Idiopathic facial nerve palsy/ Bell’s palsy

Definition:

Idiopathic (Diagnosis of exclusion), peripheral facial paralysis or paresis of acute

onset.

diagnostic criteria for Bell's palsy:

1. paralysis or paresis of all muscle groups of one side of the face

2. sudden onset (<48 hours)

3. absence of signs of CNS disease

4. absence of signs of CPA disease or ear

Epidemiology:

 the most common cause of facial nerve palsy (60-75% of F.N cases)

 M=F (except for a predominance in women < 20 & predominance in men >
age 40)

 Any age group may be affected

 Incidence:

 20 to 30 patients per 100,000 population

 Incidence rises with increasing age.

 greater in patients older than 65 years (59 of 100,000)

 lower in children younger than age 13 (13 of 100,000)

 The left = right sides of the face

  incomplete paralysis: 30%

 complete paralysis : 70%

 Bilateral paralysis :0.3% of patients

 Positive family history is present in 6-8% of patients (early age of

onset, recurrent, and have an excellent prognosis).

 Recurrence rate: 9% of cases (higher in females, D.M)

 Risk factors:

1. diabetics (angiopathy)

2. Pregnant women:

 esp in pre-eclampsia because of fluid retention).

 most commonly occurs in the 3RD trimester or immediately
postpartum

Etiology (Hypothesis):

1. Viral infection

The viral hypothesis has been the most widely accepted

however, no virus has ever been consistently isolated from the serum of
patients with Bell's palsy.
 Thus, the evidence for the viral hypothesis is indirect, relying on clinical
observations and changes in viral antibody titers
 more than 50% of pt with bell’s palsy has functional deficit of additional
cranial nerve (part of the total picture of polyneuritis) in which bell’s palsy
is the most obvious cranial nerve to be involved (most commonly ass with
glossopharyngeal + trigeminal).
 Most of the evidence supports the viral aetiology due to:

1. herpes simplex (most likely cause)

2. herpes zoster

3. Epstein-Barr virus.

4. Mumps

5. rubella

 considering there is no seasonal predilection or epidemic clustering, it is much

more likely that Bell's palsy is caused by reactivation of a latent virus rather
than direct, communicable viral infection

 the virus is usually latent in the genigulate ganglion

Summary of Pathophysiology:

Impaired axoplasmic flow from edema of the facial nerve within the fallopian canal
Secondary to a herpes simplex virus type 1 (HSV-1) reactivated from dormancy in
genigulate ganglion
 most commonly occurs in the meatal foramen:

 meatal foramen is the narrowest point of fallopian canal

 located at the junction of the internal auditory canal and the

labyrinthine portion

 The meatal foramen averaged 0.68 mm in diameter, whereas the

remainder of the fallopian canal measured 1.02 to 1.53 mm

2.microcirculatory failure of the vasa nervorum (b)

3.Vascular ischaemia

(c) Hereditary :

The fallopian canal is narrow because of hereditary predisposition and this makes
the nerve susceptible to early compression with the slightest oedema.

(d) Autoimmune disorder

T-lymphocyte changes have been observed

Histological findings:

 diffuse demyelination of the FN throughout its intratemporal course (from

distal IAC to mastoid segment)
 with the most severe findings in the labyrinthine segment and at the meatal
foramen.
 HSV1 DNA in facial perineural fluid
 Cisternal segment (intracranial part of facial nerve) is not affected
 spectrum of injury from neuropraxia-neuromtesis
 lymphocytic infilteration, neural edema, and myelin degeneration most
prominent at the labyrinth segment
 MRI demonstrates a linear uniformly enhancing facial nerve from distal IAC to
mastoid segment on contrast
Clinical Features :

 viral-like prodrome 3–4 days prior to paralysis

 Sudden Onset (less than 48 hr)
 Face becomes asymmetrical.
 Patient is unable to close his eye.
 On attempting to close the eye, eyeball turns up and out (Bell's
phenomenon).
 Tears flow down from the eye (epiphora). (lacrimation may decrease but
never absent)
 Postauricular pain: Pain in the ear may precede or accompany the nerve
paralysis.
 Hyperacusis: Some complain of noise intolerance (stapedial paralysis)
 Dysgeusia
 loss of taste (involvement of chorda tympani).
 Saliva dribbles from the angle of mouth.
  Paralysis may be complete or incomplete.

 Bell's palsy is recurrent in 3-10% of patients.

Treatment

General :

1. Reassurance.

2. Relief of ear pain b analgesics.

3.Eye Car :

a) Ophthalmology consult: exclude corneal ulcer/abrasionCare of the eye.

b) Artificial tears
c) Tape the eye closed during sleep: to protect the Eye against exposure
keratitis.

4. Physiotherapy:

 Psychological support to the patient. It has not been shown to influence

recovery.

 Active facial movements are encouraged when there is return of some

movement to the facial muscles.

Medical management

Steroids

 Prednisolone is the drug of choice.

 within 1 week, the adult dose of prednisolone is 1 mg/kg/day divided into

morning and evening doses for 5 days.

 Patient is seen on the 5th day:

 a) If paralysis is incomplete or is recovering, dose is tapered during the next
5 days.

b) If paralysis remains complete or the same,dose is continued for another 10

days and thereafter tapered in next 5 days. (Total of 20 days).

 Contraindications to use of steroids include:

1. Pregnancy
2. Diabetes
3. Hypertension
4. peptic ulcer
5. pulmonary tuberculosis
6. glaucoma
 Steroids have been found useful to prevent incidence of:

1. Synkinesis
2. crocodile tears
3. Shorten the recovery time of facial paralysis.
 Steroids can be combined with acyclovir for Herpes zoster oticus or Bell's
palsy.

Anti-virals:

 can be added if treatment is initiated within the first 72 hours;

 Beyond this time, additional efficacy is less likely.
 Valacydovir is given at a dose of 1,000 mg three times daily for 7 days
famcidovir may be given at 1,500 mg daily for 7 days.

Surgical:

 still controversial
  considered only for > 90% degeneration on ENOG in first 2 weeks of
paralysis
 postulated the maximal nerve injury occurs at the meatal foramen
 unroofing labyrinthine segment via middle fossa approach
 decompression performed within 14 days of onset significantly improves
outcome in patients with poor prognosis;
 after 14 days _ no additional benefit
 decompression of mastoid and tympanic segments has no effect on
recovery

Prognosis:

 Good prognosis since the cause of paralysis is neuropraxia

Bell's palsy

2/3 paralysis 1/3 paresis

15% no 95% full

85% recover
recovery recovery

70-85% full 15-30% partial

recovery recovery

 85-90% of the patients recover fully within 6 months.

 No further recovery is obtained after 6 months

 Poor prognostic signs:

1. Complete paralysis

2. Late onset of recovery

3. decreased tearing (dry eyes)

4. Hyperacusis

5. severe aural, anterior facial, or radicular pain

6. age older than 60 years

7. DM

8. HTN

 Recurrent facial palsy may not recover fully.

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