Sternocleidomastoid Omohyoid Entrapment of the Internal Jugular Vein Causing Vertigo and Headaches

Extracranial venous compression of the internal jugular vein (IJV) from neck structures such as the sternocleidomastoid (SCM) and omohyoid (OMH) muscles can lead to vertigo and headaches [1-4]. Because case reports of this mechanism have been limited, the pattern of clinical features that should lead to consideration of this mechanism for vertigo and headaches has not yet been delineated. The broader phenomenon of head-motion-induced vestibular symptoms is more typically diagnosed as either vestibular migraine or cervicogenic dizziness, though neither diagnosis has a structural model that leads to the treatment of a targeted pathology [5, 6]. Patients often undergo vestibular rehabilitation to adapt to their symptoms, but treatment refractoriness is common without new treatments on the horizon [7, 8]. Extracranial venous compression by muscular entrapment of the IJV in the mid-neck may be an underrecognized mechanism of head motion induced vertigo that is frequently accompanied by headache. It can be a new target for treatment. We report our experience with 12 patients with entrapment of the IJV under the SCM/OMH muscles that led to vertigo and headaches, with symptoms resolving with targeted treatment of this pathology. The mechanism for vertigo was retrograde efflux of venous blood leading to dilation of the superior and inferior petrosal sinuses and shunting down the vertebral veins. We report clinical features that should alert earlier recognition of this syndrome when non-invasive methods such as physical therapy and postural education can be initiated to avoid more invasive treatments later. Design: Clinical case series. Setting: Tertiary university-based outpatient clinic. Patients: Patients presented with intractable head motion-triggered vertigo to our team's neurotologist (Y.H.C.). Detailed history, neurological exam, vestibular function testing, audiological exams, and arterial imaging (MRA/CTA) were used to rule out primary inner ear and arterial disorders. The Academic HealthCare Information Exchange for the medical centre identified patients through an IRB-approved study who were then reviewed for availability of all diagnostic tests. Outcome measures: Report of relief of vertigo by at least 70%. Screening measures: IJV entrapment was based on dynamic quantitative Doppler ultrasound (qDUS), CT venogram (CTV) of the head and neck, a trial of physical therapy, and then ultrasound-guided (US) intramuscular onabotulinumtoxin A (BoNT-A) injections (M.G.). Digital subtraction venography was performed in all patients, and surgical decompression was performed (J.K.) if non-invasive treatment was not sufficient. Descriptions of each step are included below. Dynamic quantitative Doppler ultrasound of the IJV and subclavian vein (SCV) in neutral and stressed positions for each vessel was performed in every patient. This involved velocity measurements in head extension, flexion, right rotation, and left rotation for the IJV, as well as arm abduction at 0°, 90°, 135°, and 180° for the SCV. Dynamic stenosis was regarded as a flow velocity increase of > 300% or a drop to < 50%. On the stenosis-velocity curve, this represents a decrease in cross-sectional area of > 75%. CTV of the head and neck imaged down to the right atrium was performed in the head neutral and symptom-exacerbating head position (Figure 1). This imaging ruled out stenoses in the dural sinuses, concurrent IJV compression caused by the styloid process, and any other mediastinal or neck pathology. All patients underwent a structured course of physical therapy with a focus on ergonomic awareness and optimising posture and cervical alignment. This included strengthening of the posterior cervical chain, specific stretching of the SCM and anterior scalene muscles (ASM), as well as mobilisation of the first rib for thoracic outlet syndrome. Patients underwent physical therapy for at least 2 months initially, which typically ranged from 4 to 8 in-person sessions supplemented with a home exercise programme. Physical therapy remained the foundation of all further treatments. As we learned of the importance of the omohyoid muscle in this entrapment process, specific omohyoid stretches were subsequently added. Patients who had persistent symptoms despite physical therapy underwent a diagnostic block to the SCM and ASM. If there was short-term relief of vertigo for several hours with a lidocaine injection, the patients were given a trial of BoNT-A under a cervical dystonia protocol. Direct sonographic guidance was used to ensure the accurate placement of the needle to minimise the risk of bleeding or injury to nearby neurovascular structures for each set of injections. For the short-term block, 1.5 mL of 2% lidocaine was injected into each SCM and ASM. Patients were provided with pre- and post-injection symptom diaries to record their responses. On a severity scale of 0–10, a general guideline was to observe at least a 50% improvement in baseline vertigo severity before proceeding with BoNT-A. The initial BoNT-A injection was prepared at a concentration of 5 units per 0.1 mL (2:1 dilution of BoNT-A reconstituted in normal saline). Each injection site received 0.3 mL of volume (15 units) as the starting dose. Subsequent dosing was adjusted based on treatment response and was administered every 12 weeks. Patients who did not experience sufficient clinical improvement with BoNT-A or whose symptoms were severe enough that more rapid escalation of diagnostic testing was warranted were referred for digital subtraction intravascular venography. Using ultrasound guidance, a catheter was introduced through the common femoral vein on the affected side and advanced into the innominate vein. The IJV was selected. The catheter was advanced to the level of the base of the skull. Venography was carried out in the head neutral position and with provocative manoeuvres (head rotation or head rotation with flexion) to demonstrate extrinsic compression of the IJV. This evaluation was conducted for each IJV, and a pressure gradient measurement was taken above and below the site of compression with supplementation with intravascular ultrasound (Figure 2). Under general anaesthesia, the patient was positioned supine with a slight reverse Trendelenburg inclination. The neck was gently extended with special consideration given to ensure safe head manipulation by the anaesthesiologist during the procedure, allowing for venography to be performed in the stressed position. A longitudinal incision was made along the medial border of the SCM. The incision was deepened in the subcutaneous tissue and the platysma divided. Access was gained to the carotid sheath enabling identification and release of the IJV from surrounding tissue (Figure 3). Attention was focused on identifying the precise site of compression. The next step involved a partial myotomy of the SCM executed at the level of compression through the incision along the SCM's medial border. The omohyoid muscle, situated beneath the SCM, was sacrificed. In some cases, external venolysis was necessary to fully mobilise the vein. Ten of 12 patients were female with a median age of 44 years (range 31–74 years) and a median duration of vertigo of 1.8 years before presentation. All 12 patients had vertigo triggered by leftward head rotation; 8 were also triggered by rightward head rotation, 6 with head flexion, and 9 with head extension. All patients underwent a course of physical therapy; 8 received BoNT-A injections, which all found helpful. Five patients tried a carbonic anhydrase inhibitor; only one patient found it helpful. Four patients were symptomatic enough to proceed directly to surgery. Table 1 details the associated symptoms in the patients with IJV compression. Figure 1 details extracranial venous anatomy and IJV compressions diagnosed with dynamic Doppler ultrasound and CT venogram of the head and neck. Eight patients underwent SCM/OMH myotomy, three of whom had concurrent supraclavicular thoracic outlet decompression with anterior and middle scalenectomies, brachial plexus neurolysis, first rib resection, and pectoralis minor tenotomy. Of these eight patients, six had bilateral resections with sequential improvement ipsilateral to the side of the surgery, for example, right-sided headache, neck pain, and rightward head rotation triggered vertigo resolving with right SCM/OMH myotomy. The remaining two patients had residual contralateral symptoms and further surgery is being considered. Of the six bilaterally operated patients, five had near-resolution of baseline vertigo that allowed return to regular daily activities such as work or driving. Surgical patients were followed for 4–20 months counting from their last surgery (median 10.5 months). Four patients are being managed longitudinally with BoNT-A alone as they had at least a > 50% reduction in baseline symptom severity, all having received at least four rounds (1 year of treatment) at the date of this report. Figure 2 details normal and abnormal digital subtraction venography in three patients with muscular compression of the IJV. Figure 3 is an intraoperative view of the surgical field that shows the relationship between the IJV, SCM, OMH, and the sternohyoid muscles. This report presents a mechanism for compression of the IJV in the neck under the SCM/OMH muscles leading to head movement-triggered vertigo, headache, facial pain, neck pain, tinnitus, and myofascial pain due to retrograde venous backflow into the petrosal sinuses that drain the inner ear and into the vertebral veins that drain the cervical spinal cord. This is a potential mechanism for syndromes of vertigo and headache that follow neck trauma, muscular strain, or other causes of inflammation. Diagnosing this syndrome requires recognising the clinical features and confirming with quantitative Doppler ultrasound of the IJV and subclavian veins in stressed positions, a CTV of the head and neck in stressed positions, a trial of muscular blocks, and digital subtraction venography showing dynamic IJV compression and venous shunting. Muscular compression of the IJV frequently occurs in conjunction with other extracranial venous compression syndromes such as jugular variant Eagle's syndrome and venous TOS suggesting that symptoms occur because of cumulative loss of venous outflow pathways. Muscular entrapment in the mid-neck may also have overlapping features with jugular variant Eagle's syndrome since the compressions are in tandem and both can be induced with head rotation [2, 9, 10]. Symptoms may occur when venous pressure around eloquent structures such as the inner ear is high, shunting occurs to lower resistance tissue beds, and metabolic clearance is reduced due to inefficient venous outflow. While the formation of collateral vessels can reduce intracranial hypertension, they may also become a source of symptoms themselves. Internal jugular vein entrapment by the SCM/OMH can manifest in various eccentric head positions, but we found it to be more commonly induced by ipsilateral head rotation. In our series, leftward head rotation-induced vertigo was more common than rightward head rotation-induced vertigo. This is consistent with the generally smaller left IJV calibre in most patients, leading to less tolerance of outflow compromise [11]. Concurrent ASM tightening can worsen IJV compression since the IJV can be sandwiched between the SCM and ASM. This may explain the high co-occurrence of TOS in SCM entrapment syndrome and the response to both the SCM and ASM with BoNT-A. Concurrent SCV obstruction at the thoracic outlet may lead to elevated venous pressure at the skull base through obstruction of external jugular vein drainage and reduce the capacity for collateral flow required in the setting of an IJV obstruction. Besides head movement-induced vertigo, all of our patients experienced headaches or facial pain. Specifically, 50% experienced migraine headaches; 42% experienced a facial pain syndrome such as trigeminal neuralgia, and most patients reported headaches that were worse in the morning (Table 1). A mechanism for the facial pain could be enhanced venous shunting down the facial vein or dilation of the superior petrosal sinus, which sits over and sometimes wraps around the trigeminal nerve [12]. Pulsatile tinnitus occurred in 50% of the patients. These auditory symptoms without hearing loss, paired with vertigo, could be diagnosed as probable Meniere's disease [13]. While Meniere's disease is idiopathic, raised venous pressure around the inner ear due to a downstream obstruction should be considered a possible mechanism in intractable or atypical Meniere's presentations. Vertigo due to IJV compression induced by head rotation can be distinguished from vertebral artery stenosis, aka Bow-Hunter's Syndrome (BHS), by differences in presentation and demographics. There was a middle-aged female predominance in our jugular compression group (10 of 12 patients) whereas BHS occurs with either an equal distribution of sexes or a male predominance; the compression is due to bony malformations of the atlantooccipital junction in paediatric patients or due to vascular risk factors in older patients and is usually unilateral [1, 14, 15]. BHS is reported in high-volume vascular and neurosurgical practices at a rate of one case every 1–2 years, whereas all of our patients were diagnosed and treated within 16 months [1, 14, 16]. This is a small case series that cannot fully convey the spectrum of symptoms that occur in muscular compression of the IJV. We are also not able to determine the prevalence of these compressions in the larger population of patients who present with vestibular symptoms and headaches. Determining this prevalence would require systematically ruling out venous compression pathology in all patients who present with vestibular symptoms and headache, a process that would require a significantly larger population pool. We present our initial experience with patients with this syndrome who had venographic evidence of IJV compression in order to alert clinicians to this pathology. Prompt recognition of this process may allow earlier treatment with non-invasive measures before symptoms become intractable and surgery is needed. This case series shows a mechanism and spectrum of symptoms induced by SCM/OMH entrapment of the IJV. While we have presented a limited number of cases because they had confirmation by digital subtraction venography, the clinical syndrome exhibited by these patients could be extremely common and might be diagnosed as other conditions such as vestibular migraine, cervicogenic dizziness, and even some cases of probable Meniere's disease. Muscular compression of the IJV in the neck should be considered early in the course of a vestibular-headache syndrome before surgery becomes necessary and there is a window to treat with physical therapy or postural education. Y.-H.C. provided patient data, performed analysis, drafted the manuscript, and reviewed all drafts of the manuscript. M.G. provided patient data and reviewed all drafts of the manuscript. K.C. performed data analysis and reviewed all drafts of the manuscript. J.K. provided patient data and reviewed all drafts of the manuscript. The paper was presented in abbreviated form at the 2024 American Academy of Neurology meeting. Data are presented anonymously and in aggregate without personally identifying information. The authors declare no conflicts of interest. Tabulated anonymized data may be shared by request but because this is a clinical series and there are patient privacy laws, we cannot share primary patient data.