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Comments on the last four cranial nerves in ascending order:
The hypoglossal nerve is the motor to the tongue. The spinal accessory nerve is the motor to the sternocleidomastoid and trapezius muscles.
The cranial accessory nerve supplies the intrinsic muscles of the larynx and pharynx and all palatine muscles, except the tensor veli palatini (supplied by the mandibular branch of the trigeminal nerve). It is distributed by the vagus.
The vagus nerve proper is the principal preganglionic parasympathetic nerve. It is also the principal visceral afferent nerve.
The main features of the glossopharyngeal nerve are as follows: (1) it provides the afferent limb of the gag reflex; (2) it tells us when we have an inflamed throat; (3) it signals (tastes) bitterness from the posterior one-third of the tongue; (4) its carotid branch carries afferents from the carotid sinus, monitoring blood pressure, and from the carotid body, monitoring blood gases; and (5) it gives a clinically significant branch to the middle ear.
The hypoglossal nerve (cranial nerve (CN) XII) contains somatic efferent fibres supplying all the extrinsic and intrinsic muscles of the tongue, except for the palatoglossus, which is supplied by the pharyngeal plexus (CN X). Its nucleus lies close to the midline in the floor of the fourth ventricle and extends almost the full length of the medulla ( Fig. 18.1D ). The nerve emerges as a series of rootlets in the interval between the pyramid and the olive (pre-olivary sulcus). It crosses the subarachnoid space and leaves the skull through the hypoglossal canal. Just below the skull it lies close to the vagus and spinal accessory nerves ( Fig. 18.2 ). It descends on the superficial aspect of the carotid sheath to the level of the angle of the mandible, and then passes forwards on the surface of the hyoglossus muscle where it gives off its terminal branches.
Afferent impulses from about 100 muscle spindles in the same side of the tongue travel from the hypoglossal to the lingual nerve and are then relayed to the mesencephalic nucleus of the trigeminal nerve.
In reptiles the lingual muscles, the geniohyoid muscle, and the infrahyoid muscles develop together from the rostral mesodermal somites. The somatic efferent neurons supplying this hypobranchial muscle sheet form a continuous ribbon of cells extending from the lower medulla to the third cervical spinal segment. In mammals the hypoglossal nucleus is located more rostrally, and its rootlets emerge separately from the cervical rootlets. However, the caudal limit of the hypoglossal nucleus remains linked to the cervical motor cell column by the supraspinal nucleus , from which the thyrohyoid muscle is supplied via the first cervical ventral root. In rodents some of the intrinsic muscle fibres of the tongue receive their motor supply indirectly, from axons that leave the most caudal cells of the hypoglossal nucleus and emerge in the first cervical nerve to join the hypoglossal nerve trunk in the neck. Whether this arrangement holds for primates is not yet known.
The hypoglossal nucleus receives inputs from the reticular formation, whereby it is recruited for stereotyped motor routines in eating and swallowing. For delicate functions including articulation, most of the fibres from the motor cortex cross over in the upper part of the pyramidal decussation; the majority of the corticobulbar input fibres to the hypoglossal nucleus are more crossed, but a few remain uncrossed and supply the ipsilateral hypoglossal nucleus.
Corticobulbar/corticonuclear/supranuclear, nuclear, and infranuclear lesions of the hypoglossal nerve are described together with lesions of the accessory nerve (see Clinical Panels 18.1–18.3 .)
Supranuclear lesions of all four nerves are commonly seen following vascular strokes damaging the pyramidal tract in the cerebrum or brainstem.
The corticobulbar innervation of the hypoglossal nucleus is more crossed than uncrossed. The usual picture following a hemiplegic stroke is as follows: during the first few hours or days, the tongue, when protruded, deviates towards the paralysed side because of the stronger push of the healthy genioglossus. Later the tongue does not deviate on protrusion. However, normal hypoglossal nerve function on the affected side is not restored. Electrophysiological testing has revealed that tongue movement, in response to electrical stimulation of the crossed monosynaptic corticonuclear supply to the hypoglossal nucleus, is both delayed and weaker than normal. This, together with comparable deficiency in the corticonuclear supply to the facial nerve (which includes a motor supply to the lips), accounts for the dysarthria (slurred speech) that persists after a hemiplegic stroke.
Damage to the corticobulbar innervation of the nucleus ambiguus may cause temporary interference with phonation and swallowing.
On testing the power of the trapezius by asking the patient to shrug the shoulders against resistance, the muscle on the affected side is relatively weak. This accords with expectation. But on testing sternocleidomastoid muscle (SCM) by asking the patient to turn the head against resistance applied to the side of the jaw, the SCM on the unaffected side appears to be relatively weak. Given that electrical stimulation applied to the supranuclear supply for SCM has shown that the crossed supply is strong and monosynaptic and the uncrossed is weak and disynaptic, there appears to be an ‘SCM paradox’.
However, the most parsimonious explanation is that the prime mover for the ‘no’ headshake is not the contralateral SCM but the ipsilateral inferior oblique (obliquus capitis inferior) , a muscle within the suboccipital triangle passing from the spine of the axis to the transverse process of the atlas. Supplementary ipsilateral muscles include the splenius capitis and longissimus capitis. All three are typical spinal muscles and would be expected to share in the general muscle weakness on the affected side.
During the head rotation test, the functionally intact contralateral (healthy side) SCM does contract strongly. However, the three ipsilateral head rotators also have a tilting action at the atlanto–occipital joint. The laterally placed insertion of the SCM has strong leverage potential and is well placed to counter the tilting action of the ipsilateral muscles inserting onto the skull.
The supranuclear supply to the hypoglossal nucleus and nucleus ambiguus may be compromised bilaterally by thrombotic episodes in the brainstem in patients suffering from arteriosclerosis of the vertebrobasilar arterial system. The motor nuclei of the trigeminal nerve (to the masticatory muscles) and of the facial nerve (to the facial muscles) may also be affected. The characteristic picture, known as pseudobulbar palsy , is that of an elderly patient who has spastic (tightened) oral and pharyngeal musculature, with consequent difficulty with speech articulation, chewing, and swallowing. The gait is slow and shuffling because of involvement of corticospinal fibres descending to lower limb motor neurons.
Lesions of the hypoglossal nucleus and nucleus ambiguus occur together in progressive bulbar palsy , a variant of progressive muscular atrophy ( Chapter 16 ) in which the cranial motor nuclei of the pons and medulla are attacked at the outset. The patient quickly becomes distressed by a multitude of problems: difficulty in chewing and articulation (mandibular and facial nerve nuclei) and difficulty in swallowing and phonation (hypoglossal and cranial accessory nuclei).
Unilateral lesions at nuclear level may be caused by occlusion of the vertebral artery or of one of its branches (see Clinical Panel 19.2 ). The distribution of motor weakness is the same as for infranuclear lesions (see Clinical Panel 18.3 ).
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