C ASE R EPORT N R APPORT DE CAS Lateral medullary syndrome: a diagnostic approach illustrated through case presentation and literature review Gregory S. Day, MD, MSc* 3 ; Richard H. Swartz, MD, PhD* 4 ; Jordan Chenkin, MD, MEd 41 ; Adil I. Shamji, MD I ; David W. Frost, MD 3" # ABSTRACT accident vasculaire ce ´re ´bral. L’association entre l’infarctus du bulbe late ´ral et la dissection de l’arte `re verte ´brale fait Patients with lateral medullary syndrome classically present ressortir l’importance de reconnaı ˆtre cette premie `re affection with crossed hemisensory disturbance, ipsilateral Horner au service des urgences. Moyennant le meilleur traitement syndrome, and cerebellar signs, all of which are attributable possible, le syndrome bulbaire late ´ral porte un pronostic to infarction of the lateral medulla. However, variability in the favorable quant au re ´tablissement. presentation of this syndrome is the rule, as illustrated in this case presentation and literature review. We propose an approach to diagnosis and management of the lateral Keywords: lateral medullary infarct, lateral medullary syn- medullary syndrome and illustrate the need to integrate drome, posterior fossa, stroke, vertebral artery dissection, clinical information with an understanding of brainstem Wallenberg syndrome anatomy with the goal of determining which patients require urgent neuroimaging and acute stroke therapies. The The lateral medullary (Wallenberg) syndrome arises importance of recognition of this condition in the emergency from compromise of the posterior inferior cerebellar department is underscored by the association between lateral medullary infarction and vertebral artery dissection. artery (PICA) leading to infarction of the lateral With optimal therapy, the prognosis for recovery from lateral medulla. Patients with the complete syndrome present medullary syndrome is good. with crossed hemisensory disturbance (ipsilateral face, contralateral body), ipsilateral Horner syndrome, and ´SUME ´ RE ipsilateral cerebellar signs. A historical article published Les patients qui souffrent du syndrome bulbaire late ´ral in 1961 estimated that the syndrome accounts for 2.5% pre ´ sentent ge ´ ne ´ ralement des troubles he ´ misensoriels of ischemic strokes 1 ; however, given the diagnostic croise ´s, un syndrome de Claude Bernard-Horner homolate ´ral challenges involved, this is likely an underestimate. et des signes ce ´re ´belleux, manifestations qui re ´sultent toutes Accurate interpretation of clinical signs and symptoms is d’un infarctus du bulbe late ´ral. Toutefois, le tableau clinique critical to establishing the diagnosis and determining habituel du syndrome est variable, comme en te ´moignent un which patients require urgent neuroimaging and acute expose ´ de cas et l’examen de la documentation. Nous ferons donc e ´tat de l’approche diagnostique et de la prise en charge stroke therapies. Clinical recognition of patients with du syndrome bulbaire late ´ral, et soulignerons la ne ´cessite ´ de lateral medullary infarction is of particular importance rassembler tous les renseignements d’ordre clinique et de due to its association with vertebral artery dissection in les mettre en relation avec l’anatomie du tronc ce ´re ´bral afin 15 to 26% of cases 2,3 and the favourable prognosis de distinguer les patients devant subir d’urgence des associated with optimal management. examens en neuro-imagerie et des traitements pour un From the *Division of Neurology, Department of Medicine, University of Toronto; 3 University Health Network Hospitals; 4 Sunnybrook Health Sciences Centre; and 1 Division of Emergency Medicine, Department of Medicine, University of Toronto; I Department of Family and Community Medicine, University of Toronto; " Division of General Internal Medicine, Department of Medicine, University of Toronto and #Herbert HoPingKong Centre for Excellence in Education and Practice, University of Toronto, Toronto, ON. Correspondence to: Dr. Gregory Day, Division of Neurology, University of Toronto, Toronto Western Hospital, 399 Bathurst Street, Toronto, ON M5T 2S8; gregg.day@mail.utoronto.ca. This article has been peer reviewed. � Canadian Association of Emergency Physicians CJEM 2014;16(2):164-170 DOI 10.2310/8000.2013.131059 164 2014;16(2) CJEM N JCMU Downloaded from https://www.cambridge.org/core. IP address: 192.151.151.66, on 11 Aug 2020 at 01:51:10, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.2310/8000.2013.131059
Lateral medullary syndrome CASE PRESENTATION A B A previously well 67-year-old man presented to the emergency department (ED) with a 4-hour history of vertigo, nausea, and vomiting. He had a 50-pack-year smoking history and was not taking any medications. There was no history of neck trauma or manipulation. While in the ED, his condition deteriorated. He developed slurred speech, numbness and paresthesias of the left hemibody (with preserved facial sensation), C and difficulty swallowing liquids. His blood pressure was 195/90 mm Hg, and his pulse was regular at 66 beats/min. Cardiovascular, respiratory, and abdominal examinations were all unre- markable, and his mental status was normal. Verbal comprehension, naming, and repetition were normal; however, his speech was dysarthric. Cranial nerve examination revealed right-sided ptosis and miosis, consistent with a partial Horner syndrome. The patient’s Figure 1. A , Magnetic resonance angiogram of vertebral arteries confirming occlusion of the proximal right vertebral visual fields were normal on confrontational testing, and artery ( arrow ). B , The posterior inferior cerebellar artery is his extraocular movements were full and without visualized ( arrow ). C , Diffusion-weighted image showing an nystagmus. There was symmetrical contraction of the area of restricted diffusion in the right lateral medulla, compatible with acute ischemic infarct. muscles of facial expression. Pinprick sensation was decreased throughout the right face, and his right corneal of the brain identified an area of restricted diffusion in reflex was absent. His uvula was deviated to the left, and the right lateral medulla (Figure 1C). his gag reflex was absent. There was mild pyramidal Within 48 hours, he improved dramatically. His pattern weakness in his right arm and leg (flexors weaker speech returned to normal, his dysmetria resolved, and than extensors in the arm; extensors weaker than flexors he was able to sit unassisted. Fasting blood glucose was in the leg). Deep tendon and superficial reflexes were normal, and no arrhythmias were identified with 48 normal. Sensation to pain and temperature was decreased hours of cardiac monitoring. The patient’s dysphagia below the neck on the left side. Coordination assessment persisted, requiring placement of a gastric tube. Blood with finger-to-nose and heel-to-shin testing revealed pressure control was optimized with dual antihyper- severe right-sided dysmetria. When sitting or standing, tensive therapy (an angiotensin-converting enzyme the patient had marked truncal ataxia, with a tendency to inhibitor and a thiazide diuretic). A statin was fall to the right. He was unable to ambulate. commenced for management of newly diagnosed Routine laboratory investigations and an electrocar- diogram were normal. An unenhanced (noncontrast) dyslipidemia. Smoking cessation counselling was pro- vided, and warfarin was commenced for ongoing computed tomographic (CT) scan of the brain was anticoagulation. Ten days after admission, the patient normal. The diagnosis of lateral medullary infarction was eating modified-consistency meals and was trans- was made on clinical grounds. Acute treatment with intravenous tissue plasminogen activator was not ferred to a stroke rehabilitation centre. At 3 months postdischarge, he had recovered almost entirely offered due to the delayed presentation (clinical assess- (Modified Rankin Scale [MRS] 5 1 4 ). He no longer ment was completed 6 hours following symptom onset). Magnetic resonance angiography (MRA) of the head required the gastric tube and was ambulating indepen- and neck vessels showed occlusion of the proximal right dently. Repeat neurovascular imaging prior to the 6- month follow-up showed recanalization of the vertebral vertebral artery, suspicious for extracranial dissection (Figure 1A). The PICA was patent (Figure 1B). with artery. His warfarin was discontinued, and antiplatelet supply through collateral flow via the basilar and left therapy (acetylsalicylic acid) was prescribed for long- vertebral arteries. Magnetic resonance imaging (MRI) term secondary stroke prevention. CJEM N JCMU 2014;16(2) 165 Downloaded from https://www.cambridge.org/core. IP address: 192.151.151.66, on 11 Aug 2020 at 01:51:10, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.2310/8000.2013.131059
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