|Year : 2014 | Volume
| Issue : 4 | Page : 216-218
Bilateral facial nerve palsy in a newly diagnosed diabetic patient with associated herpes labialis
Manish Gupta1, Monica Gupta2
1 Department of Ear, Nose and Throat, Gian Sagar Medical College and Hospital, Ramnagar, Banur, Patiala, India
2 Department of Medicine, Government Medical College and Hospital, Chandigarh, India
|Date of Web Publication||13-Dec-2014|
Department of ENT, Gian Sagar Medical College and Hospital, Banur, Punjab
Source of Support: None, Conflict of Interest: None
Bilateral facial nerve palsy is a very rare condition, usually following neurologic, neoplastic, traumatic, infective or metabolic causes. We present here a case of 29-year-old male, diagnosed on admission as diabetic with herpes labialis and bilateral facial paralysis. As the differentials are extensive, diagnostic workup and subsequent treatment should be done keeping various etiological factors in mind.
Keywords: Bilateral, facial nerve, palsy
|How to cite this article:|
Gupta M, Gupta M. Bilateral facial nerve palsy in a newly diagnosed diabetic patient with associated herpes labialis. Indian J Otol 2014;20:216-8
| Introduction|| |
Bilateral facial nerve paralysis is a very uncommon clinical entity, representing less than 2% of all facial palsy cases, and has an incidence of 1 per 5 lakh population.  Bilaterality makes facial neuropathy a more ominous sign with widely varying causes that requires prompt investigation.  We hereby report a rare case of complete, bilateral, spontaneous, simultaneous, lower motor neuron facial nerve paralysis following herpes labialis in a newly diagnosed diabetic patient. We discuss the diagnostic evaluation and management of such cases.
| Case Report|| |
A 29-year-old male presented to the outpatient department with complaints of inability to chew and swallow the food, along with inability to close both eyes for the last 12 days. Due to its tendency to collect in vestibule, with every bolus, he had to press the cheek with his hands in order to swallow. He had also noticed altered taste sensation. Fifteen days back, he had undergone surgery for right renal stone under general anesthesia and the recovery was uneventful. There was history of fever with few blisters on lips 10 days back. He had no fever, headache, visual disturbance, vomiting, decreased hearing or tinnitus. There was no history of head trauma, prior diabetes or painless ulcers over genitalia. He denied any history of numbness or weakness in limbs or any prior similar illness. There was no history of exposure to ticks or recent travel abroad. He denied any history of smoking, alcohol intake, blood transfusion or sexual promiscuity.
The patient was afebrile with normal blood pressure. A crop of few blisters and erosions over left angle of mouth were noticed. Local examination revealed grade IV (House-Brackmann grading system) lower motor neuron bilateral symmetrical facial weakness. Patient was not able to close eyes, with presence of Bell's phenomenon on attempt to do so [Figure 1]. The other cranial nerve examinations were normal and there were no cerebellar signs, limb weakness or nerve thickening. Bilateral deep tendon reflexes were preserved. Rest of the general physical examination was unremarkable.
|Figure 1: Clinical picture showing patient with bilateral lower motor neuron facial paralysis (showing Bell's phenomenon) with herpes labialis lesion (marked with arrow)|
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The fasting plasma glucose and postprandial plasma glucose values were 149 and 305 g/dl, respectively. These were reconfirmed on the next day. The hematological and biochemical investigations were normal. Specialized tests like thyroid function tests, erythrocyte sedimentation rate, and angiotensin-converting enzyme level were within normal limits. The viral serology for herpes simplex virus (HSV) was positive. Venereal Disease Research Laboratory test (VDRL) and HIV serology were negative. The monospot test for infectious mononucleosis and anti-nuclear cytoplasmic antibody were also negative. Radiological investigations, including chest X-ray, ultrasound abdomen and MRI brain with temporal bone cuts were unremarkable. A computed tomography scan of the chest was done to look for sarcoidosis but was within normal limits. The test for stapedial reflex was absent for right side and present on left. The nerve conduction velocity study indicated denervation of bilateral facial nerves. Electroneurography of lower limb nerves showed normal nerve conduction bilaterally.
The patient was started on oral acyclovir 400 mg thrice a day, oral hydrocortisone 60 mg OD, parenteral ceftriaxone 1 gm I/V twice a day, esomeprazole 40 mg OD, methylcobalamin OD, artificial tear drops during day at frequent intervals and eye ointment HS. The patient was also started on combination of regular and long-acting insulin regime. Simultaneously physiotherapy, single sitting daily of electrical stimulation (intermittent galvanic mode) full face, facial exercises and ultrasound at nerve trunk site were started. The patient started showing improvement on sixth day of starting the therapy, simultaneously on both the sides and subsequently the steroids were tapered from 10 th day [Figure 2], and he was normal within one month of active treatment.
|Figure 2: Clinical picture of the same patient at 10th day of treatment showing improved eye closure and healed herpes lesions|
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| Discussion|| |
Most cases of bilateral facial paralysis reported in literature are sequential, but our case is of bilateral simultaneous facial paralysis. Bilateral facial nerve paralysis unlike unilateral palsy is rarely idiopathic or Bell's. The variety of diseases that may present with bilateral facial paralysis are Guillain-Barre syndrome,  Lyme's disease,  sarcoidosis,  brain stem encephalitis, benign intracranial hypertension, leukemia, Melkersson-Rosenthal syndrome More Details, diabetes mellitus, HIV infection,  syphilis, leprosy,  infectious mononucleosis, bilateral neurofibromas or trauma. Thus, the diagnostic workup for a patient with bilateral facial paralysis depends greatly on a meticulous history.
Adour et al. observed that 100% of their patients with idiopathic facial paralysis (Bell's palsy) had presence of antibodies to HSV.  They suggested that Bell's palsy may be caused by reactivation of HSV as evident by clinical, neurologic, laboratory and immunologic similarities between idiopathic facial paralysis and known manifestations of reactivated HSV infection, and the known neurotropism of HSV, including its presence in latent form in the trigeminal ganglia. HSV 1 and 2 is transmitted by direct mucocutaneous contact and typically present with clusters of tense blisters on an erythematous base in the perioral area. The lesions quickly evolve into erosions or ulcerations with associated crusting. Following viral replication in the skin or mucosa, intact viral nucleocapsids travel via sensory neurons to the corresponding dorsal root ganglia to establish latency. Later, a variety of stimuli can trigger reactivation. The virus travels back along the sensory neurons to the mucocutaneous surface to replicate and induce active or subclinical infection. The diagnostic laboratory tests are Tzanck smear, viral culture, antigen detection, polymerase chain reaction and immunoglobulin-specific serology. The serologic testing cannot reliably differentiate HSV-1 from HSV-2.
Diabetes has been associated with facial palsy, more prominently in those with bilateral facial palsy. In one of the first study of its kind, it was observed that diabetes was present in 28.4% patients with recurrent or bilateral facial palsy and 11.4% in those with unilateral palsy and 3.8% in healthy individuals.  This indicates that the risk of Bell's palsy is increased in patients with diabetes. Patients with diabetes are more prone to nerve degeneration, and this tendency is not age-related. , The pathogenesis of Bell's palsy is related to the tortuous course of the facial nerve through the Fallopian canal More Details. In diabetics, the Schwann cell and myelin sheath of nerves are at higher risk of damage, nerve degeneration is more severe, and the threat of sequelae-like contracture and synkinesis is increased than in nondiabetics. In another study in a series of patients with Bell's palsy, diabetes mellitus was found in 39% of the cases.  A significantly higher frequency of taste disturbances in those without diabetes was found, and thereby it was proposed that site of facial nerve lesion in diabetics appears to be distal to the chorda tympani due to localized facial nerve ischemia in the distal part of the Fallopian canal.
The prognosis of bilateral facial paralysis depends upon the exact etiology and is usually good if etiology is identified and successfully managed.  The prognosis may be worse with age over 60 years, diabetes mellitus, hypertension, pain, decreased tearing and the degree of denervation demonstrated on electrical testing. Resolution of bilateral facial paralysis may be nonsimultaneous.
| Conclusion|| |
Diagnosis of bilateral palsy involves an extensive differential diagnostic workup, and we suggest that all patients regardless of age should be screened for the possibility of diabetes. Unlike Bell's palsy, where in a large proportion of patients the cause remains unknown, bilateral disease is generally a manifestation of a systemic disease process.
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[Figure 1], [Figure 2]