Top PDF Online Learning for the Control of Human Standing via Spinal Cord Stimulation

Online Learning for the Control of Human Standing via Spinal Cord Stimulation

Online Learning for the Control of Human Standing via Spinal Cord Stimulation

therapeutically useful. This motivates the second requirement. The third property is required by the fact that the calibration sessions in which the algorithm is run will also constitute a substantial part of the patient’s therapy, and indeed, are arguably the most therapeutically useful sessions available due to the very expensive presence of highly trained clinicians and therapists. Optimally, all stimuli ever administered (including those delivered by the stimulator as the patient undertakes the tasks of daily living) should be evaluated in terms of their functional performance, such that an algorithm which takes full advantage of this opportunity for experimentation and learning may be preferable. If the algorithm operates continuously, it must treat the therapeutic effectiveness of the stimuli delivered as a substantial component of its decision-making if an effective therapy is to be applied. Furthermore, poor stimuli (those which produce low reward values, indicative of poor therapeutic performance) may produce high fatigue or confound the results of later experiments. Poor stimulus choices destroy much of the utility of the experimental or therapeutic training session. The fourth property allows for much greater flexibility in applications; the requirement of algorithms like GP-UCB that all observations be available before the next action can be selected, and thus that only one action can be pending at any time can prove to be a substantial encumbrance. In the SCI therapy setting, the data processed into the performance metric used by the algorithm is often complex and time-consuming to calculate, resulting in substantial delays between the performance of an experiment and the availability of the assessed performance on that experiment. Motion capture, for example, may take extensive hand annotation to analyze fully, and multi-channel EMG may take several minutes to process into a useful form. However, it is most efficient to assemble an experimental session which consists of an unbroken sequence of requested stimuli; this necessitates either a batch procedure or delayed selection of stimuli. Further, it is highly desirable that an active learning system have the following additional properties:
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Development of a multi-electrode array for spinal cord epidural stimulation to facilitate stepping and standing after a complete spinal cord injury in adult rats

Development of a multi-electrode array for spinal cord epidural stimulation to facilitate stepping and standing after a complete spinal cord injury in adult rats

The full potential for the use of high-density epidural elec- trode arrays in clinical and basic scientific studies cannot yet be realized due to limitations in currently available implantable stimulating electronics. The stimulators cur- rently FDA-approved for human studies are too limited in the types of stimulation that they can generate and have no capability to record evoked potentials. Currently, we are unable to detect dynamic changes in intra-spinal cord net- work interactions during stimulation. The importance of the afferent information to motor command and control cannot be overestimated, yet we have little to no informa- tion about the ascending signals that form a significant component of the CPG’s input data. Adding the ability to record from intrinsic networks of the spinal cord could re- veal a great deal about the feedback mechanisms that form the foundation for locomotor pattern generation. This will require that the technology for the electrodes be refined to provide optimal characteristics for both stimulation and recording.
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Microelectrode Implants for Spinal Cord Stimulation in Rats

Microelectrode Implants for Spinal Cord Stimulation in Rats

In recent developments, completely paralyzed human subjects were implanted with a commercially available spinal cord electrode array and stimulation package originally designed for pain suppression [22]. A combination of stimulation of specific spinal segments near the S1 spinal level, sensory information from the lower limbs, and weeks of training was sufficient to generate full weight-bearing standing. Surprisingly, these subjects also recovered some voluntary control of movements of the toe, ankle, and the entire lower limb, but only when epidural stimulation was present. This obviously cannot happen with a complete lack of communication between the brain and the spinal cord, but no activity was detectable without stimulation. It appears that very weak excitation of descending axons are capable of activating spinal motor circuits if the lumbosacral interneurons and motoneurons are made more sensitive through spinal cord stimulation. Therefore even patients with complete spinal cord injury are offered hope of regaining a range of motor functions with the help of epidural stimulation.
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Sub-threshold spinal cord stimulation facilitates spontaneous motor activity in spinal rats

Sub-threshold spinal cord stimulation facilitates spontaneous motor activity in spinal rats

[7,8]. Epidural stimulation of specific spinal segments (via caudal electrodes at ~ S1 spinal level), in combination with the sensory information from the lower limbs and weeks of stand training, was sufficient to generate full weight-bearing standing. These subjects also recovered some voluntary con- trol of movements of the toe, ankle, and the entire lower limb, but only when electrical enabling motor control (eEmc) was present. Thus, one possibility is that modulation of the excitability of the lumbosacral region of the spinal cord via eEmc, combined with the weak excitatory activity of descending axons that were not otherwise detectable, could volitionally achieve a level of excitation that was suffi- cient to activate the spinal motor circuits above the motor thresholds of a significant number of motoneurons among synergistic motor pools. These results in human subjects demonstrate that some patients clinically diagnosed as hav- ing complete paralysis can use proprioceptive information
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Functional MR Imaging of the Human Cervical Spinal Cord

Functional MR Imaging of the Human Cervical Spinal Cord

Spinal cord and CSF motion are problematic in spinal cord functional MR imaging. To correct for interimaging motion, we used a 3D rigid body alignment to align images to the first time point. The more critical motion is that within the images. Ultrafast imaging techniques, such as single-shot echo-planar imaging (EPI) with high bandwidth, is normally used to reduce this effect. With EPI, artifacts produced by motion, suscepti- bility effects, magnetic field inhomogeneity, and off-resonance are a major concern along the phase-encoding axis. Several solutions have been proposed to address this problem: reducing the acquisition time, increasing the phase-gradient amplitude or its duration, and using interleaved multishot EPI, which ac- quires the image with multiple radio-frequency excitations.
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Attenuation of Lower Thoracic, Lumbar, and Sacral Spinal Cord Motion: Implications for Imaging Human Spinal Cord Structure and Function

Attenuation of Lower Thoracic, Lumbar, and Sacral Spinal Cord Motion: Implications for Imaging Human Spinal Cord Structure and Function

All of the experiments were performed in a 3T whole-body MR im- aging system (Magnetom Trio; Siemens, Erlangen, Germany), with subjects lying supine. Using a bore-mounted laser guide, subjects were carefully positioned on the scanner bed to align their shoulders and hips and to center the yaw and roll of their heads. Before scan- ning, a pulse oximeter was also placed on the index finger to enable segmented image acquisition and peripheral pulse recording throughout each experiment. Initial 3-plane localizer images were then acquired to provide a 3D position reference for subsequent slice alignment within each subject. All of the radio-frequency pulses were transmitted with a body coil and, for the lower-thoracic, lumbar, and sacral regions of the cord, the lower elements of a spine phased-array coil were used as receivers. Alternatively, when imaging lower-cervi- cal and upper-thoracic spinal cord regions, signal intensity was re- ceived by a posterior neck coil and the upper elements of a spine phased-array coil.
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Hydrogen sulfide protects spinal cord and induces autophagy via miR-30c in a rat model of spinal cord ischemia-reperfusion injury

Hydrogen sulfide protects spinal cord and induces autophagy via miR-30c in a rat model of spinal cord ischemia-reperfusion injury

In addition, several miRNAs have also been reported to be involved in autophagy modulation by regulating the expression of autophagy-related genes [12]. Autoph- agy, a regulated process of degradation and recycling of cellular constituents, can participated in organelle turn- over and the bioenergetic management of starvation of spinal cord injury [13]. During autophagy, part of the cyto- sol or entire organelles are sequestered into autophago- somes. Autophagosomes ultimately fuse with lysosomes, thereby generating single-membraned autophagolyso- somes and degrading their content [14]. In experiments, Beclin 1, the mammalian homologue of yeast Atg6, was first described as a Bcl-2-interacting protein , and its me- diated autophagy plays an important role in the regulation of cell survival and death [15]. Additionally, microtubule- associated protein 1 light chain 3 (LC3) were previously found to promote autophagy by transforming LC3-I into LC3-II. Notably, it has been reported the early and sus- tained activation of autophagy after spinal cord injury [16] and the change in expression of these autophagy-related proteins has also been recognized in rat model of spinal cord injury [17]. Recently, autophagy has been reported to contributed to the protective effect of H2S against I/R injury in hepar [18] and colon epithelial cells [19]. Thus, we attempted to testify whether that occurs in regulation effect of H2S on spinal cord I/R injury.
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Transcranial electrical stimulation motor-evoked potentials in a spinal cord ischaemia rabbit model

Transcranial electrical stimulation motor-evoked potentials in a spinal cord ischaemia rabbit model

The 8 rabbits in the control group were used for exclusion of anaesthesia and surgery on evoked potentials and to de- termine the optimal stimulation intensity. Twenty-five rabbits were included in the spinal cord ischaemia groups. During the surgery, 3 rabbits were excluded for variation or intraoperative haemorrhage. After awakening, the rab- bits were free to eat. Urine retention was not observed. The success rate of the model was 88%. Motor-evoked po- tentials recorded from the needle electrode in the gastro- cnemius muscle in the hind leg were composed of a major initial negativity (upward deflection) followed by a positive deflection (downward deflection). Although the wave con- figuration and amplitude varied in different rabbits, the basic negative-positive waveform had good reproducibility and was high in amplitude. The typical MEP wave deflec- tions were described as N1 and P1 (Fig. 1). Very few were described as N1, P1, and N2, or more. In all of the 33 ani- mals, the latency was 12.27 ± 0.96 ms, and the amplitude was 6157.87 ± 2362.99 μV.
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The Effects of Hippotherapy on Standing Balance in Patients with Incomplete Cervical Spinal Cord Injuries: A Pilot Study

The Effects of Hippotherapy on Standing Balance in Patients with Incomplete Cervical Spinal Cord Injuries: A Pilot Study

Direct or indirect damage to the central or peripheral nervous system can reduce an individual’s ability to per- form activities of daily living [1-3]. In a significant number of spinal cord injured individuals, incomplete injury to the spinal cord may spare their descending mo- tor control pathways and allow them to retain the ability to walk [4]. However, one of the key functional deficits is poor balance; people who have sustained a spinal cord injury (SCI) lack the normal postural synergies and sen- sory-motor integration of the lower limbs and trunk that regulate upright position [5]. Balance is a somewhat am- biguous term used to describe the ability to maintain or move within a weight-bearing posture without falling [6]. Balance is a significant issue for the majority of ambula- tory patients with incomplete spinal cord injuries. Indeed, they are at increased risk of falling [7]. Because of these individuals’ poor balance, bone fractures are common [8]. The mortality rate associated with falls increases dra- matically with injury. In addition, instability and falls can be markers of poor health and declining function, and they are often associated with significant morbidity [6]. One potential way to improve balance and mobility and
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Combined Sacral Nerve Roots Stimulation and Low Thoracic Spinal Cord Stimulation for the Treatment of Chronic Pelvic Pain

Combined Sacral Nerve Roots Stimulation and Low Thoracic Spinal Cord Stimulation for the Treatment of Chronic Pelvic Pain

Some pelvic pain syndromes are very resistant to medical treatment. Several studies have demon- strated that sacral neuromodulation, which has been successfully used for the treatment of blad- der dysfunction, incontinence, urinary retention and urinary frequency [1]-[3], can be successfully used for the treatment of chronic pelvic pain [4]-[7]. Several studies have also demonstrated sig- nificant involvement of dorsal column pathways in the transmission of visceral pelvic pain [8] and the successful use of spinal cord stimulation for the treatment of chronic pelvic pain [9]. We report three cases of severe chronic pelvic pain that failed conservative treatment modalities. Placement of a combined sacral nerve roots stimulator and a low thoracic spinal cord stimulator resulted in a significant pain relief and improvement in daily life activities. We believe that this combination may help patients suffering from chronic pelvic pain resistant to medical management.
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Variable-frequency-train stimulation of skeletal muscle after spinal cord injury

Variable-frequency-train stimulation of skeletal muscle after spinal cord injury

The major finding of this study was that VFTs failed to enhance the torque-time integral in fatigued, paralyzed skeletal muscle. This could be caused by rise times that were already so fast in patients with SCI during CFT stimulation that providing an initial, brief IPI did not reduce the T20–80 or increase peak torque enough to augment the torque-time integral. The TT200 data sup- port this argument, because the advantage of the VFT over the CFT was much smaller in the SCI groups. For the VFT to have an advantage over the CFT, the T20–80 must be shorter for the VFT and/or peak torque higher to counter the fact that the VFT train is 65 ms shorter than the CFT, as the two trains have the same number of pulses. An analogy can be made to VFT stimulation in fresh muscle of AB subjects. The VFT does not augment the torque-time integral in fresh muscle, because a 60 ms increase in rise time with VFTs is not sufficient to counter the 65 ms longer train duration of the CFT. After fatigue, there is a slowing of contraction, which is made evident by much longer rise times, and the VFT exposes this by enhancing the rise time (by ~80 ms). This leads to the novel aspect of VFT stimulation, which is an increased torque-time integral despite the difference in train duration (~20%, Figure 3).
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Spinal Cord Injury Therapy through Active Learning

Spinal Cord Injury Therapy through Active Learning

control and sensation, resulting in impaired mobility and independence. While the symptoms of some patients improve over the first one to one and one-half years after injury, these improvements eventually cease (see Fawcett et al., 2007). The remaining deficits in sensory and motor function are at present generally considered to be largely irreversible, i.e., there is no cure for SCI, though a number of approaches have been developed (e.g., locomotor therapy, see Wernig and M¨ uller, 1992) which have produced gains for some patients. Interestingly, in incomplete injuries and within the general realm of motor control, the degree of recovery in the performance of individual motor tasks may be somewhat independent; this may be due to different levels of supraspinal control exercised in different motor functions, e.g., locomotion versus reaching (Courtine et al., 2005). Beyond loss of motor control and bodily sensation, a number of other problems commonly arise for SCI patients, particularly issues resulting from lack of exercise and from the disruption of the nervous system’s internal communications. These deficits can include muscle atrophy and spasticity, as well as poten- tially life-threatening autonomic problems such as failures of temperature regulation and autonomic dysreflexia. For a discussion of the many and varied autonomic deficits which result from SCI, the symposium proceedings edited by Weaver and Polosa (2006) are an excellent resource. Advances in care have meant that SCI patients who do not die immediately tend to survive for a many years (see John F. Ditunno and Formal, 1994, which contrasts early and late 20th century prognoses for SCI patients), such that therapies which partially alleviate some of their symptoms are highly desirable. Anderson (2004) surveyed 681 SCI patients and found that, among the seven options presented on the survey instrument, a near-majority of quadriplegics believed that recovery of hand and arm function would produce the greatest improvement in their quality of life, while a plural- ity of paraplegics believed that recovery of sexual function would most greatly improve the quality of theirs. A very substantial number of both populations ranked the item comprised of bladder, bowel, and autonomic dysreflexia as one of their top two potential greatest gains in quality of life. Among paraplegics, walking movement, described by the survey’s creator as inclusive of standing and other forms of exercise, also ranked highly, but its share of first or second votes was much lower among quadraplegics. Even given the limitations of the survey, it is striking that bladder, bowel, and autonomic dysreflexia concerns were so important, particularly as compared with walking and mobility.
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Original Article Retrospective analysis on temporary spinal cord stimulation in the treatment of postherpetic neuralgia

Original Article Retrospective analysis on temporary spinal cord stimulation in the treatment of postherpetic neuralgia

Temporary electrode (eight contacts) were se- lected according to the characteristic distribu- tion of the somatic ganglia. Spinal cord stimu- lators (model 3861, Medtronic) were placed in the posterior epidural space closer to the dor- sal root entry zone (DREZ) through an epidural needle placement. The third and fourth elec- trodes were placed in the most painful gang- lion segment. External stimulator (Medtronic 3625) was attached to the temporary elec- trode. An electrical current from the electrodes induced paresthesia or a tingling sensation that masks the pain. The position of the elec- trode was determined when the patients sh- owed concordant stimulation over usual pain distribution. The parameters for external stimu- lator included pulse width of 60-80 μs, fre- quency of 60-80 Hz and amplitude of 0.8-3.2 V. When the patient feels no obvious discomfort, the Tuohy needle was removed and the elec- trode wire was attached to the skin. We adjust- ed the parameters for 10 days according to the abnormal feeling of the patient. The test stimu- lation was completed within 10 days, and patients who obtained at least 50% pain relief during this period were considered to experi- ence satisfactory treatment outcome. We re- moved the temporary electrode after 10 days. Observation index
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Spinal cord stimulation for treatment of failed back surgery syndrome  two case reports

Spinal cord stimulation for treatment of failed back surgery syndrome two case reports

Conservative management included patient education, epidural steroid injections, physiotherapy and a trial of transcutaneous electrical nerve stimulation.. She obtained about 20 - 30% pa[r]

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Cannabinoids and spinal cord stimulation for the treatment of failed back surgery syndrome refractory pain

Cannabinoids and spinal cord stimulation for the treatment of failed back surgery syndrome refractory pain

This article reports a retrospective study, performed at Pain Therapy Unit of San Vincenzo Hospital of Taormina, in col- laboration with the Anesthesiology and Pain Therapy Unit and the Department of Biomedical and Dental Sciences and Morphofunctional Imaging of the University Hospital “G. Martino” of Messina. All outpatients included in the study were referred at the Pain Unit of San Vincenzo Hospital, dur- ing the period between September 2014 and January 2016. Treatments were performed in accordance with rules and ethical standards on human experimentation and the Decla- ration of Helsinki of 1964 (further revised in 2013). All the study participants gave written informed consent (including information on possible risks and side effects) for participa- tion in the research study. Every precaution was taken to protect the privacy of patients. The retrospective study was approved by the Local Ethics Committee (Comitato Etico Interaziendale della Provincia di Messina) with protocol number 61/17, and the clinical study is registered with the number NCT03210766 (www.clinicaltrials.org). Between November 2014 and December 2015, authors included the clinical records of eleven FBSS patients suffering from moderate to severe chronic pain not responsive to other treat- ment regimens (including neuromodulating techniques), and considered eligible according to the inclusion and exclusion criteria established for the study. The patients, aged between 49 and 77 years (median age 61.18 ± 10.26 years), were equally distributed (six males and five females) (Table 1). Primary inclusion criteria in this study were the diagnosis of FBSS refractory to other standard treatments. Patients who had not discontinued their previous oral analgesic therapy, at least 2 months before the beginning of the treatment with cannabinoid agonists, were excluded. The SCS therapy, unsatisfactory in terms of pain perception as observed from
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Mechanisms of escape phenomenon of spinal cord and brainstem in human rabies

Mechanisms of escape phenomenon of spinal cord and brainstem in human rabies

Formalin fixed paraffin embedded CNS tissue of 10 rabies patients processed between 1987 and 2005 were included in this study. Five rabies patients presented as furious and the remaining had paralysis. Characteristics of these patients were summarized in Table 1. All patients did not receive any intensive care support and had evidence of hypoxia and cardiovascular collapse during the last 24–36 hours before death. Post-mortem examinations were per- formed within 24 h of death. Brain and spinal cord were fixed in formalin for 7 days. Sections of frontal, temporal, hippocampus, parietal, occipital, thalamus, basal ganglia, cerebellum, midbrain, pons, medulla, cervical, thoracic, lumbosacral enlargement were subsequently embedded in paraffin, sectioned and examined for the presence of rabies virus antigen and apoptosis and MOMP.
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Control of roof plate formation by Lmx1a in the developing spinal cord

Control of roof plate formation by Lmx1a in the developing spinal cord

expressed mouse Bmp4, Bmp7 or an activated Bmp receptor, BmprIa, in chick developing spinal cords using the same parameters and conditions as described for Lmx1a. Ectopic expression of either construct resulted in a similar phenotype, including significant hypocellularity and increased apoptosis (as detected by TUNEL) within the electroporated regions (8/8 embryos). At the same time, induction of Lmx1a along the whole dorsoventral axis of the neural tube, excluding only the most ventral regions, was observed (Fig. 8A,B and data not shown). Surprisingly, activation of Bmp signaling induced expression of both MafB and Lmx1a to the same broad extent along the dorsoventral axis of the neural tube (compare adjacent sections shown on Fig. 8A,B and Fig. 8C,D). This was in contrast to exogenous Lmx1a, which could induce MafB only in a restricted dorsal domain of the neural tube (n=8 embryos). These data suggest that Bmps may not only induce Lmx1a but also induce co- factors required to make neural progenitors competent to Lmx1a roof plate inducing activity. An alternative hypothesis is that Bmps can induce roof plate via Lmx1a-independent mechanisms.
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Matrix metalloproteinases and their inhibitors in human traumatic spinal cord injury

Matrix metalloproteinases and their inhibitors in human traumatic spinal cord injury

After traumatic spinal cord injury (SCI), the initial dam- age to the parenchyma at the lesion site is followed by a complex cascade of secondary events including break- down of the blood spinal cord barrier (BSB) and infiltra- tion of blood-derived inflammatory cells, oedema, excitotoxicity and ischemia. Experimental investigations have revealed that this phase of secondary parenchymal damage spans the first 48–72 hours post injury and is fol- lowed by the removal of tissue debris over subsequent weeks. Finally, the lesion site of severely injured tissue becomes dominated by scar tissue comprised of connec- tive tissue, including Schwann cells and meningeal fibrob- lasts, and fluid-filled cysts, surrounded by a dense astroglial scar [1]. Remodelling of the extracellular matrix (ECM) plays an important role in most of these events Matrix metalloproteinases (MMPs) are a family of extra- cellular zinc- and calcium-dependent endopeptidases that degrade the extracellular matrix and other extracellular proteins [2]. The 23 mammalian MMPs can be placed into sub-groups based on structural similarities and substrate specificity and they are capable of degrading virtually all extracellular proteins. Once activated, MMPs are subject to inhibition by 4 different tissue inhibitors of metallo- proteinases (TIMPs) that bind MMPs non-covalently [3]. MMPs are involved in events requiring matrix remodel- ling in developmental processes, wound healing and repair throughout life. In the nervous system, these enzymes play a role in the migration of precursor cells to their destination and are directly involved in axonal out- growth during development [4]. However, the aberrant expression of members of this protein family is involved in disease processes such as cancer metastasis and CNS disorders including multiple sclerosis, stroke, Alzheimer's disease and trauma [4,5]. Recent experimental SCI inves- tigations have demonstrated an involvement of MMPs in the post-traumatic events. In a mouse spinal cord com- pression injury model, a significant up-regulation of 11 MMPs was demonstrated [6]. Most of the proteins, includ- ing MMP-3, -9 and -10, showed an early induction, start- ing 24 hours after injury whereas the expression of other MMPs, including MMP-2, -12 and -13, was delayed until 5 days after trauma. Further studies into the role of MMP- 12, the most markedly up-regulated MMP, demonstrated improved recovery in MMP-12 null mice, most likely due to a reduction of the lesion-induced permeability of the blood spinal cord barrier (BSB) and a reduced density of microglia/macrophages at the lesion site [6]. An investiga- tion into the role of MMP-9 in SCI showed similar results in a contusion injury model, with improved locomotor function in MMP-9 null mice as compared to wild-type animals. Again, a reduction of the lesion-induced perme- ability of the BSB and a resulting attenuation of inflam- matory cell infiltration were suggested to be the likely
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Spinal cord RB

Spinal cord RB

• Posterior gray horns contain somatic and visceral sensory nuclei • Anterior gray horns contain somatic motor nuclei. • Lateral gray horns are in thoracic and lumbar segments ; c[r]

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Stance controlled knee flexion improves stimulation driven walking after spinal cord injury

Stance controlled knee flexion improves stimulation driven walking after spinal cord injury

Considerable evidence suggests that allowing some stance phase knee flexion during pathological gait is beneficial. In studies of healthy individuals, knee flexion during loading response and weight acceptance is less than 10° at slower gait speeds typically observed in FNS walking (0.5 m/sec) [30]. But unlike normal gait, the ef- fects of a stiff knee on the leading limb (i.e. during load- ing response and mid-stance) are compounded in HNP walking by the use of a walker, ankle locking by AFO, and orthotic braces which constrain limb motion to the sagittal plane. Stimulated or locked quadriceps immedi- ately after foot contact results in knee hyperextension, which limits shock absorption [31]. Stiff leading limb during FNS gait persists through loading response phase causing hip flexion and trunk tilt toward the walking aid, an action which impedes forward progression of body center of mass [31]. During mid-stance, stiff limb re- stricted to the sagittal plane creates a compass type gait causing excessive vertical center of mass motion that re- quires excessive trunk and upper extremity effort to carry the body over the stance limb [31]. During late stance (terminal stance and pre-swing), stiff knee has implica- tions for knee flexion and forward progression during swing phase. Study of stiff legged gait has determined that delayed deactivation of knee extensors during late stance reduces peak knee flexion [32]. Furthermore, re- duced knee flexion velocity at toe-off has been identified as a key cause of limited knee flexion during swing phase [33,34], and delayed deactivation of knee extensor mus- cles can significantly diminish knee flexion velocity at toe-off [35]. These studies [32-35] examined implication of stiff knee at toe-off for gait speeds ranging from 0.9- 1.4 m/sec, which can be faster than FNS-driven gait. But unlike loading response, knee flexion during pre-swing does not diminish with decreased gait speed [30]. In FNS-only walking, turning knee extensor stimulation off before the leg is fully unloaded can lead to collapse [31]. Delayed deactivation of knee extensor stimulation creates residual tone in pre-swing that hinders knee flexion in early swing, leading to toe-drag and instability.
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