The patient came to me having already done everything right. She had sought assessment from several neurologists who diagnosed prolonged MdDS. She had kept meticulous records of her symptoms, her triggers, her patterns.
I assessed and treated her for prolonged Mal de Débarquement Syndrome (MdDS) in Adelaide. She responded well to the treatment, but vague MdDS-like sensations persisted. It did not gel. On return to Sydney, she continued pursuing answers with the support of her General Practitioner because the conventional pathway ran out of road. Her GP concluded she had exhausted the available options. The recommendation was to return to a neurologist she had already seen. She trusted her instincts and looked further.
The patient reached out to a US-based MdDS researcher, who directed her toward assessment by a venous compression specialist in Australia. Earlier this year (2026), following multidisciplinary reviews at the Chris O’Brien Lighthouse in Sydney, she underwent surgery for a C1 transverse process resection with internal jugular vein decompression, which is a rare surgery. She let me know one-week post-surgery that she was asymptomatic. It required her tenacity, finding the right people, in the right institution, and importantly asking the right questions.
Her journey raises important considerations for every clinician working with prolonged MdDS patients, and for that matter all patients; the need for compassion, curiosity, conviction, support, and non-judgmental behaviour with which we must sit. When our best treatment does not produce the expected response, are we asking all the right questions about what else might be driving the symptom picture? It is imperative we refrain from “the treatment was a failure” or “the patient failed to respond to treatment”. Be big enough to search for the answers. Go to the literature. Talk to other specialists.
I speak from experience and attest to this tenet which is the foundation of my career.
The Foundation We Work From
The current gold standard for prolonged, motion-triggered MdDS is optokinetic stimulation with passive head roll, the treatment paradigm developed by the late Dr Mingjia Dai and the late Dr Bernard Cohen at Mount Sinai, New York (Dai M, Cohen B, Cho C, Shin S, Yakushin SB. Treatment of the mal de débarquement syndrome: a 1-year follow-up. Front Neurol. 2017;8:175).
This paradigm is grounded in rigorous scientific evidence and has produced meaningful outcomes for many patients, over considerable time. It is not a general vestibular rehabilitation programme. It is a specific, evidence-based protocol developed by researchers who understand the neurological mechanisms of MdDS with unusual precision. Clinicians applying it need to understand what it is and why it works. Generalised vestibular exercises are not a substitute. It is a rare central vestibular lesion and not a peripheral vestibular lesion. I urge you not to treat this clinical population with vestibular rehabilitation exercises. It is professional and ethical to refer the patient to a clinician who is conversant with and experienced using the Dai treatment paradigm.
It is also important to be clear about the scope of the Dai treatment protocol. Prolonged, motion-triggered MdDS is the population for which this treatment was developed and validated. It is the population I work with. Non-motion triggered persistent oscillating vertigo is a separate clinical entity and does not fall within this treatment paradigm or within the scope of this article.
When Treatment Does Not Produce the Expected Response
Most clinicians working in this field will, over time, encounter the patient who does not respond as expected to the Dai protocol. The persistent rocking continues. The symptom burden does not ease. The clinical picture becomes confusing.
The instinct, sometimes, is to question the diagnosis, the patient’s compliance, or the adequacy of the treatment delivered. In my experience, the more productive instinct is to question what we may not yet have looked for.
A paper published in 2025 in Otology and Neurotology Open by Dr Yoon-Hee Cha and colleagues at the University of Minnesota has introduced a hypothesis worth taking seriously (Cha YH, Gharib M, Chan K, Karam J. Persistent oscillating vertigo from extracranial venous compression. Otology Neurotol Open. 2025;5:e065). Cha is a well-published figure in MdDS research and the lead author of the Bárány Society consensus diagnostic criteria. This paper, while limited in scale, raises a differential diagnostic consideration which physiotherapists working with vestibular and neurological patients must be aware.
What the Cha Paper Proposes
Cha and colleagues present six cases of persistent oscillating vertigo where extracranial venous compression was identified and treated with significant symptom reduction. The compression sites were the internal jugular vein (IJV) at the atlas (C1), the IJV beneath the sternocleidomastoid muscle (SCM), and the subclavian vein at the thoracic outlet. Compressions were typically bilateral and concurrent.
The proposed mechanism is that these compressions raise venous pressure around the inner ear, producing continuous peripheral vestibular stimulation and downstream central effects — generating the persistent rocking, bobbing, and swaying that defines the condition.
Interventions ranged from botulinum toxin injections to the SCM and anterior scalene muscle, through to styloidectomy, stenting, SCM partial myotomy, first rib resection, and scalenectomy. Outcomes ranged from approximately 70% to 100% symptom reduction across the six patients, with follow-up periods of 8 months to 2.5 years.
Reading the Paper Critically
This is a proof-of-principle case series, not a mechanistic study. The authors state this clearly and do not overclaim. The key methodological limitations are as follows.
Six cases cannot establish prevalence or confirm causation. The patients were drawn from a study specifically investigating venous narrowing in headache and dizziness, not from a representative prolonged MdDS cohort. The authors noted that the age and sex distribution does not align with the broader MdDS literature, where female predominance with peak onset in the fifth decade is well established. There is no control group, so whether venous compression is causally related to persistent oscillating vertigo or is an incidental finding in this population cannot be determined from this data alone.
Critically for our field: the paper states all patients underwent physical therapy before injections or surgery, but the nature of that therapy is not described. Whether any patients received optokinetic stimulation with passive head roll is not stated. The relationship between venous decompression and response to the Dai treatment paradigm is entirely unexplored.
Symptom relief does not confirm mechanism. One adverse event occurred in the series: accessory nerve injury from stenting in one patient, which resolved over six months. In a series of six, this is not insignificant.
The Broader Context: Venous Compression Syndromes Are Consistently Underdiagnosed
The challenge of identifying venous compression as an underlying driver of neurological symptoms is not unique to MdDS. Associate Professor Kenneth Lui of the Keck School of Medicine, University of Southern California, has documented multiple cases in which venous compression syndromes of the central nervous system were missed, misattributed, and in one striking case, labelled as a factitious disorder in a 17-year-old athlete who was in fact experiencing progressive limb weakness from a critically stenosed right internal jugular vein at C1 (Lui K. Venous Compression Syndromes: From Diagnosis to Treatment. University of Southern California.
Lui’s central point is one that resonates directly with my clinical concern: these conditions are difficult to diagnose because their presentations are vague, variable, and do not map neatly onto the well-characterised symptom territories of arterial occlusion. Without a high index of clinical suspicion and appropriate imaging, these patients are easily misdiagnosed or dismissed.
This is also consistent with what the surgical literature confirms. C1 transverse process resection with internal jugular vein decompression sits at the intersection of skull-base ENT surgery, vascular surgery, and neurosurgery. Very few surgeons worldwide are trained and comfortable operating where the C1 vertebra, cranial nerves, and the jugular vein converge. Patient selection is strict. Multidisciplinary review is standard. These are not procedures performed in general hospitals, and the global pool of surgeons with the necessary expertise is very small.
What This Means for Clinical Practice
My reading of the Cha paper, and of the broader venous compression literature, leads me to this position: extracranial venous compression is an uncommon condition that is difficult to diagnose, and physiotherapists working with prolonged MdDS patients are unlikely to encounter it frequently. However, we need to be aware that it exists.
Physiotherapists treating headache, and vestibular physiotherapists with an underpinning in neurological sciences, need to hold this differential in mind. When a patient with a well-established prolonged MdDS diagnosis does not respond as expected to the Dai treatment paradigm in the way the clinical evidence would predict, the appropriate next step is referral to a neurologist with a request for systematic imaging of the head, neck, chest, and abdomen.
The clinically accessible assessment findings flagged in the Cha paper are worth incorporating into your assessment of treatment-refractory patients:
Upper limb tension tests positive bilaterally warrant attention. Anterior scalene tenderness is relevant. Symptoms worsening in recumbency — present in approximately 30% of prolonged MdDS patients — may indicate internal jugular vein compromise, given that the IJV is the preferred venous outflow path when lying down. Symptom exacerbation with head turning or arm abduction is consistent with the compression sites identified in the Cha series.
Caution: None of these findings are diagnostic in isolation. Together, in a non-responding MdDS patient, they constitute a clinical signal worth pursuing.
The Question We Must Keep Asking
My patient’s story is not extraordinary in its suffering — many patients with prolonged MdDS carry a burden that is poorly understood by those around them and poorly served by the systems they move through. What is instructive about her story is the persistence, determination, time, curiosity and support required to arrive at an additional diagnosis underlying her refractory symptoms.
We cannot place that burden entirely on patients. The responsibility to keep asking why a patient is not responding sits with us as clinicians. Not every patient responds to our best treatment. Some have not yet had the right question asked about them.
Continuous clinical analysis and working in a multi-disciplinary team is not optional. It is the foundation of responsible practice and learning.
The Final Outcome
The patient had prolonged MdDS which responded well to the Dai protocol. Her apparent refractory symptoms – head pressure and dizziness – were due to a rare C1 transverse process compressing the internal jugular vein which required resection of the C1 transverse process and decompression of the vein earlier this year (2026). She let me know one-week post-surgery that she was asymptomatic.