front-page-grid Uncategorized

Bell’s palsy


Unilateral peripheral facial weakness of the VII cranial nerve.

VII nerve palsy (seventh nerve palsy)

Facial nerve palsy.

It is the most common cranial nerve disorder.

Incidence 20-30 cases per 100,00 people per year.

The incidence of idiopathic facial nerve paralysis is highest in the 15-45-year-old age group.
It has no gender predilection.

There is no preferential localization to a side of the face.

Lifetime risk 1 in 60.

Acute process suggested to be caused by inflammatory, vascular or viral reasons.

HSV type 1 (HSV-1) probably the cause of most cases.

Reactivation of herpes simplex virus and herpes zoster is postulated to account for the majority of cases: Supported by the detection of HSV-1 in the endoneural fluid.

Presence of vesicles may indicate the presence of Ramsay Hunt syndrome-zoster of the geniculate ganglion.

Inflammation of the facial nerve leads to nerve compression resulting in clinical symptoms.

Inflammation of the facial nerve results in edema leading to compression as it passes through the narrow fallopian canal in the temporal bone.
It is diagnosed by exclusion, and there is diagnostic certainty only if the resolution of facial palsy.
The initial evaluation of a patient with facial paralysis is the exclusion of a central cause by history and physical examination.
Most central causes of facial weakness, such as a lesion of the cortex or corticobulbar fibers, affect the countralateral lower half of the face well sparing the forehead and eye closure.
The upper half of the face receives bilateral upper motor neuron input from corticobulbar fibers from both cerebral hemispheres, while the lower half of the face only receives innovation from contralateral corticobulbar fibers.

Peripheral pattern facial weakness results from lesions distal to the facial nucleus in the pons and usually affects the entire ipsilateral face.

Patients with Bell’s palsy often have a drooping mouth on the affected side and often have trouble chewing because the buccinator muscle is affected.

Occurs very rarely, affecting around 40,000 Americans annually.

Some case secondary to diabetes and atherosclerosis suggesting ischemia associated the cause.

Rising incidence of Bell’s palsy with age reflects increased seroconversion to HSV-1 and the disease probably reflects reactivation from latency in the geniculate ganglion.

Responsible for 60-75% of all cases of unilateral facial paralysis.

Idiopathic facial nerve paralysis is acute in onset coming on over hours and peaks within 72 hours.
It involves the peripheral facial nerve.
It may be preceded by postauricular pain, associated with decrease in lacrimation, dysguesia, or hyperacusis.
It often resolves spontaneously over 3 to 6 weeks.
Routine imaging is not indicated in the typical presentation.

Forehead muscles are affected and the patient cannot wrinkle forehead on the side of the peripheral seventh cranial nerve abnormality.

The peripheral pattern involve lesions involving the ipsilateral facial nucleus or its exiting fascicles within the brainstem may be distinguished based on their association with all the brainstem findings including: contralateral hemiparesis, sensory loss, ataxia, nystagmus, third-six nerve palsy, or ophthalmoparesis, whereas peripheral lesions involving the facial nerve after its exit from the brain stem result in isolated complete weakness of the ipsilateral hemiface.

If the forehead muscles are spared the patient probably has a central lesion and not Bell’s palsy, the situation may be a stroke and differentiation should proceed immediately.

Peripheral facial palsy maybe accompanied by hyperacusis, decreased lacrimation or salivation, or dysgeusia, depending upon facial nerve branch involvement of the stapedius, parasympathetic innervation via the greater petrosal nerve and chorda tympani,  respectively.

In Bell’s palsy there is incomplete closure of the eyelids.

When the examiner attempts to open the patient’s eyes they deviate upward amd laterally in Bell’s palsy.

Affects genders equally and the median age of onset is 40 years , but can occur at any age.

Incidence the lowest in children below 10 years of age, increases from ages 10-29 years and stable ages 30-69, with highest rates in individuals over the age of 70 years.

Most cases between ages 30 and 45 years.

Leads to significant sequelae in approximately 20% of patients.

Sequelae include continued facial distortion, facial pain and psychological disturbances.

71% of untreated patients completely recover and 84% have complete or nearly normal recovery (Peitersen).

Patients with residual disease have moderate to severe weakness, facial contracture or synkinesis.

Poor prognosis associated with severe disease and as few as 61% of individuals with complete paresis have full recovery, while 94% of patients with an incomplete paresis have complete recovery, within 4 months of presentation (Cawthorn)

Megadose steroid therapy highly effective treatment.

Meta-analyses suggest that treatment with steroid started within seven days after the onset of complete facial paralysis results in significant improvement in facial weakness.

Morbidity rate for patients with Bell’s palsy and diabetes is 4.2% to 6.6%, which is higher than the rate of 1.7% to 5.4% in the general population.

The rate of Improvement is poorer in patients with diabetes.

Poor prognosis associated with advanced age, hypertension, impairment of taste, complete facial paralysis and the presence of pain aside from the ear.

Electrical studies reveal when excitability is retained 90% of patients recover fully, and in the absence of excitability only 20% completely recover.

Causes if acquired peripheral facial weakness include: diabetes, hypertension, HIV infection, Lyme disease, Ramsay-Hunt syndrome, Epstein-Barr virus, herpes simplex virus, B burgdorferi, hepatitis B virus, mumps virus, M pneumoniae, sarcoidosis, amyloidosis, Sjogren’s syndrome eclampsia, parotid nerve tumors and among recipients of inactivated influenza vaccine.

Rarely recurs.

MRI of the brain is rarely performed for diagnosis but the most common abnormality is enhancement of the distal intracanalicular and labyrinthine segments of the facial nerve.

Some patients have incomplete return of facial motor function and involuntary facial movements as long term process.

Use of electrically evoked stimulus and a recording device to measure the amplitude of facial muscle action potential can determine the extent of nerve degeneration.

Electrical testing should not be performed until three days after the onset of paralysis since with nerve compression or traumatic transaction axonal degeneration is not apparent for a few days.

Electroneurography is most useful when evaluation occurs within 2 weeks of complete loss of voluntary facial function.

Patients who do not have 90% degeneration within the first three weeks, 80-100% regain good function from normal to minimal facial weakness.

Patients with initial severe symptoms carry a worse prognosis than milder forms of disease, with up to 50% of patients failing to achieve complete recovery after 9 months, even with corticosteroids.

Patients with more than 90% degeneration within the first three weeks have a 50% chance of good recovery of facial function.

The faster the onset of facial degeneration the worse the prognosis.

71% of untreated patients recover completely and 84% achieve near normalization of function.

Some patients are candidates for surgical decompression when the facial nerve is compressed at the entrance to the meatal foramen, but the role of such surgery is controversial.

1-15% of patients treated with surgical decompression have permanent unilateral deafness.

Decompression should not be performed after 2 weeks after the onset of paralysis since severe degeneration of facial nerve occurs by then.

Early treatment with corticosteroids is probably effective in improving outcome of facial function and the addition of acyclovir to steroids is possibly effective.

Treatment with corticosteroids should be initiated within the first 72 hours.

Corticosteroids reduce facial nerve edema and accelerated recovery and increase the percentage of patients achieving complete recovery.

Double blind placebo controlled study of patients recruited within 72 hours of onset of symptoms randomized to receive treatment with 10 days of prednisilone, acyclovir, both agents or placebo: at 3 months percentage of patients with complete facial recovery were 83% for prednisilone group versus 63.6% among patients who did not receive prednisilone, 71.2% in the acyclovir group compared to 75.7% among patients who did not receive acyclovir: at none months 94.4% for prednisilone, 81.6% for no prednisilone, and 85.4% for acyclovir and 90.8% for no acyclovir: for both drugs 79.7% at 3 months and 92.7% at 9 months (Sullivan, F 2007).

Conclusion of the above study, early prednisilone significantly improves recovery at 3 and 9 months, while acyclovir alone or in addition to prednisilone offers no benefit.

In a meta-analysis of 10 randomized old trials antiviral agents were not efficacious in increasing portion of patients with Bell’s palsy who achieved complete recovery, regardless of baseline symptom severity (Turgeon RD et al).

35% of patients who have signs at six months and 7-12% will have a recurrent process.

Lyme disease can cause facial palsy can be seen in 50-63% of Lyme meningitis.

Bilateral facial nerve palsy differential diagnosis includes:infectious, inflammatory/autoimmune diseases such as sarcoidosis or Sjögren syndrome, and neoplastic diseases including lymphoma to us leptomeningitis and carcinomatous meningitis.

Leave a Reply

Your email address will not be published. Required fields are marked *