palsy, ipsilateral loss of taste and buccal ulceration, and a painful

vesicular eruption in the external auditory meatus. Other causes

of a lower motor neurone VII lesion include cerebellopontine

Submandibular ganglion

Stylomastoid foramen

Nucleus solitarius

Abducens nucleus

Superior salivatory

nucleus

Pterygopalatine

ganglion

Geniculate ganglion

Chorda

tympani

To facial muscles

To stapedius

muscle

Palate

Lacrimal gland

Anterior two-thirds

of the tongue

Sublingual

gland

Submandibular

gland

Mucous mambranes

of nasal and oral

cavities

Fourth ventricle

Facial nucleus

= Motor fibres

= Sensory

= Parasympathetic

Fig. 7.10 Component fibres of the facial nerve and their peripheral distribution.

Fig. 7.11 Lesions of the pons. Lesions at (1) may result in ipsilateral VI

and VII nerve palsies and contralateral hemiplegia. At (2) ipsilateral

cerebellar signs and impaired sensation on the ipsilateral side of the face

and on the contralateral side of the body may occur.

132 • The nervous system

Isolated unilateral IX nerve lesions are rare. Unilateral X nerve

damage leads to ipsilateral reduced elevation of the soft palate,

which may cause deviation of the uvula (away from the side of

the lesion) when the patient says ‘Ah’. Unilateral lesions of IX and

X are most commonly caused by strokes, skull-base fractures or

tumours. Damage to the recurrent laryngeal branch of the X nerve

due to lung cancer, thyroid surgery, mediastinal tumours and

aortic arch aneurysms causes dysphonia and a ‘bovine’ cough.

Bilateral X nerve lesions cause dysphagia and dysarthria, and may

be due to lesions at the upper motor neurone level (pseudobulbar

palsy) or lower motor neurone level (bulbar palsy; see Box 7.5).

Less severe cases can result in nasal regurgitation of fluids and

nasal air escape when the cheeks are puffed out (dysarthria and

nasal escape are often evident during history taking). Always

consider myasthenia gravis in patients with symptoms of bulbar

dysfunction, even if the examination seems normal.

information but also innervates upper pharyngeal and laryngeal

muscles. The main functions of IX and X that can be tested

clinically are swallowing, phonation/articulation and sensation

from the pharynx/larynx. In the thorax and abdomen, the vagus

(X) nerve receives sensory fibres from the lungs and carries

parasympathetic fibres to the lungs, heart and abdominal viscera.

Anatomy

Both nerves arise as several roots from the lateral medulla and

leave the skull together via the jugular foramen (see Fig. 7.5). The

IX nerve passes down and forwards to supply the stylopharyngeus

muscle, the mucosa of the pharynx, the tonsils and the posterior

one-third of the tongue, and sends parasympathetic fibres to the

parotid gland. The X nerve courses down in the carotid sheath

into the thorax, giving off several branches, including pharyngeal

and recurrent laryngeal branches, which provide motor supply

to the pharyngeal, soft palate and laryngeal muscles. The main

nuclei of these nerves in the medulla are the nucleus ambiguus

(motor), the dorsal motor vagal nucleus (parasympathetic) and

the solitary nucleus (visceral sensation; Fig. 7.13).

Examination sequence

• Assess the patient’s speech for dysarthria or dysphonia

(p. 125).

• Ask them to say ‘Ah’. Look at the movements of the

palate and uvula using a torch. Normally, both sides of the

palate elevate symmetrically and the uvula remains in the

midline.

• Ask the patient to puff out their cheeks with their lips

tightly closed. Listen for air escaping from the nose. For

the cheeks to puff out, the palate must elevate and

occlude the nasopharynx. If palatal movement is weak, air

will escape audibly through the nose.

• Ask the patient to cough; assess the strength of the

cough.

• Testing pharyngeal sensation and the gag reflex is

unpleasant and has poor predictive value for aspiration.

Instead, and in fully conscious patients only, use the

swallow test. Administer 3 teaspoons of water and

observe for absent swallow, cough or delayed cough, or

change in voice quality after each teaspoon. If there are no

problems, observe again while the patient swallows a

glass of water.

Preserved function

in upper face

Loss of

nasolabial fold

Mouth deviates

to normal side

A B

Loss of frontal

wrinkling

Loss of

nasolabial fold

Mouth deviates

to normal side

Bell’s phenomenon

Fig. 7.12 Types of facial weakness. A Right-sided lower motor neurone lesion (within facial nerve or nucleus); Bell’s phenomenon is also shown.

B Right-sided upper motor neurone lesion.

Glossopharyngeal

Sensory to pharynx

Motor to stylopharyngeus

Taste from posterior one-third

of tongue

Pharyngeal nerve

Elevators of palate and

closure of nasopharynx

Peristaltic movement of

constrictor muscles

(superior middle

and inferior)

Recurrent laryngeal

nerve

Motor to all the

intrinsic muscles

of the larynx

Spinal part of

accessory nerve

Motor to sternomastoid and

trapezius muscles

Jugular

foramen

PONS

MEDULLA IX X XI

XI

Superior laryngeal

nerve

Vagus

nerve

Internal

External

Fig. 7.13 The lower cranial nerves: glossopharyngeal (IX), vagus (X)

and accessory (XI).

Motor system • 133

7

• Ask the patient to put out their tongue. Look for deviation

or involuntary movement.

• Ask the patient to move their tongue quickly from side to

side.

• Test power by asking the patient to press their tongue

against the inside of each cheek in turn while you press

from the outside with your finger.

• Assess speech by asking the patient to say ‘yellow lorry’.

• Assess swallowing with a water swallow test (p. 132).

Unilateral lower motor XII nerve lesions lead to tongue wasting

on the affected side and deviation to that side on protrusion (Fig.

7.14). Bilateral lower motor neurone damage results in global

wasting, the tongue appears thin and shrunken and fasciculation

may be evident. Normal rippling or undulating movements may be

mistaken for fasciculation, especially if the tongue is protruded;

these usually settle when the tongue is at rest in the mouth.

When associated with lesions of the IX, X and XI nerves, typically

in motor neurone disease, these features are termed bulbar

palsy (see Box 7.5).

Unilateral upper motor XII nerve lesions are uncommon; bilateral

lesions lead to a tongue with increased tone (spastic) and the

patient has difficulty flicking the tongue from side to side. Bilateral

upper motor lesions of the IX–XII nerves are called pseudobulbar

palsy (see Box 7.5). Tremor of the resting or protruded tongue

may occur in Parkinson’s disease, although jaw tremor is more

common. Other orolingual dyskinesias (involuntary movements

of the mouth and tongue) are often drug-induced and include

tardive dyskinesias due to neuroleptics.

Motor system

Anatomy

The principal motor pathway has CNS (corticospinal or pyramidal

tract – upper motor neurone) and PNS (anterior horn cell –

lower motor neurone) components (Fig. 7.15). Other parts of

Accessory (XI) nerve

The accessory nerve has two components:

• a cranial part closely related to the vagus (X) nerve

• a spinal part that provides fibres to the upper trapezius

muscles, responsible for elevating (shrugging) the

shoulders and elevation of the arm above the horizontal,

and the sternomastoid muscles that control head turning

and flexing the neck.

The spinal component is discussed here.

Anatomy

The spinal nuclei arise from the anterior horn cells of C1–5.

Fibres emerge from the spinal cord, ascend through the foramen

magnum and exit via the jugular foramen (see Fig. 7.5), passing

posteriorly.

Examination sequence

• Face the patient and inspect the sternomastoid muscles

for wasting or hypertrophy; palpate them to assess their

bulk.

• Stand behind the patient to inspect the trapezius muscle

for wasting or asymmetry.