Cranial Nerve OSCE Examination

1. Introduction
2. General Inspection
3. Olfactory Nerve (CN I)
4. Optic Nerve (CN II)
5. Oculomotor, Trochlear and Abducens Nerves (CN III, IV, VI)
6. Trigeminal Nerve (CN V)
7. Facial Nerve (CN VII)
8. Vestibulocochlear Nerve (CN VIII)
9. Glossopharyngeal and Vagus Nerves (CN IX, X)
10. Accessory Nerve (CN XI)
11. Hypoglossal Nerve (CN XII)
12. Completing the Examination
13. Quiz

Wash your hands and don personal protective equipment if appropriate.

Introduce yourself to the patient and ensure to mention your grade e.g. 3rd year medical student/junior doctor/consultant.

Confirm the patient’s details using 3 points of identification, usually full name, date of birth and NHS or hospital number.

Obtain consent for the examination, ensuring to explain what the examination will entail. A useful explanation is that you would like to test the nerves that control the senses and movements of the head and face. Tell them that it will involve looking into the eyes, testing sensation and asking them to perform some movements.

Position the patient seated, ideally on a chair with you sitting directly opposite at roughly the same eye level so that you can compare both sides of the face symmetrically.

Ask the patient if they have any pain anywhere before you begin. Then gather the equipment you may need: a pen torch, a Snellen chart (a chart of letters that get smaller, to test sharpness of vision), Ishihara plates (pictures made of coloured dots, to test colour vision), an ophthalmoscope (a handheld light and lens for looking at the back of the eye), a cotton wisp, a neuro-tip (a single-use sharp tip for testing pinprick sensation), a 512 Hz tuning fork, a tongue depressor and a small item with a smell for olfaction (testing the sense of smell).

Begin by inspecting the patient and their surroundings from the end of the bed or across the room. Look at the face at rest for any obvious asymmetry, facial droop, ptosis (drooping of the upper eyelid) or strabismus (a squint). These can point to a cranial nerve lesion before any formal testing begins.

Note any abnormal movements such as facial twitching. Listen to the patient’s speech. Dysarthria (slurred speech) can result from weakness of the muscles supplied by several cranial nerves. A hoarse voice or a ‘bovine’ cough (a weak cough that lacks the usual explosive start) may suggest a vagus nerve problem.

Also look for any scars on the scalp or behind the ear, which may indicate previous neurosurgery. Glance at the limbs as the patient settles. Wasting (thinning of muscle), tremor or abnormal posturing can hint at a wider neurological process.

Look around the bedside for clues such as hearing aids, glasses, a white cane or other walking aids, a feeding tube (which may indicate swallowing difficulties), or prisms on spectacles used to correct double vision. These objects can give early clues to the underlying diagnosis.

The olfactory nerve is the first cranial nerve and is responsible for the sense of smell. In an OSCE it is rarely formally tested. You should always screen for it, though, by asking the patient whether they have noticed any recent change in their sense of smell or taste. The two are closely linked, as much of what we perceive as taste is actually smell.

If formal testing is required, occlude one nostril at a time and ask the patient to identify a familiar smell, such as coffee or peppermint, with their eyes closed.

Reduced or absent sense of smell is called anosmia. The commonest causes are benign: nasal and sinus disease, and viral infections of the upper airway such as the common cold. More important neurological causes include head trauma, a frontal lobe tumour, or early Parkinson’s disease (a movement disorder that causes tremor and slowness), in which anosmia can precede the motor features by years. After head trauma, the delicate olfactory nerve fibres can be sheared (torn) as they pass through the cribriform plate (the thin, sieve-like bone between the nose and the brain).

The optic nerve carries visual information from the retina (the light-sensitive layer at the back of the eye) to the brain. It is tested thoroughly because so many neurological conditions affect vision. Assessment is conventionally broken down into acuity (sharpness of vision), fields (the area you can see), pupillary responses, colour vision and fundoscopy (looking at the back of the eye).

Visual acuity is assessed using a Snellen chart at 6 metres, testing each eye individually. The patient should wear their usual glasses, to correct refractive error (such as short- or long-sightedness), which is not a neurological problem. Acuity is recorded as a fraction such as 6/6. The top number is the testing distance. The bottom number is the distance at which a person with normal sight could read that line. Reduced acuity that does not correct with a pinhole (looking through a small hole, which cancels out refractive error) suggests pathology of the eye or optic nerve.

Image - A Snellen chart, read at 6 metres to assess visual acuity. The smallest line the patient can read gives the bottom number of the recorded fraction

SimpleMed original image, credit ‘SimpleMed original’

Colour vision is tested using Ishihara plates. Loss of colour vision, particularly red desaturation (where red appears washed out), is an early and sensitive sign of optic nerve disease such as optic neuritis (inflammation of the optic nerve). In one long-term trial, about half of the people with optic neuritis developed multiple sclerosis (an immune disease that damages the coverings of nerves in the brain and spinal cord) within 15 years.

Image - An Ishihara plate used to test colour vision. A person with normal colour vision reads the number, whereas it may be invisible to someone with a colour vision deficit or early optic nerve disease

Creative commons source by Shinobu Ishihara [Public domain]

Visual fields are tested by confrontation, comparing the patient’s field to your own. Sit opposite the patient, ask them to cover one eye and look at your nose, then bring a moving finger or red hatpin in from the periphery in each quadrant.

Mapping out a field defect is one of the most useful localising tests in neurology. The pattern of loss tells you where along the visual pathway the lesion lies. A monocular field loss (loss in one eye only) localises to the eye or the optic nerve in front of the optic chiasm (where the two optic nerves meet and partly cross). A bitemporal hemianopia (loss of both outer halves) localises to the chiasm. It is classically caused by a pituitary tumour compressing the crossing nasal fibres (the fibres from the inner half of each retina). A homonymous hemianopia (loss of the same side of the field in both eyes) localises behind the chiasm. It is often due to a stroke affecting the optic tract or the optic radiation (the nerve fibres that carry the signal on to the visual cortex at the back of the brain).

Before mapping the fields formally, screen for visual inattention (also called visual neglect). With both of the patient’s eyes open, hold your hands out to either side and wiggle a finger on one hand, then the other, then both at the same time. A patient who sees each side individually but consistently misses the finger on one side when both move together has visual extinction. This is not a field defect at all but a problem of attention, typically from a parietal lobe lesion (usually after a right-sided stroke causing left-sided neglect). This screening test helps you separate true visual loss from inattention caused by damage to the cerebral cortex.

You can also map the blind spot. This is the small physiological gap in each field where the optic disc (where the optic nerve leaves the eye) meets the retina and there are no photoreceptors (light-sensing cells). Compare your blind spot with the patient’s using a red pin. An enlarged blind spot suggests a swollen optic disc. Papilloedema is a swollen optic disc caused by raised intracranial pressure (raised pressure inside the skull), so check the disc with an ophthalmoscope to find out whether this is the cause.

Image - How lesions at different points along the visual pathway produce characteristic field defects. A chiasmal lesion causes a bitemporal hemianopia, while a lesion behind the chiasm causes a homonymous hemianopia

Creative commons source by As eo [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]

Before testing the reflexes, inspect the pupils themselves, comparing their size, shape and symmetry. A small difference in size (anisocoria) can be physiological (normal). A markedly dilated pupil suggests a third nerve palsy (weakness or paralysis of the oculomotor nerve). A small pupil may point to Horner’s syndrome (a small pupil with a drooping eyelid and reduced sweating on the same side of the face) or to Argyll Robertson pupils (small pupils that constrict when the patient focuses on a near object but not in response to light).

The pupillary light reflex tests the integrity of the optic nerve (the afferent, ‘sensing’ limb) and the oculomotor nerve (the efferent, ‘responding’ limb). Shine a torch into one eye. Observe the direct response (constriction of that pupil) and the consensual response (constriction of the other pupil). The consensual response occurs because the signal is shared between both sides of the midbrain (the top part of the brainstem).

The swinging light test detects a relative afferent pupillary defect (RAPD, or Marcus Gunn pupil). Move the torch quickly from one eye to the other. Normally both pupils stay constricted. If one optic nerve is damaged, the affected pupil paradoxically dilates when the light swings onto it. This is because the weaker afferent signal from that eye produces less constriction than the consensual response it had just been receiving while the light shone in the healthy eye. A RAPD is a sign of significant optic nerve disease such as optic neuritis, or extensive retinal damage.

The accommodation reflex is tested by asking the patient to focus on a distant object and then on your finger held roughly 30 cm in front of their nose. As they switch focus to the near target, the eyes should converge and the pupils constrict.

Fundoscopy using an ophthalmoscope allows direct inspection of the optic disc and retina. Look for a swollen disc, which may be papilloedema (swelling caused by raised intracranial pressure), or a pale disc (optic atrophy), which suggests chronic optic nerve damage.

Image - Papilloedema seen on fundoscopy: the optic disc is swollen with blurred margins, indicating raised intracranial pressure

SimpleMed original image, credit ‘SimpleMed original’

These three nerves are tested together because they all control eye movements. The oculomotor nerve (CN III) supplies most of the extraocular muscles (the muscles that move the eye), raises the eyelid, and carries the parasympathetic fibres that constrict the pupil. The trochlear nerve (CN IV) supplies only the superior oblique muscle (which moves the eye down and in), and the abducens nerve (CN VI) supplies only the lateral rectus (which moves the eye outwards).

First inspect for ptosis and the resting position of the eyes. Then hold your finger about 30 cm in front of the patient. Ask them to follow it with their eyes, keeping their head still, through an ‘H’ pattern. This takes each eye through its full range of movement. Ask the patient to report any double vision (diplopia) and watch for nystagmus (involuntary rhythmic eye movements).

A complete third nerve palsy produces a characteristic picture: the eye is held ‘down and out’, there is complete ptosis, and the pupil may be fixed and dilated. A painful third nerve palsy with a blown pupil (a fixed, widely dilated pupil) is a red flag. It can be caused by a compressive lesion such as a posterior communicating artery aneurysm (a bulge in an artery at the base of the brain). The parasympathetic fibres run on the surface of the nerve, so they are compressed first. This explains the early pupil involvement. A medical cause, such as damage to the small blood vessels that supply the nerve in diabetes (a microvascular cause), tends to spare the pupil.

A fourth nerve palsy causes vertical diplopia that is worst on looking down (for example reading or descending stairs); patients often tilt their head away from the affected side to compensate. A sixth nerve palsy causes a convergent squint with the affected eye unable to abduct, producing horizontal diplopia. Because of its long intracranial course, the sixth nerve is vulnerable to raised intracranial pressure and is therefore a poor localising sign.

The trigeminal nerve is the great sensory nerve of the face and also supplies the muscles of mastication (chewing). It has three divisions: ophthalmic (V1), maxillary (V2) and mandibular (V3), which supply sensation to the forehead, cheek and jaw respectively.

Test light touch sensation with a cotton wisp (and, if indicated, pinprick with a neuro-tip) over each of the three divisions on both sides, asking the patient to compare left with right. A sensory deficit in a trigeminal distribution can be caused by a brainstem lesion, a tumour at the cerebellopontine angle (the angle between the cerebellum and the pons, the middle part of the brainstem), or herpes zoster (shingles) affecting a division.

Test the muscles of mastication by asking the patient to clench their teeth while you palpate the masseter and temporalis muscles (the chewing muscles over the angle of the jaw and the temple), then to open the jaw against resistance. A lower motor neurone lesion (damage to the nerve cells that run from the brainstem or spinal cord to the muscle) causes the jaw to deviate towards the side of the weakness when opened, because the unopposed pterygoid (a deep jaw muscle) on the normal side pushes it across.

The corneal reflex tests V1 as the afferent limb and the facial nerve (CN VII) as the efferent limb. Lightly touching the cornea (the clear front surface of the eye) with a wisp of cotton wool should cause both eyes to blink. The jaw jerk is usually absent or only slightly present. A brisk jaw jerk suggests an upper motor neurone lesion (damage to the pathway running from the brain down to the brainstem or spinal cord) above the pons.

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