Abstract Details

Title Hemi-body Hyperhidrosis as an Unusual Manifestation of Lateral Medullary Infarction Secondary to Vertebral Artery Dissection

Topic Cerebrovascular Disease and Interventional Neurology

Presentation(s) P1 - Poster Session 1 (8:00 AM-9:00 AM)

Poster/Presentation
Number 5-010

Objective To describe an uncommon presentation of lateral medullary infarction associated with contralateral hemi-body hyperhidrosis, providing clinical insight into the localization of sympathetic inhibitory pathways within the lateral medulla.

Background Lateral medullary syndrome (Wallenberg’s syndrome) typically presents with crossed sensory deficits, dysarthria, ataxia, and autonomic dysfunction such as ipsilateral Horner’s syndrome. Hyperhidrosis, however, is a rare and under-recognized manifestation.

Design/Methods NA

Results A 54-year-old man with a history of hypertension, hyperlipidemia, and chronic neck pain presented with acute right facial numbness and tingling, left hemi-body numbness and tingling, dysarthria, gait imbalance, right sided ptosis, and exacerbated right-sided neck pain. Examination confirmed crossed sensory deficits, dysarthria, gait ataxia, and partial right sided Horner’s syndrome. Notably, he exhibited pronounced hyperhidrosis of the left hemi-body. MRI revealed a right lateral medullary infarct, and vascular imaging demonstrated acute dissection of the V3 and V4 segments of the right vertebral artery. It is known that descending sympathetic fibers originate in the hypothalamus and travel ipsilaterally through the brainstem without decussation, explaining ipsilateral Horner’s syndrome when disrupted. However, interruption of descending inhibitory fibers within the lateral medulla may disinhibit contralateral sympathetic outflow, producing contralateral hyperhidrosis as observed in this case.

Conclusions Previous studies have suggested sympathetic inhibitory pathways running through the ventrolateral medulla. This case highlights contralateral hemi-body hyperhidrosis as an atypical but localizing sign of lateral medullary infarction. Recognition of this finding enhances understanding of the dual sympathetic regulatory role of the lateral medulla and may assist in more precise clinical localization of posterior circulation strokes and provide further evidence of a sympathetic modulation pathway in the lateral medulla.

Authors/Disclosures
McKethan Parker, MD PRESENTER	Dr. Parker has nothing to disclose.
Ahmed M. Koriesh, MD, FAAN	Dr. Koriesh has nothing to disclose.

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