CRANIAL NERVE LESIONS

IN THE EMERGENCY DEPARTMENT

BYRAKSHA RAMLAKHAN

OVERVIEW

Introduction

The cranial nerves1. Function2. Anatomy3. Clinical examination4. Pathologic features5. 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 NERVESCN 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

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 neuropathyTumour – orbital compressive lesionIschaemic – ischaemic optic neuropathy

OPTIC NEURITIS

Inflammation of optic nerve complete or partial loss of visionDemyelinationTriad 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, inferior oblique

PUPIL CONSTRICTION

- parasympathetic fibres to constrictor pupillae and ciliary muscles

Fig 8

ANATOMY:

Miosis -

• Parasympathetic innervation ->Edinger Westphal

• Pupil constriction in response to light relayedby optic nerve and tract superior colliculusEW 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 spinalcord 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 marginPupil 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 SRSO

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 tympaniSensory 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 bonetrigeminal ganglion3

1. Ophthalmic - cavernous sinus with CN3 SOF skin of forehead, cornea and conjunctiva2. Maxillary -infraorbital foramen skin in middle of face ,mucus membranes of mouth, palate and nasopharynx3. Mandibular with motor part of nerve foramen ovale skin of lower jaw , mucus membranes of mouth

Fig 12

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)vasculartumoursyringobulbar

-Peripheral (middle fossa)aneurysmtumourchronic meningitis

-Trigeminal ganglion (petrous temporal bone)trigeminal neuromameningiomamiddle cranial fossa fracture

-Cavernous sinusophthalmic division onlywith 3,4,6aneurysm, 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 supant• 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 SOFlateral rectus

Fig 13

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

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 foldMuscle 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. -

Progressive -3 weeks -Suspect neoplastic cause if recurrent ipsilateral facial paralysis

significant pain, prolonged symptoms, cranial nerve abnormality.

CN VIII – VESTIBULOCOCHLEAR NERVE

FUNCTION: Hearing and balance

ANATOMY: 2 components: -cochlear with afferent fibres for hearing-originate in Organ of Corticochlear nucleus in ponsbilateral transmission to -Medial geniculate bodiessuperior gyrus of temporal lobes

-vestibular with afferent fibres for balance-Begin in utricle and semicircular canalsjoin auditory fibres in facial canalenter brainstem at-Cerebellopontine angle.After entering pons-vestibular fibres run widely throughout brainstem and cerebellum

Fig 19

EXAMINATION: Hearing test Suspect partial deafness do Rinne’s and Weber’s

PATHOLOGICAL FEATURES: Unilateral hearing loss Tinnitus Vertigo and unsteadiness

AETIOLOGY:

-Unilateral nerve deafnesstumours eg acoustic neuromatrauma eg petrous temporal bone fracture

-Bilateral nerve deafnessdegenerationtoxicity eg aspirin, streptomycininfection eg rubella, syphilisMenieres 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 medullaJoin 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 thirdtongueAlso carries secretory fibres to parotid glandTenth receives sensory fibres from pharynx, larynx& innervates muscles pharynx ,larynx and palate

Fig 20

EXAMINATION:Inspect palate and uvulaAssess 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 segmentsI-nnervates trapezuis and SCM

EXAMINATION:Patient shrug shoulders and examiner attempts to push downTurn 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, syringomyeliaBilateral – 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 tongueUMN lesion usually bilateral – tongue deviates towards opposite sideNB. Has bilateral UMN innervationLMN 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, syringobulbiaPeripheral – aneurysms, tumours, trauma, meningitis (post fossa)

- tumours and lymphadenopathy (upper neck) - Arnold-Chiari malformation

-Bilateral LMNGBS, Motor neurone disease polio

MULTIPLE CRANIAL NERVE PALSIES

Anatomical course =>can be affected in groups by single lesions Syndromes:

CAVERNOUS SINUS LESION – unilateral 3,4,5,6CEREBELLOPONTINE ANGLE LESION –unilateral 5,7,8JUGULAR 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

REFERENCES1. 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