Facial palsy, or facial paralysis, can be caused by lesions of the facial nerve that disrupt motor function on one side of the face. It is commonly unilateral and can result from various etiologies like Bell's palsy, tumors, trauma, or infections. Clinical features include weakness or paralysis of facial muscles on the affected side leading to issues like eyelid drooping, inability to fully close the eye, and drooping of the mouth corner. Treatment involves facial exercises and in severe cases, surgery or implants may help restore more natural movement. Prognosis is generally good with many cases recovering normal function, but some are left with minor to severe long-term weakness or contractures.

1. FACIAL PALSY
DR.R.BALAMURUGAN
Final year p.g,M.D(PMR)

2. Facial functions

3. FACIAL PARALYSIS
• Commonly Unilateral
Nuclear- from destruction of the nucleus
• Central or cerebral orSupranuclear
• Peripheral- from a lesion of the nerve
• Supranuclear lesions usuallya part of hemiplegia,
only the lower part of the face is paralysed. The upper
part (frontalis and part of orbicularis oculi)escapes due to
bilateral representation in the cerebral cortex.Infranuclear
lesions- entire face is paralysed, as seen in bell’s palsy

4. Clinical features
Weakness or paralysis of the upper and lower facial muscles of the affected side
Drooping of ipsilateral eyelids
Inability to close the eye completely
Dry eye due to inability to close eyes completely
Excessive tearing of the eye (epiphora)
Drooping of the corner of the mouth
Ipsilateral impaired/loss of taste sensation
Difficulty with eating due to ipsilateral muscle weakness causing food to be
trapped on the affected side of the mouth
Dribbling of saliva
Altered sensation on the affected side of the face
Pain in or behind the ear
Increased sensitivity to sound (hyperacusis) on affected side if stapedius muscle is
involved

5. Clinical Testing of
Facial Nerve Functions
• 1. Observe patient Face
• during rest & movement for :
• • Asymmetry
• • Hemi facial spasm
• • Facial tics
• • blinking

7. ETIOLOGIC CLASSIFICATON OF
FACIALPALSY
• Various classification have been suggested in
this respect.
• Based on:
• Course of the nerve
• Various etiologic causes
• Degree of dysfunction observed

8. INTRACRANIAL (CENTRAL)
CAUSES
• Vascular abnormalities
• CNS degenerative diseases
• Tumours of the intracranial cavity
• Trauma to the brain
• Congenital abnormalities and agenesis

9. INTRATEMPORAL CAUSES
• Bacterial and Viral infection
• Cholesteatoma
• Trauma- blunt temporal bone trauma,
• longitudinal and horizontal fractures of the
• temporal bone and gunshot wounds.
• Tumours invading the middle ear, mastoid and
• facial nerve
• Iatrogenic causes

10. • NEUROLOGIC
• Myasthenia Gravis
• Multiple Sclerosis
• Guillain Barre syndrome
• NEOPLASTIC
• Facial nerve tumours Glomus tumours
• Meningiomas, acoustic neuroma
• Parotid tumours Temporal bone/external
• auditory meatus tumours

11. • INFECTIONS
• Otitis media, mastoiditis
• Bacterial causes
• Viral causes

12. Recurrent facial palsy
• Bell’s palsy,
• Melkersson’s syndrome,
• diabetes,
• sarcoidosis
• tumuors

13. BELL’S PALSY
• First described more than a
century ago by Sir Charles Bell
Bell palsy is certainly the most common cause
of facial paralysis worldwide

14. Viruses that have been linked to
bells palsy
• Cold sores and genital herpes (herpes simplex)
Chickenpox and shingles (herpes zoster)
• Mononucleosis (Epstein-Barr)
• Cytomegalovirus infections
• Respiratory illnesses (adenovirus)
• German measles (rubella)
• Mumps (mumps virus)
• Flu (influenza B), Hand-foot-and-mouth disease
(coxsackievirus

15. EXTRACRANIAL CAUSES
• Malignant tumours of the parotid gland
• Trauma
• Iatrogenic causes
• Primary tumours of the facial nerve
• Malignant tumours of the ascending ramus of
the mandible, pterygoid region and skin

16. Traumatic facial nerve palsy
• Second most common cause of FN
paralysis
• - Represents 15% of all cases of FN
paralysis
• - Most common cause of traumatic facial
nerve injury is temporal bone fracture

17. Bilateral simultaneous facial
palsy
• Moebius syndrome
• GB Syndrome
• Sarcoidosis
• Myotonic dystrophy
• Skull trauma
• Infectious mononucleosis
• CMV
• Acute porphyria, Botulism
• Lyme disease,Bell’s herpes simplex

18. International classification of
Diseases
• G51 Facial nerve disorders G51.0 Bell's palsy
• G51.1 Geniculate ganglionitis
• G51.2 Melkersson's syndrome
• G51.3 Clonic hemifacial spasm
– G51.31 …… right
– G51.32 …… left
– G51.33 …… bilateral
– G51.39 …… unspecified

19. • G51.4 Facial myokymia
• G51.8 Other disorders of facial nerve
• G51.9 Disorder of facial nerve, unspecified

20. RAINER SCHMELZEISEN
CLASSIFICATION
• CONGENITAL
• Moebius Syndrome
• Myotonic dystrophy
• Melkersson Rosenthal syndrome
• Congenital Cholesteatoma
• Birth injuries
• Osteopetrosis

21. HOUSE-BRACKMAN(1985)
CLASSIFICATION
• Grade I-normal function without weakness.
• Grade II-mild dysfunction with sligth facial
asymmetry with a minor degree of synkinesis.
• Grade III-moderate dysfunctions-obvious, but
not disfiguring, asymmetry with contracture
and/or
• hemifacial spasm, but residual forehead motion
and incomplete eye closure.

22. • • Grade IV-moderately severe dysfunction-
obvious, disfiguring asymmetry with lack of
forehead motion and incomplete eye closure.
• • Grade V-severe dysfunction-asymmetry at rest
and only slight facial movement.
• • Grade VI-total paralysis-complete absence of
tone ormotion.

23. Complications
• Irreversible damage to your facial nerve
• Misdirected regrowth of nerve fibers,
resulting in involuntary contraction of
certain muscles whenyou're trying to move
others (synkinesis) — forexample, when you
smile, the eye on the affected sidemay close
• Partial or complete blindness of the eye that
won't close, due to excessive dryness and
scratching of the cornea, the clear protective
covering of the eye

24. synkinesis
• Most distressing consequences of facial
paralysis.
• Synkinesis refers to the abnormal involuntary
facial movement that occurs with voluntary
movement of a different facial muscle group.
• •Abnormal regeneration of facial nerve fibers
to the facial muscle groups

25. ASSESSMENT AND PLANNING
• Cause of facial paralysis
• Functional deficit/extent of paralysis
• Time course/duration of paralysis
• Likelihood of recovery
• Other cranial nerve deficits
• Patient’s life expectancy
• Patient’s needs/expectations

26. Clinical Testing of
Facial Nerve Functions
• Blink test: Delay in blinking on one side
• 3. Testing facial movement
• i. Temporal branch:
• To wrinkle forehead, To elevate eye brow
• ii. Zygomatic branch: to screw up the eye
• iii. Buccal branch: to wrinkle the nose
• iv. Mandibular branch: to show the teeth,
toblow out the cheeks
• v. Cervical branch: by grimacing

27. EVALUATIONS OF NERVE
FUNCTION
• HISTORY is of vital importance to establish the
onset characteristics,duration and degree of
recovery.
• • Previous trauma, surgery or infection may help
in arriving at a diagnosis
• • Examination of the face at rest and movement.
• • Radiolologic evaluations
• • Nerve excitability tests.

28. Pathophysiology of
nerve injury
• Neuropraxia : Blocks flow of axoplasm
from stoma to distal axon.
• Axonotemesis : Wallerian
degeneration with intact endoneural tubules.
Neurotemesis : Wallerian
degeneration with loss of endoneural tubules .
• Transection : Complete division of the nerve .

29. Minimal
excitability test
Compare the minimal current necessary to elicit
minimal muscle contraction when applied
tobranch of facial nerve on normal side to paralyze
• Difference of 3.5mA Or greater between 2
side→ degeneration→surgical decompression

30. ELECTRICAL TESTING OF
FACIAL NERVE
• MAXIMUM STIMULATION TEST
• Pulsed electric current is delivered through a
cutaneous electrode
• Short pulse will stimulate an intact nerve & elicit
a muscular twitch.
• In paralysed facial nerve, this indicates that
lesion is neuropraxia & distal neurons have not
undergone degeneration Hence differentiates
between neuropraxia & axonotmesis:prognostic
value.

31. • No value for 1st 72 h
• Equal response
• Reduced response
• Absent response
• Frequent testing
• shows progressive ↑
• threshold →continuing
• degeneration

32. NERVE EXCITABILITY TEST
• Current required for stimulation on normal side
is compared with paralysed side.
• Disadv: even few intact fibres can elicit a
response when rest in
• undergoing degeneration.
• Muscle twitch response is subjective
• Uncomfortable procedure
• Requires patient co-operation

33. ELECTRONEUROGRAPHY
• Measures compound action potential in facial
muscles in response to facial nerve stimulation.
• Compare compound action potential of facial n.
after Supramaximal stimulation of bothsides
• The degree of degeneration is directly
proportional to the amplitude loss of measured
summation potential
• Not useful during 1st72 h,90% or more
degeneration indicate decompression within3
weeks

34. ELECTROMYOGRAPHY
• The recording of
spontaneous and voluntary muscle potentials by
needles introduced into the muscle is called
electromyography(EMG).
• Records motor unit potentials of the orbicularis
oculi & orbicularis oris muscle during rest
&voluntary contraction

35. • EMG can be used to determine:-
• 1.If a nerve in question is in fact in
continuity(volitional activity recorded)
• 2.Evidence of degenration ( fibrillation after 10-
14 days)
• 3.If there are early sign of reinnervation
(polyphasic innervation potentials after 4-6
weeks)

36. • Fibrillation potentials typically arises 2-3 weeks
following injury
• With regeneration of nerve after injury,
polyphasic
• reinnervation potential replaces fibrillation
potential
• Reinnervation potentials may precede clinical
signs of recovery by 6-12 weeks

37. Limitation of electophysiological
testing
• Electric impulse can stimulate only normal/
neuropraxic fibres and can’t distinguish b/w
axonotemesis or neurotemesis
• Provides no useful information in cases of
incomplete facial paralysis
• It fails to provide information on the
immediate post paralysis period( first 72 hours)

39. • Types of physical therapy interventions for
facial palsy
• Facial exercises, such as
• – Strengthening and Stretching,
• – Endurance,
• – Therapeutic and facial mimic exercises ("mime
• therapy")

40. • • Electrotherapy,
• • Biofeedback,
• • Transcutaneous electrical nerve stimulation
(TENS)
• • Thermal methods or massage, alone or in
• combination with any other therapy

41. Exercise therapy
• Simple movement retraining
• • Expression training- mime
• • Functional training
• • PNF
• • Massage-Efflureage,circular&fine thumb
kneading improve circulation and prevent
contracture
• Active exercise in front of mirror prevent
contracture

42. ELECTRICAL STIMULATION

43. Electrotherapy
• May have an adverse effect on recovery
• • Avoid in acute stage
• • Poor evidence to show it may be helpful in
• chronic facial paralysis.

44. Feedback
• Mirror feedback
• EMG feedback
• Lack of proprioceptors

45. Prognosis
• The Copenhagen Facial Nerve Study
found that around 71% of patients recover normal
function without treatment. Around 13% are left with
slight weakness and around 4% with severe weakness
resulting in major facial dysfunction. Contracture of
the facial muscles on the affected side was found in
17% and associated movements were found in 16%.6

46. STRAPPING

47. LATEST DEVELOPMENTS

48. BIONIC FACE
• An implantable neuroprosthetic device may one
day provide a new approach to restoring more
natural facial movement in patients with one-
sided facial paralysis (hemifacial palsy)
• Initial experiments in animals show promising
results with a "bionic face" approach to facial
reanimation -- using electrical signals from the
uninjured side of the face to trigger muscle
movement on the paralyzed side.

49. House-Brackmann scale of facial
nerve weakness
• 1-Normal
• 2-Mild Weakness
• 3-Weak but eye closes
• 4-weak with incomplete eye closure
• 5-Flicker of movement
• 6-No movement

50. THANK YOU