Introduction
The cranial nerve examination is one of the most complex and comprehensive examinations in clinical medicine. In an OSCE or exam setting, talking continuously while examining keeps the examiner engaged and demonstrates your knowledge. Develop a consistent routine and present your findings systematically as you go.
Opening the Examination
Introduce yourself, explain what you would like to do, and ask for the patient's consent. Position the patient sitting upright, at eye level with you.
CN I — Olfactory Nerve
Ask: "Have you noticed any change in your sense of smell?"
Formal testing involves presenting non-noxious odours — coffee, peppermint, or vanilla — to each nostril separately, with the patient's eyes closed. Note that noxious smells (e.g. ammonia) are detected by the trigeminal nerve (CN V), not the olfactory nerve, and can be detected even in patients with true anosmia. If a patient claims complete loss of smell, test with petrol (which is detected by CN V) to distinguish true anosmia from malingering.
Common causes of anosmia: Upper respiratory tract infection (most common), trauma (shearing of olfactory filaments), frontal lobe tumours, Parkinson's disease (early marker), COVID-19.
CN II — Optic Nerve
Visual Acuity
Use a Snellen chart at 6 metres, testing each eye separately. Allow the patient to wear their glasses if they usually wear them for distance. Record as a fraction: 6/18 means the patient can only read at 6 metres what a person with normal vision can read at 18 metres. If the patient cannot read the top line, test finger counting, hand movements, and then light perception.
Colour Vision
Use 15 Ishihara test plates at 75 cm. 13 or more out of 15 plates correctly identified is considered normal. Colour vision defects (particularly red-green) suggest optic nerve pathology (e.g. optic neuritis, glaucoma).
Visual Inattention
Stand one metre from the patient and hold up both index fingers at 50 cm, approximately shoulder-width apart. Ask the patient to look at your nose and tell you when they see fingers moving. Move each finger separately and then both together. In parietal lobe lesions — particularly of the non-dominant hemisphere — the patient may detect an isolated stimulus on either side but "extinguishes" the stimulus on the affected side when both are presented simultaneously (extinction on double simultaneous stimulation).
Visual Fields
Sit 1 metre from the patient, at the same eye level. Ask the patient to close one eye (cover with their hand or a card) and you close the corresponding eye on your side. Using your hand in the four quadrants (superior nasal, superior temporal, inferior nasal, inferior temporal), bring a moving finger in from the periphery until the patient can see it. This tests for visual field defects by confrontation. Use a moving finger for the outer field, and a small red pin for the central field to assess for scotomas. Always check the blind spot.
Common visual field defects and their localisation:
- Monocular blindness — optic nerve (ipsilateral)
- Bitemporal hemianopia — optic chiasm (e.g. pituitary tumour)
- Homonymous hemianopia — optic tract or radiation (contralateral)
- Homonymous quadrantanopia (superior) — temporal lobe (contralateral)
- Homonymous quadrantanopia (inferior) — parietal lobe (contralateral)
- Macular sparing — occipital cortex lesion
Fundoscopy
Use an ophthalmoscope to examine the optic disc (colour, margins, cup-to-disc ratio), retinal vessels (arteriovenous nipping, silver wiring, flame haemorrhages), and retina.
CN III, IV, VI — Oculomotor, Trochlear, Abducens
Eyelids and Pupils — Inspection
- Note any ptosis (drooping of the upper eyelid). Assess fatigability by asking the patient to look upwards for 30 seconds (fatigable ptosis = myasthenia gravis).
- Inspect the pupils: comment on size, shape, and symmetry. Note that a slight inequality (anisocoria) occurs in up to 20% of the normal population — in isolation and without other neurological signs, this is usually benign.
Light Reflex
Shine a bright light obliquely into one eye. Both pupils should constrict — the ipsilateral direct reflex and the contralateral consensual reflex.
Swinging Light Test
Swing the light rapidly from one eye to the other. In a normal response, both pupils remain equally constricted throughout. This test detects a relative afferent pupillary defect (RAPD), which indicates an optic nerve or severe retinal lesion on the affected side:
- Relative afferent pupillary defect (RAPD/Marcus Gunn pupil): When the light is moved from the normal eye to the affected eye, the affected pupil dilates (paradoxically) instead of remaining constricted, because the afferent signal from the affected eye is weaker.
Accommodation Reflex
Ask the patient to fixate on a distant object, then quickly on your finger held 30 cm from their face. A normal accommodation reflex consists of convergence (both eyes adduct) and constriction of both pupils.
Abnormal Pupils
- Horner's syndrome: Unilateral miosis (small pupil), slight ptosis, enophthalmos (sunken eye), and anhidrosis (absent sweating) on the affected side. Due to interruption of the sympathetic pathway — causes include Pancoast tumour, carotid artery dissection, syringomyelia, brainstem stroke.
- Argyll Robertson pupil: Small, irregular pupil that does not react to light but does react to accommodation ("accommodates but does not react"). Classic sign of neurosyphilis. Mnemonic: "like a prostitute — she accommodates but doesn't react."
- Holmes-Adie (myotonic) pupil: Large pupil with sluggish reaction to light and accommodation. Often associated with absent knee and ankle jerks (Holmes-Adie syndrome), predominantly in young women. Benign.
- CN III palsy: Unilateral ptosis, dilated and fixed pupil (the oculomotor nerve carries pupil-constricting parasympathetic fibres on its surface, making these susceptible to compression — e.g. by a posterior communicating artery aneurysm), and the eye is deviated "down and out" (lateral rectus and superior oblique are unopposed).
Eye Movements
Ask the patient to follow your finger with their eyes, keeping their head still, and to tell you if they see double vision at any point. Trace a large "H" shape to test all six directions of gaze:
- CN III (Oculomotor): Controls all EOM except lateral rectus and superior oblique — test by looking medially, superiorly (medial), and inferiorly (medial)
- CN IV (Trochlear): Controls superior oblique — tests downward gaze medially (e.g. looking down the stairs). CN IV palsy causes vertical diplopia, worse on looking down and inward.
- CN VI (Abducens): Controls lateral rectus — tests abduction. CN VI palsy causes failure to abduct the eye (convergent squint at rest); the most common EOM palsy due to its long intracranial course.
Additional Eye Movement Tests
- Cover test: Ask the patient to fixate on your nose. Cover one eye and watch for the other eye to adjust (re-fixate) — this indicates a manifest squint (tropia).
- Saccades: Rapid voluntary eye movements — ask the patient to look quickly from your nose to your finger. Impaired saccades may suggest cerebellar or frontal lobe pathology.
- Head thrust test (vestibulo-ocular reflex): Hold the patient's head with both hands and ask them to keep their eyes fixed on your nose. Rapidly rotate the head to one side. Normally the eyes remain fixed. A corrective saccade (the eyes move with the head and then flick back) indicates a vestibulo-ocular reflex defect on the side to which the head was thrust. Useful in distinguishing peripheral vestibulopathy from central causes of vertigo.
Nystagmus
Nystagmus is an involuntary rhythmical oscillatory movement of the eyes. It is assessed during smooth pursuit eye movements:
- Pendular nystagmus: Equal velocity in both directions. Usually a congenital defect.
- Jerk nystagmus: Slow drift in one direction with a rapid saccadic corrective movement in the other. Named by the direction of the fast phase.
- 1st degree: only present when the eyes are deviated in the direction of the fast component
- 2nd degree: present with eyes in the primary position (looking straight ahead)
- 3rd degree: present even with the eyes deviated in the direction of the slow component — significant pathology
- Internuclear ophthalmoplegia (INO): Lesion of the medial longitudinal fasciculus (MLF), which links the abducens nucleus (pons) with the contralateral oculomotor nucleus (midbrain). On attempted lateral gaze, the ipsilateral eye abducts but the contralateral eye fails to adduct, with nystagmus in the abducting eye. The most common cause in young people is multiple sclerosis; in older patients, stroke.
CN V — Trigeminal Nerve
Motor Component
Look for wasting of the temporalis and masseter muscles. Ask the patient to clench their teeth — feel the masseter and temporalis muscles on both sides. Ask the patient to open their mouth widely (observe for jaw deviation — deviation towards the side of weakness). Test the jaw jerk by placing your finger on the patient's slightly open chin and tapping with a tendon hammer — a brisk jaw jerk suggests an upper motor neuron lesion above the pons.
Sensory Component
Test light touch in all three divisions bilaterally: ophthalmic (V1) — forehead; maxillary (V2) — cheek; mandibular (V3) — jaw. Compare like-for-like on both sides. Also test pain sensation (sharp versus blunt using a neurological pin).
Corneal reflex: Touch the lateral cornea (not the sclera or conjunctiva) lightly with a wisp of cotton wool. The patient should blink briskly. The afferent limb is CN V (ophthalmic division) and the efferent limb is CN VII. Avoid this test in contact lens wearers. Try to avoid eliciting the menace reflex (the patient should not see the stimulus approaching).
CN VII — Facial Nerve
The facial nerve is tested by examining the muscles of facial expression and by asking about its associated functions:
Ask: "Have you noticed any change in your taste?" (the facial nerve supplies taste to the anterior 2/3 of the tongue via the chorda tympani). Formal testing involves using sweet (sugar), sour (citric acid), salty (saline), and bitter (quinine) solutions on the anterior tongue.
Ask: "Have you noticed that loud noises seem excessively loud in one ear?" (hyperacusis — the facial nerve supplies the stapedius muscle, which normally dampens loud sounds)
Ask: "Are your eyes unusually dry on one side?" (the facial nerve contributes to lacrimation)
Muscles of Facial Expression — Testing
- "Lift your eyebrows as high as possible" and "now frown" — tests frontalis and corrugator
- "Squeeze your eyes tightly shut — don't let me open them" — try gently to open the eyelids — tests orbicularis oculi
- "Show me all your teeth" — tests zygomaticus and buccinator
- "Blow your cheeks out" — no air should escape through the lips on maximal inflation — tests orbicularis oris
Upper Motor Neuron (UMN) vs Lower Motor Neuron (LMN) Facial Weakness
- LMN facial weakness (e.g. Bell's palsy, parotid tumour, Ramsay Hunt syndrome): global weakness of one side of the face, including the forehead and eye-closing muscles. The patient cannot wrinkle the forehead or close the eye on the affected side.
- UMN facial weakness (e.g. stroke): the forehead is spared because the frontalis muscle has bilateral cortical representation from both hemispheres. The patient can still wrinkle their forehead — but has weakness of the lower face contralateral to the hemisphere lesion.
CN VIII — Vestibulocochlear (Acoustic) Nerve
(See also the Ear Examination page for more detail)
Auditory Function
Test each ear separately by rubbing your fingers together near the ear (a simple bedside test) or by using a standardised voice test (whispering numbers at 60 cm from the ear). If hearing loss is detected, perform tuning fork tests to differentiate sensorineural from conductive loss:
- Rinne's test (512 Hz tuning fork): Place the vibrating fork on the mastoid process — when the patient can no longer hear it, move it to the pinna. Normally, air conduction (AC) is better than bone conduction (BC) — Rinne positive. In conductive hearing loss, BC is better than AC — Rinne negative. In sensorineural hearing loss, Rinne is positive (AC better than BC) but both are reduced.
- Weber's test (512 Hz): Place the vibrating fork on the mid-vertex (top of the head). Ask: "Which ear can you hear the tuning fork in, or is it the same in both?" Normal: heard equally in both ears. Conductive loss: lateralises to the affected (worse) ear. Sensorineural loss: lateralises to the normal (better) ear.
Vestibular Function
Ask: "Do you experience any vertigo or dizziness? When you get dizzy, does the room spin around you?"
- Hallpike manoeuvre (Dix-Hallpike test): The patient sits on the examination couch. Gently but rapidly lower the patient backwards over the edge of the couch with the head turned 45 degrees to one side, keeping the head in your hands. Maintain this position for at least 20 seconds and observe for nystagmus. Repeat to the other side. A positive test (posterior semicircular canal BPPV) shows a brief burst of upbeat-torsional nystagmus after a latency of a few seconds, which fatigues on repeated testing.
- Romberg's test: Ask the patient to stand with feet together and arms by their sides, then close their eyes. If they sway or fall, the test is positive. Falling towards the side of the lesion suggests a peripheral vestibular disorder; falling in any direction with eyes closed suggests posterior column or cerebellar disease.
- Unterberger (Fukuda stepping) test: Ask the patient to march on the spot for 30 seconds with arms extended and eyes closed. Rotation of more than 30 degrees toward one side suggests a vestibular deficit on that side.
CN IX — Glossopharyngeal Nerve
The glossopharyngeal nerve is tested via the gag reflex — place an orange stick or tongue depressor on the posterior pharyngeal wall and observe the palate rising. However, this is uncomfortable for patients and is routinely omitted in the exam unless specifically indicated.
CN IX provides: taste to the posterior 1/3 of the tongue; sensory supply to the oropharynx (afferent limb of the gag reflex); and parasympathetic supply to the parotid gland.
CN X — Vagus Nerve
Ask the patient to swallow a sip of water and observe for coughing or choking (evidence of palatal or pharyngeal weakness).
Ask the patient to say "Ah" — the palate should rise symmetrically in the midline, and the uvula should remain central. A unilateral vagus nerve lesion causes the uvula to deviate away from the side of the lesion (the weak side fails to elevate).
Listen for dysphonia (hoarse or breathy voice) — may indicate recurrent laryngeal nerve palsy (a branch of CN X), which can cause vocal cord paresis. Causes: thyroid goitre, lung apical tumour, aortic arch aneurysm, neck surgery.
CN XI — Accessory Nerve
Inspect for visible wasting of the sternocleidomastoid (SCM) or trapezius.
"Turn your head to the left/right against my hand" — hold the patient's chin to resist — tests the SCM (turning the head to the right is powered by the left SCM).
"Shrug your shoulders up — don't let me push them down" — tests the trapezius.
CN XII — Hypoglossal Nerve
Inspect the tongue at rest for wasting and fasciculations (flickering movements — indicate LMN lesion, e.g. motor neurone disease).
"Stick your tongue out for me." The tongue deviates towards the side of the lesion (the weaker side). An LMN lesion (e.g. tumour at the jugular foramen) will show ipsilateral tongue deviation with wasting and fasciculations. A UMN lesion (e.g. stroke) will show contralateral tongue deviation without wasting.
Completing the Examination
Thank the patient and assist them in redressing if needed. Present your findings systematically. State: "To complete my examination, I would like to test the peripheral nervous system and perform a full examination of any other relevant system."
Frequently Asked Questions
What is the difference between UMN and LMN facial nerve palsy?
This is one of the most frequently tested neurological distinctions in OSCE examinations. In an upper motor neuron (UMN) facial palsy (caused by stroke or other cortical/subcortical lesion), the forehead is spared because the frontalis muscle receives bilateral cortical representation. The patient can still wrinkle their forehead on the affected side but has weakness of the lower face (inability to show teeth or blow their cheeks out) contralateral to the lesion. In a lower motor neuron (LMN) facial palsy (e.g. Bell's palsy), the entire ipsilateral half of the face is affected — including the forehead and the eye-closing muscles. The patient cannot raise their eyebrow, close their eye, or move the lower face on the affected side.
What is a relative afferent pupillary defect (RAPD) and what causes it?
A relative afferent pupillary defect (RAPD), also known as a Marcus Gunn pupil, occurs when the afferent (sensory) input from one optic nerve is reduced relative to the other. In the swinging light test, when the light is moved from the normal eye to the affected eye, the affected pupil appears to dilate (paradoxically) because it is receiving less neural drive than when the consensual reflex from the normal eye was driving it. A RAPD indicates a lesion of the optic nerve (e.g. optic neuritis in MS, ischaemic optic neuropathy, severe glaucoma) or a very severe retinal lesion. It does not occur with cataract or refractive errors. A RAPD cannot be detected if there are bilateral symmetrical optic nerve lesions.
What causes internuclear ophthalmoplegia (INO)?
INO results from a lesion of the medial longitudinal fasciculus (MLF), which connects the abducens nucleus (VI) in the pons with the contralateral oculomotor nucleus (III) in the midbrain. This pathway coordinates horizontal conjugate gaze. With an MLF lesion on the right: on attempted left lateral gaze, the left eye abducts normally (driven by left CN VI), but the right eye fails to adduct (the MLF signal from the left abducens nucleus to the right oculomotor nucleus is interrupted), with nystagmus in the abducting left eye. Bilateral INO in a young person is virtually pathognomonic of multiple sclerosis. In older patients, stroke is the most common cause.
How do I distinguish peripheral from central causes of vertigo?
Key clinical features distinguishing peripheral from central vertigo: Peripheral (e.g. BPPV, vestibular neuritis, Meniere's disease): severe, episodic rotatory vertigo; prominent nausea and vomiting; unidirectional nystagmus (fast phase always in the same direction, enhanced by gaze in the direction of the fast phase); abnormal head thrust test; no other neurological signs; hearing loss may be present. Central (e.g. cerebellar stroke, MS, posterior fossa tumour): less severe but constant vertigo; may be purely positional; direction-changing nystagmus (fast phase changes direction depending on gaze direction); normal head thrust test; other cerebellar or brainstem signs (dysarthria, ataxia, diplopia); no hearing loss (usually). The HINTS examination (Head Impulse, Nystagmus pattern, Test of Skew deviation) can be used at the bedside to distinguish peripheral from central causes of acute vertigo.
What are the clinical features of a CN III (oculomotor) nerve palsy?
A complete CN III palsy presents with: ptosis (drooping of the upper eyelid — due to paralysis of the levator palpebrae superioris); dilated, fixed pupil (mydriasis — due to loss of parasympathetic constriction; the pupil-constricting fibres run on the outer surface of CN III and are particularly vulnerable to compression by an aneurysm or uncal herniation); and the eye deviated "down and out" (because the unopposed actions of the lateral rectus [CN VI] and superior oblique [CN IV] pull the eye laterally and inferiorly). A surgical CN III palsy (caused by compression, e.g. posterior communicating artery aneurysm, uncal herniation) almost always involves the pupil. A medical CN III palsy (caused by ischaemia, e.g. in diabetes) often spares the pupil because the pupil-constricting fibres are on the outer surface and the central ischaemia affects the inner fibres first.
What are the causes of anosmia?
Loss of sense of smell (anosmia) can be caused by: local nasal causes (most common) — nasal polyps, rhinitis, upper respiratory tract infection, nasal septum deviation; head trauma — shearing of the olfactory filaments as they pass through the cribriform plate; frontal lobe tumours (e.g. olfactory groove meningioma — Foster Kennedy syndrome with ipsilateral anosmia and optic atrophy, and contralateral papilloedema); neurodegenerative diseases — Parkinson's disease (anosmia is a common early marker, often predating motor symptoms by years), Alzheimer's disease; and infectious causes — COVID-19 (a particularly prominent feature of acute infection, with post-COVID smell dysfunction affecting many patients long-term). Always consider whether anosmia is unilateral or bilateral, as the differential differs.
What is Horner's syndrome and what are its causes?
Horner's syndrome results from interruption of the sympathetic pathway to the eye. It consists of: miosis (small pupil — due to loss of sympathetic pupil dilation); partial ptosis (drooping of the upper eyelid and slight elevation of the lower lid — due to loss of sympathetically innervated Muller's muscle in both lids); enophthalmos (apparent recession of the eye into the orbit); and anhidrosis (reduced sweating on the affected side of the face, if the lesion is below the superior cervical ganglion). The sympathetic pathway is a three-neuron chain from the hypothalamus to the eye. Causes by level: First-order (hypothalamus to ciliospinal centre of Budge): brainstem stroke, MS, syringomyelia; Second-order (thoracic outlet to superior cervical ganglion): Pancoast tumour (apical lung tumour), cervical rib, neck surgery; Third-order (internal carotid to orbit): carotid artery dissection or aneurysm, cavernous sinus lesion.
References
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- Aids to the Examination of the Peripheral Nervous System. 5th ed. Saunders, 2010.
- Fuller G. Neurological Examination Made Easy. 5th ed. Churchill Livingstone, 2013.
- Kanski JJ. Clinical Ophthalmology: A Systematic Approach. 8th ed. Elsevier, 2015.
- Newman NJ, Biousse V. Diagnosis and management of third nerve palsies. In: UpToDate [Internet]. 2024.
- Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Arch Neurol. 1988;45(7):737–739.
