BELL'S PALSY

Facial palsy is caused by damage to the facial nerve (i.e. cranial nerve VII) that supplies the muscles of the face. 

Types
1. Central facial palsy- Due to damage above the facial nerve nucleus
2. Peripheral facial palsy- Due to damage at or below the facial nerve nucleus

                                                                      

Anatomy of facial nerve

It is composed of approximately 10,000 neurons, 7,000 of which are myelinated and innervate the 

muscles of facial expression.

The remaining 3,000 fibres are somatosensory and secretomotor, and are known as the Nervus 

Intermedius.

COURSE OF FACIAL NERVE

1. intracranial course

-meatal course

-labyrinthine course

-tympanic course

-mastoid course

2. extracranial course

INTRACRANIAL COURSE:

Arises within brain stem

EXTRACRANIAL COURSE

Divides into 5 branches on face. They are:

Frontal, zygomatic, buccal. marginal mandibular and cervical branches.

Causes of Peripheral Facial Palsy:

1. Idiopathic or Bell's Palsy- The most common cause of facial paralysis

2. Tumor

A tumor compressing the facial nerve can cause facial paralysis

The most common tumor to cause facial palsy is acoustic neuroma (also known as vestibular 

 

schwannoma)

3. Infection

Ramsay Hunt syndrome - caused by Herpes Zoster infection- A syndromic occurrence 

of facial paralysis, herpetiform vesicular eruptions, and vestibulocochlear dysfunction

Lyme disease - caused by infection with Borrelia burgdorferi via tick bites- 10 percent of patients 

affected with lyme's disease develop facial paralysis - 25 percent of these patients present with bilateral 

facial palsy

4. Iatrogenic facial nerve damage

Occurs most commonly in temporomandibular joint replacement, mastoidectomy and 

parotidectomy

5. Congenital

6. Rare causes, including:

Neurosarcoidosis

Otitis media

Multiple sclerosis

Melkersson-Rosenthal syndrome

Guillain-Barre syndrome

7. Trauma- Especially temporal and mastoid bone fractures

BELL'S PALSY: 

Idiopathic facial palsy, also called Bell’s palsy, is  an  acute disorder of the facial nerve, which may 

begin with symptoms of  pain  in  the  mastoid  region  and  produce  full  or  partial paralysis of 

movement of one side of the face.

It is the most common diagnosis of acute facial paralysis.

ETIOLOGY:

In a study published in the Journal of neurology in 2020, the potential clinical etiologies of BP were 

classified according to 5 theories:

1. Anatomical structure

2. Viral infection

3. Ischemia

4. Inflammatory reaction

5. Acute cold exposure

THEORY ANATOMICAL STRUCTURE:

Yilmaz et al. assessed the lower internal auditory canal (IAC) inlet as well as mid-canal values in 

patients with Bel’s palsy.

Ozan and Arslan compared the diameters and cross-sectional areas of the facial nerve and IAC between 

the affected and unaffected sides of 56 patients using MRI.

Their data suggested that Bell’s Palsy generally coincides with a narrower facial canal in affected 

patients.  

THEORY OF VIRAL INFECTION:

Infection by reactivated viruses, such as the varicella zoster virus (VZV), herpes simplex virus type 1 

(HSV-1), human herpes virus 6.

The reactivation of HSV-1 is centered around the geniculate ganglion, and thus potentially linked to 

BP  -   was first outlined by McCormick in 1972.

A possible cause of HSV-1-mediated neural dysfunction is the activation of apoptotic pathways leading 

to axonal degeneration, which are driven by the axon’s local indirect and direct responses to the viruses 

themselves in susceptible phenotypes.

THEORY OF ISCHAEMIA:

Ischemia can result in thickening of the facial nerve sheath, forming one or more fibrous bands that 

cause nerve strangulation and compression, thereby hampering recovery in long standing cases.

THEORY OF INFLAMMATION:

Numerous lines of evidence have suggested that BP results from acute, inflammation-caused 

demyelination.                               

                                                           

The nerve, from the internal acoustic meatus to the stylomastoid foramen, is infiltrated by round, small 

inflammatory cells. 

This causes breakdown of myelin sheath. The myelin sheath is a layer that wraps the axons of nerve 

cells and is mainly composed of Schwann cells. Schwann cells insulate axons protruding from neurons 

in the peripheral nervous system, thus preventing the transmission of electrical impulses from one 

neuron’s axon to another’s 

Bell's Palsy, as Guillain–Barré syndrome, may be an acute demyelinating disease of the peripheral 

nervous system. As most cases of uncomplicated Bell's Palsy result in full recovery, the main lesion 

may comprise the surrounding myelin sheaths and the Schwann cells, but not the nerve itself. 

THEORY OF ACUTE COLD EXPOSURE

Subcutaneous fat serves as a defense against cold stimulation. 

Adipose tissue releases various bioactive substances, called adipokines. 

It has been proposed that adipose tissue is a member of the diffuse neuroendocrine system. 

Subcutaneous fat may serve as a line of defense against cold stimulation, which causes the release of 

various secretory factors that influence the immune system and the susceptibility to proinflammatory 

events such as Bell’s palsy. 

CLINICAL FEATURES:

-Loss of forehead wrinkles

-loss of nasolabial fold

-inability to close eye

- drooling saliva

-excessive lacrimal secretions

- loss of taste sensatio

                                                                      

EVLUATION:

History- 

onset and progress of paralysis 

associated symptoms- pain/dysgeusia

Medical history should include recent rashes, arthralgias, or fevers;

history of peripheral nerve palsy; exposure to new medications; and exposure to ticks or areas where 

Lyme disease is endemic. 

The physical examination should include:

careful inspection of the ear canal, tympanic membrane, and oropharynx

evaluation of peripheral nerve function in the extremities and palpation of the parotid gland

examination of facial muscles.

Examination of intratemporal branches of facial nerve:

Dry eye- schirmer’s test

hyperacusis from stapedius dysfunction (reflex testing)

dysguesia

decreased sensation in external auditory canal (hitselberg’s sign)

2. Examination of peripheral branches of facial nerve:

degree of weakness

presence of synkinesis

presence of spasticity

3. examine EAC, periauricular area

GRADING OF FACIAL PARALYSIS:

 1. HOUSE BRACKMANN SCALE

2. SUNNYBROOK

3. SYDNEY

4. FISCH DETAILED EVALUATION OF FACIAL SYMMETRY

5. YANAGIHARA