The Areas of the Cerebrum

 The Areas of the Cerebrum

There is a particular moment in every student's encounter with the brain when the sheet of grey matter stops being a wrinkled mass and becomes a geography. A precise strip here moves the hand. A patch two centimetres behind it feels the hand. A region on the left inferior frontal gyrus, when it dies, takes away a person's ability to speak but not their ability to understand. The cerebrum turns out to have provinces, each with its own architecture, its own wiring, and its own characteristic way of failing.

This article is a tour of those provinces. It is written for anyone who wants more than a coloured diagram with four lobes on it, medical students, psychology students, clinicians refreshing their localisation, and curious readers who want the real thing rather than the pop-science version. Throughout, I have tried to do two things at once: give you the classical map as it appears in Guyton & Hall, Kandel, Snell and Blumenfeld, and then be honest about where that classical map has been amended, complicated, or quietly overturned by the last two decades of imaging.

Because the second part matters. A great deal of what is taught about cortical areas is a nineteenth- and early-twentieth-century inheritance, Broca in 1861, Wernicke in 1874, Brodmann in 1909, Penfield in 1937, and while those findings were extraordinary, the people who made them were working with the tools they had. Modern re-examination of the very brains Broca described, and modern parcellations of the living cortex, have changed the picture in ways that textbook diagrams have been slow to catch up with.

1. Orientation: what we mean by "the cerebrum"

The cerebrum (telencephalon) is the largest division of the human brain: two hemispheres joined by the corpus callosum, each consisting of an outer mantle of grey matter- the cerebral cortex, enclosing a core of white matter within which sit the basal ganglia, the amygdala, and the lateral ventricles.

Some numbers worth holding onto, because they make the rest intelligible:

• The cortical sheet is roughly 2 to 4.5 mm thick, thinnest in primary visual cortex and thickest in primary motor cortex.
• Unfolded, it would cover approximately 2,200–2,500 cm², about the area of a large pillowcase. Roughly two-thirds of it is hidden inside the sulci.
• It contains on the order of 16 billion neurons, about 19% of the brain's ~86 billion, with the cerebellum holding far more by count (Azevedo et al., 2009; Herculano-Houzel, 2009).
• Cortical neurons are outnumbered many times over by their connections: each pyramidal neuron may receive tens of thousands of synapses.

The folding is not decorative. Gyri and sulci are the solution to a packing problem, they allow a large sheet inside a skull constrained by the pelvic outlet, and, crucially for us, the major sulci are reliable enough across individuals to serve as landmarks. Four of them do most of the work:

• The central sulcus (of Rolando), separating frontal from parietal lobe, with the precentral gyrus in front (motor) and postcentral gyrus behind (somatosensory).
• The lateral sulcus (Sylvian fissure), separating the temporal lobe below from frontal and parietal above, and hiding the insula in its depths.
• The parieto-occipital sulcus, visible mainly on the medial surface.
• The calcarine sulcus, on the medial occipital surface, around which primary visual cortex is arranged.

FrontalParietalTemporalOccipitalM1 (BA 4)S1 (BA 3,1,2) Broca (44/45) Wernicke (22)V1 (17)A1 (41/42) insula (deep)Schematic lateral view of the left hemisphere. The central sulcus (red) divides the motor strip from the sensory strip; the lateral sulcus (teal) separates the temporal lobe and conceals the insula. Diagram is conceptual, not to anatomical scale.

On this framework sit the classical lobes: frontal, parietal, temporal, occipital, plus the insula buried in the Sylvian fissure and the limbic lobe ringing the corpus callosum on the medial surface. The lobes are named after the overlying skull bones, which tells you something important: they are cranial conveniences, not functional units. No lobe does one thing. Almost every interesting function crosses lobar boundaries.

2. The six-layered cortex: why areas exist at all

The reason the cortex can be divided into areas at all is that its microscopic structure changes from place to place. Most of the cerebral cortex is neocortex (isocortex), organised in six layers running from the pial surface inward. Kandel's Principles of Neural Science and Purves' Neuroscience both treat this laminar scheme as the foundation of cortical organisation, and it repays learning properly.

Table 1. The six neocortical layers and their principal connections.
Layer	Name	Dominant cells	Principal role
I	Molecular	Few neurons; dendrites and axons	Apical dendritic tufts; horizontal integration
II	External granular	Small pyramidal, stellate	Cortico-cortical (association) output
III	External pyramidal	Medium/large pyramidal	Main source of cortico-cortical and callosal fibres
IV	Internal granular	Stellate (granule) cells	Main input layer from specific thalamic nuclei
V	Internal pyramidal	Large pyramidal (Betz cells in M1)	Main output to subcortical targets: cord, brainstem, striatum
VI	Multiform / fusiform	Varied	Feedback output to the thalamus

Two variations on this theme explain most regional differences:

• Granular cortex (koniocortex). Primary sensory areas have a hypertrophied layer IV, packed with small stellate cells receiving thalamic input. Area 17 (V1) is the extreme case, so densely input-laden that a visible white stripe, the stria of Gennari, runs through layer IV and gives striate cortex its name.
• Agranular cortex. Primary motor cortex (area 4) has essentially no layer IV and an enormously expanded layer V containing the giant Betz cells. It is an output structure, and its histology says so.

Between these poles lie the association areas, with balanced layers. This is the whole principle behind cytoarchitectonics: if the cell packing changes at a sharp boundary, you are probably looking at a functional border.

The columnar principle

Cortex is also organized vertically. Mountcastle's recordings in somatosensory cortex (1957), and Hubel and Wiesel's work in visual cortex (Nobel Prize, 1981), established that neurons in a radial column running from pia to white matter share receptive field properties, the same patch of skin, the same line orientation. The column, roughly 300–600 µm wide, is often described as the cortex's functional module. The strong version of that claim (a canonical, repeating microcircuit performing one computation everywhere) is now debated, but the basic vertical clustering is well established.

3. How the map was made- four methods, four kinds of evidence

It is worth pausing on epistemology, because the confidence with which textbooks assert "area X does Y" varies enormously depending on which of these four methods produced the claim.

3.1 Lesion–deficit correlation

The oldest method: a patient loses a function, dies, and the brain is examined. Paul Broca's 1861 presentation of the patient Leborgne, who could produce essentially one syllable, "tan", and subsequently Lelong, established the left inferior frontal gyrus as critical for articulate speech. Carl Wernicke's 1874 monograph did the same for comprehension and the posterior superior temporal gyrus. The method's strength is causality; its weakness is that lesions do not respect areal borders and that removing a node disrupts a network, not just a function.

3.2 Cytoarchitectonics

In 1909 Korbinian Brodmann published Vergleichende Lokalisationslehre der Grosshirnrinde, dividing the human cortex into numbered areas on the basis of cell architecture alone, without any knowledge of what most of them did. The numbering scheme, 1 to 52, though not all appear in humans, survives to this day, not because it is perfect but because it turned out to be startlingly predictive: areas 4, 17, 41 and 3/1/2, defined purely by histology, mapped onto motor, visual, auditory and somatosensory function respectively. Zilles and Amunts' centenary review in Nature Reviews Neuroscience (2010) is the best short account of both the achievement and its limits.

3.3 Direct electrical stimulation

Wilder Penfield, operating on awake epilepsy patients in Montreal from the 1930s, stimulated the exposed cortex and recorded what patients reported or did. Penfield and Boldrey's 1937 paper in Brain produced the somatotopic maps that became the motor and sensory homunculi, the distorted little figures with enormous hands and lips. This method is causal and millimetre-precise, but it is only ever performed on diseased brains, and stimulation can propagate along fibre tracts.

3.4 Functional and structural neuroimaging

PET from the 1980s and fMRI from the 1990s made it possible to watch the intact human cortex work. Diffusion imaging added the fibre tracts. The contemporary culmination is the Human Connectome Project's multi-modal parcellation, which used architecture, function, connectivity and topography together to delineate 180 areas per hemisphere, of which 97 had never previously been described (Glasser et al., Nature, 2016).

4. Three grades of cortical area

Before going lobe by lobe, it helps to have the functional taxonomy, which cuts across lobar boundaries and is used consistently in both Guyton & Hall and Kandel:

1. Primary areas. One modality, one topographic map, direct connection to the periphery via a specific thalamic relay (or, for motor cortex, direct output to the cord). Damage produces elementary loss: hemiparesis, hemianaesthesia, hemianopia.
2. Unimodal (secondary/association) areas. Adjacent to the primary area, still one modality, but processing complex features- movement in vision, phonemes in audition, texture in touch. Damage produces agnosia: the raw sensation is intact; the meaning is not.
3. Heteromodal (multimodal) association areas. Prefrontal, posterior parietal, and lateral temporal cortex, where modalities converge. Damage produces disorders of attention, language, planning, and self, the syndromes that are hardest to describe and most devastating to live with.

Roughly speaking, the primary areas occupy a small minority of the human cortical sheet. The overwhelming majority is association cortex, and its disproportionate expansion, particularly prefrontal and parietal, is the main structural story of human brain evolution.

5. The frontal lobe

The frontal lobe extends from the frontal pole to the central sulcus, bounded below by the lateral sulcus. It is the largest lobe, comprising roughly a third of the cortex, and it is organized as a gradient: the further forward you go, the more abstract the control.

5.1 Primary motor cortex- BA 4

M1 occupies the precentral gyrus and the anterior wall of the central sulcus, continuing onto the medial surface as the anterior part of the paracentral lobule. Its defining features:

• Agranular architecture with a prominent layer V containing Betz cells, the largest neurons in the cortex, roughly 30,000–40,000 per hemisphere. Notably, Betz cells contribute only a small fraction (on the order of 3–5%) of corticospinal axons; the tract is mostly composed of smaller pyramidal fibres, and only about 30% of the corticospinal tract originates in M1 at all, the remainder coming from premotor areas and the parietal lobe.
• Lowest stimulation threshold of any cortical region for producing movement.
• Somatotopic organization, the motor homunculus, running from the foot and leg on the medial surface (paracentral lobule) through trunk, arm and hand on the lateral convexity to face, lips and tongue near the Sylvian fissure. Representation size scales with dexterity, not muscle mass: hand and mouth dominate.

Clinical correlation

A discrete M1 lesion produces contralateral upper motor neuron weakness: initially flaccid, later spastic with hyperreflexia and an extensor plantar response. Because the leg sits on the medial surface within the anterior cerebral artery territory while the face and arm sit laterally in the middle cerebral artery territory, the pattern of weakness localises the vessel. Focal irritation instead produces a Jacksonian march, a seizure spreading along the homuncular sequence, from thumb to hand to arm to face, described by Hughlings Jackson in the 1860s and still one of the most elegant clinical proofs of somatotopy.

5.2 Premotor cortex and the supplementary motor area- BA 6

Immediately anterior to M1, area 6 divides into a lateral premotor cortex (PMC) and a medial supplementary motor area (SMA). Both project to M1 and directly to the cord, and both are concerned with movement that is prepared rather than merely executed.

• Premotor cortex is weighted toward externally guided movement- reaching toward a seen object, shaping the hand to a visible target. It is strongly linked to posterior parietal cortex, which supplies the spatial coordinates.
• SMA is weighted toward internally generated and sequenced movement. Its readiness potentials precede voluntary action by up to a second; SMA lesions produce transient akinesia and mutism, and SMA is implicated in the "alien hand" phenomena seen after medial frontal or callosal damage.
• Damage to premotor areas with intact M1 gives apraxia: the patient has the strength and the intention but cannot assemble the act.

5.3 Frontal eye field- BA 8

Anterior to premotor cortex, the frontal eye field drives contralateral saccadic gaze. Stimulation deviates the eyes away from the stimulated side; destruction causes transient deviation toward the lesion ("the patient looks at the lesion"); an irritative seizure focus drives the eyes away from it. This trio is one of the highest-yield localisation facts in clinical neurology.

5.4 Broca's area- BA 44, 45

In the inferior frontal gyrus of the dominant (usually left) hemisphere, pars opercularis (44) and pars triangularis (45) constitute Broca's area. The classical account: this is the motor programming centre for speech, and its destruction yields Broca's (expressive, non-fluent) aphasia- effortful, telegraphic, agrammatic output with relatively preserved comprehension and preserved insight, which makes it a peculiarly distressing condition.

What modern imaging did to Broca's area

Broca preserved his patients' brains intact rather than sectioning them, and they have been held at the Musée Dupuytren in Paris ever since. In 2007, Dronkers and colleagues put both brains through high-resolution MRI (Brain, 130:1432–1441). The lesions turned out to extend well beyond the inferior frontal gyrus- involving the insula, basal ganglia, and critically the superior longitudinal/arcuate fasciculus- damage Broca could not possibly have seen from the surface. Earlier CT work by Signoret et al. (1984) had already suggested as much.

The authors were explicit that this does not diminish Broca's achievement. But it does mean that the classic picture, a small cortical patch as "the speech centre", was never quite what the founding cases showed. Persistent non-fluent aphasia generally requires deeper white-matter involvement; a lesion confined to BA 44/45 often produces only transient mutism.

5.5 Prefrontal cortex- BA 9, 10, 11, 12, 46, 47

Everything anterior to the motor and premotor areas is prefrontal cortex: the most expanded region in the human brain relative to other primates, and the seat of what is loosely called executive function. It is usefully divided into three functional–anatomical sectors.

Table 2. Prefrontal sectors, functions, and characteristic deficits.
Sector	Approx. areas	Function	Lesion syndrome
Dorsolateral prefrontal (DLPFC)	9, 46	Working memory, set-shifting, planning, sustained attention, abstraction	Dysexecutive syndrome: perseveration (classically on the Wisconsin Card Sorting Test), poor planning, reduced verbal fluency, apathy
Orbitofrontal / ventromedial	11, 12, 47, 10 (medial)	Value, reward, inhibition of socially inappropriate behaviour, somatic markers in decision-making	Disinhibition, impulsivity, tactlessness, emotional shallowness, poor real-world decisions despite normal IQ
Anterior cingulate (medial)	24, 32, 33	Conflict monitoring, error detection, effort allocation, motivation, autonomic control	Akinetic mutism, abulia, apathy; bilateral damage can abolish spontaneous behaviour entirely

The orbitofrontal syndrome has a famous exemplar. In 1848 an iron tamping rod passed through the head of the railway foreman Phineas Gage, and his physician John Harlow recorded a change in personality without loss of intellect or motor function. Damasio and colleagues re-examined Gage's skull with modern computational modelling in Science (1994), locating the damage in ventromedial prefrontal cortex bilaterally. The case is frequently exaggerated in popular retellings,

Macmillan's historical work has documented how much of the lurid "no longer Gage" narrative accreted after the fact, and how substantially Gage appears to have recovered and worked afterwards- but the core localizing inference has held up.

6. The parietal lobe

Bounded by the central sulcus in front and the parieto-occipital sulcus behind, the parietal lobe is where the body and the world are assembled into a spatial framework.

6.1 Primary somatosensory cortex- BA 3a, 3b, 1, 2

S1 occupies the postcentral gyrus. Unusually among primary areas, it is a set of four adjacent strips, each with its own submodality bias and its own complete body map- a point often lost in simplified diagrams:

• 3a (in the depth of the central sulcus): muscle spindle afferents, proprioception.
• 3b: cutaneous receptors, the principal recipient of the ventral posterior thalamic projection; texture and light touch.
• 1: rapidly adapting cutaneous input; texture and motion across the skin.
• 2: deep pressure and joint position; size and shape.

The sensory homunculus runs in the same sequence as the motor one, with representation scaled to innervation density- which is why the fingertips and lips are vast and the back is small, and why two-point discrimination thresholds vary by an order of magnitude across the body.

Clinical correlation

S1 lesions impair discriminative touch, proprioception, two-point discrimination and stereognosis contralaterally, while crude pain and temperature awareness often survive- a reminder that nociception is distributed across S1, S2, insula and cingulate rather than localised to a single "pain cortex". Loss of the ability to recognise objects by touch alone with intact primary sensation is astereognosis, and points to the superior parietal lobule rather than to S1 itself.

6.2 Somatosensory association cortex- BA 5, 7

The superior parietal lobule integrates across submodalities and across the two body halves, supporting tactile object recognition and the body schema. Together with area 7 it forms the parietal terminus of the dorsal visual stream.

6.3 The inferior parietal lobule- supramarginal BA 40 and angular BA 39 gyri

This is heteromodal cortex at its most heteromodal: visual, auditory, somatosensory and vestibular information converge here, and the consequences of damage are strikingly different on the two sides.

Left (dominant) inferior parietal lobule. Lesions of the angular gyrus classically produce Gerstmann syndrome: the tetrad of agraphia, acalculia, finger agnosia and left–right disorientation. (The syndrome's status as a unitary entity has been questioned for decades- the four elements can dissociate, and some argue the clustering reflects a shared underlying white-matter bundle rather than a single cortical module- but it remains a useful bedside alert to dominant parietal pathology.) Left supramarginal damage contributes to conduction aphasia and to ideomotor apraxia.

Right (non-dominant) inferior parietal lobule. Lesions produce hemispatial neglect: the patient does not merely fail to see the left side, they fail to conceive of it- eating from one half of the plate, shaving one side of the face, drawing a clock with all twelve numbers crowded to the right. Neglect after right hemisphere damage is far more common and more persistent than after left, which is the clearest evidence that spatial attention is right-lateralised. Corbetta and Shulman's influential account locates the critical lesions at the temporo-parietal junction and in the right ventral frontal cortex, as a disruption of a ventral attention network rather than of a "neglect centre".

7. The temporal lobe

Below the Sylvian fissure lies the temporal lobe: hearing, the recognition of objects and faces, language comprehension, and, on its medial surface, the machinery of memory and emotion. It has more distinct jobs than any other lobe.

7.1 Primary auditory cortex - BA 41, 42

A1 sits on Heschl's transverse gyri, on the superior temporal plane buried within the Sylvian fissure. It is tonotopically organised: an orderly frequency map inherited from the cochlea, with low frequencies represented anterolaterally and high frequencies posteromedially. Because auditory pathways are substantially bilateral above the cochlear nuclei, unilateral A1 damage does not cause deafness, it causes subtle deficits in sound localisation and in discriminating complex sounds. This is a favourite examination point and a genuinely important clinical principle.

7.2 Wernicke's area- BA 22 (posterior part)

In the dominant hemisphere, the posterior superior temporal gyrus and surrounding cortex support the comprehension of language. Damage produces Wernicke's (receptive, fluent) aphasia: speech that is effortless, well-articulated, normally prosodic and largely meaningless, full of paraphasias and neologisms, with severely impaired comprehension and, the cruellest feature, frequently impaired insight, so the patient does not realise they are not being understood.

The classical Wernicke–Lichtheim–Geschwind model connects Wernicke's area to Broca's area through the arcuate fasciculus, and predicts that severing that connection yields conduction aphasia: fluent speech, good comprehension, but disproportionately impaired repetition. The model is a magnificent piece of nineteenth-century reasoning and it still organises bedside assessment. It is also, as a literal anatomical claim, too simple: language depends on a distributed dorsal and ventral stream architecture (Hickok and Poeppel, 2007), the boundaries of "Wernicke's area" are defined differently by different authors, and repetition deficits can follow damage at several points. Teach the model; don't believe it is the map.

7.3 The ventral visual stream- BA 20, 21, 37

The inferior and middle temporal gyri and the fusiform gyrus form the "what" pathway, running from occipital cortex forward along the ventral surface. Along this path, representations become progressively more abstract and more invariant to size, position and lighting. Two specialised regions are worth naming:

• The fusiform face area (Kanwisher, McDermott & Chun, J Neurosci, 1997), responding preferentially to faces. Bilateral or right-sided damage causes prosopagnosia- inability to recognise familiar faces despite intact vision and intact recognition by voice or gait.
• The visual word form area in the left mid-fusiform, described by Dehaene and Cohen, which becomes tuned to letter strings through literacy- a striking case of cultural learning colonising a cortical patch.

Damage further along this stream produces visual agnosia generally: the patient sees the object, can copy it, and cannot say what it is.

7.4 The medial temporal lobe- hippocampus, entorhinal and perirhinal cortex BA 28, 34, 35, 36

The medial temporal lobe is allocortex and transitional cortex rather than six-layered neocortex, and it performs a function unlike anything else in the cerebrum: the conversion of experience into durable declarative memory.

The decisive evidence is the case of H.M. (Henry Molaison), whose bilateral medial temporal lobectomy for intractable epilepsy in 1953 produced profound anterograde amnesia with largely intact intelligence, working memory and procedural learning (Scoville & Milner, J Neurol Neurosurg Psychiatry, 1957). The case established that memory is a separable faculty with a specific anatomy, and that declarative and procedural memory are dissociable systems. Subsequent work- including the discovery of place cells by O'Keefe and grid cells by the Mosers, recognised with the 2014 Nobel Prize- showed the same structures build the brain's spatial map.

The amygdala, at the anterior pole of the medial temporal lobe, attaches emotional significance, particularly threat value, to stimuli and drives autonomic and endocrine responses. Bilateral amygdalar damage impairs fear conditioning and the recognition of fear in faces.

Clinical correlation

Medial temporal structures have the lowest seizure threshold in the brain, which is why mesial temporal lobe epilepsy is the commonest focal epilepsy in adults. Its auras, a rising epigastric sensation, an olfactory hallucination, déjà vu, intense unexplained fear, are a direct clinical readout of what this cortex does.

8. The occipital lobe

The smallest lobe, and the one whose organisation we understand in the most quantitative detail.

8.1 Primary visual cortex- BA 17, V1, striate cortex

V1 lines the banks of the calcarine sulcus on the medial occipital surface. Its properties are worth memorising precisely, because they generate very specific clinical predictions:

• Retinotopic organisation. The contralateral visual hemifield is mapped point-for-point. The upper bank (cuneus) represents the inferior visual field; the lower bank (lingual gyrus) represents the superior field, the image is inverted, as at the retina.
• Cortical magnification. The macula occupies a hugely disproportionate share of V1, concentrated at the occipital pole. This is why occipital infarcts frequently spare central vision, macular sparing, the pole often receiving collateral supply from middle cerebral artery branches.
• Feature selectivity. Hubel and Wiesel showed that V1 neurons respond not to spots of light but to oriented edges, with simple, complex and hypercomplex cells arranged in orientation columns and ocular dominance columns.

Localizing visual field defects

• Complete unilateral V1 destruction → contralateral homonymous hemianopia, usually with macular sparing.
• Cuneus (above calcarine) → contralateral inferior quadrantanopia.
• Lingual gyrus (below calcarine) → contralateral superior quadrantanopia.
• Meyer's loop, in the temporal lobe → contralateral superior quadrantanopia ("pie in the sky"), a classic sign after anterior temporal lobectomy.
• Bilateral occipital infarction → cortical blindness. When the patient denies it and confabulates, that is Anton's syndrome. Conversely, some cortically blind patients show blindsight — above-chance responses to stimuli they deny seeing — attributed to retinotectal and extrastriate pathways bypassing V1.

8.2 Visual association cortex- BA 18, 19

Surrounding V1 are V2, V3, V4 and V5/MT, each with its own (usually partial) retinotopic map and its own specialisation. From these, the two great cortical streams emerge — a distinction introduced by Ungerleider and Mishkin (1982) and reframed by Goodale and Milner (1992) as a division between perception and visually guided action:

• Dorsal stream ("where/how"): occipital → posterior parietal. Spatial relations, motion, visuomotor guidance. Bilateral damage causes Balint syndrome — optic ataxia, oculomotor apraxia, and simultanagnosia.
• Ventral stream ("what"): occipital → inferior temporal. Form, colour, identity. Damage causes the agnosias.

Specific extrastriate lesions produce startlingly specific deficits: damage to V4 and its neighbours causes cerebral achromatopsia, the loss of colour perception with intact form; damage to V5/MT causes akinetopsia, in which the world is seen as a series of still frames — documented in the well-known patient described by Zihl and colleagues in 1983, who found pouring tea impossible because the liquid appeared frozen.

9. The insula and the limbic lobe

9.1 Insular cortex

Buried beneath the frontal, parietal and temporal opercula, the insula is the cortex most often omitted from teaching diagrams and most consistently activated in functional imaging. Its recognised roles:

• Interoception - the representation of the body's internal physiological state. Craig's synthesis (Nature Reviews Neuroscience, 2002) positions the posterior-to-anterior insula as a progression from raw visceral and thermal input to a subjective feeling state, with the anterior insula implicated in awareness of one's own emotional condition.
• Gustatory cortex in the anterior insula and adjacent frontal operculum.
• Visceral, autonomic and vestibular processing; also, a consistent site of pain-related activation.
• Disgust - both felt and recognised in others.

9.2 The limbic lobe

On the medial surface, the cingulate gyrus, parahippocampal gyrus, subcallosal area and hippocampal formation form a ring around the corpus callosum, Broca's le grand lobe limbique. Its cortex is largely three- to five-layered mesocortex and allocortex, phylogenetically older than neocortex.

• Anterior cingulate (24, 32, 33): conflict monitoring, error detection, effort and motivation, autonomic control, affective pain.
• Posterior cingulate and retrosplenial cortex (23, 29, 30, 31): spatial orientation, autobiographical memory, and a central hub of the default mode network described by Raichle et al. (PNAS, 2001) — the set of regions more active at rest than during externally directed tasks, and among the earliest to show metabolic change in Alzheimer's disease.
• Parahippocampal gyrus (27, 28, 34, 35, 36): the gateway between neocortex and hippocampus, and the site of scene-selective responses.
• Olfactory cortex: uniquely, olfaction reaches the piriform cortex without an obligatory thalamic relay, the one sensory exception to the thalamic rule.

10. The wiring beneath: white matter makes areas into systems

An area is defined as much by what it connects to as by what it contains. Cortical white matter carries three classes of fibre.

Table 3. Principal white matter systems of the cerebrum.
Class	Tract	Connects	Clinical relevance
Association (within hemisphere)	Arcuate / superior longitudinal fasciculus	Temporal ↔ parietal ↔ frontal	Repetition; conduction aphasia; implicated in Broca's original cases
	Inferior fronto-occipital fasciculus	Occipital ↔ frontal	Semantic processing
	Uncinate fasciculus	Anterior temporal ↔ orbitofrontal	Naming, emotional memory
	Cingulum	Along the cingulate gyrus	Limbic integration, memory
	Inferior longitudinal fasciculus	Occipital ↔ temporal	Ventral stream; visual recognition
Commissural (between hemispheres)	Corpus callosum	Homologous cortical areas	Disconnection syndromes; alien hand; callosotomy
	Anterior commissure	Anterior temporal lobes, olfactory	Spared in most callosal lesions
Projection (cortex ↔ below)	Corona radiata / internal capsule	Cortex ↔ thalamus, brainstem, cord	A tiny capsular lacune can produce a dense hemiplegia by compressing an entire homunculus into a few millimetres

The internal capsule deserves emphasis because it is the great lesson in why cortical localisation is not the whole story. In the cortex, the motor homunculus is spread across many centimetres, so a small infarct causes a small deficit. In the posterior limb of the internal capsule, the same fibres are packed into a few millimetres, and a lacunar infarct one-tenth the size produces a complete contralateral hemiplegia. Geography and vulnerability are not the same thing.

10.1 The split-brain evidence

The corpus callosum's role was revealed by the callosotomy patients studied by Roger Sperry and Michael Gazzaniga from the 1960s, work that earned Sperry a share of the 1981 Nobel Prize. With the commissures cut, a word flashed to the left visual field (right hemisphere) could not be named but could be selected by the left hand; the left hemisphere, asked why, confabulated a reason. The findings are still the sharpest demonstration that hemispheric specialisation is real and that verbal report reflects only part of what the brain knows, though modern authors caution against over-reading the small and neurologically atypical patient sample.

11. Lateralisation: two hemispheres, not two personalities

Hemispheric asymmetry is genuine and it is clinically indispensable. It is also the single most abused fact in popular neuroscience.

What is well supported:

• Language is left-lateralised in roughly 95–96% of right-handers and about 70–80% of left-handers, with the remainder showing bilateral or right-sided representation (Wada testing and subsequent fMRI series).
• The planum temporale, on the superior temporal plane, is anatomically larger on the left in the majority of brains (Geschwind & Levitsky, 1968), a structural asymmetry present before birth.
• Praxis is typically left-lateralised; spatial attention, prosody, and face processing are weighted right; hemispatial neglect is overwhelmingly a right-hemisphere syndrome.

What is not supported: the idea of "left-brained" analytical people and "right-brained" creative people. Large-scale resting-state analyses have found no evidence that individuals have globally stronger left- or right-hemisphere networks. Lateralisation is a property of specific functions within a brain, not a personality type.

12. Blood supply: the map neurology actually uses

In practice, cortical territory is most often lost by vascular boundary rather than by functional boundary, so the arterial map deserves to sit beside the functional one.

Table 4. Arterial territories of the cerebrum and their characteristic syndromes.
Artery	Cortex supplied	Syndrome if occluded
Anterior cerebral (ACA)	Medial frontal and parietal surface, paracentral lobule, anterior corpus callosum	Contralateral weakness and sensory loss worst in the leg; abulia; urinary incontinence; grasp reflex; transcortical motor aphasia if dominant
Middle cerebral (MCA)	Most of the lateral convexity: lateral motor/sensory strip (face, arm), Broca's and Wernicke's areas, inferior parietal lobule, insula	Contralateral weakness worst in face and arm; aphasia if dominant; neglect if non-dominant; gaze preference toward the lesion; homonymous hemianopia
Posterior cerebral (PCA)	Occipital lobe, inferomedial temporal lobe, thalamus	Contralateral homonymous hemianopia with macular sparing; alexia without agraphia (left PCA with splenial involvement); memory impairment; cortical blindness if bilateral
Watershed zones	ACA–MCA and MCA–PCA borders	After global hypoperfusion: "man-in-a-barrel" proximal arm weakness; transcortical aphasias

13. Where the classical map breaks and what replaced it

Everything above is the map as taught. Four contemporary findings materially qualify it, and a good article should say so plainly rather than leaving the reader with a tidy nineteenth-century picture.

13.1 Brodmann's numbers are a histological scheme, not a functional one

Brodmann's areas are sometimes cited as if they were functional units with crisp borders. They were defined by cell architecture in a small number of post-mortem brains, their boundaries vary substantially between individuals, and several of Brodmann's areas contain multiple functionally distinct subregions. Probabilistic cytoarchitectonic atlases, most prominently the Julich-Brain atlas (Amunts et al., Science, 2020), now represent areas as probability maps across many brains rather than as lines on a single specimen, which is a more honest representation of the underlying biology.

13.2 There are far more areas than 52

The Human Connectome Project's multi-modal parcellation delineated 180 areas per hemisphere using architecture, function, connectivity and topography in combination, characterizing 97 areas that had never been described before (Glasser et al., Nature, 2016). The authors were careful to call it version 1.0 and to anticipate revision. Even so, the direction of travel is clear: the cortex is finer-grained than the classical map, and individual brains deviate from any group average.

13.3 The motor homunculus is not continuous

This is the most striking recent revision, and it has not yet reached most textbooks. Using precision fMRI, Gordon and colleagues reported in Nature (2023) that the classic homunculus is interrupted: between the foot, hand and mouth effector regions lie three "inter-effector" zones with thinner cortex, distinct connectivity, and strong links to the cingulo-opercular network involved in action control, arousal, error monitoring and physiological regulation. They named this the somato-cognitive action network (SCAN), and reported convergent evidence from the three largest fMRI datasets, from macaques, and from newborns and children.

The finding has been vigorously debated, an open review by Muret, Makin and Diedrichsen questioned aspects of the interpretation, and the older literature on concentric functional zones and complex-action maps in M1 had already troubled the simple strip picture. But if it holds, the implication is substantial: M1 is not purely a somatotopic output map with a little person laid along it. It is interleaved with control machinery that integrates body and intention.

13.4 Localization has become network thinking

The deepest change is conceptual. The dominant framework is no longer "area X performs function Y" but "distributed networks, each spanning several lobes, support families of functions, and nodes participate in more than one network." The default mode, dorsal attention, ventral attention, salience, frontoparietal control and sensorimotor networks are now as much a part of the working vocabulary as the lobes themselves. Lesion studies increasingly find that the deficit correlates better with the network disrupted than with the grey matter destroyed, which is exactly what the re-imaging of Broca's own patients suggested.

None of this makes the classical map obsolete. A neurologist localising a stroke at the bedside in 2026 is still reasoning with Broca, Wernicke, Penfield and Brodmann, and reasoning well. But the map is a chart of a coastline, not a satellite photograph, and it is worth knowing which is which.

14. Summary table

Table 5. The principal cortical areas at a glance.
Area	Brodmann	Location	Function	Lesion effect
Primary motor (M1)	4	Precentral gyrus	Execution of voluntary movement	Contralateral UMN weakness
Premotor / SMA	6	Anterior to M1	Planning, sequencing of movement	Apraxia; akinesia; alien hand
Frontal eye field	8	Middle frontal gyrus	Contralateral saccades	Gaze deviation toward lesion
Broca's area	44, 45	Inferior frontal gyrus (dominant)	Speech production	Non-fluent aphasia
Dorsolateral prefrontal	9, 46	Middle frontal gyrus	Working memory, executive control	Dysexecutive syndrome
Orbitofrontal	11, 12, 47	Orbital surface	Value, inhibition, social conduct	Disinhibition, impulsivity
Anterior cingulate	24, 32	Medial surface	Conflict monitoring, motivation	Abulia, akinetic mutism
Primary somatosensory (S1)	3a, 3b, 1, 2	Postcentral gyrus	Touch, proprioception	Contralateral discriminative sensory loss
Somatosensory association	5, 7	Superior parietal lobule	Body schema, stereognosis, dorsal stream	Astereognosis; Balint syndrome if bilateral
Supramarginal gyrus	40	Inferior parietal lobule	Phonological / praxis integration	Conduction aphasia; apraxia; neglect (right)
Angular gyrus	39	Inferior parietal lobule	Reading, calculation, multimodal integration	Gerstmann syndrome (left); neglect (right)
Primary auditory (A1)	41, 42	Heschl's gyri	Tonotopic hearing	Impaired localisation; not deafness
Wernicke's area	22 (post.)	Superior temporal gyrus (dominant)	Language comprehension	Fluent aphasia with poor comprehension
Inferotemporal / fusiform	20, 21, 37	Ventral temporal	Object, face and word recognition	Visual agnosia; prosopagnosia; alexia
Medial temporal / hippocampal	28, 34, 35, 36	Medial temporal lobe	Declarative memory, spatial mapping	Anterograde amnesia
Primary visual (V1)	17	Calcarine sulcus	Retinotopic vision, edge detection	Homonymous hemianopia
Visual association	18, 19	Surrounding V1	Motion, colour, form; two streams	Achromatopsia; akinetopsia; agnosia
Insula	13–16	Depth of Sylvian fissure	Interoception, taste, autonomic, disgust	Impaired interoceptive awareness; dysgeusia

15. How to hold all of this

If you are learning this material rather than reviewing it, three organising habits make it stick far better than memorising the table above.

First, learn the sulci before the areas. Every functional claim in this article is anchored to a fold. If you can find the central sulcus, the Sylvian fissure and the calcarine sulcus on any image, three-quarters of localisation follows.

Second, learn each area through its failure. The cortex is easier to remember as a catalogue of syndromes than as a catalogue of functions, partly because the syndromes are vivid and partly because that is how the knowledge was acquired in the first place. Neglect teaches the right parietal lobe. H.M. teaches the medial temporal lobe. Gage teaches the orbitofrontal cortex.

Third, keep the resolution of your claims honest. "The left inferior frontal region is critical for fluent speech production" is well supported. "Broca's area is the speech centre" is a compression that the original evidence never quite justified. Holding the difference between those two sentences is, in the end, most of what it means to understand the cortex rather than to have memorised a diagram of it.

References and further reading

Standard texts

1. Kandel ER, Koester JD, Mack SH, Siegelbaum SA (eds). Principles of Neural Science, 6th ed. McGraw-Hill, 2021. — Parts on cortical organisation, sensory and motor systems, and language.
2. Hall JE, Hall ME. Guyton and Hall Textbook of Medical Physiology, 14th ed. Elsevier, 2021. — Chapters on the cerebral cortex, intellectual functions, learning and memory, and motor control.
3. Purves D et al. Neuroscience, 6th ed. Oxford University Press, 2018.
4. Standring S (ed). Gray's Anatomy: The Anatomical Basis of Clinical Practice, 42nd ed. Elsevier, 2020. — Cerebral hemisphere chapters.
5. Splittgerber R. Snell's Clinical Neuroanatomy, 8th ed. Wolters Kluwer, 2019.
6. Blumenfeld H. Neuroanatomy through Clinical Cases, 3rd ed. Sinauer/Oxford, 2021. — Particularly strong on vascular territories and localisation.
7. Barrett KE et al. Ganong's Review of Medical Physiology, 26th ed. McGraw-Hill, 2019.

Primary and historical literature

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9. Wernicke C. Der aphasische Symptomencomplex. Breslau: Cohn & Weigert, 1874.
10. Brodmann K. Vergleichende Lokalisationslehre der Grosshirnrinde. Leipzig: Barth, 1909.
11. Penfield W, Boldrey E. Somatic motor and sensory representation in the cerebral cortex of man as studied by electrical stimulation. Brain. 1937;60(4):389–443.
12. Mountcastle VB. Modality and topographic properties of single neurons of cat's somatic sensory cortex. Journal of Neurophysiology. 1957;20(4):408–434.
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27. Azevedo FAC et al. Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. Journal of Comparative Neurology. 2009;513(5):532–541.
28. Zilles K, Amunts K. Centenary of Brodmann's map — conception and fate. Nature Reviews Neuroscience. 2010;11(2):139–145.
29. Glasser MF, Coalson TS, Robinson EC, et al. A multi-modal parcellation of human cerebral cortex. Nature. 2016;536(7615):171–178. doi:10.1038/nature18933
30. Amunts K, Mohlberg H, Bludau S, Zilles K. Julich-Brain: a 3D probabilistic atlas of the human brain's cytoarchitecture. Science. 2020;369(6506):988–992.
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