Spinal cord injury can result in partial or complete loss of supraspinal control of sympathetic outflow below the lesion. Despite the importance of the sympathetic nervous system in autonomic dysreflexia and orthostatic hypotension, its integrity is not currently assessed in the clinical determination of lesion level - only motor and sensory pathways are examined. The aim of this thesis was to develop non-invasive means of assessing the integrity of sympathetic pathways following human spinal cord injury. Brief innocuous electrical stimuli applied to the forehead evoked cutaneous vasoconstrictor and sudomotor responses in the fingers and toes of able-bodied subjects, which were abolished by complete spinal lesions. Application of these same stimuli to the abdominal wall (below lesion) generated long-lasting cutaneous vasoconstriction (but not sweat release) and significant increases in blood pressure that accumulated with repeated stimuli. Moreover, the magnitude and duration of these spinal somatosympathetic reflexes did not depend on the number of impulses or duration of the sensory input, suggesting that only the initial part of the sensory barrage elicits reflex responses. This work has shown that cutaneous vascoconstriction provides a more robust measure of the integrity of sympathetic pathways than does sweat release. This was confirmed during natural stimulation of somatic afferents during vibroejaculation, which caused marked increases in blood pressure and marked cutaneous vasoconstriction but negligible sweat release below lesion. Muscle vasoconstrictor function below lesion was assessed by asking subjects to perform a maximal inspiratory breath-hold, which is known to cause a sustained activation of muscle vasoconstrictor neurones that counteracts the fall in blood pressure in able-bodied subjects. Blood pressure remained low in paraplegics and, especially, quadriplegics during this manouevre; importantly, heart rate showed a linear increase only in the spinal patients. In the absence of blood pressure measurements, the latter infers an interruption of descending muscle vasoconstrictor pathways. In conclusion, this thesis has demonstrated simple, non-invasive techniques that can be utilised to assess the function of the sympathetic nervous system in spinal cord injury, and highlighted the need to assess the injury in terms of the integrity of the sympathetic nervous system below the lesion level.

Spinal cord injury can result in partial or complete loss of supraspinal control of sympathetic outflow below the lesion. Despite the importance of the sympathetic nervous system in autonomic dysreflexia and orthostatic hypotension, its integrity is not currently assessed in the clinical determination of lesion level - only motor and sensory pathways are examined. The aim of this thesis was to develop non-invasive means of assessing the integrity of sympathetic pathways following human spinal cord injury. Brief innocuous electrical stimuli applied to the forehead evoked cutaneous vasoconstrictor and sudomotor responses in the fingers and toes of able-bodied subjects, which were abolished by complete spinal lesions. Application of these same stimuli to the abdominal wall (below lesion) generated long-lasting cutaneous vasoconstriction (but not sweat release) and significant increases in blood pressure that accumulated with repeated stimuli. Moreover, the magnitude and duration of these spinal somatosympathetic reflexes did not depend on the number of impulses or duration of the sensory input, suggesting that only the initial part of the sensory barrage elicits reflex responses. This work has shown that cutaneous vascoconstriction provides a more robust measure of the integrity of sympathetic pathways than does sweat release. This was confirmed during natural stimulation of somatic afferents during vibroejaculation, which caused marked increases in blood pressure and marked cutaneous vasoconstriction but negligible sweat release below lesion. Muscle vasoconstrictor function below lesion was assessed by asking subjects to perform a maximal inspiratory breath-hold, which is known to cause a sustained activation of muscle vasoconstrictor neurones that counteracts the fall in blood pressure in able-bodied subjects. Blood pressure remained low in paraplegics and, especially, quadriplegics during this manouevre; importantly, heart rate showed a linear increase only in the spinal patients. In the absence of blood pressure measurements, the latter infers an interruption of descending muscle vasoconstrictor pathways. In conclusion, this thesis has demonstrated simple, non-invasive techniques that can be utilised to assess the function of the sympathetic nervous system in spinal cord injury, and highlighted the need to assess the injury in terms of the integrity of the sympathetic nervous system below the lesion level.

Thesis (M.Nsg.) -- Flinders University, School of Nursing and Midwifery. / Typescript (bound). Includes bibliographical references (leaves 106-146). Also available online.

Thesis (M.S.)--Purdue University, 2004. / Includes bibliographical references (leaves 48-52). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Thesis--(M.S.)--University of Michigan, 1983. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaf 50).

Thesis (M.S.)--University of Wisconsin--Madison, 1970. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M. Med. Sc.)--University of Hong Kong, 1999. / Includes bibliographical references (leaves 43-48).

Thesis (PH.D.)--Michigan State University. Kinesiology, 2008. / Title from PDF t.p. (viewed on Aug. 11, 2009) Includes bibliographical references. Also issued in print.

Thesis (M.Med.Sc.)--University of Hong Kong, 1999. / Includes bibliographical references (leaves 43-48). Also available in print.

Thesis (M.S.)--Brock University, 2009. / Includes bibliographical references (leaves 42-53).