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The Cranial Nerve Exam

The cranial nerve examination is a complex mix of examination techniques designed to localise pathology to one or more of the twelve cranial nerves.
 

The Cranial Nerve Exam

Overview

  • The cranial nerve examination is a complex mix of examination techniques designed to localise pathology to one or more of the twelve cranial nerves. 

First Steps

  • Before commencing the cranial nerve exam, wash your hands, introduce yourself to the patient and gain consent.
  • Position the patient comfortably, in a sitting position. Sit directly across from the patient with your eyes level with theirs.

The Patient

    • General Inspection

    • Look around the room, particularly looking for mobility devices, orthoses or other assistance devices.
  • Look at the patient, assessing for general comfort, any scars present around the face, and their general posture.
    • Level of Consciousness

    • Gauge the patient’s level of alertness and interactivity. For a more formal measure, assess the patient’s glasgow coma scale.

I - Smell

  • The olfactory nerve (I) provides olfactory sensation. This nerve is not commonly assessed in detail, however a screening test can be performed by asking the patient to smell and identify a common scent (such as alcohol wipe, coffee or cinnamon). While loss of smell sensation - or anosmia - may be a sign of an olfactory nerve lesion, Parkinson’s disease is an important differential to keep in mind.

II - Vision

  • The optic nerve (II) provides special sensory innervation, in the form of sight.
    • Visual Acuity

    • The patient’s visual acuity is a useful screening tool for identifying visual loss, which may be caused by a variety of ocular, optic nerve or CNS disorders. Ask the patient to cover one eye (with their corrective lenses if they normally wear any), look at a Snellen chart and identify the smallest line they can read. 
    • Peripheral Visual Fields

    • The pattern of a patient’s peripheral visual field loss can aid in localising their lesion. To assess these, ask the patient to cover one eye and then slowly move a finger or white examination pin from the upper left, upper right, lower left and then lower right; ask the patient to state when they can see the finger / pen. Repeat with the other eye. The patterns of visual field loss and their corresponding pathologies are:
    • II - Vision
    • Interpretation:
    • A
      Unilateral anopia - complete loss of vision in one eyeUnilateral optic nerve lesion or ocular pathology
    • B
      Bitemporal hemianopia - loss of lateral vision in both eyesOptic chiasmal compression
    • C
      Homonymous hemianopia - loss of left or right field in one eyeContralateral optic tract lesion
    • D/E
      Homonymous quadrantanopia - loss of the left or right upper / lower quarters of vision in both eyesContralateral upper (superior loss) or lower (inferior loss) optic radiation lesion
    • F
      Homonymous hemianopia with macular sparingContralateral occipital lobe lesion
    • Central Visual Fields

    • Assess the central visual fields by asking the patient to cover on eye, and moving a red examination pin from lateral to medial. Ask the patient when they see the pin as red, and ask if it disappears at any time.
    • Colour Vision

    • In certain instances, colour vision can be assessed using Ishihara plates. There are several types of plates that may be used to differentiate between types of colour vision loss.

II & III - Pupils

  • The optic nerve (II) provides the sensory pathway of the pupillary reflexes, interfacing with the Edinger-Westphal nucleus within the midbrain, with the oculomotor nerve (III) providing the motor pathway.
    • Inspect the Pupils

    • Look at the size and equality of the pupils, for miosis (pupillary constriction), mydriasis (pupillary dilatation) or anisocoria (unequal pupils).
    • Light Reflexes

    • Shine a light into each pupil, and watch to see that both the ipsilateral (direct response) and contralateral (consensual response) pupils constrict as a result of the stimulus. Pupillary light reflexes may be absent in certain intraocular, optic (II) nerve, midbrain, oculomotor (III) nerve pathology; it may also occur due to certain medications.
    • Swinging Light Test

    • The swinging eye test is used to assess for a relative afferent pupillary defect (RAPD), a sign of an asymmetric pathology affecting the pupillary reflex pathway. Shine a light into one eye, swing it into the other eye, and so on back and forth. An RAPD is present if the affected eye dilates, or constricts briefly followed by dilatation.
    • Accomodation Reflex

    • To assess the accommodation reflex, ask the patient to focus on a distant object, such as the back wall of the room. Place a finger in front of their field of view and ask them to look at it. Unresponsiveness to light with an intact accommodation reflex is referred to as an Argyll Robertson Pupil, which is classically associated with neurosyphillis.

III, IV & VI - Eye Movement

  • Eye movement is innervated by the oculomotor (III), trochlear (IV) and abducens (VI) nerves.
    • Inspect for Ptosis

    • Look for lowering of the eyelid, either completely or partially; note whether this is unilateral or bilateral. Partial ptosis is classically a sign of Horner’s syndrome (along with miosis and anhydrosis), while complete ptosis may be due to structural, neurological or muscular disease.
    • Inspect for Strabismus

    • Strabismus refers to a misalignment of the eyes, either medially (esotropia) or laterally (exotropia). Strabismus is often quite subtle and difficult to detect, and slight angulation of the head to either side may be a sign of compensation for a subtle strabismus. The cover test can be used to further assess a patient with strabismus.
    • Look for Nystagmus

    • Nystagmus (usually referring to jerk nystagmus) is an abnormal rhythmic eye movement that commonly occurs due to vestibular, brainstem or cerebellar pathology. Ask the patient to look at your finger, held ~50cm in front of their eyes. Repeat this in the extremes of left and right lateral gaze, as well as in superior and inferior gaze. Look for slow drifting movements of the eye interspersed with corrective fast saccadic movements; note whether these movements are horizontal, vertical or torsional. 
  • Nystagmus that is transient with onset following change in position is suggestive of benign paroxysmal positional vertigo, while vertical or torsional nystagmus are suggestive of a central cause.
    • Assess the Extraocular Movements

    • Ask the patient to keep their head still and watch your finger as you move it through a modified H pattern:
    • III, IV & VI - Eye Movement
    • Ask the patient whether they have pain or double vision. Look for limitation of eye movement in any direction, which may be suggestive of specific pathology:
    • Oculomotor nerve palsy - eye deviated down and out, with ptosis, mydriasis and loss of pupillary reflexes
    • Trochlear nerve palsy - head tilted away from the side of the lesion, with the eye deviated upward and rotated outward; inability to look down
    • Abducens nerve palsy - eye deviated inward, with inability to look laterally
    • Internuclear ophthalmoplegia (INO) - inability to adduct one eye, with nystagmus in the other eye. This sign is suggestive of multiple sclerosis in younger patients, and stroke in older patients.
  • The patient may also have fatiguability of eye movements, meaning that they can initially look up but not maintain this gaze over time - this is a sign of myaesthenia gravis.

V - Facial Sensation & Jaw Muscles

  • The trigeminal nerve (V) innervates sensation of the face, corneas, nasal cavity and oral cavity. The third branch of the trigeminal nerve (the mandibular nerve) also innervates the muscles of mastication.
    • Assess Facial Sensation

    • Using a piece of cotton wool, lightly touch the patient's face over the three trigeminal areas of innervation, moving from side to side. Ask the patient if there is any area that is numb or has altered sensation in any way. Loss of sensation in the distribution of a single branch suggests a peripheral nerve lesion (V1 / V2 / V3), while complete loss of sensation on one side suggests a CNS lesion.
    • V - Facial Sensation & Jaw Muscles
    • Muscles of Mastication

    • Ask the patient to clench their teeth, and palpate the muscles of mastication. Ask the patient to open their mouth against resistance. Weakness of the muscles of mastication may be a sign of a lesion affecting the mandibular branch of the trigeminal nerve (V3), however may also occur due to an upper motor neuron lesion.
    • Jaw Jerk

    • The jaw jerk involves the mandibular branch of the trigeminal nerve (V3) as both its afferent and efferent arms. Place a finger horizontally over the chin with the mouth open, and then strike this finger with a tendon hammer. While a slight jerk may be normal, an exaggerated jerk is a sign of an upper motor neuron lesion.
    • Corneal Reflex

    • Always offer to perform the corneal reflex, however avoid this test if possible because it is very unpleasant. To test the corneal reflex, lightly touch the cornea from the side with a piece of cotton wool. Look for blinking in response to touching the cornea; lack of blinking is a sign of pathology somewhere along the reflex pathway.
    • Glabellar Tap

    • In patients with suspected Parkinsonism, perform the glabellar tap. Percuss repeatedly between the eyebrows, looking for reactive blinking. Up to five blinks are normal, however lack of habitualisation is a sign of frontal damage or Parkinsonism.

VII - Facial Movement

  • The facial nerve (VII) provides somatic motor supply for facial expression; somatic sensory supply to the external ear; taste to the anterior ⅔ of the tongue; and parasympathetic innervation of several salivery and lacrimal glands.
    • Assess for Facial Weakness

    • Inspect the patient’s face, looking for facial asymmetry, facial spasm or blepharospasm (spasm of the eyelid muscles).
  • Ask the patient to raise their eyebrows, close their eyes, puff out their cheeks and then show their teeth. Apply resistance if the movement appears to be weak. 
  • It is important to remember that eyebrow-sparing facial weakness is a sign of an upper motor neuron lesion, while eyebrow involvement is classically a sign of a facial nerve lesion - particularly Bell’s palsy or Ramsay-Hunt syndrome (herpes zoster).

VIII - Hearing

  • The vestibulocochlear nerve (VIII) supplies special sensory innervation providing feedback on both equilibrium (vestibular system) and hearing (cochlea).
  • Hearing loss may be conductive, due to external autory canal or middle ear pathology; or sensorineural, due to cochlear or neurologic pathology. The Weber and Rinne tests are used to distinguish between these two types.
    • Weber’s Test

    • The Weber test uses conduction of sound via the forehead to determine the type of hearing loss present. Place a 256hz tuning fork onto the centre of the patient's forehead, and ask whether they can hear the vibration. If heard, ask on which side the vibration is louder. If the vibration is louder in the deaf ear, then this suggests conductive hearing loss; if the vibration is louder in the normal ear then this suggests sensineural loss.
    • Rinne’s Test

    • The Rinne test compares sound heard through the ears with sound conducted via the mastoid process. Place a 256hz tuning fork onto the patient's mastoid process, and ask them to indicate when they can no longer hear the vibration. Then move the tuning fork in from of the auditory meatus and ask them whether they can still hear the sound.
  • If the sound is louder via the auditory meatus, then this is normal or may occur in patients with sensorineural hearing loss. If the sound is louder via the mastoid process, then this suggests conductive hearing loss.

IX & X - Throat

  • The glossopharyngeal nerve (IX) and vagus nerve (X) serve multiple somatic, visceral and special sensory functions. Together, they provide motor and sensory supply to the pharynx.
    • Hoarseness  & Cough

    • Listen for hoarseness while the patient speaks, and ask them to cough. A hoarse voice (also known as dysphonia) or a hoarse cough may be a sign of a vagus (X) nerve lesion, however there are many causes for these findings.

XI - Neck & Shoulders

  • The accessory nerve (XI) supplies motor innervation to laryngeal and pharyngeal muscles; the sternocleidomastoid; and the trapezius.
    • Inspect for Torticollis

    • Look for twisting of the head and neck toward a shortened sternocleidomastoid, with rotation of the chin in the opposite direction.
    • Assess the SCM and Trapezius

    • Ask the patient to turn their head against resistance (sternocleidomastoid), and then shrug their shoulders against resistance (trapezius). This tests the two major muscle groups supplied by the accessory nerve.

XII - Tongue

  • The hypoglossal nerve (XII) provides motor innervation to the intrinsic and extrinsic tongue muscles.
  • Ask the patient to open their mouth, without protuding the tongue. Look for wasting and fasciculations of the tongue.
  • Next ask the patient to protrude their tongue, looking for tongue deviation, and then ask them to move their tongue to either side. Deviation of the tongue may be a sign of ipsilateral hypoglossal nerve palsy, though may also occur with a contralateral upper motor neuron lesion, motor neurone disease or trauma.

Finishing Up

  • Thank the patient, turn around and present your findings.
  • Depending on findings, you may offer to perform an upper or lower limb examination looking for signs to confirm your suspicion.
  • Try to localise the patient’s lesion - e.g. to the cerebrum, cerebellum, brainstem, spinal cord, dorsal nerve root, peripheral nerve, neuromuscular junction or muscle. This can be difficult to begin with but with experience, signs will begin to become constellations characteristic of specific lesions.
Last updated on February 7th, 2020
 
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