3-cranial Nerves

Examination of Nervous System

Hong Zhang, MD,PhD Department of Neurology Zhongnan Hospital of Wuhan University

When approching a patient with a neurologic disorder always ask youself 1. Where is the lesion? • cerebrum • cerebellum • brainstem • spinal cord • nerve root • peripheral nerve • neuromuscular junction • muscle • not confined to one level

2. What is the cause of the lesion? • vascular • infectious • neuroplastic • degenerative • inflammatory-immunologic • congenital-developmental • traumatic • toxic • metabolic 3. Is the lesion focal, multifocal or diffuse?

Neuroanatomy through Clinical Cases • Hal Blumenfeld Yale University School of Medicine • Publishing Information: September 2001 • ISBN 0-87893-060-4

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INTRODUCTION MENTAL STATUS CRANIAL NERVES MOTOR EXAM REFLEXES COORDINATION AND GAIT SENSORY EXAM

CRANIAL NERVES

1. Olfaction (CN I) 2. Ophthalmoscopic Exam (CN II) 3. Vision (CN II) 4. Pupillary Responses (CN II, III) 5. Extraocular Movements (CN III, IV, VI) 6. Facial Sensation and Muscles of Mastication (CN V) 7. Muscles of Facial Expression and Taste (CN VII) 8. Hearing and Vestibular Sense (CN VIII) 9. Palate Elevation and Gag Reflex (CN IX, X) 10.Muscles of Articulation (CN V, VII, IX, X, XII) 11.Sternocleidomastoid and Trapezius Muscles (CN XI) 12.Tongue Muscles (CN XII)

Olfaction (CN I) • Can the patient smell coffee or soap with each nostril? • Do not use noxious odors, since they may stimulate pain fibers from CN V • CN I is often not tested unless specific pathology such as a subfrontal brain tumor is suspected

Olfaction (CN I) What is Being Tested? • Impairment can be due to 1. nasal obstruction 2. damage to the olfactory nerves in the nasal mucosa 3. damage to the nerves as they cross the cribriform plate 4. intracranial lesions affecting the olfactory bulbs

Opthalmoscopic Exam (CN II) • Examine both retinas carefully with an ophthalmoscope

Opthalmoscopic Exam (CN II) What is Being Tested? • This exam allows direct visualization of damage to 1. retina or retinal vessels 2. optic nerve atrophic changes 3. papilledema 4. other important abnormalities

Opthalmoscopic Exam (CN II) Visual Acuity • Test visual acuity for each eye separately (by covering one eye at a time) using an eye chart

Opthalmoscopic Exam (CN II) Color Vision • Test each eye separately for ability to distinguish colors • Test for red desaturation, a sign of subtle asymmetry in optic nerve function seen • In optic neuritis, by asking the patient to cover each eye alternately while looking at a red object and report any relative dullness of the color in one eye

Opthalmoscopic Exam (CN II) Visual Fields • Test visual fields for each eye by asking the patient to fixate straight ahead and to report when a finger can be seen moving in each quadrant • Alternatively, ask the patient to report how many fingers are being shown in each quadrant • More precise mapping of visual fields can be done in the laboratory for patients who will be followed over time

Opthalmoscopic Exam (CN II) Visual Extinction • Test for visual extinction on double simultaneous stimulation by asking the patients how many fingers they see when fingers are presented to both sides at the same time • In visual extinction, a form of hemineglect , patients do not report seeing the fingers on the affected (usually left) side of the visual field, although they can see fingers when they are presented to that side alone

Opthalmoscopic Exam (CN II) • In comatose or uncooperative patients, visual fields can be tested roughly using blink-to-threat, in which the examiner's fingers are moved rapidly towards the patient's eyes from each quadrant to see if a blink occurs.

Opthalmoscopic Exam (CN II) What is Being Tested? • Damage anywhere in the visual pathway from the eye to the visual cortex can cause specific deficits in the visual fields of one or both eyes • Importantly, some visual information from each eye crosses to the opposite side at the optic chiasm

Opthalmoscopic Exam (CN II) What is Being Tested? • Lesions in front of the optic chiasm (eye, optic nerve) cause visual deficits in one eye • Lesions behind the optic chiasm (optic tract, thalamus, white matter, visual cortex) cause visual field deficits that are similar for both eyes

Opthalmoscopic Exam (CN II) • Visual hemineglect or extinction is usually caused by contralateral parietal lesions, and less often by frontal or thalamic lesions • Neglect is usually more robust in lesions of the right hemisphere

Pupillary Responses (CN II, III) • First, record the pupil size and shape at rest • Next, note the direct response, meaning constriction of the illuminated pupil, as well as the consensual response, meaning constriction of the opposite pupil

Pupillary Responses (CN II, III) • In an afferent pupillary defect there is a decreased direct response caused by decreased visual function in one eye • This can be demonstrated with the swinging flashlight test, in which the light is moved back and forth between the eyes every two to three seconds

Pupillary Responses (CN II, III) • The afferent pupillary defect becomes obvious when the flashlight is moved from the normal to the affected eye, and the affected pupil dilates in response to light • Under normal conditions, the pupil constricts in response to light • Brief oscillations of pupillary size called hippus occur normally in response to light which should not be confused with an afferent pupillary defect

Pupillary Responses (CN II, III) • Finally, test the pupillary response to accommodation. Normally, the pupils constrict while fixating on an object being moved from far away to near the eyes

Pupillary Responses (CN II, III) What is Being Tested? • Direct response (pupil illuminated) is impaired in lesions of 1. ipsilateral optic nerve 2. pretectal area 3. ipsilateral parasympathetics traveling in CN III 4. pupillary constrictor muscle of the iris

Pupillary Responses (CN II, III) What is Being Tested? • Consensual response (contralateral pupil illuminated) is impaired in lesions of 1. contralateral optic nerve 2. pretectal area 3. ipsilateral parasympathetics traveling in CN III 4. pupillary constrictor muscle

Pupillary Responses (CN II, III) What is Being Tested? • Accommodation (response to looking at something moving toward the eye) is impaired in lesions of 1. ipsilateral optic nerve 2. ipsilateral parasympathetics traveling in CN III 3. pupillary constrictor muscle 4. in bilateral lesions of the pathways from the optic tracts to the visual cortex 5. Accommodation is spared in lesions of the pretectal area

Extraocular Movements (CN III, IV, VI) • Check extraocular movements (eye movements) by having the patient look in all directions without moving their head and ask them if they experiences any double vision • Test smooth pursuit by having the patient follow an object moved across their full range of horizontal and vertical eye movements

Extraocular Movements (CN III, IV, VI) • Test convergence movements by having the patient fixate on an object as it is moved slowly towards a point right between the patient's eyes • Also, observe the eyes at rest to see if there are any abnormalities such as spontaneous nystagmus (see below)or dysconjugate gaze (eyes not both fixated on the same point) resulting in diplopia (double vision)

Pupillary Responses (CN II, III) • Saccades are eye movements used to rapidly refixate from one object to another • The examiner can test saccades by holding two widely spaced targets in front of the patient (such as the examiner's thumb on one hand and index finger on the other) and asking the patient to look back and forth between the targets

Pupillary Responses (CN II, III) • Test optokinetic nystagmus (OKN) by moving a strip with parallel stripes on it in front of the patient's eyes and asking them to watch the stripes go by • Normally, rhythmic eye movements called nystagmus occur consisting of an alternating slow phase with slow pursuit movements in the direction of strip movement, and a rapid phase with quick refixations back to midline

Pupillary Responses (CN II, III) • In comatose or severely lethargic patients, the vestibulo-ocular reflex can be used to test whether brainstem eye movement pathways are intact • The oculocephalic reflex, a form of the vestibulo-ocular reflex, is tested by holding the eyes open and rotating the head from side to side or up and down

Pupillary Responses (CN II, III) • These maneuvers obviously should not be performed in cases of head injury or other cases of suspected cervical spine trauma unless complete cervical spine films are normal • The reflex is present if the eyes move in the opposite direction of the head movements, and it is therefore sometimes called doll's eyes

Pupillary Responses (CN II, III) • In awake patients, doll's eyes are usually not present because voluntary eye movements mask the reflex • The absence of doll's eyes suggests brainstem dysfunction in the comatose patient but can be normal in the awake patient • More potent stimulus of the vestibuloocular reflex used to evaluate comatose patients is caloric stimulation

Pupillary Responses (CN II, III) What is Being Tested? • Careful testing can often identify abnormalities in 1. individual muscles 2. particular cranial nerves (oculomotor, trochlear, or abducens) in their course from the brainstem to the orbit 3. brainstem nuclei 4. higher-order centers and pathways in the cortex and brainstem that control eye movements

Pupillary Responses (CN II, III) What is Being Tested? • Spontaneous nystagmus can indicate 1. Toxic or metabolic conditions such as drug overdose 2. alcohol intoxication 3. peripheral or central vestibular dysfunction

Facial Sensation and Muscles of Mastication (CN V)

• Test facial sensation using a cotton wisp and a sharp object • Also test for tactile extinction using double simultaneous stimulation

Facial Sensation and Muscles of Mastication (CN V) • The corneal reflex, which involves both CN V and CN VII • It is tested by touching each cornea gently with a cotton wisp and observing any asymmetries in the blink response

Facial Sensation and Muscles of Mastication (CN V) • Feel the masseter muscles during jaw clench • Test for a jaw jerk reflex by gently tapping on the jaw with the mouth slightly open

Facial Sensation and Muscles of Mastication (CN V) What is Being Tested? • Facial sensation can be impaired by lesions of 1. trigeminal nerve (CN V) 2. trigeminal sensory nuclei in the brainstem 3. ascending sensory pathways to the thalamus and somatosensory cortex in the postcentral gyrus

Facial Sensation and Muscles of Mastication (CN V) What is Being Tested? • The corneal blink reflex is mediated by polysynaptic connections in the brainstem between the trigeminal (CN V) and facial (CN VII) nerves • It can be impaired by lesions anywhere in this circuit

Facial Sensation and Muscles of Mastication (CN V)

What is Being Tested? • Extinction in the presence of intact primary sensation is usually caused by right parietal lesions

Facial Sensation and Muscles of Mastication (CN V) What is Being Tested? • Weakness of the muscles of mastication can be due to lesions in 1. upper motor neuron (UMN) pathways synapsing onto the trigeminal (CN V) motor nucleus 2. lower motor neurons (LMNs) of the trigeminal motor nucleus in the pons or as they exit the brainstem to reach the muscles of mastication 3. neuromuscular junction 4. muscles themselves

Facial Sensation and Muscles of Mastication (CN V) What is Being Tested? • Presence of a jaw jerk reflex is abnormal, especially if it is prominent • It is a sign of hyperreflexia associated with lesions of UMN pathways projecting to the trigeminal motor nucleus • Both the afferent and the efferent limbs of the jaw jerk reflex are mediated by CN V

Muscles of Facial Expression and Taste (CN VII) • Look for asymmetry in facial shape or in depth of furrows such as the nasolabial fold • Also look for asymmetries in spontaneous facial expressions and blinking

Muscles of Facial Expression and Taste (CN VII) Ask patient to 1. Smile 2. puff out their cheeks 3. clench their eyes tight 4. wrinkle their brow • Old photographs of the patient can often aid your recognition of subtle changes.

Muscles of Facial Expression and Taste (CN VII) • Check taste with sugar, salt, or lemon juice on cotton swabs applied to the lateral aspect of each side of the tongue • Like olfaction, taste is often tested only when specific pathology is suspected, such as in lesions of the facial nerve, or in lesions of the gustatory nucleus (nucleus solitarius)

Muscles of Facial Expression and Taste (CN VII) What is Being Tested? • Facial weakness can be caused by lesions of 1. upper motor neurons in the contralateral motor cortex or descending central nervous system pathways 2. lower motor neurons in the ipsilateral facial nerve nucleus (CN VII) or exiting nerve fibers 3. the neuromuscular junction 4. face muscles

Muscles of Facial Expression and Taste (CN VII) What is Being Tested? • The upper motor neurons for the upper face (the upper portions of the orbicularis oculi and the frontalis muscles of the forehead) project to the facial nuclei bilaterally • Upper motor neuron lesions, such as a stroke, cause contralateral face weakness sparing the forehead • Lower motor neuron lesions, such as a facial nerve injury, typically cause weakness involving the whole ipsilateral face

Hearing and Vestibular Sense (CN VIII) Hearing • Can the patient hear fingers rubbed together or words whispered just outside of the auditory canal and identify which ear hears the sound? • A tuning fork can be used to distinguish neural from mechanical conductive hearing problems

Hearing and Vestibular Sense (CN VIII) Hearing

• In the Rinne test the sound heard when holding a vibrating tuning fork just outside each ear (air conduction), is compared to the sound heard when placing the tuning fork handle on each mastoid process (bone conduction) • Normal individuals will hear the tone better by air conduction

Hearing and Vestibular Sense (CN VIII) Hearing • In conductive hearing loss, bone conduction is greater than air conduction, because bone conduction bypasses problems in the external or middle ear • In sensorineural hearing loss, air conduction is greater than bone conduction in both ears (as in normal hearing), however, hearing is decreased in the affected ear

Hearing and Vestibular Sense (CN VIII) Hearing • In the Weber test, the tuning fork is placed on the vertex of the skull in the midline, and the patient is asked to report the side where the tone sounds louder • Normally, the tone sounds equal on both sides

Hearing and Vestibular Sense (CN VIII) Hearing • In sensorineural hearing loss, the tone is louder on the normal side • In conductive hearing loss, the tone is louder on the affected side • You can verify that the tone is louder on the side of conductive hearing loss on yourself by closing each ear alternately while humming

Hearing and Vestibular Sense (CN VIII) Vestibular Sense • Vestibular sense is generally not specifically tested, except for in the following important situations 1. Patients with vertigo 2. Patients with limitations of horizontal or vertical gaze 3. Patients in coma

Hearing and Vestibular Sense (CN VIII) Patients with vertigo • Barany or Hall-Pike positional testing can help distinuish peripheral from central causes of vertigo • The patient sits on the bed or examining table, and the examiner supports the patient's head as the patient lays back with one ear down, and with the head extending over the edge of the table • This maneuver does not need to be done especially briskly

Hearing and Vestibular Sense (CN VIII) Patients with vertigo • The patient is asked to keep their eyes open and report any sensations of vertigo, while the examiner looks for nystagmus • This change of position causes maximal stimulation of the posterior semicircular canal of the ear that is down, and of the anterior semicircular canal of the ear that is up • The maneuver is also done with the other ear down

Hearing and Vestibular Sense (CN VIII) Patients with vertigo • With peripheral lesions 1. There is usually a delay of a few seconds before the onset of nystagmus and vertigo 2. The nystagmus is horizontal or rotatory and does not change directions 3. Nystagmus and vertigo then fade away within about a minute 4. If the same maneuver is repeated, there is often adaptation, so that the nystagmus and vertigo are briefer and less intense each time

Hearing and Vestibular Sense (CN VIII) Patients with vertigo In contrast, with central lesions 1. Nystagmus and vertigo may begin immediately, and there tends to be no adaptation 2. Horizontal or rotatory nystagmus can also be seen with central lesions 3. However, vertical nystagmus, nystagmus that changes directions, or prominent nystagmus in the absence of vertigo are seen only in central, and not in peripheral lesions

Hearing and Vestibular Sense (CN VIII) Patients with limitations of horizontal or vertical gaze • Testing the vestibulo-ocular reflex can help localize the lesion • As we mentioned when discussing Extraocular Muscles the vestibulo-ocular reflex can be tested in two ways • The first is using the oculocephalic maneuver, in which the eyes are held open and the head is turned rapidly either from side to side or up and down

Hearing and Vestibular Sense (CN VIII) Patients with limitations of horizontal or vertical gaze • Testing the vestibulo-ocular reflex • The second is using caloric testing, in which cold or warm water is instilled into one ear, producing asymmetric stimulation of the semicircular canals

Caloric stimulation Definition • Caloric stimulation is a test which uses differences in temperature to diagnose ear nerve damage • Caloric stimulation is done to check the acoustic nerve, which provides hearing and helps with balance

Caloric stimulation How the Test is Performed • This test stimulates the inner ear and nearby nerves by delivering cold and warm water (air) to the ear canal at different times • One ear is tested at a time • When cold water enters the ear, it should cause rapid, side-to-side eye movements called nystagmus. The eyes should move away from the cold water and slowly back • Next, warm water is placed into the ear. The eyes should now move towards the warm water then slowly away

Caloric stimulation Why the Test is Performed • This test may be recommended if you have 1. Dizziness or vertigo 2. Hearing loss that may be due to certain antibiotics 3. Certain types of anemia 4. Possible psychological causes of vertigo

Hearing and Vestibular Sense (CN VIII) Patients in coma • The vestibulo-ocular reflex is often the only way to test eye movements in these patients

Hearing and Vestibular Sense (CN VIII) What is Being Tested? • Hearing loss can be caused by lesions in 1. acoustic and mechanical elements of the ear 2. neural elements of the cochlea 3. acoustic nerve (CN VIII) • After the hearing pathways enter the brainstem, they cross over at multiple levels and ascend bilaterally to the thalamus and auditory cortex • Clinically significant unilateral hearing loss is invariably caused by peripheral neural or mechanical lesions

Hearing and Vestibular Sense (CN VIII) What is Being Tested? Abnormalities in vestibular testing can be associated with lesions in 1. vestibular apparatus of the inner ear 2. vestibular portion of CN VIII 3. vestibular nuclei in the brainstem, the cerebellum 4. pathways in the brainstem (such as the medial longitudinal fasciculus) that connect the vestibular and oculomotor systems

Palate Elevation and Gag Reflex (CN IX, X) • Does the palate elevate symmetrically when the patient says, "Aah"? • Does the patient gag when the posterior pharynx is brushed? • The gag reflex needs to be tested only in patients with suspected brainstem pathology, impaired consciousness, or impaired swallowing

Palate Elevation and Gag Reflex (CN IX, X) What is Being Tested? Palate elevation and the gag reflex are impaired in lesions involving 1. CN IX 2. CN X 3. neuromuscular junction 4. pharyngeal muscles

Muscles of Articulation (CN V, VII, IX, X, XII) Is the patient's speech 1. Hoarse ? 2. Slurred ? 3. Quiet ? 4. Breathy ? 5. Nasal ? 6. Low or high pitched? • It is often important to ask if the patient's speech has changed from baseline

Muscles of Articulation (CN V, VII, IX, X, XII) • Note that dysarthria, abnormal pronunciation of speech, is not the same as aphasia • Aphasia is an abnormality in language production or comprehension

Muscles of Articulation (CN V, VII, IX, X, XII) What is Being Tested? Abnormal articulation of speech can occur in lesions involving 1. muscles of articulation 2. neuromuscular junction 3. peripheral or central portions of CN V, VII, IX, X, or XII

Muscles of Articulation (CN V, VII, IX, X, XII) What is Being Tested? Speech production can be abnormal as a result of lesions in 1. Motor cortex 2. Cerebellum 3. Basal ganglia 4. Descending pathways to the brainstem

Sternocleidomastoid and Trapezius Muscles (CN XI) Ask the patient to 1. Shrug their shoulders 2. Turn their head in both directions 3. Raise their head from the bed 4. Flexing forward against the force of your hands

Sternocleidomastoid and Trapezius Muscles (CN XI) What is Being Tested? Weakness in the sternocleidomastoid or trapezius muscles can be caused by lesions in 1. muscles 2. neuromuscular junction 3. lower motor neurons of the accessory spinal nerve (CN XI)

Sternocleidomastoid and Trapezius Muscles (CN XI) What is Being Tested? • Unilateral upper motor neuron lesions in the cortex or descending pathways cause contralateral weakness of the trapezius, with relative sparing of sternocleidomastoid strength • This may be explained by bilateral upper motor neuron projections controlling the sternocleidomastoid, in analogy to the bilateral projections controlling the upper face

Tongue Muscles (CN XII) • Note any atrophy or fasciculations (spontaneous quivering movements caused by firing of muscle motor units) of the tongue while it is resting on the floor of the mouth • Ask the patient to stick their tongue straight out and note whether it curves to one side or the other • Ask the patient to move their tongue from side to side and push it forcefully against the inside of each cheek

Tongue Muscles (CN XII) • Fasciculations and atrophy are signs of lower motor neuron lesions • Unilateral tongue weakness causes the tongue to deviate toward the weak side • Lesions of the motor cortex cause contralateral tongue weakness

Tongue Muscles (CN XII) Tongue weakness can result from lesions of 1. tongue muscles 2. neuromuscular junction 3. lower motor neurons of the hypoglossal nerve (CN XII) 4. upper motor neurons originating in the motor cortex

A summary of the cranial nerves and their respective functioning I - Smell II - Visual acuity, visual fields and ocular fundi II,III - Pupillary reactions III,IV,VI - Extra-ocular movements, including opening of the eyes V - Facial sensation, movements of the jaw, and corneal reflexes VII - Facial movements and gustation VIII - Hearing and balance IX,X - Swallowing, elevation of the palate, gag reflex and gustation V,VII,X,XII - Voice and speech XI - Shrugging the shoulders and turning the head XII - Movement and protrusion of tongue

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