BELLS PALSY

Dr. Abdulloh Machin, dr, Sp.S(K)

Departement Neurology Faculty of Medicine Universitas Airlangga
Dr. Soetomo General Hospital– Universitas Airlangga Hospital
INTRODUCTION
• Bell’s palsy is an acute-onset peripheral facial neuropathy and is the
most common cause of lower motor neuron facial palsy
• The clinical presentation of the disorder is a rapid onset, unilateral,
lower motor neuron-type facial weakness with accompanying
symptoms of postauricular pain, dysgeusia, subjective change in facial
sensation and hyperacusis.
• Some times there are involvemeny of NV (facial sensation), N VII,
pharyngeal symptoms (NIX-X).
Anatomy of N VII
HISTORY
• Sir Charles Bell (1774–1842)  separation of sensory and motor
suplly to the face
• there is prehistoric ceramic art depicting facial palsy identified in
ancient peruvian culture
• Sydenham, Stalpart van der Wiel, Douglas, Friedreich, and Thomassen
a Thuessink describe acute idiopathic facial paralysis before Bell.
• Razi (865–925 CE), described facial palsy at length in his seminal ninth
century text ‘al-Hawi’ .
EPIDEMIOLOGY
• Bell’s palsy is a common cranial mononeuropathy
• It affects males and females equally
• incidence rates range from 11.5 to 40.2/100000
• increase in incidence of Bell’s palsy during a trial of intranasal vaccine
delivery
• The incident is higher in pregnancy, viral upper respiratory tract
infection, immunocompromised, diabetes mellitus, and hypertension
AETIOLOGY
• The cause of classical Bell’s palsy remains unclear
• Possible cause is HSV-1 infection
• The association with HSV-1 is supported by the presence of HSV-1 in
intratemporal facial nerve endoneural fluid
• possible cause of neural dysfunction due to HSV-1 is the activation of
intra-axonal degradation and apoptotic pathways
• Another possible cause is immune, infective and ischaemic
mechanisms
DIAGNOSIS
• Bell’s palsy is a clinical diagnosis
• Acute onset of unilateral lower motor neuron facial paralysis that
reaches its peak by 72 h
• Frequently accompanied by symptoms of neck, mastoid or ear pain,
dysgeusia, hyperacusis
• Involvement of posterior auricular, petrosal, chorda tympani and
stapedius nerves implicates the site of dysfunction
House-Brackmann Facial Nerve Grading System
Pemeriksaan N VII (Fasialis)
Komponen saraf VII adalah:

• komponen lakrimasi
• komponen pendengaran
• komponen perasa khusus lidah
• komponen motorik otot-otot mimic

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Pemeriksaan Lakrimasi
di nilai dengan pemeriksaan Zimmer
lakmus merah 
 canthus medialis dekat saccus lakrimalis selama 5 menit 
 mejadi biru
normalnya 15-20mm tiap menit.

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Komponen pendengaran
stetoskop loudness balance tes;
letakkan stetoskop pd kedua telinga pasien
membran stetoskop tersebut di gesek
hiperakusis pd telinga yg terganggu
ok kelumpuhan n stapedius.

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Komponen perasa lidah
2/3 depan lidah
menggunakan larutan bonstein,
 NaCl 2,5%,
 glukosa 4%,
 asam sitrat 1%, dan kinin 0,075%.
Cara pemeriksaannya adalah:
pasien diminta menutup mata ,
lidah dikeluarkan dan dibersihkan lalu
diolesi cairan bonstein tersebut, dan
pasien diminta m’sebutkan yg dia rasakan dgn
cara menulis atau menunjuk tulisan.

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Komponen motorik
NVII meliputi otot-otot mimik,
yg harus kita perhatikan saat diam dan saat bergerak,
hendaknya kita dpt menilai masing masing otot.

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Parese N VII kiri

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Px N VII

m. Orbicularis oris
M. Zygomaticus

m. frontalis m. Orbicularis oculi

m. platysma

m. Corrugator supercilii
m. risorius 15
Parese N.VII dextra

perifer sentral

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Kelainan NVII

08/27/2022 Mac, dr 17
Kelainan NVII

08/27/2022 Mac, dr 18
Classified patients into 2 groups; group 1 (good
prognosis) with HB grade 1 or 2 in the third month
of clinical follow-up and group 2 (poor prognosis)
with grade 3 or higher.
Differential diagnosis
TREATMENT
Treatment recomendation
Physiotherapy
• Heat therapy, electrostimulation, massage, mime therapy and
biofeedback
• Physiotherapy and chemo- denervation are complementary in the
treatment of synkinesis.
Prognosis
• Natural history studies have demonstrated that ∼85% of patients
experience some recovery in the first 3 weeks.
• Patients with complete facial palsy (House-Brackman grades 5–6) who
have not experienced some recovery in the first 3–4 months 
incomplete recovery
• Steroid treatment during acute phase  full recovery > 90%
•
Managing incomplete recovery
• Chronic facial palsy is a disabling condition that has a dramatic impact
on social function, emotional expression and quality of life
• Aesthetic, functional and psychological considerations need to be
addressed
• zonal-based approach ,physiotherapy, chemodenervation and
selective surgical procedures to maximise cosmetic and functional
outcome needs of patient.
• Synkinesis
• Synkinesis refers to abnormal facial muscular contraction attributed to
aberrant reinnervation of facial musculature following nerve injury.
• Treatment include physiotheraphy, biofeedback, selective chemodenervation
using botulinum toxin
• Facial reanimation
• Regional tendon transfer technique
• muscle transfer techniques that utilise the gracilis muscle
• Nerve-to-nerve transfers
Thank You