Back
ditki Logo
medical & biological sciences
All Access Pass - 1 FREE Month!
Institutional email required, no credit card necessary.
Facial Palsy (Bell's Palsy)
FREE ONE-MONTH ACCESS
Institutional (.edu or .org) Email Required
Register Now!
No institutional email? Start your 1-week free trial, now!
- or -
Log in through OpenAthens

Facial Palsy (Bell's Palsy)

Summary Examination of Facial Palsy
  • Inspection of Facial symmetry
    • The wrinkles of the forehead and the prominence or flatness of the nasolabial folds.
    • The symmetry of blinking; the eyeballs should turn up and out with each blink. This is a normal phenomenon but is not seen because of full closure of the lids if there is no weakness.
CN 7: Motor Division
Rest
  • Inspect the patient’s nasolabial folds and palpebral fissures at rest.
    • Flattening of a nasolabial fold (crease) and widening of the palpebral fissure may indicate facial weakness.
    • Note that inspection of the face at rest is neither as sensitive nor as specific as inspection of the patient’s forced smile but should be used as additional evidence of facial weakness.
Action
  • Lower face. Ask the patient to smile (or show his/her teeth).
    • On each side of the face, the corner of the patient’s mouth should pull backward and draw to one side.
    • Failure of the side of the face to move is abnormal.
    • Be aware that laughter produces a smile through different neuroanatomical pathways than a forced volitional smile.
  • Upper face. Assess the patient’s ability to tightly close his/her eyes and wrinkle his/her forehead. - Corticonuclear innervation to the upper face is different than that to the lower face (addressed in the anatomical discussion of cranial nerve 7).
Associated Evaluation of Spontaneous movements of the mouth.
    • "*Note abnormal movements such as twitching, tremor, involuntary movements and myokymia (a vermicular (worm-like) undulating movement around the eye or hemifacial spasm or oculopalatal myoclonus (rhythmic movement of the platysma muscle in conjunction with the palate)."
Facial Palsy: Bell's Palsy Variants
Regional facial nerve anatomy
  • Pons, medulla, and cervical spinal cord.
  • Skull base (the clivus)
  • Internal acoustic meatus (aka internal auditory canal) is where the facial nerve enters the petrous bone.
CN 7 Nuclei
  • The facial nucleus spans from the lower pons to the pontomedullary junction.
    • This component innervates the muscles of facial expression.
  • The superior salivatory nucleus lies just above the pontomedullary junction.
    • This component provides parasympathetic innervation to the pterygopalatine ganglion, which innervates the nasal, lacrimal, and palatine glands, and the submandibular ganglion, which innervates the submandibular and sublingual glands.
  • The solitary tract nucleus spans the height of the medulla.
    • It receives taste sensation from the anterior two thirds of the tongue.
  • Pars caudalis portion of the spinal trigeminal nucleus spans from the inferior medulla to the upper cervical spinal cord.
    • It receives sensory information from select portions of the external ear. This facial nerve component is clinically insignificant.
Manifestations of Facial Palsy
  • Clinical Exam - Facial Palsy.
  • Radiographic Image - Facial Neuropathy.
    • Hemi-facial paralysis occurs from major motor involvement.
    • The affected eye gets dry from loss of lacrimal gland secretion and there can be mouth drying; we'll soon see why drying of the eye tends not to occur in a very distal Bell's palsy.
    • There can be loss of taste.
Facial Nerve Fiber Courses
Although each fiber track has its individual course through the brainstem, basal cisterns, and skull, its easiest to learn the major motor component, first, and then simply focus on how the other fibers differ from it.*
The major motor component
  • Exits the brainstem at the pontomedullary junction as the motor root, passes through the cerebellopontine angle cistern, enters the petrous bone through the internal acoustic meatus.
  • Then gives off the stapedius nerve branch at the beginning of the mastoid segment before it drops straight down through the stylomastoid foramen where it divides into several nerve branches, which innervate the muscles of facial expression.
  • As a clinical pearl, indicate that hyperacusis, an abnormal sensitivity to loud sounds, can occur in Bell's palsy.
    • The stapedius muscle contracts the neck of the stapes, ostensibly to prevent the transmission of high-energy sounds through the middle ear ossicles, and thus it often fails in CN 7 injury.
A major differentiation between the motor division is that the other fibers exit together via the nervus intermedius (of Wrisberg); whereas the motor root exits on its own.*
The parasympathetic fibers
  • Exit the brainstem at the pontomedullary junction as the nervus intermedius, join the major motor component, divide at the geniculate ganglion (which is the sensory ganglion of CN 7) into an upper division.
  • The upper division exits the petrous bone as the greater petrosal nerve to innervate the pterygopalatine ganglion, which provides parasympathetic postganglionic innervation to the lacrimal, nasal, and palatine glands.
  • & The lower division, which continues with the major motor component until it joins the chorda tympani to innervate the submandibular ganglion, which innervates the submandibular and sublingual glands.
    • Thus, a proximal Bell's palsy will affect the upper and lower divisions of parasympathetic output and cause upper facial and oral secretions, whereas a distal lesion may only affect oral secretions.
    • This explains why there can be intense drying of the eye, so much so that the eye must be well lubricated to avoid corneal abrasion.
The taste sensation fibers
  • Follow the exact same course as the lower division parasympathetic fibers, except they innervate taste sensation of the anterior 2/3rds of the tongue.
    • Thus, both proximal and distal Bell's palsy can affect taste.
The clinically insignificant sensory fibers to the external ear
  • Follow the major motor component to its exit at the stylomastoid foramen.
Ramsay Hunt syndrome
  • Herpes zoster reactivation in the geniculate ganglion (the sensory ganglion) triggers a Bell's palsy.
  • The zoster vesicles may or may not be visible on the palate, tongue, or external acoustic meatus.
  • Importantly, in Ramsay hunt, there is CN 8 involvement, as well, so patients manifest with hearing loss and vertigo in association with their CN 7 injury, because CN 8 runs through the internal acoustic meatus along with CN 7; thus herpes zoster activation in the geniculate ganglion affects both CNs.
  • The chorda tympani is the nerve bundle of the lower parasympathetic fibers and the taste fibers.
    • It merges with the lingual nerve, a branch of the mandibular division of the trigeminal nerve, which carries sensory afferent information from the floor of the mouth.
  • This helps explain why Bell's palsy commonly causes facial dysthesias (sensory abnormalities) even though CN 7, itself, doesn't supply facial sensation.
The CN 7 Anatomical Segments
  • In the meatal segment, CN 7 passes through the internal acoustic meatus.
  • In the labyrinthine segment, it enters the facial canal.
    • This segment terminates at the geniculate ganglion, which is identified by its abrupt bend, the external genu.
  • In the horizontal (aka tympanic) segment, CN 7 runs posteriorly (horizontally).
  • In the mastoid segment CN 7 drops straight down and exits the skull through the stylomastoid foramen.
Common causes of Bell's palsy
  • Idiopathic, most often, (meaning the primary cause isn't identified).
  • If a cause is identified, it's typically Herpes Zoster, which is why anti-viral therapy is used in conjunction with prednisone to treat Bell's palsy.
    • Lyme disease is a common infectious cause of Bell's palsy.
  • Bell's Palsy can be a manifestation of autoimmune disorders, such as Neurosarcoidosis and Sjögren's disease.
  • Physical damage of CN 7 is also an important a cause, from traumatic causes but also non-traumatic compressive causes, such as tumor.
AAN Practice Guideline
  • Gronseth GS, Paduga R. Evidence-based guideline update: Steroids and antivirals for Bell palsy. Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology 2012;79:2209–2213.
CONCLUSIONS
  • "For patients with new-onset Bell palsy, steroids are highly likely to be effective and should be offered to increase the probability of recovery of facial nerve function (2 Class I studies, Level A) (risk difference 12.8%-15%). For patients with new-onset Bell palsy, antiviral agents in combination with steroids do not increase the probability of facial functional recovery by >7%. Because of the possibility of a modest increase in recovery, patients might be offered antivirals (in addition to steroids) (Level C). Patients offered antivirals should be counseled that a benefit from antivirals has not been established, and, if there is a benefit, it is likely that it is modest at best."

Related Tutorials