Case reports in neurology · 2026
Facial Diplegia Guillain-Barre Syndrome Variant Initially Presenting as a Stroke Mimic: Evolution from Unilateral Central-Appearing Facial Weakness to Bilateral Facial Palsy - A Case Report.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Alqatati Fadel, Mesilhy Rowan, Ghabashneh Mohammad, Jaber Kholoud Riyad, Al-Abdulla Noora, Sanosi Amin S, Parampil T Shibu Kandalam
Аннотация
INTRODUCTION: Facial diplegia is an uncommon regional variant of Guillain-Barre syndrome (GBS). It may initially resemble acute cerebrovascular disease when facial weakness appears unilateral or central in pattern.
CASE PRESENTATION: A 48-year-old Sri Lankan man with untreated hypertension, obesity, and newly recognized diabetes presented approximately 18 h after onset of slurred speech and persistent left facial weakness. Initial examination suggested a left central facial palsy, although incomplete left eye closure was also present. Non-contrast computed tomography and same-day brain magnetic resonance imaging with angiography, performed approximately 25 h after symptom onset, showed no acute infarction, hemorrhage, vascular occlusion, dissection, or significant stenosis. Over the next 48 h, facial weakness progressed to bilateral lower motor neuron facial palsy with mild dysphagia and weak gag reflex, while limb strength remained preserved. Cerebrospinal fluid showed albuminocytologic dissociation. Dedicated contrast-enhanced magnetic resonance imaging of the internal auditory canals showed no facial nerve enhancement; bilateral linear enhancement represented vascular enhancement. Electrodiagnostic testing showed facial motor terminal latency abnormalities, prolonged bilateral blink reflex responses, and facial muscle EMG abnormalities supportive of a facial diplegia GBS variant. Campylobacter testing and anti-ganglioside antibody testing were not performed. He received intravenous immunoglobulin 0.4 g/kg/day for 5 days and gradually improved.
CONCLUSION: Facial diplegia GBS may initially trigger an acute stroke evaluation when early facial weakness appears unilateral or central. Repeated neurological examination, cerebrospinal fluid analysis, and neurophysiology are essential when persistent symptoms and negative neuroimaging argue against a vascular syndrome.
CASE PRESENTATION: A 48-year-old Sri Lankan man with untreated hypertension, obesity, and newly recognized diabetes presented approximately 18 h after onset of slurred speech and persistent left facial weakness. Initial examination suggested a left central facial palsy, although incomplete left eye closure was also present. Non-contrast computed tomography and same-day brain magnetic resonance imaging with angiography, performed approximately 25 h after symptom onset, showed no acute infarction, hemorrhage, vascular occlusion, dissection, or significant stenosis. Over the next 48 h, facial weakness progressed to bilateral lower motor neuron facial palsy with mild dysphagia and weak gag reflex, while limb strength remained preserved. Cerebrospinal fluid showed albuminocytologic dissociation. Dedicated contrast-enhanced magnetic resonance imaging of the internal auditory canals showed no facial nerve enhancement; bilateral linear enhancement represented vascular enhancement. Electrodiagnostic testing showed facial motor terminal latency abnormalities, prolonged bilateral blink reflex responses, and facial muscle EMG abnormalities supportive of a facial diplegia GBS variant. Campylobacter testing and anti-ganglioside antibody testing were not performed. He received intravenous immunoglobulin 0.4 g/kg/day for 5 days and gradually improved.
CONCLUSION: Facial diplegia GBS may initially trigger an acute stroke evaluation when early facial weakness appears unilateral or central. Repeated neurological examination, cerebrospinal fluid analysis, and neurophysiology are essential when persistent symptoms and negative neuroimaging argue against a vascular syndrome.