Document Type




Format of Original

9 p.

Publication Date




Source Publication

Clinical Neurophysiology

Source ISSN


Original Item ID

doi: 10.1016/j.clinph.2007.10.013; PubMed Central: PMCID 2267914



To determine if sympathetically mediated vasoconstriction in the lower extremities is injury level dependent. Although sympathetic responses have been measured in the limbs of people with high and low level SCI using blood flow measurements, including Doppler ultrasound and venous plethysmography, a direct comparison between injury levels has not been made.


Volunteers with chronic SCI were grouped according to injury level. Above T6: high level (HL, n = 7), and T6 and below: low level (LL, n = 6). All subjects had complete motor and sensory loss. Leg arterial flows were recorded by venous occlusion plethysmography, and continuous heart rate and mean arterial pressure (MAP) were measured. The conditioning stimulus consisted of transcutaneous stimulation to the arch of the contralateral foot.


HL and LL subjects demonstrated a significant decrease in arterial conductance during stimulation with no significant difference found between groups. As expected, only group HL demonstrated a significant increase in MAP.


These results support our hypothesis that local (leg) sympathetic responses are similar for both high and low level SCI.


While low level SCI does not typically present with autonomic dysreflexia, bouts of increased reflex sympathetic activity could have ramifications for metabolism as well as renal and motor system function


Accepted version. Clinical Neurophysiology, Vol. 119, No. 2 (February 2008): 466–474. DOI. © Elsevier 2008. Used with permission.

NOTICE: this is the author’s version of a work that was accepted for publication in Clinical Neurophysiology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Clinical Neurophysiology, VOL 119, ISSUE 2, February 2008, DOI.