Cerebral hemispheres
Cerebral hemispheres on imaging: cortex, white matter, internal capsule and limbic lobe
On CT and MRI the hemispheres are a cortical ribbon over white matter tracts that converge on the internal capsule. CPSP asks you to name the gyrus or tract from a landmark or deficit, and to recognise white matter and developmental diseases by where they sit and why.
Finding the landmarks
- Central sulcus: on high axial images the hand knob, an inverted omega projecting backwards from the precentral gyrus, lies just in front of it. The precentral gyrus is usually thicker than the postcentral.
- Insula: cortex hidden in the depth of the lateral sulcus with MCA branches on its surface. Going inwards: insula, extreme capsule, claustrum, external capsule, putamen.
- Loss of the insular ribbon (grey–white blurring) is often the earliest CT sign of a proximal MCA infarct. Early CT is mainly to exclude haemorrhage.
- The AC–PC line joins the anterior and posterior commissures; it is the standard axial reference.
Cortical areas and their lesions
| Area | Site | Lesion |
|---|---|---|
| Primary motor (4) | Precentral gyrus; leg on the medial surface (ACA), hand and face laterally (MCA) | Contralateral weakness; hand, face and tongue have the largest representation, the trunk the least |
| Frontal eye field (8) | Middle frontal gyrus | Destruction: eyes look towards the lesion |
| Broca (44, 45) | Left inferior frontal gyrus | Slow, effortful speech, comprehension intact |
| Orbitofrontal | Above the orbits | Disinhibition, poor judgement |
| Anterior cingulate | Above the corpus callosum | Bilateral damage gives akinetic mutism |
| Primary sensory (3, 1, 2) | Postcentral gyrus | Loss of position sense, two-point touch, stereognosis |
| Angular gyrus | Left inferior parietal | Alexia with agraphia, finger agnosia, acalculia, left–right confusion |
| Right parietal | Non-dominant | Neglect |
| Wernicke (22) | Posterior left superior temporal gyrus | Fluent, meaningless speech, poor comprehension |
| Primary auditory (41, 42) | Transverse temporal gyri | Poor sound localisation, not deafness |
| Primary visual (17) | Banks of the calcarine sulcus | Homonymous hemianopia with macular sparing |
| Fusiform gyrus | Inferior occipitotemporal | Prosopagnosia |
- Aphasias: conduction aphasia (arcuate fasciculus) loses repetition; transcortical aphasias (watershed infarcts) keep repetition; global aphasia follows MCA stem occlusion.
- Alexia without agraphia: left occipital cortex plus splenium (left PCA).
White matter
| Fibre type | Examples | Join |
|---|---|---|
| Association | Arcuate fasciculus, cingulum, uncinate | Areas in one hemisphere |
| Commissural | Corpus callosum (rostrum, genu, body, splenium), anterior commissure | The two hemispheres |
| Projection | Corona radiata, internal capsule | Cortex to and from deep and lower centres |
- Diffusion tensor colour maps: red left to right, green front to back, blue up and down.
- Callosal agenesis: widely separated parallel lateral ventricles, dilated occipital horns, high-riding third ventricle.
- Newborn MRI: unmyelinated white matter is brighter than cortex on T2, the reverse of adults; the posterior limb of the internal capsule is myelinated at term.
Internal capsule
| Part | Between | Contents | Main supply |
|---|---|---|---|
| Anterior limb | Caudate head and lentiform | Frontopontine fibres, anterior thalamic radiation | Lenticulostriate; recurrent artery of Heubner |
| Genu | At the bend | Corticobulbar fibres | Lenticulostriate |
| Posterior limb | Thalamus (medial) and lentiform (lateral) | Corticospinal and sensory fibres | Lenticulostriate; anterior choroidal |
| Retrolenticular | Behind the lentiform | Optic radiation | Anterior choroidal |
- A small capsular infarct gives pure motor hemiplegia of face, arm and leg equally.
- Months after a large infarct, Wallerian degeneration shrinks the ipsilateral cerebral peduncle.
White matter disease: location explains mechanism
| Disease | Pattern | Why |
|---|---|---|
| Multiple sclerosis | Ovoid FLAIR lesions perpendicular to the ventricles (Dawson fingers), callososeptal interface, juxtacortical, infratentorial | Inflammation and demyelination around the medullary veins, which run radially from the ventricles |
| Small-vessel disease | Periventricular and deep white matter, spares U-fibres | Arteriolosclerosis of penetrating arteries from hypertension |
| CADASIL | Confluent change in anterior temporal poles and external capsules; young normotensive adult with migraine with aura, strokes, mood change, family dementia | NOTCH3 mutation on chromosome 19; granular osmiophilic material in arteriole walls |
| PML (JC virus) | Asymmetric, involves subcortical U-fibres, no enhancement | Oligodendrocyte infection in immunosuppression |
| Diffuse axonal injury | Small dark foci on susceptibility imaging at the grey–white junction, splenium and dorsolateral brainstem; near-normal initial CT, persistent coma | Shear from rotational acceleration: tissues of different density move differently and axons tear. Brainstem involvement carries the worst prognosis |
| Periventricular leukomalacia | Preterm baby; white matter loss beside the trigones, irregular ventricles | Arterial border zone of the immature brain; leg fibres pass closest to the ventricles, so spastic diplegia (legs worse than arms); severe PVL spreads outwards to involve arm fibres |
| Marchiafava–Bignami | Middle layers of the corpus callosum | Alcohol, malnutrition |
Developmental disorders of the cortex
| Disorder | Imaging | Mechanism |
|---|---|---|
| Lissencephaly | Smooth brain, thick cortex, shallow vertical Sylvian fissures (figure-of-eight outline) | Arrested neuronal migration (LIS1, DCX); cannot be diagnosed before about 26 weeks, when the normal fetal brain is still smooth |
| Nodular heterotopia | Nodules lining the ventricles, isointense to grey matter | Neurons failed to leave the germinal zone |
| Schizencephaly | Full-thickness cleft from ventricle to surface lined by grey matter; open-lip (CSF-filled) or closed-lip (look for a ventricular dimple) | Early injury to the germinal zone; presents with hemiparesis and seizures |
| Sturge–Weber syndrome | Gyriform ("tram-track") cortical calcification and hemiatrophy under a leptomeningeal angioma, usually parieto-occipital; port-wine stain in V1 | Abnormal pial veins cause chronic venous ischaemia of the underlying cortex, which calcifies; glaucoma on the same side |
Limbic lobe and frontal connections
- Cingulate and parahippocampal gyri, hippocampus, amygdala, fornix and mammillary bodies. The Papez circuit runs hippocampus, fornix, mammillary body, anterior thalamic nucleus, cingulum, entorhinal cortex, back to the hippocampus.
- The dorsomedial (mediodorsal) thalamic nucleus is reciprocally connected with the prefrontal cortex and amygdala, serving emotion, judgement and memory. The anterior nucleus is the Papez relay; the dorsomedial is the prefrontal relay.
- Hippocampal sclerosis: small hippocampus, high T2 signal, lost internal structure; imaged in the oblique coronal plane perpendicular to the hippocampus.
- Alzheimer disease: earliest atrophy in the entorhinal cortex and hippocampus; amyloid plaques and flame-shaped tau tangles.
- Frontotemporal dementia (Pick type): disinhibited behaviour, knife-edge atrophy of frontal and anterior temporal gyri; silver-staining round cytoplasmic Pick bodies made of aggregated tau protein.
- HSV-1 encephalitis: asymmetric medial temporal, insular and cingulate swelling, sparing the basal ganglia.
Remember Name the capsule part by its neighbours: anterior limb by the caudate, posterior limb by the thalamus, both with the lentiform lateral.
Exam trap Repetition preserved means a transcortical aphasia, not Broca or Wernicke aphasia.
Exam trap Small-vessel disease in a young normotensive adult is not hypertensive until the temporal poles are checked for CADASIL.
How FCPS asks about this
- MS lesions perpendicular to the ventricles: perivenular inflammation around medullary veins.
- Coma after a crash with near-normal CT, dark foci at the grey–white junction: diffuse axonal injury from rotational shear.
- Preterm child with spastic diplegia: periventricular leukomalacia; leg fibres lie nearest the ventricles.
- Smooth brain with figure-of-eight outline: lissencephaly from arrested neuronal migration.
- Port-wine stain with gyriform calcification: Sturge–Weber; venous ischaemia under a pial angioma.
- Thalamic nucleus linked with prefrontal cortex: dorsomedial nucleus.
- Knife-edge frontotemporal atrophy: frontotemporal dementia with tau inclusions.
Test yourself on this topic
5 of the 83 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
On a midline sagittal MRI, a small round white matter bundle lies in the anterior wall of the third ventricle, just in front of the columns of the fornix. A line from it to a second bundle above the cerebral aqueduct is used as the standard reference plane for axial brain imaging. What is the first bundle?
Answer: Anterior commissure
The anterior commissure crosses the midline in the lamina terminalis region, just in front of the columns of the fornix, and links the olfactory areas and the anterior temporal lobes. The posterior commissure crosses just above the opening of the cerebral aqueduct, below the pineal. The line joining them (the AC-PC line) is the standard reference plane for axial imaging and stereotactic surgery. The optic chiasm lies lower, at the junction of the anterior wall and floor of the third ventricle.
AC-PC line
- Anterior commissure: in front of fornix columns
- Posterior commissure: above the aqueduct
- AC-PC line = axial reference
- Used in stereotaxy
Remember Front of the third ventricle: anterior commissure.
Exam trap The anterior commissure is not part of the corpus callosum; it is a separate small commissure.
Why the other options are wrong
- Posterior commissure This is the second bundle, above the aqueduct.
- Rostrum of corpus callosum Lies higher, at the front of the corpus callosum.
- Optic chiasm Lies lower, at the front of the floor of the third ventricle.
- Mammillothalamic tract Runs within the hypothalamus and thalamus, not across the midline.
A 60-year-old man dies six months after a large left MCA infarct involving the motor cortex. At autopsy the left cerebral peduncle and the left side of the ventral pons are shrunken and pale on myelin staining. What is the explanation?
Answer: Wallerian degeneration of corticospinal fibres
When cortical neurons die in an infarct, their axons separated from the cell bodies degenerate along their whole length, a process called Wallerian degeneration, with breakdown of myelin cleared by macrophages. The corticospinal fibres from the left motor cortex descend through the left internal capsule, cerebral peduncle and ventral pons, so these shrink and lose myelin on the same side as the infarct over months. On MRI the same tract becomes T2 bright. Crossed cerebellar diaschisis affects the opposite cerebellar hemisphere, mainly as reduced metabolism.
Wallerian degeneration
- Axons die distal to the cell body
- Follows the corticospinal tract
- Same side peduncle and pons shrink
- Develops over months
Remember Old cortical infarct with a small same-side peduncle: Wallerian degeneration.
Exam trap Wallerian degeneration is ipsilateral to the infarct, above the pyramidal decussation.
Why the other options are wrong
- New infarct in basilar perforator territory A new infarct would show acute necrosis, not slow shrinkage along a tract.
- Demyelination from multiple sclerosis MS would not follow one tract exactly beneath an old infarct.
- Crossed cerebellar diaschisis Affects the opposite cerebellum, not the peduncle.
- Central pontine myelinolysis Symmetrical central pontine damage after rapid sodium correction.
Which lobe of cortex lies hidden in the depth of the lateral sulcus, covered by the frontal, parietal and temporal opercula, with branches of the middle cerebral artery running over its surface?
Answer: Insula
The insula is a lobe of cortex that becomes buried during development as the surrounding frontal, parietal and temporal lobes grow over it, forming opercula. It forms the floor of the lateral sulcus, and branches of the middle cerebral artery (M2) run over its surface in the Sylvian fissure. Deep to the insula lie the extreme capsule, claustrum, external capsule and putamen. The transverse temporal gyri lie on the upper surface of the temporal lobe, not in the floor of the sulcus.
Insula
- Floor of the lateral sulcus
- Covered by opercula
- MCA M2 branches over it
- Deep to it: claustrum and putamen
Remember Open the Sylvian fissure and the insula is the floor.
Exam trap The insula is cortex, not deep grey matter, even though it lies deep on imaging.
Why the other options are wrong
- Claustrum A thin grey sheet deep to the insula, not cortex on the surface.
- Transverse temporal gyrus Lies on the upper surface of the temporal lobe within the sulcus.
- Lentiform nucleus Deep grey matter, separated from the insula by capsules and claustrum.
- Uncus Medial temporal lobe structure near the tentorial notch.
Which structures together form the corpus striatum?
Answer: Caudate and lentiform nuclei
The corpus striatum is the caudate nucleus together with the lentiform nucleus, named for the grey and white striations where bridges of grey matter cross the internal capsule. The lentiform nucleus is itself made of the putamen laterally and the globus pallidus medially. The caudate and putamen, which have the same cell structure and connections, form the striatum (neostriatum), the input part of the basal ganglia. The globus pallidus is the paleostriatum and the main output.
Corpus striatum
- Corpus striatum = caudate + lentiform
- Lentiform = putamen + globus pallidus
- Striatum = caudate + putamen
- Globus pallidus = main output
Remember Corpus striatum: caudate plus lentiform.
Exam trap Do not confuse the corpus striatum (caudate plus lentiform) with the striatum (caudate plus putamen).
Why the other options are wrong
- Putamen and globus pallidus These form the lentiform nucleus, only part of the corpus striatum.
- Thalamus and caudate nucleus The thalamus is not part of the striatum.
- Claustrum and putamen The claustrum is a separate thin sheet lateral to the putamen.
- Subthalamus and substantia nigra Functionally linked basal ganglia, but not part of the corpus striatum.
A 7-year-old girl with a port-wine stain over the left forehead and upper eyelid has seizures, atrophy of the left cerebral hemisphere and gyriform calcification along the left occipital and parietal cortex. What causes the cortical calcification?
Answer: Chronic venous ischaemia under a pial angioma
In Sturge-Weber syndrome, a somatic GNAQ mutation produces a facial port-wine stain in the ophthalmic (V1) territory and a leptomeningeal (pial) venous angioma over the same side of the brain. The angioma has poor venous drainage, so the underlying cortex suffers chronic venous congestion and ischaemia, leading to neuronal loss, atrophy and calcification of the cortex in a gyriform 'tram-track' pattern. Congenital CMV gives periventricular calcification, not one-sided gyral calcification.
Sturge-Weber syndrome
- V1 port-wine stain
- Ipsilateral pial angioma
- Tram-track cortical calcification
- Somatic GNAQ mutation
Remember Forehead port-wine stain plus seizures: look for gyral calcification.
Exam trap Glaucoma on the side of the port-wine stain is a common and treatable association.
Why the other options are wrong
- Calcified tubers of the cortex Tuberous sclerosis tubers are scattered and not with a V1 port-wine stain.
- Healed congenital CMV infection Gives periventricular calcification and microcephaly.
- Calcified cortical arteriovenous malformation AVMs have feeding arteries and draining veins; this is a pial venous angioma.
- Dystrophic calcification after meningitis Meningitis does not give one-sided gyral calcification with a facial stain.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Brain, Cerebral hemispheres, cortex, white matter and internal capsule; limbic lobe