11/13/24, 6\:59 PM Guide | Cranial nerve examination

Cranial nerve examination

Table of contents
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0\:00 10\:28

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.
Con
Brie
Gain consent to proceed with the examination.
Ask the patient to sit on a chair, approximately one arm's length away.
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Ask the patient if they have any pain before proceeding with the clinical examination.

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.
General inspection

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.
Olfaction can be tested more formally using di
Pennsylvania smell identi
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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
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.
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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).
3. Assess if they can count the number of
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”).
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Assess visual acuity using a Snellen chart
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
Optic nerve (CN II) pathology usually causes a decrease in acuity in the a
disc swelling from raised intracranial pressure), does not usually a

Pupillary re

With the patient seated, dim the lights in the assessment room to allow you to assess pupillary re
Direct pupillary re
Assess the direct pupillary re
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 re
Consensual pupillary re
Assess the consensual pupillary re
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 re
being tested.
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Assess direct and consensual pupillary light re
Swinging light test
Move the pen torch rapidly between the two pupils to check for a relative a
Perform the swinging light test
Accommodation re
1. Ask the patient to focus on a distant object (clock on the wall/light switch).
2. Place your
3. Ask the patient to switch from looking at the distant object to the nearby
4. Observe the pupils, you should see constriction and convergence bilaterally.
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Assess the accomodation re
Pupillary light re
Each a
The a
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 e
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 e
ciliary sphincter and enable pupillary constriction.
Normal pupillary light re
provide an indirect way of assessing their function\:
The direct pupillary re
The consensual pupillary re
The swinging light test is used to detect relative a
Abnormal pupillary responses
Relative a
pupils equally (due to the dual e
damaged, partially or completely, both pupils will constrict less when light is shone into the a
the healthy eye. The pupils, therefore, appear to relatively dilate when swinging the torch from the healthy to the
a
a
optic neuropathy such as optic neuritis, unilateral advanced glaucoma and compression secondary to tumour or
abscess.
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Unilateral e
of the e
light entering either eye (due to loss of ciliary sphincter function). The consensual light re
would still be present as the a
oculomotor nerve) of the una

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 di
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.
1. Ask the patient to cover one of their eyes.
2. Then ask the patient to read the numbers on the Ishihara plates. The
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 identi
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
Colour vision de
Colour vision de
Optic neuritis\: results in a reduction of colour vision (typically red).
Vitamin A de
Chronic solvent exposure
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Visual neglect/inattention

Visual neglect (also known as visual inattention) is a condition in which an individual develops a de
one side (hemispace) of their visual . 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. It should be noted that visual neglect is not caused by optic
nerve pathology, however, it is useful in the context of a cranial nerve examination to di
the optic nerve (true visual
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
hands moving.
3. Hold your hands out laterally, with each occupying one side of the patient's visual
4. Take turns wiggling a
5. Finally wiggle a
Interpretation
Visual inattention is present when there is neglect of one hemispatial
hemispacial
Visual extinction is present when the patient can’t identify one of the moving
simultaneously. They can, however, identify each of them when they’re wiggled individually. Again, during simultaneous
bilateral wiggling, people will usually fail to see the
Assess for visual inattention

Visual

This method of assessment relies on comparing the patient's visual
you need to position yourself, the patient and the target correctly (see details below).
you need to have normal visual
Visual
1. Sit directly opposite the patient, at a distance of around 1 metre.
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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
assessment can be completed with an Amsler chart.
6. Position the hatpin (or another visual target such as your
essential for the assessment to work).
7. Assess the patient's peripheral visual
slowly move the target towards the centre, asking the patient to report when they
but the patient cannot, this would suggest the patient has a reduced visual
8. Repeat this process for each visual
9. Document your
Assess the patient's peripheral visual
Types of visual
Bitemporal hemianopia\: loss of the temporal visual
hemianopia typically occurs as a result of optic chiasm compression by a tumour (e.g. pituitary adenoma,
craniopharyngioma).
Homonymous
tumour, abscess (i.e. pathology a
hemianopias if half the vision is a
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).
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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).
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
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

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 o
fundoscopy guide for more details.
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CN III, CN IV, CN VI

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
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

Brie
trochlear, abducens, vestibular nerve pathology).
1. Hold your
the primary position for any deviation or abnormal movements.
2. Ask the patient to keep their head still whilst following your
any double vision or pain.
3. Move your
4. Observe for any restriction of eye movement and note any nystagmus (which may suggest vestibular nerve pathology or
stroke).
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.
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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 a
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
Trochlear nerve palsy (CN IV)
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 a

Assessment of strabismus

Strabismus is a condition in which the eyes do not properly align with each other when looking at an object. Pathology
a
Light re
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 light re
If the ocular alignment is normal, the light re
De
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Corneal light re
Cover test
The cover test is used to determine if a heterotropia (i.e. manifest strabismus) is present.
1. Ask the patient to
2. Occlude one of the patient's eyes and observe the contralateral eye for a shift in
If there is no shift in
alignment).
If there is a shift in
3. Repeat the cover test on the other eye.
The direction of the shift in
Interpretation of the cover test
Direction of eye at rest
The direction of shift in
opposite eye is occluded
Type of tropia
present
Temporally (i.e. laterally or
outwards)
Nasally (i.e. medially or inwards) Nasally (i.e. medially or
inwards)
Temporally (i.e. laterally or outwards) Superiorly (i.e. upwards) Inferiorly (i.e. downwards) Inferiorly (i.e. downwards) Superiorly (i.e. upwards) Exotropia
Esotropia
Hypertropia
Hypotropia
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Cover test

Trigeminal nerve (CN V)

The trigeminal nerve (CN V) transmits both sensory information about facial sensation and motor information to the muscles of
mastication.
The trigeminal nerve has three sub-divisions, each of which has its own broad set of functions (not all are covered below)\:
Ophthalmic (V )\: carries sensory information from the scalp and forehead, nose, upper eyelid as well as the conjunctiva and
1
cornea of the eye.
Maxillary (V )\: carries sensory information from the lower eyelid, cheek, nares, upper lip, upper teeth and gums.
2
Mandibular (V )\: carries sensory information from the chin, jaw, lower lip, mouth, lower teeth and gums. Also carries motor
3
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
de
Ask the patient to close their eyes and say 'yes' each time they feel you touch their face.
Assess the sensory component of V , V and V 1 2 3
supplied by each branch\:
by testing light touch and pinprick sensation across regions of the face
Forehead (lateral aspect)\: ophthalmic (V )
1
Cheek\: maxillary (V )
2
Lower jaw (avoid the angle of the mandible as it is supplied by C2/C3)\: mandibular branch (V )
3
You should compare each region on both sides of the face to allow the patient to identify subtle di

Motor assessment

Use the muscles of mastication to assess the motor component of V \:
3
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 e
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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.

Re

Jaw jerk re
The jaw jerk re
response is exaggerated in patients with an upper motor neuron lesion. Both a
re
To assess the jaw jerk re
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
4. Tap your
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 re
The corneal re
consensual blinking). The a
mediated by the temporal and zygomatic branches of the facial nerve.
To assess the corneal re
1. Clearly explain what the procedure will involve to the patient and gain consent to proceed.
2. Ask the patient to turn their eyes away from the direction you are going to approach (e.g. if you're on the patient's right, ask
them to look to the left).
3. The sclera shares the same innervation as the cornea (V1) and thus, to reduce the risk of causing corneal damage it is
reasonable to
assessment by gently touching the edge of the cornea (the sclera may be less sensitive, particularly in patients who wear
contact lenses).
4. 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 re
behind the test.
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Assess light touch sensation (V1)

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\:
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\:
" R a i s e Raised eyebrows\: assesses frontalis -
Closed eyes\: assesses orbicular oculi -
Blown out cheeks\: assesses orbicularis oris -
y o u r e y e b r o w s a s i f y o u' r e s u r p r i s e d .
"
" S c r u n c h u p y o u r e y e s a n d d o n' t l e t m e o p e n t h e m .
"
" B l o w o u t y o u r c h e e k s a n d d o n' t l e t m e d e
"
Smiling\: assesses levator anguli oris and zygomaticus major -
" C a n y o u d o a b i g s m i l e f o r m e ?"
Pursed lips\: assesses orbicularis oris and buccinator -
" C a n y o u t r y t o w h i s t l e ?"
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Inspect the face for asymmetry
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 a
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.
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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.

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.
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Perform gross hearing assessment

Rinne's test

1. Place a vibrating 512 Hz tuning fork
sure the contact is
2. Con
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)
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Place a vibrating 512 Hz tuning fork on the mastoid process

Weber’s test

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 " W h e r e d o y o u h e a r t h e s o u n d ?"
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 a
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.
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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 e
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 re

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

CN IX and CN X

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
The vagus nerve transmits motor information to several muscles of the mouth which are involved in the production of speech
and the e
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 una
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 ine
glossopharyngeal (a
Gag re
The gag re
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
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the re
To perform the gag re
1. Stimulate the posterior aspect of the tongue and oropharynx which in healthy individuals should trigger a gag re
absence of a gag re
Inspect the soft palate and uvula

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).
Source\: geekymedics.com
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