Article

Comparison of Single Bout Effects of Bicycle Training Versus Locomotor Training on Paired Reflex Depression of the Soleus H-Reflex After Motor Incomplete Spinal Cord Injury

Department of Physical Therapy, University of Florida, Gainesville, FL, USA.
Archives of physical medicine and rehabilitation (Impact Factor: 2.18). 08/2009; 90(7):1218-28. DOI: 10.1016/j.apmr.2009.01.022
Source: PubMed

ABSTRACT To examine paired reflex depression changes post 20-minute bout each of 2 training environments: stationary bicycle ergometer training (bicycle training) and treadmill with body weight support and manual assistance (locomotor training).
Pretest-posttest repeated-measures.
Locomotor laboratory.
Motor incomplete SCI (n=12; mean, 44+/-16y); noninjured subjects (n=11; mean, 30.8+/-8.3y).
All subjects received each type of training on 2 separate days.
Paired reflex depression at different interstimulus intervals (10 s, 1 s, 500 ms, 200 ms, and 100 ms) was measured before and after both types of training.
(1) Depression was significantly less post-SCI compared with noninjured subjects at all interstimulus intervals and (2) post-SCI at 100-millisecond interstimulus interval: reflex depression significantly increased postbicycle training in all SCI subjects and in the chronic and spastic subgroups (P<.05).
Phase-dependent regulation of reflex excitability, essential to normal locomotion, coordinated by pre- and postsynaptic inhibitory processes (convergent action of descending and segmental inputs onto spinal circuits) is impaired post-SCI. Paired reflex depression provides a quantitative assay of inhibitory processes contributing to phase-dependent changes in reflex excitability. Because bicycle training normalized reflex depression, we propose that bicycling may have a potential role in walking rehabilitation, and future studies should examine the long-term effects on subclinical measures of reflex activity and its relationship to functional outcomes.

0 Bookmarks
 · 
70 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Postactivation depression is decreased in patients with spasticity and partially restored by physical exercise in spinal cord injured patients. Up until now, the possibility to modulate postactivation depression with motor training has never been explored in subjects with spasticity following brain lesions. Postactivation depression, assessed as frequency related depression of soleus H-reflex, was investigated before and after robotic-assisted gait training in a group of seven subjects with spastic hemiparesis following hemispheric stroke. Patients received three sessions per week of robotic-assisted gait training for a period of 4 weeks (12 sessions in total). Postactivation depression was measured before the treatment (T0), after the first session (T1) and after the last session (T2). Postactivation depression was quantified as the ratio between H-reflex amplitude at 1Hz and at 0.1Hz. The greater the 1Hz/0.1Hz ratio, the smaller the postactivation depression. Following robotic-assisted gait training, the 1Hz/0.1Hz ratio decreased from 0.79±0.26 at T0 to 0.56±0.18 at T1 and 0.58±0.13 at T2. Post hoc analysis showed a significant difference between T0 and T1 and between T0 and T2, stating an increase of postactivation depression. No significant differences were found between T1 and T2. This study provides the first demonstration that physical exercise can determine a partial normalization of postactivation depression in hemiparetic patients with spasticity following unilateral hemispheric stroke.
    Gait & posture 04/2013; 38(4). DOI:10.1016/j.gaitpost.2013.03.011 · 2.58 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Spasticity is the velocity-dependent increase in muscle tone due to the exaggeration of stretch reflex. It is only one of the several components of the upper motor neuron syndrome (UMNS). The central lesion causing the UMNS disrupts the balance of supraspinal inhibitory and excitatory inputs directed to the spinal cord, leading to a state of disinhibition of the stretch reflex. However, the delay between the acute neurological insult (trauma or stroke) and the appearance of spasticity argues against it simply being a release phenomenon and suggests some sort of plastic changes, occurring in the spinal cord and also in the brain. An important plastic change in the spinal cord could be the progressive reduction of postactivation depression due to limb immobilization. As well as hyperexcitable stretch reflexes, secondary soft tissue changes in the paretic limbs enhance muscle resistance to passive displacements. Therefore, in patients with UMNS, hypertonia can be divided into two components: hypertonia mediated by the stretch reflex, which corresponds to spasticity, and hypertonia due to soft tissue changes, which is often referred as nonreflex hypertonia or intrinsic hypertonia. Compelling evidences state that limb mobilisation in patients with UMNS is essential to prevent and treat both spasticity and intrinsic hypertonia.
    BioMed Research International 01/2014; 2014:354906. DOI:10.1155/2014/354906 · 2.71 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Spasticity is evident in both humans and animals following spinal cord injury (SCI) and can contribute to significant functional limitation and disruption in quality of life of patients with this disorder. This mini-review describes a number of preclinical and clinical studies that promise to improve outcomes for, especially in terms of spasticity and hyper-reflexia, patients with SCI. A gold standard for the quantification of spasticity has proved elusive, but the combination of H-reflex frequency dependent depression and a novel stretch reflex (SR) windup protocol have the potential to provide new insights. As the pathophysiology of hyper-reflexia and spasticity continue to be investigated, the documented onset in the animal model of SCI provides critical time points for further study into these complex mechanisms. The positive effects of a passive exercise protocol and several potential pharmacological interventions are reviewed as well as a novel potential mechanism of action. Further work is needed to determine additional mechanisms that are involved in SCI, and how to optimize multiple therapies to overcome some of the deficits induced by SCI.
    06/2010; 1(2):160-169. DOI:10.2478/v10134-010-0021-z

Full-text

Download
0 Downloads
Available from
Mar 12, 2015
Available from