Bell’s palsy

Presentation about Bells Palsy

1. Bell’s Palsy Dr. Ishfaq Ahmad BDS, BCS, MCPS, MS

2. Bell’s palsy is a lower motor neuron disease of the facial nerve (cranial nerve VII) characterized by acute unilateral peripheral facial weakness involving muscles innervated by the facial nerve. Bilateral weakness is very rare and occurs in less than 1% of patients .

3. Incidence Incidence: 20 per 100,000 persons, with equal numbers of men and women, incidence increases with age . Common condition affecting 15-to 45-year-old age group There is no predilection for either side of the face . It occurs more commonly in patients with diabetes and in pregnant women. Patients who have had one episode of Bell’s palsy have an 8 % risk of recurrence. About 10% of those with Bell’s palsy have a family history of the condition.

4. Etiology The cause is unknown, but site of damage is probably the portion of facial nerve lying within the facial canal ( stylomastoid ). Inflammation of facial nerve in the canal with demyelination and edema further hazards with blood supply. Inflammation of the nerve initially results in a reversible neurapraxia , but ultimately Wallerian degeneration ensues. Herpes zoster virus , the  varicella zoster virus  and the  Epstein–Barr virus . Reactivation of an existing (dormant) viral infection has been suggested as a cause of acute Bell's palsy . Risk factors include  diabetes , a recent  upper respiratory tract infection , and  pregnancy .

5. Causes of facial palsy Extracranial causes • Bell’s palsy • Malignant parotid neoplasms • Parotid surgery • Sarcoidosis ( Heerfordt’s syndrome) • Misplaced local anaesthetic • Melkersson –Rosenthal syndrome

6. Intracranial causes • Strokes • Cerebral tumours • Multiple sclerosis • HIV infection • Lyme disease • Ramsay Hunt syndrome • Trauma to the base of the skull

7. Clinical features no history of trauma, local infection , tumor, or CNS disease. peripheral dysfunction of the facial nerve, involving all distal branches . The onset is usually abrupt and maximal facial weakness is observed at 24–72 hours. Generally , the unilateral facial weakness is complete. Numbness or pain around the ear on the affected side reduction in taste on the affected side ; altered taste on the anterior two-thirds of tongue Drooping of the corner of the mouth on the affected side loss of facial creases hyperacusis (hypersensitivity to sounds) inability to close eyelid on the affected side.

8. Upper Motor Neuron vs Lower Motor Neuron If the forehead is not affected (i.e. the patient is able to raise fully the eyebrow on the affected side) then the facial palsy is likely to be an upper motor neuron (UMN) lesion. [3]  Paralysis which includes the forehead, such that the patient is unable to raise the affected eyebrow, is a lower motor neuron (LMN) lesion. The facial nerve lower motor neurons pass from its motor nucleus in the pons to the facial muscles. In lower motor neuron lesions, such as Bell’s palsy, there is impairment of contraction of all facial muscles. The cause is usually extracranial . The facial nerve upper motor neurons pass from the primary motor cortex in the frontal lobe to the pons, but the muscles of the upper part of the face receive stimuli from both sides of the brain, whereas the muscles of the lower face are only activated by the contralateral cortex. Thus , the upper face is controlled by both sides of the brain, and when there is upper motor neuron damage, for instance from a stroke, the lower face is more affected. Emotional movements of the face, the blink reflex and ability to wrinklethe forehead may remain normal.

9. Clinical test for diagnosis Function of the facial nerve is tested by asking the patient to perform facial movements. When asked to close the eyes, the lids on the affected side cannot be brought together, but the eyeball rolls up normally since the oculomotor nerves are unaffected. When the patient is asked to smile, the corner of the mouth on the affected side is not pulled upward and the normal lines of expression are absent (Fig . 38.1). The wrinkling round the eyes that accompanies smiling is also not seen on the affected side, and the eye remains staring, indicating a lower motor neurone disorder . Speech and taste are affected, the latter a result of loss of chorda tympani fibre function in the facial nerve. At rest, saliva may drool from the mouth

10. Differential diagnosis Some of the relatively common conditions that have to be ruled out for before diagnosing Bell’s palsy are Ramsay Hunt syndrome tumors affecting facial nerve diabetes mellitus sarcoidosis Lyme neuroborreliosis .

11. Investigations Electromyography can confirm the presence and severity of nerve damage . Radiographic evaluation of the cerebellopontine angle , internal acoustic canal and mastoid region can be undertaken to eliminate presence of tumors.

12. Treatment Steroids Corticosteroids  such as  prednisone   Antivirals antivirals  (such as  aciclovir ) when combined with corticosteroids . Eye protection Tear-like eye drops or eye ointments and patches or taping Physiotherapy  Facial exercises such as trying to raise the eyebrows, opening and closing the eyes, blowing, and whistling. To reduce  pain , heat can be applied Electrical stimulation for Bell's palsy . Surgery Smile surgery  or smile reconstruction is a surgical procedure that may restore the smile for people with facial nerve paralysis. Alternative medicine   acupuncture and   hyperbaric oxygen therapy

13. Prognosis Most people with Bell's palsy start to regain normal facial function within 3 weeks After a follow-up of at least one year or until restoration, complete recovery had occurred in more than two-thirds (71%) of all patients. better prognosis for young patients, aged below 10 years old, while the patients over 61 years old presented a worse prognosis. [17] Major possible complications of the condition are chronic loss of taste ( ageusia ), chronic facial  spasm , facial pain and corneal infections. Another complication can occur in case of incomplete or erroneous regeneration of the damaged facial nerve. During regrowth, nerves are generally able to track the original path to the right destination—but some nerves may sidetrack leading to a condition known as  synkinesis . For instance, regrowth of nerves controlling muscles attached to the eye may sidetrack and also regrow connections reaching the muscles of the mouth. In this way, movement of one also affects the other. For example, when the person closes the eye, the corner of the mouth lifts involuntarily. Around 9% of people have some sort of ongoing problems after Bell's palsy, typically spasm, contracture,  tinnitus  or hearing loss during facial movement or crocodile-tear syndrome. This is also called gustatolacrimal reflex or  Bogorad's syndrome  and involves the sufferer shedding tears while eating. This is thought to be due to  faulty regeneration  of the facial nerve, a branch of which controls the lacrimal and salivary glands. Gustatorial sweating can also occur.

14. DISTURBANCES OF TASTE AND SMELL Loss of taste Dysgeusia is abnormal taste, hypogeusia reduced taste and ageusia , loss of taste. Loss of smell Anosmia and hyposmia have many causes. Sudden onset of taste loss indicates a likely neurological problem and is a significant sign meriting urgent investigation. A slow onset is usually associated with nasal disease such as hay fever, deviated septum, chronic rhinosinusitis and nasal polyps that either cause mucosal inflammation or prevent air circulating to the olfactory sensors high in the nose. Less common causes include hypothyroidism, Cushing’s syndrome, stroke , vitamin B12 deficiency and alcohol abuse.