Ear - Chapter 3 (Facial nerve paralysis) Flashcards
Causes of facial nerve paralysis
A- Upper motor neuron lesion (central or supra nuclear) Lesion of the pyramidal tract above the facial nucleus due to embolism, thrombosis, Hemorrhage, Brain tumors, encephalitis and head trauma.
B- Lower motor neuron lesion (peripheral) due lesions at or below the nucleus :
* Intracranial :
- Pons (at the nucleus) : usually associated with 6th nerve palsy e.g Hemorrhage, tumors, meningitis
- At cerebello-pontine angle (usually associated with 8th nerve palsy) e.g Acoustic neuroma, meningioma, congenital cholesteatoma.
* Cranial (intratemporal) :
1- Idiopathic : Bell’s palsy : the commonest cause of LMN facial paralysis.
2- Traumatic :
- During mastoidectomy.
- During stapedectomy.
- Tight pack after ear surgery.
- Postauricular incision in children where the facial nerve is superficial.
- Operation for congenital anomalies of the external and middle ear due to abnormal course of the facial nerve.
- Fracture skull base (Transverse).
- Skull base surgery.
3- Inflammatory :
a- Otitis media :
- Acute otitis media may cause facial paralysis if there is congenital dehiscence of the bony facial canal.
- Chronic suppurative otitis media may cause facial paralysis due to erosion by cholesteatoma.
- Chronic specific otitis media (T.B or syphilis).
b- Otitis externa :
- Malignant otitis externa.
- Viral : herpes zoster oticus (Ramsy-Hunt syndrome)
4- Neoplastic :
- Benign tumours of the middle ear e.g glomus tumours.
- Malignant tumours of the middle ear e.g squamous cell carcinoma.
- Acoustic neuroma.
* Extra cranial (infra temporal)
- Trauma : cut wound of the face, parotid gland surgery and birth injury.
- Inflammation e.g sarcoidosis and peripheral neuritis.
- Tumors: malignant, parotid.
2 types of facial nerve lesions
1- Neuropraxia :
* Due to minor trauma.
* It is reversible conduction block.
* No damage to the nerve sheath or axon.
* Complete recovery occurs within one month.
2- Wallerian degeneration: due to severe trauma :
a- Axonotmesis :
* Degeneration of nerve axon (the nerve sheath remains intact)
* The nerve axon grows inside the sheath (1 mm/day).
* Recovery may be incomplete occurs within 2-3 months.
b- Neurotmesis :
* Degeneration of both nerve axon and sheath
* Recovery is always incomplete and delayed within one year.
Diagnosis of F.N paralysis (LMN or UMN lesion)
- Lesion is peripheral at or below the nucleus.
- Paralysis of the upper and lower parts of the face.
- Paralysis of voluntary and emotional muscles.
- Hypotonia (flaccid paralysis).
- Atrophy of the muscles.
- No hemiplegia.
VS - Lesion is central above the nucleus.
- Paralysis of lower part only. *
- Paralysis of voluntary muscles only. **
- Hypertonia (spastic paralysis).
- No atrophy of the muscles. ***
- Hemiplegia is common.
(* The upper half is not paralyzed because it is supplied by pyramidal fibers from both sides.
** Emotional e.g. laughing is intact because they are controlled by extra pyramidal fibers.
*** Because the muscles are not denervated.)
Diagnosis of F.N paralysis (level of the lesion )
1- Supra nuclear : UMN F. paralysis.
2- Nuclear (pons) :
- LMN- Facial paralysis +
- Paralysis of VΙ nerve (diplopia)
- Pontine manifestations
- Loss of taste on anterior 2/3 of the tongue.
- Loss of lacrimation.
- Hyperacusis = intolerance of loud sound due to paralysis of stapedius muscle.
3- Supra geniculate (at CPA and internal auditory meatus) :
- LMN paralysis of the facial muscles.
- Loss of taste on the anterior 2/3 of the tongue.
- Loss of salivation from the submandibular salivary gland.
- Loss of lacrimation.
- 8th cranial nerve palsy (SNHL).
- No hyperacusis due to associated SNHL.
4- At the geniculate :
- LMN facial paralysis.
- Loss of taste from anterior 2/3 of the tongue.
- Loss of saliva.
- Loss of lacrimation.
- Hyperacusis (phonophobia).
5- Tympanic (Horizontal) segment :
- LMNL.
- Loss of taste on ant 2/3 of the tongue.
- Hyperacusis.
- Lacrimation is intact.
6- Mastoid (vertical) segment :
- Above the chorda tympani LMN facial paralysis + loss of taste of ant 2/3 of the tongue.
- Below the chorda tympanic LMNL facial paralysis.
7- Below stylomastoid foramen (extracranial) LMN facial Paralysis (facial muscles)
Examination :
A- Motor tone (i.e. at rest) :
* Loss of forehead corrugations (occipito-frontalis).
* Loss of the naso-labial fold (levator anguli oris).
* Drooping of the angle of the mouth (levator anguli oris).
* Drippling of saliva (orbicularis oris).
B- Motor power (i.e. during active movements):
* Inability to elevate the eyebrow (occipito-frontalis).
* Inability to close the eye firmly (orbicularis occuli).
* Inability to whistle (orbicularis oris).
* Inability to blow (buccinator).
* Deviation of the mouth to the healthy side on smiling (levator anguli oris).
Diagnosis of F.N paralysis (Investigations )
To evaluate the followings :
1- The cause of paralysis :
a. Radiological: CT, MRI of the temporal bone and brain.
b. Audiological : to determine type of deafness associated with facial paralysis.
2- The level of the lesion :
a- Test for lacrimation (Schrimers test) : placing small blotting paper in the conjunctival fornix of each eye and measuring lacrimation. If there are 25% reduction of the affected eye as compared to normal. This means a lesion at or above the geniculate ganglion.
b- Tympanometery (Stapedius reflex) : If lost it means lesion above the nerve to stapedius.
c- Taste test : taste sensation of the anterior 2/3 of the tongue by putting sugar or salt on the protruded tongue or by using electrogustometry. If taste lost it means lesion above the chorda tympani.
d- Submandibular salivary flow test : It is diminished on the affected side.
3- The condition of the nerve and muscles evaluated by :
Electrodiagnosis :
1- Value :
* Differentiate between neuopraxia and denervation
* Gives idea a bout prognosis
* Determine time of surgical interference
2- Types :
A- Nerve excitability test (NET) :
* The facial nerve is stimulated by an electrode placed over the stylomastoid foramen.
* The examiner measures (by his eyes) the intensity of electrical current, which can produce minimal twitches of the facial muscles.
* A difference between the two sides of 3.5 milli-Ampere → indicates partial degeneration.
* Complete loss of excitability : total degeneration.
B- Electro-neuronography (ENoG) :
* The facial nerve is stimulated by an electrode placed over the stylomastoid foramen.
* The examiner measures (by an electrode) the response of the facial muscles to maximum electrical stimulation.
* A difference between the two sides of more than 90% indicates degeneration.
* It provides more accurate results than the nerve excitability test.
C- Electro-myography (EMG) :
* A recording electrode is inserted into the facial muscles.
* The examiner records the electrical activities within the facial muscles.
* The presence of fibrillation potentials indicate degeneration, while the presence of polyphasic potentials indicate regeneration.
* It is of no value during the first two weeks of paralysis.
Treatment of F.N. paralysis
A) Conservative :
1- Treatment of the cause.
2- Care of the eye :
- To avoid keratitis, dryness (due to loss of blinking and lacrimation)
- Eye drops, ointment and glasses.
3- Care of the paralyzed muscles :
- To avoid disuse atrophy
- Massage of the facial muscles
- Active muscular exercises when recovery begins
B) Facial rehabilitation :
A. Dynamic :
- When facial muscles are still liable to regain motor activity of the face.
- Hypoglossal-facial anastomosis (between hypoglossal and facial nerve).
- Facio–facial anastomosis (between facial nerves of both sides).
B. Static :
- When facial muscles are fibrosed to improve the appearance of the face during rest (cosmotic).
- Fascia lata slings: to elevate the angle of the mouth.
- Implantation of temporalis muscle in the cheek.
BELL’S PALSY
(Idiopathic Facial Paralysis)
* Sudden LMN facial paralysis of unknown etiology.
* The commenst cause of LMN facial paralysis.
Etiology :
Unknown – edema of the nerve due to :
* Vascular : usually follows exposure to cold air currents- causing spasm of vasa nervosa of the nerve.
* Viral : reactivation of dormnant herpes simplex virus.
* Auto-immune.
Pathology :
Nerve compression at or just above stylomastoid foremen.
Clinical picture :
* Sudden LMN facial paralysis.
* Unilateral.
* Partial or complete.
* May be preceded by viral prodroma, pain around the ear.
Investigations : See before (level and condition of nerve).
Treatment :
1- General : care of the eye and muscles.
2- Medical :
* Steroids, high doses for 2 weeks.
* Anti viral (acyclovir) may be used
3- Surgical :
* Decompression of the nerve: after 2 weeks of medical treatment and 90% of n. fibers are degenerated.
* Facial rehabilitation (mentioned)
* Prognosis 75% of cases (neuropraxia) shows complete recovery within 3 months.