Late contralateral hyperhidrosis in lateral medullary infarcts

• Published in: Stroke (1970) Vol. 27; no. 5; pp. 991 - 995
• Main Authors: ROUSSEAUX, M, HURTEVENT, J. F, BENAIM, C, CASSIM, F
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.05.1996; American Heart Association, Inc
• Subjects: Adult; Biological and medical sciences; Cerebral Infarction - physiopathology; Disorders of higher nervous function. Focal brain diseases. Central vestibular syndrome and deafness. Brain stem syndromes; Electric Stimulation; Female; Follow-Up Studies; Functional Laterality; Humans; Hyperhidrosis - etiology; Male; Median Nerve - physiology; Medical sciences; Medulla Oblongata; Middle Aged; Nervous system (semeiology, syndromes); Neurology; Reflex; Skin - innervation; Sympathetic Nervous System - physiopathology; Time Factors; Human; Cerebral infarction; Skin disease; Nervous system diseases; Cardiovascular disease; Cerebral disorder; Vascular disease; Case study; Symptomatology; Hyperhidrosis; Central nervous system disease; Diseases of the autonomic nervous system; Cerebrovascular disease; Sweat gland disease
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.STR.27.5.991

This study describes unilateral increases of sweating reactions observed in the months after contralateral medullary infarct; evaluation of sympathetic cutaneous response may help to explain sweating disorders. After the discovery of the clinical phenomenon in one case, patients admitted between 1990 and 1993 were systematically evaluated clinically and electrophysiologically. In a group of five patients presenting with lateral or dorsal medullary lesions, two exhibited an increase of contralateral sweating reactions that appeared 6 to 8 months after stroke, were elicited by effort and exposure to heat and stress, and were more severe over the forehead, face, and upper trunk. In one case, this was clinically associated with an absence of sweating on the side of the lesion. During the late phase after stroke, in three patients presenting with lateral medullary lesions, electrophysiological evaluation revealed significant asymmetry of the sympathetic skin response, which was higher on the side contralateral to the lesion than on the ipsilateral side. In one patient, no response could be elicited by stimulations applied on the side of the lesion. Contralateral hyperhidrosis can be observed in the late phase after lateral medullary infarct and is likely due to lesion of the sympathetic pathway passing through the lateral medulla, which inhibits sudomotor neurons. Evaluation of sympathetic skin response may help to explain such clinical disorders.