Challenge Case Report: Left-Sided Headache & Dizziness
Clinical Presentation
Mr O, age 57 with no significant past medical history, was brought to the emergency department (ED) by emergency medical services (EMS) with left-sided headache and dizziness. He reports that symptoms began 8 hours earlier, at which time he went to sleep. When he awoke 3 hours later, he felt “off balanced” and walked to the bathroom with difficulty. Mr O noted that when he ran his hands under the sink he noticed his right hand couldn’t feel the hot water.
The stroke team was alerted upon Mr O’s arrival, in consideration of his presentation and lack of prior history. He was not taking any anticoagulating medications. His initial vital signs were notable for blood pressure of 162/85 mm Hg, but were otherwise unremarkable. He was afebrile with a normal heart rate, respiration, oxygen saturation, and fingerstick blood glucose level.
On physical examination, Mr O had repeated throat clearing, fluent speech with mild dysarthria, left-sided Horner syndrome with left eyelid ptosis, and left eye miosis. He had left lower facial weakness and decreased sensation to pinprick on the right side of his face in the V1-V3 distribution. Other notable findings include left side dysmetria and dysdiadochokinesia, horizontal nystagmus, and truncal ataxia. Mr O had a National Institute of Health Stroke Scale (NIHSS) score of 6 (3 for left-sided complete hemifacial paralysis, 1 for decreased sensation, 1 for left-sided dysmetria, and 1 for dysarthria).
Diagnostic Testing and Imaging Studies
Complete blood count and blood and urine chemistry were ordered, and results showed no significant abnormalities in electrolytes, renal function, cardiac enzymes, coagulation panel, or cell counts. The only notable laboratory findings were mildly elevated hemoglobin A1c at 6.6%, hypertriglyceridemia at 191 mg/dL, and elevated low-density lipoprotein (LDL) level at 116 mg/dL.
Mr O’s ECG showed normal sinus rhythm with first-degree atrioventricular (AV) block, left axis deviation, and left ventricular hypertrophy with QRS widening (Figure 1). His chest radiograph showed enlarged cardiac silhouette and prominent ascending aorta but no other abnormality (Figure 2). Head CT without contrast showed global cerebral atrophy but no hemorrhage or other acute findings were observed. Head and neck CT angiography demonstrated a hypoplastic left vertebral artery with occlusion at the C2-C3 level to the level of the origin of the left posterior inferior cerebellar artery (PICA) (Figure 3). No other significant stenosis or large vessel occlusion were identified. Brain CT perfusion was within normal limits.
Challenge Questions
1. What area of the brainstem is usually affected by Wallenberg Syndrome?
a. Medial lemniscus
b. Lateral medulla
c. Lateral pons
d. Lower midbrain
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The correct answer is B: the lateral medulla is usually affected by Wallenberg syndrome.
2. Which artery is most likely affected by Wallenberg Syndrome?
a. Basilar artery
b. Anterior inferior cerebellar artery
c. Vertebral artery
d. Anterior spinal artery
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The correct answer is C: the vertebral artery is most likely affected by Wallenberg syndrome.
Case Resolution
Mr O was not eligible for treatment with tissue plasminogen activator (tPA) because of the time that had passed since his symptoms began (ie, he was outside the tPA window). The neurointervention team was consulted for potential endovascular intervention, but thrombectomy was not recommended because of the difficulty in accessing the left vertebral artery. There was also a risk of pushing the thrombus further into the basilar artery.
A heparin drip was recommended and initiated in the ED. Mr O was admitted to the intensive care unit (ICU) for further and frequent neurologic monitoring and medical management with permissive hypertension (goal of <220/120 mm Hg). Brain MRI was obtained emergently and showed an acute infarct of the posterior left lateral medullary velum, compatible with a diagnosis of Wallenberg syndrome (Figure 4). An associated thrombosis of the left distal vertebral artery was also identified.
In the ICU, Mr O had treatment with insulin for newly diagnosed diabetes and amlodipine for hypertension. Atorvastatin was started for secondary stroke prevention, and on Mr O’s third day in the hospital, a plan was made for bridge therapy before initiating an oral anticoagulant. Evaluation related to this plan, however, determined that Mr O was at high risk for bleeding because of his job as a construction worker. As a result, his heparin drip was stopped and dual antiplatelet therapy with aspirin and clopidogrel was initiated. Although Mr O had only mild improvement of persistent symptoms, he remained neurologically and hemodynamically stable during his hospital stay and was discharged on hospital day 5 with arrangements made for home-based physical therapy. Mr O was counseled to follow up with his primary care provider for diabetes and hypertension and with neurology in 3 months.
Discussion
Wallenberg syndrome is most commonly secondary to an occlusion of the intracranial vertebral artery, followed by the PICA, leading to a lateral medullary infarction.4,5 In this case, both the vertebral artery and left PICA were affected. Lateral medullary infarction inadvertently leads to damage to the vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguus, and sympathetic fibers.6
Mr O had dizziness, nystagmus, sense of disequilibrium, and left-sided ataxia and dysmetria suggestive of involvement of the vestibular nuclei. He also had decreased pinprick sensation on the right side of his face, suggesting involvement of the spinal trigeminal nucleus, which is atypical, because it is usually the ipsilateral face that is affected. Ipsilateral sensory abnormality in the face and contralateral limbs are common in lateral medullary infarcts. Less commonly, sensory abnormalities may be solely contralateral, as this case.7 Decreased pinprick sensation on the right upper and lower extremities suggests involvement of the lateral spinothalamic tract. Mild dysarthria and repeated throat clearing are suggestive of involvement of the nucleus ambiguus. Mr O also had ipsilateral ptosis, which could be due to involvement of the sympathetic fibers. The most common reason that leads to Wallenberg syndrome is ischemia of the vertebral artery from embolism or a thrombus. However, the second most common reason is vertebral artery dissection caused by mechanical trauma or cervical spinal manipulation.
The diagnosis of Wallenberg syndrome can easily be missed because affected individuals may present with vertigo only. Unless a detailed neurologic exam is performed, findings such as ataxia and sensory abnormalities can be missed easily. If a Wallenberg syndrome lesion involves the whole PICA territory, cerebellar infarction with edema, mass effect, and herniation are common. Considering the potentially dangerous and fatal neurologic sequelae, Wallenberg syndrome is a very important cannot-miss diagnosis. First-line treatment is tPA if the patient presents within the tPA window.
Clinicians caring for people with Wallenberg syndrome should consult with neurointerventional radiology for further recommendations. Endovascular intervention with thrombectomy is also a consideration, depending on the size of the vessel involved and ease of access. MRI should be obtained as quickly as possible to evaluate the extent of the infarct and whether there is salvageable area for endovascular intervention. When presentation is not within the tPA window and endovascular thrombectomy is not possible, as for Mr O, heparin and permissive hypertension are warranted.
Good recovery occurs in most cases of Wallenberg syndrome, with gait instability as the most common long-term sequelae.
Conclusion
It is imperative to recognize a Wallenberg stroke because it is a diagnosis that can be easily missed due to its often subtle presentation; and yet it can result in a devastating outcome. For example, in a person who presents with a chief complaint of dizziness, a cursory exam—especially in the ED—could miss truncal ataxia which may mean a posterior circulation or cerebellar stroke is not considered in the differential until the patient herniates. What is notable about this case is precisely the relatively benign presentation of the patient , who was alert, oriented, and had fluent speech.
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