Cranial Nerve Examination – OSCE Guide

geekymedics.com/cranial-nerve-exam/

Dr David Bargiela

Cranial nerve examination frequently appears in OSCEs. You’ll be expected to assess a

subset of the twelve cranial nerves and identify abnormalities using your clinical skills.
This cranial nerve examination OSCE guide provides a clear step-by-step approach to
examining the cranial nerves, with an included video demonstration.

Download the cranial nerve examination PDF OSCE checklist, or use our interactive
OSCE checklist. If you want to learn more about the cranial nerves, check out our
summary. You may also be interested in our guide to dermatomes and myotomes or our
paediatric neurological examination guide.

Gather equipment
Gather the appropriate equipment to perform cranial nerve examination:

Pen torch
Snellen chart
Ishihara plates
Ophthalmoscope and mydriatic eye drops (if necessary)
Cotton wool
Neuro-tip
Tuning fork (512hz)
Glass of water

Introduction
Wash your hands and don PPE if appropriate.

Introduce yourself to the patient including your name and role.

Confirm the patient’s name and date of birth.

1/34
Briefly explain what the examination will involve using patient-friendly language.

Gain consent to proceed with the examination.

Ask the patient to sit on a chair, approximately one arm’s length away.

Ask the patient if they have any pain before proceeding with the clinical examination.

You might also be interested in our OSCE Flashcard Collection which contains over
2000 flashcards that cover clinical examination, procedures, communication skills
and data interpretation.

General inspection
Perform a brief general inspection of the patient, looking for clinical signs suggestive of
underlying pathology:

Speech abnormalities: may indicate glossopharyngeal or vagus nerve pathology.

Facial asymmetry: suggestive of facial nerve palsy.
Eyelid abnormalities: ptosis may indicate oculomotor nerve pathology.
Pupillary abnormalities: mydriasis occurs in oculomotor nerve palsy.
Strabismus: may indicate oculomotor, trochlear or abducens nerve palsy.
Limbs: pay attention to the patient’s arms and legs as they enter the room and take
a seat noting any abnormalities (e.g. spasticity, weakness, wasting, tremor,
fasciculation) which may suggest the presence of a neurological syndrome).

Look for objects or equipment on or around the patient that may provide useful insights
into their medical history and current clinical status:

Walking aids: gait issues are associated with a wide range of neurological
pathology including Parkinson’s disease, stroke, cerebellar disease and myasthenia
gravis.
Hearing aids: often worn by patients with vestibulocochlear nerve issues (e.g.
Ménière’s disease).
Visual aids: the use of visual prisms or occluders may indicate underlying
strabismus.
Prescriptions: prescribing charts or personal prescriptions can provide useful
information about the patient’s recent medications.

Olfactory nerve (CN I)

The olfactory nerve (CN I) transmits sensory information about odours to the central
nervous system where they are perceived as smell (olfaction). There is no motor
component to the olfactory nerve.

Ask the patient if they have noticed any recent changes to their sense of smell.

2/34
Olfaction can be tested more formally using different odours (e.g. lemon, peppermint), or
most formally using the University of Pennsylvania smell identification test. However, this
is unlikely to be required in an OSCE.

Causes of anosmia
There are many potential causes of anosmia including:

Mucous blockage of the nose: preventing odours from reaching the olfactory
nerve receptors.
Head trauma: can result in shearing of the olfactory nerve fibres leading to
anosmia.
Genetics: some individuals have congenital anosmia.
Parkinson’s disease: anosmia is an early feature of Parkinson’s disease.
COVID-19: transient anosmia is a common feature of COVID-19.

Optic nerve (CN II)

The optic nerve (CN II) transmits sensory visual information from the retina to the brain.
There is no motor component to the optic nerve.

Inspect the pupils

The pupil is the hole in the centre of the iris that allows light to enter the eye and reach
the retina.

Assess pupil size:

Normal pupil size varies between individuals and depends on lighting conditions
(i.e. smaller in bright light, larger in the dark).
Pupils are usually smaller in infancy and larger in adolescence.

Assess pupil shape:

Pupils should be round, abnormal shapes can be congenital or due to pathology

(e.g. posterior synechiae associated with uveitis).
Peaked pupils in the context of trauma are suggestive of globe injury.

Assess pupil symmetry:

Note any asymmetry in pupil size between the pupils (anisocoria). This may be
longstanding and non-pathological or relate to actual pathology. If the pupil is more
pronounced in bright light this would suggest that the larger pupil is the abnormal
pupil, if more pronounced in dark this would suggest the smaller pupil is abnormal.
Examples of asymmetry include a large pupil in oculomotor nerve palsy and a small
and reactive pupil in Horner’s syndrome.

3/34
 Inspect the pupils

Visual acuity

Assessment of visual acuity (distance)

Begin by assessing the patient’s visual acuity using a Snellen chart. If the patient
normally uses distance glasses, ensure these are worn for the assessment.

1. Stand the patient at 6 metres from the Snellen chart.

2. Ask the patient to cover one eye and read the lowest line they are able to.

3. Record the lowest line the patient was able to read (e.g. 6/6 (metric) which is
equivalent to 20/20 (imperial)).

4. You can have the patient read through a pinhole to see if this improves vision (if vision
is improved with a pinhole, it suggests there is a refractive component to the patient’s
poor vision).

5. Repeat the above steps with the other eye.

Recording visual acuity

Visual acuity is recorded as chart distance (numerator) over the number of the lowest line
read (denominator).

If the patient reads the 6/6 line but gets 2 letters incorrect, you would record as 6/6 (-2).

If the patient gets more than 2 letters wrong, then the previous line should be recorded as
their acuity.

When recording the vision it should state whether this vision was unaided (UA), with
glasses or with pinhole (PH).

Further steps for patients with poor vision

If the patient is unable to read the top line of the Snellen chart at 6 metres (even with
pinhole) move through the following steps as necessary:

1. Reduce the distance to 3 metres from the Snellen chart (the acuity would then be
recorded as 3/denominator).

2. Reduce the distance to 1 metre from the Snellen chart (1/denominator).

4/34
3. Assess if they can count the number of fingers you’re holding up (recorded as
“Counting Fingers” or “CF”).

4. Assess if they can see gross hand movements (recorded as “Hand Movements” or
“HM”).

5. Assess if they can detect light from a pen torch shone into each eye (“Perception of
Light”/”PL” or “No Perception of Light”/”NPL”).

Assess visual acuity using a Snellen chart

Re-assess visual acuity using a pinhole

Assess visual acuity using number of fingers

Assess visual acuity using hand movements

5/34
 Assess visual acuity using perception of light

Causes of decreased visual acuity

Decreased visual acuity has many potential causes including:

Refractive errors
Amblyopia
Ocular media opacities such as cataract or corneal scarring
Retinal diseases such as age-related macular degeneration
Optic nerve (CN II) pathology such as optic neuritis
Lesions higher in the visual pathways

6/34
Optic nerve (CN II) pathology usually causes a decrease in acuity in the affected eye. In
comparison, papilloedema (optic disc swelling from raised intracranial pressure), does not
usually affect visual acuity until it is at a late stage.

Pupillary reflexes

With the patient seated, dim the lights in the assessment room to allow you to assess
pupillary reflexes effectively.

Direct pupillary reflex

Assess the direct pupillary reflex:

Shine the light from your pen torch into the patient’s pupil and observe for pupillary
restriction in the ipsilateral eye.
A normal direct pupillary reflex involves constriction of the pupil that the light is
being shone into.

Consensual pupillary reflex

Assess the consensual pupillary reflex:

Once again shine the light from your pen torch into the same pupil, but this time
observe for pupillary restriction in the contralateral eye.
A normal consensual pupillary reflex involves the contralateral pupil constricting as
a response to light entering the eye being tested.

Assess direct and consensual pupillary light reflexes

Assess consensual pupillary reflex

Swinging light test

Move the pen torch rapidly between the two pupils to check for a relative afferent
pupillary defect (see more details below).

7/34
 Perform the swinging light test

Perform the swinging light test

Relative afferent pupillary defect 15

Relative afferent pupillary defect 15

Accommodation reflex

1. Ask the patient to focus on a distant object (clock on the wall/light switch).

2. Place your finger approximately 20-30cm in front of their eyes (alternatively, use the
patient’s own thumb).

3. Ask the patient to switch from looking at the distant object to the nearby finger/thumb.

4. Observe the pupils, you should see constriction and convergence bilaterally.

8/34
 Assess the accommodation reflex

Assess the accommodation reflex

Pupillary light reflex

Each afferent limb of the pupillary reflex has two efferent limbs, one ipsilateral and one
contralateral.

The afferent limb functions as follows:

Sensory input (e.g. light being shone into the eye) is transmitted from the retina,
along the optic nerve to the ipsilateral pretectal nucleus in the midbrain.

The two efferent limbs function as follows:

Motor output is transmitted from the pretectal nucleus to the Edinger-Westphal

nuclei on both sides of the brain (ipsilateral and contralateral).
Each Edinger-Westphal nucleus gives rise to efferent nerve fibres which travel in
the oculomotor nerve to innervate the ciliary sphincter and enable pupillary
constriction.

Normal pupillary light reflexes rely on the afferent and efferent pathways of the reflex arc
being intact and therefore provide an indirect way of assessing their function:

The direct pupillary reflex assesses the ipsilateral afferent limb and the
ipsilateral efferent limb of the pathway.
The consensual pupillary reflex assesses the contralateral efferent limb of the
pathway.
The swinging light test is used to detect relative afferent limb defects.

Abnormal pupillary responses

9/34
 Relative afferent pupillary defect (Marcus-Gunn pupil): normally light shone into
either eye should constrict both pupils equally (due to the dual efferent pathways
described above). When the afferent limb in one of the optic nerves is damaged,
partially or completely, both pupils will constrict less when light is shone into the
affected eye compared to the healthy eye. The pupils, therefore, appear to relatively
dilate when swinging the torch from the healthy to the affected eye. This is termed a
relative…. afferent… pupillary defect. This can be due to significant retinal damage
in the affected eye secondary to central retinal artery or vein occlusion and large
retinal detachment; or due to significant optic neuropathy such as optic neuritis,
unilateral advanced glaucoma and compression secondary to tumour or abscess.
Unilateral efferent defect: commonly caused by extrinsic compression of the
oculomotor nerve, resulting in the loss of the efferent limb of the ipsilateral pupillary
reflexes. As a result, the ipsilateral pupil is dilated and non-responsive to light
entering either eye (due to loss of ciliary sphincter function). The consensual light
reflex in the unaffected eye would still be present as the afferent pathway (i.e. optic
nerve) of the affected eye and the efferent pathway (i.e. oculomotor nerve) of the
unaffected eye remain intact.

Relative afferent pupillary defect (RAPD) 1

Relative afferent pupillary defect (RAPD) 1

Colour vision assessment

Colour vision can be assessed using Ishihara plates, each of which contains a coloured
circle of dots. Within the pattern of each circle are dots which form a number or shape
that is clearly visible to those with normal colour vision and difficult or impossible to see
for those with a red-green colour vision defect.

How to use Ishihara plates

If the patient normally wears glasses for reading, ensure these are worn for the
assessment.

10/34
1. Ask the patient to cover one of their eyes.

2. Then ask the patient to read the numbers on the Ishihara plates. The first page is
usually the ‘test plate’ which does not test colour vision and instead assesses contrast
sensitivity. If the patient is unable to read the test plate, you should document this.

3. If the patient is able to read the test plate, you should move through all of the Ishihara
plates, asking the patient to identify the number on each. Once the test is complete, you
should document the number of plates the patient identified correctly, including the test
plate (e.g. 13/13).

4. Repeat the assessment on the other eye.

Assess colour vision using an Ishihara chart at arms length

Ensure the patient can read the Ishihara test plate

Ask the patient to read the numbers on the Ishihara plates

Colour vision deficiencies

Colour vision deficiencies can be congenital or acquired. Some causes of acquired colour
vision deficiency include:

Optic neuritis: results in a reduction of colour vision (typically red).

Vitamin A deficiency
Chronic solvent exposure

Visual neglect/inattention

11/34
Visual neglect (also known as visual inattention) is a condition in which an individual
develops a deficit in their awareness of one side of their visual field. This typically
occurs in the context of parietal lobe injury after stroke, which results in an inability to
perceive or process stimuli on one side of the body. The side of the visual field that is
affected is contralateral to the location of the parietal lesion. It should be noted that visual
neglect is not caused by optic nerve pathology and therefore this test is often not
included in a cranial nerve exam.

Assessment

To assess for visual neglect:

1. Position yourself sitting opposite the patient approximately 1 metre away.

2. Ask the patient to remain focused on a fixed point on your face (e.g. nose) and to state
if they see your left, right or both hands moving.

3. Hold your hands out laterally with each occupying one side of the patient’s visual field
(i.e. left and right).

4. Take turns wiggling a finger on each hand to see if the patient is able to correctly
identify which hand has moved.

5. Finally wiggle both fingers simultaneously to see if the patient is able to correctly
identify this (often patients with visual neglect will only report the hand moving in the
unaffected visual field – i.e. ipsilateral to the primary brain lesion).

Assess for visual inattention

Assess for visual inattention

Visual fields
This method of assessment relies on comparing the patient’s visual field with your own
and therefore for it to work:

12/34
 you need to position yourself, the patient and the target correctly (see details
below).
you need to have normal visual fields and a normal-sized blindspot.

Visual field assessment

1. Sit directly opposite the patient, at a distance of around 1 metre.

2. Ask the patient to cover one eye with their hand.

3. If the patient covers their right eye, you should cover your left eye (mirroring the
patient).

4. Ask the patient to focus on part of your face (e.g. nose) and not move their head or
eyes during the assessment. You should do the same and focus your gaze on the
patient’s face.

5. As a screen for central visual field loss or distortion, ask the patient if any part of your
face is missing or distorted. A formal assessment can be completed with an Amsler
chart.

6. Position the hatpin (or another visual target such as your finger) at an equal distance
between you and the patient (this is essential for the assessment to work).

7. Assess the patient’s peripheral visual field by comparing to your own and using the
target. Start from the periphery and slowly move the target towards the centre, asking the
patient to report when they first see it. If you are able to see the target but the patient
cannot, this would suggest the patient has a reduced visual field.

8. Repeat this process for each visual field quadrant, then repeat the entire process for
the other eye.

9. Document your findings.

Assess the patient's peripheral visual fields

13/34
 Assess the patient's peripheral visual fields

Types of visual field defects

Types of visual field defects

Bitemporal hemianopia: loss of the temporal visual field in both eyes resulting in
central tunnel vision. Bitemporal hemianopia typically occurs as a result of optic
chiasm compression by a tumour (e.g. pituitary adenoma, craniopharyngioma).
Homonymous field defects: affect the same side of the visual field in each eye
and are commonly attributed to stroke, tumour, abscess (i.e. pathology affecting
visual pathways posterior to the optic chiasm). These are deemed hemianopias if
half the vision is affected and quadrantanopias if a quarter of the vision is affected.
Scotoma: an area of absent or reduced vision surrounded by areas of normal
vision. There is a wide range of possible aetiologies including demyelinating
disease (e.g. multiple sclerosis) and diabetic maculopathy.
Monocular vision loss: total loss of vision in one eye secondary to optic nerve
pathology (e.g. anterior ischaemic optic neuropathy) or ocular diseases (e.g. central
retinal artery occlusion, total retinal detachment).

Blind spot
A physiological blind spot exists in all healthy individuals as a result of the lack of
photoreceptor cells in the area where the optic nerve passes through the optic disc. In
day to day life, the brain does an excellent job of reducing our awareness of the blind spot
by using information from other areas of the retina and the other eye to mask the defect.

Blind spot assessment

1. Sit directly opposite the patient, at a distance of around 1 metre.

2. Ask the patient to cover one eye with their hand.

3. If the patient covers their right eye, you should cover your left eye (mirroring the
patient).

14/34
4. Ask the patient to focus on part of your face (e.g. nose) and not move their head or
eyes during the assessment. You should do the same and focus your gaze on the
patient’s face.

5. Using a red hatpin (or alternatively, a cotton bud stained with fluorescein/pen with a red
base) start by identifying and assessing the patient’s blind spot in comparison to the size
of your own. The red hatpin needs to be positioned at an equal distance between you
and the patient for this to work.

6. Ask the patient to say when the red part of the hatpin disappears, whilst continuing to
focus on the same point on your face.

7. With the red hatpin positioned equidistant between you and the patient, slowly move it
laterally until the patient reports the disappearance of the top of the hatpin. The blind spot
is normally found just temporal to central vision at eye level. The disappearance of the
hatpin should occur at a similar point for you and the patient.

8. After the hatpin has disappeared for the patient, continue to move it laterally and ask
the patient to let you know when they can see it again. The point at which the patient
reports the hatpin re-appearing should be similar to the point at which it re-appears for
you (presuming the patient and you have a normal blind spot).

9. You can further assess the superior and inferior borders of the blind spot using the
same process.

Assess the patient's blind spot

The blind spot is located just temporal to central vision at eye level

15/34
 Map out the patient's blind spot and compare to your own

Fundoscopy
In the context of a cranial nerve examination, fundoscopy is performed to assess the
optic disc for signs of pathology (e.g. papilloedema). You should offer to perform
fundoscopy in your OSCE, however, it may not be required. See our dedicated
fundoscopy guide for more details.

Oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves
The oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves transmit
motor information to the extraocular muscles to control eye movement and eyelid
function. The oculomotor nerve also carries parasympathetic fibres responsible for
pupillary constriction.

Eyelids
Inspect the eyelids for evidence of ptosis which can be associated with:

Oculomotor nerve pathology

Horner’s syndrome
Neuromuscular pathology (e.g. myasthenia gravis)

Eye movements
Briefly assess for abnormalities of eye movements which may be caused by underlying
cranial nerve palsy (e.g. oculomotor, trochlear, abducens, vestibular nerve pathology).

1. Hold your finger (or a pin) approximately 30cm in front of the patient’s eyes and ask
them to focus on it. Look at the eyes in the primary position for any deviation or abnormal
movements.

2. Ask the patient to keep their head still whilst following your finger with their eyes. Ask
them to let you know if they experience any double vision or pain.

3. Move your finger through the various axes of eye movement in a ‘H’ pattern.

4. Observe for any restriction of eye movement and note any nystagmus (which may
suggest vestibular nerve pathology or stroke).

16/34
 Assess eye movements

Assess eye movements

Actions of the extraocular muscles

Superior rectus: primary action is elevation, secondary actions include adduction
and medial rotation of the eyeball.
Inferior rectus: primary action is depression, secondary actions include adduction
and lateral rotation of the eyeball.
Medial rectus: adduction of the eyeball.
Lateral rectus: abduction of the eyeball.
Superior oblique: depresses, abducts and medially rotates the eyeball.
Inferior oblique: elevates, abducts and laterally rotates the eyeball.

Oculomotor, trochlear and abducens nerve palsy

Damage to any of the three cranial nerves innervating the extraocular muscles can result
in paralysis of the corresponding muscles.

Oculomotor nerve palsy (CN III)

The oculomotor nerve supplies all extraocular muscles except the superior oblique
(CNIV) and the lateral rectus (CNVI). Oculomotor palsy (a.k.a. ‘third nerve palsy’),
therefore, results in the unopposed action of both the lateral rectus and superior oblique
muscles, which pull the eye inferolaterally. As a result, patients typically present with a
‘down and out’ appearance of the affected eye.

Oculomotor nerve palsy can also cause ptosis (due to a loss of innervation to levator
palpebrae superioris) as well as mydriasis due to the loss of parasympathetic fibres
responsible for innervating to the sphincter pupillae muscle.

Trochlear nerve palsy (CN IV)

17/34
The only muscle the trochlear nerve innervates is the superior oblique muscle. As a
result, trochlear nerve palsy (‘fourth nerve palsy’) typically results in vertical diplopia
when looking inferiorly, due to loss of the superior oblique’s action of pulling the eye
downwards. Patients often try to compensate for this by tilting their head forwards and
tucking their chin in, which minimises vertical diplopia. Trochlear nerve palsy also causes
torsional diplopia (as the superior oblique muscle assists with intorsion of the eye as the
head tilts). To compensate for this, patients with trochlear nerve palsy tilt their head to the
opposite side, in order to fuse the two images together.

Abducens nerve palsy (CN VI)

The abducens nerve (CN VI) innervates the lateral rectus muscle. Abducens nerve
palsy (‘sixth nerve palsy’) results in unopposed adduction of the eye (by the medial rectus
muscle), resulting in a convergent squint. Patients typically present with horizontal
diplopia which is worsened when they attempt to look towards the affected side.

Assessment of strabismus

Strabismus is a condition in which the eyes do not properly align with each other when
looking at an object. Pathology affecting the oculomotor, trochlear or abducens nerves
can cause strabismus.

Light reflex test (a.k.a. corneal reflex test or Hirschberg test)

1. Ask the patient to focus on a target approximately half a metre away whilst you shine a
pen torch towards both eyes.

2. Inspect the corneal reflex on each eye:

If the ocular alignment is normal, the light reflex will be positioned centrally and
symmetrically in each pupil.
Deflection of the corneal light reflex in one eye suggests a misalignment.

Cover test

The cover test is used to determine if a heterotropia (i.e. manifest strabismus) is present.

1. Ask the patient to fixate on a target (e.g. light switch).

2. Occlude one of the patient’s eyes and observe the contralateral eye for a shift in
fixation:

If there is no shift in fixation in the contralateral eye, while covering either eye, the
patient is orthotropic (i.e. normal alignment).
If there is a shift in fixation in the contralateral eye, while covering the other eye, the
patient has a heterotropia.

3. Repeat the cover test on the other eye.

18/34
The direction of the shift in fixation determines the type of tropia; the table below
describes the appropriate interpretation.

Interpretation of the cover test

Direction of eye The direction of shift in fixation of the Type of

at rest unoccluded eye when the opposite eye is tropia
occluded present

Temporally (i.e. Nasally (i.e. medially or inwards) Exotropia

laterally or
outwards)

Nasally (i.e. Temporally (i.e. laterally or outwards) Esotropia

medially or
inwards)

Superiorly (i.e. Inferiorly (i.e. downwards) Hypertropia

upwards)

Inferiorly (i.e. Superiorly (i.e. upwards) Hypotropia

downwards)

Cover test interpretation

Trigeminal nerve (CN V)

The trigeminal nerve (CN V) transmits both sensory information about facial sensation
and motor information to the muscles of mastication.

19/34
The trigeminal nerve has three sub-divisions, each of which has its own broad set of
functions (not all are covered below):

Ophthalmic (V1): carries sensory information from the scalp and forehead, nose,
upper eyelid as well as the conjunctiva and cornea of the eye.
Maxillary (V2): carries sensory information from the lower eyelid, cheek, nares,
upper lip, upper teeth and gums.
Mandibular (V3): carries sensory information from the chin, jaw, lower lip, mouth,
lower teeth and gums. Also carries motor information to the muscles of mastication
(masseter, temporal muscle and the medial/lateral pterygoids) as well as the tensor
tympani, tensor veli palatini, mylohyoid and digastric muscles.

Sensory assessment

First, explain the modalities of sensation you are going to assess (e.g. light
touch/pinprick) to the patient by demonstrating on their sternum. This provides them with
a reference of what the sensation should feel like (assuming they have no sensory
deficits in the region overlying the sternum).

Ask the patient to close their eyes and say ‘yes’ each time they feel you touch their face.

Assess the sensory component of V1, V2 and V3 by testing light touch and pinprick
sensation across regions of the face supplied by each branch:

Forehead (lateral aspect): ophthalmic (V1)

Cheek: maxillary (V2)
Lower jaw (avoid the angle of the mandible as it is supplied by C2/C3): mandibular
branch (V3)

You should compare each region on both sides of the face to allow the patient to identify
subtle differences in sensation.

Motor assessment
Use the muscles of mastication to assess the motor component of V3:

1. Inspect the temporalis (located in the temple region) and masseter muscles (located at
the posterior jaw) for evidence of wasting. This is typically most noticeable in the
temporalis muscles, where a hollowing effect in the temple region is observed.

2. Palpate the masseter muscle (located at the posterior jaw) bilaterally whilst asking the
patient to clench their teeth to allow you to assess and compare muscle bulk.

3. Ask the patient to open their mouth whilst you apply resistance underneath the jaw to
assess the lateral pterygoid muscles. An inability to open the jaw against resistance or
deviation of the jaw (typically to the side of the lesion) may occur in trigeminal nerve
palsy.

Reflexes

20/34
Jaw jerk reflex

The jaw jerk reflex is a stretch reflex that involves the slight jerking of the jaw upwards in
response to a downward tap. This response is exaggerated in patients with an upper
motor neuron lesion. Both afferent and efferent pathways of the jaw jerk reflex involve the
trigeminal nerve.

To assess the jaw jerk reflex:

1. Clearly explain what the procedure will involve to the patient and gain consent to
proceed.

2. Ask the patient to open their mouth.

3. Place your finger horizontally across the patient’s chin.

4. Tap your finger gently with the tendon hammer.

5. In healthy individuals, this should trigger a slight closure of the mouth. In patients with
upper motor neuron lesions, the jaw may briskly move upwards causing the mouth to
close completely.

Corneal reflex

The corneal reflex involves involuntary blinking of both eyelids in response to unilateral
corneal stimulation (direct and consensual blinking). The afferent branch of the corneal
reflex involves V1 of the trigeminal nerve whereas the efferent branch is mediated by the
temporal and zygomatic branches of the facial nerve.

To assess the corneal reflex:

1. Clearly explain what the procedure will involve to the patient and gain consent to
proceed.

2. Gently touch the edge of the cornea using a wisp of cotton wool.

3. In healthy individuals, you should observe both direct and consensual blinking. The
absence of a blinking response suggests pathology involving either the trigeminal or facial
nerve.

The corneal reflex is not usually assessed in an OSCE scenario, however, you should
offer to test it and understand the purpose behind the test.

21/34
Assess light touch sensation (V1)

Assess light touch sensation (V2)

Assess light touch sensation (V3)

Assess pinprick sensation (V1, V2, V3)

Assess masseter muscle bulk

22/34
 Mouth opening against resistance

Assess jaw jerk reflex

Assess corneal reflex

Facial nerve (CN VII)

The facial nerve (CN VII) transmits motor information to the muscles of facial expression
and the stapedius muscle (involved in the regulation of hearing). The facial nerve also
has a sensory component responsible for the conveyance of taste from the anterior two-
thirds of the tongue.

Sensory assessment
Ask the patient if they have noticed any recent changes in their sense of taste.

Motor assessment

Hearing changes

Ask the patient if they have noticed any changes to their hearing (paralysis of the
stapedius muscle can result in hyperacusis).

Inspection

Inspect the patient’s face at rest for asymmetry, paying particular attention to:

23/34
 Forehead wrinkles
Nasolabial folds
Angles of the mouth

Facial movement

Ask the patient to carry out a sequence of facial expressions whilst again observing for
asymmetry:

Raised eyebrows: assesses frontalis – “Raise your eyebrows as if you’re

surprised.”
Closed eyes: assesses orbicular oculi – “Scrunch up your eyes and don’t let me
open them.”
Blown out cheeks: assesses orbicularis oris – “Blow out your cheeks and don’t let
me deflate them.”
Smiling: assesses levator anguli oris and zygomaticus major – “Can you do a big
smile for me?”
Pursed lips: assesses orbicularis oris and buccinator – “Can you try to whistle?”

"Raise your eyebrows"

"Tightly close your eyes and don't let me open them"

"Blow out your cheeks"

24/34
 "Purse your lips"

"Smile for me"

Facial nerve palsy

Facial nerve palsy presents with unilateral weakness of the muscles of facial expression
and can be caused by both upper and lower motor neuron lesions.

Facial nerve palsy caused by a lower motor neuron lesion presents with weakness of
all ipsilateral muscles of facial expression, due to the loss of innervation to all muscles on
the affected side. The most common cause of lower motor neuron facial palsy is Bell’s
palsy.

Facial nerve palsy caused by an upper motor neuron lesion also presents with
unilateral facial muscle weakness, however, the upper facial muscles are partially spared
because of bilateral cortical representation (resulting in forehead/frontalis function being
somewhat maintained). The most common cause of upper motor neuron facial palsy is
stroke.

Bell's palsy 2, 3

Vestibulocochlear nerve (CN VIII)

The vestibulocochlear nerve (CN VIII) transmits sensory information about sound and
balance from the inner ear to the brain. The vestibulocochlear nerve has no motor
component.

25/34
Gross hearing assessment

Preparation

Ask the patient if they have noticed any change in their hearing recently.

Explain that you’re going to say 3 words or 3 numbers and you’d like the patient to
repeat them back to you (choose two-syllable words or bi-digit numbers).

Assessment

1. Position yourself approximately 60cm from the ear and then whisper a number or word.

2. Mask the ear not being tested by rubbing the tragus. Do not place your arm across the
face of the patient when rubbing the tragus, it is far nicer to occlude the ear from behind
the head. If possible shield the patient’s eyes to prevent any visual stimulus.

3. Ask the patient to repeat the number or word back to you. If they get two-thirds or more
correct then their hearing level is 12db or better. If there is no response use a
conversational voice (48db or worse) or loud voice (76db or worse).

4. If there is no response you can move closer and repeat the test at 15cm. Here the
thresholds are 34db for a whisper and 56db for a conversational voice.

5. Assess the other ear in the same way.

Whisper a number 60cm from the ear

Mask the ear not being tested by rubbing the tragus

Rinne’s test
1. Place a vibrating 512 Hz tuning fork firmly on the mastoid process (apply pressure to
the opposite side of the head to make sure the contact is firm). This tests bone
conduction.

26/34
2. Confirm the patient can hear the sound of the tuning fork and then ask them to tell you
when they can no longer hear it.

3. When the patient can no longer hear the sound, move the tuning fork in front of the
external auditory meatus to test air conduction.

4. Ask the patient if they can now hear the sound again. If they can hear the sound, it
suggests air conduction is better than bone conduction, which is what would be expected
in a healthy individual (this is often confusingly referred to as a “Rinne’s positive” result).

Summary of Rinne’s test results

These results should be assessed in context with the results of Weber’s test before any
diagnostic assumptions are made:

Normal result: air conduction > bone conduction (Rinne’s positive)

Sensorineural deafness: air conduction > bone conduction (Rinne’s positive) –
due to both air and bone conduction being reduced equally
Conductive deafness: bone conduction > air conduction (Rinne’s negative)

Place a 512 Hz tuning fork on the mastoid process

Ask the patient to tell you when they can no longer hear it

When the patient can no longer hear the sound, moving the tuning fork in front of
the external auditory meatus to test air conduction

Weber’s test

27/34
1. Tap a 512Hz tuning fork and place in the midline of the forehead. The tuning fork
should be set in motion by striking it on your knee (not the patient’s knee or a table).

2. Ask the patient “Where do you hear the sound?”

These results should be assessed in context with the results of Rinne’s test before any
diagnostic assumptions are made:

Normal: sound is heard equally in both ears.

Sensorineural deafness: sound is heard louder on the side of the intact ear.
Conductive deafness: sound is heard louder on the side of the affected ear.

A 512Hz tuning fork is used as it gives the best balance between time of decay and tactile
vibration. Ideally, you want a tuning fork that has a long period of decay and cannot be
detected by vibration sensation.

Tap a 512Hz tuning fork and place in the midline of the forehead

Conductive vs sensorineural hearing loss

Conductive hearing loss occurs when sound is unable to effectively transfer at any
point between the outer ear, external auditory canal, tympanic membrane and middle ear
(ossicles). Causes of conductive hearing loss include excessive ear wax, otitis externa,
otitis media, perforated tympanic membrane and otosclerosis.

Sensorineural hearing loss occurs due to dysfunction of the cochlea and/or

vestibulocochlear nerve. Causes of sensorineural hearing loss include increasing age
(presbycusis), excessive noise exposure, genetic mutations, viral infections (e.g.
cytomegalovirus) and ototoxic agents (e.g. gentamicin).

Vestibular testing – “Unterberger” or “Turning test”

Ask the patient to march on the spot with their arms outstretched and their eyes
closed:

Normal result: the patient remains in the same position.

Vestibular lesion: the patient will turn towards the side of the lesion

Vestibular testing – “Head thrust test” or “Vestibular-ocular reflex”

Before performing this test you need to check if the patient has any neck problems and if
so you should not proceed.

28/34
1. Explain to the patient that the test will involve briskly turning their head and then gain
consent to proceed.

2. Sit facing the patient and ask them to fixate on your nose at all times during the test.

3. Hold their head in your hands (one hand covering each ear) and rotate it rapidly to the
left, at a medium amplitude.

4. Repeat this process, but this time turn the head to the right.

The normal response is that ocular fixation is maintained. In a patient with loss of
vestibular function on one side, the eyes will first move in the direction of the head
(losing fixation), before a corrective refixation saccade occurs towards your nose.

Turning test

Glossopharyngeal (CN IX) and vagus (CN X) nerves

The glossopharyngeal nerve transmits motor information to the stylopharyngeus
muscle which elevates the pharynx during swallowing and speech. The
glossopharyngeal nerve also transmits sensory information that conveys taste from the
posterior third of the tongue. Visceral sensory fibres of CN IX also mediate the afferent
limb of the gag reflex.

The vagus nerve transmits motor information to several muscles of the mouth which
are involved in the production of speech and the efferent limb of the gag reflex.

The glossopharyngeal and vagus nerves are assessed together because of their closely
related functions.

Assessment

Ask the patient if they have experienced any issues with swallowing, as well as any
changes to their voice or cough.

Inspection

Ask the patient to open their mouth and inspect the soft palate and uvula:

Note the position of the uvula. Vagus nerve lesions result in deviation of the uvula
towards the unaffected side.

29/34
Ask the patient to say “ahh“:

Inspect the palate and uvula which should elevate symmetrically, with the uvula
remaining in the midline. A vagus nerve lesion will cause asymmetrical elevation of
the palate and uvula deviation away from the lesion.

Ask the patient to cough:

Vagus nerve lesions can result in the presence of a weak, non-explosive sounding
bovine cough caused by an inability to close the glottis.

Swallow assessment

Ask the patient to take a small sip of water (approximately 3 teaspoons) and observe
the patient swallow. The presence of a cough or a change to the quality of their voice
suggests an ineffective swallow which can be caused by both glossopharyngeal (afferent)
and vagus (efferent) nerve pathology.

Gag reflex

The gag reflex involves both the glossopharyngeal nerve (afferent) and the vagus nerve
(efferent). This test is highly unpleasant for patients and therefore the swallow test
mentioned previously is preferred as an alternative. You should not perform this test in an
OSCE, although you may be expected to have an understanding of what cranial nerves
are involved in the reflex.

To perform the gag reflex:

1. Stimulate the posterior aspect of the tongue and oropharynx which in healthy
individuals should trigger a gag reflex. The absence of a gag reflex can be caused by
both glossopharyngeal and vagus nerve pathology.

Assess soft palate and uvula

Assess cough

30/34
 Assess swallow

Accessory nerve (CN XI)

The accessory nerve (CN XI) transmits motor information to the sternocleidomastoid
and trapezius muscles. It does not have a sensory component.

Assessment

To assess the accessory nerve:

1. First, inspect for evidence sternocleidomastoid or trapezius muscle wasting.

2. Ask the patient to raise their shoulders and resist you pushing them downwards: this
assesses the trapezius muscle (accessory nerve palsy will result in weakness).

3. Ask the patient to turn their head left whilst you resist the movement and then repeat
with the patient turning their head to the right: this assesses the sternocleidomastoid
muscle (accessory nerve palsy will result in weakness).

Assess trapezius strength

Assess sternocleidomastoid strength

Hypoglossal nerve (CN XII)

31/34
The hypoglossal nerve (CN XII) transmits motor information to the extrinsic muscles of
the tongue (except for palatoglossus which is innervated by the vagus nerve). It does not
have a sensory component.

Assessment

To assess the hypoglossal nerve:

1. Ask the patient to open their mouth and inspect the tongue for wasting and
fasciculations at rest (minor fasciculations can be normal).

2. Ask the patient to protrude their tongue and observe for any deviation (which
occurs towards the side of a hypoglossal lesion).

3. Place your finger on the patient’s cheek and ask them to push their tongue against
it. Repeat this on each cheek to assess and compare power (weakness would be present
on the side of the lesion).

Inspect the tongue at rest

Inspect protruded tongue

Assess tongue power

Hypoglossal nerve palsy

Hypoglossal nerve palsy causes atrophy of the ipsilateral tongue and deviation of the
tongue when protruded towards the side of the lesion. This occurs due to the overaction
of the functioning genioglossus muscle on the unaffected side of the tongue.

32/34
 Left hypoglossal nerve palsy 4

To complete the examination…

Explain to the patient that the examination is now finished.

Thank the patient for their time.

Dispose of PPE appropriately and wash your hands.

Summarise your findings.

Example summary
“Today I examined Mrs Smith, a 64-year-old female. On general inspection, the patient
appeared comfortable at rest, with normal speech and no other stigmata of neurological
disease. There were no objects or medical equipment around the bed of relevance.”

“Examination of all twelve cranial nerves was unremarkable.”

“In summary, these findings are consistent with a normal cranial nerve examination.”

“For completeness, I would like to perform the following further assessments and
investigations.”

Further assessments and investigations

Full neurological examination including the upper and lower limbs.

Neuroimaging (e.g. MRI head): if there are concerns about space-occupying lesions
or demyelination.
Formal hearing assessment (including pure tone audiometry): if there are concerns
about vestibulocochlear nerve function.

Reviewer

Dr Gemma Maxwell

Neurology Registrar

References

33/34
1. Jonathan Trobe, M.D. Adapted by Geeky Medics. RAPD. Licence: CC BY.
2. Andrea Kamphuis. Adapted by Geeky Medics. Bell’s palsy. Licence: [CC BY-SA
4.0].
3. Andrea Kamphuis. Adapted by Geeky Medics. Bell’s palsy. Licence: [CC BY-SA
4.0].
4. Mukherjee SK, Gowshami CB, Salam A, Kuddus R, Farazi MA, Baksh J. Adapted
by Geeky Medics. Hypoglossal nerve palsy. Licence: CC BY.

34/34