CRANIAL NERVE LESIONS - PowerPoint Presentation

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CRANIAL NERVE LESIONS IN THE EMERGENCY DEPARTMENTBYRAKSHA RAMLAKHAN

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OVERVIEW

Introduction

The cranial nerves

1. Function

2. Anatomy

3. Clinical examination

4. Pathologic features

5.

Aetiology

Multiple

cranial nerve lesions

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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

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INTRODUCTION - ANATOMY

Figure 1:Major nuclei of the cranial nerves

Figure 2

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THE CRANIAL NERVESCN I – OLFACTORY NERVE

FUNCTION: SENSE OF SMELLANATOMY: - 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 presentPATHOLOGICAL FEATURES: Unilateral anosmiaAETIOLOGY: Trauma – skull fracture or shear injury Tumour – Frontal lobe masses

Fig 3

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CN II – OPTIC NERVE

FUNCTION : VISIONANATOMY: - 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 - FundiPATHOLOGICAL FEATURES: Unilateral/Bilateral visual loss Visual field defects

Fig 4

Fig 5

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Figure 6: The Visual Fields and Optic Pathways

Figure 7: Visual Field Defects

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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

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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

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ANATOMY:

Miosis - Parasympathetic innervation ->Edinger Westphal Pupil constriction in response to light relayed by optic nerve and tract  superior colliculus EW nucleus in midbrainEfferent motor fibres from oculomotor nucleuswall of cavernous sinus with CN 4,5a,6Iridoconstrictor fibres -ciliary ganglionPostganglionic fibres innervate iris

Figure 9: Pupillary constriction to light

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Mydriasis

- Sympathetic innervation to eyeFibres from hypothalamus to ciliospinal centre and synapse in spinal cord at C8, T1 & T2Exit anterior ramus in thoracic trunk & synapse in superior cervical ganglion in neckNeurones travel with internal carotid artery to eye

Figure 10: Oculo Sympathetic Pathway

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CLINICAL EXAMINATION: - Pupils – light reflex (direct and consensual)

- Accommodation - Eye movements (diplopia and nystagmus)ACCOMMODATIONNeural circuit to visual cortex and backInvolves parasympathetic component of CNIIIStimulates smooth muscle of ciliary body to contract → lens changes shapePupil constrictsArgyll Robertson pupil → absent light reflex with intact accommodation (midbrain lesion)

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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

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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

-

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MEDICAL VS SURGICAL 3

rd

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

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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

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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

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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 ponsProprioceptive nucleus in midbrainPain and temperature nucleus descends through medulla to reach upper cervical cordCerebellopontine angle  temporal lobe in middle cranial fossaPetrous temporal bonetrigeminal ganglion31. 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

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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

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-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

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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antSubarachnoid 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

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PATHOLOGICAL FEATURES: Inability to move eye laterally

Diplopia on lateral gazeAETIOLOGY: -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

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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

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ANATOMY:

Nucleus lies in ponsLeaves pons with CN8 through cerebellopontine angleEnters facial canal and becomes geniculate ganglionGives off nerve to stapediusChorda tympani (taste from and two thirds of tongue) joins nerve in facial canalLeaves skull via stylomastoid foramenEnters parotid gland and divides to supply muscles of facial expression

Fig 16

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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

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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

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Bells Palsy

(60-70% of acute unilateral facial paralysis)Idiopathic facial paralysis?viral cause – herpesAbrupt onset LMN paresis progresses over 1-7 days to complete paralysisAssociated s& s – ear pain, decreased tearing, hyperacusis ,impairment of tasteMedical Rx – corticosteriods (1mg/kg per day for 7-10 days) oedema of nerve confined within facial canal causes/contributes to nerve injuryDiabetics have 29% risk of being affected

Fig 18 : Bell’s Palsy

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UPPER MOTOR NEURON

-vascular, tumours

TRAUMATIC

-T

emporal

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

.

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CN VIII – VESTIBULOCOCHLEAR NERVE

FUNCTION: Hearing and balanceANATOMY: 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

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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

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CN IX – GLOSSOPHARYNGEAL NERVE & VAGUS NERVES

FUNCTION: General sensation and taste to posterior third of tongue Motor supply to stylopharyngeusANATOMY: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 11thEmerge 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

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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

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CN XI – ACCESSORY NERVE

FUNCTION: Motor supply to sternocleidomastoid and trapezius muscles

ANATOMY:

-Central portion arises in medulla close to nuclei of 9

th

,10

th

,12

th

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

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CN XII – HYPOGLOSSAL NERVE

FUNCTION: Motor supply to intrinsic and extrinsic muscles of tongueANATOMY:Arises from medulla and leaves skull via hypoglossal foramenEXAMINATION:Inspect tongue – wasting and fasciculationsPATHOLOGICAL 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

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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

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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

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REFERENCES

Talley NJ, O’Connor S. Clinical Examination. 5

th

ed.Elsevier;2006

Rosen P. Emergency Medicine : Concepts and

Clinical practice 7

th

ed. Mosby

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THE END