Guillain-Barré Syndrome (GBS), or Acute Inflammatory Demyelinating Polyneuropathy (AIDP), presents with varying degrees of motor, sensory, autonomic, bulbar, and balance involvement. 

In this case, we present a 22-year-old female with depression and rapidly progressive postpartum type 1 diabetes mellitus (positive GAD65 antibodies), complicated by neuropathy (gastroparesis, neurogenic bladder), frequent episodes of diabetic ketoacidosis (DKA), and severe cachexia. During an admission for DKA which was precipitated by a viral respiratory infection, she developed acute bilateral facial weakness (involving forehead, eye closure, and lower face), distal sensory loss, and diffuse areflexia—present for three weeks prior to evaluation. 

Cerebrospinal fluid (CSF) analysis showed albuminocytologic dissociation [(protein level: 122 mg/dL, WBC count: 0)] on two lumbar punctures. Inflammatory markers, including CRP and ESR, were elevated. CSF protein electrophoresis showed increased gamma globulin without oligoclonal bands or M spike. An extensive workup including Lyme antibody panel, HIV, RPR, ANA, SSA/SSB, ganglioside antibodies, and ACE (serum and CSF) was negative. Soluble IL-2 receptor alpha was elevated (1,981 pg/mL). Brain MRI with and without contrast (including IAC protocol) revealed bilateral enhancement of the facial nerves without leptomeningeal involvement. 

Top differential diagnoses included neurosarcoidosis, Lyme disease, HIV, and the rare Facial Diplegia with Paresthesia (FDP) variant of GBS. After extensive evaluation, she received IVIG (2 g/kg ideal body weight) with noted improvement within a week.