ICM 2 Cranial nerve 7&8

CN 7 assessment
Facial expression
Ask about crocodile tears
Ask about noise intolerance
Ask about taste

Facial nerve palsy UMN vs LMN

Upper motor neuron palsy
Forehead spared
Cortical lesions eg CVA, Tumour
Lower motor neuron lesion
Forehead affected
Lesion sites include:
Nucleus
Cerebellar pontine angle
Facial canal
Parotid

Facial nerve UMN course

Path
Motor cortex
Internal capsule
Cerebral peduncle
Pons
Bilateral cortical innervation to Nuclei
Subject to CVA, MS, Tumor, Lacunar infarcts

Facial nerve LMN course

Nucleus
Cerebellar pontine angle
Internal auditory meatus in
temporal bone
Facial canal in temporal bone past
middle ear branch to stapedius &
chorda tympani exits
Out through stylomastoid foramen &
through parotid gland

Facial nerve conditions LMN

1) Facial nerve nucleus
May be assoc with CN6 palsy
and corticospinal tracts.
Contralateral hemipareisus
Causes vascular, inflammatory
and occasionally infiltrative
2) Cerebellopontine angle syndrome
CN 5,6,7,& 8 affected.
Acoustic neuroma , meningiomas,
metastases, cholesteotomas
3) Facial canal:
prone to ischaemia and compression
due to poor blood supply and small
calibre. Fractured temporal bone, infection
eg otitis externa or suppurative otitis, Zoster
infection ( Ramsey Hunt), Bells
4) Parotid region: Malignancy
Facial Nerve Bells palsy
Incidence: 20/100,000 per year (1)
Age: Risk increases with age.
Sex: equally affected
Predisposing factors: weak associations
with diabetes and hypertension, risk is three

times greater during pregnancy,

Pathology: Detection of herpes simplex virus type I
DNA in endoneurial fluid is present in most patients . May be primary
infection or reactivation.
Inflammation of facial nerve in facial canal
Unilateral facial weakness develops over hours, maximum loss
within 21 dys, recovery within 6 mo
Associated with hyperacusis and loss of taste
Treatment
Steroids and antivirals
Complications
Crocodile tears, smiling causes eye closure
Differential
CP angle tumor, Ramsey Hunt syndrome, Lyme disease
Note:
Diagnosis:
Diffuse facial nerve involvement with facial muscle paralysis, with or
without loss of taste on the anterior 2/3rds of the tongue, or altered
secretions of the lacrimal and salivary glands.
Onset is acute, over 24-48 hours; maximal weakness is within 3 weeks
or less from the first day of visible weakness; recovery is within 6
months to some extent.
Differential diagnosis:
A diagnosis of Bells palsy is doubtful if some facial function has not
returned within 3-4 months (5). Additional investigation is required.
Prolonged, slowly progressive or facial palsy affecting only one or two
branches could suggest malignancy.
Herpes Zoster is diagnosed if vesicles can be seen around the external
meatus. Occasionally, herpes zoster is seen without vesicles (zoster
sine herpete). A history of dermatomal pain or dysasthesia may be
suggestive of this diagnosis.
Investigations:
There is no gold standard diagnostic investigation
Electrodiagnostic studies help determine prognosis: Compound muscle
action potential (CMAP) at 10 days; those with 10% of normal CMAP
have a poor prognosis, those with 2% have a very poor prognosis (6);
facial nerve stimulation is most useful within two weeks after
progression to complete facial paralysis if surgery is contemplated.
Imaging is indicated if a malignancy is suspected. This may be
prompted by atypical signs, slow progression beyond three weeks, no
improvement at six months, facial twitch or spasm preceding paralysis
(which suggests nerve irritation from tumour). Treatment

Conservative educate the patient and reassure them that they have
not had a stroke! Monitor the patient to ensure this is Bells palsy and
there is no sinister underlying cause.
Medical If quickly diagnosed within 2-3 days, high dose steroids with
or without antivirals can be used. Steroids improve the rate of
complete recovery . Regardless of this, eye care is important this can
include artificial tears for dry eyes and taping the eyes shut at night to
prevent exposure keratitis.
Complications:
Failure to recover: prognosis depends on the degree of initial weakness
- the less the better.
Synkinesis this is where the regenerating facial nerve fibres are
thought to erroneously innervate different targets. Examples include
eyes closing whilst muscles of the mouth contract, lacrimation during
eating (crocodile tears) or smiling causing eye closure.
Recurrence this is uncommon, and occurs in around 1 in 10 people.
Ramsey Hunt syndrome
Varicella Zoster reactivation
in geniculate ganglion
Pain pre-auricular pain
Vesicles in external auditory
meatus
Clinical presentation
Ear pain, rash, facial paralysis,
loss of taste, vertigo, hearing loss
Treatment
Steroids and antivirals
Complications
Cerebellopontine angle tumour
Most common is vestibular schwannoma
Assoc Neurofibromatosis type 2( if bilateral)
Clinical
Pressure on adjoining structures CN5, 6,7,&8
Pressure develops over months
Eventual BSt infiltration and raised ICP
Also meningiomas, astrocytomas
Cerebellopontine angle tumors :Vestibular schwannoma

Vestibular schwannoma(acoustic neuroma)

Benign primary intracranial tumour
Incidence 1;100,000, M=F
5-10% intracranial neoplasms

Clinical
5th-6th decadeCN8 deafness,
tinnitus, vertigo
CN7 LMN paralysis in face
CN6 Diplopia
CN5 parasthesias of face and
inside mouth
B st compression
Raised ICP

Vestibulocochlear nerve
Composed of vestibular nerve and
Cochlear nerve
Symptoms of nerve deficit include
sensorineural deafness, vertigo, nausea
and vomiting

Symptoms and causes of 8th nerve dysfunction

Sensorineural deafness
Presbyacussis
Acoustic neuroma
Vertigo
Benign positional vertigo
Labyrinthitis
Menieres disease
Dizziness Types:

Presyncope - lightheadedness; sensation one is about to

pass out
Vertigo - illusion of movement; usually rotational can be
an illusion of
tilting or swaying
Disequilibrium - general sense of imbalance when walking

CAUSES of

VERTIGO

Drug- induced vertigo: Loop diuretics, Streptomycin,

Salicylate, Alcohol
Benign paroxysmal positional vertigo (BPPV)
Menieres disease
Perilymphatic fistula
Acoustic neuroma
Herpes zoster oticus
Vestibular neuronitis
Neurolabyrinthitis - also has hearing loss
Labyrinthine ischemia
Inferior cerebellar infarction
Vertebrobasilar transient ischemic attacks
Benign paroxysmal positional vertigo
Sudden onset vertigo typically with head movement
No hearing loss
Causes :
Otolith loose in semicircular canals
Incidence 64:100,000 ( ememdicine)
F>M, older persons
Tested using Hallpike test
Note:
Hallpike test: In this test, the patient is placed in the headhanging position after turning the head to the side. After a
short delay of a few seconds, nystagmus and reproduction of
the vertigo occurs and typically resolves within 30-60 seconds.
The neurologic examination is otherwise unremarkable.

Acute Vestibular Syndrome

Caused by rapid, unilateral injury

of peripheral or central vestibular structures

Causes
Viral Vestibular Neuritis(normal hearing)
Neurolabyrinthitis ( hearing affected)
Infarction & Hemorrhage
of inferior cerebellum

Note: Labyrinthitis is an inflammatory disorder of the inner ear,

or labyrinth. Clinically, this condition produces disturbances of
balance and hearing to varying degrees and may affect 1 or
both ears. Bacteria or viruses can cause acute inflammation of
the labyrinth in conjunction with either local or systemic
infections. Autoimmune processes may also cause
labyrinthitis.
MENIERE S DISEASE

Idiopathic endolymphatic hydrops

disorder of inner ear
Mechanism:
Distortion of membranous
labyrinth due to over accumulation
of endolymph
Incidence : in 40- 60 year old age group
Clinical triad of :
Vertigo: lasts from 20 min to few
hours (Horizontal or rotatory
nystagmus with vertigo)
Tinnitus
Sensoneuronal hearing loss: low frequencies
sounds
Associating symptoms: nausea, vomiting & anxiety

Note: hormonal imbalance, trauma, and various infections (eg,

otosyphilis and Cogans syndrome [interstitial keratitis]).[4, 5]
Autoimmune diseases, such as lupus and rheumatoid arthritis,
may cause an inflammatory response within the labyrinth.

8th nerve assessment

Webers and Rinnes test
To determine conduction vs.
sensorineural deafness
Assess for nystagmus

8th nerve exam Conductive deafness

Webers
Sound lateralizes to affected ear
Rinnes
Bone conduction>air conduction in
affected ear
Causes
block to air conduction eg cerumen,
middle ear infection ( otitis media),
perforated ear drum

8th nerve exam Sensorineural deafness

Webers
Sound lateralizes to better ear
Rinnes
AC>BC in better ear

 Causes
Presbyacussis, drugs (gentamicin,
neomycin)Menieres disease, acoustic neuroma,
Congenital Rubella
SUMMARY:
Cranial nerves 7 & 8 originate in the pons and pass out at the
cerebellar pontine angle.
8th nerve assessment is by Webbers and Rinnes test
7 & 8 are compressed by cerebellar pontine angle tumours
Vertigo is an important symptom and has several causes