Identification and assessment of Electronic Aids for Daily Living considered essential by persons with high level tetraplegia: a case series.

Although assistive technology (AT) is recognized as a basic human right, access to AT, and particularly electronic aids to daily living (EADL), is limited. We aimed to understand how persons with high level spinal cord injury (SCI) prioritize EADL needs and assess satisfaction and efficacy of self-identified EADL. Thus, in this case series, we recruited three participants with C4, C5 or C6 SCI receiving in-patient SCI rehabilitation. Each received dedicated occupational therapy-based assistance in identifying EADL items within an unrestricted envelope of support ($5000 CDN) for use in maximizing physical independence and supporting their return to community-based living. Items identified were categorized by need (emergency/security; home environment control; or virtual access to the outside world). Each participant selected distinct EADL. Evaluation of selected EADL items indicated very high satisfaction. The selected EADL contributed to participants' returns to employment, community life, or reduced requirements for attendant services. These findings suggest that identification of essential technology should reflect the unique needs of each person and the context in which it will be used. These findings also support use of mainstream technology to meet EADL needs of individuals with limited physical abilities.

Initial spinal cord injury (SCI) rehabilitation should provide individualized identification and selection of electronic aids for daily living (EADL) for those with very minimal arm and hand function, including mainstream voice-activated technologies, to increase independence and function.Individualized self-selection of EADL, rather than general prescription-based provision of EADL, is most appropriate for identifying key EADL that will enhance function and independence in the community.Support from occupational therapists with expertise in SCI rehabilitation can provide expertise in identifying and setting up EADL, including in the community, to ensure selected EADL function as intended.

Lumbar V3 interneurons provide direct excitatory synaptic input onto thoracic sympathetic preganglionic neurons, linking locomotor, and autonomic spinal systems.

Although sympathetic autonomic systems are activated in parallel with locomotion, the neural mechanisms mediating this coordination are incompletely understood. Sympathetic preganglionic neurons (SPNs), primarily located in the intermediate laminae of thoracic and upper lumbar segments (T1-L2), increase activation of tissues and organs that provide homeostatic and metabolic support during movement and exercise. Recent evidence suggests integration between locomotor and autonomic nuclei occurs within the brainstem, initiating both descending locomotor and sympathetic activation commands. However, both locomotor and sympathetic autonomic spinal systems can be activated independent of supraspinal input, in part due to a distributed network involving propriospinal neurons. Whether an intraspinal mechanism exists to coordinate activation of these systems is unknown. We hypothesized that ascending spinal neurons located in the lumbar region provide synaptic input to thoracic SPNs. Here, we demonstrate that synaptic contacts from locomotor-related V3 interneurons (INs) are present in all thoracic laminae. Injection of an anterograde tracer into lumbar segments demonstrated that 8-20% of glutamatergic input onto SPNs originated from lumbar V3 INs and displayed a somatotopographical organization of synaptic input. Whole cell patch clamp recording in SPNs demonstrated prolonged depolarizations or action potentials in response to optical activation of either lumbar V3 INs in spinal cord preparations or in response to optical activation of V3 terminals in thoracic slice preparations. This work demonstrates a direct intraspinal connection between lumbar locomotor and thoracic sympathetic networks and suggests communication between motor and autonomic systems may be a general function of the spinal cord.

Spinal electrical stimulation to improve sympathetic autonomic functions needed for movement and exercise after spinal cord injury: a scoping clinical review.

Spinal cord injury (SCI) results in sensory, motor, and autonomic dysfunction. Obesity, cardiovascular disease, and metabolic disease are highly prevalent after SCI. Although inadequate voluntary activation of skeletal muscle contributes, it is absent or inadequate activation of thoracic spinal sympathetic neural circuitry and suboptimal activation of homeostatic (cardiovascular and temperature) and metabolic support systems that truly limits exercise capacity, particularly for those with cervical SCI. Thus, when electrical spinal cord stimulation (SCS) studies aimed at improving motor functions began mentioning effects on exercise-related autonomic functions, a potential new area of clinical application appeared. To survey this new area of potential benefit, we performed a systematic scoping review of clinical SCS studies involving these spinally mediated autonomic functions. Nineteen studies were included, 8 used transcutaneous and 11 used epidural SCS. Improvements in blood pressure regulation at rest or in response to orthostatic challenge were investigated most systematically, whereas reports of improved temperature regulation, whole body metabolism, and peak exercise performance were mainly anecdotal. Effective stimulation locations and parameters varied between studies, suggesting multiple stimulation parameters and rostrocaudal spinal locations may influence the same sympathetic function. Brainstem and spinal neural mechanisms providing excitatory drive to sympathetic neurons that activate homeostatic and metabolic tissues that provide support for movement and exercise and their integration with locomotor neural circuitry are discussed. A unifying conceptual framework for the integrated neural control of locomotor and sympathetic function is presented which may inform future research needed to take full advantage of SCS for improving these spinally mediated autonomic functions.

The ability of heart rate or perceived exertion to predict oxygen uptake varies across exercise modes in persons with tetraplegia.

STUDY DESIGN: Descriptive study. OBJECTIVES: To examine grouped and intra-individual relationships between 1) exercise intensity and heart rate (EI-HR); 2) EI and oxygen uptake (EI-VO2); 3) VO2 and HR (VO2-HR); and 4) perceived exertion and VO2 (PE-VO2) in persons with tetraplegia (C4/5-C8) during different modes of exercise. SETTING: Community in Winnipeg, Canada. METHODS: Participants exercised at 3 graded intensities during arm ergometry (ERG), wheeling indoors on cement (MWC), or hand-cycling outdoors (HC). EI (Watts, km/hr) and VO2, HR and PE were recorded. RESULTS: 22 persons completed ERG, 14/22 also completed MWC and 5/22 completed ERG, MWC and HC. Regression analysis of grouped data showed a significant relationship between EI-VO2 but not for EI-HR or HR-VO2. Intra-individual analyses showed a strong correlation (r or ρ > 0.7) for VO2-HR for 16/22 during ERG. In the participants completing multiple exercise modes, a strong VO2-HR relationship was present in 12/14 in ERG, but in only 6/14 in MWC. The 5 persons exercising with all 3 modes had a strong HR-VO2 relationship in 5/5 for ERG, 2/5 in MWC and 1/5 in HC. A strong relationship for PE-VO2 was observed in a higher proportion of participants (versus HR-VO2) during MWC (9/14) and HC (2/4). CONCLUSION: Within the same individual, the HR-VO2 relationship varies across modes, despite exercising over similar ranges of steady-state VO2. HR appears less able to predict VO2 compared to PE. Based on these new findings, systematic investigation of the HR-VO2 relationship across modes of exercise in tetraplegia is warranted.

Energy Expenditure as a Function of Activity Level After Spinal Cord Injury: The Need for Tetraplegia-Specific Energy Balance Guidelines.

The World Health Organization recognizes obesity as a global and increasing problem for the general population. Because of their reduced physical functioning, people with spinal cord injury (SCI) face additional challenges for maintaining an appropriate whole body energy balance, and the majority with SCI are overweight or obese. SCI also reduces exercise capacity, particularly in those with higher-level injury (tetraplegia). Tetraplegia-specific caloric energy expenditure (EE) data is scarce. Therefore, we measured resting and exercise-based energy expenditure in participants with tetraplegia and explored the accuracy of general population-based energy use predictors. Body composition and resting energy expenditure (REE) were measured in 25 adults with tetraplegia (C4/5 to C8) and in a sex-age-height matched group. Oxygen uptake, carbon dioxide production, heart rate, perceived exertion, and exercise intensity were also measured in 125 steady state exercise trials. Those with motor-complete tetraplegia, but not controls, had measured REE lower than predicted (mean = 22% less, p < 0.0001). REE was also lower than controls when expressed per kilogram of lean mass. Nine had REE below 1200 kcal/day. We developed a graphic compendium of steady state EE during arm ergometry, wheeling, and hand-cycling. This compendium is in a format that can be used by persons with tetraplegia for exercise prescription (calories, at known absolute intensities). EE was low (55-450 kcal/h) at the intensities participants with tetraplegia were capable of maintaining. If people with tetraplegia followed SCI-specific activity guidelines (220 min/week) at the median intensities we measured, they would expend 563-1031 kcal/week. Participants with tetraplegia would therefore require significant time (4 to over 20 h) to meet a weekly 2000 kcal exercise target. We estimated total daily EE for a range of activity levels in tetraplegia and compared them to predicted values for the general population. Our analysis indicated that the EE values for sedentary through moderate levels of activity in tetraplegia fall well below predicted sedentary levels of activity for the general population. These findings help explain sub-optimal responses to exercise interventions after tetraplegia, and support the need to develop tetraplegia-specific energy-balance guidelines that reflects their unique EE situation.

A new conceptual framework for the integrated neural control of locomotor and sympathetic function: implications for exercise after spinal cord injury.

All mammals, including humans, are designed to produce sustained locomotor movements. Many higher centres are involved in movement, but ultimately these centres act upon a core "rhythm-generating" network within the brainstem-spinal cord. In addition, endurance-based locomotor exercise requires sympathetic neural support to maintain homeostasis and to provide needed metabolic resources. This review focuses on the roles and integration of these 2 neural systems. Part I reviews the cardiovascular, thermoregulatory, and metabolic functions under spinal sympathetic control as revealed by spinal cord injury at different levels. Part II examines the integration between brainstem-spinal sympathetic pathways and the neural circuitry producing motor rhythms. In particular, the rostroventral medulla (RVM) contains the neural circuitry that (i) integrates heart rate, contractility, and blood flow in response to postural changes; (ii) initiates and maintains cardiovascular adaptations for exercise; (iii) provides direct descending innervation to preganglionic neurons innervating the adrenal glands, white adipose tissue, and tissues responsible for cooling the body; (iv) integrates descending sympathetic drive for energy substrate mobilization (lipolysis); and (v) is the relay for descending locomotor commands arising from higher brain centres. A unifying conceptual framework is presented, in which the RVM serves as the final descending supraspinal "exercise integration centre" linking the descending locomotor command signal with the metabolic and homeostatic support needed to produce prolonged rhythmic activities. The role and rationale for an ascending sympathetic and locomotor drive from the lower to upper limbs within this framework is presented. Examples of new research directions based on this unifying framework are discussed.

Neurochemical excitation of thoracic propriospinal neurons improves hindlimb stepping in adult rats with spinal cord lesions.

Using an in vitro neonatal rat brainstem-spinal cord preparation, we previously showed that cervicothoracic propriospinal neurons contribute to descending transmission of the bulbospinal locomotor command signal, and neurochemical excitation of these neurons facilitates signal propagation. The present study examined the relevance of these observations to adult rats in vivo. The first aim was to determine the extent to which rats are able to spontaneously recover hindlimb locomotor function in the presence of staggered contralateral hemisections (left T2-4 and right T9-11) designed to abolish all long direct bulbospinal projections. The second aim was to determine whether neurochemical excitation of thoracic propriospinal neurons in such animals facilitates hindlimb stepping. In the absence of intrathecal drug injection, all animals (n=24) displayed some degree of hindlimb recovery ranging from weak ankle movements to brief periods of unsupported hindlimb stepping on the treadmill. The effect of boluses of neurochemicals delivered via an intrathecal catheter (tip placed midway between the rostral and caudal thoracic hemisections) was examined at post-lesion weeks 3, 6 and 9. Quipazine was particularly effective facilitating hindlimb stepping. Subsequent complete transection above the rostral (n=3) or caudal (n=2) hemisections at week 9 had no consistent effect on drug-free locomotor performance, but the facilitatory effect of drug injection decreased in 4/5 animals. Two animals underwent complete transection at T3 as the first and only surgery and implantation of two intrathecal catheters targeted to the mid-thoracic and lumbar regions, respectively. A similar facilitatory effect on stepping was observed in response to drugs administered via either catheter. The results indicate that partial spontaneous recovery of stepping occurs in adult rats after abolishing all long direct bulbospinal connections, in contrast to previous studies suggesting that hindlimb stepping after dual hemisections either does not occur or is observed only if the second hemisection surgery is delayed relative to the first. The results support the hypothesis that artificial modulation of propriospinal neuron excitability may facilitate recovery of motor function after spinal cord injury. However, whether this facilitation is due to enhanced transmission of a descending locomotor signal or is the result of excitation of thoracolumbar circuits independent of supraspinal influence, requires further study.

Neurochemical excitation of propriospinal neurons facilitates locomotor command signal transmission in the lesioned spinal cord.

Previous studies of the in vitro neonatal rat brain stem-spinal cord showed that propriospinal relays contribute to descending transmission of a supraspinal command signal that is capable of activating locomotion. Using the same preparation, the present series examines whether enhanced excitation of thoracic propriospinal neurons facilitates propagation of the locomotor command signal in the lesioned spinal cord. First, we identified neurotransmitters contributing to normal endogenous propriospinal transmission of the locomotor command signal by testing the effect of receptor antagonists applied to cervicothoracic segments during brain stem-induced locomotor-like activity. Spinal cords were either intact or contained staggered bilateral hemisections located at right T1/T2 and left T10/T11 junctions designed to abolish direct long-projecting bulbospinal axons. Serotonergic, noradrenergic, dopaminergic, and glutamatergic, but not cholinergic, receptor antagonists blocked locomotor-like activity. Approximately 73% of preparations with staggered bilateral hemisections failed to generate locomotor-like activity in response to electrical stimulation of the brain stem alone; such preparations were used to test the effect of neuroactive substances applied to thoracic segments (bath barriers placed at T3 and T9) during brain stem stimulation. The percentage of preparations developing locomotor-like activity was as follows: 5-HT (43%), 5-HT/N-methyl-D-aspartate (NMDA; 33%), quipazine (42%), 8-hydroxy-2-(di-n-propylamino)tetralin (20%), methoxamine (45%), and elevated bath K(+) concentration (29%). Combined norepinephrine and dopamine increased the success rate (67%) compared with the use of either agent alone (4 and 7%, respectively). NMDA, Mg(2+) ion removal, clonidine, and acetylcholine were ineffective. The results provide proof of principle that artificial excitation of thoracic propriospinal neurons can improve supraspinal control over hindlimb locomotor networks in the lesioned spinal cord.

Propriospinal transmission of the locomotor command signal in the neonatal rat.

Long direct bulbospinal projections are known to convey descending activation of locomotor networks. Less is understood about the role, if any, of propriospinal mechanisms in this function. Here we review our recent studies on propriospinal neurons in the in vitro neonatal rat brainstem-spinal cord preparation. Neurochemical suppression of synaptic activity in the cervicothoracic spinal cord blocked locomotor-like activity, suggesting synaptic relays make a critical contribution to descending transmission of the locomotor signal. Staggered contralateral hemisections in the cervicothoracic region, intended to eliminate all long direct bulbospinal transmission, failed to suppress locomotion, suggesting the propriospinal system alone is sufficient. Midsagittal lesion experiments showed that locomotor-related commissural components are required for rhythm generation in response to electrical stimulation of the brainstem and are redundantly distributed. No single segment was essential, although a bi-directional gradient was noted, centered on the thoracolumbar junction. These results strongly favor a role for propriospinal mechanisms in the activation of locomotion and suggest that propriospinal neurons are a logical target for interventions to restore locomotor function after spinal cord injury.

Contribution of commissural projections to bulbospinal activation of locomotion in the in vitro neonatal rat spinal cord.

Commissural projections are required for left-right coordination during locomotion. However, their role, if any, in rhythm production is unknown. This study uses the neonatal rat in vitro brain stem-spinal cord model to examine the rostrocaudal distribution of locomotor-related commissural projections and study whether commissural connections are needed for the generation of hindlimb rhythmic activity in response to electrical stimulation of the brain stem. Midsagittal lesions were made at a wide range of rostrocaudal levels. Locomotor-like activity persisted in some preparations despite midsagittal lesions extending from C(1) to the mid-L(1) level or from the conus medullaris to the T(12/13) junction. In some preparations, midsagittal lesions throughout the entire spinal cord had no effect on locomotor-like activity if two or three contiguous segments remained intact. Those bridging segments had to include the T(13) and/or L(1) levels. These observations suggested that commissural projections in the thoracolumbar junction region were critical. However, locomotor-like activity was also elicited in preparations with limited midsagittal lesions focused on the thoracolumbar junction (T(12) through L(1) or L(2) inclusive). In other experiments, locomotor-like activity was evoked by bath-applied 5-hydroxytryptamine (5-HT) and N-methyl-d-aspartate (NMDA). Appropriate side-to-side coordination was observed, even when only one segment remained bilaterally intact. Commissural projections traversing the thoracolumbar junction region were most effective. In combination, these results suggest that locomotor-related commissural projections are redundantly distributed along a bi-directional gradient that centers on the thoracolumbar junction. This commissural system not only provides a robust left-right coordinating mechanism but also supports locomotor rhythm generation in response to brain stem stimulation.

Propriospinal neurons are sufficient for bulbospinal transmission of the locomotor command signal in the neonatal rat spinal cord.

We recently showed that propriospinal neurons contribute to bulbospinal activation of locomotor networks in the in vitro neonatal rat brainstem-spinal cord preparation. In the present study, we examined whether propriospinal neurons alone, in the absence of long direct bulbospinal transmission to the lumbar cord, can successfully mediate brainstem activation of the locomotor network. In the presence of staggered bilateral spinal cord hemisections, the brainstem was stimulated electrically while recording from lumbar ventral roots. The rostral hemisection was located between C1 and T3 and the contralateral caudal hemisection was located between T5 and mid-L1. Locomotor-like activity was evoked in 27% of the preparations, which included experiments with staggered hemisections placed only two segments apart. There was no relation between the likelihood of developing locomotor-like activity and the distance separating the two hemisections or specific level of the hemisections. In some experiments, where brainstem stimulation alone was ineffective, neurochemical excitation of propriospinal neurons (using 5-HT and NMDA) at concentrations subthreshold for producing locomotor-like activity, promoted locomotor-like activity in conjunction with brainstem stimulation. In other experiments, involving neither brainstem stimulation nor cord hemisections, the excitability of propriospinal neurons in the cervical and/or thoracic region was selectively enhanced by bath application of 5-HT and NMDA or elevation of bath K(+) concentration. These manipulations produced locomotor-like activity in the lumbar region. In total, the results suggest that propriospinal neurons are sufficient for transmission of descending locomotor command signals. This observation has implications for regeneration strategies aimed at restoration of locomotor function after spinal cord injury.

Equipment and modifications that enabled infant child-care by a mother with C8 tetraplegia: a case report.

PURPOSE: In the past, rehabilitative effort after spinal cord injury has focused on maximizing physical functioning related to activities of daily living and self-care, with less emphasis on issues such as care-giving. The number of women becoming pregnant and rearing children after spinal cord injury has increased in recent years, but descriptions of equipment and modifications used in child-care are scarce. Equipment and techniques that enable physical independence in providing infant-care by persons with low-level tetraplegia has not previously been described. METHODS: This case report describes the modified equipment and physical strategies used by a mother with C8 tetraplegia to physically care for her young infants. Relevant issues of physical function were identified, potential sources for equipment and techniques were reviewed, and then the equipment and technique solutions were formulated. RESULTS: Attachment arms and brackets were made so that a lightweight stroller could be attached directly to the mother's manual wheelchair, a crib was modified with sliding Lexan doors so that it could be accessed at wheelchair level, and a table with sides was designed and built to act as a play surface where the mother could independently place an infant. All other pieces of baby-care equipment were commercially available and the mother developed strategies for their use without modification. CONCLUSION: With the exception of bathing, using the tools and techniques described, this mother was able to achieve physical independence in providing her children's infant care.

Propriospinal neurons contribute to bulbospinal transmission of the locomotor command signal in the neonatal rat spinal cord.

This study examines whether propriospinal transmission contributes to descending propagation of the brainstem locomotor command signal in the in vitro neonatal rat spinal cord. Using double bath partitions, synaptic transmission was suppressed in the cervicothoracic region while monitoring locomotor-like activity on lumbar ventral roots evoked by either chemical or electrical stimulation of the brainstem. Locomotor-like activity induced by electrical stimulation was more stable (cycle period coefficient of variation (CV) 11.7 +/- 6.1%) than the rhythm induced by chemical stimulation (CV 31.3 +/- 6.4%). Ca(2+)-free bath solution, elevated Mg(2+) ion concentration, excitatory amino acid receptor antagonists (AP5 and/or CNQX), and the muscarinic receptor antagonist, atropine, were used in attempts to block synaptic transmission. Each of these manipulations, except muscarinic receptor blockade, was capable of blocking locomotor-like activity induced by brainstem stimulation. However, locomotor-like activity induced by higher intensity electrical stimulation of the brainstem (1.2-5 times threshold) was relatively refractory to synaptic suppression using AP5 and CNQX, and Ca(2+)-free solution was more effective if combined with high Mg(2+) (15 mm) or EGTA. Enhancement of neuronal excitation in the cervicothoracic region, using Mg(2+)-free bath solution, facilitated brainstem activation of locomotor-like activity in the lumbar cord, consistent with a propriospinal mechanism of locomotor signal propagation. Blockade of brainstem-induced locomotor-like activity was related to the number of cervicothoracic segments exposed to synaptic suppression, being most effective if five or more segments were included. These results provide direct evidence that propriospinal pathways contribute to bulbospinal activation of the locomotor network in the in vitro neonatal rat brainstem-spinal cord preparation, and suggest that a propriospinal system is recruited in parallel with long direct projections that activate the locomotor network.

Is NMDA receptor activation essential for the production of locomotor-like activity in the neonatal rat spinal cord?

Previous work has established that in vitro bath application of N-methyl-D-aspartic acid (NMDA) promotes locomotor activity in a variety of vertebrate preparations including the neonatal rat spinal cord. In addition, NMDA receptor activation gives rise to active membrane properties that are postulated to contribute to the generation or stabilization of locomotor rhythm. However, earlier studies yielded conflicting evidence as to whether NMDA receptors are essential in this role. Therefore in this study, we examined the effect of NMDA receptor blockade, using D-2-amino-5-phosphono-valeric acid (AP5), on locomotor-like activity in the in vitro neonatal rat spinal cord. Locomotor-like activity was induced using 5-hydroxytryptamine (5-HT), acetylcholine, combined 5-HT and NMDA receptor activation, increased K(+) concentration, or electrical stimulation of the brain stem and monitored using suction electrode recordings of left and right lumbar ventral root discharge. We also studied the effect on locomotor capacity of selectively suppressing NMDA receptor-mediated active membrane properties; this was achieved by removing Mg(2+) ions from the bath, which in turn abolishes voltage-sensitive blockade of the NMDA receptor channel. The results show that, although NMDA receptor activation may seem essential for locomotor network operation under some experimental conditions, locomotor-like rhythms can nevertheless be generated in the presence of AP5 if spinal cord circuitry is exposed to appropriate levels of non-NMDA receptor-dependent excitation. Therefore neither NMDA receptor-mediated nonlinear membrane properties nor NMDA receptor activation in general is universally essential for locomotor network activation in the in vitro neonatal rat spinal cord.

Psychogenic and pharmacologic induction of the let-down reflex can facilitate breastfeeding by tetraplegic women: a report of 3 cases.

Although an increasing number of women are becoming pregnant and rearing children after spinal cord injury (SCI), scant literature exists on breastfeeding after injury. In particular, it is unclear whether women with SCI above T7 can sustain breastfeeding in a manner similar to neurologically intact nursing mothers. A functional let-down reflex is required to provide adequate milk to a nursing infant. Infant suckling activates tactile receptors in the breast, and this signal is carried via afferent nerves in the T4-6 dorsal roots to the spinal cord and then to neurons in the hypothalamus, which release oxytocin into the bloodstream. Oxytocin triggers milk ejection from the breast. Suckling-induced afferent stimuli are absent in women with SCI above T4 and are reduced if the injury is between T4 and T6. This report describes the breastfeeding practices of 3 tetraplegic women and shows that breastfeeding can be maintained for extended periods (12-54 wk) after delivery. Two women required active mental imaging and relaxation techniques, or oxytocin nasal spray, to facilitate the let-down reflex. These findings suggest that although an absence of suckling-induced afferent stimuli may impair the let-down reflex, long-term breastfeeding can be maintained.

A reliable technique for the induction of locomotor-like activity in the in vitro neonatal rat spinal cord using brainstem electrical stimulation.

The use of brainstem electrical stimulation (BES) to evoke locomotion in in vivo preparations, such as the decerebrate cat, is well established. In contrast, despite the popularity of in vitro rodent spinal cord models, BES has not been adapted for routine induction of locomotion in these preparations. We describe a simple and reliable method of inducing locomotor-like activity in the in vitro neonatal rat spinal cord using BES. Relatively large amplitude (0.5-10mA), long duration (4-20ms) and low frequency (0.8-2.0Hz) pulses were delivered through a metal-in-glass electrode placed in contact with the ventral surface of the brainstem, without the need for precise targeting of specific sites. During continuous BES, locomotor-like activity (0.15-0.63Hz) persisted for over 45min. Episodes of locomotor-like activity could be recruited repeatedly for hours, using short periods (60s) of BES alternating with brief rest periods. Additional observations confirmed that the rhythmogenic effect of BES is mediated by excitation of spinal projections at the brainstem level, rather than spinal cord activation due to electrotonic spread of stimulus from the brainstem electrode. Endogenous activation of locomotor networks using BES offers important advantages over bath-applied application of neurochemicals to induce stepping in the in vitro rat model.