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Cranial nerve palsies Last updated: May 9, 2022

Summary

Cranial nerve palsy is characterized by a decreased or complete loss of function of one or more cranial nerves. Cranial nerve palsies can
be congenital or acquired. Multiple cranial neuropathies are commonly caused by tumors, trauma, ischemia, or infections. While
diagnosis can usually be made based on clinical features, further investigation is often warranted to determine the specific etiology.
Contrast-enhanced MRI is usually the preferred imaging modality to evaluate the affected nerve and any soft tissue abnormalities. A
CT scan may be indicated to evaluate for bony lesions and fractures that may be compressing the nerve. Management is mainly aimed at
treating the underlying etiology. Surgery may be indicated for individuals with severe disability (e.g., acute traumatic cranial nerve
palsies, persistent symptoms despite conservative measures). Spontaneous resolution over months may occur, especially in cranial nerve
palsies secondary to microangiopathy.
Facial nerve palsy is covered in detail separately.

Cranial nerve types and functions

Overview of cranial nerves and their function [1]

Cranial nerve Nerve type Function

I Olfactory nerve Sensory Smell

II Optic nerve Sensory Vision

Afferent limb of the pupillary light reflex

III Oculomotor Motor (somatic) Eyelid opening (indirect): levator palpebrae superioris muscle

nerve Eye movement

Superior rectus muscle: elevation, intorsion, and adduction

Inferior rectus muscle: depression and extorsion

Medial rectus muscle: adduction
Inferior oblique muscle: extorsion, elevation, and abduction

Motor ( Pupillary constriction

parasympathetic) Pupillary sphincter (Edinger-Westphal nucleus and muscarinic receptors)
Efferent limb of the pupillary light reflex
Accommodation: ciliary muscle

IV Trochlear nerve Motor Eye movement: superior oblique muscle (intorsion, depression, and abduction) [2]

V Trigeminal nerve Sensory Facial sensation: ophthalmic (CN V1), maxillary (CN V2), mandibular nerve (CN V3)
Innervation of:
Mucous membranes of the oral and nasal cavity and the soft and hard palate
Teeth

Temporomandibular joint
Meninges
Anterior wall of the external auditory canal

Somatosensation of anterior ⅔ of the tongue

Afferent limb of the corneal and lacrimation (nasociliary branch)
Afferent limb of the jaw jerk reflex (muscle spindle from masseter)

Motor (only Muscles of mastication

mandibular nerve) Masseter, temporalis, medial pterygoid muscles close the jaw
Lateral pterygoid muscles open the jaw
Efferent limb of the jaw jerk reflex (masseter)

Innervation of:
Tensor tympani muscle (contraction dampens loud sounds)
Tensor veli palatini muscle
Anterior belly of the digastric muscle
Mylohyoid muscle

VI Abducens nerve Motor Eye movement: lateral rectus muscle: abduction

VII Facial nerve Sensory Taste: anterior ⅔ of the tongue (chorda tympani)
Innervation of:
Tympanic membrane (chorda tympani)

Skin behind the ear (posterior auricular branch)

Motor (somatic) Facial expression

Eyelid closing: orbicularis oculi

Efferent limb of the corneal reflex (temporal branch, bilaterally)

Jaw opening: posterior belly of the digastric muscle
Hyoid elevation: stylohyoid muscle

Efferent limb of the acoustic reflex (stapedius muscle) → auditory volume modulation

Motor ( Salivation: submandibular and sublingual glands

parasympathetic) Lacrimation: lacrimal gland

Efferent limb of the lacrimation

VIII Vestibulocochlear Sensory Balance and equilibrium: vestibular nerve

nerve Hearing: cochlear nerve

IX Glossopharyngeal Sensory Taste perception: posterior ⅓ of the tongue (lingual branch)

nerve Somatosensation: posterior ⅓ of the tongue, middle ear, and Eustachian tube (tympanic nerve)
Afferent limb of the gag reflex
Visceral sensation: carotid sinus (baroreceptors for blood pressure)

Chemoreception: carotid body (chemoreceptors for PaO, PaCO2, and pH)

Motor (somatic) Swallowing: pharyngeal muscles (CN IX and CN X)

Innervation of stylopharyngeus muscle (elevation of pharynx/larynx)

Motor ( Salivation: parotid gland

parasympathetic)

X Vagus nerve Sensory (somatic) Posterior wall of the external auditory canal
Supraglottic region, larynx, trachea (cough reflex)

Sensory (visceral) Taste perception: supraglottic region

Visceral sensation: aortic body (baroreceptors for blood pressure), lung, stomach, liver,
kidneys, intestines up to left colonic flexure
Chemoreception: aortic body (chemoreceptors for PaO and PaCO)

Motor (somatic) Swallowing: pharyngeal muscles (glossopharyngeal and vagus nerves)

Middle and inferior pharyngeal constrictor muscles: passage of bolus
Palatoglossus muscle: elevates posterior tongue upon swallowing
Efferent limb of the gag reflex
Speech: laryngeal muscles (recurrent laryngeal branch)

Motor ( SA and AV node: ↓ heart rate

parasympathetic) Blood vessels: vasodilation
Visceral function: promotes the motility of the esophagus, stomach, intestines (up to the
splenic flexure)

XI Accessory spinal Motor Head turn: sternocleidomastoid muscle

nerve Shoulder elevation: trapezius muscle

XII Hypoglossal Motor Tongue protrusion: intrinsic and extrinsic muscles of the tongue

nerve

“Some Say Marry Money, But My Brother Says Big Brain Matters More:” CN I is sensory, CN II is sensory, CN III is motor,
CN IV is motor, CN V is both (mixed), CN VI is motor, CN VII is both (mixed), CN VIII is sensory, CN IX is both (mixed), CN X
is both (mixed), CN XI is motor, and CN XII is motor.

CN VII (Seven) controls Salivation by innervating Submandibular and Sublingual glands.

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Origin and pathways of the cranial nerves

Gross anatomy

Origin and pathways of the cranial nerves

Cranial Nerve origin Foramina/Structures Cranial nerve nuclei Destination Pathway

nerve

CN I Olfactory Cribriform plate - Lateral stria → Olfactory receptor cells (first order
epithelium telencephalon neurons) → fila olfactoria → penetrate
of the cribriform plate of the ethmoid bone →
Medial stria →
nasal olfactory bulb → olfactory tract
amygdala
mucosa (second order neurons) → (split into
two) lateral portion connects directly
with telencephalon (prepyriform area),
medial portion connects with
amygdala [3]

Only cranial nerve with no thalamic

relay to cortex

CN II Retinal Optic canal Lateral geniculate Visual cortex on the Ganglion cells of the retina →
ganglion nucleus occipital lobe optic nerve → optic canal (sphenoid
cells bone) → optic chiasm (
middle cranial fossa)
Fibers from nasal retina: cross at
the optic chiasm
Fibers from temporal retina:
continue ipsilaterally at the
optic chiasm

Optic chiasm → optic tract → projects

to pretectal area, superior colliculi ,
suprachiasmatic nuclei, and
lateral geniculate nucleus
Lateral geniculate nucleus → optic
radiation
Upper optic radiation: fibers from
superior retinal quadrants →
parietal lobe → visual cortex
Lower optic radiation: fibers from
inferior retinal quadrants →
temporal lobe (Meyer loop) → visual
cortex

Visual cortex on the occipital lobe:

comprises the calcarine sulcus
between lingual and cuneus gyrus
[4]

CN III Midbrain Lateral Somatic: oculomotor Ocular and orbital Somatic: efferent fibers from
cavernous sinus nucleus muscles oculomotor nucleus → red nuclei →
medial aspect of the cerebral peduncle
Superior orbital Visceral: Edinger-
fissure Westphal nucleus Visceral: Edinger-Westphal nucleus →
preganglionic parasympathetic fibers
join CN III in the basilar segment
Interpeduncular fossa → between
posterior cerebral artery and
superior cerebellar artery →
dura mater → lateral wall of
cavernous sinus → (together with
sympathetic fibers from internal
carotid plexus) superior orbital fissure
→ division into superior and inferior
branch [5]
Superior branch
Superior rectus and
levator palpebrae superioris

Sympathetic fibers →
superior tarsal muscle
Inferior branch
Inferior rectus, medial rectus,
and inferior oblique muscle
Preganglionic parasympathetic
fibers → ciliary ganglion →
sphincter pupillae and
ciliary muscles

CN IV Posterior Lateral Trochlear nucleus Contralateral Trochlear nucleus in the posterior

midbrain cavernous sinus superior oblique midbrain → fibers cross within
muscle midbrain → subarachnoid space →
Superior orbital
through dura mater → lateral wall of
fissure
cavernous sinus →
superior orbital fissure → contralateral
superior oblique muscle [6]

CN V Pons CN V1: Three sensory nuclei CN V1: frontonasal One motor nucleus: motor root passes
superior orbital skin and inferiorly to the sensory root
fissure Mesencephalic mucous membranes Three sensory nuclei: sensory root on
nucleus:
CN V2: CN V2: maxillary the anterior pons at the middle
proprioception
foramen skin and cerebellar peduncle → trigeminal
rotundum Principal sensory mucous membranes ganglion → divides into 3 nerves:
nucleus: fine Ophthalmic nerve (CN V1): lateral
CN V3: CN V3: mandibulary
touch and wall of cavernous sinus → recurrent
foramen ovale skin and
pressure from the tentorial branch (supplies tentorium
(skull) mucous membranes,
face and teeth cerebelli) → superior orbital fissure
muscles of
→ division into three branches that
Spinal trigeminal mastication
provide sensory innervation to the
nucleus: pain,
skin and mucous membranes of
temperature, and
light touch frontonasal structure [7]
sensations Upper eyelid and conjunctiva,
cornea, ciliary bodies, iris
One motor nucleus
Scalp, forehead
Frontal, ethmoid, and
sphenoid sinuses
Superior anterior nasal cavity,
bridge of nose

Parasympathetic and sensory

fibers to lacrimal gland
Sympathetic fibers to
dilator pupillae muscle
Maxillary nerve (CN V2): lateral
wall of cavernous sinus→
foramen rotundum → division into
branches that provide sensory
innervation to the skin and
mucous membranes of maxillary
structures [8]
Lower eyelid and conjunctiva

Inferior posterior portion of the

nasal cavity, lateral nose
Upper lip, cheeks, maxillary sinus
, upper teeth, and gingiva,
superior palate
Postganglionic parasympathetic
fibers from the
pterygopalatine ganglion (from
CN VII): lacrimal gland, nasal
mucous glands
Mandibular nerve (CN V3)
Sensory root →
foramen ovale (skull) →
infratemporal fossa → 4 branches
that provide sensory innervation
to the skin and
mucous membranes of
mandibular structures

Sensory innervation of:

Lower third of the face,
including chin and lower lip
Buccal membranes,
mandibular teeth, and gingiva
Anterior ⅔ of the tongue

Anterior auricle, external

meatus, and tympanic
membrane
Autonomic fibers via
submandibular ganglion to
submandibular and sublingual
glands
Parasympathetic fibers from
the chorda tympani (from
CN VII): taste in the anterior
⅔ of the tongue

Parasympathetic fibers from

CN IX to parotid gland
Motor root runs along trigeminal
cave → joins sensory root →
foramen ovale (skull) [9]
Muscles of mastication:
masseter, medial pterygoid,
temporalis , and
lateral pterygoid muscles
Tensor tympani muscle

Tensor veli palatini muscle

Anterior belly of
digastric muscle
Mylohyoid muscle

CN VI Dorello canal Abducens nucleus Lateral rectus Abducens nucleus (caudal pons) →
muscle through the dura mater →
Medial
Dorello canal → medial wall of
cavernous sinus
cavernous sinus →
superior orbital fissure →
lateral rectus muscle [10]

CN VII Stylomastoid Facial motor nuclei Muscles of Intracranial: large motor and small
foramen sensory root exit the brain in the
Solitary nucleus
cerebellopontine angle →
(gustatory
internal acoustic meatus → roots fuse
sensation)
in the facial canal → geniculate
Salivatory nuclei ( ganglion → branches:
parasympathetic) Greater petrosal nerve:
parasympathetic fibers to mucous
glands of the oral cavity, nose, and
pharynx as well as the
lacrimal gland
Nerve to stapedius: motor fibers to
stapedius muscle of the middle ear

Chorda tympani: sensory fibers to

the anterior ⅔ of the tongue,
parasympathetic fibers to the
submandibular and sublingual
glands

Exits facial canal via

stylomastoid foramen
Extracranial: travels anterior to the
outer ear
Posterior auricular nerve: Motor
fibers to intrinsic and extrinsic
muscles of the outer ear
Sensory fibers to a small area
around the concha of the auricle

Motor branches to posterior belly

of the digastric muscle and
stylohyoid muscle
Travels through parotid gland →
within parotid gland, CN VII splits into
five branches that innervate the
muscles of (e.g., orbicularis oculi,
platysma) [11]

CN Internal auditory Vestibular nuclei Cochlear pathway: Vestibular nuclei complex and ventral
meatus complex auditory cortex and dorsal cochlear nuclei form the
VIII
vestibulocochlear nerve →
Ventral and dorsal Vestibular pathway:
internal auditory meatus at the
cochlear nuclei vestibular cortex
cerebellopontine angle → splits in
vestibular nerve and the cochlear
nerve [12]

Cochlear pathway: outer and inner

hair cells (from the organ of Corti)
→ bipolar neurons of the spiral
(cochlear) ganglion → cochlear
nerve → ventral and dorsal nuclei →
superior olivary nucleus →
lateral lemniscus → inferior
colliculus → medial geniculate body
→ auditory radiations →
primary auditory cortex (transverse
temporal gyri of Heschl) and
amygdala → auditory association
cortex

Vestibular pathway: hair cells of the

otolith organs and the three
semicircular canals → bipolar
neurons of the vestibular ganglion →
vestibular nerve → vestibular nuclei
complex → cerebellum (
flocculonodular lobe), nuclei of
CN III, CN IV, and CN VI ,
reticular formation , spinal cord,
and thalamus → vestibular cortex

CN IX Medulla Jugular foramen Inferior salivatory
nucleus
Solitary nucleus
Spinal nucleus of the
trigeminal nerve
Nucleus ambiguus
Pharyngeal mucosa
Postolivary sulcus → jugular foramen
(along with CN X and CN XI) →
superior and inferior (petrous) ganglia
Tympanic nerve: sensory and
parasympathetic fibers
Sensory fibers to middle ear,
internal surface of the tympanic
membrane, and Eustachian tube
Parasympathetic fibers to
parotid gland

Descends anterolateral to the internal

carotid artery
Motor innervation of
stylopharyngeus muscle
Carotid sinus nerve: sensory fibers
to carotid sinus and body
Enters pharynx between superior and
middle pharyngeal constrictors [13]
Divides into several sensory
branches
Unites with vagus fibers →
pharyngeal plexus: sensory
innervation of oropharyngeal
mucosa

Taste and sensation to posterior

⅓ of the tongue
Tonsillar plexus: sensory
innervation of palatine tonsils

CN X Jugular foramen Nucleus ambiguus: Multiple viscera, Cranium: postolivary sulcus →

responsible for
Esophageal hiatus
motor output and
parasympathetic
output to the heart
and motor
innervation of the
upper part of
gastrointestinal
tract (including
pharynx, larynx,
upper esophagus)
Nucleus solitarius:
responsible for
visceral sensory
input (e.g., due to
bowel distention,
signaling from
baroreceptors due
to pressure increase)
and taste sensation
Dorsal nucleus of
vagus nerve:
responsible for
parasympathic
output to viscera
(heart, lungs, and
upper GI)
Spinal trigeminal
nucleus
including the larynx,
pharynx, esophagus,
heart, lungs, and
greater part of the
intestine
jugular foramen (together with CN IX
and CN XI) → sensory innervation of
external auditory canal and external
ear
Neck: carotid sheath → inferior of the
internal jugular vein and
common carotid artery
Right vagus nerve: anterior of the
subclavian artery → thorax
Left vagus nerve: between left
common carotid and left
subclavian arteries → thorax
Branches
Pharyngeal branches: motor
innervation of pharyngeal and
soft palate muscles
Afferent fibers to root of tongue
and epiglottis: minor role in taste
sensation
Superior laryngeal nerve: splits
into 2 branches
Internal laryngeal nerve:
passes underneath the
mucosa of the piriform recess,
sensory innervation of
laryngopharynx and larynx
above the vocal cords
External laryngeal nerve:
motor innervation of
cricothyroid muscle
Right recurrent laryngeal nerve:
under right subclavian artery

Left recurrent laryngeal nerve:

under aortic arch
Both recurrent laryngeal nerves
ascend to larynx
Motor innervation of majority
of intrinsic laryngeal muscles

Sensory innervation of larynx

below the vocal fold

Thorax
Right vagus nerve forms posterior
vagal trunk → runs along the dorsal
esophagus
Left vagus nerve forms anterior
vagal trunk → runs along the ventral
esophagus
Both trunks form oesophageal
plexus: motor innervation of
esophageal smooth muscles

Cardiac plexus
Parasympathetic fibers →
regulation of heart rate (SA node
and AV node)
Sensory fibers: visceral sensation
of heart
Pulmonary plexus: visceral
sensation of lungs
Abdomen: via esophageal hiatus →
anterior and posterior vagal trunk →
parasympathetic and sensory
innervation of lower esophagus,
stomach, small intestine, and large
intestine up to the splenic flexure

CN XI Enters: Spinal accessory Sternocleidomastoid Spinal portion: ventral horn of C1–

foramen magnum nucleus (C1–C5) and trapezius C5/C6 spinal nerve roots → form
muscles spinal part of the accessory nerve
Exits: Nucleus ambiguus
→ enters cranial cavity via
jugular foramen
foramen magnum → posterior
cranial fossa → meets the cranial
portion of the accessory nerve → exits
via jugular foramen → descends
along internal carotid artery → motor
fibers to sternocleidomastoid muscle
→ through posterior triangle of the
neck → motor fibers to
trapezius muscle
Cranial portion: lateral aspect of the
medulla oblongata → meets spinal part
of the accessory nerve →
jugular foramen → combines with CN X
at its inferior ganglion [14]

CN XII Hypoglossal canal Hypoglossal nucleus Muscles of the Hypoglossal nucleus → preolivary
tongue sulcus → hypoglossal canal → inferior
of angle of the mandible → crosses
internal and external carotid arteries
→intrinsic and
extrinsic muscles of the tongue
[15]

CN I–IV are located in the midbrain, V–VIII in the pons,and IX–XII in the medulla.

The nuclei located in the medial brainstem are factors of 12, except 1 and 2 (i.e., CN III, CN IV, CN VI, and CN XII).

“Standing Room Only”: CN V1 exits through Superior orbital fissure, CN V2 exits through foramen Rotundum, and CN V3
exits through foramen Ovale.

The sulcus limitans in the 4 ventricle separates the CN Motor nuclei in the Medial part of the brain stem (basal plate) from
the sensory nuclei in the Lateral part (aLar plate).

3D Anatomy

Clinical approach to cranial nerve palsy

Confirm the diagnosis clinically with a cranial nerve examination.

Consider further evaluation for underlying etiology based on clinical suspicion.

General principles of imaging [16][17][18]

MRI (without and with IV contrast)

Usually the preferred first-line imaging modality for direct imaging of the nerve(s)

Can also identify soft tissue etiologies (e.g., cavernous sinus thrombosis in CN III–VI palsy)

CT with IV contrast

Preferred for the evaluation of bony lesions or skeletal trauma (e.g., orbital fractures, skull base fractures)

Preferred first line imaging modality to evaluate sinonasal pathology (e.g., in CN I palsy)

MR angiography: Consider for patients with vascular pathology (e.g., aneurysm).

Laboratory studies (e.g., CBC, inflammatory markers, and antigen-specific ANAs) as needed to evaluate for neoplastic, infectious,
inflammatory, or autoimmune etiologies

Electromyography (EMG): can be used to assess the severity of nerve injury

Fibrillation potentials: indicate nerve degeneration

Polyphasic potentials: indicate nerve regeneration

Absence of motor action potentials (on EMG in combination with electroeurography): surgical intervention likely needed

Consult neurology and other relevant specialties.

Management depends on addressing underlying etiology; spontaneous recovery may occur.

Olfactory nerve palsy (I)

Etiology

Acquired

Most commonly due to trauma to the lateral and occipital regions (e.g., ethmoid bone fracture)

Intracranial space-occupying lesion (e.g., meningioma)

Infection (e.g., meningitis)

Congenital

Primary: congenital anosmia

Secondary in diseases such as Kallmann syndrome and primary ciliary dyskinesia

Clinical features [16][19]

Anosmia (hyposmia or dysosmia may be present instead)

Sudden anosmia typically occurs secondary to trauma.

Progressively worsening anosmia is suggestive of an obstructive lesion or a neurodegenerative disease-

Altered perception of taste

Diagnostics [16][17][20][21]

Cranial nerve examination

Diagnosis is clinical and based on:

Comprehensive history
[20]
Cranial nerve examination: inability to identify certain smells (e.g., peppermint, coffee)

Assess for common differential diagnoses of olfactory dysfunction, such as sinonasal pathology. [21]

Perform a head and neck exam.

Consult otolaryngology for nasal endoscopy.

Further evaluation [20]

Evaluate for the underlying etiology.

Imaging [16][17][18]

CT maxillofacial region (with IV contrast): preferred for trauma or suspected sinonasal pathology not confirmed on nasal endoscopy

MRI head (without and with IV contrast): preferred for a suspected primary neurological etiology [18]

Laboratory studies as needed : to evaluate for other etiologies as guided by clinical probability

Treatment

Consult neurology.

Address any treatable causes identified.

Consider a trial of olfactory training. [20][22][23]

A self-administered therapy in which the patient exposes themselves to 4 different odors for ∼10 seconds twice daily for about 12–
24 weeks.

Associated with improved olfactory sensitivity, especially in olfactory dysfunction secondary to trauma, infections, and
neurodegenerative diseases.
[20][21]
Spontaneous recovery (typically over months to years) can occur in up to half the patients with anosmia.

Counsel patients on coping strategies such as monitoring for signs of spoiled food and installing smoke and gas detectors.
[24]

Optic nerve palsy (II)

Etiology

Acquired

Ischemic optic neuropathy (i.e., caused by microvascular disease)

Inflammation (optic neuritis): multiple sclerosis, sarcoidosis, viral infections (e.g., measles, mumps)

Trauma

Tumors: e.g., optic nerve glioma, pituitary adenoma

 Elevated intracranial pressure: e.g., hydrocephalus

Ischemia: e.g., giant cell arteritis [25]

Malnutrition: vitamin B deficiency

Drugs: sildenafil, amiodarone, ethambutol

Toxins: e.g., ethyl alcohol, mercury, lead

Congenital

Primary: optic nerve hypoplasia

Secondary: infantile nystagmus, sensory strabismus

Clinical features [16]

Impaired vision, including blindness (may start as night blindness), depending on the site of the lesion

Features of the underlying disease, such as: [26]

Uhthoff phenomenon in multiple sclerosis

Jaw claudication and headache in giant cell arteritis

Diagnostics [16][26]

Cranial nerve examination

Diagnosis is clinical and based on a comprehensive ocular examination as part of the cranial nerve examination, which includes:

Assessment of pupillary response, visual field exam, and visual acuity tests
[17]
Complete transection: ipsilateral blindness and loss of direct and indirect pupillary reflex
[4]
Pituitary adenoma (compression to the optic chiasm): bitemporal hemianopia

Unilateral optic nerve dysfunction: relative afferent pupillary defect [25][26]

Fundoscopy: findings depend on the underlying etiology and include

Papillitis

Papilledema in ↑ ICP

Optic atrophy in compression (e.g., tumor)

Further evaluation

Consider further evaluation for underlying etiology based on clinical findings.

Imaging [17]

CT head: initial evaluation of trauma or orbital complications of sinusitis

MRI brain and orbits: initial evaluation of suspected tumor, optic neuritis, or neurodegenerative diseases

Laboratory studies as needed, such as: [27][28]

ESR and CRP (to assess for giant cell arteritis)

ANA and antigen-specific ANAs

Toxic exposure tests

Treatment [16][26]

Address any underlying etiologies identified.

Consult neurosurgery and/or ophthalmology.

Traumatic CN II palsy: Options include surgery, high-dose corticosteroids, and observation.

Oculomotor nerve palsy (III)

Etiology

Etiology of CN III palsy

Structure Etiology Clinical features

Oculomotor Ischemic stroke (posterior cerebral artery) The corticospinal tract is usually also affected, causing syndromes characterized
by ipsilateral oculomotor palsy and contralateral hemiparesis:
nuclei Multiple sclerosis
Benedikt syndrome
Weber syndrome
Unilateral lesion of the oculomotor nucleus can cause bilateral
superior rectus muscle palsy. [29]

Basilar segment Aneurysm of the Headache

posterior communicating artery Paralytic squint
Skull base fracture Pupillary involvement: nonreactive, dilated pupil (blown pupil)
Basal meningitis

Transtentorial herniation (uncal herniation) Abducens nerve palsy

Features of elevated intracranial pressure (e.g., coma, blown pupil)
Hutchinson pupil

Intracavernous Cavernous sinus thrombosis CN IV, CN V (CN V1, CN V2), and/or CN VI palsy

segment Tolosa-Hunt syndrome

Internal carotid artery aneurysms
Large parasellar tumors (e.g., meningioma)

Intraorbital Tumors within the orbital cavity Loss of vision

segment Trauma Pain

Orbital cellulitis Proptosis

Palsies associated with CN IV and/or CN VI

Nonreactive pupil

Isolated Ischemic microangiopathy (e.g., diabetic Paralytic squint

cranial mononeuropathy, hypertension)
oculomotor Pupillary involvement: typically sparing the pupil
nerve palsy Multiple sclerosis
Myasthenia gravis
Giant cell arteritis

High-speed deceleration injuries [16]

Parasympathetic fibers of CN III are located superficially and motor fibers are located centrally. Parasympathetic fibers
are more susceptible to compressive lesions (e.g., uncal herniation, aneurysm of the posterior communicating artery).
Motor fibers are more susceptible to ischemia (e.g., vasculitis, diabetes, atherosclerosis).

Clinical features [30]

Horizontal diplopia that worsens when the head is turned away from the side of the lesion

Ptosis

Light sensitivity

Additional features may be present, depending on the etiology and the level of the oculomotor nerve lesion.

Diagnostics [16][30]

Cranial nerve examination

Diagnosis is clinical and based on a comprehensive ocular examination as part of the cranial nerve examination.

Assessment of extraocular muscle function : Lesions of the motor portion typically produce paralytic squint.

Down-and-out gaze: affected eye looks outwards (exotropia) and downwards (hypotropia)

Adduction weakness

Assessment of pupillary response (afferent: CN II; efferent: CN III)

Lesions of the autonomic (parasympathetic) portion result in loss of the pupillary reflex.

See also “Physiology and abnormalities of the pupil” for details on oculomotor nerve lesions and drugs that affect pupillary size.

Oculomotor nerve palsy leaves you down and out.

Impaired pupillary reaction with relative sparing of motor function is typically seen in compressive lesions. Prominent
motor dysfunction with sparing of the pupil is typically seen in ischemic lesions. However, pupillary findings cannot
reliably distinguish between the etiologies of oculomotor palsy. [27][31][32]

Further evaluation

Evaluate for underlying etiology based on clinical findings.

Clinical findings Likely underlying etiology Further evaluation

Complete palsy with dilated Suggestive of a compressive lesion (e.g., Obtain urgent MRI brain and orbits with

pupil posterior communicating artery aneurysm) [30] MR angiography [17][31][33]

OR Consult neurosurgery depending on findings.

Incomplete palsy regardless If MRI is normal, consult neurology and/or

of pupillary findings ophthalmology and consider a lumbar puncture.

Complete palsy with a normal
pupillary reflex (pupillary
sparing)
Suggestive of ischemic microangiopathy, especially in Initial neuroimaging may not be routinely required.
patients > 50 years of age with atherosclerotic risk factors [17][30][31][32]
[17][30][34]
Consult neurology and/or ophthalmology.

Assess risk factors for atherosclerosis or arteritis; e.g.,

[30]

Check blood pressure and blood glucose.

Consider additional laboratory studies (e.g., CBC,
ESR, lipid profile, ANA, syphilis diagnostics) as
needed.
Consider MRI brain if signs of pupillary involvement
develop, or if there is no recovery after 6–8 weeks.
[17][30]

MRI brain and orbits should also be obtained in patients ≤ 50 years old with a history of cancer and additional neurologic
findings, including nonisolated cranial nerve palsy. [33]

Treatment [16][30]

Compressive lesions

Immediate neurosurgery referral for management

[35][36]
Posterior communicating artery aneurysm requires urgent neurosurgical clipping or endovascular coiling

Consider strabismus surgery if symptoms do not improve after treatment of the underlying cause.

Ischemic microangiopathy or demyelinating lesions:

Medical management with control of the underlying disease

Ischemic CN III palsy typically resolves spontaneously within 6–8 weeks. [17][30]

Prism glasses or an eye patch can be used to improve diplopia while awaiting resolution.

Motor fibers are in the Middle of CN III, while Parasympathetic fibers are on the Periphery of the nerve.

Trochlear nerve palsy (IV)

Etiology

Acquired

Microvascular damage (diabetes, hypertension, arteriosclerosis)

Cavernous sinus thrombosis

Trauma

Congenital: fourth nerve palsy

Clinical features

Vertical or oblique diplopia

Exacerbated on downgaze (e.g., reading, walking downstairs) away from side of affected muscle [37]

Worsens when patient turns the head towards the paralyzed muscle → compensatory head tilt to the opposite side of the lesion

With damage to the CN IV, you cannot look at the floor.

Diagnostics

Cranial nerve examination

Diagnosis is clinical, based on cranial nerve examination, which includes: [37][38]

Assessment of extraocular muscle function

Extorsion of the eye

Inability to depress and abduct the eyeball simultaneously

Park-Bielchowsky test: ipsilateral hypertropia that worsens on contralateral gaze and ipsilateral head tilt

Imaging [17][33]

Not routinely required

Consider MRI brain and orbits in consultation with a neurologist in the following situations

History of trauma

Patients ≤ 50 years old with a history of cancer and additional neurologic findings, including nonisolated cranial nerve palsy

Persistent palsy after 3 months (in all age groups)

Progression of symptoms

Treatment [16][39]

Consult neurology and ophthalmology.

Symptoms often resolve spontaneously within six months of onset.

Prism glasses or an eye patch can be used to improve diplopia while awaiting resolution.

Surgical realignment may be needed for persistent CN IV palsy.

Trigeminal nerve palsy (V)

Etiology

Tumor

Vascular compression

Trauma, including maxillofacial or oral surgery, and mandibular molar extractions

Inflammation of the nerve

Cavernous sinus thrombosis

Clinical features
Clinical features depend on the site of the lesion and can include (see “Localizing features of CN V palsy” for details):

Altered sensation over the face and tongue

Weakness in muscles of mastication

Hearing impairment

Diagnostics [16][40]

Cranial nerve examination

Diagnosis is clinical, based on ear examination, nose and throat examination, and cranial nerve examination.

Assess for decreased facial sensation to light touch, pain (can also be increased), and/or temperature (CN V1, V2).

Assess for diminished/absent corneal reflex or lacrimation (CN V1).

Assess muscles of mastication (CN V3) for:

Signs of atrophy

Decreased strength (e.g., open mouth against resistance)

Jaw jerk reflex

Localizing features of CN V palsy

Peripheral trigeminal nerve Ophthalmic nerve ( Absent corneal reflex (afferent limb)

lesions CN V1 Loss of sensation in the ipsilateral forehead

Maxillary nerve (CN V2) Loss of sensation in the ipsilateral midface

Mandibular nerve ( Anesthesia of the ipsilateral lower ⅓ of the face and anterior ⅔ of the tongue

CN V3 Paresis of ipsilateral muscles of mastication

Deviation of jaw towards the side of the lesion due to unopposed action from the
opposite pterygoid muscle
Diminished/absent jaw jerk reflex (CN V3)

Lesion of the tensor tympani branch Hearing impairment (particularly affecting low-pitched sounds)

Lesions of the trigeminal nerve nuclei (depending on the Ipsilateral weakness of muscles of mastication and/or ipsilateral loss of sensation

nuclei affected)

The primary features of trigeminal neuropathy are numbness and/or weakness in the areas of trigeminal nerve
innervation, whereas the primary feature of trigeminal neuralgia is intermittent sharp pain in the same area without
sensory or motor deficits. [40]

Further evaluation

Consider further evaluation for underlying etiology based on clinical findings.

Imaging [16][17][40]

Not routinely required if the underlying etiology is clear (e.g., peripheral paresthesia following mandibular molar extraction)

History of head trauma: Consider CT head and skull base.

Suspected intracranial hemorrhage, tumor, cavernous sinus thromboss : MRI head (without and with contrast)

Laboratory studies (as needed): e.g., CBC, ESR, RPR, ANA and antigen-specific ANAs

Treatment [16][40]

Consult neurology and maxillofacial surgery.

Traumatic CN V palsy (e.g., following dental surgery) often resolves spontaneously within six months of symptom onset.

Treat the underlying cause (e.g., see “Treatment of cavernous sinus thrombosis”).

Screen for and treat complications.

Monitor for tongue and mouth injuries due to decreased sensation.

Screen for inadequate nutrition due to weak mastication.

Consider biofeedback training for chronic pain and weakness.

Screen for corneal edema due to absent corneal reflex; consider protective contact lenses.

Screen for symptoms of depression.

Abducens nerve palsy (VI)

Etiology [10][41]

Acquired

Trauma (e.g., at the superior orbital fissure)

Pseudotumor cerebri

Cavernous sinus thrombosis

Space-occupying lesion causing downward pressure (e.g., tumor)

Diabetic neuropathy

Giant cell arteritis (GCA)

Congenital: Duane syndrome (a rare type of strabismus characterized by an impaired abduction and ptosis on adduction) [42]

Abducens nerve palsy is the most common ocular cranial nerve palsy.

Clinical features

Horizontal diplopia that worsens when looking at distant objects

Inability to look laterally in the affected eye

Features of the underlying cause

Diagnostics [41][43]

Cranial nerve examination

Diagnosis is clinical, based on the examination of the extraocular muscles as part of the cranial nerve examination.

Esotropia: medial deviation of the affected eye at primary gaze

Inability to abduct the affected eye

Further evaluation [41]

Evaluate for underlying etiology based on clinical findings.

[17][33][41][43]
MRI head and orbits (with IV contrast) if any of the following are present:

Patients < 50 years of age

History of cancer

No ischemic risk factors

Additional neurologic findings, including nonisolated cranial nerve palsy

No evidence of resolution after 3 months

Evaluation of all other patients (or patients with normal neuroimaging): [41][43]

Consult neurology and/or ophthalmology.

Assess for ischemic risk factors : e.g., Check blood pressure, blood glucose, lipid profile, ESR.

Assess for underlying infection, autoimmune etiologies, or mimics (e.g., thyroid eye disease, myasthenia gravis) as needed.

CBC, ANA

Syphilis diagnostics,

Thyroid function tests, AChR antibody levels

Consider lumbar puncture.

Treatment

Consult neurology and ophthalmology.

Treat the underlying etiology.

Complete resolution of isolated CN VI palsy is seen in 75–88% of patients within 6 months of symptom onset. [41]

Prism glasses or eye patching may be considered to manage disabling diplopia.

Consider strabismus surgery for chronic CN VI palsy.[44]

Facial nerve palsy (VII)

See “Facial nerve palsy.”

Vestibulocochlear nerve palsy (VIII)

Etiology

Bacterial meningitis (most common cranial nerve palsy)

Lyme disease

Tumor (e.g., acoustic neuroma, neurofibromatosis type 2)

Trauma: basilar skull fracture (damage to the CN VIII within the internal acoustic meatus → symptoms of vestibular and cochlear
nerve damage)

Clinical features

Hearing loss

Vertigo

Motion sickness [45]

Tinnitus

Diagnostics [46][47]

Cranial nerve examination

Diagnosis is clinical, based on a comprehensive examination of the ears, hearing, and vestibular system, as part of the
cranial nerve examination.

Evaluation of cochlear nerve function (Rinne test, Weber test, audiometry) : sensorineural hearing loss

Evaluation of vestibular nerve function (HINTS exam, vestibular function tests): features of peripheral vertigo (see “Peripheral vs.
central vertigo”)

Abnormal head impulse test

Horizontal nystagmus; gaze fixation suppresses nystagmus

Skew deviation is absent

If a tuning fork is unavailable, a hum test may be used as an alternative to the Weber test [47]

In patients with sudden hearing loss, audiometry should be performed within 14 days from the onset of symptoms. [47]

Further evaluation

Consider further evaluation for underlying etiology based on clinical findings.

Laboratory studies as needed: e.g., CBC, ANA, or testing for Lyme disease, syphilis, TB, or HIV
[17]
Imaging: MRI of brain and brainstem with contrast (to assess for, e.g., vestibular schwannoma, multiple sclerosis, TIA)

Treatment [47]

Consult neurology and/or otolaryngology.

Treatment is aimed at resolving underlying causes (e.g., surgical excision and/or radiation for a tumor).

Consider expectant management with scheduled repeat audiometry to assess for spontaneous recovery.

For severe sensorineural hearing loss, consider initial treatment with prednisone within two weeks of symptom onset. [47]

Glossopharyngeal nerve palsy (IX)

Etiology

Idiopathic

Compression (e.g., aneurysm, tumor, retropharyngeal abscess)

Trauma (skull base fractures)

Clinical features
Isolated CN IX palsy is rare and may be asymptomatic due to shared sensory and motor nuclei with adjacent nerves. [48]

Throat and ear pain (glossopharyngeal neuralgia)

Mild dysphagia

Altered taste over the posterior aspect of the tongue

Difficulty swallowing

Lesions that affect the glossopharyngeal nerve typically also affect the vagus nerve because the two nerves exit the
jugular foramen in close proximity. [16][48]

Diagnostics [48]

Cranial nerve examination

Diagnosis is clinical, based on the cranial nerve examination.

Ipsilateral diminished or absent gag response (afferent limb).

Loss of taste in the posterior third of the tongue.

Sensory loss over the soft palate, upper pharynx, and posterior third of the tongue (including loss of taste sensation)

Further evaluation

Consider high-resolution MRI orbit, face, and neck, in conjunction with MRI head (without and with IV contrast) to assess for
underlying etiology. [17][18][49]

Treatment

Consults [48]

Neurology for all patients

Otolaryngology for patients with laryngeal or pharyngeal symptoms (for laryngoscopy)

Speech therapy as needed

Address suspected underlying cause if identified.

Consider acute pain management with adjuvant analgesics for glossopharyngeal neuralgia. [49]

Vagus nerve palsy (X)

Etiology

Trauma (skull base fractures)

Diabetes

Inflammation

Aortic aneurysms

Tumors

Surgery (e.g, recurrent nerve injury during thyroidectomy)

Clinical features

Nasal speech

Dysphagia, aspiration

Vocal cord paralysis, manifesting as:

Dysphonia (hoarseness) in unilateral recurrent laryngeal nerve palsy

Aphonia and inspiratory stridor in bilateral recurrent laryngeal nerve palsy

Features of gastroparesis, e.g., postprandial bloating

Lesions that affect the vagus nerve typically also affect the glossopharyngeal nerve because the two nerves exit the
jugular foramen in close proximity. [16][48]

Diagnostics [16][48][50]

Cranial nerve examination

Perform a focused HEENT examination and cranial nerve examination, assessing for:

Diminished or absent gag reflex (efferent limb) and/or cough reflex (afferent limb; impulses travel via the internal laryngeal nerve)

Uvular deviation: Articulating "ahh" will cause the uvula to deviate away from the affected side.

Flaccid paralysis and ipsilateral lowering of soft palate

Pharyngeal dysfunction: Ask the patient to swallow some water; choking or difficulty swallowing indicated dysfunction.

Tachycardia (resting heart rate > 100 beats per minute)

Consult otolaryngology for evaluation of larynx and pharynx, including: [48][50]

Indirect laryngoscopy: to identify vocal cord palsy (unilateral or bilateral)

Fiberoptic nasopharyngoscopy: to evaluate the upper respiratory tract for structural abnormalities or foreign bodies

Isolated palsy of the recurrent laryngeal nerve(s) indicates that the site of the lesion is most likely distal to the hyoid bone.
More proximal lesions manifest with dysphagia, nasal speech, palatal paralysis, and uvular deviation. [17][48]

Dysphonia in a patient with a neck mass, dyspnea, stridor, progressive neurological symptoms, history of tobacco use, or
history of surgery on the head, neck, or chest requires urgent evaluation by an otolaryngology specialist to evaluate for a
potentially serious underlying etiology. [50]

Further evaluation [16][17][18]

Based on clinical and laryngoscopic findings, consult neurology and consider further evaluation, including:

MRI brain and brainstem: to evaluate for proximal or intracranial etiologies, such asstroke or neoplasms

CT neck and proximal chest (with IV contrast): to evaluate for distal etiologies, such as thyroid, neck mass, or thoracic aortic aneurysm

Treatment
Depending on the etiology and severity of symptoms may include: [48][50]

Expectant management

Voice therapy

Laryngeal framework surgery

Thyroplasty

Injection laryngoplasty

Bilateral vocal cord palsy with stridor and dyspnea is a potentially airway-threatening condition. Consult otolaryngology
urgently to secure the airway (e.g., via tracheostomy). [51]
Accessory nerve palsy (XI)

Etiology

Iatrogenic: most commonly from surgery of lateral cervical region; , especially posterior border of sternocleidomastoid muscle (e.g.,
resection of posterior cervical lymph nodes, radical neck dissection)

Trauma (e.g., sternoclavicular joint dislocation, acromioclavicular joint dislocation)

Tumor

Clinical features [52]

Shoulder pain and heaviness

Difficulty or inability to raise hand overhead

Neckline asymmetry

Diagnostics [16][17]

Cranial nerve examination

Diagnosis is clinical, based on the cranial nerve examination.

Inspect upper back, shoulder, and neck

Paresis, atrophy, and/or asymmetry of the trapezius muscle

Ipsilateral shoulder drooping

Lateral winging of the scapula

Paresis, atrophy, and/or asymmetry of the sternocleidomastoid

Assess the trapezius muscle.

Ask the patient to shrug their shoulders.

CN IV palsy results in weakness during elevation of the ipsilateral shoulder.

Assess the sternocleidomastoid muscle.

Ask the patient turn their head from side to side.

CN IV palsy results in weakness in turning the head towards the contralateral side

Muscular atrophy is a late sequelae of CN XI palsy. [52]

Further evaluation

Consider further evaluation for underlying etiology based on clinical findings. Studies may include:

Imaging (i.e.,MRI orbit, face, neck or CT neck with IV contrast): to evaluate for possible underlying compressive etiology (e.g.,
malignancy) [17][18]

Electromyography (EMG): to assess severity of impairment

Accessory nerve palsy should be part of the differential diagnosis of neck and shoulder pain.

Treatment [16]

Consult neurology and/or head and neck or plastic surgery.

[52]
Conservative measures can be considered for patients with mild dysfunction and/or evidence of improvement on follow-up.

Pain control with arm sling

Physical therapy to strengthen shoulder girdle musculature

Surgical measures (e.g., nerve grafting, neurolysis) [52][53]

May be preferred for acute traumatic causes with severe dysfunction

Consider within 6 months of onset if there is poor response to conservative management

Hypoglossal nerve palsy (XII)

Etiology

Tumors (e.g., glomus jugulare)

Trauma

Occipital condyle fractures, skull base fractures

Iatrogenic trauma (e.g., neck dissection, endotracheal intubation, laryngeal mask airway) [54]

Dissection of the internal carotid artery

Stroke

Deymyelination

Clinical features

Dysarthria

Difficulty swallowing

Atrophy and fasciculation of the tongue on the side of the lesion

Diagnostics [17]

Cranial nerve examination

Diagnosis is clinical, based on the cranial nerve examination. Ask the patient to:

Press tongue against each cheek: Pressure to the cheek of the affected side might be increased.

Stick out their tongue

Deviation of the tongue to the ipsilateral side when protruded due to weakness of the ipsilateral tongue muscles.

Signs of unilateral lower motor neuron damage: tongue atrophy, fasciculations, or asymmetry

Further evaluation

Consider further evaluation to identify lesion location and underlying etiology based on clinical findings. Studies may include:

Imaging [17][18]

MRI head and neck (without and with IV contrast) : to locate nerve lesion and possible etiologies

CT skull base and neck with IV contrast: may be performed in conjunction with MRI to evaluate the foramina and skull base (e.g., for
fractures, skull base tumors)

Electromyography (EMG): to assess severity of of nerve damage

Treatment [16]

Consult neurology and speech language pathology.

Consider early surgery in acute nerve injury. [16]

Unilateral nerve injury

May spontaneously resolve within 6 months.

Advise patients to chew on the unaffected side.

Bilateral nerve injury: Consider enteral feeding strategies for swallowing difficulty.

Multiple cranial neuropathies

Overview of multiple cranial neuropathies [55][56][57]

Condition Affected cranial nerve Etiology Clinical features

Chronic Any Infection (Lyme disease, Insidious or subacute headache, fever, and neck stiffness
tuberculosis,
meningitis Additional symptoms depend on which CN is involved
cryptococcosis)
Inflammation (e.g.,
sarcoidosis, SLE, neoplasm)

Jugular foramen CN IX, CN X, and CN XI Glomus tumor Loss of taste in the posterior third of the tongue (CN IX)

syndrome Schwannoma Impaired speech and swallowing: paralysis of vocal cords,

palate, and pharyngeal muscles (CN X)
Meningioma
Impaired head turning and shoulder elevation: weakness of
Metastatic tumor
the trapezius and sternocleidomastoid muscles (CN XI)
Cholesteatoma

Cavernous sinus CN III, CN IV, CN V1, CN V2, Neoplasm or inflammation Impaired movement of the eye: paralysis of
and CN VI (e.g., Tolosa-Hunt extraocular muscles (CN III, CN IV, CN VI)
syndrome
syndrome) Horner syndrome
Intracavernous aneurysms Decreased sensation of the upper face (CN V1, CN V2)
Cavernous sinus
See “Skull base syndromes.”
thrombosis

Cerebellopontine CN V, CN VI, CN VII, CN VIII, Neoplasms of the Impairment of facial sensation (CN V)
CN IX, CN X cerebellopontine angle
angle syndrome Tinnitus
Vestibular
schwannoma Progressive sensorineural hearing loss

Meningioma Gait disequilibrium

Metastases Vertigo is uncommon.

Cholesteatoma See “Skull base syndromes.”

Guillain-Barré Any (most commonly CN III, Autoimmune inflammation Facial droop (CN VII)
CN VII, CN IX, CN X) of peripheral cranial nerves
syndrome Dysphonia, dysarthria, and dysphagia (CN IX and CN X)

Ophthalmoplegia and diplopia (CN III)

Multiple Any cranial nerve can be Autoimmune inflammation Vision loss (CN II)
affected of the cranial nerves
sclerosis Internuclear ophthalmoplegia (INO)
CN II impairment ( Ischemic stroke
retrobulbar neuritis) is a
common feature

References

1. Erman AB, Kejner AE, Hogikyan ND, Feldman EL. Disorders of cranial nerves IX and X. Semin Neurol. 2009; 29 (1): p.85–92. doi:
10.1055/s-0028-1124027 . | Open in Read by QxMD

2. Tubbs RS. Nerves and Nerve Injuries. Academic Press ; 2015

3. Khaku A, Patel V, Zacharia T, Goldenberg D, McGinn J. Guidelines for Radiographic Imaging of Cranial Neuropathies. Ear Nose
Throat J. 2017; 96 (10-11): p.E23-E39. doi: 10.1177/0145561317096010-1106 . | Open in Read by QxMD
4. Blumenfeld A, Nikolskaya G. Glossopharyngeal Neuralgia. Curr Pain Headache Rep. 2013; 17 (7). doi: 10.1007/s11916-013-
0343-x . | Open in Read by QxMD

5. Policeni B et al.. ACR Appropriateness Criteria ® Cranial Neuropathy. J Am Coll Radiol. 2017; 14 (11): p.S406-S420. doi:
10.1016/j.jacr.2017.08.035 . | Open in Read by QxMD

6. Morillon P, Bremner F. Trochlear nerve palsy.. Br J Hosp Med (Lond). 2017; 78 (3): p.C38-C40. doi:
10.12968/hmed.2017.78.3.C38 . | Open in Read by QxMD

7. Sharma AK, Kim DD, Fraser JA. Pearls & Oy-sters: Paradoxical Head Tilt in a Congenital Fourth Nerve Palsy. Neurology. 2021;
97 (3): p.e320-e323. doi: 10.1212/wnl.0000000000012082 . | Open in Read by QxMD

8. Murchison AP. Neuroimaging and Acute Ocular Motor Mononeuropathies. Arch Ophthal. 2011; 129 (3): p.301. doi:
10.1001/archophthalmol.2011.25 . | Open in Read by QxMD

9. Lueck CJ. Infranuclear ocular motor disorders. Elsevier ; 2011 : p. 281-318

10. The abducens nerve (CN VI). https://teachmeanatomy.info/head/cranial-nerves/abducens-nerve/ . Updated: March 13, 2019.
Accessed: April 2, 2019.

11. Elder C, Hainline C, Galetta SL, Balcer LJ, Rucker JC. Isolated Abducens Nerve Palsy: Update on Evaluation and Diagnosis. Curr
Neurol Neurosci Rep. 2016; 16 (8). doi: 10.1007/s11910-016-0671-4 . | Open in Read by QxMD
12. Duane syndrome. https://rarediseases.org/rare-diseases/duane-syndrome/ . . Accessed: April 6, 2017.

13. Chan J, Albretson J. Causes of isolated recurrent ipsilateral sixth nerve palsies in older adults: a case series and review of the
literature. Clinical Ophthalmology. 2015 : p.373. doi: 10.2147/opth.s78319 . | Open in Read by QxMD

14. Peragallo JH, Bruce BB, Hutchinson AK, et al. Functional and Motor Outcomes of Strabismus Surgery for Chronic Isolated
Adult Sixth Nerve Palsy. Neuro-Ophthalmology. 2014; 38 (6): p.320-325. doi: 10.3109/01658107.2014.957780 . | Open in
Read by QxMD

15. Stachler RJ, Francis DO, Schwartz SR, et al. Clinical Practice Guideline: Hoarseness (Dysphonia) (Update). Otolaryngology–
Head and Neck Surgery. 2018; 158 (1_suppl): p.S1-S42. doi: 10.1177/0194599817751030 . | Open in Read by QxMD
16. Li Y, Garrett G, Zealear D. Current Treatment Options for Bilateral Vocal Fold Paralysis: A State-of-the-Art Review. Clinical and
experimental otorhinolaryngology. 2017; 10 (3): p.203-212. doi: 10.21053/ceo.2017.00199 . | Open in Read by QxMD
17. Chandawarkar RY, Cervino LA, Pennington GA. Management of Iatrogenic Injury to the Spinal Accessory Nerve. Plast Reconstr
Surg. 2003; 111 (2): p.611-617. doi: 10.1097/01.prs.0000041943.47622.eb . | Open in Read by QxMD
18. Olarte M, Adams D. Accessory nerve palsy.. Journal of Neurology, Neurosurgery & Psychiatry. 1977; 40 (11): p.1113-1116. doi:
10.1136/jnnp.40.11.1113 . | Open in Read by QxMD

19. Setter K, Voloshin I, Bigliani L. Operative Treatment of Spinal Accessory Nerve Palsy. Techniques in Shoulder and Elbow
Surgery. 2004; Volume 5 (Issue 1): p.25-36.
20. Smith JH, Cutrer FM. Numbness matters: A clinical review of trigeminal neuropathy. Cephalalgia. 2011; 31 (10): p.1131-1144.
doi: 10.1177/0333102411411203 . | Open in Read by QxMD

21. Shah AC, Barnes C, Spiekerman CF, Bollag LA. Hypoglossal nerve palsy after airway management for general anesthesia: an
analysis of 69 patients. Anesth Analg. 2015; 120 (1): p.105-120. doi: 10.1213/ANE.0000000000000495 . | Open in Read by
QxMD

22. Blumenfeld H. Neuroanatomy Through Clinical Cases. Wiley-Blackwell ; 2010

23. Yanovitch T, Buckley E. Diagnosis and management of third nerve palsy. Curr Opin Ophthalmol. 2007; 18 (5): p.373-378. doi:
10.1097/icu.0b013e328270b8db . | Open in Read by QxMD

24. Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy. Lippincott Williams & Wilkins ; 2013

25. Tamhankar MA, Biousse V, Ying G-S, et al. Isolated Third, Fourth, and Sixth Cranial Nerve Palsies from Presumed Microvascular
versus Other Causes. Ophthalmology. 2013; 120 (11): p.2264-2269. doi: 10.1016/j.ophtha.2013.04.009 . | Open in Read by
QxMD

26. Fang C, Leavitt JA, Hodge DO, Holmes JM, Mohney BG, Chen JJ. Incidence and Etiologies of Acquired Third Nerve Palsy Using a
Population-Based Method. JAMA Ophthalmology. 2017; 135 (1): p.23. doi: 10.1001/jamaophthalmol.2016.4456 . | Open in
Read by QxMD

27. Sadagopan KA, Wasserman BN. Managing the patient with oculomotor nerve palsy. Curr Opin Ophthalmol. 2013; 24 (5): p.438-
447. doi: 10.1097/icu.0b013e3283645a9b . | Open in Read by QxMD

28. Steiner T, Juvela S, Unterberg A, Jung C, Forsting M, Rinkel G. European Stroke Organization Guidelines for the Management of
Intracranial Aneurysms and Subarachnoid Haemorrhage. Cerebrovasc Dis. 2013; 35 (2): p.93-112. doi: 10.1159/000346087
. | Open in Read by QxMD

29. Thompson BG, Brown RD, Amin-Hanjani S, et al. Guidelines for the Management of Patients With Unruptured Intracranial
Aneurysms. Stroke. 2015; 46 (8): p.2368-2400. doi: 10.1161/str.0000000000000070 . | Open in Read by QxMD

30. Carroll CG, Campbell WW. Multiple Cranial Neuropathies. Seminars in Neurology. 2009; 29 (1): p.53-65.

31. Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré syndrome. Lancet. 2016; 388 : p.717-727. doi: 10.1016/ S0140-
6736(16)00339-1 . | Open in Read by QxMD

32. Multiple Sclerosis (MS). https://www.merckmanuals.com/professional/neurologic-disorders/demyelinating-disorders/multiple-

sclerosis-ms . Updated: August 1, 2016. Accessed: April 6, 2017.
33. Peripheral Vestibular Nystagmus. https://www.aao.org/bcscsnippetdetail.aspx?id=d20f8ad8-845e-46fc-b7ed-7d00216c2726
. . Accessed: April 6, 2017.

34. Thomas Brandt, Marianne Dieterich. The dizzy patient: don't forget disorders of the central vestibular system. Nature Reviews
Neurology. 2017; 13 (6): p.352-362. doi: 10.1038/nrneurol.2017.58 . | Open in Read by QxMD
35. Chandrasekhar SS, Tsai Do BS, Schwartz SR, et al. Clinical Practice Guideline: Sudden Hearing Loss (Update). Otolaryngology–
Head and Neck Surgery. 2019; 161 (1_suppl): p.S1-S45. doi: 10.1177/0194599819859885 . | Open in Read by QxMD
36. The olfactory nerve (CN I) and olfactory pathway. https://teachmeanatomy.info/head/cranial-nerves/olfactory-cni/ .
Updated: December 24, 2018. Accessed: April 2, 2019.

37. The optic nerve (CN II) and visual pathway. https://teachmeanatomy.info/head/cranial-nerves/optic-cnii/ . Updated: October
19, 2018. Accessed: April 2, 2019.

38. The oculomotor nerve (CN III). https://teachmeanatomy.info/head/cranial-nerves/oculomotor/ . Updated: March 13, 2019.
Accessed: April 2, 2019.

39. The trochlear nerve (CN IV). https://teachmeanatomy.info/head/cranial-nerves/trochlear-nerve/ . Updated: March 13, 2019.
Accessed: April 2, 2019.

40. The opthalmic division of the trigeminal nerve (CNV1). https://teachmeanatomy.info/head/nerves/ophthalmic-nerve/ .

Updated: December 22, 2017. Accessed: April 3, 2019.

41. The opthalmic division of the trigeminal nerve (CNV2). https://teachmeanatomy.info/head/nerves/maxillary-nerve/ .

Updated: December 24, 2018. Accessed: April 3, 2019.

42. The opthalmic division of the trigeminal nerve (CNV3). https://teachmeanatomy.info/head/nerves/mandibular-nerve/ .

Updated: April 2, 2018. Accessed: April 3, 2019.

43. The facial nerve (CN VII). https://teachmeanatomy.info/head/cranial-nerves/facial-nerve/ . Updated: December 31, 2017.
Accessed: April 4, 2019.

44. The vestibulocochlear nerve (CN VIII). https://teachmeanatomy.info/head/cranial-nerves/vestibulocochlear/ . Updated:

August 7, 2018. Accessed: April 4, 2019.

45. The glossopharyngeal nerve (CN IX). https://teachmeanatomy.info/head/cranial-nerves/glossopharyngeal-nerve/ . Updated:

January 2, 2018. Accessed: April 4, 2019.

46. The accessory nerve (CN XI). https://teachmeanatomy.info/head/cranial-nerves/accessory/ . Updated: January 2, 2018.
Accessed: April 4, 2019.

47. The hypoglossal nerve (CN XII). https://teachmeanatomy.info/head/cranial-nerves/hypoglossal/ . Updated: January 20, 2019.
Accessed: April 4, 2019.

48. Bähr M, Frotscher M. Duus' Topical Diagnosis in Neurology. Thieme Medical Pub ; 2012

49. Ahmed HU. A case of mistaken muscles. BMJ. 2002; 324 (7343): p.962-962. doi: 10.1136/bmj.324.7343.962 . | Open in Read
by QxMD

50. Wrobel BB, Leopold DA. Smell and taste disorders.. Facial Plast Surg Clin North Am. 2004; 12 (4): p.459-68, vii. doi:
10.1016/j.fsc.2004.04.006 . | Open in Read by QxMD

51. Bromley SM. Smell and taste disorders: a primary care approach.. Am Fam Physician. 2000; 61 (2): p.427-36, 438.

52. Malaty J, Malaty IA. Smell and taste disorders in primary care. Am Fam Physician. 2013; 88 (12): p.852-9.

53. Pellegrino R, Han P, Reither N, Hummel T. Effectiveness of olfactory training on different severities of posttraumatic loss of
smell. Laryngoscope. 2019; 129 (8): p.1737-1743. doi: 10.1002/lary.27832 . | Open in Read by QxMD

54. Pekala K, Chandra RK, Turner JH. Efficacy of olfactory training in patients with olfactory loss: a systematic review and meta-
analysis. International Forum of Allergy & Rhinology. 2015; 6 (3): p.299-307. doi: 10.1002/alr.21669 . | Open in Read by
QxMD

55. Pinto JM. Olfaction. Proc Am Thorac Soc. 2011; 8 (1): p.46-52. doi: 10.1513/pats.201005-035rn . | Open in Read by QxMD

56. Vodopivec I, Rizzo JF. Ophthalmic manifestations of giant cell arteritis. Rheumatology. 2018; 57 (suppl_2): p.ii63-ii72. doi:
10.1093/rheumatology/kex428 . | Open in Read by QxMD

57. Riordan-Eva P. Clinical assessment of optic nerve disorders. Eye (Lond). 2004; 18 (11): p.1161-1168. doi:
10.1038/sj.eye.6701575 . | Open in Read by QxMD

58. Behbehani R. Clinical approach to optic neuropathies.. Clin Ophthalmol. 2007; 1 (3): p.233-46.

59. DIAGNOSIS: How are vestibular disorders diagnosed?. https://vestibular.org/understanding-vestibular-disorder/diagnosis ..

Accessed: April 4, 2019.

60. The vagus nerve (CN X). https://teachmeanatomy.info/head/cranial-nerves/vagus-nerve-cn-x/ . Updated: January 28, 2019.
Accessed: April 4, 2019.

61. Gastroparesis Diagnosis. https://www.ucsfhealth.org/conditions/gastroparesis/diagnosis.html . . Accessed: April 9, 2019.

62. Bedside Water-Swallow Testing for Dysphagia. https://www.jwatch.org/na41936/2016/07/28/bedside-water-swallow-

testing-dysphagia . Updated: July 28, 2016. Accessed: April 9, 2019.

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