BELL’S PALSY
| A | Vasodilators and ACTH | |
| B |
Physiotherapy and electrical stimulation |
|
| C |
Increase steroid dosage |
|
| D |
Electrophysiological nerve testing |
A case of bells palsy on steroids shows no improvement after 2 weeks; the next step in management should be:
| A |
Vasodilators and ACTH |
|
| B |
Physiotherapy and electrical stimulation |
|
| C |
Increase steroid dosage |
|
| D |
Electrophysiological nerve testing |
This appears to be the most reasonable and appropriate action to be taken once the initial steroid therapy is failed.
| A |
Tensor tympani |
|
| B |
Levator palatii |
|
| C |
Tensor veli palatini |
|
| D |
Stapedius |
Hyperacusis (Phonophobia) occurs due to undue sensitivity to loud sounds.
- Stapedius muscle dampens excessive vibrations of the stapes caused by high pitched sounds in order to protect the internal ear.
- If this protective reflex is not elicited it indicates stapedius paralysis and results in hyperacusis.
| A |
Post operative |
|
| B |
Trauma |
|
| C |
Ramsay Hunt syndrome |
|
| D |
Bells palsy |
Most common cause of lower motor neuron facial palsy is:
| A |
Cholesteatoma |
|
| B |
Cerebello-pontine angle tumours |
|
| C |
Bell’s palsy |
|
| D |
Postoperative (ear surgery) |
Bell’s palsy is paralysis of:
| A |
UMN V nerve |
|
| B |
UMN VII nerve |
|
| C |
LMN V nerve |
|
| D |
LMN VII nerve |
True regarding Bell’s palsy is all except
| A |
Steroids are used |
|
| B |
U/L facial weakness |
|
| C |
Role of herpes simplex in etiology |
|
| D |
Immediate surgical decompression is required |
Which of the following is not true about Bell’s palsy?
| A |
Acute onset |
|
| B |
Always recurrent |
|
| C |
Spontaneous remission |
|
| D |
Increased predisposition in Diabetes Mellitus |
Bells Palsy
- It is the commonest cause of facial palsy in adults
- Lower motor neuron type paralysis
- It is idiopathic in nature°
- Bells palsy manifests as an acute, unilateral paresis or paralysis of the face.
- The onset and evolution are rapid – typically less than 48 hours.
- The incidence reaches a maximum between the ages 15 and 45 years. It has a predominance in women younger than 20 years and a slight predominance in men older than 40 years, although it is more or less equaL°
- Recurrence rate of Bells palsy is 4.5-15%
- Familial incidence = 4.1%
- Bells palsy is uncommon in pregnancy, however the prognosis is significantly worse in pregnant women with Bells palsy than among non pregnant women with palsy.
- Several authors have also demonstrated, a correlation between diabetes mellitus and Bells palsy in developing countries.
- Infectious causes have also been implicated in the origin of Bells palsy – viz:
FISV 1 and HSV 2, human herpes
Varicella zoster virus
Influenza B
Adenovirus
Cox sackie virus
– Epstein Barr virus
Recently it has been demonstrated that an inactivated intranasal influenza vaccine increased the risk of Bells palsy.
- Normal function is usually regained within 3 months in about 2/3 rd of patients
- No further recovery is expected after a period of 6 months.
- Majority of the patients with Bell’s palsy recover completely
Surgical decompression of facial nerve in Bells palsy is needed only in indicated cases, i.e.
- In case of complete paralysis and
- If electroneurography of facial nerve shows >90% of degeneration. When done it should be within 2 weeks of onset of palsy.
| A |
Hemiparesis and contralateral facial nerve paralysis |
|
| B |
Combined paralysis of the facial, trigeminal, and abducens nerves |
|
| C |
Idiopathic ipsilateral paralysis of the facial nerve |
|
| D |
Facial nerve paralysis with a dry eye |
- Bells paralysis is a LMN type of facial nerve palsy of unknown etiology i.e. idiopathic nature.
- Lower motor neuron type of palsy causes ipsilateral paralysis therefore bells palsy causes ipsilateral facial paralysis.
- Other neurological examinations are normal in Bells palsy
All of the following are seen in bell’s palsy except:
| A |
Ipsilateral-facial palsy |
|
| B |
Ipsilateral-loss of taste sensation |
|
| C |
Hyperacusis |
|
| D |
Ipsilateral ptosis |
Bell’s palsy is an acute onset lower motor neuron type of palsy – there will be Ipsilateral loss of :
- Taste sensation, lacrimation and salivation
- Facial paralysis
- Noise intolerance (hyperacusis)
- Eye balls will turn up and out (Bells phenomenon) on attempting to close eyes but ptosis will not be seen.
In Bells palsy – Facial paralysis is usually preceeded by pain behind the ear.
Bell’s palsy patient comes on day 3. Treatment given would be:
| A | Intratympanic steroids | |
| B |
Oral steroids + vitamin B |
|
| C |
Oral steroids + Acyclovir |
|
| D |
Vitamin B Vasodilator |
Medical Management
I. Steroid therapy:
- Oral prednisolone has been used extensively to treat patients with Bells palsy.
- Proof of efficacy is however controversial.
- Steroids are considered useful because they have an anti inflammatory response.
- Because the cost of therapy is less and it has low risk of side effects, predinosolone is commonly started at the initial visit
- Initiation of therapy during the first 24 hours of symptom confers a higher likelihood of recovery
II. Antiviral therapy:
- It represents a newer adjunct in treating acute facial palsy of viral origin (Both Bells palsy and Ramsay hunt syndrome)
- Oral acyclovir is the DOC
- Some studies have shown that patients who receive prednisolone plus oral acyclovir have a higher recovery rate and reduced rates of synkinesis in comparison to those who receive prednisolone alone.
- Based on above evidence most surgeons advocate combination of steroids and antiviral drugs.
The usual recommended regime is predisolone 1mg/kg/day for five days followed by a ten day taper and oral acyclovir (200-400 mg 5 times daily) for ten days.
Physical Management
Includes :
Electrical stimulation: It is done to maintain membrane conductivity and reduce muscle atrophy
- It is generally used in patients left with partial defects
Eye care:The cornea is vulnerable to drying and foreign body irritation in acute facial palsy due to orbicularis oculi dysfunction. So measures conferring corneal protection are recommended such as
- Artificial tears drops at daytime
- Ocular ointment at night
- Use of sunglasses etc
In long standing cases: Reducing the area of exposed cornea by implanting a gold weight in the upper lid (tarsorapphy) is done.
Surgical Management
Nerve decompression
- Axonal ischemia can be reduced by the decompression of nerve segments presumed to be inflammed and entrapped.
- Decompression of the facial nerve is done in cases who have a poor prognosis for complete recovery with medical treatment alone.

