Overview
Two linked half-lectures on brainstem motor control of the head. The first covers how the cortex drives brainstem motor nuclei through the corticobulbar tract, and works through the motor functions and lesion patterns of the trigeminal (V), facial (VII), accessory (XI) and hypoglossal (XII) nuclei, plus the secretomotor role of VII and the reflexes routed through the facial motor nucleus. The second covers the ocular motor nuclei (III, IV, VI), the extraocular muscles they supply and the effects of their LMN lesions, the pupillary light and accommodation reflexes, and the cortical and brainstem machinery that produces conjugate gaze. The unifying theme is that bilateral cortical input protects some targets from UMN lesions while unilaterally innervated targets are not protected, so the pattern of deficit localises the lesion.
Corticobulbar versus corticospinal organisation
- The neocortex is somatotopically arranged: neurons in the arm region contribute to the corticospinal tract, neurons in the face region form the corticobulbar tract.
- Corticobulbar fibres descend via the internal capsule and basis pedunculi and synapse, mostly bilaterally, on brainstem motor nuclei including the trigeminal motor nucleus and the facial motor nucleus in the pons. Other targets shown along the path are the pontine and medullary reticular formation, nucleus ambiguus, and the hypoglossal nucleus.
- Corticospinal fibres continue through the pyramid of the medulla, decussate at the pyramidal decussation, and become the lateral corticospinal tract, reaching limb muscles via the cervical and lumbosacral ventral roots. A ventral corticospinal tract is also shown.
- Consequence: bilaterally innervated targets (muscles of mastication, upper face, sternocleidomastoid) show only slight weakness after a UMN lesion, whereas unilaterally (contralaterally) innervated targets (lower face, genioglossus, trapezius) are clearly weak.
Trigeminal motor nucleus (V)
- Location: pons, at the level of the trigeminal nerve, alongside the chief sensory nucleus. Seen in section as the motor nucleus of V with the trigeminal nerve fibres leaving via the motor root; the pontine trigeminal nucleus lies adjacent.
- Supplies muscles derived from the 1st (mandibular) branchial arch, so it is a branchial motor nucleus. Branchial arches appear at 26 +/- 1 and 28 +/- 1 days in the embryo, with mandibular arch, hyoid arch, third and fourth arches.
- Target muscles: the muscles of mastication, named as temporalis, masseter, medial pterygoid and lateral pterygoid.
- UMN lesion: slight weakness only, because the nucleus receives bilateral cortical input.
- LMN lesion (motor root or nucleus): ipsilateral muscle atrophy progressing to paralysis. Clinically the jaw deviates to one side on opening, toward the weak/paralysed side.
Facial motor nucleus (VII) and the course of the facial nerve
- Location: pons at the level of the facial colliculus. The facial nerve fibres form a genu that loops around the abducens nucleus to raise the facial colliculus in the floor of the IVth ventricle; the medial longitudinal fasciculus lies at the midline, and the spinal V nucleus nearby.
- Supplies muscles derived from the 2nd branchial arch, so it too is a branchial motor nucleus.
- Course: brainstem to internal acoustic meatus, geniculate ganglion, through the petrous temporal bone, exiting at the stylomastoid foramen; branches then fan out through the parotid gland.
- Five terminal branches to the muscles of facial expression: temporal, zygomatic, buccal, mandibular, cervical (with a branch to occipitofrontalis).
- Other motor targets: stapedius (dampens the stapes), platysma, stylohyoid and the posterior belly of digastric, described as superficial neck, swallowing and floor of mouth (the last shared with V).
- Bedside testing of VII: “Smile”, “Close your eyes tight and don’t let me open them”, “Puff up your cheeks”.
Upper versus lower face and lesion patterns
- The part of the facial nucleus innervating the upper face receives bilateral cortical input; the part innervating the lower face receives only crossed (contralateral) input.
- UMN lesion: paralysed contralateral lower face with a normal upper face, because the upper-face part of the nucleus still receives ipsilateral cortical input. Clinically the brow still wrinkles on the affected side.
- UMN lesions can show emotional hypermimia: dissociation between a weak asymmetric voluntary smile and a more symmetric spontaneous/emotional smile.
- LMN lesion (VII nerve or facial nucleus): atrophy and paralysis of both the upper and lower face on the same side. Example given is Bell’s palsy affecting the left VII, with loss of left forehead wrinkling, drooping of the left mouth corner, failure of the left eye to close (lagophthalmos) and the mouth drawn to the right, later shown resolving. A winking-face drawing is used as a test case and identified as a right-sided LMN lesion of VII or its nucleus.
Reflexes involving the facial motor nucleus
Efferent limb in all three is the facial motor nucleus and VII.
| Stimulus | Afferent path | Efferent to |
|---|---|---|
| Pain/cornea (“corneal reflex”) | V1 to nucleus of the spinal tract of V | Orbicularis oculi |
| Loud noise | VIII to cochlear nucleus | Stapedius |
| Sour taste | VII + IX to nucleus of tractus solitarius | Muscles of facial expression |
Secretomotor functions of VII
- Preganglionic parasympathetic fibres leave in the nervus intermedius from the superior salivatory nucleus (which includes the lacrimal nucleus). These nuclei sit just caudal to the facial motor nucleus.
- Lacrimal pathway: greater petrosal nerve, nerve of the pterygoid canal, pterygopalatine ganglion, then via maxillary V (V2) to the lacrimal gland (and the nose).
- Salivary pathway: chorda tympani, joining the lingual nerve, to the submandibular and sublingual glands.
- The parotid gland is not supplied by VII: its secretomotor fibres come from the inferior salivatory nucleus via nerve IX to the otic ganglion.
Accessory nerve (XI)
- Cranial root: fibres from the nucleus ambiguus in the medulla, join the vagus, exit via the jugular foramen, supplying muscles of the larynx and pharynx via the internal ramus.
- Spinal root: fibres from the accessory nucleus in the ventral horn of spinal segments C1 to C5, ascend through the foramen magnum, join the cranial root briefly at the jugular foramen, then separate as the external ramus to supply trapezius and sternomastoid.
- Testing: shoulder shrug tests trapezius (from the spinal accessory nucleus); turning the head against the examiner’s hand tests the sternocleidomastoid on the side opposite the examiner’s hand.
- UMN lesion: contralateral weakness of trapezius with relative sparing of sternocleidomastoid, which is bilaterally innervated in the same way as the upper face.
Hypoglossal nucleus (XII)
- Location: medulla, at the midline near the floor of the IVth ventricle; the hypoglossal fibres curve ventrally and laterally between the medial lemniscus and the pyramid to exit.
- Motor to the tongue, with genioglossus the muscle demonstrated for protrusion.
- LMN lesion (XII nerve or nucleus): the protruded tongue deviates markedly toward the weak side, with visible atrophy.
- UMN lesion: only slight deviation and weakness of the contralateral side, since there is some bilateral cortical input.
Ocular motor nuclei and the extraocular muscles
- Three cranial nerves move the eye: oculomotor (III), trochlear (IV), abducens (VI), all seen emerging on the anterior brainstem.
- Nuclei, classified by functional column: Edinger-Westphal nucleus (general visceral motor) and oculomotor nucleus (general somatic motor), both feeding CN III; trochlear nucleus (general somatic motor) to CN IV; abducens nucleus (general somatic motor) to CN VI.
- Muscle-to-nerve rule: LR6SO4, lateral rectus by VI and superior oblique by IV; all the rest plus levator palpebrae superioris by III.
- Directions of pull (left eye): superior rectus (III) up, inferior oblique (III) up and out, medial rectus (III) medially, lateral rectus (VI) laterally, superior oblique (IV) down and in, inferior rectus (III) down.
- The obliques insert behind the axis of rotation of the eye (unlike the recti) and so have their major effects on the adducted eye.
- The superior oblique runs through the trochlea.
Origins and LMN lesion effects
- VI (abducens): nucleus in the caudal pons beneath the facial colliculus, with the MLF at the midline. LMN lesion gives failure of abduction of the affected eye, apparent on attempting to look in that direction, with diplopia (double vision).
- IV (trochlear): nucleus in the midbrain at the level of the inferior colliculus, near the MLF. LMN lesion paralyses superior oblique, giving trouble with vision when looking downwards with the eye adducted, hence difficulty walking down stairs and reading (scanning down a page).
- III (oculomotor): nuclei in the midbrain at the level of the superior colliculus, below the periaqueductal grey. The oculomotor nucleus is a collection of paired sub-nuclei devoted to each muscle; the Edinger-Westphal nucleus sends preganglionic parasympathetic fibres to the ciliary ganglion in each orbit.
- LMN lesion of III affects three things at once: eye movements (very restricted, with the eye pulled laterally by the unopposed lateral rectus of VI), eyelid opening (weak levator palpebrae superioris, giving ptosis) and pupillary constriction (loss of parasympathetic supply, giving a fixed dilated pupil). Lost muscles are SR, IR, MR, IO, levator palpebrae superioris and the pupillary constrictor.
Warning
Slide 48 asks the class what the direct and consensual light responses would be if tested in the affected right eye of a patient with a III palsy. No answer is given anywhere in the slides.
Parasympathetic innervation within the eye
Fibres from the ciliary ganglion innervate:
- the pupillary constrictor muscle;
- the ciliary muscle, whose activation “rounds up” the lens (makes it more convex), that is, accommodation.
Pupillary light reflex
- Requires an intact brainstem but does not require cortical “consciousness”.
- Shining a light in one eye constricts the stimulated pupil (direct response) and the contralateral pupil (consensual response).
- Pathway: afferents in CN II, on their way to the thalamus, synapse with the Edinger-Westphal nucleus on both sides; the efferent limb runs in CN III to the ciliary ganglion and then to the pupillary constrictor muscle of each eye. The route passes via the pretectal area at the level of the superior colliculus, with bilateral connections to both Edinger-Westphal nuclei; other retinal fibres go to the lateral geniculate nucleus.
- Related visual-pathway point: fibres from both nasal retinae cross at the optic chiasm, so a pituitary tumour compressing the chiasm causes loss of both temporal visual fields, that is, bitemporal hemianopia.
Accommodation (near) reflex
- Part of the near reflex for close focus, with three components: accommodation (lens rounding), eyes turning medially (convergence), and pupil constriction.
- Unlike the light reflex it requires cortex, because it is triggered by blurring on the retina: retina to optic chiasma to lateral geniculate nucleus to primary visual cortex and visual association cortex, then a descending cortical pathway back through the pretectal area to the Edinger-Westphal nucleus and via III and the ciliary ganglion to the eye.
Cortical initiation of eye movements
- Frontal eye field (middle frontal gyrus, anterior to the central sulcus): voluntary movements, for example to foveate a target; drives the eyes to the opposite side; always saccadic. With a lesion the eyes “look at the side of the lesion”.
- Occipital eye field (occipital cortex, V1 plus association areas): involuntary movements such as tracking; fixation and smooth pursuit to keep the fovea fixed on a target.
Brainstem gaze centres and conjugate movement
- The eye-movement task is to coordinate six pairs of muscles and correlate them with movements of the head and body and with movements of objects in the visual field.
- There are NO direct connections between the cortical initiation centres and nuclei III, IV and VI. Signals relay first to gaze centres in the brainstem, then travel via the medial longitudinal fasciculus (MLF), which links the nuclei and runs from midbrain to cervical spinal cord.
- Vertical gaze centre: pretectal area.
- Lateral gaze centre: PPRF (paramedian pontine reticular formation), lying medial to nucleus VI in the caudal pons. It inhibits antagonist muscles via interneurons and receives vestibular information (from nucleus VIII) to compensate for head position.
- Worked example, “look left and up”, initiated by the right frontal eye field: activate the lateral gaze centre (PPRF) to drive the left lateral rectus and the right medial rectus; also activate both vertical gaze centres so that both superior recti and both inferior obliques are active for the upward component. The result is conjugate eye movement (muscles listed on the diagram: right SR, right IO, right MR; left SR, left IO, left LR).
Self-test
- Contrast the cortical innervation of the corticobulbar system with that of the lateral corticospinal system.
- Explain why a UMN lesion affecting the trigeminal motor nucleus causes only slight weakness, whereas an LMN lesion causes paralysis.
- Predict the direction of jaw deviation on mouth opening in a unilateral LMN trigeminal motor lesion, and explain the finding in terms of the muscles affected.
- List the five terminal branches of the facial nerve to the muscles of facial expression.
- List the non-facial-expression muscles supplied by the facial motor nucleus, with the function attributed to each on the slides.
- Distinguish the facial findings of a UMN facial lesion from those of an LMN facial lesion, and explain the anatomical basis of the difference.
- Define emotional hypermimia and say which lesion type it accompanies.
- State the afferent path and the efferent target for each of the three reflexes routed through the facial motor nucleus.
- Describe the pathway by which secretomotor fibres reach the lacrimal gland.
- Explain why the parotid gland is not affected by a lesion of the facial nerve trunk.
- Describe the origin and course of the spinal root of the accessory nerve, including the segments involved.
- Predict the pattern of weakness in an UMN lesion affecting XI, and explain why sternocleidomastoid is relatively spared.
- Describe the effect of an LMN lesion of XII on tongue protrusion and contrast it with a UMN lesion.
- State which cranial nerve supplies each extraocular muscle, and give the mnemonic used.
- Explain why the oblique muscles have their major effects on the adducted eye.
- Describe the clinical picture of an LMN lesion of IV and the everyday activities it disrupts.
- Describe the three deficits produced by an LMN lesion of III and give the mechanism of each.
- Describe the steps of the pupillary light reflex from stimulus to bilateral constriction.
- Explain why the consensual response occurs even though only one eye is illuminated.
- Explain why the accommodation reflex requires cortex when the light reflex does not, and list the three components of the near reflex.
- Predict the visual field defect caused by a pituitary tumour and explain it from the chiasmal anatomy.
- Distinguish the frontal eye field from the occipital eye field by function and by the effect of a lesion.
- Name the vertical and lateral gaze centres and state where the lateral gaze centre lies.
- Describe how the brainstem produces the conjugate movement “look left and up” after initiation by the right frontal eye field.
Answers
Reveal answers
- Corticobulbar neurons come from the face region of the neocortex and project mostly bilaterally, via the internal capsule and basis pedunculi, onto brainstem motor nuclei such as the trigeminal and facial motor nuclei. Corticospinal neurons come from the arm region, descend through the pyramid, decussate at the pyramidal decussation and continue as the crossed lateral corticospinal tract to the limbs.
- The trigeminal motor nucleus receives bilateral cortical input, so losing one side leaves the other cortex still driving it, giving only slight weakness. An LMN lesion removes the only motor supply to the muscle, causing ipsilateral atrophy and paralysis.
- The jaw deviates toward the weak/paralysed side on opening. The muscles of mastication supplied by V are affected, with the lateral pterygoid highlighted as the protruding/opening muscle.
- Temporal, zygomatic, buccal, mandibular and cervical (plus a branch to occipitofrontalis).
- Stapedius (dampens the stapes), platysma (superficial neck), stylohyoid and the posterior belly of digastric (swallowing and floor of mouth, the last shared with V).
- A UMN lesion paralyses the contralateral lower face while the upper face is normal, because the upper-face part of the nucleus keeps ipsilateral cortical input; the lower-face part receives only crossed input. An LMN lesion paralyses both upper and lower face on the same side with atrophy, as in Bell’s palsy where the eye fails to close and the forehead does not wrinkle.
- Emotional hypermimia is the dissociation in which a spontaneous/emotional smile is more symmetric than a weak voluntary smile; it accompanies a UMN lesion.
- Corneal/pain: afferent V1 to the nucleus of the spinal tract of V, efferent to orbicularis oculi. Loud noise: afferent VIII to the cochlear nucleus, efferent to stapedius. Sour taste: afferent VII and IX to the nucleus of tractus solitarius, efferent to the muscles of facial expression.
- Preganglionic fibres from the lacrimal nucleus (part of the superior salivatory nucleus) travel in the nervus intermedius, then the greater petrosal nerve, the nerve of the pterygoid canal, to the pterygopalatine ganglion, and postganglionic fibres reach the lacrimal gland via the maxillary nerve (V2).
- Parotid secretomotor fibres arise from the inferior salivatory nucleus and travel via nerve IX to the otic ganglion, not via VII.
- The spinal root arises from the accessory nucleus in the ventral horn of spinal segments C1 to C5, ascends through the foramen magnum, joins the cranial root briefly at the jugular foramen, then separates as the external ramus to supply trapezius and sternomastoid.
- Contralateral weakness of trapezius with relative sparing of sternocleidomastoid, because sternocleidomastoid is bilaterally innervated in the same way as the upper face.
- An LMN lesion of XII causes marked deviation of the protruded tongue toward the weak side with atrophy. A UMN lesion causes only slight deviation and weakness, because of some bilateral cortical input.
- Lateral rectus by VI and superior oblique by IV (mnemonic LR6SO4); superior rectus, inferior rectus, medial rectus, inferior oblique and levator palpebrae superioris by III.
- Because the obliques insert behind the axis of rotation of the eye, unlike the recti, so their action is best seen when the eye is adducted.
- Paralysis of superior oblique, giving difficulty with vision when looking downwards with the eye adducted, so trouble walking down stairs and reading (scanning down a page).
- Very restricted eye movements with the eye pulled laterally by the unopposed lateral rectus (VI); ptosis from weakness of levator palpebrae superioris; a fixed dilated pupil from loss of the parasympathetic supply to the pupillary constrictor.
- Light stimulates the retina; afferents run in CN II toward the thalamus and pass via the pretectal area at the level of the superior colliculus, synapsing with the Edinger-Westphal nucleus on both sides; efferents leave in CN III to the ciliary ganglion of each orbit; postganglionic fibres contract the pupillary constrictor, producing direct constriction in the stimulated eye and consensual constriction in the other.
- Because the afferent input reaches the Edinger-Westphal nuclei on both sides, so both III nerves are activated regardless of which eye is illuminated.
- The accommodation reflex is triggered by blurring on the retina, which must be processed by primary visual and visual association cortex before a descending pathway reaches the pretectal area and the Edinger-Westphal nucleus; the light reflex needs only an intact brainstem and no cortical consciousness. The near reflex components are accommodation, medial movement of the eyes and pupil constriction.
- Bitemporal hemianopia, that is loss of both temporal visual fields, because the fibres from both nasal retinae cross at the optic chiasm and are compressed there.
- The frontal eye field drives voluntary, always saccadic movements to the opposite side (for example to foveate a target); with a lesion the eyes “look at the side of the lesion”. The occipital eye field drives involuntary movements: fixation and smooth pursuit tracking that keep the fovea fixed.
- Vertical gaze centre is the pretectal area; lateral gaze centre is the PPRF (paramedian pontine reticular formation), lying medial to nucleus VI in the caudal pons.
- There is no direct cortical connection to III, IV and VI, so the right frontal eye field signal relays to the brainstem gaze centres and then travels via the MLF. The PPRF is activated to drive the left lateral rectus and the right medial rectus for leftward gaze, and both vertical gaze centres are activated so that both superior recti and both inferior obliques act for the upward component, giving a conjugate movement. The PPRF also inhibits the antagonists via interneurons.