Cranial Nerve Examination

Examination of the Cranial Nerves:

The first thing in learning how to examine the cranial nerves is to learn what they are and have a system for examining them that you do every time you do a cranial nerve examination. Then with practice it becomes second nature:

CN I- olfactory nerve

CN II- optic nerve

CN III- oculomotor nerve

CN IV- trochlear nerve

CN V- trigeminal nerve

CN VI- abducens nerve

CN VII- facial nerve

CN VIII- vestibulocochlear nerve

CN IX- glossopharyngeal nerve

CN X- vagus nerve

CN XI- spinal accessory nerve

CN XII- hypoglossal nerve

Anatomical Landmarks:

Where each cranial nerve exits the skull:
Cribriform plate- olfactory nerve
Optic canal- optic nerve
Superior orbital fissure- oculomotor, troclear, abducens and ophthalmic division of trigeminal nerve
Foramen rotundum- maxillary division of trigeminal nerve
Foramen ovale- mandibular division of trigeminal nerve
Internal auditory meatus- facial and vestibulocochlear nerves
Stylomastoid foramen- main portion of the facial nerve
Jugular foramen- glossopharyngeal, vagus and spinal accessory nerves
Hypoglossal canal- hypoglossal nerve

Cranial Nerve I- Olfactory nerve

Sense of smell or olfaction.

Important anatomical concepts:

  1. Olfactory sensation is perceived in the limbic system which includes the amygdala, hippocampus and uncus.
  2. Patients with anosmia often report a decreased taste sensation because of the important contribution of olfaction to the perception of flavour.

How to test it:

The sense of smell is tested using a non-pungent stimulus such as a mild perfume. It is important to test each nostril separately.

Patterns of abnormality:

  1. Unilateral anosmia may signify a meningioma of the olfactory groove.
  2. Bilateral anosmia is seen in inflammation of the nasal mucosa such as rhinitis or the common cold.
  3. Parkinson disease- one of the earliest signs of Parkinson disease is anosmia.
  4. This occurs because dopamine is one of the neurotransmitters involved in the olfactory bulb.
  5. Loss of sense of smell can also be caused by head trauma which damages the olfactory nerves as they penetrate the cribriform plate of the ethmoid.
  6. Foster-Kennedy syndrome- large lesion of the olfactory sulcus region (typically a meningioma) can cause anosmia together with optic atrophy on one eye because of the ipsilateral tumour compression and contralateral papilloedema due to the raised intra-cranial pressure.

Cranial Nerves II, III, IV and VI are all dealt with in the section on examination of eyes.

Cranial Nerve V- Trigeminal nerve


  1. Sensation to the face, forehead, part of the oral mucosa and a large part of the meninges- divided in to the ophthalmic, maxillary and mandibular divisions.
  2. Motor function to the muscles of mastication- temporal muscle, masseter and pterygoids. Also gives motor innervation to the tensor tympani muscle.
  3. Jaw jerk
  4. Corneal reflex

Important anatomical concepts:

  1. For the sensory nerve- the ophthalmic division shares a border with the greater occipital nerve of cervical origin at the vertex of the head. The mandibular nerve shares a border with the third cervical nerve at the chin.
  2. Each branch of the trigeminal nerve synapses in the semilunar ganglion which is the primary sensory neuron for the trigeminal nerve. Therefore, if there is a lesion at the semilunar ganglion sensation from all of the side of the face will be affected. After leaving the semilunar ganglion the fibres divide in to those concerned with nociception and those with tactile sensation.
  3. The spinal nucleus of the trigeminal nerve is where the nociceptive fibres synapse and the trigeminothalamic tract originates. The main sensory nucleus of the trigeminal nerve is where sensory fibres concerned with tactile sensation on the face synapse and then join the medial lemniscus.
  4. The mesencephalic nucleus is where proprioception from the muscles of mastication is mediated. This nucleus is also important in the afferent arc of the jaw jerk.
  5. The motor nucleus of the trigeminal nerve is bilaterally innervated by the corticobulbar tract. Therefore, a unilateral lesion of the corticobulbar tract does not cause paralysis of the masticatory muscles.
  6. Jaw jerk- the afferent impulse is triggered by contraction of the masseter muscle spindle and travels along the mandibular nerve to the mesencephalic nucleus of the trigeminal nerve. There the impulse is reflected through its efferent axon and monosynaptically transmits to the ipsilateral motor nucleus of the trigeminal nerve which then causes contraction of the masseter muscle.
  7. Corneal reflex- polysynaptic reflex. Afferent limb formed by the trigeminal nerve, efferent by the facial nerve. A nociceptive impulse from the cornea is transmitted through the ophthalmic nerve to the spinal nucleus of the trigeminal nerve. The impulse arising from this is transmitted to the ipsilateral as well as contralateral facial nucleus causing bilateral eye closure.

How to test it:

Sensory nerve- Pain, temperature and tactile sensation are tested in each division and compared to the other side. As this nerve also supplies the oral mucosa it is important to also ask about numbness of the mouth or tongue. Maxillary nerve for the upper half and mandibular nerve for the lower half of the oral mucosa.

Motor nerve- Observe volume of the masticatory muscles. Palpation of these muscles with the teeth clenched may also reveal some atrophy. Ask the patient to open the mouth. In unilateral paralysis of the lateral pterygoid muscle the jaw will deviate towards the weakness.

Jaw jerk- The jaw is tapped downwards while the mouth is kept slightly open. The response can be seen as jaw elevation or contraction of the masseter. This reflex is of more clinical use when it is exaggerated. This is because it can be difficult to elicit even in normal subjects. Enhancement of this reflex suggests hyperexcitability of motor neurons in the motor nucleus of the trigeminal nerve in the pons. This can occur because of bilateral lesions of the corticobulbar tracts or impairment of the upper motor neurons innervating those motor nuclei. Enhancement of the jaw jerk in the context of other bulbar symptoms suggests a pseudobulbar palsy.

Corneal reflex- A twisted string of tissue is used to gently touch the cornea from the lateral visual field and the response can be judged by observing closure of the eyelids. Touching the sclera will not elicit the response as there are no nociceptive fibres on the sclera.

Patterns of abnormality:

Disorders of the trigeminal nerve are quite uncommon except for trigeminal neuralgia. In this case the examination of sensation on the face will be normal. There is often no cause found for this but it can be a presentation of multiple sclerosis. Sensory loss in the distribution of the trigeminal nerve warrants a brain scan. A lesion of the trigeminal nuclei in the brainstem causes ipsilateral sensory loss on the face as the primary sensory fibres do not cross before entering the nucleus. A lesion of the trigeminal nucleus in the pons often also affects the spinothalamic fibres so this causes ipsilateral loss of sensation on the face and contralateral loss on the body.

Cranial Nerve VII- Facial nerve.


  1. Main branch- Motor function to the muscles of facial expression.
  2. Nervus intermdius (one of the branches) carries fibres for parasympathetic (tears and salivation), visceral sensory (taste) and general somatosensory functions.
  3. Taste sensation to the anterior 2/3 of the tongue
  4. Parasympathetic input to the salivary and lacrimal glands.
  5. Somatosensory branches provide sensation to the inner aspect of the earlobe and external auditory meatus.

Important anatomical concepts:

  1. Lesions of the cortex or corticobulbar tracts cause contralateral face weakness that spares the forehead.
  2. Lesions of the facial nucleus, nerve fascicles in the brainstem or peripheral nerve cause ipsilateral weakness of the entire side of the face- this most commonly occurs in Bells palsy. Other associated symptoms with a lower motor neuron Bells palsy would include reduced lacrimation (from interruption of the parasympathetic fibres) and hyperacusis (from stapedius muscle weakness).
  3. Ramsay-Hunt syndrome is where the geniculate ganglion (which is the primary sensory ganglion for the facial nerve) is inflamed- usually in the context of varicella zoster infection. Here there will be a lower motor neuron facial nerve palsy in addition to a vesicular rash in the inner ear lobe and the external auditory meatus associated with neuralgia, numbness and sensory loss in that region.
  4. The facial nerve travels alongside the abducens nerve through the cerebellopontine angle before reaching the internal auditory meatus where it then travels with the vestibulocochlear nerve.
  5. There are 5 main branches- the temporal, zygomatic, buccal, mandibular and cervical branches. There are a few smaller branches innervating a few small muscles.
  6. Parasympathetic fibres go from the superior salivatory nucleus to the sphenopalatine ganglion and from there to the lacrimal glands and the nasal mucosa.
  7. It is the chorda tympani branch that joins the lingual nerve and synapses in the submandibular ganglion to then send parasympathetic fibres to the salivary glands.

How to test it:

Firstly observe the face for any asymmetry.

Then ask the patient to close the eyes shut tightly and raise the eyebrows- you can test the strength gently by asking the patient to keep the eye closed as you gently try and open it. Ask the patient to show you their teeth or blow out their cheeks.

Do not ask the patient to smile in testing muscles of facial expression as the mimetic muscles employed for laughing and crying are also controlled by the basal ganglia, hypothalamus and cingulate gyrus.

Taste can be tested with sugar and salt on each side of the tongue although this is not routinely tested at the bedside.

The sensory branches are not tested routinely in the clinical setting. It is just important to know the area that may become involved in a Ramsay-Hunt syndrome.

Similarly, the parasympathetic function can really only be tested by the shirmer test to measure adequate lacrimation.

Patterns of abnormality:

  1. Upper motor neuron facial nerve palsy- spares the forehead. Seen most commonly in a stroke. Assess for associated symptoms such as involvement of arm or speech etc.
  2. Lower motor neuron facial nerve palsy- involves entire half of face including forehead. Look in the external auditory meatus for lesions that may be seen in Ramsay Hunt syndrome.
  3. Millard-Gubler syndrome- this is a combination of a unilateral lower motor neuron facial nerve palsy and a contralateral hemiplegia. This is due to an intramedullary lesion in the pons.
  4. Bilateral facial paralysis is uncommon but if seen the following causes need to be considered- sarcoidosis, Lyme disease or leprosy.

Cranial Nerve VIII- Vestibulocochlear nerve


  1. Hearing- through the cochlear portion of the nerve
  2. Balance- through the vestibular portion of the nerve

Important anatomical concepts:

  1. Unilateral hearing loss is not seen in lesions in the central nervous system proximal to the cochlear nuclei- auditory information ascends bilaterally in the brainstem.
  2. The cochlea is supplied by CN VIII to modulate the sensitivity of the hair cells in response to sounds of varying intensities. Reflex pathways from the vestibular nuclei project to the facial and trigeminal nuclei to contract stapedius (CN VII) and tensor tympani (CN V) muscles to dampen the response of the middle ear to loud sounds.
  3. Vestibular pathways are important for adjustment of posture, muscle tone and eye position in response to movements of the head in space.

How to test:

  1. Hearing can be tested with various sounds such as whispering or a ticking watch. However, the standard would be to use a tuning fork.Rinnes test is where you place a vibrating tuning fork on the mastoid process and then move it to outside the external auditory canal and ask the patient at which point it is louder? It should be louder in front of the external auditory canal as air conduction should be louder than bone conduction.Webers test is where the vibrating tuning fork is placed in the centre of the forehead and the patient is asked to which side is the sound louder? This test is interpreted with the Rinne test. If the sound localizes to the right ear for example this means there is either conductive hearing loss in the right ear or sensorineural hearing loss in the left ear.
  2. Dix-Hallpike positional testing is a useful exam that can help distinguish peripheral from central causes of dizziness. Here the patient sits at the edge of the bed. The examiner gently but rapidly brings the head towards the edge of the bed and turns to one side so one ear is down and the head extends over the edge of the bed. The patient is asked to keep the eyes open and report any symptoms of vertigo. The examiner observes for any nystagmus. Then it is repeated to the other side. This test only needs to be done if the presenting complaint is one of vertigo. This is not part of the standard neurological examination. This test is used to distinguish between peripheral and central causes of vertigo. For a peripheral cause such as benign paroxysmal positional vertigo the dizziness comes on around 2- 5 seconds after head turning. For central causes it comes on immediately.
  3. Vestibulo-ocular reflex- this reflex is mediated through the medial and superior vestibular nuclei and medial longitudinal fasciculus to the abducens, oculomotor and trochlear nuclei. The VOR allows eye movements to adjust for the changes in head position- it is described in the section on eye movements.
  4. March test- patients are asked to step with the eyes closed and arms out in front. Rotation by more than 45 degrees is abnormal. The rotation usually occurs to the side of the lesion.

Patterns of abnormality:

  1. Unilateral hearing loss can occur as a result of a lesion of the external auditory canal, middle ear, cochlea, 8th nerve or cochlear nuclei.
  2. Conductive hearing loss- lesion of external auditory canal or middle ear. Here the patient will hear the sound louder with the tuning fork on the mastoid process than in front of the external auditory canal. The most common causeof conductive hearing loss is wax in the ear. Other causes could be otitis, tympanic membrane perforation and sclerosis of the middle ear ossicles.
  3. Sensorineural hearing loss- lesion of the cochlea or 8th nerve. Causes of sensorineural hearing loss include exposure to loud sounds, meningitis, ototoxic drugs, head trauma, viral infections, ageing, Menieres disease andcerebellopontine angle tumours.
  4. With an acoustic neuroma the most common first symptom will be unilateral deafness, tinnitus and unsteadiness as CN VIII is compressed in the cerebellopontine angle. The next nerve to be compressed as it grows is the trigeminal causing facial pain and sensory loss. There may be a subtle decrease in the corneal reflex. Only large tumours compress the facial nerve so facial weakness tends to be a much later symptom.
  5. Dizziness is a very commonly encountered though non-specific symptom. It is firstly important to distinguish if it is dizziness as in room spinning versus lightheadedness as in the feeling of pre-syncope. Then when you have established that it is dizziness the next thing to decide is if it is due to peripheral or central causes. For peripheral causes dizziness may be the only symptom or there may be associated tinnitus or deafness. For central causes pay close attention to any accompanying symptoms or signs such as diplopia, sensory symptoms, weakness, dysarthria, impaired coordination or impaired consciousness. If any of these symptoms are present then urgent brain imaging looking at the brain stem and cerebellum is warranted.

Cranial Nerve IX: Glossopharyngeal Nerve


  1. Motor supply to the stylopharyngeus muscle- this elevates the pharynx during talking and swallowing and contributes to the gag reflex (afferent limb).
  2. Parasympathetic supply to the parotid glands.
  3. Sensation from the middle ear, region near the external auditory meatus, pharynx and posterior 1/3 of tongue.
  4. Taste from the posterior 1/3 of tongue.
  5. Chemoreceptors and baroreceptors of carotid body.

Cranial Nerve X: Vagus Nerve


  1. Motor supply to pharyngeal muscles, upper oesophageal muscles and laryngeal muscles.
  2. Recurrent laryngeal nerve is a branch of the vagus nerve that supplies all of the intrinsic muscles of the larynx except the cricothyroid.
  3. Gag reflex (efferent limb).
  4. Sensation from pharynx, meninges and a small portion near the external auditory meatus.
  5. Parasympathetic fibres of the vagus nerve innervate the visceral organs such as cardiovascular system, bronchus and lung, oesophagus, small intestine, large intestine proximal to the middle of the transverse colon, liver, gallbladder, pancreas and others. This nerve plays a huge role in blood pressure control.
  6. General visceral sensation is also conveyed to the central nervous system through the vagus nerve- for examples the feelings of satiety and hunger.

Cranial Nerve XII: Hypoglossal Nerve


  1. Motor innervation to all tongue muscles, except for palatoglossus which is supplied by the vagus nerve.

How to test:
Cranial nerves IX, X and XII are all tested together.

  1. Examination of the tongue- Observe for muscle atrophy and/or fasciculations. If it is unilateral it suggests a lesion of the ipsilateral medulla or hypoglossal nerve.
  2. The gag reflex is elicited by stroking the posterior pharynx with a cotton swab.
  3. Soft palate function can be assessed by asking the patient to say “ah” as you observe for elevation of the soft palate with a pen light.
  4. For testing phonation you can ask the patient to repeat the same sound such as mi-mi-mi for a labial sound, ga-ga-ga for a palatal sound and la-lala for a lingual sound.
  5. This is also a good time to observe for palatal myoclonus which can be seen in certain types of stroke (involving Guillain-Mollaret triangle) or in genetic conditions such as Alexander disease.

Important anatomical concepts:

  1. In a unilateral hemispheric lesion the tongue will protrude to the contralateral (weak) side. Lesions of the hypoglossal nucleus and exiting fascicles cause ipsilateral tongue weakness. The tongue will deviate to the weak side. This is because the genioglossus muscle receives unilateral innervation from the contralateral motor cortex.
  2. In a unilateral lesion of cranial nerve X or the nucleus ambiguous the uvula and palate will deviate toward the normal side while the soft palate on the abnormal side hangs abnormally low.
  3. The nucleus ambiguus and hypoglossal nucleus both receive bilateral innervation from the motor cortices and so a unilateral lesion should not cause dysphagia and dysarthria. In vascular lesions there may still be mild dysphagia- this owes to the hypothesis of hemisphere dominance for swallow.
  4. When blood pressure drops it is sensed through the baroreceptors which signal the vagus nerve to decrease parasympathetic outflow and thereby increase heart rate and in turn this normalizes the blood pressure. The opposite happens when the baroreceptors sense a decrease in blood pressure.
  5. Injury to the recurrent laryngeal nerve can occur during surgery of the neck such as carotid endarterectomy, cervical disc surgery or thyroid surgery or during cardiac surgery as the left nerve loops around the aorta. This nerve can also be damaged by apical lung tumours during its looping course through the upper thoracic cavity. When damaged it produces vocal cord paralysis and hoarseness.
  6. Brainstem nuclei involved in laughing and crying include CN VII, IX, X and XII. Lesions of corticobulbar pathways in the subcortical white matter or brainstem can occasionally produce a bizarre syndrome called pseudobulbar affect. Here patients will exhibit uncontrollable bouts of laughter or crying without feeling the usual associated emotions. This may be likened to an “upper motor neuron” disorder in which there is abnormal reflex activation of laughter and crying circuits in the brainstem leading to emotional incontinence.

Patterns of abnormality:

  1. The tongue deviates to the weaker side.
  2. The uvula and soft palate deviate toward the normal side and the soft palate on the abnormal side hangs low.
  3. A bulbar palsy is manifested by dysarthria and dysphagia that is associated clinically with tongue atrophy and fasciculations and a normal jaw jerk.
  4. A pseudobulbar palsy causes similar symptoms (dysphagia and dysarthria) without the tongue atrophy or fasciculations and will usually be associated with a brisk jaw jerk. The term comes from the fact that it looks like a lesion of the medulla but it is not- it is a lesion of the corticobulbar tracts that synapse at the medulla- in effect it is an upper motor neuron problem with the corticobulbar pathways.

Cranial Nerve XI- Spinal Accessory Nerve:


Motor supply to the sternocleidomastoid and upper trapezius muscles. The left sternocleidomastoid turns the head to the right and vice versa for the right muscle. When both sternocleidomastoid muscles are contracted together they extend the neck.

Important anatomical concepts:

  1. This nerve arises from the upper five or six segments of the cervical cord.
  2. The sternocleidomastoid is considered to be innervated by the ipsilateral motor cortex. There may be bilateral innervation. Upper motor neuron lesions that would involve this nerve will cause contralateral trapezius weakness and spare the sternocleidomastoid muscles.
  3. The spinal accessory nerve lies in the posterior triangle of the neck and is susceptible to injury by lymph node biopsies in the neck.

How to test it:

For the sternocleidomastoid- ask the patient to turn the head to the right against resistance to assess the left sternocleidomastoid and then the left for the right sternocleidomastoid.

For trapezius- ask the patient to shrug the shoulders against resistance.

Patterns of abnormality:

  1. A biopsy of a cervical lymph node in the neck can damage the spinal accessory nerve. The lesion will be distal to the branch that goes to the sternocleidomastoid. There will be drooping of the shoulder at rest.


The Neurologic Examination. Scientific basis for clinical diagnosis. Shibasaki H and Hallett M.

Neuroanatomy through clinical cases. Blumenfeld H.

Cranial Nerve Examination

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