Compression of the internal jugular vein (IJV) by the transverse process of the atlas (C1) represents an underrecognized cause of cerebral venous outflow obstruction that can lead to a spectrum of symptoms, including headache, tinnitus, and intracranial hypertension [2,3,9]. While surgical approaches such as styloidectomy have a good clinical outcome, non-invasive strategies such as endovascular stenting have emerged as a promising therapeutic approach to restore venous patency and alleviate symptoms [7,9]. In this report, we highlight the role of stenting as an effective treatment strategy for IJV compression secondary to C1 impingement, supported by pre- and postoperative imaging demonstrating the venous narrowing and subsequent restoration of vascular patency following stent placement.

A 73-year-old male presented to our outpatient clinic with persistent dizziness, episodic vertigo, horizontal nystagmus, and gait instability that had progressively worsened over the course of several months. Physical examination was notable for signs consistent with peripheral vestibular dysfunction.

Brain magnetic resonance imaging (MRI) was performed, where hyperintensity with contrast enhancement was observed in the posterior periventricular fossa of the fourth ventricle, reported by the interpreting neuroradiologist as dilated ependymal veins (Fig. 1). A possible vascular anomaly, such as an arteriovenous fistula, had to be ruled out, for instance, a computed tomography (CT) angiography was performed. No fistulas or arteriovenous malformations (AVMs) were observed, but a significant compression of the left IJV at the level of the C1 transverse process was evidenced (Fig. 2).

A digital subtraction angiography was done to better visualize the arterial and venous blood flow, confirm the venous stenosis, and rule out other possible vascular pathologies. Normal arterial cerebral flow was observed, however, in the venous phase, a significant stenosis of the left IJV was noted with evident increased collateral flow as compared to the right side, where venous drainage is smooth through the IJV, as shown in Fig. 3. A femoral vein access was successfully achieved, manometry of the left IJV was performed proximal and distal to the stenosis, demonstrating a 10 mmHg gradient across the stenosis (Fig. 2), consistent with venous hypertension. Balloon angioplasty was subsequently performed using a 5×15 mm TransForm^® balloon (Stryker Neurovascular, Fremont, CA) followed by a 7×60 mm Passeo^® balloon (Biotronik, Lake Oswego, OR) without any complications. Control angiographic images after the angioplasty demonstrated that blood flow was notably better (Fig. 4A, B). Post-operatively, the patient reported a significant improvement in symptoms.

After two weeks of progressive symptom worsening, follow-up Doppler ultrasound and CT venography confirmed hemodynamic compromise, showing reduced venous outflow from the left IJV. Given the refractory nature of the patient’s symptoms and the vascular abnormality, a stenting angioplasty was planned. Using a 6F femoral introducer, the femoral vein was canalized through which a 4F guidewire was successfully passed and cephalically pushed through the iliac vein, inferior vena cava, and superior vena cava, reaching the left IJV bulb to finally access the stenosed site. With the aid of an exchange guidewire, a 10×40 mm Venovo venous stent (BD, Tempe, AZ) was deployed successfully with the objective of restoring vascular patency and adequate venous blood flow (Fig. 5A, B). No complications were encountered, and a follow-up CT with 3-dimensional reconstruction showed resolution of the stenosis and good stent apposition as shown in Fig. 6. Clinically, the patient reported marked improvement in vertigo and stability, with immediate resolution of nystagmus.

This case illustrates a rare etiology of extracranial venous stenosis causing peripheral vestibular symptoms. It underscores the value of detailed imaging in the evaluation of atypical vertigo presentations and highlights the role of endovascular stenting as a minimally invasive solution to vascular compressive pathologies.

Cerebral venous outflow disorders are diseases that impair brain venous drainage derived from stenoses intra- or extracranially, often leading to symptoms similar to those seen in idiopathic intracranial hypertension [1]. Headache, tinnitus, dizziness, and visual disturbances are some of the common symptoms experienced by patients with these disorders. The IJV, an extracranial portion of the brain’s cerebral drainage system, can be compressed or occluded due to distinct etiologies, including thrombosis, vasculitis, or extrinsic compression. Extrinsic compression has been reported to occur by tumors, the digastric muscle, and near bony prominences such as the C1 transverse process and styloid process [5]. The latter has been reported in several case reports and series. Clinically, the venous hypertension caused by this type of compression often presents with headache, dizziness, pulsatile tinnitus, and visual impairment, consistent with the above-mentioned cerebral venous outflow disorders [10]-12]. It is well recognized that relieving the pressure from the stenosed section improves symptoms. Styloidectomy still predominates as the most common surgical procedure done in these patients [9]. C1 transverse process resection has also proved to be a potentially effective treatment strategy [4]. However, minimally invasive surgery is an increasingly popular approach in many vascular and cerebrovascular pathologies as they have been demonstrated to be less morbid, they decreased inpatient stay and postoperative complications. There is scarce data regarding pure endovascular treatment of IJV compression by a C1 transverse process [6-8]. Reviews have concluded that styloidectomy has a slightly better outcome compared to pure endovascular stenting, however, endovascular patient cohorts are small to make a clear conclusion regarding this surgical approach [8]. Some authors have recommended a staged approach to treat styloidogenic jugular venous compression by first removing the styloid process and subsequently performing stent angioplasty if symptoms recur [6]. Some others have referred to endovascular treatment as a future promise, emphasizing that it is effective, but complications and symptom recurrence are of concern [2]. Upon the revolving controversy between surgical or endovascular treatment, the decision as to whether to resolve the stenosis surgically or endovascularly should rely on the whole clinical scenario, including compression severity, symptom severity, and patient preferences. In our case, the patient had daily disabling symptoms that prompted correction, however the patient completely refused any invasive surgical treatment. The possibility of treating endovascularly was proposed and agreed upon after further discussion. Although no guidelines are available for this particular clinical entity, we believe that endovascular angioplasty and stenting are a good option for cases in which compression is mild to moderate and the surgical approach is refused by the patient or otherwise in high surgical risk patients. Here we present a case of peripheral vertigo caused by an IJV compression caused by the C1 transverse process, in which stenting was successfully done and symptoms resolved without the need for surgical styloidectomy or C1 process resection.

Extrinsic compression of the IJV, causing cerebral venous hypertension symptoms, is rarely related to C1 transverse process interference. Endovascular stenting is unusually approached as a standard therapy because styloidectomy and transverse process resection predominate. Although not thoroughly studied yet, this case demonstrates that a minimally invasive endovascular venous stenting could be enough to relieve symptoms in a patient with this rare extracranial compressive vascular pathology. However, future studies such as clinical trials or prospective cohorts are needed to adequately measure clinical impact and long-term outcomes of this approach.