech was lost. A lesion of 8 to 10 mm could abolish speech, while one ten times larger only impaired it (Brazis 2011, p. 1). The map is real, but individual brains differ in how they use it, and this variation is now read as an early sign of cortical plasticity.

Testing language

At the bedside, test language in six parts, which are fluency, comprehension, repetition, naming, reading and writing. A school-aged child can name pictures, follow a command with several steps, repeat a phrase, read a sentence and write their name. Each pattern of loss points to a different part of the left hemisphere. One well-known disconnection shows how literally the map can work. A lesion of the left visual cortex and the back of the corpus callosum leaves a patient able to write but unable to read, even what they have just written (Pearl 2014, p. 28).

Delayed language or lost language

With a child, ask first whether language was ever gained, and only then where the lesion is. A child whose language has always been behind most likely has a developmental language disorder, once hearing has been checked and nothing else in the story points elsewhere. That kind of delay does not localize to a focal lesion. In most people the back of the left inferior frontal gyrus is larger than the right, but this asymmetry is not found in autism or developmental language disorder (Brazis 2011, p. 493). A child who loses words they once had, over hours or days, has an acquired aphasia. That is a localizing sign, and it needs an urgent explanation.

Recovery after early injury

Children injured early in life often regain more language than adults with similar lesions, because the developing brain can reorganize. The recovery varies and is rarely complete in every respect. No published figure will fit the child in front of you, so offer the family close follow-up of their own child's progress rather than a percentage.

Key points

  • The left hemisphere is dominant for language in almost all right-handers (Pearl 2014, p. 10).
  • Broca saw that the size of a lesion did not predict how much speech was lost, an observation now read as evidence of cortical plasticity (Brazis 2011, p. 1).
  • Language that was never gained suggests a developmental disorder, whereas language that is lost is an acquired, localizing sign.
  • Children often recover more language than adults after early injury, but the course is variable, so avoid promising numbers.

Check your understanding

A 5-year-old whose speech was normal for age last week now speaks in short, effortful phrases, cannot name a cup or a key, and has a slightly weak right hand. Which reading is most accurate?

Select an answer to reveal the explanation


05

Aphasia as four switches

Aphasia as four switchesEvery patient below describes the same picture. Set the four bedside tests and see which syndrome, and which part of the brain, fits the result.
Speech
Comprehension
Repetition
Naming
A picture: a girl's kite is stuck in a tree; her brother climbs a ladder to fetch it, and the ladder wobbles.

"Kite... tree... boy... up. Ladder... wobble."

Broca (expressive) aphasia. Inferior frontal lobe, dominant hemisphere.

After Pearl 2014, p. 20 (Table 2.1), with conduction and mixed transcortical aphasia from Brazis 2011, pp. 524 and 448. The adult classification; acquired aphasia in children does not always follow it. Sample speech is ours.

Once you know a child has lost language, ask which part has gone. The answer rests on Broca's area in the frontal lobe, Wernicke's area in the temporal lobe, and the pathway between them, which Wernicke said could cause aphasia wherever it was interrupted (Brazis 2011, p. 2).

Four bedside tests

Four tests do the work (Pearl 2014, pp. 18-20).

  • Fluency: is speech effortful and sparse, or does it flow?
  • Comprehension: can the child carry out a spoken command without copying you?
  • Repetition: can the child say a phrase back word for word?
  • Naming: can the child name a cup, a key, a shoe?

Each combination corresponds to a classic syndrome (Pearl 2014, p. 20, Table 2.1). Nonfluent speech with understanding preserved is Broca aphasia, from the dominant frontal lobe. Fluent speech with understanding lost is Wernicke aphasia, from the dominant temporal lobe (Pearl 2014, pp. 18-19). Losing both gives global aphasia, usually from a large lesion.

Repetition then splits each of these patterns in two. Preserved repetition means the lesion has spared the core language areas and lies in the cortex around them, which gives the transcortical motor and sensory aphasias (Pearl 2014, p. 20). Fluent speech and good understanding with failed repetition is conduction aphasia. Speech stays intelligible but contains sound errors, and the lesion usually lies around the supramarginal gyrus or the pathway linking the language areas (Brazis 2011, p. 524).

Naming fails in nearly every aphasia, so anomia alone localizes poorly (Pearl 2014, p. 20).

Go deeper: Aphasia from the thalamus

When output and understanding both fail but repetition survives, the pattern is a mixed transcortical aphasia (Pearl 2014, p. 20). Even the dominant thalamus, a deep gray structure rather than language cortex, can cause aphasia. It is usually a mixed transcortical picture that tends to improve over weeks (Brazis 2011, p. 448; Pearl 2014, p. 20).

Using the figure

In the figure, the child always describes the same picture, a kite stuck in a tree and a brother on a wobbling ladder, so every difference in what the child says comes from the lesion you chose.

Conditions that mimic aphasia

Slurred speech made of well-built sentences is dysarthria, a disorder of articulation rather than of language (Pearl 2014, p. 20). Neither cerebellar mutism, the silence that can follow removal of a cerebellar tumor, nor the speech of a confused, encephalopathic child should be read as a cortical aphasia (Pearl 2014, p. 20).

Applying adult syndromes to children

The four tests and their syndromes come from adult patients. A child's acquired aphasia may not sort as neatly, sit where an adult's would, or recover on an adult's schedule. Use the scheme to describe what you hear, and be cautious about predicting from it.

Watch it at the bedside
Expressive aphasia

Halting, effortful speech made mostly of nouns and verbs, with frustration and good comprehension.

NeuroLogic Exam, Larsen & Stensaas. CC BY-NC-SA. Source · Credits

Key points

  • Fluency, comprehension, repetition and naming are the four bedside tests that sort the aphasias (Pearl 2014, p. 20, Table 2.1).
  • Preserved repetition places the lesion in the cortex around the language core, as in the transcortical aphasias (Pearl 2014, p. 20).
  • Fluent speech and good understanding with failed repetition is conduction aphasia (Brazis 2011, p. 524), and a dominant thalamic lesion gives a mixed transcortical picture that improves over weeks (Brazis 2011, p. 448).
  • Anomia on its own is relatively nonlocalizing (Pearl 2014, p. 20).
  • Dysarthria, cerebellar mutism after posterior fossa surgery and encephalopathy can all imitate aphasia (Pearl 2014, p. 20).

Check your understanding

A 12-year-old is recovering from a left hemisphere injury. She talks in full sentences at a normal rate and carries out three-step commands. Asked to repeat "the ladder wobbles", she says "the lather... the ladder wobbers" and gives up. Naming is patchy, with sound errors. How do you classify her language, and what does it suggest about the lesion?

Select an answer to reveal the explanation


06

Perinatal brain injury

In the nineteenth century both William Little and Sigmund Freud wrote on the origins of cerebral palsy (George 1992). Cerebral palsy is a lasting disorder of movement and posture caused by injury to the developing brain, before or around birth or in early infancy. Two patterns of early injury are common enough that every child neurologist should recognize them from the examination alone. In both, the shape of the deficit reflects where the injury fell.

Early hand preference and perinatal stroke

A stroke around the time of birth often goes unnoticed in the newborn period, and the first sign may be a baby who reaches with only one hand. Hand preference before the first birthday is abnormal and points to weakness of the other hand, because true handedness develops only after twelve months (Utah PediNeuroLogic Exam). The child later shows a hemiplegia, with the arm and hand more affected than the leg, a fisted hand, and a leg that circumducts when walking (DeMyer, p. 340). Those are the proportions of the lateral cortex and the middle cerebral territory.

Spastic diplegia after premature birth

The premature brain is vulnerable in a different place. Its characteristic injury is periventricular leukomalacia, damage to the white matter around the lateral ventricles, often with injury to neurons and axons as well (Volpe 2009). The fibers for the legs pass closest to the ventricles on their way down from the medial cortex, so they are caught first. The result is spastic diplegia, with severe spasticity in the legs, little in the arms, and little or no trouble with speech or swallowing. Double hemiplegia is the reverse, with the arms weaker than the legs and with pseudobulbar palsy (DeMyer, p. 340). Children with spastic diplegia walk on their toes, scissor their legs or walk in a crouch.

Deep gray matter injury

Injury to the basal ganglia and thalamus around birth, classically from hypoxia, produces a third pattern, in which slow writhing movements are mixed with spasticity (DeMyer, p. 340). Its anatomy is covered with the loops in Module 8.

At the bedside

When an infant shows an early hand preference, examine the neglected hand for tone, reflexes and fisting, and ask about the pregnancy and delivery. When a child born early walks on the toes with stiff legs and good hands, the history and the proportions point to the periventricular white matter before any imaging does.

Watch it at the bedside
Diplegic gait

Spastic, weak legs swung around in circumduction on both sides, with the arms much less affected.

NeuroLogic Exam, Larsen & Stensaas. CC BY-NC-SA. Source · Credits

Key points

  • Hand preference before the first birthday is abnormal and points to weakness of the other hand (Utah PediNeuroLogic Exam).
  • Hemiplegic cerebral palsy after perinatal stroke affects the arm more than the leg, with a fisted hand and a circumducting leg (DeMyer, p. 340).
  • Periventricular leukomalacia is the characteristic white-matter injury of prematurity (Volpe 2009).
  • Spastic diplegia affects the legs much more than the arms and spares speech and swallowing, whereas in double hemiplegia the arms are weaker than the legs (DeMyer, p. 340).

Check your understanding

A 7-month-old reaches for every toy with the left hand. The right hand is often fisted with the thumb tucked in, and the right arm reflexes are brisker than the left. The pregnancy and birth were uneventful at term. What is the most likely explanation?

Select an answer to reveal the explanation

Module quiz

5 vignettes

Read every section first. The quiz unlocks when the last section has been on screen.

Sign-off · with a faculty reader

The resident maps the visual fields of two children and names the lesion site in each, with a faculty member.

Read and watch

These sites are free but grant no reuse licence, so this module links to their pages rather than copying their figures.

Sources

  1. Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2011.
  2. Pearl PL, Emsellem HA. Neuro-Logic: A Primer on Localization. New York: Demos Medical; 2014.
  3. Biller J, Gruener G, Brazis PW. DeMyer's The Neurologic Examination: A Programmed Text. 6th ed. New York: McGraw-Hill.
  4. Volpe JJ. Brain injury in premature infants: a complex amalgam of destructive and developmental disturbances. Lancet Neurol. 2009;8(1):110-124. PMID 19081519 ↗
  5. Larsen PD, Stensaas SS. PediNeuroLogic Exam: A Neurodevelopmental Approach. University of Utah; updated 2020. Videos CC BY-NC-SA. link ↗
  6. George MS. Changing nineteenth century views on the origins of cerebral palsy: W. J. Little and Sigmund Freud. J Hist Neurosci. 1992;1(1):29-37. PMID 11618412 ↗

The interactive figures are calculated from our own models of the anatomy, and exam videos are from the University of Utah NeuroLogic Exam (CC BY-NC-SA); see credits. For education. Not for clinical decision-making; consult primary sources and your attending.