• cranial nerves;
  • examination;
  • neurological


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  2. Abstract
  3. Supporting Information

Examination of the cranial nerves is an integral and important part of a complete neurological examination. Historically, these skills were crucial for diagnosing specific lesions. With the development of modern imaging modalities, the significance of clinical examination techniques has perhaps been undermined. The authors present an overview of each cranial nerve with a concise summary of examination techniques. Clin. Anat. 27:25–30, 2014. © 2013 Wiley Periodicals, Inc.

Medicine is a Science of Uncertainty and an Art of Probability

(William Osler)

Examination of the cranial nerves is an integral and important part of a complete neurological examination. Historically, these skills were crucial for diagnosing specific lesions. This made diagnostic medicine an art of “probability” and treatment during those early years “a science of uncertainty.” With the development of modern imaging modalities, the significance of clinical examination techniques has perhaps been undermined. In particular, skills in neurological examination are often considered challenging to learn by medical students and junior clinicians. However, a systematic and consistent approach allows a complete and thorough examination to be performed in a timely manner. The authors present an overview of each cranial nerve with a concise summary of examination techniques.

Olfactory Nerve (CN I)

Anatomy snapshot

As the name implies, the olfactory nerve serves the sense of olfaction or smell. Its fibers arise in the mucous membranes of the nose and pass through the cribriform plate of the ethomoid bone to synapse in the olfactory bulb. From here, the olfactory tract follows the ventral surface of the frontal lobe and ends in the olfactory trigone. The olfactory tract lies in the olfactory sulcus on the orbital surface of the frontal lobe. Most axons follow the lateral olfactory stria and end in the pyriform cortex (uncus, entrohinal area, and limen insulae). The medial olfactory striae terminate in the anterior olfactory nucleus and in the region of the anterior perforated substance. Olfaction is the only sensation not directly connected to the thalamus. It is important to note that the true neural networks subserving olfaction are probably much more complex as olfaction is closely integrated with memory, emotions and alimentary pleasures.


Testing of olfaction is often overlooked in clinical examination. Anosmia can be the only localizing sign of lesions in basi-frontal areas compromising the olfactory pathways. It should be noted that anosmic patients do not always complain about loss of smell, but rather about altered taste.

The clinical examination begins with assessing the external appearance of the nose to look for any obvious deformity. One nostril should be occluded to facilitate separate testing of each side. While a range of products can be used for testing, it is more practical to use commonly accessible items such as coffee, orange peel, vanilla etc. Noxious stimuli are detected by sensory fibers of the trigeminal nerve and pungent smells are best avoided. If anosmia is detected, an examination of the nasal passages should be considered to rule out nasal polyps and mucosal thickening. Common causes of anosmia include respiratory tract infection, increasing age, head injury, olfactory groove meningioma and following meningitis.

Optic Nerve (CN II)

Anatomy snapshot

This is a purely sensory nerve. It is a unique fiber pathway and not a peripheral nerve and it connects the retina to the brain. The first order neurons are activated by the rods and cones in the retina, the true peripheral nerves in this instance. These bipolar cells synapse with ganglion cells, which converge to the optic disc and form the optic nerve. Each optic nerve passes through the optic canal and joins its counterpart to form the chiasm. The spatial orientation of fibers from different parts of the fundi is preserved so that fibers from the lower part of the retina are found in the inferior part of the chiasm and vice versa. Of note, the papillomacular bundle, which originates in the peripheral portions of the optic nerve located slightly inferior and lateral, becomes more centrally located at the level of the chiasm. Fibers from the temporal visual field cross over at the chiasm but fibers from the nasal fields do not. From the chiasm the optic tract reaches three destinations: (1) the lateral geniculate body for relay to the visual cortex in the occipital cortex; (2) pretectal nuclei for papillary reflexes to light; and (3) the superior colliculi for body reflexes to light.

The optic radiation from the lateral geniculate body divides before reaching the visual cortex. The fiber tracts that originate from the upper retinal quadrants pass through the internal capsule and course within the parietal and occipital lobes to terminate on the cuneus. The lower retinal fibers pass through the internal capsule and sweep around the temporal horn of the lateral ventricle forming Meyer's loop, eventually terminating in the lingual gyrus.


Each eye should be tested separately in assessments of visual acuity, visual fields, and fundoscopy.

Visual acuity

As refractory errors are not part of cranial nerve examination, the patient should use any optical aids to which they are accustomed. A hand-held eye chart or a Snellen chart can be used. During the examination, one eye should be completely covered with a small card. The examiner should be mindful that patients with impaired vision may tend to turn their head, thus inadvertently looking with the covered eye. Depending on the Snellen chart used, the patient should be tested at a distance of 20 feet (6 m) or 10 feet (3 m). The patient is asked to read progressively smaller letters until consistent perception is no longer possible. In a patient who has uncorrected visual acuity of less than 20/20 (6/6) vision, the pinhole test can be performed using a piece of cardboard with a tiny (2 mm) perforation. Improved vision indicates refractory error. If a patient is unable to read the largest letters on the chart, he or she should be asked to count fingers held up in front of them. Failing this, recognition of hand movement is tested. In cases of severe visual impairment, light perception should be tested using a pen torch.

Visual fields

Visual fields can be examined by confrontation using the examiner's finger or colored pen, but a red pen allows a more detailed assessment to be made. Using a waggling finger can reduce the sensitivity of the test in the peripheral field and can fail entirely to assess the central fields (Fig. 1).


Figure 1. CN II lesions and associated visual field deficits.

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The examiner should ensure that his/her line of sight is level with that of the patient. The patient is instructed to look directly at the examiner's eye while the nontested eye remains covered with a piece of cardboard (or the patient's hand). The red pen should be brought in from four directions diagonally towards the center of the visual field. The patient should state when the colored pen becomes clearly detectable. As this examination relies on comparative evaluation, the examiner should ensure that the red pen is always equidistant from each individual. An enlarged blind spot can also be mapped by asking about disappearance of the pen around the center of the field of vision, but this can be more challenging to test.


Fundoscopic examination is performed using the ophthalmoscope to assess the optic disc and retina while the patient is looking into the distance. Regular practice is required to achieve competence, particularly when examining patients with undilated pupils.

Oculomotor, Trochlear, and Abducens Nerves (CN III, IV, and VI)

Anatomy snapshot

Cranial nerves III, IV, and VI provide motor innervations to extra-ocular muscles. The oculomotor nucleus is situated in the periaqueductal gray at the level of the superior colliculus. The oculomotor nerve provides somatic motor inputs to all the extra-ocular muscles except the lateral rectus (abducens nerve) and superior oblique (trochlear nerve). Pupil size depends on a balance between sympathetic (midriasis) and parasympathethic (miosis) tone. The parasympathetic innervation is through the Edinger Westphal nucleus located dorsal to CN III. Preganglionic parasympathetic fibers travel to the ciliary ganglion where postganglionic fibers relay to the pupil and ciliary muscle. Sympathetic innervation to the eyes travels from the hypothalamus via the ciliospinal center in the spinal cord at C8, T1, and T2 to the superior cervical ganglion in the neck. From here the sympathetic fibers travel with the internal carotid artery into the cavernous sympathetic plexus. This in turn travels within the ophthalmic division of the trigeminal nerve to innervate the eye through the long and short ciliary nerves. Of note, the sympathetic plexus also innervates the tarsal muscles and the orbital muscle of Müller.

The trochlear nerve (CN IV) is located immediately beneath and lateral to the occulomotor nerve in the mesencephalon. The fibers decussate in the anterior medullary velum of the aqueduct of Sylvius. They then travel forward to pierce the dura, which forms the lateral wall of the cavernous sinus, below the oculomotor nerve.

The abducens nerve (CN VI) arises from the pons ventral to the fourth ventricle. Its fibers emerge ventrally between the pons and medulla, and then ascend between the pons and the clivus. Dorello's canal channels the nerve towards the cavernous sinus where the nerve courses in close proximity to the carotid artery.



The size, shape, and symmetry of pupils should be noted on inspection. An irregular pupil can suggest previous surgery or traumatic injury. Direct and indirect pupillary responses to light should be elicited. The direct response is the constriction that occurs when the pupil is exposed to light. The consensual or indirect response refers to the simultaneous constriction of the opposite pupil. The torch should be moved in an arc from pupil to pupil to assess for an afferent pupillary defect. This is also known as the Marcus Gunn sign, where the affected pupil dilates paradoxically after a short time when the light source is moved from a normal to an abnormal eye.

The light reflex and resting pupil size are dependent on light perception by at least one eye. If both eyes are blind owing to a lesion anterior to the lateral geniculate bodies, both pupils will be fixed and nonreactive to light. If blindness is secondary to destruction of the visual cortex the light reflex will be preserved.

Accommodation refers to the pupillary constriction that occurs as the patient attempts to converge his or her eyes. To test this, the patient is initially asked to look into the far distance and then asked to focus on the tip of his or her nose. Causes of an absent light reflex with an intact accommodation reflex include a midbrain lesion or a ciliary ganglion lesion. In very rare cases, failure of accommodation only can occur after a midbrain lesion or cortical blindness.

Eye Movements

Failure of movement, diplopia and nystagmus are assessed in this examination. The examiner should be 30–40 cm in front of the patient and a hat pin should be moved in an “H” pattern. Patients should be asked to follow the target with their eyes without moving their heads. Look for failure of movement and ask about diplopia. If any abnormity is detected, each eye should be tested individually.

Diplopia is an early sign of extraocular muscle weakness. The false image is usually paler, less distinct and more peripheral. The patient should be asked if the images are side by side or one above the other. A side by side position indicates only the lateral and medial recti are involved. To assess the muscles involved, the direction in which image separation is maximal should be established. Image separation is greatest in the direction of the purest muscle action of the weak muscle. At the point of maximal image separation, cover one eye. Disappearance of the false image indicates that the covered eye is responsible.

Table 1. Common Mistakes in Cranial Nerve Examination
Cranial NerveCommon Mistakes in Examination
IOnly use easily recognizable agents like coffee, rosewater
IIDo not forget to inquire about eye glasses and use them
III, IV, VIExamination is performed too close to the patient; Target moves too fast during examination; Patient is allowed to move head
VConjunctiva is touched instead of cornea; Corneal reflex can be mildly inhibited in contact lens wearers; Movement of the examiner triggers reflex blinking
VIIPtosis is not due to weakness of facial paresis
VIIIAlways inspect the ear for hearing aids, scars etc
IX,X-Be mindful of aspiration risks when testing swallowing
XII-Facial paresis or asymmetry may give the misleading impression of an asymmetrical tongue during protrusion

Trigeminal Nerve (CN V)

Anatomy snapshot

The trigeminal nerve is the largest cranial nerve and has both sensory and motor fibers. It emerges from the pons and runs within the cerebellopontine angle. At the petrous temporal bone, it forms the trigeminal ganglion housed within Meckel's cave. The trigeminal ganglion gives rise to three divisions. The ophthalmic division (V1) runs within the lateral wall of the cavernous sinus to enter the orbital fissure superior to supply the skin of the forehead and the cornea and conjunctiva. The maxillary division (V2) supplies the skin in the middle of the face, mucous membranes in the upper part of the mouth palate and the nasopharynx. The mandibular division (V3) runs with the motor part of the nerve and leaves the skull through the foramen ovale to supply the skin of the lower jaw and muscles of mastication (temporalis, masseter, pterygoids).


The three trigeminal divisions are tested using a cotton wool ball and blunt tip needle sequentially on the forehead, malar eminence and lower face over the mandible, while comparing sides. Loss of pain sensation will result in the pin prick feeling dull. The area of dullness should be mapped. Light touch can be tested with cotton wool, but temperature is rarely tested except in syringobulbia.

Corneal reflex testing is simple to perform but potential problems must be recognized. The assessor should ideally be positioned to the side or behind the patient to avoid a blink reflex, which can be triggered by sudden movements in the patient's visual field. A wisp of cotton is used to touch the cornea gently while the patient is gazing towards the distance. The examiner should ask if the patient felt the corneal contact and look for blinking in both eyes. Reflex blinking of both eyes is a normal response. If blinking occurs only in the contralateral eye, this can indicate ipsilateral seventh nerve palsy.

The motor component of the trigeminal nerve can be assessed by examining the function of the temporalis, masseteric and pterygoid muscles. With the patient clenching, the temporalis and masseteric muscles are palpated to assess for tone and muscle bulk. The strength of these muscles can be tested by asking the patient to bite on a wooden tongue depressor. The depth of the bite marks can be used to assess muscle strength. The patient can also be asked to hold the mouth open while the examiner attempts to force it shut. This test assesses the strength of the pterygoid muscles.

An exaggerated jaw reflex can be a valuable sign indicating an upper motor neuron lesion. After an index finger is placed on the chin and a tap with the tendon hammer elicits any reflex. Normally there is slight closure of the mouth or no reflex at all.

Facial Nerve (CN VII)

Anatomy snapshot

The facial nerve is predominantly a motor nerve with parasympathetic and sensory components. The sensory division is separate from the motor division and is sometimes referred to as the “nervus intermedius.” The motor nucleus is located ventral and medial to the abducens nucleus in the pons. The fibers then loop around the abducens nucleus before exiting the ponto-medullary junction with the eighth cranial nerve to enter the internal acoustic meatus above the eighth nerve. After entering the facial canal the nerve enlarges to become the geniculate ganglion. The corda tympani, which contain the taste fibers from the anterior two thirds of the tongue, join the nerve in the facial canal. The facial nerve exits the skull at the stylomastoid foramen and divides into its terminal branches within the parotid gland to supply the muscles of facial expression. The efferent parasympathetic fibers initiate salivation, lacrimation and mucous membrane secretion. These fibers travel in the corda tympani nerve to supply the submandibular, submaxillary, and lacrimal glands.


The facial nerve provides innervation for the muscles of facial expression. Close observation of a patient's face can yield the initial clues of asymmetrical expression (e.g., flattening of the nasolabial groove) in a patient with facial nerve palsy. The upper part of the face is relatively spared in facial paresis of an upper motor neuron pattern owing to bilateral cortical representation. This can be tested by instructing the patient to look upwards, which can exaggerate the wrinkling the forehead. Next, the patient should be asked to close both eyes tightly while the examiner attempts to force open each eye to test strength. To assess the muscles of expression in the lower face, the patient is asked to show his/her teeth and to “puff out” the cheeks, and then the cheeks are palpated to determine any difference in tone. A lower motor neuron lesion results in paresis/paralysis of all the ipsilateral facial muscles.

Unilateral upper motor neuron facial nerve paresis can commonly result from vascular lesions or tumors. A lower motor neuron pattern of facial paresis is seen in Bell's palsy, multiple sclerosis and tumors (e.g., meningiomas and vestibular schwannomas) that compress the facial nerve. Bilateral facial nerve weakness is uncommon. Causes include Guillain–Barre syndrome, sarcoidosis and bilateral parotid disease.

Vestibulocochlear Nerve (CN VIII)

Anatomy snapshot

This nerve is sensory, specialized for sound reception and balance. Fibers for hearing originate in the hair cells of the organ of Corti. They travel towards the bipolar cells of the spiral ganglion within the cochlea. The nerve emerges from the cochlea and passes through the internal acoustic meatus to enter the upper medulla at its junction with the pons. The fibers terminate in the cochlear nuclei located in the pons. Fibers for balance originate in the maculae of the utricle and saccule and the cristae of the ampullae of the semicircular canals. Impulses travel to the bipolar cells of Scarpa's ganglion. The vesibular nerve emerges through the internal auditory meatus to join the auditory fibers in the facial canal. The nerve eventually enters the brainstem at the ponto-medullary junction and relays in the vestibular nuclei.



Test one ear at a time. A simple test would involve blocking the contralateral ear with a finger and whispering numbers in the ipsilateral ear. Numbers such as 68 can be used to test for high tone and 100 for low tone. Whispering should be performed at the end of respiration at distance of 60 cm to standardize the examination. If any deficits are noted, Rinne's and Weber's tests are performed.

Rinne's test

A 256 Hz tuning fork is struck and placed on the mastoid process. The patient is requested to indicate when the sound is no longer audible. As soon as the sound is extinguished, the tuning fork is placed next to the external auditory meatus to assess whether it can be heard. In a patient with normal hearing, air conduction should be greater than bone conduction, so the patient should be able to hear the tuning fork next to the ear after it is no longer audible against the mastoid. With conductive deafness, the patient will not be able to hear the tuning fork when it is moved next to the external auditory meatus. In sensorineural deafness, the mastoid and external auditory meatus components are equally reduced.

Weber's test

A 256-Hz tuning fork is placed in the middle of the forehead and the sound is heard from there. In sensorineural deafness the sound is heard better in the normal ear. A patient with conduction deafness finds the sound louder in the abnormal ear.

Vestibular system

A bedside examination of the vestibular system is difficult to perform. This system can be assessed indirectly, without performing specialized tests such as Hallpike's maneuver, by assessing the patient's gait and looking for nystagmus.

Glossopharyngeal Nerve (CN IX)

Anatomy snapshot

As the name implies, this nerve originates from the medulla and innervates primarily the muscles of the tongue and pharynx. The nerve emerges from the medulla as three to six rootlets between the inferior olive and the inferior cerebellar peduncle. It exits through the jugular foramen within a separate dural sheath (lateral and anterior to CNs X and XI). The glossopharyngeal nerve then travels within the carotid sheath and ultimately terminates in the lateral pharyngeal wall. The nerve provides both sensory and motor innervations to structures in the glossopharynx. Efferent nerves innervate the stylopharyngeus muscle. Autonomic fibers supply the parotid gland and mucous membranes of the posterior inferior mouth and membranes through the tympanic nerve (Jacobson's nerve).

Afferent fibers arise from the retroauricular region with tactile, thermal and noxious stimuli from the mucous membranes of the posterior third of the tongue, the tonsils, and the Eustachian tube. Taste sensation is carried from the posterior tongue region. Hering's nerve, a special visceral afferent nerve, arises just below the jugular foramen. It innervates the carotid sinus and body and brings chemo- and baro-receptor inputs to the medulla. Together with collateral inputs via the vagal nerve, the glossopharyngeal-vagal reflex slows the heart rate or lowers blood pressure.


Clinical examination of the glossopharyngeal nerve is typically performed in conjunction with the vagus nerve, as separate testing is challenging. A unilateral lesion in the glossopharyngeal nerve can manifest as loss of the ipsilateral gag reflex, carotid body and sinus reflex and taste in the posterior region of the tongue. In practice, only the gag reflex is assessed. The examiner should explain the procedure thoroughly and state that it may be uncomfortable, so that the patient knows what is to be expected prior to testing. With a tongue depressor, the back of the throat is touched gently on one side. This normally triggers the gag reflex. If this is weakened or absent, the patient should be asked if the sensation was felt equally on both sides.

Vagus Nerve (CN X)

Anatomy snapshot

The vagus nerve also originates in the medulla and innervates multiple structures. The Latin root of its name translates as “wandering,” reflecting its long and wide distribution. The nerve exits just below the glossopharyngeal nerve in the medulla. It courses towards the jugular foramen, posterior and medial to CN IX, then travels down in the carotid sheath. Like the glossopharyngeal nerve, this nerve contains both afferent and efferent projections. The efferent innervations convey general visceral efferents to the thorax, abdominal viscera, and muscles of the pharynx and larynx. Afferents arise from the external ear, external auditory canal, surface of the tympanic membrane, pharynx, larynx, trachea, esophagus and viscera of the thorax and abdomen.


The vagus nerve is typically evaluated in conjunction with the glossopharyngeal nerve. The examiner should take note of the patient's voice during conversation. An isolated recurrent laryngeal nerve (branch of the vagus nerve) palsy results in a hoarse voice. When the patient is asked to cough, the failure of vocal cord closure produces a hollow “bovine” sound. Unilateral vagus nerve lesions result in hoarseness, dysphagia and dyspnea secondary to loss of branchiomeric muscle innervations. While testing the gag reflex, the examiner should note the position of the uvula and look for symmetrical elevation of the soft palate to exclude uvular deviation away from the side of the vagus nerve lesion. A simple bedside swallowing assessment can also be performed by asking the patient to drink small sips of water. Patients with bulbar palsy can be at risk of aspiration. Bilateral vagal nerve injuries are usually fatal owing to laryngeal paralysis, which results in airway obstruction and asphyxia.

Spinal Accessory Nerve (CN XI)

Anatomy snapshot

The spinal accessory nerve is formed from cranial and spinal contributions. The spinal roots arise from the ventral horn cells in the cord from C1-C5 and travel cranially through the foramen magnum. These fibers travel in turn to the clivus, turning laterally towards and then exiting through the jugular foramen after joining the cranial portion discussed above.

The spinal portion of the nerve innervates the sternocleidomastoid and upper part of the trapezius through somato-motor fibers. The cranial portion communicates with the jugular ganglion of the vagus nerve, and innervates the intrinsic muscles of the pharynx through the recurrent laryngeal nerve branch.


A lesion or injury to the cranial portion of the spinal accessory nerve is difficult to distinguish from one of the vagal nerve, as described above. Hence, clinical examination focuses on the bulky muscles innervated by the spinal portion of the nerve. The tone and bulk of the sternocleidomastoid and trapezius muscles are initially examined by close observation and palpation. The trapezius is tested by asking the patient to shrug their shoulders while applying resistance. In severe cases of ipsilateral trapezius muscle atrophy, shoulder sag with downward and outward rotation of the scapula can be observed. The sternocleidomastoid is assessed by asking the patient to turn his/her head against resistance applied to the side of the face. In cases of unilateral palsy, the patient is unable to turn the head to the side opposite the lesion as the sternocleidomastoid muscle is weak.

Hypoglossal Nerve (CN XII)

Anatomy snapshot

The hypoglossal nerve provides motor innervation to the tongue musculature. The hypoglossal nucleus resides primarily in the medulla oblongata. The exiting fibers emerge from a sulcus between the pyramid and inferior olive. The nerve then enters the hypoglossal canal and exits towards the angle of the mandible. It subsequently courses anteriorly to supply both the intrinsic and extrinsic tongue muscles.


The tongue is carefully inspected for signs of atrophy and asymmetry. With atrophy the tongue starts to lose its bulk at the tip and the border area. This progresses until it appears wrinkled. The patient is then asked to protrude the tongue; there is tongue deviation towards the side of the lesion in pathological conditions. Fasciculations may be seen in patients with motor neuron disease (amyotrophic lateral sclerosis). While the tongue is at rest, fasciculations usually persist while resting tremors abate. Power is examined by having the patient press the tip of the tongue against each cheek while the examiner tries to dislodge it. With facial weakness, tongue deviation can appear to be produced when none is present. Hence, manual elevation of the weak side of the face can be helpful in eliminating this finding.

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