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

Abstract

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.

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.

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.