Document Type

Article

Language

eng

Format of Original

9 p.

Publication Date

2-2008

Publisher

Elsevier

Source Publication

Clinical Neurophysiology

Source ISSN

1388-2457

Original Item ID

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

Abstract

Objective

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.

Methods

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.

Results

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.

Conclusions

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

Significance

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

Comments

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.

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