The document discusses facial nerve disorders and paralysis, detailing both central and peripheral causes, with central causes including brain abscesses and strokes, while peripheral causes primarily involve idiopathic lesions and infections. It highlights acoustic neuroma as a common tumor affecting the facial nerve, outlines diagnostic methods, and treatment options like surgery and corticosteroids. Additionally, the document covers conditions such as Bell's palsy and Ramsay Hunt syndrome, including their clinical features, diagnosis, and management strategies.

1. FACIAL NERVE
DISORDERS
ENT Specialist :- Dr.Ayman Al-hyari
ENT Resident:- Dr.Amro Al-amleh

2. Causes of facial nerve
paralysis
 The cause may be central or peripheral.
 Central:
 Brain abscess
 Pontine gliomas
 Poliomyelitis
 Multiple sclerosis
 Cerebrovascular strokes
 If symptoms or signs of other cranial nerve deficits
are present, central and systemic cause should be
suspected

3.  Sparing of forehead movement is considered to
be characteristic of central lesion but is always
the cause.
 Isolated lower facial palsy is not necessarily
indicative of central lesion Peripheral lesion of
temporal branch of facial nerve.
 Partial palsy of one or two branches suggests
diseas localized distal to stylomastoid foramen
and parotid malignancy should be suspected.

4. Peripheral causes
 Peripheral lesions are more common , 70% of them are of the
idiopathic variety may involve the nerve in its intracranial,
intratemporal or extratemporal parts.
 Intracranial part :-
 Cerebellopontine Angle Tumors:
 Acoustic neuroma (Vestibular Schwannoma )
 Intratemporal Part
 Idiopathic: Bell’s palsy, recurrent facial palsy and Melkersson’s
syndrome
 Infection: Acute and chronic suppurative otitis media, Herpes zoster
oticus, tuberculosis and malignant otitis externa
 Surgical trauma: mastoid and middle ear surgery and parotid surgery.
 Accidental trauma: Fractures of temporal bone
 Neoplasms: Malignancy of external and middle ear,
rhabdomyosarcoma, histiocytosis, leukemia, glomus tumors, facial nerve
neuroma, metastasis to temporal bone (from cancer of breast, bronchus,

5. Peripheral causes
 Parotid: Malignancy, surgery, accidental injury and
birth trauma.
 Congenital: Compression injury, Mobius
syndrome, lower lip paralysis
 Systemic Diseases:
 Diabetes mellitus
 Sarcoidosis (Heerfordt’s syndrome)
 Leprosy
 guillain-Barre syndrome
 Lyme’s disease
 infectious mononucleosis

6. ACOUSTIC NEUROMA

7. (Acoustic neuroma (AN
 Acoustic neuroma (AN) is the most common (80%) CPA
tumor and constitutes 10% of all the brain tumors.
 This benign, encapsulated eighth nerve tumor is
extremely slow growing. The unilateral tumors are more
common. In patients of neurofibromatosis bilateral tumors
are seen.
 Acoustic neuroma arises from the Schwann cells of the
vestibular nerve twice as often as from the cochlear
nerve. It reaches the CPA after eroding and widening
IAC.
 Anterosuperiorly it involves the CN V and inferiorly
involves the Ix, x and xI CN, which lie in jugular foramen.

9. Classification of size
 It is based on the size of largest extrameatal
diameter.
 If tumor entirely within the meatus without any
extension out of porus, the term intrameatal 
size zero.
Size (mm)gradeClassification
0IntrameatalGrade 0
1-10SmallGrade 1
11-20MediumGrade 2
21-30Moderately largeGrade 3
31-40LargeGrade 4
>40GiantGrade 5

10. Clinical features
 Asymptomatic AN occurs in about 2% of the population.
The cases of progressive unilateral
sensorineural hearing loss (SNHL) and
unilateral tinnitus must be investigated to
rule out AN.
 „Onset  Growth of AN is slow and patient’s history may
extend over several years.
 „Age  Patients are usually in age group of 40–60
years.
 Sex  Female to male ratio is 3:2.
 „90% of patient , the first symptom Progressive unilateral
SNHl with or without tinnitus.
 5-10% of cases, patients present with sudden

11.  Vestibular symptoms: Imbalance or unsteadiness occurs in 50% of patients.
 „Facial nerve: Sensory fibers are more sensitive and affected early. Motor
fibers are more resistant so are affected late.
 Numbness of posterior aspect of concha, (Histeliberger’s sign)
 Loss of taste anterior 2/3 tongue.
 Schirmer’s test: Reduced lacrimation.
 Blink reflex: It is delayed may be early manifestation.
 „CN V: The first extracanalicular nerve to be involved is trigeminal.
 Reduced corneal sensitivity.
 Numbness or paresthesia of face.
 „CN IX and X Dysphagia, hoarseness of voice and nasal regurgitation of fluid.
Palatal, pharyngeal and laryngeal paralysis.
 Brainstem and cerebellum signs and symptoms.

12. Diagnosis
1. Audiometry
 Hearing loss is more marked in high frequencies and
Poor speech discrimination.
2.Caloric test
 Diminished or absent response in 92% of patients.
3. Gadolinium-enhanced MRI
 Thin section gadolinium-enhanced MRI is the gold
standard for diagnosis of acoustic neuroma and is
superior to CT scan. Intracanalicular tumor of a few
millimeters size can be diagnosed.

13. Differential diagnosis
A—GAMES
 Acoustic neuroma
 Glomus tumor
 Arachnoid cyct
 Meningioma
 Epidermoid
 Schwannoma

14. Treatment
 The treatment of first choice is surgical
removal.
 The second choice is gamma knife surgery.
 Radiotherapy and chemotherapy do not have
any role in the treatment.

15. IDIOPATHIC (BELL’S)
PALSY

16. Bell’s palsy
 The term Bell’s palsy should be reserved for
cases of facial paralysis in which search for
another cause is negative.
 Diagnostic criteria for Bell’s palsy
 Paralysis of all muscle groups on one side of face.
 Sudden onset.
 Absence of signs of CNS disease.
 Absence of signs of ear disease.
 Absence of signs CPA disease.
 Within 72 hours rapidly develop LMN facial
weakness.

17.  Annual incidence  2o – 32.7 per 100,000
 Peak incidence  B/W ages of 15-45 years
 Both sexes are equally affected, especially
B/W 20-40 years
 Predominance in women younger than 2o years
 Predominance in men older than 40 years
 Familial incidence 4.1%
 „It accounts for over 50% of acute facial
palsies.

18. Recurrence rates
 Recurrence rates : Bell’s palsy is recurrent in (4.5-15 %) 13% of
patient.
 38% are ipsilateral side
 62% are contralateral side

 Mean interval of 10 years B/W recurrences of Bell’s palsy.
 Patient with recurrence 2.5 times more likely to have + family
history.
 Recurrence is common in herpes smiplex type 1 infection.
 30% of patients with ipsilateral recurrence , tumor involving the
facial nerve was cause  tumor must be suspected in every
patient with ipsilateral recurrence.
 Contralateral side recurrence is almost benign.

19. Risk factors
 „Bell’s palsy is more common pregnancy with
majority of cases being in 3rd trimester.
 Increased in ECF (retention of fluid)  nrve
oedema and subsequent compression within
fallopian canal
 Prognosis for pregnant women is better than non-
pregnant women  once child has been
delivered , the clinical picture tends to improve.
 Diabetes (angiopathy) and

20. Etiology
 „The Etiology of Bell’s palsy remains unclear.
 1. Viral infection triggers immunological response resulting in damage
to facial nerve.
 Herpes simplex virus type 1
 Herpes simplex virus type 2
 Varicella-zoster virus
 Epstein-Barr virus
 Influenza type B virus, intranasal influenza vaccine increse the risk of Bell’s
palsy
 Adenovirus, Coxsackie virus.
 Clinical samples of facial nerve endoneurial fluid and posterior auricular
muscle analyed using PCR
 HSV-1 detected in 79% of patient with Bell’s palsy but not in Ramsay-Hunt
syndrome
 HSV-1 Is major agent in Bell’s palsy
 HSV-1 genomic DNA in 86% of autpsied geniculate ganglion samples taken

21. Etiology
 2. Vascular ischemia:
 Primary ischemia may be induced by cold or emotional
stress.
 Secondary ischemia. Increased capillary permeability
that leads to exudation of fluid, edema and compression
of microcirculation of the nerve.
 „3. Hereditary : About 10% of patients give positive family
history. The narrow fallopian canal can make the nerve
susceptible to early compression at the slightest edema.
 „4. Autoimmunity: T-lymphocyte changes have been
seen.

22. Clinical features
 This sudden onset of complete or incomplete
isolated unilateral lower motor neuron facial palsy
may present with following features:
 „Inability to close eye.
 Bell’s phenomenon: When patient tries to close the eye,
eyeball turns up.
 Dribbling of saliva from the angle of mouth.
 Asymmetrical face.
 Epiphora: Tears flowing down from the eye.
 Earache: Ear pain may precede or accompany the facial
palsy.
 Hyperacusis: Sensitivity to loud sounds due to stapedial
palsy.
 Diminished taste sensation: It may occur due to the
involvement of chorda tympani.

24. Diagnosis
 Diagnosis of Bell’s palsy is usually clinical and by
exclusion.
 Patient requires careful history and examination to
exclude other known causes of facial paralysis.
 Electrophysiologiacl tests are not used in assessment of
incomplete paralysis which has high probability of full
recovery.
 Imaging is only recommended if:-
 Presentation is atypical
 Alternative diagnosis is suspected
 Surgical decompression is planned
 Recover is incomplete at 6 months

25. Treatment
Regular electrophysiological assessment is important to know the
extent of nerve damage and determine the need of surgical
decompression.
A. General Measures.
 1. Reassurance.
 2. Analgesics: For the relief of ear pain.
 3. Eye Care: Eye must be protected against exposure keratitis.
 Artificial tears (methylcellulose drops) every 1–2 hours and 4–5
times per day.
 Eye ointment followed by patching or taping the eye.
 Cover for the eye in night.
 Protect the eye from wind, foreign bodies and drying with glasses
and moisture chambers.
 4. Physiotherapy: The facial muscles massage though does not
influence recovery, gives psychological support. Active facial
movements should be encouraged.

26. B. Medical Treatment
 1. Steroids: Prednisolone 1 mg/kg/day divided into
morning and evening doses for 10 days depending
upon whether the paralysis is incomplete or is
recovering. Thereafter the doses are tapered in
next 5–10 days.
 2. Oral Acyclovir: 400 mg 5 times daily for 10 days.
 3. Other drugs: Vasodilators, vitamins, mast cell
inhibitors and antihistaminics have not been found
useful.

27. Prognosis
 Majority of the patients (85–90%) recover fully.
 „95% patients of incomplete Bell’s palsy recover
completely.
 „The chances of complete recovery are better when
clinical recovery begins within three weeks of onset.
 Poor prognosis
 Complete paralysis at onset
 Incomplete paralysis with late onset of recovery
 Old age
 Absent stapedius reflex

28. MELKERSSON–ROSENTHAL
SYNDROME

29.  Melkersson–Rosenthal syndrome is
rare neurological disorder characterized by
 Recurring facial paralysis
 Swelling of the face and lips (usually the upper
lip) and
 Fissured tongue

31. RAMSAY HUNT
SYNDROME

32. Ramsay hunt Syndrome
 Definition:- Peripheral facial nerve palsy
accompanied by erythematous vesicular rash on ear
or in mouth.
 Mechanism:- Reactivation of the latent VZV virus in
geniculate ganglion  virus starts to replicate in
ganglion and then travels down and affect
 Facial nerve
 Inner ear
 Spiral ganglion
 Vestibular ganglion.
 Varicella-Zoster virus remains latent in geniculate
ganglia for decades after attack of acute
Chickenpox.
 Stimuli for viral reactivation: Immunosuppression,

33. Signs and symptoms
 Severe otalgia. Precede facial nerve paralysis.
 „Painful erythematous vesicular rash in the ear
canal and concha, behind pinna and or soft
palate. Later vesicles rupture and form crusts.
 „Unilateral LMN facial palsy.
 „About 25% patients have vertigo, nystagmus,
tinnitus and hearing loss.
 Involvement of the trigeminal nerve can cause
numbness of the face.

34. Diagnosis
Clinical presentation and confirmed by
 Rising of titers of antibodies to VZV.
 „PCR to detect VZV DNA in vesicle fluid or
cerebrospinal fluid (CSF).
 Gadolinium-enhanced MRI of temporal bone and
CSF examination have no diagnostic or
prognostic value

35. Prognosis
 Worse than Bell’s palsy
 Persistent weakness observed in 30-50% of
patients
 Only 10% recover completely after complete loss
of function without treatment.

36. Treatment
 Combination of steroids and antiviral agents for
longer period of time, 2-3 weeks.
 Significant improvement in patients treated with
prednisone and acyclovir within 3 days of onset.
 Patients treated with prednisone less likely to
progress to compete facial paralysis
 „Prednisone 1 mg/kg/day for 5 days followed by 10-day
taper.
 I.V 250 mg three times daily of oral Acyclovir 800 mg 5
times daily
 „Topical antibiotic/steroid ear drops.
 „Eye care.
 Surgical decompression is not indicated

37. TEMPORAL BONE
FRACTURE

38. Basal skull fracture
A basilar skull fracture is a break of a bone in the base of the
skull
 The break is of at least one of the following bones:
 Temporal bone
 Occipital bone
 Sphenoid bone
 Frontal bone
 Ethmoid bone
 They are divided into anterior fossa, middle fossa, and posterior
fossa fractures.
The temporal bone fracture is encountered in 75% of
all basilar skull fractures and may be longitudinal,
transverse or mixed, depending on the course of the
fracture line in relation to the longitudinal axis of

39. Symptoms and signs
 Basal skull fractures are often not detectable with skull x-rays or even CT
scan. Basal skull fractures are most frequently diagnosed by clinical
findings:
 Battle's sign (mastoid ecchymosis) – bruising of the mastoid
process of the temporal bone. is an indication of fracture of middle
cranial fossa of the skull.
 Raccoon eyes (periorbital ecchymosis) – bruising around the eyes,
i.e. "black eyes“ may be bilateral or unilateral. If bilateral, it is highly
suggestive of basilar skull fracture, with a positive predictive value of
85%. They are most often associated with fractures of anterior cranial
fossa.
 CSF rhinorrhea
 CSF otorrhoea
 Cranial nerve palsy
 Bleeding (sometimes profuse) from the nose and ears

42. (Classification)Temporal bone
fractures
 Fracture of the petrous temporal bone is usually
classified according to the
 Main direction of the fracture plane and/or
 Involvement of the otic capsule.
Direction
 According to orientation of fracture line relative to
axis of petrous ridge
 Longitudinal fractures 80-90%
 Transverse fractures 10-20%
 Mixed /oblque fractures
 Longitudinal fractures are more common and have
better outcomes.

45. Otic capsule involvement
 Other classifications have been proposed as being
more clinically relevant, specifically focusing on
whether or not the otic capsule is involved.
 Otic capsule sparing
 Otic capsule disrupting
 Involvement of the otic capsule is predictor of more
serious complications including :-
 facial nerve paralysis  2 times more likely
 cerebrospinal fluid leak  4 times
 Profound sensorineural hearing loss 7 times
 epidural hematoma and subarachnoid hemorrhage

46.  Facial nerve palsy complicates 7% of
Temporal bone fractures, depending on type of
trauma and fracture pattern.
 Facial nerve injuries occur in
 10-25% of Longitudinal fractures
 Perigeniculate region most commonly involved
 38-50% of Transverse fractures
 Labrynthine and mastoid segament are most
commonly involved

47.  High-resolustion CT-can is investigation of
choice
 Electroneuronography ( ENoG)

48. Management in early stage
 Excellent prognosis and surgical exploration not
indicated in :-
 Patients with normal facial nerve function at
presentation , regardless of they developed delayed
palsy.
 Patients with acute onset incomplete palsy without
progression.
 Surgical exploration is indicated in :-
 Cases of acute complete paralysis and ENoG shows
greater than 90% denervation within 6 days.
 Incomplete palsy progress to compete palsy over
time

49. Management in early stage
 ENoG is not helpful after 3 weeks.
 Decision based on CT finding and
electromyographic results.
 If no return of facial function is observed 6-12
months after injury  exploration to remove any
fragments of bone and fibrosis that impede
regeneration.

50. Complications
 Facial nerve involvement
 facial nerve palsy
 Ossicular chain disruption
 Otic capsule involvement
 vertigo and sensorineural hearing loss
 Cerebrospinal fluid (CSF) disruption
 CSF otorrhea or CSF rhinorrhea
 Meningitis
 Post-traumatic cholesteatoma

51. IATROGENIC INJURY

52. Middle ear and mastoid surgery
 The incidence of facial nerve palsy has been
reported to be between 0.6-3.6 %.
 The most common site of injury is distal to
tympanic segment including second genu.
 Second most common site is mastoid
segment.

53. Management
 If facial palsy is observed intra-operatively 
exploration with decompression.
 If complete facial palsy observed immediately
post-operatively and nerve was identified  few
hours of observation will usually allow for LA-
induced weakness.
 If paralysis is incomplete  oral steroid and
observed clinically.  progression to full paralysis
 exploration.

54. FACIAL NERVE PARALYSIS AS
COMPLICATIONS OF EAR
INFECTION

55. 1. Otitis Media
 Facial nerve paralysis complicate both acute otitis
media and CSOM.
 Mechanisms include :-
 Direct involvement through fallopian canal
dehiscences of canaliculi for neurovascular
connection.
 Fallopian canal osteitis with bone erosion and nerve
involvement
 Inflammatory edema leading to compression and
ischemia of facial nerve
 Demyelination of facial nerve caused by bacterial
toxins.

56. Tratment
 Acute otitis media
 Antibiotic therapy
 Steroid may be used
 Myringotomy with insertion of ventilation tube
 CSOM
 Mastoid exploration anf facial nerve
decompression.

57. 2. Malignant otitis externa
 It is invasive pseudomonas or Aspergillus
infection of ear canal  lead to skull base
osteomyelitis.
 It mainly afflicts immunocompromised patients.
 Facial palsy indicates advancing infection and
invasion through bony-cartilaginous junction and
the fissures of santorini and posteriorly to
stylomastoid foramen.

58. Treatment
 Ciprofloxacin 750mg twice per day is antibiotic
of choice for 6-8 weeks
 Cases attributed to aspergillus infection need
systemic antifungal therapy.
 Surgical management is not indicated.

60.  A 30-year-old female presents to your office
with recurrent orofacial edema, recurrent facial
palsy, and lingua plicata (fissured tongue). The
most likely diagnosis is
A. Conradi-Hunerman syndrome
B. Cogan syndrome
C. Reichert syndrome
D. Melkersson-Rosenthal syndrome
E. Raeder syndrome

61.  Which of the following tests is used to predict
facial nerve function or return 6 to 12 weeks
before clinical evidence of return of function?
A. nerve excitability test
B. maximum stimulation test
C. electromyography
D. nerve conduction time
E. trigeminofacial reflex