Unilateral facial paralysis is a relatively common condition with an incidence of 20–25 per 100,000 population. However, simultaneous bilateral facial palsy (facial diplegia) is an extremely rare clinical entity and occurs in 0.3–2% of facial paralysis patients (1). The annual incidence is approximately 1 per 5 million (2).
A 78-year-old diabetic patient presented to the emergency room of our hospital with dysarthry and bilateral symmetrical facial weakness. He was unable to show his teeth, close his eyelids, or dilate his cheeks. From the neurologic examination, there were no other important findings, except for a minor instability during walking. The patient did not refer head injury or febrile viral infection in the recent past. We made the presumptive diagnosis of bilateral peripheral facial paralysis. Five weeks after his admission to our hospital, he made a full recovery. We have to note that glucocorticoids were not administered to him.
His full blood count, erythrocyte sedimentation rate, liver function tests, tumor markers, thyroid hormones, serum protein immunoelectrophoresis, serum ACE levels, C-reactive protein, and rapid protein reagent (RPR) were all within normal limits. HbA1c was 7.0%, and the autoantibody screen was negative. Purified protein derivative was 5 mm. Serological tests for varied infectious agents, including herpes simplex virus (HSV)-I and -II, Varicella-Zoster virus (VZV), Epstein-Barr, Coxsackie, HIV-I and -II, cytomegalovirus (CMV), and hepatitis B viruses, as well as Mycoplasma and Borrelia Burgdorferi, were all negative.
Lumbar puncture revealed a normal pressure. Glucose, protein, and white blood count of the cerebrospinal fluid (CSF) were all within normal limits. Furthermore, stains and cultures for microorganisms were negative, as were tests for viruses (HSV and HSV-II, VZV, amd CMV), Borrelia Burgdorferi, and syphilis (venereal disease reaction level [VDRL] test).
Magnetic resonance imaging (MRI) of the brain and computed tomography (CT) scans of the head, thorax, and abdomen were all normal.
Facial diplegia may have diverse etiologies and may prove to be a diagnostic dilemma. The most common causes are bilateral Bell’s palsy, Lyme disease, Guillain-Barre syndrome, sarcoidosis, Moebious syndrome, leukemia, viral infections, syphilis, basilar skull fractures, and pontine gliomas.
The most common infectious cause of facial diplegia is Lyme disease, caused by Borrelia Burgdorferi(3). Regarding the case presented, the IgG antibodies against this agent in serum, as well as in CSF, were negative. Other rare infectious causes include syphilis and Mycoplasma (4). However, VDRL tests in CSF and RPR in serum were negative, while antibody titer against Mycoplasma was negative.
Guillan-Barre syndrome is thought to be a postinfectious inflammatory polyradiculoneuritis. Up to 50% of the fatal cases have bilateral facial paralysis (5). The diagnosis is made on lumbar puncture (with a typically elevated protein in the absence of a raised number of cells) and peripheral areflexia. Our patient had neither peripheral muscle weakness nor areflexia, and the CSF examination was normal.
Basilar skull fractures and pontine gliomas were excluded by means of both brain CT and MRI. Because there was no hilar adenopathy on chest CT and because serum ACE levels were normal, sarcoidosis was rejected.
Bilateral Bell’s palsy does not seem to be a plausible diagnosis because our patient had neither a preceding viral infection nor the characteristic symptoms of this condition (facial numbness or pain, change in taste, numbness of the tongue, hyperacusis, etc.).
Diabetes has previously been associated with facial diplegia (4,6,7). According to Adour, Wingerd, and Doty (7), diabetes was present in 28.4% of 67 patients with recurrent or bilateral facial palsy. A plausible explanation could be that diabetic patients are more prone to nerve degeneration. In another series of 43 patients with bilateral seventh nerve palsy, there was one case associated with diabetes (4). Thus, having excluded all the other possible causes of this disorder after extensive evaluation, we could assume that the most likely cause of facial diplegia in the case presented is diabetes.
In conclusion, bilateral facial paralysis may be due to a life-threatening condition and, therefore, the practitioner should be aware of the diagnostic possibilities that cause this extremely rare condition. A review of the literature reveals that diabetes is associated with facial diplegia and should always be included in the differential diagnosis of this condition.
