A 32-yr-old active duty woman presented to the emergency room 2 d after snowboarding where she fell multiple times with one particular hard fall on the back of her head, but no loss of consciousness and she continued snowboarding. She presented with a right-sided occipital headache, along with right shoulder and neck pain, intermittent vertigo, and a general ill feeling. She had no significant medical history, and her only medication was a combined oral contraceptive. Physical examination, including a detailed neurologic examination, was normal except for a blood pressure of 154/98 mm Hg. Computerized tomography angiography (CTA) and magnetic resonance imaging (MRI) imaging obtained revealed a right vertebral artery dissecting aneurysm (VADA) in segment V2 measuring 3 mm with focal stenosis (Fig.A–C).
She was admitted for observation under the neurosurgery service and discharged 24 h later. She was placed on 500-mg naprsoyn twice a day, robaxin 500 mg every 6 h as needed, and 325 mg of aspirin daily. She was to follow-up with her primary care provider and have a repeat magnetic resonance angiography (MRA).
At follow-up with her primary care manager (PCM), she stated her pain was worse upright but relieved lying down. No lumbar puncture was performed. She also had elevated blood pressures of 156/100 mm Hg in the right arm and 136/100 mm Hg in the left arm. Her physical examination remained normal. She was started on 25 mg of propranolol and was evaluated for fibromuscular dysplasia with an MRA of her renal arteries, which results reported as normal. Symptoms gradually improved over a 3-wk time span. Propranolol was stopped at this time as her blood pressure normalized.
Follow-up imaging with MRA at 7 wk showed interval improvement and an adequately patent right vertebral artery with minimal luminal irregularity. Final follow-up imaging 3 months later was reported as normal. Her aspirin was stopped at this time.
In VADA, a disruption occurs at the intimal layer of the vessel (1). This allows the weakened vessel wall to balloon out as blood begins to push through between the vasa intima and media, creating an aneurysm that can result in an intramural hematoma (1). Additionally, this disruption can result in narrowing of vessel caliber producing stenosis (1). Our patient had both an aneurysm and intramural hematoma as seen in Figure A–C.
Vertebral artery dissecting aneurysm is thought to be an exceedingly rare disease with a reported incidence of 5 per 100,000, but it is more likely to be under diagnosed and more common than previously thought (2–6). Vertebral artery dissecting aneurysm is an important diagnosis because of the high association with ischemic stroke, especially in the young adult population (2). It represents about 25% of cases in the age ranges of 18 to 45 yr, second only to cardiac embolism (3,7). Some literature uses the term spontaneous VADA in description of cases occurring in sports, but we would argue that this would be a misnomer and better described as a traumatic VADA. Our case of VADA with snowboarding is unique; three cases to date have previously mentioned VADA with snow sports similar to our patient, but both were part of a retrospective database review (8,9). Additionally, no cases in the literature describe a postepisodic interval of hypertension following VADA without preceding history.
The vertebral artery is sectioned into V1 to V4 in ascending fashion. It comes off of the subclavian arteries and then ascends through the transverse foramen. At the C2 transverse foramen, it swings out laterally before medializing to enter the cranium. There is risk for injury at each of these sections, but the most common is between the atlas and axis of the cervical spine—the V3 section, which is depicted in Figure D (10,11). The V4 section is intracranial and has a higher association with subarachnoid bleeding and additional morbidity (1). A proposed pathophysiology for injury is that the combination of a wider atlas and the available rotation that occurs at the atlantoaxial joint, which is about 40 degrees, increases the risk for injury to the artery (12). Additionally, there is an available 30 degrees of extension at the atlantooccipital joint which could factor in.
The proposed mechanism is that when extremes of motion are reached, combined with impact or force such as in sports, high velocity cervical rotational manipulation, cough or sneeze, a tensile force on the vessel results in an injury to the innermost layer of the vessel, the intima. A tear here allows for a false lumen to be created as blood pools and pushes between the intima and media. Given the limited anatomical space, the effect of this presents similar to a stenosis with decreased blood flow to the brain. The presentation can vary because there is often anatomical variations of collateral flow with only 42% of people having a complete Circle of Willis (13). There is some evidence that there is an undiagnosed and yet to be named connective tissue disorder in about 20% of cases, where named connective tissue disorders such as Marfan’s and Ehler’s Dahnlos only account for between 1% and 5% (14).
After the inciting event, the symptoms may occur relatively quickly or take hours to develop. The most common symptom is a headache, which is seen in up to 75% of patients (15,16). When headache pain is localized to the occipital area and combined with posterior neck pain in the presence of athletic participation, a clinician should consider VADA in their differential diagnosis (15,16). The decrease of cerebral blood flow can result in a variety of symptoms that include tinnitus, vertigo, nausea, unilateral, facial numbness, dizziness, diplopia, ataxia, and dysarthria (17,18). A more obvious and severe presentation would be an infarct with the two most common sites being: lateral medullary and cerebellar (18). The lateral medullary can present as a loss of pain and temperature sensation of the contralateral trunk and ipsilateral face often with accompanying dysphagia (18). Cerebellar infarct is more likely to present with dizziness and vertigo (19).
A young patient presenting with a sudden occipital headache with any combination of the following six factors should make a clinician suspect VADA: no apparent risk factors for arteriosclerosis, posterior neck pain, face pain, any focal neurological signs, athletic participation, or recent high-velocity cervical rotational manipulation (20). On physical examination, one should look for any eye or facial findings, such as miosis, impaired conjugate adduction of the affected side eye, nystagmus, ptosis, vertigo, and sensory loss as these neurological signs would greatly increase the pretest probability of VADA. Additionally, one should also examine the extremities for weakness and sensory loss. Even isolated atypical headaches or neck pain should raise the suspicion of VADA, as one prospective case-control study on cervical artery dissection found these symptoms to be present in 24 of 24 of patients (21). When suspecting VADA, one might consider starting with an ultrasound, but prior studies have shown only a 70% to 80% sensitivity for VADA, so this should be done only as an adjunct to MRA, and only if it does not delay completion of the MRA (22–25). Typically, CT angiography would be the diagnostic test of choice for vertebral arterial dissection with a sensitivity of 100% and specificity of 98%, but MRI/MRA provides several advantages (15). An MRI/MRA is able to more easily demonstrate an intramural hematoma and has no radiation exposure (18). A reasonable approach would be to obtain an MRI/MRA and if concern still remains about a VADA, then a CT angiography should be pursued (11,15). There is controversy on the best management strategy of VADA. Given that it is not commonly diagnosed, it becomes difficult to perform a substantial comparison study of the two treatment approaches: conservative with antiplatelet/anticoagulation versus surgical endovascular stenting. A conservative treatment regimen either uses antiplatelet or anticoagulation with ideal treatment lasting 3 to 6 months (5,26). The goal is to prevent stenosis from thrombosis and embolization resulting in a ischemic stroke during this time, and this method has been shown successful with recurrence or new symptoms occurring between 1% and 10% (1,4,5,26). A randomized control study of 250 patients found no difference between anticoagulation versus antiplatelet (4). Another recent study looking at 370 carotid and vertebral artery dissection also showed no difference (26). The body of literature for surgical intervention currently lacks any randomized control trials and surgery carried a 10% complication rate in one meta-analysis for treatment of VADA (27,28). Endovascular techniques may be best used with recurrent ischemia despite conservative management or intracranial dissection (29). Although most cases can be managed conservatively, we would recommend consultation with a vascular surgeon or neurosurgeon as various studies range from 1% to 20% of subjects needing later surgical intervention (1,4,5,26).
If VADA is caught early before an ischemic stroke then long-term complications are unlikely. There is about a 2% to 4% chance that individuals will develop a new or recurrent ischemic stroke or transient ischemic attack within 3 months of VADA or internal carotid arterial dissection (1,30–32). Therefore, it would be wise to perform follow-up imaging with MRA at the 3-month time frame. Also, the majority of patients who develop serious morbidity have a good chance for significant recovery (1,32). Ultimately, the prognosis is based on lesion location, quality of the collateral blood supply, and the amount of neurological insult (33).
For a young individual presenting with posterior neck pain, occipital headache, neurological symptoms, and recent athletic participation, such as snowboarding, one should consider the diagnosis of VADA. Advanced imaging with either MRI/MRA or CT angiography is required in the evaluation. Vertebral artery dissecting aneurysm management requires consultation to a surgical specialty. Evidence-based recommendations are lacking on optimal treatment.
The authors declare no conflict of interest and do not have any financial disclosures.
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