Spinal inhibitory mechanisms following cord transection in man
Spinal inhibitory mechanisms following cord transection in man
Clinical spasticity is found in many pathological conditions and is generally thought to be due to a failure in the control of motoneurone (MN) output. A convenient method of estimating MN output is offered by the soleus H-reflex. This has been used in the past to examine the effect of conditioning stimuli in MN activity in an attempt to develop a neurophysiological definition of spasticity. One such conditioning protocol is known as D1 and has been clearly defined in normal subjects. Traumatic cord section would seem to offer a useful experimental model by excluding uncontrollable descending influences. Most injuries of this type are, however, not complete. Fifty spinal injury patients with established, clinically complete lesions were included in the initial study. Despite gross spasticity they were found not to have abnormally excitable MNs as judged by H-reflex data. D1 inhibition was very significantly increased in these subjects. The development of this abnormality was then studied by examining patients immediately after injury whilst still in spinal shock. This period of profound reflex depression as measured by tendon jerk was found to be associated in most cases with H-reflex preservation and this was of clear prognostic significance. The D1 abnormality was always immediately fully present whenever there was an H-reflex to test it on. Some patients were receiving Functional Electrical Stimulation (FES). This had no effect on their neurophysiological data but features of the quadriceps EMG were noted which may be of use in monitoring this treatment. Some aspects of antispasmodic therapy were examined but little precise information was forthcoming. Combined H-reflex and urological data supported earlier work in suggesting that these patients had a second, neurophysiological, lesion distal to the anatomical one. The principle conclusions of this work were then combined to yield a proposed neurological mechanism to explain the neurophysiological findings.
University of Southampton
Benfield, John Edward Charles
1990
Benfield, John Edward Charles
Benfield, John Edward Charles
(1990)
Spinal inhibitory mechanisms following cord transection in man.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
Clinical spasticity is found in many pathological conditions and is generally thought to be due to a failure in the control of motoneurone (MN) output. A convenient method of estimating MN output is offered by the soleus H-reflex. This has been used in the past to examine the effect of conditioning stimuli in MN activity in an attempt to develop a neurophysiological definition of spasticity. One such conditioning protocol is known as D1 and has been clearly defined in normal subjects. Traumatic cord section would seem to offer a useful experimental model by excluding uncontrollable descending influences. Most injuries of this type are, however, not complete. Fifty spinal injury patients with established, clinically complete lesions were included in the initial study. Despite gross spasticity they were found not to have abnormally excitable MNs as judged by H-reflex data. D1 inhibition was very significantly increased in these subjects. The development of this abnormality was then studied by examining patients immediately after injury whilst still in spinal shock. This period of profound reflex depression as measured by tendon jerk was found to be associated in most cases with H-reflex preservation and this was of clear prognostic significance. The D1 abnormality was always immediately fully present whenever there was an H-reflex to test it on. Some patients were receiving Functional Electrical Stimulation (FES). This had no effect on their neurophysiological data but features of the quadriceps EMG were noted which may be of use in monitoring this treatment. Some aspects of antispasmodic therapy were examined but little precise information was forthcoming. Combined H-reflex and urological data supported earlier work in suggesting that these patients had a second, neurophysiological, lesion distal to the anatomical one. The principle conclusions of this work were then combined to yield a proposed neurological mechanism to explain the neurophysiological findings.
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Published date: 1990
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Local EPrints ID: 458317
URI: http://eprints.soton.ac.uk/id/eprint/458317
PURE UUID: f4286ef0-aafa-4ae2-8fd6-ec3402091ac7
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Date deposited: 04 Jul 2022 16:46
Last modified: 04 Jul 2022 16:46
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Author:
John Edward Charles Benfield
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