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Sensory feedback is an important training tool that is utilized when implementing a motor learning task as a means of combating hypertonia which results from spinal cord injury. In many studies which utilize animals for obvious ethical reasons, there was a demonstration of the importance of sensory feedback in retraining locomotion after injury. These studies reported some sensory aspects necessary for effective training to be stretch-sensitive receptors in the hip flexors of the cat (Grillner & Rossignol 1978), and the stretch-sensitive receptors for the ankle extensor muscles also in the cat (Duysens & Pearson 1980). Fouad & Pearson (2004) discussed the necessity of cutaneous signals for skilled locomotor activity.
In addition to sensory feedback, a regular training schedule appears to be a necessary component of training. Improved stepping occurred in transected neonatal rats that were trained regularly on a treadmill for 15 min per day for 12 weeks compared to the same age animals that were untrained, or compared to animals that had been trained to stand reflexively to improve postural, rather than locomtor, control. (Edgerton et al., 2006). Adult spinalized mice were trained on a treadmill and demonstrated hind limb stepping in fourteen days following transection (Leblond et al., 2003). In contrast, stepping in adult spinalized rats has not been demonstrated with training.
Barbeau & Rossignol (1987) demonstrated improved hind-limb function (described as EMG activity of the hindlimb retaining the characteristics of the intact animal) with implementation of a regular treadmill training program in adult spinalized cats. In addition, one study (Dietz et al., 1995) revealed that treadmill training in patients with complete SCI increased the magnitude of the EMG patterns in lower extremity muscles presumably associated with changes to the neuronal network in the spinal cord. These authors reported that the changes observed cannot be reduced to simple enhancement of the stretch reflexes (Dietz et al., 1995).
The neuronal circuit must be exposed to afferent and intraspinal activation patterns similar to the desired outcome. That is, the motor performance goal of standing and stepping are different and require different training regimens suggesting task specific training is essential.
Retention of functional gains is an essential motor learning concept when implementing a training program. After complete transection, it has been shown that there is a loss in stepping capacity and reflex normalization if training is stopped. De Leon et al. (1999) demonstrated retention in functional acquisition when he evaluated stepping retention in spinal cats after cessation of training for six weeks after a twelve week training session. However, significant reduction in stepping capacity was observed when training was stopped for twelve weeks. Interestingly, three of the cats were retrained to step after losing the ability to step with cessation of training. The cats demonstrated a more rapid recovery of stepping during the second training session compared to the original skill acquisition (De Leon et al., 1999).
Wirz et al. (2001) examined leg extensor muscle EMG activity in a group of patients with an incomplete SCI and a group of patients with complete SCI over the course of daily 15 minute body-weight supported treadmill training for an average of 137 days. The patients that were able to use their locomotion ability and translate the function to over ground ambulation did not change the EMG activity or had marginal changes. The patients that had complete SCI were not able to initiate stepping over ground after training, and the EMG significantly fell over time after training.
In a chronic patient with a complete injury, normalization of the H-reflex was demonstrated with motorized bicycle training after sixteen weeks of training and return of hypertonia was evident after training had stopped over the course of three weeks (Kiser et al., 2005). This research suggests that once normalization has been achieved after chronic injury, continual training is necessary to maintain normalization of reflexes.
Research has demonstrated that sensory feedback produced by a regular exercise training program that is task specific has improved hind limb locomotor function in complete SCI models of the rat and the cat, and incomplete injuries in the human population. The research indicates the necessity of a training program that includes sensory feedback, a regular schedule, and task specific training, all suggestive of extensive plasticity in spinal circuitry.
There are multiple forms of training that have been implemented following spinal cord injury including treadmill training, swimming, bicycling, and standing. Partial weight bearing training (PWBT) has been utilized in human patients with SCI to effect changes in locomotor function. Improvements in actual locomotion have been induced in (Baekelandt et al., 1994). After several days of voluntary wheel running, normal rats were tested and found to have increased levels of BDNF mRNA in the hippocampus, cerebellum and cortex (Neeper et al, 1995). Other authors have found mRNA changes for BDNF after exercise in the lumbar spinal cord following SCI (Gomez-Pinilla et al., 2001).
Several neurotransmitters including ACh and GABA could affect BDNF expression as the neurotransmitters influence “glutamate-mediated signaling” in the hippocampus (Cotman & Berchtold, 2002). GABA has been suggested to be influential in the cortical reorganization process discussed by Jacobs & Donoghue (1991).
BDNF levels are decreased after contusion injury in the rat for mRNA levels that were measured in the spinal cord and the soleus muscle and have been shown to be up-regulated in the spinal cord after exercise. However, only treadmill training of the three exercise regimes evaluated (treadmill, swimming and standing) facilitated normalization of the peripheral BDNF levels and normalized sensory changes observed (Hutchinson et al., 2004). Therefore, it could be necessary to alter BDNF levels in both the spinal cord and peripheral muscle to influence sensory, and possibly motor, function.
Recent attention has focused on the role of insulin-like growth factor-1 (IGF-1) in the recovery of locomotion after incomplete injury and the effects of exercise in complete injuries. IGF-1 is a survival factor for neurons and oligodendrocytes and plays a role in neuronal growth and differentiation in the brain (Arsenijevic 1998). IGF-1 given peripherally induces BDNF mRNA in the brain (Carro et al., 2000).
It has been shown that patients with a chronic SCI have lower plasma (IGF-1) levels than normal adults (Bauman et al. 2006). IGF-1 given subcutaneously improved locomotion recovery in rats with an incomplete spinal cord injury, and alterations in circulating IGF-1 levels decreased functional gains that had been observed in an “enriched” environment (Koopmans et al., 2006). Gomes et al. (2006) linked exercise, specifically swimming, with IGF-1 serum levels in his comparison of diabetic rats exercised for six weeks compared with diabetic sedentary controls.
There is modulation of the spinal circuitry with performance of a motor task and changes can be observed quickly or require weeks or months to be observed (Edgerton et al., 2006). The medical community expects the intensity of physical therapy to have the greatest impact during the first year following an incomplete SCI or a traumatic brain injury. This time frame is usually extended in the case of a pediatric patient considering that the central nervous system has increased plasticity throughout development. Fawcett (2006) reported that the critical period when the spinal cord is more plastic declines at around five years of age for a child. Although the concept of a critical period (for recovery) is established in development and understood to occur immediately after injury, the critical period has not been established after injury. There are limited studies addressing the impact of training in the acute phase versus the chronic phase.
Yilmaz et al. (2005) completed a study with forty one patients that suffered a SCI and found that these patients demonstrated sensory, motor (incomplete patients only), and functional independence measure (FIM) score changes for a period of eighteen months. Giangregorio et al. (2005) initiated PWBT in five patients in the acute phase after SCI (within two to six months after injury) and they trained two times a week. The authors concluded that training resulted in partial reversal of muscle atrophy but did not influence bone loss. Shields (2002) demonstrated prevention of fiber type changes by assessing the fatigue index in one patient case study after an acute SCI. Prevention was demonstrated in the soleus muscle after implementing a training regime of repetitive electrical stimulation to one lower extremity while comparing the untrained other lower extremity over a period of a year.
The literature suggests that there is a window of optimal initiation of treatment and training, and that treatment outside the window of time can be futile. When discussing time course, human studies have shown that administration of the anti-inflammatory steroid methylprednisolone is moderately successful if given within eight hours of injury, and is ineffective otherwise (Bracken, 1990). Rodent transplantation work has also suggested that this window of time exists when determining the time frame essential for optimal outcomes. The literature suggests multiple time courses for initiation of cellular transplants including a four day delay after injury to delays of up to four months.
Studies (Humm et al., 1998 & Kozlowski et al., 1996) have shown that initiating exercise after cerebral ischemia can be detrimental to outcomes if training is initiated too quickly. Humm (1999) suggested that tissue around the lesion is vulnerable to increased excitatory neurotransmitter release for the first seven days after insult. These studies suggest that initiation of exercise should not begin for days after injury.
On the other hand, Werning et al. (1995) suggests that a long delay before the onset of training in the human population can reduce the benefits of the training program. Therefore, the timing of the initiation of the training appears to be vital to the outcomes produced, in that training should not be initiated immediately after surgery (within several days after injury) nor should the initiation be delayed for too long a period of time. The exact range of these time frames (during which they produce beneficial effects) has not been demonstrated.
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