Marin-Amat syndrome: a comprehensive review of pathophysiology, clinical presentation, and management

Marin-Amat syndrome is a rare, acquired facial synkinesis characterized by involuntary eyelid closure upon jaw opening. It is historically confused with other types of synkinesis, despite distinct underlying mechanisms. This scoping review aims to clarify the pathophysiology, clinical presentation, and optimal treatment modalities for Marin-Amat syndrome.

A comprehensive search was conducted on PubMed, Scopus, Embase, and Web of Science databases following PRISMA-ScR guidelines. Studies published from inception to January 2026 were screened. Inclusion criteria were restricted to cases of acquired synkinesis manifesting as eyelid closure triggered by jaw movement. Congenital syndromes were excluded.

Twenty articles met inclusion criteria, comprising 37 patients. The mean age was 55.8 ± 23.3 years. Bell's palsy was the most common etiology (73.0%), followed by iatrogenic or surgical injury (8.1%), trauma (8.1%), COVID-19-associated palsy (8.1%), and vascular causes (2.7%); latency to onset ranged from approximately 24 days to 40 years. Electrophysiologic and clinical descriptions supported active orbicularis oculi co-contraction consistent with post-paralytic synkinesis, with a margin reflex distance-1 reduction of roughly 0.5-2.5 mm on jaw opening. Botulinum toxin type A directed at the orbicularis oculi produced effective but transient control. Selective preseptal orbicularis myectomy or resection, frequently combined with levator advancement or plication when concomitant ptosis was present, achieved durable resolution and high satisfaction without reported recurrence.

Marin-Amat syndrome is a distinct clinical entity resulting from aberrant regeneration of the facial nerve. Botulinum toxin is effective for temporary management, while surgical myectomy combined with ptosis correction represents the definitive treatment for long-term functional and aesthetic restoration.