Brainstem Cross-Sections and Lesions — Midbrain, Pons and Medulla Syndromes

The brainstem joins the cerebrum to the spinal cord and cerebellum. From above down it has three parts — midbrain, pons and medulla oblongata — and it carries the nuclei of 10 of the 12 cranial nerves (all except I and II). Every level contains three kinds of structure: cranial nerve nuclei and fascicles, long tracts passing through (corticospinal, medial lemniscus, spinothalamic), and local nuclei (red nucleus, substantia nigra, olive, vestibular nuclei).

The corticospinal tract decussates at the lower end of the medulla (pyramidal decussation), and the dorsal column pathway crosses as the medial lemniscus in the lower medulla. A brainstem lesion therefore sits above these crossings. It damages a cranial nerve on its own side but the limb pathway destined for the opposite side. That gives the hallmark of a brainstem lesion: ipsilateral cranial nerve palsy + contralateral hemiplegia — a crossed or alternating hemiplegia.

The midbrain surrounds the cerebral aqueduct, which joins the third and fourth ventricles and is ringed by periaqueductal grey. Behind the aqueduct lies the tectum with the paired superior and inferior colliculi (corpora quadrigemina); in front lies the tegmentum; the most anterior part is the crus cerebri (cerebral peduncle base), carrying corticospinal, corticonuclear and corticopontine fibres, with the substantia nigra between crus and tegmentum.

All the ventral and paramedian midbrain syndromes share an ipsilateral third nerve palsy — ptosis, an eye that rests down and out (unopposed lateral rectus and superior oblique) and, if the upper fascicles are involved, a dilated pupil. What is added depends on how far back the lesion reaches: the crus (hemiplegia), the red nucleus (tremor, ataxia) or the dorsal midbrain (vertical gaze).

Parinaud syndrome is classically caused by a pineal gland tumour pressing on the dorsal midbrain, though midbrain infarction, haemorrhage, multiple sclerosis and obstructive hydrocephalus also cause it. Neoplastic causes dominate in children and young adults; vascular causes in older patients. Downgaze is classically preserved and the vestibulo-ocular reflex is spared.

The pons has a bulging basilar (ventral) part — corticospinal fibres broken into bundles by transverse pontocerebellar fibres, with the basilar artery in the basilar groove on its surface — and a dorsal tegmentum forming the upper floor of the fourth ventricle. It joins the cerebellum through the middle cerebellar peduncles, the largest of the three.

• Upper pons: trigeminal (V) motor and principal sensory nuclei; CN V, the largest cranial nerve, exits the anterolateral upper pons.
• Lower pons: abducens (VI) and facial (VII) nuclei in the tegmentum near the pontomedullary junction. This region underlies the facial colliculus in the floor of the fourth ventricle.
• Pontomedullary groove: VI, VII and VIII emerge from medial to lateral.
• Throughout: medial lemniscus behind the corticospinal fibres, spinothalamic tract more laterally, MLF next to the midline.

Millard-Gubler syndrome (ventral pontine syndrome, 1858) is the textbook crossed palsy of the lower pons: a lesion of the basis pontis involving the facial (VII) fascicles and the corticospinal tract gives an ipsilateral lower motor neuron facial palsy with contralateral hemiplegia. The abducens (VI) is often involved too (ipsilateral lateral rectus palsy and diplopia), though it was not part of the original description. Sensory tracts are usually spared. In older patients the cause is mostly vascular — occlusion of basilar artery branches to the caudal pons; in the young, tumours, infections such as tuberculosis and neurocysticercosis, and demyelination.

Locked-in syndrome is quadriplegia and bulbar palsy (and often loss of body sensation) from brainstem damage — most commonly the anterior (ventral) pons — with preserved consciousness, vertical eye movements, blinking and hearing. The ventral pons is supplied by the basilar artery, so basilar thrombosis is the classic cause; trauma with vertebrobasilar injury is another.

The sparing makes anatomical sense: the lesion is ventral, so the reticular activating system in the dorsal tegmentum (consciousness) and the midbrain vertical gaze centres above the lesion survive, while horizontal gaze — organised in the pons around the abducens nucleus — is lost. Patients communicate with vertical eye movements or blinks. The diagnosis is easily missed because it looks like coma or akinetic mutism; a 'motor' score on the Glasgow Coma Scale will badly underestimate awareness.

The anterior medulla carries the pyramids on either side of the anterior median fissure; at its lower end most corticospinal fibres cross in the pyramidal decussation to form the lateral corticospinal tract. Lateral to the pyramids are the olives. The hypoglossal nerve (XII) emerges from the sulcus between the pyramid and the olive; IX, X and XI emerge from the postolivary groove in that order from above down. The medulla meets the spinal cord at the foramen magnum.

Lateral medullary syndrome (Wallenberg) is ischaemia of the dorsolateral medulla, most often from occlusion of the vertebral artery or the posterior inferior cerebellar artery (PICA). It is the commonest brainstem stroke syndrome you will be asked about, and its signs map neatly onto lateral structures.

Medial medullary syndrome (Dejerine) is infarction of the medial medulla, most often atherothrombotic occlusion of paramedian branches of the anterior spinal artery or the vertebral artery. Its triad is ipsilateral hypoglossal palsy (the tongue deviates towards the lesion, a lower motor neuron sign) + contralateral hemiparesis (pyramid) + contralateral loss of vibration and proprioception (medial lemniscus). It is rare — about 1% of cerebral infarcts — and the full triad is seen in only a minority.

Acute management follows the usual posterior-circulation stroke pathway — see stroke management. Bulbar weakness makes swallow assessment and aspiration prevention an early priority in lateral medullary stroke.