Hemifacial spasm: a nodal, stretch-mediated paradigm beyond neurovascular compression.

BACKGROUND: Hemifacial spasm (HFS) has traditionally been interpreted as a neurovascular compression syndrome, in which arterial contact at the root exit zone induces focal demyelination and hyperexcitability of the facial nerve. Although this framework underpins the clinical success of microvascular decompression (MVD), multiple consistent observations remain difficult to reconcile with a purely compression-based mechanism, including the high prevalence of neurovascular contact in asymptomatic individuals, the rapid and reproducible reversibility of symptoms after surgery, and the limited and inconsistent morphological evidence for demyelination.

METHODS: This review integrates clinical, electrophysiological, anatomical, and biomechanical findings to re-examine the pathophysiology of HFS, with particular focus on the transitional zone at the central-peripheral myelin interface.

RESULTS: Structural discontinuity and elastic mismatch at the transitional zone increase susceptibility to mechanical perturbation, identifying the transitional node of Ranvier as a critical site of vulnerability.

CONCLUSIONS: I propose a revised framework-Stretched Cranial Nerve Syndrome (SCNS)-in which HFS reflects mechanically induced, reversible nodal dysfunction arising from chronic stretch and altered neurovascular geometry. This framework provides a coherent and internally consistent explanation for observations insufficiently accounted for by compression-based models, offering a more integrative mechanistic understanding of HFS.