Bell’s Bell’s

PalsyPalsyAlso known as/

a. Idiopathic facial paralysisb. Peripheral Facial Paralysis

c. Refrigeration Palsyd. Prosoplegia

Bell’sBell’s Palsyparalysis of cranial

nerve VII (the facial nerve)

resulting in inability to

control facial muscles on the affected side.

Named afterScottish anatomist Sir Charles Bell

(1774-1842), who first described the syndrome along with the anatomy and function of the facial nerve in 1821.

AnatomyThe facial nerve (seventh cranial nerve)

has 2 components. The larger portion comprises efferent fibers that stimulate the muscles of facial expression. The smaller afferent portion contains taste fibers to the anterior two thirds of the tongue, secretomotor fibers to the lacrimal and salivary glands, and some pain fibers.

Definition of bell’s palsy

Most common acute mononeuropathy (disease involving only one nerve), and is the most common cause of acute facial nerve paralysis.

LMN lesion of CN VII which occurs at or beyond the stylomastoid foramen is commonly referred to as a Bell's Palsy.

Unilateral, peripheral facial paresis or paralysis that has an abrupt onset and no detectable cause.

Facial paralysis of acute onset presumed to be due to a non-suppurative inflammation of unknown etiology of the facial nerve within its canal above the stylomastoid foramen.

incidence

75% of lesions of facial nerve fall into category of Bell’s Palsy The problem can occur at any age, but rarely affects people

under the age of 15 or over the age of 60. Annual incidence of Bell's palsy is 15 to 30 per 100,000

persons. Equal numbers of men and women affected. There is no

predilection for either side of the face. Bell's palsy has been described in patients of all ages, with

peak incidence noted in the 40s. Occurs more commonly in patients with diabetes and in

pregnant women. Patients who have had one episode of Bell's palsy have an 8

percent risk of recurrence.1,2 Each year, about 40,000 Americans develop Bell's palsy Between 8 percent and 10 percent will experience a recurrence

of the signs and symptoms, sometimes on the opposite side of the face.

And a small number of people never recover and continue to have some signs and symptoms for life.

etiologyetiologyIt is due to an acute inflammation edema

involving the nerve within its canal. It may be caused by any of the following:

1) exposure to cold and chill 2) secondary to viral (herpes simplex type1 and 2,

herpes zoster) human herpesvirus (HHV); varicella-zoster virus (VZV);influenza B; adenovirus; coxsackievirus; Ebstein-Barr virus; hepatitis A, B, and C viruses; cytomegalovirus (CMV);

3) Rubella infection 4) Diabetes 5) acute respirator tract infection 6) tumor which invade the temporal bone 7) fractures of the temporal bone

etiologyetiology

8) lymphocytes- mediated hypersensitivity phenomenon

9) middle ear infection 10)meningitis 11) hemorrhage 12)infectious dse:

13)middle ear surgery14) Genetics: A family history of Bell's

palsy has been reported in approximately 4% of cases. Inheritance in such cases may be autosomal dominant with low penetration. Which predisposing factors are inherited is unclear.

Theories regarding the cause 1) hereditary- due to the size of the

diameter of the facial canal 2) vascular ischemic theory 3) viral theory

Pathogenic process From the course of the illness, it is

presumed that the acute non-suppurative inflammation of unknown etiology cause swelling and/ or edema and hyperemia of the nerve sheath, with compression of the axons in the narrow facial canal, thus strangulating them.

Pathophysiology

A popular theory proposes that inflammation and swelling of the facial nerve results in compression of the nerve within the temporal bone.

The facial nerve courses through a portion of the temporal bone commonly referred to as the facial canal. The first portion of the facial canal, the labyrinthine segment, is narrowest; the meatal foramen in this segment has a diameter of only about 0.66 mm. Given the tight confines of the facial canal, it seems logical that inflammatory, demyelinating, ischemic, or compressive processes may impair neural conduction at this site.

PathwayThe path of the facial nerve is complex; this

may be the reason the nerve is vulnerable to injury. Two portions of the facial nerve leave the brain at the cerebellopontine angle, traverse the posterior cranial fossa, dive into the internal acoustic meatus, pass through the facial canal in the temporal bone, then angle sharply backwards, where they pass behind the middle ear and exit the cranium at the stylomastoid foramen. From here, the facial nerve bisects the parotid gland, and then terminal branches extend from the parotid plexus to innervate the muscles of facial expression.

anatomyanatomyComponent• Brachial Motor

• Visceral Motor

• Visceral Sensory

• Point’s of Comparison

• Etiology• UMNL/LMNL• Types of Lesion• Distribution• Paralysis

• Nerve Affected• Skin Condition

Primary cell bodyFacial Nucleus

Superior salivary Gland

Geniculate ganglionBell’s Palsy

UnknownLMNLPeripheral or

NuclearOne side,ipsilateralUpper & lower

quadrantVIIdry

CourseTemporal bone facial

side

a. Greater superficialpetrosal to sphenopalatine ganglion

b. Chorda typani to submaxillary ganglion

Internal Acoustic Meatus

Peripheral termination

ms of expressionHyoid elevatorsa. Glands of nose,

palate,lacrimalb.

Submaxillary,and sublingual glands

Anterior taste buds

Central facial Paralysis

CVA, tumors,vascular lesionUMNLcentral, or supernuclearOne side or contralateralLower quadrantNo specific nervedry

• Marked facial asymmetry

• Atrophy of facial muscles

• Eyebrow droop

• Smoothing out of forehead and nasolabial folds

• Drooping of the mouth corner

• Uncontrolled tearing

• Loss of efferent limb of conjunctival reflex (cannot close eye)

• Lips cannot be held tightly together or pursed

• Diificulty keeping food in mouth while chewing on the affected side

Onset Within a day or two after exposure, there

may be slight fever, pain behind the ear, and pain and stiffness in the neck. The onset is sudden or acute, and often, the patient awakens to find the face paralyzed. A feeling of stiffness and numbness but sensory testing is normal. About ½ of the cases attain maximum paralysis in 48 hours and practically all cases in 5 days.

Affected patients develop unilateral facial paralysis over one to three days with forehead involvement and no other neurologic abnormalities. Symptoms typically peak in the first week and then gradually resolve over three weeks to three months.

Signs and symptoms

These depends upon the location of the lesion

A. Lesion 1. Outside the stylomastoid

foramen. As is it a lower motor neuron lesion, the muscles of the both lower and upper part of the ipsilateral face are involved in a flaccid paralysis forehead cannot be wrinkled

lesion1

• Widened palpebral fissure is lost to paralysis of the orbicularis palpebrum

• Upper eyelid closes slowly due to pull of gravity• Bell’s Phenomenon – eyeball rotates upward and outward when

attempting to close the eye• Blink or corneal reflex (-) in ipsilateral side• Oculogyric auricular reflex (drawing back of ear on extreme lat.

Gaze• Tears are apt to roll doen the cheek• Obliterated nasolabial fold, unwrinkled brow, angle of the mouth

sags and the side of the face is expressionless• Mouth is drawn to the opposite side• Salivamay dribble from the mouth and food gathers between

cheek and gums• Paralyzed lip may give an assymetric appearance and push the

tongue to the opposite side• Atrophy is present, although rarely apparent because of small ms

bulk• Electrical reaction of degeneration appears in 10-14 days,

depends upon the extent of damage

b. Lesion 2

In facial canal involving the chorda tympani all signs of Lesion 1 is present as well as:

• Loss of taste in the anterior 2/3 of tongue• Reduced salivation on affected side

c. Lesion 3

Higher than the facial canal involving the stapedius muscle. + all signs of lesion 1 and 2

• Hyperacusis-pain sensitivity to loud sounds– Increased acuity of hearing

d. Lesion 4

Higher involving the geniculate + all signs of Lesions 1,2&3*Pain behind the ear*Herpes of the typanum and concha may precede the palsy*Ramsay hunt syndrome

• Herpetic eruptions on the ipsilateral eardrum, post. Part of auricle, tympanic membrane, external auditory canal, pinna, or on the soft palate

• Facial paralysis• Ipsilateral deafness

e. Lesion 5

in the internal auditory meatus + all the signs of Leisons 1-4

• Sign’s of Bell’s Palsy• Deafness (CN8 involvement)• Tinnitus• Defective vestibular response

f. Lesion 6

At the immergence of CNVII from ponsInvolvement of CNV & CN8May also invove CNVI,XI,XII

• Marcus-Gunn or jaw winking phenomenon- seen in the congenital ptosis,elevation of ptotic eyelid on the mov’t of jaw to the contaralateral

• Marin Amat Syndrome- closure of the eye occurs when patient open the mouth forcefully and maximally

dx• Electrodiagnostic testing with nerve conduction studies

and electromyography allow for the determination of the presence or absence of a motor response within 1 week of onset. A motor response upon stimulation of the facial nerve is a good prognostic indicator. Electrodiagnostic testing is also useful later in the course of Bell's palsy to evaluate aberrant regeneration. In addition, the preservation of taste perception and submandibular salivary flow along with the presence of a motor response on electrodiagnostic testing are all associated with a more favorable recovery.

• MRI imaging • CSF analysis • Submandibular salivary flow rates are typically not

evaluated routinely in patients with Bell's palsy. However, it has been shown that a flow rate greater than 50% of normal correlates with complete recovery of facial function.15

• Titers for Lyme disease and herpesviruses, primarily varicella-zoster virus and herpes simplex virus type 1 herpes, should be obtained in patients presenting with new-onset Bell's palsy, particularly when clinical symptoms support these infectious etiologies.

• No specific laboratory tests exist to confirm the diagnosis of Bell's palsy. Clinical setting determines tests that may be of value. Results of the following laboratory tests may confirm or suggest other potential causes in the differential diagnosis:– Complete blood count– Erythrocyte sedimentation rate– Thyroid function studies– Lyme titer– Serum glucose level– Rapid plasma reagin (RPR) or Venereal Disease

Research Laboratory (VDRL) test– Human immunodeficiency virus (HIV) antibodies– Cerebral spinal fluid analysis– Immunoglobulin M (IgM), immunoglobulin G (IgG), and

immunoglobulin A (IgA) titers for CMV; rubella; HSV; hepatitis A virus; hepatitis B virus; hepatitis C virus; VZV; M pneumoniae; and Borrelia burgdorferi

prognosis

• Depends on severity of lesion• Total actual deficit may not be

determined for about 7-10 days because damaged fibers may conduct during the process of degeneration, and undestroyed fibers may not function temporarily

• Spontaneous recovery may take place in mild cases

txThe evidence for many therapies is based on a study

released by the Quality Standards Subcommittee of the American Academy of Neurology (AAN) in 2001 which established practice parameters regarding the effectiveness of corticosteroids, antivirals, and decompression surgery as treatment for Bell's palsy.16 While the evidence for various therapies is not definitive, several treatments offer some benefit.

• Prednisone • The use of oral prednisone in the treatment of Bell's palsy has

been the subject of much debate. • Acyclovir and prednisone –maximal effect on dx within

3days of onset

• In patients with facial nerve palsy secondary to Lyme disease, a 2- to 4-week course of amoxicillin or doxycycline should be started. In some patients with acute onset of Bell's palsy, a reactivation of herpes viruses, primarily varicella-zoster virus and herpes simplex virus type 1 may be involved. Antiviral medications can be used in these patients.

• Eye patching and use of eye drops These measures, which minimize the risk of corneal irritation

and abrasion, are recommended when the patient cannot fully close the eye on the affected side.

• Facial retraining Facial retraining exercises may help to facilitate facial

movement for some patients although this approach is still very controversial. A recent small study of 24 patients with long-standing paralysis who received neuromuscular facial retraining demonstrated improved symmetry in dual-channel electromyographic readings and increased facial movement.19

• Botulinum toxin Botulinum toxin (Botox) can be used to treat the crocodile

tears associated with Bell's palsy. Hyperlacrimation can be very problematic for patients and botulinum toxin may help these patients. Injections are to the submandibular salivary gland or periglandular area. The effect lasts 3 to 4 months and may require reinjection. The most common side effect, which is probably due to diffusion of the botulinum toxin, is increased weakness of the eyelid (ptosis).

• Facial nerve decompression surgery Facial nerve decompression has been evaluated and has been

performed in some patients with prolonged Bell's palsy. Patients in whom less aggressive treatments have failed and have not recovered satisfactory function may choose to have this surgical procedure. However, there are no evidence-based recommendations for its use.16 Permanent unilateral sensorineural deafness has been reported as the most common side effect of this procedure; thus, surgery is not recommended in most patients, although it may still be an option for some.20

PT management

• IR• ES• Facial massage• Facial excercise• Taping

Good prognosis

1. Recovery of taste in 1st week2. Incomplete paralysis in the 1st 5-7

days 3. EMG shows there are motor units

voluntary control in CNVII w/in few days after onset

4. Return to voluntary motor power at the end of 3 weeks from onset

Poor prognosis

1. Age > than 602. Hypertension3. DM4. Hyperacusis5. Diminished lacrimation6. Complete paralysis7. No motor detectable by needle electrode

exploration of facial musculature8. Inexcitable CNVII,spontaneous fibrillation w/in 2-

3 weeks (+) wallerian degeneration9. Evidence of denervation after 10 days