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
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