The location and characteristics of the thermal sudomotor pathways in the human brainstem: A reappraisal

Published:January 28, 2019DOI:


      • Two descending pathways related to human thermal sweating were confirmed.
      • The pathway descending in the dorsolateral tegmentum facilitates thermal sweating.
      • The plausible inhibitory pathway descends in the dorsal paramedian portion.
      • Unilateral brainstem lesions rarely cause anhidrosis,
      • Tendency of lower body swearing preservation suggest that some fiber may cross.


      To elucidate location and characteristics of the central thermoregulatory sudomotor pathway in the human brainstem, thermoregulatory sweating (TS) in 91 patients with focal brainstem lesions was studied. TS was symmetric or minimally asymmetric in 40 subjects (Group S), and was apparently asymmetric in 51 patients (Group AS). In Group AS, the main abnormality was ipsilateral segmental hypohidrosis with a varying extent, involving predominantly the upper half of the body. Lesion locations, correlations between thermoregulatory sweat test results, and other autonomic and somatic functions were compared between the groups. The results suggested following: (1) The hypothalamospinal pathway related to TS may pass through the posterior hypothalamus and descend in the dorsolateral part of the brainstem, near the spinal trigeminal and spinothalamic tracts; (2) the pathway may descend together with those related to oculosympathetic and vasoconstrictor systems, but each of these may form distinct fiber groups; (3) the majority of the central TS fibers may reach ipsilateral sudomotor sympathetic neurons of the spinal cord, even though some fibers may cross at various levels; (4) in this descending pathway, somatotopic arrangements corresponding to each of the spinal sympathetic segments must be present; (5) There may be another fiber group passing through the central to dorsal paramedian portions of the brainstem, and lesions of these fibers also result in asymmetric TS, but seldom in oculosympathetic dysfunction. This second pathway probably exerts contralateral inhibitory influence on TS, but its origin, intracerebral course and exact physiological function require further clinical investigations.


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