BELLS PALSY

Dr. BUDI OETOMO W, Akp, Sp.S, Sp.KL, PhD

Letkol Laut (K) NRP. 9692 / K

A. Definition:
Bells Palsy is the acute onset of an isolated peripheral facial
paralysis.
B. Etiology & Pathology:
Etiology: unknown is believed to be the result of a viral
infection involving the geniculate ganglion.
Pathologic changes inflammation & edema of the
facial nerve in facial canal.

C. Clinical Features:
- Initial feature often pain in or behind the ipsilateral ear suggesting
an ear infection.
- Frequently history of exposure to cold temperature or drafts preceding
the onset.
- Usually appreciated for the first time on awakening in the morning.
- Often excess watering of the eye (crocodile tears) inability to move
secretions across the cornea to the lacrimal duct.
- Involvement the chorda tympani may be loss of taste.

D. Diagnostic procedures:
- Some determination of prognosis can be obtained by observation of
evoked responses on stimulating the facial nerve as it emerges from the
stylomastoid foramen.
*Good evoked response indicates good prognosis.
*Complete loss of excitability indicates poorer prognosis.
E. Tx:
- Initial discomfort : Aspirin or Aspirin + Codeine.
- Corticosteroid controversial.
*Single-dose of Medrol (methylprednisolone) 80 mg initially with a
gradual reduction of dosage over the seven-day periode.
F. Prognosis:
- Majority: complete recovery over 2-3 wks.

REFERENCES:
1. Gilroy, Basic Neurology 2nd ed., McGraw-Hill Inc., 1992, p.356,
1992.
2. Bradley et al, Pocket Companion to Neurology in Clinical Practice
3rd ed., 2000, p.542-543.

GUILLAIN BARRE SYNDROME

(GBS)
# Ref.:
1. Gilroy J: Basic Neurology. 2nd ed.Mcgraw-Hill Inc., 1992, pp.377378.
2. Marshall RS: On Call Neurology. W.B. Saunders Company, 1997,
pp. 197-198.

A. DEFINITION :
GBS is : - monophasic, acute inflammatory demyelinating
polyneuropathy = acute or subacute progressive
polyradiculoneuropathy.
- symmetric, ascending polyneuropathy (rare type:
descending).
- frequently occurring 1 to 3 wks (occasionally up to 8 wks)
after an acute infection.

B. ETIOLOGY & PATHOPHYSIOLOGY:

1. Often follows a non-specific respiratory or gastrointestinal illness.
2. Also after a number of specific infection such as:
- cytomegalovirus
- campylobacter jejuni
- Epstein-Barr virus
- mycoplasma
- enterovirus
- after immunization.
3. Is believed to be due to lymphocytic sensitization to peripheral
nerve antigen.

C. CLINICAL FEATURES:
- > 50% of cases have a clear history of an upper resp. tr. infection
1-3 wks prior to the onset of neuropathy.
- Often begins with myalgia or paresthesias of the lower limbs
weakness.
- of them, which ascends to involve pelvic girdle, abdominal
thoracic & upper limbs muscles.
- Examination shows :
* muscles weakness symmetric.
* loss of tone & flaccidity
* stretch reflexes absent
* bilateral N. VII frequently involved.
* other cranial nerve : - N. III Ptosis.
- N. X Dysphagia
- N. III, IV, VI Diplopia.
* sensory involvement varies.

* The paralysis :
- may progress for 10 days then remain unchanged
2 wks.
- Recovery phase much slower & take from 6 months
to 2 yrs.
D. COMPLICATIONS:
- respiratory failure
- retention of urine
- Orthostatis hypotension.
- Papilledema.
- Death resp. insufficiency or intercurrent infection.

E. VARIANTS:
- may occasionally present with a descending paralysis of pharyngeal
cervical brachial muscles.
- paraparesis with normal strength & reflexes in the upper limbs and an
initial severe midline back pain.
F. DIAGNOSTIC PROCEDURES:
1. CSF protein after the 1st wk & continues to for several wks.
2. Nerve conduction velocities : < 60 % of normal most cases.

G. DD:
1. Poliomyelitis:
- Initial fever + severe myalgia asymmetric flaccid paralysis.
- CSF : pleocytosis.
- Sensory: N.
2.Periodic paralysis:
- sudden onset of general paralysis.
- respiratory involvement: ( - )
- hypo- or hyperkalemia.
3. Myasthenia gravis:
- ascending paralysis: ( - )

H. TREATMENT:
1. Good nursing care.
2. Retention of urine catheterization.
3. Resp. insuff. endotracheal intubation + respirator.
4. Physical Tx.
5. Corticosteroid.
6. Plasmapheresis.
I. PROGNOSIS:
- Recovery may take years.
- Few cases partial recovery.