Traumatic vertebral artery dissection and Wallenberg syndrome after a motorcycle collision

Wallenberg syndrome is also called lateral medullary syndrome or posterior inferior cerebellar artery syndrome. The clinical presentations include ipsilateral Horner syndrome, ipsilateral cerebellar signs, and the hypalgesia of ipsilateral face and contralateral body. A considerable number of cases of Wallenberg syndrome were reported to be associated with vertebral artery dissection (VAD). Nowadays, the preferred imaging tool comes down to magnetic resonance imaging because it provides high spatial resolution, which is especially important for assessment of lesions in posterior fossa. The optimal treatment of VAD remains controversial. Most patients receive conservative treatments with anticoagulants or antiplatelet drugs. Overall, most cases have good prognosis. However, the rarity and various presentations of VAD may challenge emergency physicians in making correct diagnosis in the emergency department. Hence, maintaining a high index of suspicion is needed for an early diagnosis, especially in young people without risk factors attributing to cerebrovascular accident. Wallenberg syndrome is also called lateral medullary syndrome or posterior inferior cerebellar artery (PICA) syndrome. The clinical presentations include ipsilateral Horner syndrome, ipsilateral cerebellar signs, and hypalgesia of ipsilateral face and contralateral body. Like its name, the typical occlusive vessel is the PICA. However, a considerable number of cases of Wallenberg syndrome were reported to be associated with vertebral artery dissection (VAD) [1]. Two most common causes of nonspontaneous VAD were reported as spinal manipulation and trivial trauma [2]. This article reports a case of traumatic VAD presented with PICA syndrome after a motorcycle collision. A 38-year-old man experienced mild neck tenderness after a motorcycle collision. He had worn a helmet and fell down to the left when he became involved in a minor traffic accident. There was no initial loss of consciousness or vomiting. He did not seek medical help immediately. Ten hours later, he developed sudden onset of vertigo, nausea, dysarthria, unsteady gait, and numbness at the right side of his body. He lost consciousness and became apneic on the way to our hospital. Intubation with ventilation support for this patient was performed by an emergency medical technician in the ambulance, and he became conscious soon. Upon arriving at our emergency department, he had a Glasgow Coma Scale of E4V_TM5, a blood pressure of 121/66 mm Hg, a heart rate of 110 beats/min, and a body temperature of 36°C. The patient did not have a history of any systemic disease. Right horizontal nystagmus, ptosis, and hemifacial anhydrosis were noted. Right dysmetria and subjective numbness over the right side of the face and left side of the body and the limb were also described. Bilateral muscle power score was 5, and Barbinski signs showed normal values. There was no obvious ecchymosis or hematoma seen over his neck or body. The radiographic examinations of the chest, lateral view of the cervical spine, and anterio-posterior view of the pelvis were unremarkable. The electrocardiography disclosed normal sinus rhythm, and laboratory results were all within normal limits. The patient still experienced occipitonuchal pain. Based on the clinical presentations, brainstem or cerebellar infarction was highly suspected. Magnetic resonance imaging (MRI) of the brain showed that there were areas of hypointensity on T₁-weighted images and hyperintensity on T₂-weighted images at the right half of the medulla oblongata and the inferior cerebellar peduncle (Fig. 1). Magnetic resonance angiography (MRA) disclosed markedly decreased signal in the entire right vertebral artery (VA) with irregularity from its origin to the intradural segment, suggesting high-grade stenosis and dissection of the entire right VA (Fig. 2). Computed tomography (CT) angiography of the head and neck disclosed a filling defect with luminal dilation over the right VA. An intraluminal flap was also visible (Fig. 3). The result of angiography demonstrates total occlusion of the right extraspinal VA (V3) and intracranial VA (V4) (Fig. 4). The patient was admitted to the intensive care unit for further observation and management. Diplopia, dysphagia, and hiccup developed after he was admitted. A nasogastric tube was placed because of swallowing difficulty. Aspiration pneumonia ensued, but he recovered after adequate antibiotic therapy. After anticoagulant therapy and other conservative treatments, he was discharged 17 days later with sequelae of unstable gait and difficulty in swallowing. Nasogastric tube was not indicated anymore based upon videoesphagrographic evidence 3 months later. Vertebral artery dissection may be spontaneous or traumatic. Aside from chiropractic manipulation, trivial trauma resulting in traumatic VAD was also reported [2]. According to a case series, clinical symptoms consistent with VAD started in 55% of patients within 12 hours after neck manipulation [3]. Vertebrobasilar artery dissection typically occurs in adults with a mean age of 44 years [4-5]. The cardinal symptoms include occipital headache or neck pain and symptoms of vertebrobasilar circulation ischaemia. However, many cases reported presented with delayed emerging neurologic symptoms and signs after a trauma episode [6-7]. However, brain CT and CT angiography still have limitations to detect small infarctions in brain stem or cerebellum. They show only the consequence of VAD, for example, subarachnoid hemorrhage (SAH). In the past, the golden standard to diagnose VAD relied on angiography [8]. Nowadays, the preferred imaging tool comes down to MRI because it provides high spatial resolution, which is especially important for posterior fossa lesion assessment [9]. Combined with MRA, MRI may clearly demonstrate the stenotic vessel and decide the age of intravascular hematoma [10]. The optimal treatment of VAD remains controversial [11]. Some researches recommended the application of anticoagulants for extracranial VAD without SAH because of high risk of recurrent emboli event [12-13]. Surgical intervention and endovascular treatment are reserved for VAD complicated with SAH [4,14-16]. With conservative managements, most cases have good prognosis [17]. The dissecting vessel will recanalize in a few weeks or months [18]. Poor prognosis is associated with SAH and those with basilar artery involvement [14-16]. Vertebral artery dissection should be considered as a cause of posterior circulation infarction in patients with a head or neck injury history, even it is trivial. The rarity and various presentations of VAD may challenge emergency physicians in making diagnoses. We want to remind emergency department physicians to maintain a high index of suspicion, especially in young people without risk factors attributing to cerebrovascular accident.