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This book brings together researchers from several of the most exciting areas of spinal cord plasticity research. Format Hardcover. See details.
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Buy It Now. Add to cart. Be the first to write a review About this product. About this product Product Information The spinal cord has long been viewed as largely a conduit for neural impulses from the body to the brain and the brain to the body, with various reflexes hard wired in the structure to allow for low level control.
The past two decades of the 20th century have seen a very different view of the spinal cord emerging from the laboratories of various disciplines. Studies rooted in physiology, psychology, rehabilitation, pain control and regeneration have begun to show that the spinal cord contains neurons whose functional capacities are highly plastic. Collectively, they present not only findings in their areas, but a perspective of the broader emerging picture of spinal cord neural plasticity. Additional Product Features Number of Volumes.
Spinal Plasticity; R. Grau, R. Willis, Jr. Reggie Edgerton, et al. Bouyer, S. Wernig, et al. Show More Show Less. Any Condition Any Condition. Furthermore, BWS robotic-assisted step training also decreased biomechanical measures of reflexive joint stiffness in the ankle of SCI patients [ 17 ].
Given that some of the individual SCI patients in these studies had either motor complete or sensory-motor complete SCIs, it is likely that the plasticity in the spinal cord occurred with little or no descending supraspinal input [ 14 ]. These findings support the notion that spinal neuronal networks of patients with clinically complete, motor complete, or motor incomplete SCI have the potential to undergo a reorganization of spinal neural circuits, improve spinal reflex function, and improve walking function with BWS robotic-assisted step training.
The most notable sign of spinal plasticity following BWS robotic-assisted step training in SCI patients was the re-emergence of walking phase modulation of the soleus H-reflex [ 12 ], which can be viewed as a net plasticity of multiple spinal networks [ 14 ]. The patients tested in this study had chronic clinically complete, motor complete, and motor incomplete SCI and received an average of 45 training sessions, five days per week for one hour per day.
Following training, the soleus H-reflex was depressed at late stance, stance-to-swing transition, and swing phase initiation, allowing for a smooth transition from the stance to swing phase [ 12 ]. The soleus H-reflex remained depressed at early and mid-swing phases of the gait cycle, which fostered a reciprocal activation of the ankle flexors and extensors.
The training reorganized spinal locomotor neural networks, evoking a functional amplitude modulation of the soleus H-reflex and therefore a more natural step progression. Moreover, the BWS robotic-assisted step training altered the amplitude and onset of muscle activity during walking, decreased step duration, and improved the gait speed [ 12 ].
While it was concluded that the primary source of the neuronal plasticity observed in these studies is located in spinal locomotor networks, plasticity of supraspinal connections with spinal locomotor networks may also be altered [ 12 ]. However, regardless of the precise location of neuronal plasticity, these studies show that patients with clinically complete, motor complete, or motor incomplete SCI have the potential for an adaptive reorganization of spinal neural pathways and improved walking function following BWS robotic-assisted step training [ 12 — 16 ].
Larger scale neurophysiological studies are needed to comprehensively characterize spinal plasticity in patients with different types and levels of SCI. Furthermore, no significant improvements in walking or sit-to-stand ability were observed after the training as assessed by the six-minute walk test, the timed up and go test, and the sit-to-stand test [ 14 ]. These results are similar to studies investigating cortical plasticity in patients groups, where there is not necessarily a correlation between cortical plasticity and clinical improvement [ 21 , 22 ].
However, the lack of relationship between changes in spinal plasticity and functional recovery is also likely due to the low sample sizes and therefore a lack of statistical power, the variable number of training sessions between patients, and also due to the sensitivity to changes in the clinical tests used for assessing improvements in walking function, highlighting the need for further research on this topic [ 14 ].
Spinal plasticity was also induced following operant conditioning training of simple spinal reflex pathways for muscles of the lower leg elicited by electrical stimulation [ 23 — 27 ] and a simple robotic actuator device [ 28 — 30 ]. Spinal reflex conditioning can alter the size of spinal reflexes and leads to functionally beneficial alterations in the modulation of reflexes during dynamic activities in both healthy individuals and patients with SCIs [ 24 — 27 ].
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Studies in monkeys and rats show that soleus H-reflex conditioning is associated with plasticity at multiple sites in the spinal cord and brain, including changes in motoneuron properties and spinal interneurons [ 24 — 27 ]. While conditioning protocols can target plasticity to specific neural pathways, the benefits of the conditioning appear to be much more widespread than what can be attributed to the specific pathway. For example, unilaterally decreasing the size of the soleus H-reflex in SCI patients led to faster and more symmetrical gait in these patients, as well as an increase in the modulation of muscle activity bilaterally [ 24 , 25 , 27 ].
Therefore, specific conditioning protocols can be designed to target specific deficits in patients [ 23 ]. While operant conditioning of spinal reflex pathways elicited by electrical stimulation may be beneficially incorporated into lower limb robot-mediated therapies in order to induce beneficial spinal plasticity in normal, patient, and athlete populations, operant conditioning of the human soleus stretch reflex has been successful using a simple robotic mechanical actuator device. Indeed, soleus spinal stretch reflex pathways can be both increased up-conditioned and decreased down-conditioned in healthy participants in the same way as soleus H-reflexes using a mechanical actuator system [ 25 ].
Following successful soleus stretch reflex up-conditioning in healthy individuals, afferent feedback is enhanced leading to an increase in stiffness around the ankle joint [ 28 — 30 ]. Similar reflex conditioning protocols may also benefit elderly or patient populations with an elevated risk of falling [ 29 ].
A recent review of robotic therapy for rehabilitation suggests that lower extremity robotic therapies are in their relative infancy compared with upper limb robotic therapy [ 29 ]. While a recent meta-analysis including 23 trials with a total of patients showed a small additional value for robot-assisted gait training combined with conventional training compared to conventional training alone, especially for the more severely affected patients, the effectiveness of this form of training could clearly be further improved [ 31 ].
With more knowledge about the underlying neurophysiology and spinal plasticity in SCI and brain-injured patients following robotic training assessed via specific neurophysiological techniques, the training may possibly be more targeted for specific patients in order to maximize recovery.
Indeed, there is evidence for plasticity in a number of spinal reflex pathways in stroke and SCI patients following BWS robotic-assisted step training, with many spinal pathways becoming more like healthy controls in terms of phase modulation and amplitude during locomotion [ 12 — 16 , 18 ]. Furthermore, operant conditioning of soleus stretch reflexes using a simple robotic actuator device provide a promising direction of future research given the stability improvements in healthy subjects and the functional improvements observed in patients following targeted conditioning of the H-reflex [ 23 — 30 ].
Alterations in spinal pathways have the advantage that they are directly linked to motor behaviour and as such one may not only quantify the responses electrophysiologically, but also behaviourally for example, a change in the forces or torques around the target joint [ 2 , 32 ]. To date, the majority of studies continue to report reflex response sizes from electromyographic EMG data, likely since early reports indicated that the behavioural response varies from one elicited reflex to the next [ 17 , 33 , 34 ].
Regardless of the outcome measure, the importance of the spinal cord from a clinical perspective resides in the fact that it forms the final pathway to the ensuing behaviour. Therefore, the appropriate guidance of spinal cord plasticity likely plays a major role in restoring useful function following a central nervous system insult such as SCI or stroke [ 35 , 36 ].
However, any alterations at the level of the spinal cord will also have an influence and on the converse be influenced by changes in higher-level structures [ 25 , 37 ]. For example, the operant conditioning protocol mentioned previously not only up and down-regulates the size of the H- and stretch reflex, but also significantly affects more complex behaviors beyond the conditioned pathway such as improvements in walking [ 25 , 37 ].
Indeed, spinal and supraspinal plasticity underlies operant conditioning [ 16 ]. In conclusion, many pathways may be affected by the rehabilitation intervention both within the spinal cord as well as within other areas of the central nervous system and as such, a clear definition of spinal plasticity remains elusive.
Spinal plasticity in robot-mediated therapy for the lower limbs
The neurophysiological methods that can be used to assess spinal plasticity are based on the utilization of spinal reflexes to probe the spinal networks. These reflexes include for example, the H-reflex, the stretch reflex, and withdrawal reflexes. However it is important to note that all spinal reflexes are under the control from higher centers, being modulated in a task specific manner. Eliciting H-reflexes and withdrawal reflexes require the use of electrical stimulation, which is not a natural part of a robotic device.
The technology needed to elicit stretch reflexes could, on the other hand, be integrated in a robot and thereby be used to routinely assess training-induced spinal plasticity. In a clinical setting, typically, tendon taps are applied to investigate where along the spinal cord an injury has occurred.
These are then repeated as the rehabilitation program progresses to assess for any changes. While tendon taps are useful tools to reveal the level of a lesion, the inability to reproduce the same tapping force and speed from one trial to the next makes it impossible to be implemented in a reliable manner. For this purpose, when eliciting the stretch reflex, it is necessary to use tools that allow a precise extension of the muscle or tendon such as an actuator system that imposes joint rotations [for review, please see 38 ].
In this sense, rehabilitation robots should have the ability to induce such joint rotations. Stretch reflexes elicited by joint rotations have the additional benefit that they result in a more natural, asynchronous input to the central nervous system, directly activating muscle afferent receptors. Furthermore, stretch reflexes also change with targeted training [ 28 — 30 ].
The following elements should be quantified when assessing spinal plasticity utilizing the stretch reflex:. The stretch reflex size in terms of a the EMG response in a defined window following the stretch onset with regards to the baseline EMG and b the force or torque produced around the respective joint.
Assessing the changes in the amplitude of stretch reflexes offers an objective method for measuring spinal plasticity in the central nervous system provided they are due to neural effects and not changes in the state of the muscle.
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The stretch reflex can be typically separated into two or three clearly defined peaks [ 39 , 40 ]. The initial short-latency response represents the monosynaptic excitation of motoneurons in the spinal cord [ 41 ], while the middle-latency component is likely mediated by group II afferents [ 42 ]. In contrast, a transcortical pathway likely contributes to the long-latency component [ 40 , 43 — 46 ].
Related Spinal Cord Plasticity: Alterations in Reflex Function
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