Bifacial weakness with paresthesias (BFP) secondary to trauma: a case report

This case details the diagnosis and treatment process of a patient with bilateral facial nerve palsy accompanied with limb sensory disturbance secondary to head trauma, who was ultimately diagnosed with Bifacial weakness with paresthesias (BFP) , a rare variant of Guillain-Barré Syndrome(GBS) . The patient underwent plasma exchange therapy and showed favorable recovery . In this article, for the first time we report a case of BFP secondary to trauma.

💡 Research Summary

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This case report describes a 47‑year‑old man who developed bilateral facial nerve palsy and distal limb paresthesias following a motor‑vehicle accident. Initially, the facial weakness was attributed to direct traumatic injury because imaging revealed bilateral temporal bone fractures, a left temporal lobe hematoma, and fluid collections in the mastoid processes, while the facial nerve canals appeared intact. The patient received intravenous dexamethasone for four days without improvement. On the third day of admission to the authors’ department, a neurologist noted diminished tendon reflexes and raised the possibility of Guillain‑Barré syndrome (GBS). Cerebrospinal fluid analysis demonstrated classic albumin‑cytologic dissociation (elevated protein with normal cell count), and serology was positive for anti‑GM2 IgM antibodies, supporting an immune‑mediated neuropathy. The combination of bilateral facial weakness, distal sensory loss, and absent reflexes fulfilled the criteria for the rare GBS variant known as bifacial weakness with paresthesias (BFP).

The patient was treated with five sessions of plasma exchange. Clinical improvement began on day 22 after onset of facial paralysis; at two months he showed partial recovery of facial symmetry, and by six months he achieved near‑complete restoration of eye closure, forehead wrinkling, and nasolabial folds, corresponding to House‑Brackmann grade I. This outcome mirrors the favorable prognosis reported in previous BFP series, where most patients recover well with standard GBS therapies (intravenous immunoglobulin or plasma exchange).

The report emphasizes several key points. First, bilateral facial palsy after head trauma is rare and is usually classified as either immediate (direct nerve transection, compression, or avulsion) or delayed (edema, vascular compromise, or hematoma within the facial canal). However, clinicians must remain vigilant for non‑traumatic etiologies, especially when additional neurological signs such as diminished reflexes or distal paresthesias are present. Second, the presence of distal limb sensory symptoms is a hallmark of BFP and often overlooked; in this case, careful history‑taking eventually uncovered the limb numbness. Third, anti‑GM2 IgM positivity, although not specific, can support the diagnosis of an immune‑mediated process in the appropriate clinical context.

The authors review the literature on bilateral facial palsy after trauma, noting that most reported cases involve direct nerve injury and are managed surgically or with steroids. In contrast, post‑traumatic GBS is exceedingly uncommon, with only isolated case reports linking surgery or severe injury to subsequent GBS. This case represents the first documented instance of BFP precipitated by trauma, expanding the spectrum of triggers for this GBS variant.

Clinically, the report advocates for a systematic neurological assessment of any patient with bilateral facial weakness after trauma, including evaluation of tendon reflexes, sensory examination of the limbs, and cerebrospinal fluid analysis when GBS is suspected. Early initiation of immunomodulatory therapy can hasten recovery and improve functional outcomes. The authors conclude that attributing bilateral facial palsy solely to mechanical injury may lead to missed or delayed diagnosis of treatable immune neuropathies, and that comprehensive work‑up is essential for optimal patient care.