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. 2025 Apr 15:15910199251332399. Online ahead of print. doi: 10.1177/15910199251332399

Transient vocal cord paralysis after transverse Sinus stenting

Ethan A Miller 1,, Abhay Moghekar 2, Philippe Gailloud 3
PMCID: PMC11999988  PMID: 40232300

Abstract

We report the case of a young woman diagnosed with idiopathic intracranial hypertension, who did not tolerate long-term pharmacologic treatment and was deemed a candidate for transverse sinus stenting (TSS). Following the procedure, she developed transient palsies of the 10th and 11th cranial nerves. She underwent orotracheal examination and brain magnetic resonance imaging, which ruled out a local structural etiology or brainstem pathology. Her symptoms resolved spontaneously and she returned to baseline neurologic functioning within 12 weeks. Her presentation was likely caused by nerve compression in the jugular foramen by the stent delivery system.

Keywords: Transverse sinus, stent, cerebral angiography, interventional neuroradiology, idiopathic intracranial hypertension

Letter

Idiopathic intracranial hypertension principally affects young women and may result in headache, visual disturbance, and pulsatile tinnitus. Typical radiological findings include ocular globe flattening, optic nerve tortuosity, an empty sella, and transverse sinus (TS) stenoses. 1 TS stenting (TSS) is considered a safe and efficient therapeutic option for patients with intracranial hypertension caused by TS stenoses.2,3 We report here the case of a patient who underwent TSS that resulted in transient vocal cord paralysis.

A 49-year-old woman without significant medical history, presented with headaches, transient visual obscurations, and right-sided pulsatile tinnitus. She underwent an extensive workup to rule out secondary causes of her symptoms, including a negative brain magnetic resonance imaging (MRI). MRV showed hypoplasia of the left TS and severe stenosis of the right TS. A neuro-ophthalmic evaluation revealed grade 1 papilledema, and a lumbar puncture demonstrated an elevated opening pressure of 29 cmH2O. She was initially managed with lifestyle modifications and pharmacological measures, including acetazolamide. As her symptoms persisted over several years, and concerns for adverse effects from the medication arose, she sought alternative treatment options, and was referred to our service for TSS.

Dural sinus venography confirmed the presence of bilateral TS stenoses, with a pressure gradient of 4 mmHg under general anesthesia. Two overlapping 6 by 40 mm self-expandable stents were deployed across the right TS stenosis Figure 1. The endovascular platform consisted of a long 6-French sheath placed in the right internal jugular vein and an intermediate catheter advanced across the stenosis. Following the procedure and after extubation, she reported dysphagia and dysphonia. Flexible nasopharyngolaryngoscopy revealed a right vocal cord paralysis. Trapezius weakness was also noted on the right.

Figure 1.

Figure 1.

Imaging obtained during the TSS procedure: (A) DSA, superior sagittal sinus injection, posteroanterior projection, confirming the presence of bilateral TS stenoses. (B) DSA, non-subtracted lateral projection, demonstrating the overlapping stents deployed in the right TS. TS: transverse sinus; TSS: transverse sinus stenting

A compressive injury of the recurrent laryngeal nerve by the endotracheal tube was considered unlikely because of the involvement of multiple cranial nerves. MRI obtained ruled out a brainstem ischemic injury. Therefore, intraprocedural compression of the 10th and 11th cranial nerves by the stent delivery platform within the boundary of the jugular foramen seemed the best explanation for our patient's symptoms. This mechanism was, in that instance, possibly made likelier by the need to use an intermediate catheter to facilitate the progression of the stent delivery system, a technique only used in our practice when initial attempts at advancing the stent by itself have failed (i.e., less than 10% of cases). Fortunately, her symptoms resolved spontaneously, and she returned to baseline neurologic functioning within 12 weeks. One year post-stenting, she remains without headache, papilledema, or pulsatile tinnitus.

In summary, we report a case of transient palsies of the 10th and 11th cranial nerves following TS stenting, which was likely due to nerve compression within the jugular foramen, caused by the stent delivery system.

Footnotes

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Ethical considerations: No IRB approval was required for this letter and all personal information was anonymized.

Funding: The authors received no financial support for the research, authorship, and/or publication of this article.

References

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