8. Neuroanatomy

The cerebral cortex on CT is read not as the histological six-layered ribbon it is, but as a band of soft tissue a few Hounsfield units denser than the white matter it caps. Cortical gray matter measures approximately $37$–$45\,\mathrm{HU}$, white matter approximately $25$–$35\,\mathrm{HU}$, and this difference of roughly $7$–$12\,\mathrm{HU}$—driven by the higher water and lower lipid (myelin) content of gray matter, and by its denser capillary bed and consequent higher blood volume—is the entire physical basis of the gray–white differentiation on which brain-window interpretation rests. Because the separation is so narrow, it must be displayed on a deliberately tight window (width $\approx 80$, level $\approx 35$–$40\,\mathrm{HU}$); on a wide window the cortex and white matter merge into an undifferentiated gray, and the earliest sign of cytotoxic edema, the loss of gray–white distinction, vanishes. This is why the expert reads acute stroke and trauma on a narrow window and frequently on a dedicated, even narrower, stroke window.

Lobar anatomy is recovered through reproducible landmarks rather than memorized slices. The Sylvian fissure separates the frontal and parietal lobes above from the temporal lobe below and houses the middle cerebral artery; on axial images its posterior horizontal ramus points toward the supramarginal and angular gyri. The central sulcus is the reader's keystone for sensorimotor localization and is identified on high axial images by a constellation of signs: the posteriorly directed “hook” of the precentral (motor) gyrus into the superior frontal sulcus (the superior frontal sulcus sign), the thicker precentral gyrus lying just anterior to the thinner postcentral gyrus, and the bifurcation of the superior frontal sulcus meeting the precentral sulcus. The parieto-occipital fissure, best appreciated on sagittal and the highest axials, divides parietal from occipital lobe, and the calcarine sulcus along the medial occipital surface marks the primary visual cortex. The insula sits deep within the Sylvian fissure, flanked by the claustrum and extreme/external capsules, and its ribbon is a sensitive early-ischemia territory.

Functional anatomy maps onto these landmarks with clinical force. The precentral gyrus is primary motor cortex with its inverted homunculus, the leg medial in the paracentral lobule and the face lateral near the operculum; the postcentral gyrus mirrors it for somatosensation. Broca's area occupies the posterior inferior frontal gyrus of the dominant hemisphere and Wernicke's area the posterior superior temporal gyrus, so an aphasic syndrome immediately lateralizes and roughly localizes the insult. The mesial temporal lobe (hippocampus, parahippocampus) subserves memory and is the seizure-onset zone of mesial temporal sclerosis.

Vascular territory is the organizing principle for cortical pathology, because the cortex fails along arterial boundaries. The anterior cerebral artery supplies the medial frontal and parietal cortex down to the parieto-occipital fissure and the paracentral lobule, so an ACA infarct preferentially weakens the contralateral leg. The middle cerebral artery supplies the lateral convexity, including motor and sensory cortex for face and arm and the perisylvian language areas, making it the dominant stroke territory clinically. The posterior cerebral artery supplies the occipital lobe and inferomedial temporal lobe, so PCA infarction produces homonymous hemianopia. Between these territories lie the watershed zones—the anterior watershed between ACA and MCA and the posterior between MCA and PCA—which infarct under global hypoperfusion and produce the classic parasagittal “man-in-a-barrel” pattern. The expert search pattern sweeps the cortical ribbon symmetrically side-to-side for focal loss of gray–white distinction, sulcal effacement, or insular ribbon loss, anchored to vascular territory; the dominant pitfall is satisfaction of search after one finding and the anchoring bias that reads subtle early edema as artifact, the two cognitive errors most often implicated in missed early infarction.

Beneath the cortex, the deep gray nuclei and the white-matter highways that thread between them constitute the most information-dense region of the axial brain CT, and reading it well demands that density, somatotopy, and vascular supply be held simultaneously in mind. On a brain-window axial image at the level of the third ventricle and foramen of Monro, the basal ganglia and thalamus present as a paired, roughly symmetric array. From medial to lateral on each side lie the caudate head (indenting the frontal horn), the anterior limb of the internal capsule, the globus pallidus and putamen together forming the wedge-shaped lentiform nucleus, the external capsule, the thin claustrum, the extreme capsule, and the insular cortex. The thalami sit medially, flanking the third ventricle, separated from the lentiform nucleus by the posterior limb of the internal capsule. Gray nuclei follow cortical density ($\approx 35$–$45\,\mathrm{HU}$); the globus pallidus is the conspicuous exception, frequently and benignly calcified in adults, and physiologic basal ganglia and pineal/habenular and choroid plexus calcification must not be mistaken for pathology, though symmetric, age-inappropriate, or florid mineralization raises Fahr disease, prior toxic/metabolic insult, or hypoparathyroidism.

The internal capsule is the structure whose anatomy most directly predicts clinical syndrome, and its CT recognition is non-negotiable. On axial images it forms a boomerang opening laterally, its anterior limb between caudate and lentiform, its posterior limb between thalamus and lentiform, and its genu at the apex pointing medially. The descending corticospinal and corticobulbar fibers occupy the posterior limb and the genu in an orderly somatotopy, face and arm anterior, leg posterior, so a small lesion confined to the posterior limb can abolish contralateral hemibody strength out of all proportion to its size—the anatomical reason a pure motor lacune is so devastating. The anterior limb carries frontopontine and thalamocortical fibers; the retrolenticular portion carries the optic radiation toward the occipital cortex, so a lesion there clips the visual field.

Vascular supply explains why this region is the epicenter of small-vessel disease. The lentiform nucleus, much of the internal capsule, and the caudate are perfused by the lenticulostriate arteries, tiny end-arterial perforators arising at right angles from the proximal middle cerebral (M1) and anterior cerebral segments; the thalamus is supplied by perforators from the posterior cerebral and posterior communicating arteries (thalamoperforators, thalamogeniculate, and the artery of Percheron variant that, when occluded, infarcts both paramedian thalami). These perforators have no collateral, so chronic hypertension drives the lipohyalinosis that produces lacunar infarcts (sharply marginated, $\le 15\,\mathrm{mm}$ CSF-density cavities in exactly these locations) and the Charcot–Bouchard microaneurysms whose rupture causes the prototypical hypertensive deep hemorrhage. This is the mechanistic link the reader must make: a hyperdense ($50$–$80\,\mathrm{HU}$) acute hematoma centered in the putamen or thalamus in a hypertensive patient is hypertensive in origin until proven otherwise, whereas a lobar location shifts the differential toward amyloid angiopathy, underlying tumor, or vascular malformation. The expert search pattern interrogates the deep gray symmetrically for subtle hypodensity (early lacune or large-territory infarct involving the lentiform), for the hyperdensity of acute blood, and for the obscuration of the normally crisp lentiform margin—the “lentiform nucleus sign” of early MCA-territory ischemia. The recurrent pitfalls are dismissing a small deep hypodensity as a Virchow–Robin space when it is an acute lacune, and overlooking the insular ribbon and lentiform obscuration that together herald a large proximal MCA occlusion.

The posterior fossa is simultaneously the most clinically unforgiving and the most technically degraded compartment on head CT, and the reader's discipline here is what most distinguishes expert performance. It is bounded by the petrous temporal bones, the clivus, and the occipital bone, and roofed by the tentorium cerebelli; within it sit the brainstem and cerebellum, surrounded by the basal cisterns. The dense surrounding bone is the source of the chief technical limitation: beam-hardening and photon-starvation streak artifact (the Hounsfield bar between the petrous pyramids) degrades the brainstem on axial images, mimics or masks hemorrhage and infarct, and is the physical reason posterior-fossa pathology is disproportionately missed. Thin sections, coronal and sagittal reconstruction, and, on modern photon-counting systems, the rejection of the electronic-noise floor mitigate but do not abolish this.

The brainstem is read in three rostrocaudal segments, each with a characteristic axial silhouette and cranial-nerve census. The midbrain at the level of the tentorial incisura shows the paired cerebral peduncles anteriorly, the tegmentum, and the tectum (the superior and inferior colliculi) posteriorly, framing the cerebral aqueduct; the interpeduncular and ambient cisterns surround it, and effacement of these cisterns is the earliest CT sign of transtentorial (uncal) herniation. The pons bulges ventrally against the clivus, with the fourth ventricle behind it and the cerebellar peduncles tethering it to the cerebellum; the basilar artery grooves its anterior surface. The medulla tapers to the cervicomedullary junction at the foramen magnum. The brainstem houses the corticospinal tracts ventrally and the cranial-nerve nuclei dorsally, so its compact anatomy means small lesions yield crossed syndromes (ipsilateral cranial nerve, contralateral long tract) that localize precisely; the basilar perforator supply makes it a target of small-vessel infarction and of the catastrophic basilar-occlusion syndrome.

The cerebellum comprises two hemispheres and the midline vermis, its surface folia giving a finer texture than the cerebrum, and its deep nuclei (notably the dentate) occasionally calcifying. The vermis is the keystone of axial and especially sagittal orientation and the site whose congenital malformations (Dandy–Walker, Chiari) are defined. Functionally the cerebellar hemispheres coordinate ipsilateral appendicular movement and the vermis governs truncal and gait stability, so a hemispheric lesion produces ipsilateral dysmetria while a vermian lesion produces a wide-based ataxia. The cerebellopontine angle cistern, between the lateral pons/cerebellum and the petrous bone, transmits cranial nerves VII and VIII into the internal auditory canal and is the cardinal location of the vestibular schwannoma and the epidermoid; it must be inspected on every study and is a classic blind spot.

The clinical mechanics that make this compartment dangerous are anatomical. The posterior fossa is a small, rigid, poorly compliant box, so even modest mass—an expanding cerebellar infarct with cytotoxic swelling, a hypertensive cerebellar hematoma, a tumor—rapidly produces two lethal consequences: upward transtentorial herniation of the vermis through the incisura and, more commonly, downward tonsillar herniation through the foramen magnum, and obstructive hydrocephalus from fourth-ventricular compression. The reader therefore evaluates not only the parenchyma but the fourth ventricle (patent, effaced, or shifted), the basal cisterns (the prepontine and quadrigeminal cisterns in particular), and the tonsillar position relative to the foramen magnum. The expert search pattern deliberately slows over the brainstem and CP angles, reconstructs in multiple planes to defeat streak artifact, and treats any fourth-ventricular effacement as an emergency; the dominant pitfalls are inattentional blindness to a CP-angle mass, attributing a genuine brainstem hypodensity to beam-hardening artifact, and failing to recognize that a small-volume but strategically located cerebellar lesion is a neurosurgical emergency because of the box it sits in.

The ventricular system is the cerebrospinal-fluid–filled core of the brain, and on CT its value is twofold: it is a near-water-density internal landmark ($0$–$15\,\mathrm{HU}$, the slight positivity over pure water reflecting protein content and partial-volume averaging with adjacent parenchyma) against which density abnormalities stand out, and its size, configuration, and symmetry are among the most sensitive integrators of intracranial mass effect available to the reader. CSF is produced principally by the choroid plexus (whose glomus, in the atria of the lateral ventricles, calcifies normally and asymmetrically in adults) at roughly $500\,\mathrm{mL/day}$, circulates through the ventricles and cisterns, and is resorbed at the arachnoid granulations and along perineural and lymphatic routes; the total CSF volume of $\approx 150\,\mathrm{mL}$ turns over several times daily, so any obstruction along the pathway manifests quickly as upstream dilatation.

The paired lateral ventricles are C-shaped and read region by region: frontal (anterior) horns indented laterally by the caudate heads and separated in the midline by the septum pellucidum; the body roofed by the corpus callosum; the atrium (trigone) containing the calcified glomus and giving off the occipital horn posteriorly and the temporal horn anteroinferiorly into the medial temporal lobe. The temporal horns deserve specific attention: they are normally slit-like and barely visible, so symmetric temporal-horn dilatation is an early and reliable sign of obstructive hydrocephalus, while focal dilatation of one temporal horn flags a trapped ventricle or adjacent mass. The lateral ventricles drain through the paired foramina of Monro into the slit-like, midline third ventricle, which sits between the thalami (often bridged by the massa intermedia) and whose anteroinferior recesses (optic, infundibular) abut the suprasellar region and whose floor is the hypothalamus. The third ventricle communicates through the narrow cerebral aqueduct of Sylvius—the system's tightest point and therefore the commonest site of obstruction—with the fourth ventricle, a rhomboid space between the dorsal pons/medulla and the cerebellar vermis. The fourth ventricle exits to the subarachnoid space through the midline foramen of Magendie and the paired lateral foramina of Luschka, beyond which CSF enters the cisterns.

This serial architecture dictates the central interpretive distinction: obstructive (non-communicating) versus communicating hydrocephalus. Obstruction within the ventricular system dilates the spaces proximal to the block and spares those distal: aqueductal stenosis or a tectal/pineal mass enlarges the lateral and third ventricles while the fourth stays normal; a fourth-ventricular or posterior-fossa mass enlarges all four. Communicating hydrocephalus, from impaired subarachnoid resorption (post-hemorrhagic, post-meningitic, or carcinomatous), dilates the entire system including the fourth ventricle and effaces the cortical sulci. Acute obstructive hydrocephalus is recognized not only by ventricular enlargement disproportionate to sulcal size but by transependymal CSF migration—periventricular interstitial hypodensity, most marked around the frontal horns—as pressurized CSF is forced across the ependyma into the white matter. This must be distinguished from the ex-vacuo ventricular enlargement of atrophy, in which sulci enlarge in proportion, and from normal-pressure hydrocephalus, in which ventricles enlarge out of proportion to sulci without a transependymal gradient and with a characteristically widened callosal angle.

The ventricular system is also a direct readout of midline shift and herniation: a unilateral mass effaces the ipsilateral ventricle and shifts the septum pellucidum across the midline, while entrapment of the contralateral ventricle (by obstruction of its foramen of Monro) paradoxically dilates it. The expert quantifies shift at the septum pellucidum and the pineal, treats new ventricular asymmetry as mass effect until proven otherwise, and inspects the temporal horns and the third-ventricular recesses where early dilatation hides. The recurrent pitfalls are attributing genuine hydrocephalus to atrophy (and vice versa), overlooking subtle temporal-horn rounding, and missing the intraventricular hemorrhage or colloid cyst at the foramen of Monro that produces acute, sometimes positional, obstruction.

The skull base is read on bone-window CT as a topographic map of three descending terraces—the anterior, middle, and posterior cranial fossae—perforated by foramina that are not merely holes but the obligate conduits through which cranial nerves and vessels leave the cranium, so that a lesion at a given foramen produces a predictable neuropathy and a given neuropathy directs the reader to a specific foramen. Cortical bone measures several hundred to over a thousand Hounsfield units and is displayed on a wide bone window (width $\approx 2000$, level $\approx 500$); the foramina appear as lucent defects, and their symmetry, margins, and content are the substance of the examination. Coronal and sagittal reconstruction is essential because many foramina course obliquely and are foreshortened on axial images.

The anterior cranial fossa floor is formed by the orbital plates of the frontal bone and the cribriform plate of the ethmoid, through whose perforations the olfactory nerve fibers (CN I) pass; a cribriform fracture is the anatomical substrate of post-traumatic anosmia and CSF rhinorrhea. The optic canal, in the lesser wing of the sphenoid, transmits the optic nerve (CN II) and the ophthalmic artery. The middle cranial fossa, built on the greater wing and body of the sphenoid, is the foramen-rich terrace. The superior orbital fissure transmits the oculomotor (III), trochlear (IV), abducens (VI), and the ophthalmic division of the trigeminal (V1) nerves together with the superior ophthalmic vein, so a lesion there yields the orbital-apex/superior-orbital-fissure syndrome of ophthalmoplegia with V1 sensory loss. Medial to it, the foramen rotundum carries V2 to the pterygopalatine fossa and the foramen ovale carries V3 (and the lesser petrosal nerve) to the masticator space—a perineural highway for head-and-neck tumor spread that the reader must trace. The foramen spinosum transmits the middle meningeal artery, the vessel whose laceration produces epidural hematoma. The carotid canal conveys the internal carotid artery, and the foramen lacerum lies over its anteroinferior course.

The posterior cranial fossa terrace contains the largest and most clinically dense apertures. The internal auditory canal transmits the facial (VII) and vestibulocochlear (VIII) nerves, and asymmetric IAC widening is the bony clue to a vestibular schwannoma. The jugular foramen transmits the glossopharyngeal (IX), vagus (X), and accessory (XI) nerves together with the internal jugular vein and the inferior petrosal sinus; its pars nervosa and pars vascularis arrangement, and the normal asymmetry of the jugular bulb, must be distinguished from a glomus jugulare tumor that permeatively erodes the foraminal margins. The hypoglossal canal carries CN XII through the occipital condyle, so condylar pathology yields tongue deviation. The foramen magnum transmits the medulla–spinal cord junction, the vertebral arteries, and the spinal roots of CN XI.

The clinical leverage of this anatomy is that cranial-nerve syndromes are localizing. Cavernous-sinus and superior-orbital-fissure lesions cluster III, IV, V1, and VI; a jugular-foramen mass clusters IX, X, and XI (Vernet syndrome); and isolated deficits point to a single canal. The skull base is also the principal route of perineural tumor spread—adenoid cystic and squamous carcinomas creep along V2 through foramen rotundum and V3 through foramen ovale, and along VII—so the expert inspects each foramen for enlargement, asymmetric soft tissue, or loss of the normal fat plane, and specifically compares the two foramina ovale and rotundum side-to-side. The recurrent pitfalls are reading the skull base only on soft-tissue windows (missing the bony erosion that is the earliest sign), overlooking subtle foraminal asymmetry, failing to trace perineural spread retrograde toward the brainstem, and mistaking a normal asymmetric jugular bulb or pneumatized variant for disease.

The three meningeal layers are largely below the spatial and contrast resolution of unenhanced CT as discrete membranes, yet they define every extra-axial compartment, and the reader interprets them indirectly through the shape, margins, and anatomical limits of the collections and enhancement patterns that occupy the spaces they bound. Understanding the meninges is therefore less about seeing them than about predicting how blood, pus, tumor, or CSF will be constrained by them—and that prediction is the single most useful tool for localizing an extra-axial process and narrowing its differential.

The dura mater is the thick, tough outer layer, adherent to the inner table of the skull and composed functionally of two leaves: an outer periosteal layer fused to bone and an inner meningeal layer that reflects inward to form the major dural folds—the falx cerebri between the hemispheres, the tentorium cerebelli between the supratentorial brain and the posterior fossa, and the diaphragma sellae. Where the two dural leaves separate, they enclose the venous dural sinuses (superior sagittal, transverse, sigmoid, straight, cavernous). The dura is densely innervated and is the pain-sensitive structure responsible for the headache of meningeal irritation. Its key interpretive role is in the epidural space: the epidural compartment is only a potential space because the periosteal dura is fused to bone at the sutures, so an arterial epidural hematoma—classically from a middle meningeal artery torn by a temporal-bone fracture—strips the dura off the skull but cannot cross suture lines, producing the characteristic biconvex, lentiform, sharply marginated hyperdense collection that respects sutures but can cross the midline and the tentorium because the dura, not the suture, is its boundary.

The arachnoid mater is the delicate, avascular middle layer that bridges loosely over the sulci and follows the inner meningeal dura. Between the dura and arachnoid lies the subdural space, a potential space traversed by the bridging cortical veins that drain into the dural sinuses; rupture of these thin-walled, low-pressure veins—readily produced by the rotational acceleration of trauma or by trivial injury in the atrophic, vein-stretched brain of the elderly—fills the subdural space with venous blood. Because the subdural space is bounded by the arachnoid (which drapes over sulci) and not by the skull sutures, the resulting subdural hematoma is crescentic (concave toward the brain), spreads diffusely over the convexity crossing suture lines, but cannot cross the midline falx or the tentorium. This lentiform-versus-crescentic, suture-respecting-versus-falx-respecting dichotomy is the anatomical heart of distinguishing epidural from subdural hemorrhage, and it follows directly from which membrane bounds which space. Subdural collections also evolve in density—hyperdense when acute ($50$–$80\,\mathrm{HU}$), isodense to cortex at one to three weeks (a dangerous phase recognized by inward displacement of the gray–white junction and effaced sulci rather than by the collection itself), and hypodense when chronic—so density timestamps the bleed, and a mixed-density collection signals rebleeding.

The pia mater is the innermost layer, intimately applied to the cortical surface and following every sulcus and the penetrating vessels into the Virchow–Robin perivascular spaces. Between the pia and arachnoid lies the subarachnoid space, which contains the circulating CSF, the cisterns, and the major cortical arteries. Subarachnoid hemorrhage therefore fills the sulci and basal cisterns with hyperdense blood, conforming to the contours of the brain surface rather than displacing it—the reader looks for hyperdensity outlining the sulci, the Sylvian and interhemispheric fissures, and especially the basal cisterns (suprasellar, ambient, interpeduncular), where aneurysmal hemorrhage concentrates. Leptomeningeal (pia-arachnoid) enhancement that follows the sulci into their depths indicates meningitis or carcinomatosis, whereas thick, nodular pachymeningeal (dural) enhancement that does not enter the sulci indicates a dural process such as intracranial hypotension, meningioma, or dural metastasis—again, the pattern localizes to a meningeal layer. The expert search pattern scrutinizes the extra-axial spaces along the entire convexity, the falx and tentorium, and every basal cistern for thin or isodense collections, judges every collection by its shape and anatomical limits, and on any enhanced study classifies meningeal enhancement as leptomeningeal versus pachymeningeal. The recurrent pitfalls are missing the isodense subacute subdural by failing to register the displaced gray–white junction, overlooking a thin convexity or interhemispheric subdural, and failing to scrutinize the basal cisterns for the subtle subarachnoid blood that, if missed, returns as a fatal aneurysmal rebleed.