Central-type facial palsy (C-FP) is frequently observed in patients with upper lateral medullary infarction.¹ The corticobulbar tract of the facial nerve descends to the ventromedial upper medulla, where it decussates and ascends in the dorsolateral medulla to synapse with the contralateral facial nucleus.^2-4 Consequently, C-FP can be present in the ipsilateral dorsolateral upper medullary lesion or in the contralateral ventral medullary lesion. Additionally, although rare, peripheral facial palsy (P-FP) can occur due to a lesion involving the facial infranuclear region of the caudal pons extending from the dorsolateral upper medulla.^2,3 We report the case of a patient with P-FP and ipsilateral dorsolateral cervicomedullary infarction.

A 74-year-old man with a history of hypertension and diabetes visited the emergency room due to difficulty closing his left eye and drooping of the mouth on the left side. No signs of infection were observed in the week prior. Neurological examination revealed House-Brackmann grade III P-FP on the left side and mild dysarthria (Fig. 1A). Ocular movements were normal. Horner’s sign, nystagmus, ataxia, limb muscle weakness, and sensory symptoms were also observed. Diffusion-weighted brain imaging revealed hyperintensities in the left dorsolateral portion of the cervicomedullary junction (Fig. 1B–E). His symptoms gradually improved over the course of three weeks.

The facial nucleus is located in the dorsolateral caudal pons. It has been noted that P-FP in medullary lesions can be explained by the involvement of adjacent lower pontine region, which contains the facial nucleus or facial nerve fascicles.^1,3 In our patient, the lesion was located in the ipsilateral dorsolateral cervicomedullary junction. To date, P-FP secondary to cervicomedullary infarction has not been reported. We were unsure whether the P-FP in our patient was caused by a cervicomedullary lesion or was coincidental with isolated Bell’s palsy. Additional cases are required to confirm this hypothesis.