The Cranial Nerve Exam
February 15th, 2021
On this page:First StepsThe PatientI - SmellII - VisionII & III - PupilsIII, IV & VI - Eye MovementV - Facial Sensation & Jaw MusclesVII - Facial MovementVIII - HearingIX & X - ThroatXI - Neck & ShouldersXII - TongueFinishing Up
The cranial nerve examination is a complex mix of examination techniques designed to localise pathology to one or more of the twelve cranial nerves.
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.
- 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 (cranial 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 (cranial nerve II) provides special sensory innervation, in the form of sight.
- 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:
- AUnilateral anopia - complete loss of vision in one eyeUnilateral optic nerve lesion or ocular pathology
- BBitemporal hemianopia - loss of lateral vision in both eyesOptic chiasmal compression
- CHomonymous hemianopia - loss of left or right field in one eyeContralateral optic tract lesion
- D/EHomonymous 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
- FHomonymous 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.
- 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.
- Always offer to perform fundoscopy as part of the cranial nerve exam, though note that the yield of this will be limited without dilation of the pupils. Look for signs of hypertensive retinopathy or diabetic retinopathy.
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).
- 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.
- 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:
- 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.
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.
- 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.
- 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.
- 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 â…” 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).
The External Ear
- Inspect the external ear for periauricular vesicles (a sign of Ramsay-Hunt syndrome / herpes zoster infection), and then palpate for mastoid tenderness.
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.
- To start with, whisper numbers into the patient's ear from approximately 1m and ask them to repeat the numbers. This can be used as a screening test for auditory loss.
- 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.
- 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.
Inspect the Throat
- Ask the patient to say 'ahh', looking for abnormal displacement of the uvula (which may be neurologic or due to a peritonsillar abscess) and asymmetric palate rise (which may be mechanical or due to a vagus nerve lesion).
The Pharyngeal Reflex
- Offer to perform the pharyngeal (or gag) reflex, however this should be avoided in most circumstances as this is extremely uncomfortable. To assess the pharyngeal reflex, ask the patient to open their mouth, and gently touch the soft palate with a tongue depressor. An absent gag reflex is a sign of a lower motor neuron lesion, such as bulbar palsy; an exaggerated pharyngeal reflex is probably normal - however may be a sign of pseudobulbar palsy.
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.
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.
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Acierno M. Ophthalmoscopy for the Neurologist. The Neurologist. 2001 Jul; 7(4): 234-251.Adhab R, Saade HS, Kikano R, Ferzli J, Tarcha W, Riachi N. Pure ipsilateral central facial palsy and contralateral hemiparesis secondary to ventro-medial medullary stroke. Journal of the Neurological Sciences. 2013; 332: 154-155.Ahmad K, Wright M, Lueck CJ. Ptosis. Practical Neurology. 2011; 11: 332-340.Anderson DR. Standard Perimetry. Ophthalmol Clin N Am 2003;16: 205-212.Armaly MF. The size and location of the normal blind spot. Arch Ophthalmol. 1969; 81(2):192-201.Athanasiov PA. Prabhakaran VC, Selva D. Non-traumatic Enophthalmos: a Review. Acta Ophthalmologica. 2008 June; 86(4): 356-364.Bagheri A, Fallahi M, Abrishami M, Salour H, Aletaha M. Clinical features and outcomes of treatment for fourth nerve palsy. Journal of ophthalmic & vision research. 2010;5:27-31.Bhargava A, Banakar BF, Pujar GS, Khichar S. A study of Guillain-Barré syndrome with reference to cranial neuropathy and its prognostic implication. Journal of neurosciences in rural practice. 2014;5:S43-S47.Bolanos I, Lozano D, Cantu C. Internuclear ophthalmoplegia: causes and long‐term follow‐up in 65 patients. Acta neurologica scandinavica. 2004 Sep;110(3):161-5.Bussell MA, Heady J. Unexpected Quinsy. British Dental Journal. 2007; 203: 227-228.Castiglia PT. Strabismus. Journal of Paediatric Health Care. 1994; 8: 236-238.
Chen G, Wang X, Wang L, Zheng J. Arterial compression of nerve is the primary cause of trigeminal neuralgia. Neurological Sciences. 2014;2013;35:61-66.Childs SG. Muscle Wasting. Orthopaedic Nursing. 2003; 22(4): 251-257.
Dacso CC, Bortz DL. Significance of the Argyll Robertson pupil in clinical medicine. The American journal of medicine. 1989 Jan 1;86(2):199-202.Danchaivijitr C, Kennard C. Diplopia and Eye Movement Disorders. J Neurol Neurosurg Psychiatry. 2004; 75: 24-31.Daniels SK. Neurological Disorders Affecting Oral, Pharyngeal Swallowing. GI Motility online. 2006. Available from: http://www.nature.com/gimo/contents/pt1/full/gimo34.html.Davidson TM, Jalowayski A, Murphy C, Jacobs RD. Evaluation and Treatment of Smell Dysfunction. The Western Journal of Medicine. 1987 April; 146(4): 434-438.De Foer B, Kenis C, Van Melkebeke D, et al. Pathology of the vestibulocochlear nerve. European Journal of Radiology. 2010;74:349-358.Desai J, Swash M. Fasciculations: What Do We Know of Their Significance?, Journal of Neurological Sciences. 1997; 152 S1: S43-S48.Fiore DC. Pain in the Quiet (Not Red) Eye. American Family Physician. 82(1): 69-72.Gaddipati RV, Meyer DR. Eyelid Retraction, Lid Lag, Lagophthalmos, and Von Graefe’s Sign: Quantifying the Eyelid Features of Grave’s Ophthalmopathy. Ophthalmology 2008. 115: 1083-1088.Gates P. The rule of 4 of the brainstem: a simplified method for understanding brainstem anatomy and brainstem vascular syndromes for the non‐neurologist. Internal medicine journal. 2005 Apr;35(4):263-6.Gattey D. The Pupil Examination in the Trauma Patient. Journal of Emergency Nursing. 2004 Oct; 30(5): 512-513.Gottlob I. Nystagmus. Current Opinion in Ophthalmology. 2001; 12: 378-383.Granick MS, Martuza RL, Ojemann RG, Parker SW, Montgomery WW. Cerebellopontine angle meningiomas: clinical manifestations and diagnosis. Annals of Otology, Rhinology & Laryngology. 1985 Jan;94(1):34-8.
Grieg MH. Otoscopy for the GP. Current Therapeutics. 1999; 40(6): 79-87.Hardy LG, Rand G, Rittler MC. Tests for Detection and Analysis of Color Blindness I: An Evaluation of the Ishihara Test. Arch Ophthalmol. 1945: 34(4): 295-302.Haslam RH. Clinical neurological examination of infants and children. Handb Clin Neurol. 2013; 111: 17-25.Haughton PM, Pearce JM. Observations on the Rinne Test. Lancet. 1982 April; 8276(319): 829-830.Idro R, Otieno B, White S, Kahindi A, Fegan G, Ogutu B et al. Decorticate, Decerebrate and Opisthotonic Posturing and seizures in Kenyan Children with Cerebral Malaria. Malaria Journal. 2005; 4(57).Isaacson B. Hearing Loss. Medical Clinics of North America. 2010 Sept; 94(5): 973-988.
Jäger HR, Miszkiel KA. Pathology of the optic nerve. Neuroimaging clinics of North America. 2008;18:243-259.Jolles J, Houx PJ, Verhey FRJ, Vreeling FW. Primitive reflexes in Parkinson's disease. Journal of neurology, neurosurgery and psychiatry. 1993;56:1323-1326.Jung WS, Kwon SW, Park SU, Moon SK, Park JM, Ko CN et al. Electroacupuncture for Decorticate Rigidity of the Upper Limbs in a Patient with Anoxic Brain Damage. Case Reports in Medicine. 2013; 1-4.Kannikeswaran N, Mahajan PV, Kamat D. Acute Facial Symmetry. Clinical Paediatrics. 2006; 45: 289-292.Kawasaki A. Anisocoria. Neuro-Ophthalmology. 2009 Aug; 15(4): 218-235.Keane JR. Internuclear ophthalmoplegia: unusual causes in 114 of 410 patients. Archives of neurology. 2005 May 1;62(5):714-7.Keane JR. Twelfth-nerve palsy: analysis of 100 cases. Archives of neurology. 1996 Jun 1;53(6):561-6.Keane JR. Vertical Diplopia. Seminars in Neurology. 2008;6:147-154.Kiely PM, Kowal L. Review of Facial Muscle Spasms. Clinical and Experimental Optometry. 1997; 80(2): 59-61.Kieser JA. Anatomical Knowledge and Clinical Evaluation of the Muscles of Mastication. Clinical Anatomy. 2000; 13(2): 94-96.Lee AG, Al-Zubidi N, Beaver HA, Brazis PW. An Update on Eye Pain for the Neurologist. Neurologic Clinics. 2014 May; 32(2): 489-505.
Levenson JH, Kozarsky A. Visual Acuity Change. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 111.Liebman SD. Strabismus. New England Journal of Medicine. 1964; 271: 1258-1260.Lima MA, Maranhao-Filho P. What is the essential neurological examination? Arq Neuropsiquiatr 2012; 70(12): 939-941.Lueck CJ. Nystagmus. Practical Neurology. 2005 Oct; 288-291.Lyden P. The Endovascular Procedure-Specific Neurological Examination Scheme. J Endovasc Ther. 2011; 18: 538–539.Lynch GS, Schertzer JD, Ryall JG. Therapeutic Approaches for Muscle Wasting Disorders. Pharmacology and Therapeutics. 2007 Mar; 113(3): 461-487.Manon-Espaillat R, Ruff RL. Dissociated weakness of sternocleidomastoid and trapezius muscles with lesions in the CNS. Neurology. 1988; 38: 796–797.Merino PS, Rojas PL, GÃ³mez De LiaÃ±o, Pilar S, Fukumitsu HM, YÃ¡Ã±ez JM. Bilateral superior oblique palsy: etiology and therapeutic options. European journal of ophthalmology. 2014;24:147.Moore FG, Chalk C. The essential neurologic examination: what should medical students be taught? Neurology. 2009; 72: 2020-2023.Moylan JS, Reid MB. Oxidative Stress, Chronic Disease and Muscle Wasting. Muscle & Nerve. 2007; 35:411-429.Nadol JB. Hearing Loss. New England Journal of Medicine. 1993; 329: 1092-1102.Nicolson SE, Chabon B, Larsen KA, Kelly SE, Potter AW, Stern TA. Primitive reflexes associated with delirium: a prospective trial. Psychosomatics. 2011;52:507.Obuchowska I, Mariak Z. Homonymous hemianopsia. Klinika oczna. 2012;114:226.Ongerboer de Visser BW, Moffie D. Effects of Brain-Stem and Thalamic Lesions on the Corneal Reflex: An Electrophysiological and Anatomical Study. Brain. 1979; 102: 595-608.Park U, Kim S, Hwang J, Yu YS. Clinical features and natural history of acquired third, fourth, and sixth cranial nerve palsy. Eye. 2008;22:691-696.Parry LA. Hemiatrophy of the Tongue. Lancet. 1900 Feb: 537.Perkin GD. Neuro-ophthalmological syndromes for neurologists. Journal of Neurology, Neurosurgery & Psychiatry. 2004 Dec 1;75(suppl 4):iv20-3.Pierrot-Deseilligny C, Milea D. Vertical Nystagmus: Clinical Facts and Hypotheses. Brain. 2005 Jun; 128(6): 1237-1246.Poppen JL. Exophthalmos. The American Journal of Surgery. 1944; 64(1): 64-79.Rainsbury JW, Aldren CP. Facial Nerve Palsy. Clinical Otolaryngology. 2007 Feb; 32(1): 38-40.Sanders RD, Gillig PM. Cranial nerve I: olfaction. Psychiatry (Edgmont (Pa. : Township)). 2009;6:30.Sharshar T, Citerio G, Andrews PJ, Chieregato A, Latronico N, Menon DK, Puybasset L, Sandroni C, Stevens RD. Neurological examination of critically ill patients: a pragmatic approach. Report of an ESICM expert panel. Intensive Care Med. 2014 Feb. Smith SA, Smith SE. Bilateral Horner's syndrome: detection and occurrence. Journal of neurology, neurosurgery, and psychiatry. 1999;66:48-51.Stahl JS, Leigh RH. Nystagmus. Current Neurology and Neuroscience Reports. 2001; 1: 471-477.Thompson EO, Smoker WR. Hypoglossal nerve palsy: a segmental approach. Radiographics. 1994 Sep;14(5):939-58.
Thompson HS, Kardon RH. The argyll robertson pupil. Journal of neuro-ophthalmology. 2006 Jun 1;26(2):134-8.Thompson HS. Adie's syndrome: some new observations. Transactions of the American Ophthalmological Society. 1977;75:587.Timmis P. Exophthalmos. Journal of Otolaryngology and Otology. 1957 Nov; 71(11): 744-753.Tomczak KK, Rosman NP. Torticollis. J Child Neurol. 2013 March; 28(3): 365-378.Toro J, Reyes S. Tongue Fasciculationsin Amyotrophic Lateral Sclerosis. NEJM. 2014 Jul; 371(5).Toulgoat F, Sarrazin JL, Benoudiba F, et al. Facial nerve: from anatomy to pathology. Diagnostic and interventional imaging. 2013;94:1033-1042.Vilensky JA. The neglected cranial nerve: Nervus terminalis (cranial nerve N). Clinical Anatomy. 2014;27:46-53.Virgo JD, Plant GT. Internuclear ophthalmoplegia. Practical neurology. 2017 Apr 1;17(2):149-53.