Brainstem anatomy
Brainstem: midbrain, pons, medulla, cranial nerve nuclei and brainstem syndromes
Brainstem anatomy for FCPS Part 1: cranial nerve nuclei at each level, internal landmarks, gaze centres and the classic crossed stroke syndromes. Covers Weber, Benedikt, Millard-Gubler, INO, one-and-a-half, lateral and medial medullary syndromes and herniation.
One of the most tested topics in past papers
Why brainstem lesions give crossed signs
- Cranial nerve nuclei and their fibres lie on the same side as the nerve, while long motor and sensory tracts have not yet crossed (corticospinal crosses at the lower medulla, medial lemniscus fibres have already crossed in the medulla, spinothalamic fibres crossed in the cord). A small lesion therefore causes an ipsilateral cranial nerve palsy with contralateral hemiplegia or sensory loss.
- The cranial nerve involved tells you the level; whether it is medial (motor) or lateral (sensory, cerebellar, sympathetic) tells you the artery.
Nuclei at each level
| Level | Nuclei | Other landmarks |
|---|---|---|
| Midbrain | III (with Edinger–Westphal), IV | Cerebral peduncles, substantia nigra, red nucleus, aqueduct, periaqueductal grey, superior and inferior colliculi |
| Pons | V (motor and main sensory), VI, VII, superior salivatory, VIII (vestibular and cochlear, extend into medulla) | Pontine nuclei, facial colliculus, locus coeruleus, MLF, PPRF |
| Medulla | IX, X, XII, nucleus ambiguus, dorsal vagal nucleus, inferior salivatory, nucleus tractus solitarius, spinal trigeminal nucleus | Pyramids, olive, nucleus raphe magnus, area postrema |
- Rule of four: two nerves above the brainstem (I, II), two in the midbrain (III, IV), four in the pons (V–VIII), four in the medulla (IX–XII). Motor nuclei of nerves that divide evenly into 12 (III, IV, VI, XII) lie near the midline.
- Trochlear (IV) is the only cranial nerve to leave the dorsal surface of the brainstem, and it decussates first. Its nucleus lies at the level of the inferior colliculus, so a nuclear lesion weakens the opposite superior oblique.
- Facial colliculus: a bump on the floor of the fourth ventricle formed by facial motor fibres looping round the abducens nucleus. A lesion here causes an LMN facial palsy plus a horizontal gaze palsy to the same side.
- In the basilar pons, the transverse fibres are pontocerebellar axons from pontine nuclei crossing to the opposite middle cerebellar peduncle; corticospinal bundles run longitudinally between them.
Midbrain structures and functions
- Superior colliculus: visual reflexes, reflex turning of eyes and head towards a sudden stimulus (tectospinal tract); vertical gaze centres lie nearby.
- Inferior colliculus: obligatory relay in the auditory pathway before the medial geniculate body. Hearing is bilateral above the cochlear nuclei, so central lesions rarely cause one-sided deafness.
- Periaqueductal grey: stimulation produces strong analgesia through the raphe magnus, whose serotonin fibres descend to the dorsal horn and excite enkephalin interneurones.
- Red nucleus: motor coordination with cerebellar input via the superior peduncle.
Pontine nuclei worth knowing
- Superior salivatory nucleus (VII): parasympathetic supply to the lacrimal gland (greater petrosal, pterygopalatine ganglion) and submandibular and sublingual glands (chorda tympani, submandibular ganglion). The inferior salivatory nucleus (IX) supplies the parotid via the lesser petrosal nerve and otic ganglion. So a lesion of the superior salivatory nucleus causes a dry eye and less submandibular saliva with normal parotid flow.
- Locus coeruleus: main noradrenergic nucleus. Opioids suppress it; in opioid withdrawal it fires excessively, causing sweating, tachycardia, piloerection, dilated pupils, yawning and diarrhoea. Clonidine, an alpha-2 agonist, calms it.
Horizontal gaze: PPRF, abducens nucleus and MLF
- To look right, the right PPRF drives the right abducens nucleus. This nucleus holds motor neurones for the right lateral rectus and internuclear neurones whose axons cross and ascend in the left MLF to the left medial rectus subnucleus of III.
| Lesion | Result |
|---|---|
| Abducens nerve | Only the ipsilateral lateral rectus is weak |
| Abducens nucleus (or PPRF) | Neither eye can look to that side (ipsilateral horizontal gaze palsy) |
| MLF (internuclear ophthalmoplegia) | Eye on the side of the lesion fails to adduct; opposite eye shows abducting nystagmus; convergence preserved |
| One-and-a-half syndrome (abducens nucleus plus MLF, same side) | Ipsilateral eye cannot move horizontally at all; opposite eye can only abduct, with nystagmus |
- Convergence survives an INO because the medial rectus subnucleus and its convergence input are intact. Bilateral INO in a young adult suggests multiple sclerosis; in older people, a stroke.
Brainstem stroke syndromes
| Syndrome | Site and artery | Ipsilateral | Contralateral |
|---|---|---|---|
| Weber | Ventral midbrain (PCA branches) | III palsy | Hemiplegia (peduncle) |
| Benedikt | Midbrain tegmentum, red nucleus | III palsy | Tremor, involuntary movements, ataxia |
| Parinaud | Dorsal midbrain (pineal tumour) | Upgaze palsy, light–near dissociation, convergence–retraction nystagmus | – |
| Millard–Gubler / Foville | Caudal ventral pons (paramedian basilar) | VI (or gaze palsy) and LMN VII | Hemiplegia |
| Lateral pontine | AICA | Facial palsy, deafness, facial sensory loss, ataxia, Horner | Body pain and temperature loss |
| Lateral medullary (Wallenberg) | PICA or vertebral artery | Facial pain and temperature loss, Horner, ataxia, dysphagia and hoarseness (nucleus ambiguus), vertigo | Body pain and temperature loss |
| Medial medullary | Anterior spinal or vertebral branches | Tongue deviates to the lesion (XII) | Hemiplegia, loss of proprioception |
| Locked-in | Basilar occlusion, ventral pons | – | Quadriplegia and anarthria; consciousness and vertical eye movements preserved |
- Lateral medullary syndrome has no hemiplegia because the pyramids are medial. Neck pain after vigorous neck manipulation followed by these signs points to vertebral artery dissection.
- Pontine haemorrhage: rapid coma, pinpoint pupils, hyperpyrexia, quadriplegia.
Herniation and secondary brainstem damage
- Uncal (transtentorial) herniation compresses the ipsilateral III nerve (dilated pupil, the parasympathetic fibres lie superficially) and the ipsilateral peduncle (contralateral weakness).
- Kernohan notch phenomenon: the shift pushes the opposite cerebral peduncle against the tentorial edge, so weakness appears on the same side as the mass and the dilated pupil. This is a false localising sign; the pupil is the better guide to the side of the clot.
- Duret haemorrhages: downward displacement of the brainstem tears the paramedian perforating branches of the basilar artery, causing linear midline bleeds in the midbrain and upper pons. Usually fatal.
- Tonsillar herniation (coning) compresses the medulla: Cushing reflex (hypertension, bradycardia, irregular breathing), then apnoea.
Bulbar versus pseudobulbar palsy
| Feature | Bulbar (LMN, medulla) | Pseudobulbar (bilateral UMN) |
|---|---|---|
| Tongue | Wasted, fasciculating | Small, stiff, spastic |
| Jaw jerk | Absent or normal | Brisk |
| Speech | Nasal | Slow, strained, spastic |
| Emotion | Normal | Emotional lability |
| Causes | MND, Guillain–Barré, syringobulbia, polio | Bilateral strokes, MND, MS |
Vital centres and reticular formation
- Respiratory centres (medulla and pons), vasomotor centre (medulla), vomiting centre; the chemoreceptor trigger zone in the area postrema lies outside the blood–brain barrier.
- The nucleus tractus solitarius receives taste (VII, IX, X) and visceral afferents from baroreceptors and chemoreceptors.
- The ascending reticular activating system in the upper pons and midbrain maintains wakefulness; lesions here cause coma.
Remember Cranial nerve on the side of the lesion, long tract on the other: the nerve gives the level, medial versus lateral gives the artery.
Exam trap A left uncal herniation can give a left dilated pupil with left hemiparesis (Kernohan notch); operate on the side of the pupil.
Exam trap An abducens nucleus lesion causes a gaze palsy to that side, not just a lateral rectus palsy.
How FCPS asks about this
- Vertigo, dysphagia, hoarseness, left face and right body pain loss, left Horner: left PICA (lateral medullary syndrome).
- Left III palsy with right hemiplegia: left ventral midbrain (Weber); with right-sided tremor instead, red nucleus (Benedikt).
- Right VI and LMN VII palsy with left hemiplegia: right caudal pons.
- MS, right eye cannot adduct on left gaze, convergence normal: right MLF.
- Only cranial nerve leaving the dorsal brainstem: trochlear; its nucleus supplies the opposite superior oblique.
- Opioid withdrawal symptoms eased by clonidine: overactive locus coeruleus.
- Midline brainstem bleeds after a temporal mass: Duret haemorrhages from torn paramedian basilar perforators.
Test yourself on this topic
5 of the 44 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A teenager with a pineal tumour cannot look upwards, and his pupils constrict on convergence but not to light. Which region is compressed?
Answer: Dorsal midbrain
Parinaud (dorsal midbrain) syndrome: compression of the pretectal region and superior colliculi, typically by a pineal tumour (germinoma) or hydrocephalus, causes vertical (upward) gaze palsy, light-near dissociation (pupils react to accommodation but not to light), convergence-retraction nystagmus and eyelid retraction (Collier's sign). The aqueduct is also compressed, causing obstructive hydrocephalus. Argyll Robertson pupils (neurosyphilis) also show light-near dissociation but are small and irregular.
Parinaud syndrome
- Dorsal midbrain; pineal tumour
- Upgaze palsy, light-near dissociation
- Convergence-retraction nystagmus, lid retraction
- Aqueduct compression → hydrocephalus
Remember Pineal pushes on the eyes' up switch.
Why the other options are wrong
- Ventral pons Causes locked-in syndrome.
- Lateral medulla Wallenberg syndrome.
- Cerebellar vermis Truncal ataxia.
- Optic chiasm Bitemporal hemianopia.
A hypertensive man with a large pontine haemorrhage has pinpoint pupils that still constrict slightly to bright light under a magnifier. Naloxone has no effect. What is the mechanism of the small pupils?
Answer: Loss of descending sympathetic fibres
Descending sympathetic fibres from the hypothalamus run through the lateral pontine tegmentum to the cord. A pontine lesion interrupts them on both sides, so the dilator pupillae loses its tone and the unopposed parasympathetic supply from the midbrain makes the pupils tiny. Because the midbrain and the light reflex pathway are intact, the pupils still react a little. Destroying the Edinger–Westphal nucleus would instead make the pupils large.
Pontine pupils
- Pinpoint, still reactive
- Loss of sympathetic fibres in pons
- Parasympathetic unopposed
- Midbrain lesion: mid-position, fixed
Remember Pinpoint pupils not reversed by naloxone: think pons.
Exam trap Hyperpyrexia with pinpoint pupils and coma should prompt you to think of pontine haemorrhage, not only opioids.
Why the other options are wrong
- Destruction of the Edinger–Westphal nucleus Would cause dilated, fixed pupils.
- Opioid receptor stimulation Naloxone gave no response.
- Damage to both optic tracts Would abolish the light reflex.
- Irritation of the ciliary ganglia Not a recognised cause of miosis in stroke.
A left lateral medullary infarct causes left limb ataxia. Which of the following structures is damaged?
Answer: Left inferior cerebellar peduncle
The inferior cerebellar peduncle forms part of the lateral wall of the medulla. It carries the dorsal spinocerebellar tract, olivocerebellar climbing fibres and vestibulocerebellar fibres into the cerebellum on the same side. A lateral medullary infarct damages it, giving ipsilateral limb ataxia. Because cerebellar hemispheres control the same side of the body, the ataxia is on the side of the lesion.
Cerebellar peduncles
- Inferior: medulla, input (spinal, olive)
- Middle: pons, pontocerebellar
- Superior: midbrain, main output
- Hemisphere lesion: same-side ataxia
Remember Lateral medulla carries the inferior peduncle: same-side ataxia.
Exam trap Climbing fibres from the opposite inferior olive enter through the inferior peduncle.
Why the other options are wrong
- Left superior cerebellar peduncle Leaves at the midbrain level; not in the medulla.
- Right middle cerebellar peduncle Lies in the pons, not the medulla.
- Left medial lemniscus Medial medullary; carries proprioception, not cerebellar input.
- Right dentate nucleus Deep nucleus in the cerebellum, not damaged by a medullary infarct.
A 26-year-old woman with multiple sclerosis has weakness of the whole right side of her face, including the forehead, and neither eye can look to the right. Limb power is normal. Where is the lesion?
Answer: Right facial colliculus (dorsal pons)
In the dorsal pons, fibres of the facial nerve loop around the abducens nucleus, raising the facial colliculus in the floor of the fourth ventricle. A small plaque here damages both: the facial fibres give an ipsilateral lower motor neurone facial palsy, and the abducens nucleus (which drives the ipsilateral lateral rectus and, through the MLF, the opposite medial rectus) gives a horizontal gaze palsy to the same side. A ventral pontine lesion would add a contralateral hemiplegia.
Facial colliculus
- Facial fibres loop round the abducens nucleus
- Lesion: ipsilateral LMN facial palsy
- Plus ipsilateral horizontal gaze palsy
- No limb signs (dorsal pons)
Remember Face and gaze to one side lost: dorsal pons.
Exam trap A nucleus lesion gives a gaze palsy; a nerve lesion only weakens one lateral rectus.
Why the other options are wrong
- Right ventral pons (basis pontis) Would add contralateral hemiplegia from the corticospinal tract.
- Right cerebellopontine angle Causes deafness and facial weakness, not a gaze palsy.
- Left frontal eye field Gives contralateral lower face weakness and eye deviation, not a full LMN palsy.
- Right medial longitudinal fasciculus Causes failure of adduction of one eye only.
During brainstem death testing, 50 mL of ice-cold water is run into each ear canal in turn, with the drum seen to be intact. Neither eye moves. Which pathway has been shown to be absent?
Answer: Vestibular nuclei to III and VI nuclei
The caloric (vestibulo-ocular) test cools the horizontal semicircular canal and alters firing in the vestibular nerve. In a patient with an intact brainstem, vestibular nuclei in the pons and medulla drive the abducens and oculomotor nuclei through the medial longitudinal fasciculus, so the eyes deviate towards the cold ear. No movement on either side shows that this pontomedullary and midbrain circuit is not working. Because it tests the brainstem itself, it is one of the core reflexes in brainstem death testing.
Caloric test
- Ice water cools horizontal canal
- Vestibular nuclei to III and VI via MLF
- Intact brainstem: eyes turn towards cold ear
- No movement: brainstem reflex absent
Remember Cold water, no eye movement: vestibulo-ocular arc lost.
Exam trap Wax or a perforated drum must be excluded, and some drugs can suppress the reflex.
Why the other options are wrong
- Optic nerve to Edinger–Westphal nucleus This is the pupillary light reflex arc.
- Trigeminal nucleus to facial nucleus This is the corneal (blink) reflex arc.
- Cerebellar vermis to red nucleus Not part of the caloric reflex.
- Frontal eye field to PPRF Cortical voluntary gaze; absent in any coma.
Where this sits in the CPSP syllabus
- Paper 1: Neuroanatomy, Brainstem: midbrain, pons, medulla and cranial nerve nuclei; brainstem syndromes
- Surgery & Allied, Paper 2: Cranium and brain, Brainstem: midbrain, pons, medulla and cranial nerve nuclei; brainstem syndromes
- Medicine & Allied, Paper 2: Central nervous system, Brainstem: midbrain, pons, medulla and cranial nerve nuclei; brainstem syndromes