M.V.D.L. Sathyanarayana*, D.Radhika**, K.V.Murali Mohan***
*Assistant Professor of Ophthalmology, **Assistant Professor of Anatomy, ***Professor and HOD of Pathology, R.I.M.S. Medical College, Kadapa, A.P., India
ABSTRACT
Facial nerve supplies to muscles of face and responsible for both forcible and smooth closure of eye lids and facial expressions. Facial nerve has three nuclei; 1. Main motor nucleus 2. parasympathetic nucleus 3. sensory nucleus .Motor nucleus supplies to muscles of face and responsible for facial expression and closure of eyelids. Facial nerve carries taste sensations from anterior 2/3 rd of tongue and cutaneous sensations from external auditory metus.In present case patient had sudden onset of left side facial palsy which completed over 24 -36 hours. She underwent lateral tarsal strip surgery, lee medial canthoplasty of lower lid and recession of upper lid retractors of left eye and had good cosmetic and symptomatic improvement.
Key words: Facial nerve, Ectropion, Lagophthalmos,Medial canthoplasty, Lateral tarsal strip surgery.
Correspondence Address:
M.V.D.L. Sathyanarayana
Assistant Professor of Ophthalmology Non teaching staff quarters
First floor, House no-F1-1 R.I.M.S Medical College Campus Kadapa, Andhra Pradesh, India Cell no: 09440367590
Email: [email protected] INTRODUCTION
Bell’s palsy is an acute idiopathic , unilateral, most common, peripheral, lower motor neuron facial nerve paralasis. It is named after Scottish anatomist Charless Bells. Possible etiology includes viral infections particularly herpes simplex, diabetes mellitus , hypertension. The symptoms on effected side typically include inability to close the eyes & to smile.
Lower eye lid may turn outwards. Wrinkle the fore head &whistle effected. Speech may be mildly slurred.
Tearing occur because eye doesnot close completely.
Taste sensation diminished on front half of the tongue.
Sounds may appear on louder side. Most people develop maximum weakness within 48 hours. Bilateral involvement in less than 1%. Recurrence & bilateral involvement suggests myasthenia gravis. Incidence of bell’s palsy 20 to 30 cases per one lakh people per year.
A strong family history found in 2to 4% of cases.
Incidence equal in both sexes . Average age onset 20 to 40 years but may occur at any age[1]. Incidence is lowest in children under 10 years. Left & right sides of
the face involved with equal incidence. One in 60 people being effected during life time. Incidence is higher in pregnant women. 71% of untreated patients will completely recover; 84% are complete or nearly normal recovery within 6 months.
Prognosis depends on age over 55 years, no recovery by 3 weeks, hypertension, diabetes mellitus, pregnancy, complete facial weakness & parotid tumors. Goal of treatment is preventing sequelae2. Both corticosteroids & antiviral agents used as treatment strategies medically. Mime therapy in the form of physiotherapy is another option of treatment. Surgical treatment required to improve cosmotic appearance.
CASE REPORT
Kamalamma female 60 years presented with watering of left eye and inability to close left eye for the last 3 years Figure 1. On examination drooping of left half of face, deviation of mouth towards right side, loss of wrinkles on left half of fore head, severe paralytic ectropion of left lower eye lid and lagophthalmos left eye. Left eye is pesudophakia and right eye has immature senile cataract. Patient has good Bells phenomenon. Visual acuity in right eye is 6/60 and in left eye is 6/12.Blood pressure is 130/80 mm of Hg. No sensory or motor deficits noted. Taste sensations from anterior two thirds of tongue normal.
No h/o hyperacusis.
A clinical diagnosis of Bell’s palsy with severe paralytic ectropion of lower lid and lagophthalmos left eye was made. Routine hematological investigations like TC,DC,ESR and biochemical investigations like blood sugar, renal function tests, serum calcium were normal. H.I.V was negative, V.D.R.L was non reacting.
X ray chest p. a was normal. C.T scan brain was normal. Syringing was patent in both eyes. Lee medial canthoplasty, lateral tarsal strip and recession of upper lid retractors done under local anesthesia to improve cosmetic appearance and symptoms Figure 2.
Post-operative period was uneventful. Skin sutures removed on 7th day.
in inability to control facial muscles on effected side.
Several conditions like brain tumors, stroke, Lyme’s disease, HSV Type 1,diabetes mellitus, sarcoidosis, brucellosis, Ramsay Hunt syndrome, Gullian –Barre syndrome, Leprosy, Melkersson-Rosenthal syndrome can cause acute fascial nerve palsy. If no specific cause can be identified the condition is called Bell’s palsy. It is named after Scottish anatomist Charless Bells. Bell’s palsy is the most common acute mononeuropathy and is the most common cause of acute facial nerve paralysis.
Bell’s palsy is usually self-limiting and unilateral.
Bilateral cases occur in 1% of cases1.It affects approximately 1 person in 60 during a lifetime. Familial inheritance in 4-14%cases5.It is three times more common In pregnant women than non-pregnant women.[6].Four times more common in diabetics than general population7.
Facial nerve nuclei are in brainstem and facial nerve supplies all muscles concerned for facial expression. Sensory component is through nervous intermedius. It conveys taste sensations from anterior two thirds of tongue and cutaneous impulses from anterior wall of external auditory metus. Motor nucleus lies anterior and lateral to abducens nucleus.
It is thought that an inflammatory condition leads to swelling of facial nerve. During its course, as nerve travels through a narrow bony canal beneath ear swollen nerve compressed, leads to nerve inhibition and damage or death. No readily identifiable cause for Bell’s palsy has been found. Exposure to trauma, environmental factors, metabolic and emotional disorders, emotional stress, environmental stress (e.g.
cold), physical stress (e.g. trauma) etc. may precede onset.
Corticosteroids have been found to improve outcome while anti-viral drugs have not3.Most of people recover sponteously and achieve near normal function.
Facial nerve controls a number of functions like blinking, closing the eyes, smiling, frowning, lacrimation and salivation, innervates stapedius and carries taste sensations from anterior two thirds of tongue. Onset of Bell’s palsy is abrupt and maximum weakness attained in 48 hours.Pain in ear may precede the paralysis for a day or two. Taste sensations may be lost unilaterally and hyperacusis may present.
Bell’s palsy characterized by facial drooping on effected half, inability to control movements of facial muscles, paralytic ectropion, inability to close upper lid, exposure keratitis and its complications. The paralysis is of lower motor neuron type.
Fig:2. Lee medial Canthoplasty & Lateral Tarsal Strip Surgery.
DISCUSSION
Bell’s palsy or idiopathic facial nerve palsy is dysfunction of cranial nerve V11 (the facial) that results
Fig:1. Paralytic Ectropion lower lid & Lagophtholmos.
Preoperative
Post operative
14 KV Mural Mohan 56-58.pmd 57 8/27/2012, 6:39 PM
Clinician should determine whether fore head muscles are spared. Fore head muscles receive innervations from both hemispheres of brain. In upper motor neuron type of facial palsy fore head muscles are spared. But Bell’s palsy is lower motor neuron type and fore head muscles are involved. The degree of nerve damage can be assessed using House - Brackmann scoring.
Bell’s palsy is a diagnosis of exclusion; by elimination of other reasonable possibilities. No specific cause can be ascertained. Bell’s palsy is commonly referred to as idiopathic or cryptogenic I.e.
unknown cause. Morris A. M ,et. al described that a large number of patients (45%) are not referred to a specialist, which suggest that Bell’s palsy is considered by physicians to be a straight forward diagnosis that is easy to manage4.Since diagnosis of Bells palsy is by exclusion it requires through investigations specialist opinion before starting treatment.
Investigations: E.S.R, Blood Sugar, Lyme titer, ACE levels, chest imaging studies, lumbar puncture, Gadolinium enhanced M.R.I scan, H.I.V screening, V.D.R.L, F.T.A -ABS . Electro diagnostic tests like stapedius reflux test, electromyography, audiography may help in accessing prognosis.
TREATMENT
Medical therapy: Systemic therapy with oral steroids such as prednisolone significantly improves recovery at 6 months and is recommended.
Anti-viral like acyclovir proscribed due to theoretical link between Bell’s palsy and herpes simplex and varicella zoster virus3.
Local therapy- Topical lubricants eye drops, lubricant eye ointments at night, advised to wear dark glasses in outdoors, Occluding lids with tape, external eye lid weights, Punctual plugs, Injecting Botullinum toxins into upper lid and lower lid retractors. Topical antibiotics and cycloplegic if exposure keratitis present.
SURGICAL THERAPY
A. Correcting lower lid droop and ectropion - Face lift, Lee medial canthoplasty, lateral tarsal strip surgery, Facial sling with facia lata, recession of lower lid retractors.
B. Correcting lagophthalmos - Implantable devices like gold plate surgery, Trasorrhaphy, transpositioning temporalis muscle, reinnervation of facial nerve, upper lid retractor recession . C. Correcting brow ptosis - By direct or indirect
brow lifts.
D. Correcting cheek ptosis - By mid face lift.
Prognosis: Prognosis is usually better for younger individuals and in patients older than 60 years prognosis is worse. Even without any treatment Bell’s palsy tend to carry good prognosis. In a 1982 study when no treatment was available, of 1,011 patients, 85%
showed first signs of recovery within three weeks after onset. For the other 15% recovery occurred 3-6 months later. After a follow-up of at least one year or until restoration, complete recover had occurred in more than two thirds (71%) of al patients. Recovery was judged moderate in 12% and poor in 4% of patients4. the patients who regain movements within the first two weeks nearly always remit entirely. When remissions does not occur until the 3rd week or later, patients develop complications5.
Major complications are chronic taste loss (ageusia), chronic facial spasm exposure keratitis and its complications, during regeneration some nerves may side track leading to silkiness and around 6% of patients exhibit crocodile tear syndrome or gustatolacrimal reflux syndrome.
Although defined as mononeurotic, patients diagnosed with Bell’s palsy may have myriad of neurological symptoms including facial tingling, moderate or severe headache, neck pain ,memory problems, balance problems, ipsilateral limb parasthesias, ipsilateral limb weakness that are unexplained by facial nerve dysfunction. This is yet an enigmatic facet of this condition.
REFERENCES
1. M.A. Nanavaty, A.R. Vasavada and P.D. Gupta . Tears in Old Age Indian Journal of Gerontology.2005; Vol. 19, No. 4. pp 393 -414.
2. N Julian Holland, Graeme M Weiner. Recent developments in Bell’s palsy. BMJ. 2004;329:553.
3. Sullivan FM, Swan IR,Donnan PT,et al ,Early treatment with Prednisolone or acyclovir in Bell’s palsy.N.Engl. J . Med. 2007;357 (16):1598-607.
4. Peitersen E . The natural history of Bell’s palsy.Am J Otol 1982;4 (2): 107-11.
5. Roob G, Fazekas F, Hartung HP .Peripheral facial palsy : etiology,diagnosis and treatment. Eur . Neurol.1999; 41 (1):3-9.
6. Peitersen E, Andersen P .Spontaneous course of 220 peripheral non traumatic facial palsies. Acta Otolaryngol.1966;Suppl. 224:296.
7. Doner F, Kutluhan S .Familial idiopathic facial palsy. Eur Arch Otorhinolaryngol.2000; 257 (3):
117-119.