Clinical Examination of the cranial nerves

I Olfactory nerve
Function: Olfaction - the sense of smell

Anosmia is loss of the sense of smell

The olfactory nerves are not normally tested at the bedside. One always asks the question "How
is your sense of smell and taste?" [The flavours of food, which we commonly refer to as their
taste, are actually sensed by the olfactory nerves; taste itself is confined to salt, sweet, bitter and
sour]. On occasion you will encounter a patient who complains of a loss of the sense of smell,
usually in the form of an inability to taste food. Sometimes you will meet patients who tell you
they lost their sense of smell many years ago and cannot remember anything that might account
for it. These patients are unlikely to be suffering from a serious disorder and are also unlikely to
recover. Anosmia of recent origin, however, should cause concern.

Firstly, in all cases, it is necessary to outrule various disorders of the nose, especially those
causing nasal obstruction [eg nasal polyps]. The olfactory nerves may then require formal testing.
You will refer the patient to an ENT clinic for this specialised assessment, which is carried out as
follows.

Testing for anosmia

The nostril of the side not being tested is blocked up with cotton wool. A succession of vials of
fluid with different odours is presented to the side being tested and the patient is asked to
identify or describe the smell. Many individuals with an excellent sense of smell still find it
difficult to describe the scent so it may be necessary to ask the patient “Is it coffee? Is it mint?”
and so on. A report on the patient’s responses and the consultant’s opinion follows.

Causes
In practice there are only two important causes of anosmia of recent origin:
Bilateral anosmia is seen the aftermath of head injury, with or without radiological evidence of
fracture of the anterior cranial fossa of the skull.
Unilateral anosmia may be an early sign of a brain tumour such as a meningioma pressing on
the olfactory tract.

II Optic nerve
Functions: Vision, visual reflexes
Malfunction: Visual loss, loss of visual reflexes

Testing the visual fields

Be aware that a lesion of any part of the visual pathway, from retina to visual cortex, will result
in visual loss. Consequently, the finding of visual loss does not localise the lesion to the optic
nerve; the history and other findings will provide other essential evidence. In addition, patients
with considerable visual loss may be quite unaware of it; you should test the visual fields in any
patient whose history suggests the possibility of visual loss. At the bedside the visual fields are
tested by confrontation perimetry, as follows:

You and the patient sit opposite one another at a suitable distance, about knee to knee or a little
further apart. Cover one of your eyes with your hand [say left eye, left hand] and ask the patient
to cover one eye [right eye, right hand]. Ask the patient to keep the gaze of his open eye on your
open eye while you do the same. Now stretch your right arm out to the right with the index
finger upraised, at a point equidistant between you both, until it is outside your field of vision.
The test now starts. Warn the patient to tell you when he notices your finger. Start wagging your
finger and bring it medially, keeping it equidistant between you both. The patient should notice
your moving finger at about the same time as you do, otherwise there is a lateral visual field
defect [in one or other of you!]. The manoeuvre is repeated in an appropriate fashion to test the
medial, superior and inferior fields. In testing the medial visual field in the example above it is
probably advisable to use your right hand to occlude your left eye and use your left hand as the
stimulus, because the elbow and forearm movement of the right arm will be visible in other visual
quadrants and might allow the patient to guess when you finger is moving.

Mechanical perimetry
If you find, or suspect you have found, a visual field defect you may need to have it further
assessed or quantified. You will refer the patient to an ophthalmogy clinic. Perimetry is a detailed
evaluation of the visual fields carried out in a manner very similar to confrontation but using a
special apparatus lending much greater precision. Perimetry gives a precise evaluation of the
visual fields of both eyes. Combined with other clinical information it can lead to a precise
localisation of the lesion in the visual pathway.

Testing the visual reflexes

The pupillary light reflex is best conducted in conditions of reduced luminosity; if the ambient
light is bright the pupil may already be constricted. Sometimes it may be necessary to shade the
eyes from bright light for about 15-30 seconds to allow the eye to adapt before testing. Place one
hand on the patients forehead and use your thumb to keep the eyelid open to prevent the reflex
blinking that might otherwise occur. Suddenly shine a bright light on the pupil; both pupils
should constrict briskly [consensual light reflex].

Pathway for the pupillary light reflex.

1 Rods and cones of the retina respond to light and project to the bipolar neurons of the retina
2 Bipolar neurons project to the ganglion neurons of the retina
3 Ganglion neurons project to the pretectal neurons of the midbrain
4 Pretectal neurons project to the accessory oculomotor [Edinger-Westphal, EW] nuclei of both
sides
5 EW neurons project to the neurons of the ciliary ganglion [of its own side]
6 Neurons of ciliary ganglion control the constrictor [sphincter] pupillae muscle
The structures involved are the retina, optic nerve, optic chiasma, optic tract, midbrain [pretectal
nuclei, commissural fibres, EW nuclei], oculomotor nerve, ciliary ganglion and constrictor pupillae
muscle. If the reflex is intact, then all the structures listed above are intact; otherwise at least one
must be damaged. The pupillary light reflex is thus a somewhat crude - but useful - test of the
function of the optic nerve, brainstem and oculomotor nerve.

The reflex may be tested in conscious or unconscious individuals since the cerebral cortex is not
involved in the pathway. There is a world of difference in the significance of this test in
conscious individuals and those with reduced levels of consciousness. The fully conscious patient
with an absent light reflex may have some serious problem such as a damaged oculomotor nerve,
but is not about to die. At the other extreme, a deeply unconscious patient [head injury, stroke]
with widely dilated pupils and no light reflex [fixed dilated pupils] may be very close to death.

Be particularly careful in carrying out this test on people who are partially conscious. Many of
these are suffering from some drug overdose, typically alcohol. They are often so uncooperative
that it is difficult, [but rarely impossible] to carry out the test. In addition the pupils of someone
who is very drunk are dilated and the pupillary light reflex is sluggish. There are two problems. If
you find that the dilated pupils are not reacting, when in fact they there are reacting sluggishly,
you will cause a major scare that there is an intracranial bleed and will unnecessarily mobilise
busy senior staff. If you find that the pupils are reacting sluggishly, when in fact they are not
reacting at all, an intracranial bleed may be missed, with fatal consequences. You must be very
determined to successfully carry out the test.

The accomodation reflex [near reflex, near response] can only be carried out in conscious
cooperative patients, since the pathway involves the cerebral cortex. Ask the patient to focus on
a distant object, say the opposite wall for about 10 seconds. Then ask him to focus on the tip of
your finger, which you place in the midline about 6 -9 inches from his eyes. The pupils should
converge [conjugate convergence] and constrict [miosis]. In addition the lens becomes more
convex [accomodation], though this is something you cannot observe.

An intact accomodation reflex depends on the following elements that form the pathway for the
reflex. [Note: some details of the pathway remain obscure, and what follows is what is generally
agreed.]
1 Rods and cones of the retina respond to light and project to the bipolar neurons of the retina.
2 Bipolar neurons project to the ganglion neurons of the retina.
3 Ganglion neurons project to the neurons of the lateral geniculate nucleus [LGN] of the
thalamus.
4 LGN neurons project to the neurons of the visual cortex.
5 Visual cortex neurons project to the frontal eye fields [FEF] via long association fibres.
6 Some FEF neurons project to the pretectal nuclei via fibres passing through the anterior limb of
the internal capsule, with onward projections to the ciliary ganglion, causing miosis and
accomodation, as in the light reflex.
7 Other FEF neurons synapse on the gaze centres of the pons, causing conjugate convergence of
the eyes.

The structures involved are the retina, optic nerve, optic chiasma, optic tract, lateral geniculate
body, visual cortex, association fibres to frontal eye fields, fibres to pretectal nuclei via anterior
limb of internal capsule, midbrain [pretectal nuclei, commissural fibres, EW nuclei], oculomotor
nerve, ciliary ganglion, ciliaris muscle, constrictor pupillae muscle and the medial recti. If the
reflex is intact, then all the structures listed above are intact; otherwise at least one must be
damaged.

Oculogyric nerves [III, IV, VI]

The nerves controlling the internal and external muscles of the eye can be affected in an
extraordinary range of diseases, ranging through trauma, infection, tumour, endocrine problems,
vascular problems and a wide variety of more esoteric medical conditions. Eye signs are
ubiquitous in medical practice, and the ability to quickly recognise them, associate them with
other signs and symptoms, thereby rapidly reaching an initial diagnosis, is one of the hallmarks of
the expert clinician. Underlying this expertise is a knowledge of the actions of the muscles
themselves, the anatomy of the nerves that supply them and the CNS structures involved in the
overall control of eye movements; the frontal eye fields, the gaze centres and the medial
longitudinal fasciculus. At a basic level it is essential to realise that all of the oculogyric nerves are
motor [voluntary or autonomic] and that a lesion of any nerve or its control centres will result in
ophthalmoplegia.

Ophthalmoplegia
Ophthalmoplegia means weakness or total paralysis of eye muscles.

Internal ophthalmoplegia means paralysis of the internal ocular muscles, i.e. dilator pupillae
muscle [sympathetic], the sphincter pupillae muscle or the ciliaris muscle [parasympathetic]. It
may be complete [all muscles] or partial [sympathetic or parasympathetic].

The eyes normally move together in one direction [left, right, up, down]; this is conjugate
movement. Conjugate ophthalmoplegia means paralysis of the ocular muscles responsible for
moving the eyes together in a particular direction. The lesion is inside the CNS and there are two
typical scenarios. [1] In the immediate aftermath of a stroke or other major intracranial vascular
event, the eyes of the unconscious patient are directed towards the side of the lesion, due to the
unopposed activity of the healthy cerebral hemisphere. Later, this sign disappears. [2] Tumours
in the pons near the abducent nucleus cause a similar clinical picture, often associated with an
ipsilateral facial paralysis. To understand these signs you should review the structures involved
in the overall control of eye movements; the frontal eye fields, the gaze centres and the medial
longitudinal fasciculus. Conjugate convergence of the eyes normally occurs when looking at a near
object; sometimes this is impaired or lost due to a midbrain lesion or Parkinson’s disease, a less
common example of conjugate ophthalmoplegia.

Nuclear ophthalmoplegia is paralysis of ocular muscles due to a lesion involving the nuclei of the
oculogyric nerves. The distinctive feature is that the visual axes do not remain parallel. Paralysis
of individual muscles is variable, depending on the site of the lesion, which is usually a tumour.
This is not a common cause of ophthalmoplegia.

Ophthalmoplegia of muscular origin is principally seen in myasthenia gravis and in the

exophthalmia associated with certain diseases of the thyroid gland.

Ophthalmoplegia associated with lesions of individual oculogyric nerves is discussed with the
individual nerves below.

Ptosis is drooping of the eyelid, be it partial or complete. Complete ptosis [as in oculomotor
paralysis] is perfectly obvious since the eye is closed and cannot be voluntarily opened. Partial
ptosis [as in Horner's syndrome] is easily missed unless you actively look for it.

Mydriasis is pupillary dilatation, due to loss of the parasympathetic supply to the sphincter
[constrictor] pupillae muscle and unopposed activity of the dilator pupillae muscle. Mydriasis is
easily missed unless you actively look for it.

Miosis is pupillary constriction, due to loss of the sympathetic supply to the dilator pupillae
muscle and unopposed activity of the sphincter [constrictor] pupillae muscle. Miosis is easily
missed unless you actively look for it

Diplopia is double vision, usually due to loss of alignment of the visual axes, in turn often due to
paralysis of oculogyric nerves. The degree of diplopia varies with the direction in which the
patient looks.

The integrity of the nerve supply of the individual oculogyric muscles is tested by asking the
patient to keep the gaze fixed on the tip of your finger while you move it left, right, up and
down. The eyes should move together [conjugate movement].

Sympathetic nerve supply of the eye

Sympathetic fibres to levator palpebrae superioris enter the oculomotor nerve as it passes
through the carotid sinus. Sympathetic fibres to the dilator pupillae enter the ophthalmic nerve
and reach the muscle via the nasociliary nerve and its long ciliary branches.

III Oculomotor nerve:

Functions: Motor [voluntary] to 4 of the 6 intrinsic muscles of the eyeball [inferior oblique,
superior, inferior and medial rect] and the levator palpebrae superioris muscle; motor
[parasympathetic] to ciliary and sphincter pupillae muscles; motor [sympathetic] to the levator
palpebrae superioris muscle [via fibres of the carotid nerve that join the oculomotor nerve as it
traverses the cavernous sinus].

Complete paralysis of the oculomotor nerve

Complete ptosis, due to loss of the voluntary and sympathetic motor supply to the levator
palpebrae superioris muscle.
The eye is directed inferiorly and laterally ["down and out"] due to unopposed activity of
superior oblique and lateral rectus muscles.
Dilated pupil due to loss of the parasympathetic motor supply to the sphincter pupillae muscle
and unopposed sympathetic activity.
Diplopia, [which is not apparent to the patient until the affected eyelid is opened] except when
looking down and out to the affected side.
Loss of the pupillary light reflex
Loss of the near reflex

Partial paralysis of the oculomotor nerve

There are a number of conditions in which some fibres of the oculomotor nerve are damaged while
others are spared. The most important is seen in the Hutchinsonian pupil which is a syndrome
caused by raised intracranial pressure, typically due to extradural haemorrhage. Classically, a
blow to the temple results in concussion from which the patient soon recovers and appears well
[the lucid interval]. However, the middle meningeal artery is bleeding and an extradural
haematoma develops. As the haematoma expands and intracranial pressure rises, consciousness is
again lost. Often there is no lucid interval because the haematoma develops before the concussion
is over. Pressure is transmitted to the oculomotor nerve and affects its parasympathetic fibres
first. There is a brief initial pupillary constriction, representing irritation [hyperactivity] of the
nerve, rapidly followed by pupillary dilatation. The pupillary constriction is rarely observed
because it is so transient. The sequence is repeated on the opposite side. The end result is a
deeply unconscious patient with bilateral fixed dilated pupils; brainstem death soon follows. The
entire scenario can develop rather slowly or with terrifying rapidity. The only answer is to drill a
hole through the skull and evacuate the haematoma, thus decompressing the brain. Clearly, the
sooner the eye signs are recognised the sooner the diagnosis will be reached and the sooner life-
saving treatment can be started. Awareness of the syndrome is fundamental and time is of the
essence. “The early recognition of a progressive neurological deficit is the sine qua non of
successful neurosurgical intervention.” [Schwartz]

IV Trochlear nerve
Function: Motor to superior oblique muscle of eye

Paralysis of the trochlear nerve causes weakness of downwards gaze with diplopia most marked
when walking down stairs. The patient may develop a head tilt to compensate for the diplopia.

VI Abducent nerve
Function: Motor to lateral rectus muscle of eye

Paralysis of the abducent nerve causes inability to abduct the eye, which is deviated medially due
to unopposed activity of the medial rectus, leading to diplopia. When the paralysis is due to a
lesion of the abducent nucleus in the pons there is usually involvement of the adjacent facial
nucleus. Consequently, when the lateral rectus alone is affected, the lesion is anterior to the pons.
The abducent nerve has the longest intracranial course of any cranial nerve and is often the first
nerve to suffer in a generalised rise in intracranial pressure, causing a “false localising sign”.

V Trigeminal nerve
Functions: Motor to the first arch muscles; sensory to much [but not all] of skin of face and
scalp, and to many deep structures in the central and lower thirds of the face.

Motor tests
Clench jaw while examiner palpates temporalis and masseter
Open jaw against resistance
Assess protraction and retraction

Trismus is painful spasm of the first arch muscles - the masseter in particular. Causes include
inflammatory conditions of the oropharyngeal region such as quinsy [peritonsillar abscess],
dental abscess and also tetanus ["lockjaw"]. In the early stages the spasm may be provoked by
tapping on the masseter.

Sensory tests
Cotton wool and needle to sensory distribution of V
You need to know the sensory distributions of the three divisions of the trigeminal nerve in order
to test each individually. In practice, one routinely applies the stimulus on the skin over the sites
of emergence of the supra-orbital, infra-orbital and mental nerves on the face.

Va Ophthalmic division of Trigeminal (V) nerve: Sensory to upper face including frontal sinus,
and probably also to muscles of scalp and forehead and eye muscles.
Vb Maxillary division of Trigeminal (V) nerve: Sensory to middle of face, including nasal sinuses,
roof of mouth and teeth and probably sensory to facial muscles.
Vc Mandibular division of Trigeminal (V) nerve: Motor to first arch muscles; Sensory to lower
face, including floor of mouth, oral part of tongue [ordinary sensation] and teeth; also sensory to
muscles of first arch.

The jaw jerk reflex is tested by asking the patient to let his jaw go slack as you place a finger
transversely across his chin. Tap your finger with a patellar hammer to cause downward
movement of the jaw. The normal response is elevation of the jaw due to reflex contraction of the
masseter and temporalis muscles. The afferent limb of the reflex consists of sensory branches of
the mandibular nerve innervating the stretch receptors of the TMJ and the muscle spindles of the
masseter and temporalis muscles. The efferent limb consists of motor fibres of the mandibular
nerve to the muscles.The afferent fibres synapse on the motor mandibular nucleus in the pons,
either directly or via the supratrigeminal nucleus. The jaw jerk reflex is essentially a test of the
mandibular nerve and the pons. The jaw jerk reflex can be difficult to elicit in a normal individual
and is not particularly brisk. It is not routinely tested. If the jaw jerk reflex is exaggerated it
suggests an upper motor neuron lesion above the pons. The chief value of the test is in comparing
it with the upper limb tendon reflexes. If both are exaggerated the lesion is above the pons; if only
the upper limb reflexes are exaggerated the lesion lies below the pons and likely below the
foramen magnum .

The corneal reflex is tested by touching the cornea with a wisp of cotton wool. The normal
response is reflex blinking of both eyes. The afferent limb of the reflex consists of long ciliary
branches of the ophthalmic division of the trigeminal nerve travelling from the cornea and
projecting to the brainstem. The efferent limb consists of facial motor fibres projecting to the
orbicularis oculi muscle. The synaptic connections between the two limbs are not known but
presumably are mediated by collaterals of the central processes of the opthalmic nerve synapsing
on the facial motor nuclei OR by by collaterals from the spinal nucleus of V that synapse on the
facial motor nuclei. The corneal reflex is therefore a test of the ophthalmic division of the
trigeminal nerve, the brainstem and the motor part of the facial nerve. It is not a routine bedside
test. Its most common use is during the administration of general ansesthesia, as an assessment of
the depth of brainstem depression.

VII Facial nerve

Functions: Motor to second arch muscles; secretomotor to lacrimal, nasal, submandibular and
sublingual glands; Sensory to oral part of tongue and to soft palate[taste] and to skin of ear.

Motor tests
Ask the patient to show his teeth [this is a test of the muscles opening the oral aperture].
Ask the patient to close his mouth and puff out his cheeks [this is a test of the orbicularis oris
and buccinator muscles]
Ask the patient to close his eyes tightly [this is a test of the orbicularis oculi]
Ask the patient to raise his eyebrows and to frown [these are tests of the occipitofrontalis]

In a lower motor neuron lesion, as typified by Bell's palsy, all the muscles supplied by the facial
nerve are paralysed because the entire nerve is affected. The patient may complain of
hyperacusis [loss of stapedius] and - ageusia - loss of taste [chorda tympani] on the affected side.
Lacrimal and salivary secretions are also reduced but the patient is not usually aware of this
because of other functioning lacrimal and salivary glands. The skin of the affected side of the face
may appear unusually smooth. [This will not be noticed unless you carefully compare both sides
of the face; in a young person no difference may be seen.] The patient will be unable to open the
oral aperture on the affected side. The patient will be unable to close the eye but may turn up the
eyeball in an effort to cooperate with your request to close the eye. Upon attempting to close the
oral aperture and puff out the cheeks, air will escape on the affected side. The patient will be
unable to raise the eyebrow or wrinkle the forehead on the affected side.

Partial damage to the facial nerve or its branches may occur, in which case not all of the above
signs may be present. For instance, in surgical division at parotidectomy the occipitalis,
auriculares, stapedius stylohyoid and posterior belly of digastric will still be intact.
In an upper motor neuron lesion [loss of the corticonuclear pathway to the facial motor nucleus]
the upper facial muscles [occipitofrontalis and perhaps orbicularis oculi] are not affected, because
the upper part of the facial motor nucleus receives bilateral cortical inputs. In addition, the limbic
inputs of both sides are intact, so that emotional movement of the facial muscles [eg smiling] still
occur. Facial nerve secretomotor activity, taste and somatic sensation are unaffected since the
upper motor neurons have nothing to do with these functions.

VIII Vestibulocochlear nerve

Functions: Hearing, balance

Patients with disturbance of vestibular nerve function complain of vertigo and nystagmus. Refer
to ENT clinic.
Cochlear nerve dysfunction may cause deafness and [rarely] tinnitus.

Deafness can be recognised and crudely assessed by speaking to the patient in a normal voice or a
whisper at various distances while one of the patient’s ears is occluded.

Tuning fork tests help distinguish conduction deafness [eg middle ear disease, wax in the ear]
from nerve deafness [lesion of the cochlear nerve]. These tests rely on the fact that in nerve
deafness air conduction and bone conduction are both reduced while in conduction deafness air
conduction is reduced but bone conduction is actually enhanced.

In Weber’s test a vibrating tuning fork is applied to the centre of the forehead or vertex and the
patient is asked if he hears it in the midline or in one ear. Normally the sound is heard in the
midline. In conduction deafness it is localised in the affected ear. In nerve deafness it is localised
in the unaffected ear.

In Rinne’s test a vibrating tuning fork is applied to the mastoid process, while the examiner
occludes the patient’s ear. The patient is asked to say when the sound stops and the examiner
then places the fork at the external acoustic meatus. In conduction deafness the sound cannot be
heard after bone conduction has ceased. In nerve deafness the reverse is true.

IX Glossopharyngeal nerve
Functions: Motor to third arch muscles; secretomotor to parotid gland; Sensory to pharyngeal
part of tongue [taste and ordinary sensation], to pharynx including tonsil, to middle ear and skin
of eardrum and to organs monitoring BP and pH.

The gag reflex [pharyngeal reflex] is performed by touching the side of the pharynx, near the
tonsil; the normal response is constriction of the pharynx. The palatal reflex is performed by
touching the palate, and the normal response is for the palate to rise on that side. In both tests
the stimulus is detected by the glossopharyngeal afferent fibres and the response is effected
primarily by the vagus. These reflexes therefore test both nerves. They are not routinely
performed because they cause nausea, and are unpleasant for the patient. However, if you need
to outrule involvement of the glossopharyngeal or vagus nerves, they should be performed.

Taste can be tested and sometimes must be, but it is an elaborate procedure, which will not be
described here.

X Vagus nerve
Functions: Motor to fourth and sixth arch muscles; motor to heart, respiratory and digestive
organs; Sensory to pharyngeal part of tongue [taste and ordinary sensation], to heart, respiratory
and digestive organs including pharynx and larynx; sensory to skin of eardrum and to organs
monitoring BP and pH.

Palatal elevation is simply tested by asking the patient to say “aaah” while you observe the
palate.
The gag and palatal reflexes may also be tested as described above.
If the laryngeal branches of the vagus are affected there may be an altered voice. Laryngoscopy
may reveal vocal cord paralysis.
Major involvement of the vagus nerve leads to a combination of problems, among which
disturbances of speech and swallowing are the most prominent [nucleus ambiguus].

XI Accessory nerve [spinal part]

Functions: Motor to sternomastoid and trapezius muscles

Muscle wasting in long-standing cases

Turn head to the side against resistance [sternomastoid]
Shrug shoulders against resistance [trapezius]
Shoulder retraction [trapezius]
Place hand on head [trapezius]

XII Hypoglossal nerve

Functions: Motor to intrinsic muscles of tongue

Atrophy of the tongue in long-standing cases

Deviation to affected side upon protrusion

Summary of cranial nerve testing, for desparados

[These are the absolute basic requirements; if you know them all you can’t fail]

I
Ask the patient about the senses of smell and taste. Don’t test. Refer to ENT clinic as necessary.

II
Visual fields [perimetry]
Visual reflexes
Fundoscopy to outrule retinal disease [but you won’t be asked to do it]

III
Complete ptosis
Diplopia upon lifting the eyelid
Eye down and out
Pupillary dilatation
Absent visual reflexes

IV
Weakness of downward gaze
Diplopia

V
A lesion of any division is accompanied by sensory loss in its cutaneous distribution [which you
must know]

In addition:

Va
Corneal reflex absent

Vb
Palatal sensation reduced or absent

Vc
Jaw movements
Jaw jerk

VI
Diplopia
Medial deviation of eye

VII
Observe facial skin creases and facial movements, including emotional movements
Test strength of certain facial muscles
Corneal reflex

VIII
Vestibular signs: refer to ENT clinic
Deafness: simple assessment and tuning fork tests [you will still end up referring most of these
patients to the ENT clinic]
IX
Gag reflex
Palatal reflex
[Taste testing]

X
Listen to speech [normal speech nearly always means normal vagus]
Gag reflex
Palatal reflex
Palatal elevation

XI
Shrug shoulders [against resistance]
Turn chin to shoulder [against resistance]

XII
Muscle wasting
Deviation of protruded tongue

Typical assessment in a practical examination

Example 1

Q Describe the symptoms and signs of a lesion of the Oculomotor nerve.

A Complete ptosis, diplopia when the eyelid is opened, eye is “down and out”, mydriasis,
absent pupillary light reflex, absent accommodation reflex. Demonstrate the pupillary light reflex.

Example 2

Q Describe the symptoms and signs of a lesion of the Accessory nerve

A Wasting of the trapezius [in long-standing cases], inability to elevate the shoulder, subjectively
and as demonstrated by the examiner applying downwards pressure while asking the patient to
raise his shoulders.