Lateral medullary syndrome

• Diaphragm pacing for central hypoventilation syndrome due to unilateral cerebellomedullary infarction: illustrative case
• Endovascular treatment of a craniocervical junction dural arteriovenous fistula associated with lateral medullary syndrome: A case report
• Collaboration Between Emergency Medicine and Optometry Aids in Diagnosing Atypical Wallenberg Syndrome in a 37-Year-Old Female
• A Case of Wallenberg Syndrome Presenting With Thunderclap Headache and Delayed Diagnosis Due to Negative Findings on Two MRI Examinations
• Mastering Vacuum Swallowing to Improve Pharyngeal Bolus Passage by Creating Negative Pressure in the Esophagus: A Case Report of Two Patients
• Lateral Medullary Infarction Presenting as Opalski Syndrome Associated with Headache Attributed to Orthostatic Hypotension
• A Delayed Onset of Lateral Medullary Syndrome: A Case Report
• Urinary Retention and Body Lateropulsion by Lateral Medullary Infarction: A Case Report

Lateral medullary syndrome (also called Wallenberg syndrome and posterior inferior cerebellar artery syndrome) is a disorder in which the patient has a constellation of neurologic symptoms due to injury to the lateral part of the medulla, resulting in tissue ischemia and necrosis.

Classically attributed to PICA occlusion, but in 80–85 % of cases the vertebral artery is also involved ¹⁾. No cases have been reported arising from brainstem hemorrhage.

This syndrome is characterized by sensory deficits affecting the trunk (torso) and extremities on the opposite side of the infarction and sensory deficits affecting the face and cranial nerves on the same side with the infarct. Specifically, there is a loss of pain and Thermoception on the contralateral (opposite) side of the body and ipsilateral (same) side of the face. This crossed finding is diagnostic for the syndrome.

Clinical symptoms include swallowing difficulty, or dysphagia, slurred speech, ataxia, facial pain, vertigo, nystagmus, Horner's syndrome, diplopia, and possibly palatal myoclonus.

Affected persons have difficulty in swallowing (dysphagia) resulting from involvement of the nucleus ambiguus, as well as slurred speech (dysarthria) and disordered vocal quality (dysphonia) . Damage to the spinal trigeminal nucleus causes absence of pain on the ipsilateral side of the face, as well as an absent corneal reflex.

The spinothalamic tract is damaged, resulting in loss of pain and temperature sensation on the opposite side of the body. The damage to the cerebellum or the inferior cerebellar peduncle can cause ataxia. Damage to the hypothalamospinal fibers disrupts sympathetic nervous system relay and gives symptoms analogous to Horner syndrome.

Nystagmus and vertigo may result in falling, caused from involvement of the region of Deiters' nucleus and other vestibular nuclei. Onset is usually acute with severe vertigo.

Palatal myoclonus may be observed due to disruption of the central tegmental tract.

Abstract A 65-year-old woman presented with sudden, severe frontal headache and nausea, initially without neurological deficits. MRI scans at presentation and 8 hours later were normal. However, progression to vertigo, right facial sensory disturbance, and dysphagia led to further imaging, which revealed a lateral medullary infarction—confirming Wallenberg syndrome. This rare case highlights thunderclap headache as an unusual initial manifestation of posterior circulation stroke.

1. Clinical Presentation and Diagnostic Surprise

The patient's presentation deviated from the classical signs of lateral medullary syndrome. Rather than vertigo or ataxia, she experienced a thunderclap headache, prompting initial concern for subarachnoid hemorrhage (SAH). However, no SAH was found, and neurological symptoms evolved over hours.

This delayed evolution underscores that thunderclap headache can, in rare instances, precede medullary infarction—a fact not widely appreciated in clinical practice.

2. Imaging Challenges in Posterior Circulation Stroke

Despite two MRIs performed within the first 8 hours, no abnormalities were detected initially. This aligns with known limitations of diffusion-weighted imaging (DWI) in the posterior fossa, where small infarcts may evade early detection due to technical factors.

Diagnostic Pearl: In evolving posterior circulation syndromes, a normal early MRI does not exclude infarction.

Comment: Repeat MRI was appropriately performed based on symptom progression. However, inclusion of high-resolution vessel wall imaging could have excluded subtle vertebral artery dissection with greater confidence.

3. Diagnostic Pitfalls and Missed Opportunities

This case reinforces a crucial teaching point: progressive neurological signs should override early negative imaging, especially in posterior fossa stroke.

Comment: A lumbar puncture could have been considered initially to rule out SAH, given the thunderclap onset. However, the development of focal signs reoriented suspicion toward ischemic stroke.

4. Treatment and Hospital Course

The patient received dual antiplatelet therapy (DAPT)—appropriate for minor non-cardioembolic stroke per CHANCE and POINT trials. Persistent dysphagia required prolonged admission and transfer to a rehabilitation center by hospital day 27.

Comment: Early speech therapy and consideration of PEG feeding should be standard in brainstem strokes with severe dysphagia.

5. Clinical Takeaways

• Thunderclap headache may rarely signal posterior circulation infarction—not only SAH.
• Initial MRI may be falsely negative in posterior fossa infarcts.
• Repeat imaging is warranted in evolving or unexplained brainstem syndromes.
• Clinical vigilance must override early negative radiology.

Conclusion

This case expands the known presentations of Wallenberg syndrome, urging caution against premature exclusion of ischemic stroke in the face of negative early imaging. It is a powerful reminder that progressive symptoms demand ongoing reassessment, and that stroke syndromes may start subtly, or unusually ²⁾

A 53-year-old female patient presenting with impaired Thermoception on the left half of her body, from the neck down, following a small infarction of the right midlateral medulla. The chronological changes in the patient's introspection regarding impairment of thermoception and the results of detailed somatosensory tests, including thermal sense, are shown in this report.

Thorough somatosensory tests, personal descriptions of symptoms, and electrophysiological quantification of similar cases are needed to improve our understanding of the neurological separation of the sensations of pain and temperature at the medullary level ³⁾.

A case of a 64-year-old female with acute-onset vertigo, nausea, and vomiting. In an emergency imaging examination, the results of computed tomography (CT) and diffusion weighted imaging (DWI) were negative. However, on 1 day post-hospital admission, a small acute infarct in the posterolateral aspect of the left medulla was detected by DWI. Extra attention should be payed to the false-negative imaging results to avoid diagnosis and treatment delay ⁴⁾.