CRANIAL NERVE LESIONS
IN THE
EMERGENCY DEPARTMENT
BY
RAKSHA RAMLAKHAN
OVERVIEW
 Introduction
 The cranial nerves
1. Function
2. Anatomy
3. Clinical examination
4. Pathologic features
5. Aetiology
 Multiple cranial nerve lesions
INTRODUCTION

Challenging for the EP

Aetiology represent a wide spectrum of pathology

Rapid evaluation for signs and symptoms that are life threatening
 Haemorrhage
 Infarct
 Mass lesion or inflammation with raised intracranial pressure
 Consider neoplasms, toxic, metabolic and infectious causes

ABC’S

Frequent re-evaluation if a central cause not excluded

Consultation with neurosurgeon and/or neurologist based on clinical evaluation and imaging
INTRODUCTION - ANATOMY
Figure 1:Major nuclei of the cranial nerves
Figure 2
THE CRANIAL NERVES
CN I – OLFACTORY NERVE
FUNCTION: SENSE OF SMELL
ANATOMY: - Fibres arise in mucous membrane of nose
- Cribriform plate of ethmoid
- Synapse in olfactory bulb
- Olfactory tract under frontal lobe
- Terminates in medial temporal lobe on same side
EXAMINATION: - Not routinely tested
3
- Test each nostril separately with bottles containing essences of familiarFig
smells
- Examine nasal passages if anosmia present
PATHOLOGICAL FEATURES: Unilateral anosmia
AETIOLOGY: Trauma – skull fracture or shear injury
Tumour – Frontal lobe masses
CN II – OPTIC NERVE

FUNCTION : VISION

ANATOMY: - Extends from retina for 5cm
- Passes through optic foramen
- Joins nerve from other side to form optic chiasm
- Fibres from temporal visual fields cross in chiasm
whereas those in nasal fields do not
- Optic tract to lateral geniculate body
- Fibres form optic radiation  posterior part of internal capsule
Ends in visual cortex of occipital lobe

CLINICAL EXAMINATION: - Visual acuity
- Visual fields
- Fundi

PATHOLOGICAL FEATURES: Unilateral/Bilateral visual loss
Visual field defects
Fig 4
-
Fig 5
Figure 6: The Visual Fields and Optic Pathways
Figure 7: Visual Field Defects

AETIOLOGY:
Trauma – traumatic optic neuropathy
Tumour – orbital compressive lesion
Ischaemic – ischaemic optic neuropathy
OPTIC NEURITIS
Inflammation of optic nerve  complete or partial loss of vision
Demyelination
Triad of loss of vision, eye pain and impairment of accurate colour vision
Causes

Multiple sclerosis

Toxic – ethambutol, chloroquine, nicotine, alcohol

Metabolic – vitamin B12 deficiency

Ischaemia – diabetes, temporal arteritis, atheroma

Familial

Infective – infectious mononucleosis
CN III – OCULOMOTOR NERVE

FUNCTION :
MOVES THE EYES
- motor fibres to levator palpebrae, superior rectus, medial rectus, inferior rectus,
oblique
Fig 8
PUPIL CONSTRICTION
- parasympathetic fibres to constrictor pupillae and ciliary muscles
inferior

ANATOMY:
Miosis •
Parasympathetic innervation ->Edinger Westphal
•
Pupil constriction in response to light relayed
by optic nerve and tract  superior colliculus
EW nucleus in midbrain
•
Efferent motor fibres from oculomotor nucleus
 wall of cavernous sinus with CN 4,5a,6
 Iridoconstrictor fibres -ciliary ganglion
•
Postganglionic fibres innervate iris
Figure 9: Pupillary constriction to light
Mydriasis •
Sympathetic innervation to eye
•
Fibres from hypothalamus to ciliospinal centre and synapse in spinal
cord at C8, T1 & T2
•
Exit anterior ramus in thoracic trunk & synapse in superior cervical
ganglion in neck
•
Neurones travel with internal carotid artery to eye
Figure 10: Oculo Sympathetic
Pathway

CLINICAL EXAMINATION: - Pupils – light reflex (direct and consensual)
- Accommodation
- Eye movements (diplopia and nystagmus)
ACCOMMODATION





Neural circuit to visual cortex and back
Involves parasympathetic component of CNIII
Stimulates smooth muscle of ciliary body to contract → lens changes shape
Pupil constricts
Argyll Robertson pupil → absent light reflex with intact accommodation (midbrain lesion)

PATHOLOGICAL FEATURES:
Ptosis caused by loss of levator palpebrae function
Eye deviated laterally and down
Diplopia
Dilated non reactive pupil
Loss of accommodation
Figure 11: Features of CNIII lesion

AETIOLOGY:
TRAUMA

Herniation of temporal lobe through tentorial opening ->compression and stretch injury
CENTRAL CAUSES

Vascular lesions in brainstem

Tumours

Demyelination
PERIPHERAL CAUSES

Compressive lesions
-intracranial aneurysms (on posterior comm artery)
-tumour
-meningitis
-nasopharyngeal carcinoma
-orbital lesions

Ischaemia/ Infarction
-diabetes mellitus
-arteritis
-migraine
-
MEDICAL VS SURGICAL 3rd NERVE PALSY
SURGICAL
•
•
•
•
•
Post communicating artery aneurysm
Pupillary involvement
Why?
Leakage of blood from aneurysm dome -- nerve across outer margin
Pupil fibres located very superficially
Cerebral angiography – definitive test
LP – Blood in CSF, inflammation, infection, neoplasm
MEDICAL
•
•
•
•
•
•
•
•
Pupil sparing
Hallmark of ischaemic lesions - central core of the nerve
Micro vascular disease, insufficiency of vasa nervosa
Frequent in >60yrs and atherosclerotic risk factors
Workup for eg DM,HYPERTENSION (if no evidence of aneurysm)
Spontaneous remission in 6-8 weeks
NSAIDS for pain
Symptomatic Rx
CN - IV TROCHLEAR NERVE

FUNCTION: Motor to superior oblique muscle – intorts ,depresses and abducts globe

ANATOMY:
-Nucleus in tegmentum of midbrain
-Exits from dorsal aspect
-Courses between post cerebral and superior cerebellar arteries before entering cavernous
sinus
-Enters orbit through superior orbital fissure ,crosses medially over LPS and SRSO

EXAMINATION: Ask patient to turn eye in and then try to look down

PATHOLOGICAL FEATURES: Inability to move eye downward and laterally
Diplopia
Patients tilt head toward unaffected eye to overcome inward
rotation of affected eye

AETIOLOGY: Trauma
A = involved (right) eye is elevated on forward gaze
B = extent of elevation is increased with adduction
C= extent of elevation is decreased with abduction
D = Elevation is increased with head tilting to the affected
side
E = Elevation is decreased with head tilting in the opposite
direction
CN V – TRIGEMINAL NERVE

FUNCTION: Motor to muscles of mastication and tensor tympani
Sensory to face, scalp, oral cavity (teeth and tongue)

ANATOMY:



Motor nucleus and sensory nucleus for touch in pons
Proprioceptive nucleus in midbrain
Pain and temperature nucleus descends through medulla to
reach upper cervical cord
Cerebellopontine angle  temporal lobe in middle cranial fossa
Petrous temporal bonetrigeminal ganglion3


Fig 12
1. Ophthalmic - cavernous sinus with CN3 SOF skin of forehead, cornea and conjunctiva
2. Maxillary -infraorbital foramen skin in middle of face ,mucus membranes of mouth, palate and nasopharynx
3. Mandibular with motor part of nerve  foramen ovale skin of lower jaw , mucus membranes of mouth
 EXAMINATION:
-Corneal reflex
-Facial sensation
-Motor – clench teeth and palpate masseter
-Jaw Jerk
 PATHOLOGICAL FEATURES:
-Partial facial anaesthesia
-Episodic facial pain with triggers eg eating and brushing teeth
 AETIOLOGY:
-Trauma – facial bone fracture
Trigeminal neuralgia
-Idiopathic, Vascular compression of root
-Episodic unilateral facial pain with triggers
-Normal findings on head and neck examination and no neurological
deficits
-Central causes (pons, medulla and upper cervical cord)
vascular
tumour
syringobulbar
-Peripheral (middle fossa)
aneurysm
tumour
chronic meningitis
-Trigeminal ganglion (petrous temporal bone)
trigeminal neuroma
meningioma
middle cranial fossa fracture
-Cavernous sinus
ophthalmic division only
with 3,4,6
aneurysm, tumour, thrombosis
CN VI – ABDUCENS NERVE

FUNCTION: Motor supply to lateral rectus muscle (abducts the eye)

ANATOMY:
•
•
•
•
•
•
•
Leaves brainstem at junction of the pons and medulla, medial to facial nerve.
Runs supant
Subarachnoid space emerges from brainstem.
Pons and clivus, dura -between dura and skull.
Tip of petrous temporal bone  enter cavernous sinus.
Alongside internal carotid artery.
Enters orbit SOFlateral rectus
Fig 13

PATHOLOGICAL FEATURES: Inability to move eye laterally
Diplopia on lateral gaze
Fig 14
note in (A) that the affected (right)
eye is adducted at rest
- note in (B) that the affected (right)
eye cannot abduct
 AETIOLOGY:
-Tumour e.g. lesions in cerebellopontine angle
-Cavernous sinus lesions e.g. vascular
-Elevated intracranial pressure from any cause
-Vascular
-Metabolic (Wernicke-Korsakoff syndrome)
-Subarachnoid space lesions (haemorrhage, infection, inflammation, tumour)
-Inflammatory (post viral, demyelinating, giant cell arteritis)
CN VII – FACIAL NERVE

FUNCTION: Motor to muscles of facial expression
Parasympathetic stimulation of lacrimal, submandibular and sublingual glands
Sensation to anterior two thirds of tongue, ear canal and tympanic membrane
Figure 15: Muscles of facial expression

ANATOMY:







Nucleus lies in pons
Leaves pons with CN8 through cerebellopontine angle
Enters facial canal and becomes geniculate ganglion
Gives off nerve to stapedius
Chorda tympani (taste from and two thirds of tongue) joins nerve in facial canal
Leaves skull via stylomastoid foramen
Enters parotid gland and divides to supply muscles of facial expression
Fig 16
 EXAMINATION:
Inspect for facial asymmetry – unilateral drooping of corner of mouth
-- smoothing of wrinkled forehead and nasolabial fold
Muscle power – look up to wrinkle forehead
- shut eyes tightly
- smile to compare nasolabial grooves

•
PATHOLOGICAL FEATURES:
Hemifacial paralysis
-LMN (level of nucleus or nerve root) leaves entire side of face paralyzed
-UMN (above level of brainstem nucleus) preserves forehead musculature
(due to bilateral cortical representation)
Figure 17: Left UMN facial
weakness
•
•
Abnormal taste
Sensory deficit around ear

AETIOLOGY:
INFECTION
Ramsay Hunt Syndrome
•
•
•
•
Herepes zoster oticus
unilateral facial paralysis, herpetiform vesiicular eruption, vestibulocochlear dysfunction
Rx similar
Lower incidence of facial recovery and possible sensorineural loss
Lyme Disease
Bacterial infections
Bells Palsy
•
(60-70% of acute unilateral facial paralysis)
•
Idiopathic facial paralysis
•
?viral cause – herpes
•
Abrupt onset LMN paresis progresses over 1-7 days to complete paralysis
•
Associated s& s – ear pain, decreased tearing, hyperacusis ,impairment of taste
•
Medical Rx – corticosteriods (1mg/kg per day for 7-10 days)
oedema of nerve confined within facial canal causes/contributes
to nerve injury
•
Diabetics have 29% risk of being affected
Fig 18 : Bell’s Palsy
UPPER MOTOR NEURON
-vascular, tumours
TRAUMATIC
-Temporal bone fracture with nerve transection
-Surgical exploration if evidence
-Sudden onset of complete unilateral facial paralysis
-Loss of electrical activity
-Evidence of displaced fracture involving the facial canal.
NEOPLASTIC
-Tumors of the facial nerve , along course of nerve that invade or compress the nerve.
-3 weeks
-Suspect neoplastic cause if recurrent ipsilateral facial paralysis
significant pain, prolonged symptoms, cranial nerve abnormality.
-Progressive
CN VIII – VESTIBULOCOCHLEAR
NERVE

FUNCTION: Hearing and balance

ANATOMY: 2 components:
-cochlear with afferent fibres for hearing
-originate in Organ of Corticochlear nucleus in ponsbilateral transmission to
-Medial geniculate bodiessuperior gyrus of temporal lobes
-vestibular with afferent fibres for balance
-Begin in utricle and semicircular canalsjoin auditory fibres in facial canalenter brainstem at
-Cerebellopontine angle.After entering pons-vestibular fibres run widely throughout brainstem
and cerebellum
Fig 19

EXAMINATION:

PATHOLOGICAL FEATURES: Unilateral hearing loss
Tinnitus
Vertigo and unsteadiness

AETIOLOGY:
Hearing test
Suspect partial deafness do Rinne’s and Weber’s
-Unilateral nerve deafness
tumours eg acoustic neuroma
trauma eg petrous temporal bone fracture
-Bilateral nerve deafness
degeneration
toxicity eg aspirin, streptomycin
infection eg rubella, syphilis
Menieres Disease
CN IX – GLOSSOPHARYNGEAL
NERVE & VAGUS NERVES

FUNCTION: General sensation and taste to posterior third of tongue
Motor supply to stylopharyngeus
 ANATOMY:
Nerve fibres from nuclei in medulla form multiple nerve rootlets as they exit the medulla
Join to form 9 and 10 CN and also contribute to 11th
Emerge from skull through jugular foramen.
9th receives sensory fibres from nasopharynx, pharynx middle and inner ear and post third
tongue
Also carries secretory fibres to parotid gland
Tenth receives sensory fibres from pharynx, larynx
& innervates muscles pharynx ,larynx and palate
Fig 20
 EXAMINATION:
Inspect palate and uvula
Assess hoarseness and swallowing
 PATHOLOGICAL FEATURES:
Unilateral 10th nerve palsy
–uvula drawn to one side
--loss of palatal elevation
 AETIOLOGY:
-Central causes
vascular, tumours, motor neurone disease
-Peripheral cause
aneurysms at base of skull, tumours, GBS, chronic meningitis
CN XI – ACCESSORY NERVE

FUNCTION: Motor supply to sternocleidomastoid and trapezius muscles
 ANATOMY:
-Central portion arises in medulla close to nuclei of 9th,10th,12th nerves
-Provides motor fibres to vagus
-Spinal portion from upper 5 cervical segments
I-nnervates trapezuis and SCM
 EXAMINATION:
Patient shrug shoulders and examiner attempts to push down
Turn head to side against resistance of examiners hand

PATHOLOGICAL FEATURES: Downward and lateral rotation of scapula and shoulder drop
 AETIOLOGY:
Unilateral – trauma, tumours near jugular foramen, polio, syringomyelia
Bilateral – motor neurone disease, polio, GBS
CN XII – HYPOGLOSSAL NERVE

FUNCTION: Motor supply to intrinsic and extrinsic muscles of tongue
 ANATOMY:
Arises from medulla and leaves skull via hypoglossal foramen
 EXAMINATION:
Inspect tongue – wasting and fasciculations
 PATHOLOGICAL FEATURES:
Deviation of tongue
UMN lesion usually bilateral – tongue deviates towards opposite side
NB. Has bilateral UMN innervation
LMN lesion – tongue deviates towards side of lesion/weaker affected side
- fasciculation wasting and weakness
- bilateral causes dysarthria
Fig 21

AETIOLOGY:
-Bilateral UMN – Vascular, motor neurone disease, tumours
-Unilateral LMN –
Central – vascular eg thrombosis of vertebral artery, syringobulbia
Peripheral – aneurysms, tumours, trauma, meningitis (post fossa)
- tumours and lymphadenopathy (upper neck)
- Arnold-Chiari malformation
-Bilateral LMN
GBS, Motor neurone disease polio
MULTIPLE CRANIAL NERVE
PALSIES


Anatomical course =>can be affected in groups by single lesions
Syndromes:
CAVERNOUS SINUS LESION – unilateral 3,4,5,6
CEREBELLOPONTINE ANGLE LESION –unilateral 5,7,8
JUGULAR FORAMEN LESION – unilateral 9,10,11
PSEUDOBULBAR PALSY
 Combined bilateral UMN lesions of 9,10,12
 Long tract signs
 Causes – bilateral cerebrovascular disease, MS, Motor neurone disease
BULBAR PALSY
 Combined bilateral LMN lesions of 9,10,12
 Wasted tongue
 Causes – GBS syndrome, brainstem infarction.polio
REFERENCES
1.
Talley NJ, O’Connor S. Clinical Examination. 5th ed.Elsevier;2006
2.
Rosen P. Emergency Medicine : Concepts and Clinical practice 7th ed. Mosby
THE END