Vertebral Artery Dissection Induced by Fitness Video Game Exercise: A Case Report

Introduction

Vertebral artery dissection (VAD) is a significant cause of ischemic stroke in young adults, often triggered by mechanical stressors such as trauma, sudden neck rotation, or hyperextension [1–3]. However, in some cases, no clear precipitating event is identified.

In recent years, home fitness video games have gained popularity, particularly among sedentary individuals seeking an accessible way to incorporate physical activity [4]. One such game, Ring Fit Adventure (Nintendo Co., Ltd.), integrates structured exercise routines with interactive gaming elements [4]. The game utilizes a resistance-equipped controller, the “Ring-Con”, which requires pushing (adduction) and pulling (abduction) movements, alongside exercises [4]. Some of these movements, including overhead pushing and pulling or excessive trunk extension and rotation, may exert significant mechanical stress on the cervical vasculature. However, the potential role of gaming-related exercise as a risk factor for VAD remains largely unexplored.

Here, we report a case of a young woman with no regular exercise habit who developed VAD following exercise with Ring Fit Adventure. She initially experienced acute neck pain, followed days later by sensory deficits and visual field disturbances due to embolic stroke. This case highlights the need to consider high-intensity fitness video gaming as a possible risk factor for VAD.

Case Report

A 25-year-old woman with no significant medical history, smoking, alcohol use, or regular medication had a predominantly sedentary lifestyle. She had recently started playing Ring Fit Adventure and had been engaging in weekly sessions of approximately 1 hour. Symptom onset occurred after 3 weeks of intermittent gameplay. On the day of symptom onset, she experienced sudden left-sided neck pain while repeatedly performing overhead pushing and pulling movements with the Ring-Con controller. As there were no associated symptoms such as dizziness or headache, she applied a topical analgesic patch and continued her usual activities.

Two days later, she developed sudden-onset numbness in her left upper and lower limbs, accompanied by visual field deficit in her left eye. She was transported to the emergency department, where neurological examination revealed left homonymous hemianopia and reduced pain and temperature sensation on the left side of her body. On arrival, her vital signs were stable: blood pressure was 138/72 mmHg, heart rate 76 bpm, respiratory rate 16 breaths/min, oxygen saturation 99% on room air, and body temperature 36.7°C. Laboratory findings showed normal complete blood count, normal coagulation profile (PT-INR 1.02, APTT 32.1 s), and no evidence of hypercoagulability. Lipid profile was within normal range: total cholesterol 176 mg/dL, low-density lipoprotein (LDL) 104 mg/dL, high-density lipoprotein (HDL) 52 mg/dL, triglycerides 85 mg/dL. Fasting blood glucose and HbA1c were also normal (HbA1c 5.3%). No evidence of systemic inflammation, infection, autoimmune disease, or underlying vascular risk factors was found.

Brain MRI demonstrated an acute ischemic stroke in the right occipital lobe on diffusion-weighted imaging (Figure 1A). Magnetic resonance angiography (MRA) revealed occlusion of the right posterior cerebral artery (PCA) (Figure 1B) and poor visualization of the left vertebral artery (Figure 2A). Time-of-flight (TOF)-MRA source images showed a crescent-shaped isointense structure along the left vertebral artery lumen, consistent with VAD with an intramural thrombus (Figure 2B).

Endovascular thrombectomy was promptly performed for the right PCA occlusion, followed by intra-arterial urokinase (120 000 units over 10 minutes). Dual antiplatelet therapy with aspirin (100 mg/day) and clopidogrel (75 mg/day) was initiated alongside intravenous argatroban (30 mg/day for 3 days).

By the following day, her visual field defect had improved to left superior quadrantanopia, and her sensory deficits had partially resolved. Follow-up MRI showed no new infarcts, recanalization of the right PCA, and improved visualization of the left vertebral artery. She continued rehabilitation and was discharged on hospital day 14 with only mild superior quadrantanopia.

At 4-month follow-up, her antiplatelet regimen was transitioned to single antiplatelet therapy with clopidogrel. MRI demonstrated persistent but improved stenosis of the left vertebral artery and continued vascular remodeling. At 18 months post-discharge, she had only a minor scotoma in the upper left visual field, with complete resolution of other neurological deficits.

Discussion

This case highlights a rare instance of ischemic stroke secondary to VAD, potentially triggered by video game-based exercise. VAD is a major cause of ischemic stroke in young adults, with an estimated incidence of 1–1.5 per 100 000 individuals [1,3]. While mechanical stressors such as trauma and sports-related injuries are well-documented risk factors [1–3], the present case suggests that repetitive upper-body exertion using a gaming controller may also contribute.

VADs are typically categorized as either traumatic – resulting from major external forces – or spontaneous, occurring without significant trauma. While our case lacks a clear traumatic event, the repetitive mechanical stress during gameplay may represent a form of stress-induced spontaneous dissection in an otherwise healthy individual. Sudden engagement in high-intensity physical activity, particularly in sedentary individuals without prior conditioning, may impose excessive stress on vascular structures, increasing the risk of adverse events such as arterial dissection. Although exergaming is generally considered a safe form of physical activity, recent studies have noted that certain high-intensity movements may pose musculoskeletal and vascular risks, particularly in untrained individuals [5].

The overhead pressing movement with the Ring-Con required for Ring Fit Adventure primarily trains the shoulder, trapezius, and neck muscles and places mechanical stress on the vertebral arteries, which may lead to endothelial damage and subsequent arterial dissection, especially in individuals who are not accustomed to high-intensity exercise. Notably, MRA revealed no features suggestive of underlying vasculopathies such as fibromuscular dysplasia, reinforcing the likelihood that extrinsic mechanical stress during exercise was the principal trigger in this case.

Previous reports have documented VAD cases linked to repetitive or strenuous activities that involve cervical hyperextension or rotational stress, including yoga poses such as the shoulder stand or headstand, weightlifting exercises involving overhead presses, and overhead sports like volleyball or tennis [6–8]. The patient in our case engaged in repeated overhead pushing and pulling motions using a resistance-based controller, mimicking the biomechanical stress patterns seen in those activities. This context further supports the plausibility of exercise-induced VAD, even in non-traditional settings such as exergaming.

Unlike conventional sports-related injuries that involve sudden neck movements, this case indicates that even repetitive muscle contractions can induce sufficient mechanical stress to compromise vertebral artery integrity. Mechanically induced VAD typically results from shear forces acting on the vertebral artery during neck rotation, hyperextension, or repetitive muscular strain [3]. These stresses can cause a tear in the intimal layer, allowing blood to enter the arterial wall and form an intramural hematoma, which may compress the true lumen or lead to thromboembolism [3].

Ultrasound examination of the vertebral arteries was not performed in this case. While MRA provided sufficient diagnostic information, the absence of ultrasound limits a multimodal imaging approach and reduces the opportunity to assess dynamic vascular changes or intimal abnormalities in real-time. Recent literature on vascular dissections underscores the diagnostic value of sonographic features in detecting intimal injury, even in non-cervical arteries [9]. Although focused on abdominal aortic dissection, these principles may inform understanding of arterial wall shear stress mechanisms involved in cervical dissections. Moreover, Arning et al provide a comprehensive overview of VAD imaging, including Doppler ultrasound findings and MRI characteristics such as crescentic intramural hematoma and tapered occlusion [10], which were consistent with our case. These references highlight both the mechanical vulnerability of the vertebral artery and the utility of multimodal imaging in confirming dissection.

This case underscores the need for awareness regarding the potential cerebrovascular risks associated with gaming-based exercise, not only among clinicians and game users but also among the general public. Home fitness video games offer the advantage of accessible physical activity without specialized equipment [3]. However, improper form or excessive exertion may pose health risks. Although the temporal association between the onset of symptoms and the gaming activity suggests a possible contributory role, a definitive causal relationship between the fitness video game and VAD cannot be conclusively established in this single case.

Conclusions

This case highlights the potential for high-intensity video game-based exercise to induce VAD, particularly in sedentary individuals. As home fitness gaming continues to grow in popularity, clinicians should remain aware of possible cerebrovascular complications. Moreover, the general public should be advised that abrupt or strenuous physical activity – even when gamified – can pose risks when performed without proper conditioning or technique.