Stroke in a golfer is not the first diagnosis that comes to mind when a patient presents with posterior circulation symptoms following a round of golf. It is not the second. The presentation is unusual, the mechanism is non-obvious, and the connection between a golf swing and a vertebral artery injury requires a chain of anatomical reasoning that is easy to miss under time pressure in an emergency setting.
The 2007 paper published in Surgical Neurology documenting vertebral artery dissection following golf-related rotational cervical trauma — the case that gave the condition its colloquial name — drew attention to a mechanism of cerebrovascular injury that had been underrecognized in the clinical literature and underappreciated in emergency neurology practice.
Vertebral Artery Anatomy and Vulnerability
The vertebral arteries are the posterior circulation's primary supply. They arise from the subclavian arteries, ascend through the transverse foramina of the cervical vertebrae, converge at the pontomedullary junction to form the basilar artery, and supply the brainstem, cerebellum, occipital lobes, and portions of the thalamus.
This anatomical course creates a specific vulnerability. As the vertebral arteries ascend through the transverse foramina — bony channels in the cervical vertebrae — they are subject to mechanical forces generated by neck movement. At the C1–C2 level, where the artery exits the transverse foramen and curves to enter the skull, it is particularly exposed to rotational and extension forces because this is the segment where mobility is greatest and bony protection least effective.
The artery at this level can be compressed, stretched, or torn when the neck undergoes extreme or rapid rotation — particularly rotation combined with extension. The result is arterial dissection: a tear in the intimal layer of the vessel wall that allows blood to enter and track between the vessel wall layers, creating a mural hematoma that can narrow or occlude the lumen, generate thrombus, or cause embolic events in the posterior circulation.
"The vertebral artery at C1–C2 is the most mechanically exposed segment of the posterior circulation. It sits where movement is greatest and protection is least — a combination that makes it uniquely vulnerable to rotational trauma."
The Golf Swing as a Dissection Mechanism
The golf swing is one of the most biomechanically demanding rotational movements in recreational sport. A full driver swing generates cervical rotation approaching 90 degrees, combined with lateral flexion and extension, completed in a fraction of a second with considerable muscular force behind it.
For the vast majority of golfers, this movement is performed thousands of times without consequence. The vertebral arteries accommodate the mechanical demands through the elasticity of youth, the adaptations of habitual motion, and the structural integrity of healthy arterial walls.
Dissection risk is elevated in several specific contexts:
- Pre-existing arterial wall abnormalities — including fibromuscular dysplasia, connective tissue disorders such as Ehlers-Danlos syndrome or Marfan syndrome, and age-related arterial wall changes that reduce elasticity and increase vulnerability to mechanical stress
- Extreme or forceful swing mechanics — particularly in golfers who generate high rotational velocity or who use technique involving exaggerated neck extension at follow-through
- Cervical degenerative disease — osteophytes or disc disease at C1–C2 or adjacent levels can reduce the available space for the vertebral artery during rotation, increasing mechanical contact and shear forces
- Repeated minor trauma — a single swing may not cause dissection, but repetitive mechanical stress across a round or season may accumulate to a threshold where arterial wall integrity fails
The case documented in the Surgical Neurology paper described a patient who developed posterior circulation stroke symptoms following golf activity, with imaging demonstrating vertebral artery dissection at the C1–C2 level consistent with rotational cervical trauma. The case contributed to a small but growing literature on sport-related vertebral artery dissection and helped establish golf as a recognized — if uncommon — mechanism.
The Clinical Presentation
Vertebral artery dissection presenting after golf activity is a diagnostic challenge because the temporal relationship between the precipitating activity and symptom onset is not always immediate. Dissection can produce symptoms within minutes, but in some cases thromboembolism from the dissection site reaches the posterior circulation hours after the initiating event — by which point the patient and examining physician may no longer associate current symptoms with earlier physical activity.
The classic posterior circulation stroke syndrome includes:
Wallenberg syndrome (lateral medullary syndrome): Ipsilateral facial numbness and contralateral body numbness, ipsilateral Horner syndrome, dysphagia, hoarseness, vertigo, and ataxia. This constellation results from infarction of the lateral medulla and is one of the most recognizable syndromes in clinical neurology — but it is incomplete in many patients, and partial presentations are common.
Cerebellar infarction: Sudden onset gait ataxia, limb dysmetria, nausea, vomiting, and headache. Can mimic acute vestibular neuritis in presentation, leading to misdiagnosis particularly in the emergency department.
Occipital infarction: Visual field deficits, cortical blindness, visual disturbances.
Posterior headache: Severe sudden-onset headache, often occipital or cervical in location, is a recognized early symptom of vertebral artery dissection and can precede ischemic symptoms by hours.
What makes the golf-related presentation particularly susceptible to delayed diagnosis is that patients frequently attribute early symptoms — dizziness, neck pain, headache — to exertion, dehydration, or musculoskeletal strain from the game itself. The diagnostic window for effective intervention may narrow during this period of misattribution.
Diagnostic Approach
When vertebral artery dissection is suspected — whether sport-related or otherwise — the diagnostic workup follows a relatively standardized pathway, though the specific imaging modality depends on institution, patient factors, and clinical urgency.
MRI with MRA (Magnetic Resonance Angiography)
The combination of MRI and MRA is the most commonly used initial imaging approach in patients who are neurologically stable. MRI can demonstrate the mural hematoma characteristic of dissection — the T1-hyperintense crescent sign — while MRA provides vascular anatomy and identifies luminal stenosis or occlusion. Diffusion-weighted imaging identifies acute ischemic infarcts in the posterior circulation.
CT with CTA (Computed Tomography Angiography)
CTA provides rapid, high-resolution vascular imaging and is often the first-line modality in acute or unstable presentations. It is less sensitive than MRI for detecting small infarcts in the posterior fossa due to beam-hardening artifact from the surrounding bone, but it reliably demonstrates arterial dissection and luminal compromise.
Conventional Digital Subtraction Angiography
The historical gold standard for cerebrovascular imaging, DSA is now reserved for cases where non-invasive imaging is inconclusive or where endovascular intervention is being considered. The characteristic angiographic findings of dissection include the string sign — a long, smooth narrowing of the arterial lumen — and the double lumen sign where contrast enters the false lumen.
Ultrasound
Carotid and vertebral Doppler ultrasound can demonstrate abnormal flow in accessible segments of the vertebral artery but has limited visualization of the C1–C2 level and the intracranial segment. It is inadequate as a sole diagnostic modality when dissection is clinically suspected.
Management Considerations
The management of vertebral artery dissection has evolved considerably since the condition was first systematically characterized, and several areas of genuine clinical controversy remain.
Antithrombotic therapy
The central therapeutic question in vertebral artery dissection is whether to use anticoagulation or antiplatelet therapy to prevent thromboembolic stroke from the dissection site. Heparin followed by warfarin was historically preferred on the grounds that it would prevent thrombus formation and propagation within the false lumen. Antiplatelet agents were considered as an alternative in patients at higher hemorrhagic risk.
The CADISS trial — a randomized comparison of anticoagulation versus antiplatelet therapy in cervical artery dissection — found no significant difference in outcomes between the two approaches, with both groups having low recurrent stroke rates. Many centers have moved toward antiplatelet therapy as first-line treatment given comparable efficacy and a simpler management profile.
Duration of treatment
Standard practice involves three to six months of antithrombotic therapy, a duration based on the observation that arterial healing typically occurs within this timeframe and the risk of new embolic events diminishes as the dissection site heals. Vascular imaging at three to six months can demonstrate healing, persistent stenosis, or pseudoaneurysm formation that may influence decisions about ongoing treatment.
Pseudoaneurysm management
Vertebral artery dissection can result in pseudoaneurysm formation at the dissection site — a contained outpouching of the vessel wall through the torn intima. Pseudoaneurysms carry uncertain rupture risk and uncertain embolization risk, and their management remains controversial. Observation, antiplatelet therapy, and endovascular treatment with stenting or coil occlusion have all been employed depending on pseudoaneurysm size, location, and clinical context.
Sport-Related Vertebral Artery Dissection: The Broader Literature
Golf is not the only sport associated with vertebral artery dissection, and the Surgical Neurology paper sits within a broader — if sparse — literature on sport and activity-related posterior circulation injury.
Recognized associations include:
- Yoga — particularly positions involving cervical extension and rotation such as shoulder stand, plough, and certain backbend variations. Case reports span decades and multiple countries.
- Chiropractic cervical manipulation — one of the more extensively studied associations, with a literature examining the causal relationship between high-velocity cervical manipulation and vertebral artery injury.
- Archery — the sustained cervical rotation required to aim has been associated with vertebral artery compression and dissection in case reports.
- Swimming — particularly the freestyle stroke, which involves repetitive unilateral cervical rotation for breathing.
- Weightlifting — extreme cervical loading and the Valsalva maneuver during heavy lifts have been reported as contributing factors.
- Contact sports — rugby, wrestling, and American football generate direct cervical trauma with obvious potential for vascular injury.
What these cases share is a mechanism involving rotational or extension forces applied to the cervical spine with sufficient velocity, force, or repetition to compromise vertebral artery integrity at its most vulnerable segment.
Why This Paper Matters
The clinical value of the Surgical Neurology paper on golfer's stroke lies less in its description of a new disease than in its contribution to pattern recognition. Vertebral artery dissection following golf activity is not common — but it is not vanishingly rare either, and the consequence of missing the diagnosis in the acute setting is a preventable stroke.
Every clinician who has read this paper and registered the association between golf activity and posterior circulation symptoms is more likely to ask the right questions, order the right imaging, and diagnose the condition before the window for intervention closes.
"Case reports are often dismissed as the lowest form of clinical evidence. But for uncommon mechanisms of common catastrophes, a well-documented case series is sometimes the only evidence that will ever exist — and it is sufficient to change clinical practice."
That is what the University of Pittsburgh Neurosurgery citation of this paper reflects. Institutional academic neurosurgery programs include it in their reference literature not because it established a treatment protocol but because it expanded the differential diagnosis — and in cerebrovascular emergency medicine, that is a meaningful contribution.
Accessing the Full Paper
The complete Surgical Neurology paper on golf-induced stroke from vertebral artery dissection is available to subscribers of the Surgical Neurology Online archive. It should be read alongside the broader literature on cervical artery dissection — including the CADISS trial, the systematic reviews on sport-related vertebral artery injury, and the case series on chiropractic-associated dissection — for full context on the clinical and mechanistic landscape in which this case was documented.

