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Ann Med Surg (Lond)
Ann Med Surg (Lond)
MS9
Annals of Medicine and Surgery
2049-0801
Lippincott Williams & Wilkins Hagerstown, MD

10.1097/MS9.0000000000000260
00038
3
Case Reports
Lateral medullary syndrome: uncommon form of brainstem stroke
Ahmed Ibrahim Abdiwahid MD drabdiwahid00@gmail.com

Bakir Ahmet MD drcu2001@gmail.com

http://orcid.org/0000-0002-6039-5054
Osman Sidow Nor MD ziidoow113@gmail.com

Mohamed Ali Abdiladhif MD cabdiladiif9@gmail.com

Farah Osman Mohamed MD mfhidig@gmail.com

Ahmed Abdulkadir MD Abdulkadirahmedharaf@gmail.com

http://orcid.org/0000-0001-7236-1524
Sheikh Hassan Mohamed MD dr.m.qalaf@gmail.com

Department of Neurology, Mogadishu Somali Turkish Training and Research Hospital, Mogadishu, Somalia
* Corresponding author. Address: Department of Neurology, Mogadishu Somali Turkish Training and Research Hospital, Mogadishu, Somalia. Tel: +2525615681600. E-mail address: abdiwahid00@gmail.com (A. Ahmed Ibrahim).
3 2023
17 2 2023
85 3 542544
28 9 2022
8 1 2023
Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc.
2023
https://creativecommons.org/licenses/by-nc-sa/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. http://creativecommons.org/licenses/by-nc-sa/4.0/

Introduction and Importance:

Lateral medullary syndrome (LMS) is a less common form of a brainstem stroke. It is the result of occlusion of the posterior inferior cerebellar artery (PICA). It is caused by atherosclerosis, thrombosis, or emboli from another source.

Case Presentation:

A 60-year-old male patient presented to the emergency department with vertigo, vomiting, slurred speech, hiccups, and left-side weakness associated with paresthesia for 1 day. He had a past medical history of uncontrolled hypertension and a smoking habit. The neurological examination revealed ataxia, and left hemiparesis associated with paresthesia. A cranial nerve examination revealed slight right-sided ptosis, mouth deviation, and loss of sensory sensation on the right side of the face. Brain MRI showed right medullary infarct consistent with LMS. Electrocardiogram, echocardiography, and vertebral artery color Doppler were normal. He was admitted to the neurology ward and was treated with low molecular weight heparin 60 mg subcutaneously, aspirin 300 mg, neuroprotective agents, and antihypertensive treatment. After 6 days of medical treatment, his condition has improved massively (dysarthria and dysphagia disappeared). He was discharged for physical rehabilitation.

Clinical Discussion:

LMS (Wallenberg syndrome) is one of the brainstem stroke syndromes caused by occlusion of PICA. Vertigo, vomiting, dysphagia, dysarthria, ipsilateral ataxia, Horner’s syndrome, and contralateral hemiparesis define this syndrome. Brain MRI is necessary for diagnosis alongside clinical syndrome.

Conclusion:

LMS is a rare form of brainstem stroke and carries a favorable prognosis if early hospitalization and treatment is applied. Brain MRI, including diffusion sequence, is the most useful diagnostic tool for detecting LMS.

Keywords:

brainstem stroke
lateral medullary syndrome
PICA
OPEN-ACCESSTRUE
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pmcHighlights

Lateral medullary syndrome (Wallenberg syndrome) is one of the rare forms of brainstem stroke syndromes caused by the occlusion of posterior inferior cerebellar artery.

This syndrome is characterized by ipsilateral ataxia, Horner’s syndrome, vertigo, dysphagia, dysarthria, and contralateral hemiparesis.

Along with the clinical scenario, a brain MRI with diffusion is required for the diagnosis of this syndrome.

Here we presented a 60-year-old male patient with the lateral medullary syndrome who was successfully treated.

Introduction

In 1808 Gaspard Vieusseux first reported the lateral medullary syndrome (LMS). It was between 1895 and 1905 when Wallenberg described this syndrome in detail both clinically and via autopsy1. LMS (Wallenberg syndrome) is one of the less common forms of brainstem stroke syndromes caused by infarction of the dorsolateral medulla due to occlusion of the posterior inferior cerebellar artery, a branch of the vertebral artery2,3.

Patients with this syndrome present with crossed hemisensory/motor deficits (e.g. ipsilateral face, contralateral body), ipsilateral Horner syndrome, and vertigo, nausea, vomiting, ataxia, dysphagia, hiccups, and dysarthria4. Some other associated, less common neurological presentations include nystagmus, diplopia, and possibly palatal myoclonus5. Recognition of this syndrome is of particular importance due to some similarities with other brainstem strokes. Brain MRI, including diffusion sequence, is the mainstay of diagnosis of posterior circulation infarcts, including LMS6,7. This syndrome has a favorable prognosis if the diagnosis is made and early treatment is initiated8. Here, we present a 60-year-old male patient who was admitted to our neurology department due to lateral medullary infarction consistent with Wallenberg syndrome.

Case presentation

A 60-year-old male patient presented to the emergency department with vertigo, vomiting, hiccups, ataxia, and left-side hemiparesis associated with paresthesia for 1 day. The patient also had slurred speech and dysphagia. He had a past medical history of uncontrolled hypertension and had used khat (Catha edulis) and cigarette smoking for 40 years.

On examination, the patient looks lethargic and not oriented to time, place, and person. His Glasgow coma scale was 9/15 (eye – 3, verbal – 3, and motor – 3). On admission, his blood pressure of 156/85 mmHg and a pulse rate of 89 beats per minute. Other vital signs were unremarkable. The neurological examination revealed truncal ataxia, and left-side hemiparesis with power 4/5 associated with paresthesia. His speech was dysarthric, but his comprehension was intact. He had moderate dysphagia. His palate was midline and did not deviate. Plantar reflex resulted in plantar flexion of all the toes (Babinski sign negative). Coordination assessment with finger-to-nose and heel-to-shin testing revealed severe right-sided dysmetria. When sitting, the patient had marked truncal ataxia, with a tendency to fall to the right. All deep tendon reflexes and plantar reflexes were normal.

A cranial nerve examination revealed slight ptosis of the right side, mouth deviation, and loss of sensory sensation on the right side of the face. Other systemic examinations were unremarkable. Brain MRI diffusion showed a right medullary infarct consistent with Wallenberg syndrome (see Fig. 1). Electrocardiogram, echocardiography, and chest X-ray showed normal findings. Carotid and vertebral artery color Doppler did not show any significant stenosis or narrowing.

Figure 1 (A, B) Diffusion brain MRI showing diffusion restriction (hyperintensity in diffusion-weighted imaging and hypointensity in apparent diffusion coefficient) in the right lateral medulla consistent with Wallenberg syndrome.

Due to a delay in hospital arrival, the patient missed the golden hours of thrombolytic treatment with a tissue plasminogen activator. He was admitted to the neurology ward and was treated with low molecular weight heparin, 60 mg subcutaneously, aspirin 300 mg, amilodipine 10 mg, and other neuroprotective agents. After 6 days of hospital treatment, his condition has improved massively (dysarthria and dysphagia have almost disappeared). He was discharged for physical rehabilitation. At the outpatient follow-up 1 month later, the ataxia resolved, and the patient continued physical rehabilitation. This case has been reported in line with the Surgical CAse REport (SCARE) 2020 criteria9.

Discussion

LMS is a rare form of ischemic stroke that is frequently caused by thrombosis or embolism from the heart or large arteries10. Hemorrhage, dissection of the vertebral artery, cavernous angioma, and malignancies are additional causes of this syndrome11. The majority of cases reported in LMS stroke registries have vertebral artery dissection and large artery atherosclerosis as major risk factors12,13. In younger patients, vertebral artery dissection is the major risk factor for LMS or those with a history of trauma, whereas in adult patients, atherosclerosis is the major risk factor, more specifically hypertension, diabetes, and coronary artery disease14,15. LMS is the most prevalent brainstem ischemic stroke syndrome, yet less common when compared to other forms of stroke. 75% of LMS cases are atherothrombotic in large arteries, 17% are cardioembolic, and the remaining 8% are due to vertebral artery dissection16,17.

LMS patients have different clinical presentations depending on the affected anatomic structure. These include gaze abnormalities, vertigo, ataxia, nausea and vomiting, a nasal voice, dysphonia, hoarseness, reduced pain and temperature sensations on the same side of the face, and contralateral body weakness (this is due to damage to the crossing corticospinal tract). Also, there may be an absence of taste sensation, decreased gag reflex, and dysphagia18,19. Our case had vertigo, vomiting, dysphagia, hiccups, ataxia, and left-sided hemiparesis associated with paresthesia, slight ptosis, mouth deviation, and loss of sensory sensation on the right side of the face. In our approach to diagnosing this case, we did a perfect neurological examination. According to the patient, the neurological examination findings were consistent with LMS, but in order to confirm it, we did a diffusion brain MRI and showed a right lateral medullary infarction.

As with other forms of ischemic stroke, patients with LMS who come to the emergency room within 4.5 h of the onset of symptoms can benefit from an intravenous tissue plasminogen activator if there are no contraindications. Furthermore, for secondary prevention, anticoagulation, antiplatelet, and risk factor control are required7,20,21. The patient was not given a tissue plasminogen activator due to a delay in the thrombolytic therapy period. He was admitted to the neurology ward and treated with low molecular weight heparin 0.6 subcutaneously, aspirin 300 mg, amlodipine 10 mg, and other neuroprotective agents. After a week of hospital treatment, his condition has improved massively (dysarthria and dysphagia have almost disappeared). He was discharged for physical rehabilitation. At the outpatient follow-up 1 month later, the ataxia resolved, and he was in physical rehabilitation.

Conclusion

Identification of symptoms and signs associated with LMS is crucial for the diagnosis of this syndrome. The outcome of patients with this syndrome is variable, and recovery may take several weeks or months following treatment. Early recognition and management are vital for better recovery. The current case had significant improvement after successful management.

Ethical approval

Ethical approval is not required in our institution. However, written informed consent was obtained from the patient for the publication of this case report and the accompanying image.

Patient consent

Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Sources of funding

The authors declared that this study received no financial support.

Author contribution

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Conflicts of interest disclosure

The authors declare no conflicts of interest.

Research registration unique identifying number (UIN)

Name of the registry: NA.

Unique identifying number or registration ID: NA.

Hyperlink to your specific registration (must be publicly accessible and will be checked): NA.

Guarantor

Abdiwahid Ahmed Ibrahim, the corresponding author.

Provenance and peer review

Not commissioned, externally peer-reviewed.

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

Published online 17 February 2023
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