Title : Atypical vernet syndrome following trauma: The overlooked role of internal jugular vein thrombosis
Abstract:
Introduction: Vernet syndrome, or jugular foramen syndrome, is characterised by dysfunction of cranial nerves IX, X, and XI due to lesions affecting the jugular foramen. While common causes include tumours, infections, and vascular anomalies, trauma-induced Vernet syndrome remains a clinical rarity. Even more uncommon is the involvement of internal jugular vein (IJV) thrombosis as a secondary pathophysiological mechanism in post-traumatic cranial neuropathy. We report a rare and atypical presentation of Vernet syndrome following penetrating neck trauma, in which adjacent IJV thrombosis contributed significantly to the clinical presentation.
Case Presentation: A 40-year-old previously healthy male presented to the emergency department following a high-velocity road traffic accident that resulted in a penetrating injury to the right side of the neck. He was hemodynamically stable but reported progressive dysphagia and hoarseness shortly after the trauma. Neurological examination revealed findings consistent with involvement of cranial nerves IX, X, and XI: uvular deviation to the left indicating right palatal weakness, right vocal cord paralysis confirmed by laryngoscopy, and weakness of the right sternocleidomastoid and trapezius muscles. No deficits in other cranial nerves or sensory-motor systems were noted.
Diagnostic Evaluation: High-resolution CT imaging revealed a skull base fracture involving the right jugular foramen. MRI with venography further identified thrombosis of the right internal jugular vein adjacent to the fracture site. The presence of IJV thrombosis in the setting of jugular foramen involvement suggested a dual mechanism for cranial nerve dysfunction—direct mechanical injury from trauma and secondary compressive or ischemic neuropathy due to venous thrombosis.
Management and Outcome: The patient was initiated on anticoagulation therapy, and over time, there was gradual improvement in bulbar symptoms. Follow-up imaging showed partial resolution of the thrombus, though some deficits, including mild hoarseness and dysphagia, persisted.
Conclusion: This case underscores the importance of considering vascular complications such as internal jugular vein thrombosis in the differential diagnosis of post-traumatic Vernet syndrome. Early identification through advanced imaging techniques, such as MR venography, is crucial for timely intervention. In trauma patients presenting with lower cranial nerve palsies, awareness of such atypical mechanisms can lead to more accurate diagnosis and potentially improved functional outcomes.
