Mandibular division of trigeminal
Abducens nerve (inferior petrosal sinus)
cerebelli and the roof of the trigeminal cave have been removed.
Hyposmia or anosmia (reduction or loss of the sense of
smell) may result from upper respiratory infection, sinus
disease, damage to the olfactory filaments after head injury or
infection, local compression (by olfactory groove meningioma,
for example; see Fig. 7.29C) or invasion by basal skull
tumours. Disturbance of smell may also occur very early in
Parkinson’s and Alzheimer’s diseases. Patients often note
hypogeusia/ageusia (altered taste) with anosmia too, as taste
is crucially influenced by the sense of smell.
Parosmia is the perception of pleasant odours as
unpleasant; it may occur with head trauma or sinus
infection, or be an adverse effect of drugs. Olfactory
hallucinations may occur in Alzheimer’s disease and focal
Optic (II), oculomotor (III), trochlear (IV)
The V nerve conveys sensation from the face, mouth and part of
the dura, and provides motor supply to the muscles of mastication.
The cell bodies of the sensory fibres are located in the trigeminal
(Gasserian) ganglion, which lies in a cavity (Meckel’s cave) in
the petrous temporal dura (see Fig. 7.5). From the trigeminal
• Ask the patient to let their mouth hang loosely open.
• Place your forefinger in the midline between lower lip and
• Percuss your finger gently with the tendon hammer in a
downward direction (Fig. 7.8), noting any reflex closing of
• An absent, or just present, reflex is normal. A brisk jaw
jerk occurs in pseudobulbar palsy (Box 7.5).
The ophthalmic branch leaves the ganglion and passes forward
to the superior orbital fissure via the wall of the cavernous sinus
(see Fig. 8.3). In addition to the skin of the upper nose, upper
eyelid, forehead and scalp, V1 supplies sensation to the eye
(cornea and conjunctiva) and the mucous membranes of the
sphenoidal and ethmoid sinuses and upper nasal cavity.
The maxillary branch (V2) passes from the ganglion via the
cavernous sinus to leave the skull by the foramen rotundum.
It contains sensory fibres from the mucous membranes of
the upper mouth, roof of pharynx, gums, teeth and palate
of the upper jaw and the maxillary, sphenoidal and ethmoid
The mandibular branch (V3) exits the skull via the foramen ovale
and supplies the floor of the mouth, sensation (but not taste)
to the anterior two-thirds of the tongue, the gums and teeth of
the lower jaw, mucosa of the cheek and the temporomandibular
joint, in addition to the skin of the lower lips and jaw area, but
not the angle of the jaw (see Fig. 7.6).
The motor fibres of V run in the mandibular branch (V3) and
innervate the muscles of mastication: temporalis, masseter and
medial and lateral pterygoids.
Four aspects need to be assessed: sensory, motor and two
• Ask the patient to close their eyes and say ‘yes’ each time
they feel a light touch (you use a cotton-wool tip for this
test). Do this in the areas of V1, V2 and V3.
• Repeat using a fresh neurological pin, such as a Neurotip,
• Compare both sides. If you identify an area of reduced
sensation, map it out. Does it conform to the distribution
of the trigeminal nerve or branches? Remember the angle
of the jaw is served by C2 and not the trigeminal nerve,
but V1 extends towards the vertex (see Fig. 7.6).
• ‘Nasal tickle’ test: use a wisp of cotton wool to ‘tickle’ the
inside of each nostril and ask the patient to compare. The
normal result is an unpleasant sensation easily appreciated
• Inspect for wasting of the muscles of mastication (most
• Ask the patient to clench their teeth; feel the masseters,
• Ask the patient to open their jaw and note any deviation;
the jaw may deviate to the paralysed side due to
contraction of the intact contralateral pterygoid muscle.
Routine testing of the corneal reflex is unnecessary, but may
be relevant when the history suggests a lesion localising to
the brainstem or cranial nerves V, VII or VIII. The afferent limb
is via the trigeminal nerve, the efferent limb via the facial
• Explain to the patient what you are going to do and ask
them to remove their contact lenses, if relevant.
• Gently depress the lower eyelid while the patient looks up.
• Lightly touch the lateral edge of the cornea with a wisp of
• Look for both direct and consensual blinking.
Fig. 7.7 Testing the corneal reflex. The cotton-wool wisp should touch
the cornea overlying the iris, not the conjunctiva, and avoid visual stimulus.
Fig. 7.8 Eliciting the jaw jerk.
7.5 Comparison of bulbar and pseudobulbar palsy
Bulbar palsy Pseudobulbar palsy
Level of motor lesion Lower motor
Speech Dysarthria Dysarthria and dysphonia
Swallowing Dysphagia Dysphagia
Emotional lability Absent May be present
from the lateral pontomedullary junction in close association with
the VIII nerve (Fig. 7.11); together they enter the internal acoustic
meatus (see Fig. 7.5). At the lateral end of the meatus the VII
nerve continues in the facial canal within the temporal bone,
exiting the skull via the stylomastoid foramen. Passing through
the parotid gland, it gives off its terminal branches. In its course
in the facial canal it gives off branches to the stapedius muscle
and its parasympathetic fibres, as well as being joined by the
taste fibres of the chorda tympani (see Fig. 7.10).
Examination is usually confined to motor function; taste is
• Inspect the face for asymmetry or differences in blinking or
eye closure on one side. Note that minor facial asymmetry
is common and rarely pathological.
• Watch for spontaneous or involuntary movement.
• For the following actions it is often easiest to demonstrate
the actions yourself and ask the patient to copy you,
• Ask the patient to raise their eyebrows and observe for
symmetrical wrinkling of the forehead (frontalis muscle).
• Ask the patient to screw their eyes tightly shut and resist
you opening them (orbicularis oculi).
• Ask the patient to bare their teeth (orbicularis oris).
• Ask the patient to blow out their cheeks with their mouth
closed (buccinators and orbicularis oris).
Sensory symptoms include facial numbness and pain. Unilateral
loss of sensation in one or more branches of the V nerve may
result from direct injury in association with facial fractures
(particularly V2), local invasion by cancer or Sjögren’s syndrome.
Lesions in the cavernous sinus often cause loss of the corneal
reflex and V1 or V2 cutaneous sensory loss. Cranial nerves III, IV
and VI may also be involved (see Fig. 8.3). Trigeminal neuralgia
causes severe, lancinating pain, typically in the distribution of V2
or V3. Reactivation of herpes varicella zoster virus (chickenpox)
can affect any sensory nerve, but typically either V1 or a thoracic
dermatome (Fig. 7.9). In herpes zoster ophthalmicus (affecting V1)
there is a risk of sight-threatening complications. Hutchinson’s
sign, vesicles on the side or tip of the nose, may be present.
Clinically significant weakness of the muscles of mastication
is unusual but may occur in myasthenia gravis, with fatigable
The facial nerve supplies the muscles of facial expression (frontalis,
orbicularis oculi, buccinators, orbicularis oris and platysma) and
carries parasympathetic fibres to the lacrimal, submandibular and
sublingual salivary glands (via nervus intermedius). It receives
taste sensation from the anterior two-thirds of the tongue (via
the chorda tympani; Fig. 7.10).
From its motor nucleus in the lower pons, fibres of the VII nerve
pass back to loop around the VI nerve nucleus before emerging
spinal root left C5. D Thoracic spinal root right T8.
angle tumours (including acoustic neuroma), trauma and
parotid tumours. Synkinesis (involuntary muscle contraction
accompanying a voluntary movement: most commonly, twitching
of the corner of the mouth with ipsilateral blinking) is a sign of
aberrant reinnervation and may be seen in recovering lower
In unilateral VII nerve upper motor neurone lesions, weakness
is marked in the lower facial muscles with relative sparing of the
upper face. This is because there is bilateral cortical innervation
of the upper facial muscles. The nasolabial fold may be flattened
and the corner of the mouth drooped, but eye closure is
usually preserved (Fig. 7.12B). Hemifacial spasm presents with
synchronised twitching of the ipsilateral eye and mouth.
Bilateral facial palsies are less common, but occasionally occur,
as in Guillain–Barré syndrome, sarcoidosis, or infection such as
Lyme disease, HIV or leprosy. Facial weakness, especially with
respect to eye closure, can also be found in some congenital
myopathies (facioscapulohumeral or myotonic dystrophies).
Distinct from VII nerve palsies, Parkinson’s disease can cause loss
of spontaneous facial movements, including a slowed blink rate,
and involuntary facial movements (levodopa-induced dyskinesias)
may complicate advanced disease.
Involuntary emotional movements, such as spontaneous
smiling, have different pathways and may be preserved in the
Vestibulocochlear (VIII) nerve
Glossopharyngeal (IX) and vagus (X) nerves
The IX and X nerves have an intimate anatomical relationship.
Both contain sensory, motor and autonomic components. The
glossopharyngeal (IX) nerve mainly carries sensation from the
pharynx and tonsils, and sensation and taste from the posterior
one-third of the tongue. The IX nerve also supplies the carotid
chemoreceptors. The vagus (X) nerve carries important sensory
In a unilateral lower motor neurone VII nerve lesion, there is
weakness of both upper and lower facial muscles. Bell’s palsy
is the term used to describe an idiopathic acute lower motor
neurone VII nerve paralysis, often preceded by mastoid pain. It
may be associated with impairment of taste and hyperacusis
(high-pitched sounds appearing unpleasantly louder than normal).
Bell’s phenomenon occurs when a patient closes their eyes:
as eye closure is incomplete the globe can be seen to roll
upwards, to avoid corneal exposure (Fig. 7.12A). Ramsay Hunt
syndrome occurs in herpes zoster infection of the geniculate (facial)
ganglion. This produces a severe lower motor neurone facial
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
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.
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.
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).
• Assess the patient’s speech for dysarthria or dysphonia
• 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
• 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
• 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
B Right-sided upper motor neurone lesion.
Taste from posterior one-third
Fig. 7.13 The lower cranial nerves: glossopharyngeal (IX), vagus (X)
• Ask the patient to put out their tongue. Look for deviation
• Ask the patient to move their tongue quickly from side to
• 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
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.
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
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
The spinal component is discussed here.
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
• Face the patient and inspect the sternomastoid muscles
for wasting or hypertrophy; palpate them to assess their
• Stand behind the patient to inspect the trapezius muscle
• Ask the patient to shrug their shoulders, then apply
downward pressure with your hands to assess the
• Test power in the left sternomastoid by asking the patient
to turn their head to the right while you provide resistance
with your hand placed on the right side of the patient’s
chin. Reverse the procedure to check the right
• Test both sternocleidomastoid muscles simultaneously by
asking the patient to flex their neck. Apply your palm to
Isolated XI nerve lesions are uncommon but the nerve may
be damaged during surgery in the posterior triangle of the neck,
penetrating injuries or tumour invasion. Wasting of the upper fibres
of trapezius may be associated with displacement (‘winging’) of the
upper vertebral border of the scapula away from the spine, while
the lower border is displaced towards it. Wasting and weakness
of the sternomastoids are characteristic of myotonic dystrophy.
Weakness of neck flexion or extension, the latter causing head
drop, may occur in myasthenia gravis, motor neurone disease
and some myopathies. Dystonic head postures causing antecollis
(neck flexed), retrocollis (neck extended) or torticollis (neck twisted
to one side) are not associated with weakness.
The XII nerve innervates the tongue muscles; the nucleus lies
in the dorsal medulla beneath the floor of the fourth ventricle.
The nerve emerges anteriorly and exits the skull in the hypoglossal
canal, passing to the root of the tongue (see Fig. 7.5).
• Ask the patient to open their mouth. Look at the tongue at
rest for wasting, fasciculation or involuntary movement.
Fig. 7.14 Left hypoglossal nerve lesion. From Epstein O, Perkin GD, de
Bono DP, et al. Clinical Examination. 2nd edn. London: Mosby; 1997.
The group of muscle fibres innervated by a single anterior
horn cell forms a ‘motor unit’. A lower motor neurone lesion
causes weakness and wasting in these muscle fibres, reduced
tone (flaccidity), fasciculation and reduced or absent reflexes.
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