Brainstem and cerebellum
Brainstem, cerebellum and cranial nerves on imaging: lesions and posterior fossa masses
Brainstem lesions give crossed signs: a cranial nerve palsy on the side of the lesion and limb signs on the other side. CPSP asks you to localise these lesions, name the cerebellar parts and recognise classic posterior fossa masses.
Surface anatomy on MRI
- Midbrain: cerebral peduncles in front, tectum (superior and inferior colliculi) behind the aqueduct. III leaves the interpeduncular fossa; IV is the only nerve from the dorsal surface and crosses, so a trochlear nucleus lesion weakens the opposite superior oblique.
- Pons: basilar part with transverse pontocerebellar fibres crossing to the opposite middle cerebellar peduncle (the large bundles sweeping back lateral to the fourth ventricle). The facial colliculus in the floor of the fourth ventricle is VI nucleus looped by VII fibres.
- Medulla: XII rootlets leave the groove between pyramid and olive; IX, X and XI leave behind the olive.
- Internal acoustic meatus in cross-section: facial nerve anterosuperior, cochlear nerve anteroinferior, two vestibular nerves posterior.
Localising brainstem lesions
| Site | Ipsilateral | Contralateral |
|---|---|---|
| Ventral midbrain | III palsy | Hemiplegia |
| Midbrain tegmentum (red nucleus) | III palsy | Tremor, involuntary movements |
| Dorsal midbrain (pineal tumour) | Upward gaze palsy, pupils react to near not light | None |
| Ventral pons, both sides (basilar thrombosis) | Locked-in: only blinking and vertical eye movement | Quadriplegia |
| Caudal ventral pons | VI and VII palsy | Hemiplegia |
| Facial colliculus | Horizontal gaze palsy (VI nucleus) and full facial weakness | None |
| Lateral pons (AICA) | Facial palsy, deafness (labyrinthine artery), ataxia | Body pain loss |
| Medial medulla | XII: tongue deviates towards the lesion | Hemiplegia, loss of position sense |
| Lateral medulla (PICA or vertebral artery, on the side of the Horner) | Face pain and temperature loss (spinal trigeminal nucleus and tract), Horner (descending sympathetic fibres), dysphagia and hoarseness (nucleus ambiguus), ataxia (inferior peduncle), vertigo | Body pain and temperature loss |
- Worked example: vertigo, dysphagia, hoarseness, loss of pain and temperature on the left face and right body and a left Horner syndrome mean a left lateral medullary infarct: left PICA (Wallenberg syndrome). The face is ipsilateral because the spinal trigeminal tract has not yet crossed; the body is contralateral because the spinothalamic tract crossed in the cord.
- MLF lesion (internuclear ophthalmoplegia): the eye on the side of the lesion cannot adduct, the other eye has abducting nystagmus, convergence is preserved. MLF plus VI nucleus gives the one-and-a-half syndrome.
- Pupils in coma: midbrain damage gives mid-position fixed pupils; pontine damage gives pinpoint pupils.
Brainstem nuclei worth knowing
- Mesencephalic nucleus of V: primary sensory cell bodies inside the CNS; afferent limb of the jaw jerk.
- Superior salivatory: lacrimal, submandibular, sublingual (VII). Inferior salivatory: parotid (IX). Nucleus ambiguus: pharynx and larynx.
- A single midline oculomotor subnucleus supplies both levators, so a nuclear III lesion causes bilateral ptosis.
- Compressive III palsy (posterior communicating aneurysm, uncal herniation) dilates the pupil early because pupillary fibres lie on the surface; diabetic III palsy spares the pupil.
- VI palsy is a false localising sign of raised pressure (long course over the petrous apex), and the first nerve hit by a clival chordoma (midline, very bright on T2).
- Uncal herniation can press the opposite peduncle on the tentorium, giving weakness on the side of the mass; the dilated pupil is the reliable side.
Cranial nerves at the skull base
| Nerve | Imaging and clinical point |
|---|---|
| II | Injured within the optic canal after brow trauma (RAPD, normal fundus); the subarachnoid sheath along the nerve explains papilloedema |
| V | V1 supplies the forehead, upper eyelid and the side and tip of the nose (nasociliary branch); shingles there (with Hutchinson sign) threatens the eye. Ganglion in Meckel cave at the petrous apex; V3 through foramen ovale. Cavernous sinus lesions spare V3. Tumour such as nasopharyngeal carcinoma spreading through the foramen ovale damages V3: the masseter, temporalis and pterygoids shrink and turn to fat (compare with the healthy side). Angle of the jaw is C2–C3, not V |
| VII | LMN palsy: whole half face. Hyperacusis and taste loss mean a lesion above the nerve to stapedius. Perineural spread: thick enhancing nerve. Superficial in newborns (no mastoid) |
| IX | Gag afferent; carries carotid sinus afferents, so glossopharyngeal neuralgia can cause bradycardia and syncope |
| XI | Crosses the posterior triangle superficially (on levator scapulae): lymph node biopsy there can injure it, giving trapezius weakness, inability to shrug and difficulty abducting above the horizontal (trapezius rotates the scapula) |
| XII | LMN lesion: wasting and deviation towards the lesion (hypoglossal canal) |
- Corneal reflex: afferent V1, efferent VII; its loss is an early sign of a large cerebellopontine angle tumour.
- Neurovascular compression: trigeminal neuralgia, usually the superior cerebellar artery; hemifacial spasm, AICA at the root exit zone of VII.
Cerebellum
| Part | Lesion |
|---|---|
| Flocculonodular lobe and vermis | Truncal ataxia, broad-based gait, nystagmus (alcohol affects the anterior vermis) |
| Hemispheres | Ipsilateral limb ataxia |
The three peduncles carry the following fibres.
| Peduncle | Main fibres |
|---|---|
| Superior | Output from dentate to opposite red nucleus and thalamus |
| Middle | Input from opposite pontine nuclei |
| Inferior | Spinocerebellar and olivocerebellar (climbing) fibres |
- Cortex sends output only through Purkinje cells to the deep nuclei; phenytoin causes Purkinje loss and atrophy.
- Dentate, red nucleus and opposite inferior olive form a loop: a pontine bleed can later enlarge the olive (T2 bright) with palatal tremor.
Posterior fossa and degenerative patterns
| Lesion | Clue |
|---|---|
| Medulloblastoma | Child with morning vomiting and truncal ataxia; midline vermis mass, hyperdense on CT and restricting on diffusion because of high cellularity with scant cytoplasm (small round blue cells); seeds through CSF, so image the whole spine before surgery |
| Pilocytic astrocytoma | Child, cyst with mural nodule in a hemisphere |
| Haemangioblastoma | Adult, cyst with enhancing nodule touching pia; VHL; erythropoietin gives polycythaemia |
| Diffuse midline glioma | Child, expanded pons engulfing the basilar artery, little enhancement |
| Multiple system atrophy | Hot cross bun pons (loss of transverse pontocerebellar fibres) |
| Progressive supranuclear palsy | Midbrain atrophy, hummingbird sign |
| Osmotic demyelination | Trident-shaped central pons, corticospinal tracts spared |
| Joubert syndrome | Molar tooth: long thick superior peduncles |
| Superficial siderosis | Dark coating on brainstem and cerebellum; deafness and ataxia |
| Dysplastic cerebellar gangliocytoma | Striated pattern; PTEN (Cowden) |
| Cavernous malformation (cavernoma) | Sudden diplopia or numbness that improves; popcorn mixed-signal core with a complete dark haemosiderin rim that blooms on susceptibility imaging; no flow voids, angiographically occult; often beside a developmental venous anomaly, which is left alone |
| Tuberculoma | Young adult from an endemic area with fever and weight loss; ring-enhancing lesions, often conglomerate, with a T2 dark centre (caseation) and no diffusion restriction (unlike pyogenic abscess); may enlarge paradoxically on treatment |
| Ataxia telangiectasia | Cerebellar atrophy in a child with ataxia from walking age, conjunctival telangiectasia, sinopulmonary infections, low IgA, raised AFP; ATM defect impairs repair of DNA double-strand breaks, so minimise ionising radiation and avoid standard radiotherapy doses |
Cerebellopontine angle
| Mass | Clue |
|---|---|
| Vestibular schwannoma | From the vestibular nerve; widens the internal meatus, "ice cream cone"; loss of the corneal reflex is an early sign. Bilateral schwannomas (with meningiomas) in a young adult mean NF2: merlin gene on chromosome 22 |
| Meningioma | Broad dural base, dural tail |
| Epidermoid | CSF-like on T1 and T2 but bright on diffusion, wraps round vessels |
Craniovertebral junction and neural crest
- Basilar invagination: the dens projects more than a few millimetres above Chamberlain line (back of the hard palate to the posterior lip of the foramen magnum) and indents the medulla, causing neck pain, dysphagia and long-tract signs; neck flexion at intubation can worsen it.
- Neural crest derivatives: sensory ganglia of cranial nerves V, VII, IX and X and the dorsal root ganglia, autonomic ganglia, Schwann cells, adrenal medulla, melanocytes, C cells, pharyngeal arch cartilages and the leptomeninges. This explains why neurocutaneous syndromes affect skin, nerves and adrenals together.
Remember Cranial nerve signs point to the side of the lesion; long-tract signs point away from it.
Exam trap The tongue deviates towards a lower motor neurone XII lesion; with an upper motor neurone lesion it deviates away and is not wasted.
Exam trap The cerebellum receives through the middle peduncle and sends out through the superior peduncle.
How FCPS asks about this
- Left face and right body pain loss, Horner, dysphagia, hoarseness: left PICA (lateral medullary syndrome).
- Shingles of forehead, eyelid and nasal tip: ophthalmic division (V1).
- Cannot shrug after posterior triangle node biopsy: accessory nerve.
- Midline vermis mass in a child, dense on CT, restricted diffusion: medulloblastoma; high cellularity.
- Bilateral vestibular schwannomas: NF2, merlin on chromosome 22.
- Clival mass bright on T2 with diplopia: chordoma; abducens first.
- Popcorn lesion with haemosiderin rim: cavernous malformation.
Test yourself on this topic
5 of the 90 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 64-year-old man has a small acute infarct in the dorsal midbrain at the level of the superior colliculi, close to the midline. He has a left third nerve palsy, but both upper eyelids droop. Why are both lids affected?
Answer: One midline subnucleus supplies both levators
The oculomotor nuclear complex lies in the dorsal midbrain, ventral to the aqueduct, at the level of the superior colliculus. Most subnuclei serve the muscles of the same eye, but the levator palpebrae of both sides are supplied by a single midline central caudal subnucleus, and each superior rectus subnucleus supplies the opposite eye. A lesion of the nuclear complex therefore causes bilateral ptosis, whereas a lesion of one oculomotor nerve after it leaves the nucleus causes ptosis on one side only. This helps localise a third nerve palsy to the nucleus.
Oculomotor nuclear lesion
- Complex lies ventral to the aqueduct
- Single central caudal subnucleus: both levators
- Superior rectus subnucleus: opposite eye
- Nuclear lesion: bilateral ptosis
Remember Third nerve palsy with both lids drooping: the lesion is in the nucleus.
Exam trap Myasthenia gravis also causes bilateral ptosis and can mimic a nuclear third nerve lesion.
Why the other options are wrong
- Each levator gets fibres from both oculomotor nerves Each nerve supplies only its own levator once outside the brainstem.
- The sympathetic fibres to both lids cross here Sympathetic fibres to the lids do not cross in the midbrain.
- The facial nucleus for both lids lies here The facial nerve closes the eye; it does not lift the lid.
- Both trochlear nerves supply the levators The trochlear nerve supplies only the superior oblique.
A 58-year-old man has brief stabbing pains in the right throat and ear set off by swallowing, from a vascular loop compressing the glossopharyngeal rootlets. During two attacks his pulse fell to 35/min and he fainted. Why does pain in this nerve cause fainting?
Answer: It carries carotid sinus afferents
Glossopharyngeal neuralgia causes paroxysmal stabbing pain in the tonsil, back of the tongue, throat and ear, triggered by swallowing, often from a PICA loop compressing the nerve's root entry zone. The ninth nerve also carries afferents from the carotid sinus baroreceptors through the carotid sinus nerve. The abnormal burst of afferent discharge is read by the brainstem as high blood pressure, triggering a strong vagal efferent response with bradycardia and hypotension. The efferent limb is the vagus, not the glossopharyngeal nerve.
Glossopharyngeal neuralgia
- Throat and ear pain on swallowing
- PICA at the root entry zone
- IX carries carotid sinus afferents
- Reflex vagal bradycardia and syncope
Remember Neuralgia plus fainting: carotid sinus afferents in IX.
Exam trap Carotid sinus afferents run in IX, but aortic arch afferents run in X; do not mix them up.
Why the other options are wrong
- It carries vagal efferents to the heart The vagus, not the ninth nerve, carries the cardiac efferents.
- It supplies the sinoatrial node directly The ninth nerve does not supply the heart.
- It carries sympathetic fibres to the heart Cardiac sympathetics come from the thoracic chain.
- It supplies the aortic arch receptors Aortic arch afferents travel in the vagus.
Eight months after a haemorrhage in the left pontine tegmentum that cut the central tegmental tract, a 45-year-old woman develops rhythmic movements of her soft palate. Which structure has undergone delayed hypertrophic degeneration?
Answer: Inferior olivary nucleus
The dentate nucleus, red nucleus and inferior olive are connected in the Guillain-Mollaret triangle. The central tegmental tract runs from the red nucleus region through the pontine tegmentum to the ipsilateral inferior olive. When a lesion interrupts this tract, the olive loses its input and undergoes a peculiar transsynaptic degeneration in which its neurons enlarge and vacuolate, months after the injury. The clinical sign is palatal tremor (myoclonus); on MRI the olive is enlarged and T2 bright.
Hypertrophic olivary degeneration
- Guillain-Mollaret triangle
- Lesion of central tegmental tract
- Olive enlarges months later
- Palatal tremor
Remember Palatal tremor after a brainstem lesion: think of the inferior olive.
Exam trap The enlarged olive is a delayed consequence, not a new tumour or infarct.
Why the other options are wrong
- Nucleus ambiguus Lies deeper in the medulla and does not enlarge after tegmental lesions.
- Hypoglossal nucleus Lies near the floor of the fourth ventricle, not behind the pyramid laterally.
- Inferior cerebellar peduncle Lies dorsolaterally and does not enlarge after this injury.
- Spinal trigeminal nucleus Lies dorsolaterally and does not enlarge after this injury.
Which cranial nerve emerges as a row of rootlets from the groove between the pyramid and the olive on the front of the medulla?
Answer: Hypoglossal nerve
The hypoglossal nerve emerges as a series of rootlets from the preolivary sulcus, the groove between the pyramid and the olive on the front of the medulla. The glossopharyngeal, vagus and cranial accessory rootlets emerge further back, from the postolivary sulcus behind the olive. The abducens leaves at the pontomedullary junction near the midline. The hypoglossal rootlets then join and leave the skull through the hypoglossal canal.
Medullary nerve exits
- Preolivary sulcus: XII
- Postolivary sulcus: IX, X, XI
- Pontomedullary junction: VI, VII, VIII
- XII leaves by the hypoglossal canal
Remember In front of the olive: XII. Behind the olive: IX, X, XI.
Exam trap Do not confuse the preolivary sulcus with the anterior median fissure between the pyramids.
Why the other options are wrong
- Glossopharyngeal nerve Emerges behind the olive.
- Vagus nerve Emerges behind the olive.
- Accessory nerve Emerges behind the olive and from the upper cervical cord.
- Abducens nerve Emerges at the pontomedullary junction, above the olive.
A 30-year-old woman has neck pain, difficulty swallowing and clumsy hands. Sagittal MRI shows the tip of the dens 9 mm above a line drawn from the back of the hard palate to the posterior margin of the foramen magnum, indenting the front of the medulla. What is the diagnosis?
Answer: Basilar invagination
The line from the posterior hard palate to the opisthion is Chamberlain line, and the tip of the dens normally lies no more than a few millimetres above it. In basilar invagination the margins of the foramen magnum are pushed upwards so the dens projects into the posterior fossa and compresses the medulla. This can cause lower cranial nerve palsies, such as dysphagia, and myelopathy. It may be congenital or follow bone softening, as in Paget disease, osteogenesis imperfecta or rheumatoid arthritis.
Basilar invagination
- Dens tip well above Chamberlain line
- Line: hard palate to opisthion
- Compresses the medulla
- Causes: congenital, Paget, OI, rheumatoid
Remember Dens poking above Chamberlain line: basilar invagination.
Exam trap Flexion of the neck can worsen medullary compression; avoid it during intubation.
Why the other options are wrong
- Chiari I malformation Shows tonsillar descent below the foramen magnum, not a high dens.
- Atlantoaxial subluxation Shows a widened atlanto-dens interval rather than upward migration.
- Os odontoideum Shows a separate ossicle in place of the dens tip.
- Klippel-Feil syndrome Shows fused cervical vertebrae with a short neck.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Brain, Brainstem and cerebellum; cranial nerves
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