Discussion
Most cases of unilateral LMN facial nerve palsy are idiopathic, referred to as Bell’s palsy. However, cases of bilateral LMN facial nerve palsy are predominantly attributed to underlying systemic conditions [4]. GBS is an autoimmune-mediated polyradiculoneuropathy characterized by rapidly evolving ascending weakness, mild sensory loss, and hypo- or areflexia, progressing to a nadir over up to four weeks. Evaluation of cerebrospinal fluid demonstrates albuminocytologic dissociation in 90% of cases. Acute inflammatory demyelinating polyneuropathy (AIDP) is the most common form of GBS in which the immune attack is directed at peripheral nerve myelin. Besides this classic presentation, there are clinical variants based on the types of nerve fibers involved (motor, sensory, sensory and motor, cranial or autonomic), the predominant mode of fiber injury (demyelinating versus axonal), and the presence of alteration in consciousness (5). Acute motor axonal neuropathy (AMAN) is unique as there is no sensory involvement, and the reflexes are preserved. Acute Motor and Sensory Axonal Neuropathy (AMSAN), Miller Fisher Syndrome (MFS), Bickerstaff encephalitis, pharyngeal-cervical-brachial weakness, pan-dysautonomia, pure sensory GBS, sixth nerve palsy with paresthesia and facial diplegia with paresthesia (FDP) are the other rare variants of GBS [6]. Isolated facial diplegia is a rare variant of GBS, with only a few cases described so far. Deep tendon reflexes are generally absent but rarely can be present or even exaggerated (7) As in the case of our patient, ankle reflexes were absent, and knee and upper limb reflexes were decreased. Diagnosis of GBS is based on clinical examination, CSF analysis and neurophysiological studies. CSF shows albuminocytological dissociation as also seen in our case. NCV and EMG are helpful in establishing a diagnosis of GBS [8], however may often have nonspecific EMG findings in patients with facial diplegia. Treatment of GBS includes supportive care and disease modifying therapy with intravenous immunoglobulin (IVIG) or plasma exchange (PE) [9]. Commonly, bilateral FN palsy will initially start from one side and progress to involve the other side subsequently. Our case is rare due to the synchronous presentation of bilateral facial involvement on the initial presentation. Approximately 80% of patients diagnosed with GBS are able to independently walk at six months with complete recovery of motor strength in 60% of patients at one year [10]. Up to 10% of patients with GBS may experience relapses with increased weakness. Our case was unique as the onset of facial palsy was sudden on both sides and not associated with any distal paresthesia and later progressed to absent ankle reflexes and decreased knee and upper extremity reflexes. Absence of deep tendon reflexes, albuminocytological dissociation of CSF, nerve conduction study findings, and improvement with IVIG favored a diagnosis of GBS variant, while all other possible differentials were ruled out through appropriate tests.