Bevel: Case Report

Unilateral Non Recurrent Bellís Palsy Along With Unusual Occurrence in Six Year Old Male Child: A Review of Three Case Reports

Shalini Gupta, Kavita Nitish Garg, Anurag Tripathi, OP Gupta


Facial nerve palsy results in the loss of facial expression and is most commonly caused by a benign self- limiting inflammatory condition known as Bells palsy. Bellís palsy (spontaneous idiopathic facial paralysis), which is the most common facial nerve disease, has a sudden onset. Bell's palsy most commonly occurs in females in their teens and twenties. The distribution is almost equal in the thirties, with a slight predominance in males over 40 years. The annual incidence of Bellís palsy in the Western world is approximately 20/l 00 000. Untreated Bell's palsy leaves some patients with major facial dysfunction and a reduced quality of life. It is essential to rule out other causes of facial paralysis before making the definitive diagnosis, which implies the intervention. Bellís palsy has been termed a diagnosis of exclusion. The article presents three case reports of manifestation of Bells palsy.


Keywords: Neurologic Manifestations; Facial Paralysis; Bell Palsy; Facial Neuropathy, Idiopathic Acute; Facial Nerve Diseases; Lower/Upper Motor Neuron.


Shalini Gupta, Kavita Nitish Garg, Anurag Tripathi, OP Gupta. Unilateral Non Recurrent Bellís Palsy Along With Unusual Occurrence in Six Year Old Male Child: A Review of Three Case Reports. International Journal of Oral & Maxillofacial Pathology; 2013:4(1):54-59. ©International Journal of Oral and Maxillofacial Pathology. Published by Publishing Division, Celesta Software Private Limited. All Rights Reserved.


Received on: 22/08/2012 Accepted on: 20/12/2012



Bell's palsy (BP) is defined as a lower motor neuron palsy of acute onset and idiopathic origin.1 It has an acute onset and is almost always a mononeuritis.2 The incidence is about 20/year/100,000 population3, and leads to a considerable disturbance in social activities among patients4. Although the actual cause of BP is unknown, the widely accepted mechanism is inflammation of the facial nerve during its course through the bony labyrinthine part of the facial canal, which leads to compression and demyelination of the axons and disruption of blood supply to the nerve itself.5 Since BP is a facial paralysis of unknown origin, it is essential to rule out other causes of facial paralysis before making the definitive diagnosis, which implies the intervention. BP has been termed a diagnosis of exclusion.6


Presented here are three case reports on unilateral bellís palsy in different age group of males along with unusual occurrence of BP in 6-year old male child which is much less reported in literature


Case Report 1

A 45-year-old male was brought to the outpatient department with a chief complaint of facial asymmetry on the right side of his face. There was no history of trauma or preceding viral illness. He was unable to close his left eye completely and even he was not able to lift left side of lip since 1month (Fig 1a & b). His past medical history was unremarkable. His physical and mental growth was normal for his age. He was not on any medication and his medical records were up to date for immunizations. On physical examination he appeared to be of moderate built. His tympanic temperature was normal. Pulse and blood pressure measurements were within the normal range for his age. His left eye remained partially open even when he blinked. There was no cervical lymphadenopathy. His tonsils were not inflamed. Facial nerve examination revealed that he was not able to blow his cheeks, incomplete closure of eyelids and complete weakness on the left side of the face. There was no loss of taste or sensation. His higher function and the rest of the cranial nerve examination were normal. A clinical diagnosis of Bell's palsy was made. Artificial tear was prescribed. He was referred to the physiotherapist. He was prescribed with prednisolone 60mg (calculated according to 1mg/kg) for six days which was supposed to be taken in equally divided dosage of 30 mg twice in a day. Subsequently the dosage was tapered for 4 days and stopped. He was followed up regularly in the outpatient clinic for six months. He recovered completely without any residual weakness (Fig 1c).

Case Report 2

A 65-year-old man was referred for physical therapy evaluation and management of his right facial muscle weakness. His primary care physician and a neurologist had diagnosed idiopathic Bellís palsy, and the patient was seeking further management of his persisting facial pain and paralysis. The patientís complaints included unremitting left facial paralysis (14 months), severe facial pain, regional facial numbness, hyperacusis (increased loudness of sounds in right ear), and excess tearing from his left eye. He was not able to close his left eye completely and not able lift his left side of lip (Fig 1d). Although when patient was asked to smile his lip was deviated on unaffected side and while opening his mouth was deviated on unaffected side (Fig 1e). Even on asking to raise his eyelids, he was not able raise left eyelid (Fig 1f).


The patient reported that the facial paralysis developed over a period of two to four weeks and there was no improvement in the paralysis over the subsequent 14 months. The facial pain started after the facial paralysis and was the most disturbing symptom for which he was now seeking evaluation and treatment. He was given predisolone 50mg (calculated according to 1mg/kg) for six days which was supposed to be taken in equally divided dosage of 25 mg twice in a day. Subsequently the dosage was tapered for four days and stopped.


Case Report 3

This case involved six years, two months old male. The mother called the pediatric dentist to report that her son's lips "twisted when he smiled." Examination revealed that when the child was asked to smiled, his lips are deviated on left unaffected side and he was not able to close his right eye (Fig 1g & h). When patient was asked to open his mouth, the mouth was deviated towards unaffected side (Fig 1i).


The patient had been seen regularly by the pediatric dentist for three months for preventive and restorative care and space maintenance. The intraoral examination revealed no etiology for facial nerve paralysis. Otology examination showed no signs of upper airway infection, and the middle ear impedances were within normal limits and did not suggest any kind of middle ear effusion. The patient was under symptomatic treatment. No corticosteroid treatment was prescribed.


Facial nerve palsy results in the loss of facial expression and is most commonly caused by a benign self-limiting inflammatory condition known as BP.7 BP accounts for around 72% of facial palsies.8 Scottish surgeon anatomist Sir Charles Bell (1774-1842) described this as a syndrome of complete facial paralysis in a lecture 'On the nerves: giving an account of some experiments on their structure and functions, which lead to a new arrangement of the system' to the Royal Society of London in 1821. Almost a century later, the management and aetiology of BP is still a subject of controversy.1 BP leaves more than 8,000 people in the United States each year with permanent, potentially disfiguring facial weakness.9


Although the actual cause of BP is unknown, but the proposed mechanism thought to be are inflammation of the facial nerve,5 microcirculatory failure of the vasonervorum, viral infection, ischemic neuropathy, autoimmune reactions10-13 surgical procedure such as local anesthesia,14,15 tooth extraction,16-18 infections,19,20 pre pros≠thetic procedures, excision of tumors or cysts, surgery of TMJ,21,22 surgical treatment of facial fractures and cleft lip/palate23 are among the proposed etiologies. The literature also reports three mechanisms, in which a dental procedure could damage a nervous structure: direct trauma to nerve from a needle, intraneural hematoma formation or compression and local anaesthetic toxicity.24


The symptoms of BP include pain and numbness on the affected side of the face, especially in the temple, mastoid area, and along the angle of the mandible.25 The mouth may be dry due to decreased salivary secretion and altered taste sensation over the anterior two-thirds of the tongue and incomplete hyperaesthesia over the trigeminal nerve distribution as well as hyperacusis on the affected side.2,26 The signs of BP include widening of the palpebral fissure, flattening of the nasolabial fold, and drooping of one corner of the mouth when smiling. These signs occur on the same side of the face as the lesion. There may be an inability to wrinkle half of the forehead, to close one eye completely and to purse the lips.25,26


The histopathology of the facial nerve one week after the onset of Bell's palsy is also has been reported which reported that the entire nerve was infiltrated by inflammatory cells. Myelin breakdown, axonal changes and edema were also reported suggesting viral neuritis.27 On opening the sheath of the nerve, which is found to consist of several layers, the outer layer being thick and the inner layers being very thin indeed, the nerve trunk when eventually exposed appears to be unduly constricted at the level of the stylomastoid foramen. In cases of Bell's palsy the narrowing of nerve appears more obvious than normal, possibly because of the swelling of the nerve above this level.


Figure 1: The patient photographs showing the facial features of bells palsy. The first case report showing the left side with a Bellís sign resulting in failure to close eye and deficit of facial muscle on affected side (a), unable to lift left side of lips (b) and was able to close his eyes after treatment (c). The second case was unable to close left side of the eye and lift left side of lip while smiling (d), deviation of mouth on unaffected side (e) and was unable to raise left eyebrows along with watery eyes (f). The third case showed right side of the face with a Bellís sign (g), deviation of lips on unaffected side (h) and deviation of mouth while opening to unaffected side (i).


At and just above the site of the constriction one or more thin haemorrhagic streaks running longitudinally upwards for about 2mm in the long axis of the nerve are also been reported. Above the constriction the nerve itself swells out often beyond the confines of the sheath; and this swelling may extend upwards for 0-5 to 1cm. before tapering off to its normal calibre. In this swollen segment there may be one or more pink-tinged patches while in case of long-standing paralysis, the nerve trunk is reduced to a shrunken and reddened strand that was adherent to the sheath.28


The proper history and physical examination provide the key to the diagnosis of BP. Most patients do not require any laboratory testing. However, patients who have persistent weakness without significant improvement requires further investigations like imaging, hearing testing and laboratory investigations. Cerebrospinal fluid testing is helpful if infection or malignancy is suspected; however, in case of Bell palsy cerebrospinal fluid tends to show mild and inconsistently elevated cell counts and protein levels. Electro diagnostic testing is not routinely done in Bell palsy. It is not very reliable when BP is in the initial stages; however, after 2 weeks, it may detect denervation and demonstrate nerve regeneration.29


Treatment of BP is still controversial.29 Clinical and electrophysiological assessment should be done. Clinical evaluation for both the severity of paralysis and the presence of complication is the first step before the start of treatment or rehabilitation. The most popular method for assessing the severity or paralysis is the facial nerve grading system according to House and Brackmann30 (Table I).



Degree of Function

Percentage of Function















Moderately Severe








Total Paralysis



Table 1: Facial nerve grading system

*A centimeter is divided into four equal parts.


On the affected side of the face, maximal voluntary lateral movement of the corner of the mouth is measured 0-4, and elevation of the eyebrow is measured 0-4, resulting in a sum from 0/8 to 8/8


Corticosteroids are the most commonly used agents for reducing inflammation and edema in the nerve sheath.31 Both transmastoid subtotal decompression and combined transmastoid-middle cranial fossa total decompression approach have been advocated.32 Early surgery including surgical decompression of the facial nerve may be recommended within 2 weeks following the onset of BP, if electroneurography revealed >90% degeneration of facial nerve fibres.33


It has also been recommended to use local superficial heat therapy (i.e. hot packs or infrared rays) for 15min/session for the facial muscles prior to electrical stimulation. Massage which has been frequently been prescribes for facial palsy, improves circulation and may prevent contracture.34 Short wave diathermy (SWD) has been suggested as treatment of BP however, some may not recommend its use in BP because there is acute viral inflammation of the facial nerve in its early stage35 and heating of inflamed nerve may be contraindicated.36 Treatment of hyperbaric oxygen, through the inhalation of 100% oxygen under high pressure (at pressure 2.8 times greater than normal atmosphere), may possible be considered as one of the physical modalities. It was reported that this modality has induce better recovery than prednisone treatment in BP patients.37


Bell's palsy is a self-limiting condition with a favorable prognosis. Although the etiology of BP is unknown there are strong indications of a viral origin which triggers a neuropathy leading to facial nerve compression and paralysis in the facial canal proximal to the stylomastoid foramen. The most important thing the dentist can do is make a prompt and appropriate referral because early detection of intracranial pathology may improve the prognosis especially in case of children.



We would like to thank all the staff members of the KGMC, Lucknow for their constant support and encouragement.


Author Affiliations

1.Dr.Shalini Gupta, Associate Professor, 2.Dr.Kavita Nitish Garg, Senior Resident, Department of Oral Pathology, 3.Dr.Anurag Tripathi, Assistant Professor, Department of Oral Medicine, CSMMU (KGMU), Lucknow, 4.Dr.OP Gupta, Assistant Professor, Department of Surgery, Career Institute of Medical Sciences, Lucknow, UP, India.



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Corresponding Author

Dr.Shalini Gupta,

Associate Professor,

Department of Oral Pathology,


Lucknow, UP, India.

Ph: +919453556510

E mail:,






Source of Support: Nil, Conflict of Interest: None Declared.


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