Non-syndromic Developmental Facial Palsy Co-occurring With Chiari I Malformation: Parallel Manifestations of a Shared Prenatal Disturbance?

Congenital facial palsy most commonly results from perinatal trauma. Developmental causes are rare and typically occur within syndromic constellations such as Möbius, Goldenhar, or CHARGE (coloboma, heart defects, atresia choanae, retarded growth, genital abnormalities, ear anomalies). Non-syndromic developmental facial palsy (DFP) is exceedingly uncommon and is thought to arise from disturbances in facial motor nucleus development, the intrapontine facial nerve tract, or its vascular supply. Chiari I malformation (CM-I) is characterized by ≥5 mm cerebellar tonsillar descent below the foramen magnum, producing posterior fossa crowding and impaired cerebrospinal fluid dynamics. CM-I-associated cranial neuropathies, including facial nerve involvement, have been reported in the setting of secondary structural pathology such as syringomyelia, syringobulbia, or basilar invagination. We report a 37-year-old woman with a lifelong House-Brackmann grade III left facial palsy, documented at first cry and stable since birth, who presented with a six-month history of Valsalva-exacerbated occipital headaches, positional vertigo, and posterior cervical allodynia. Magnetic resonance imaging demonstrated 12-mm tonsillar ectopia with brainstem compression, without syrinx, syringobulbia, or basilar invagination, and incidentally revealed a thin elevated corpus callosum with mild ventricular prominence. Posterior fossa decompression with suboccipital craniectomy, C1 laminectomy, and autologous duraplasty resolved her CM-I symptoms. After an extensive literature review, we found no prior reports of non-syndromic DFP coexisting with CM-I in the absence of syringomyelia, syringobulbia, basilar invagination, or syndromic features. Although coincidence cannot be excluded, the corpus callosum and ventricular findings suggest a shared prenatal disturbance. These features may reflect parallel manifestations affecting overlapping developmental programs during ontogeny, rather than a direct causal relationship. A systematic framework comprising neuroimaging, electrodiagnostics, and targeted genomic profiling in similar cases may elucidate a developmental pattern from isolated coincidence, with potential implications for early surveillance.