1. CRANIAL NERVE LESIONS
IN THE
EMERGENCY DEPARTMENT BY
RAKSHA RAMLAKHAN

2. OVERVIEW Introduction The cranial nerves 1. Function 2. Anatomy
3. Clinical examination
4. Pathologic features
5. Aetiology
Multiple cranial nerve lesions

3. 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

4. INTRODUCTION - ANATOMY
Figure 1:Major nuclei of the cranial nerves
Figure 2

5. 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 - Test each nostril separately with bottles containing essences of familiar smells - Examine nasal passages if anosmia present PATHOLOGICAL FEATURES: Unilateral anosmia AETIOLOGY: Trauma – skull fracture or shear injury Tumour – Frontal lobe masses
Fig 3

6. 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

7. Figure 6: The Visual Fields and Optic Pathways
Figure 7: Visual Field Defects

8. 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

9. CN III – OCULOMOTOR NERVE
FUNCTION : MOVES THE EYES
- motor fibres to levator palpebrae, superior rectus, medial rectus, inferior rectus, inferior oblique
PUPIL CONSTRICTION
- parasympathetic fibres to constrictor pupillae and ciliary muscles
Fig 8

10. Parasympathetic innervation ->Edinger Westphal
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

11. Sympathetic innervation to eye
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

12. 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)

13. Eye deviated laterally and down Diplopia Dilated non reactive pupil
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

14. 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 -

15. MEDICAL VS SURGICAL 3rd NERVE PALSY
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

16. 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

17. 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

18. 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
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
Fig 12

19. 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

20. -Central causes (pons, medulla and upper cervical cord) vascular tumour syringobulbar -Peripheral (middle fossa) aneurysm 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

21. 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

22. PATHOLOGICAL FEATURES: Inability to move eye laterally
Diplopia on lateral gaze
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)
Fig 14
note in (A) that the affected (right) eye is adducted at rest
- note in (B) that the affected (right) eye cannot abduct

23. 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

24. Leaves pons with CN8 through cerebellopontine angle
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

25. Inspect for facial asymmetry – unilateral drooping of corner of mouth
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

26. 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

27. (60-70% of acute unilateral facial paralysis)
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

28. 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 Progressive -3 weeks
-Suspect neoplastic cause if recurrent ipsilateral facial paralysis
significant pain, prolonged symptoms, cranial nerve abnormality.

29. 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

30. EXAMINATION: Hearing test
Suspect partial deafness do Rinne’s and Weber’s
PATHOLOGICAL FEATURES: Unilateral hearing loss
Tinnitus
Vertigo and unsteadiness
AETIOLOGY:
-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

31. 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

32. 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

33. 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

34. 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

35. 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

36. 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

37. REFERENCES
Talley NJ, O’Connor S. Clinical Examination. 5th ed.Elsevier;2006
Rosen P. Emergency Medicine : Concepts and Clinical practice 7th ed. Mosby

38. THE END