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New approaches to locomotor rehabilitation in spinal cord injury.

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New Approaches to Locomotor
Rehabilitation in Spinal Cord Injury
The article by Dietz and colleagues El] in this issue
should be seen as part of the efforts of an ongoing
collective quest to find better approaches to locomotor
rehabilitation involving locomotor training /2-4} and
pharmacotherapy [ 2 , 5,6}.This article suggests, as others before 17, S}, that locomotor training improves the
locomotor performances of spinal cord-in jured (SCI)
patients with incomplete lesions, and that pharmacotherapy may be beneficial in locomotor rehabilitation.
We will first point out that there is already a solid
experimental background justifying the use of drugs
and locomotor training in locomotor rehabilitation of
SCI patients, and then discuss some of the results presented by Dietz and coworkers.
Since the end of the last century, it has been known
that cats and dogs can, after a complete spinal transection at the low-thoracic level, display well organized
bilateral and reciprocal stepping movements of their
hindlimbs when they are held in the air by the thorax
or when they are placed on the ground while supporting their weight. Studies of adult spinal cats demonstrated that when the animals are placed on a moving
treadmill in the first week or so after the lesion, the
hindlimbs could display some weak walking movements greatly enhanced by unspecific perineal stimulation. After a few weeks of daily training, the cats could
walk with their hindlimbs without any further assistance while their forelimbs stood on a fued platform
and their tails were held to improve lateral stability.
Cats can follow speeds of up to 1 m/sec with proper
plantar foot placement and weight support of the hindquarters; step length and cycle duration are close to
those obtained in the same cats before acquiring spinal
lesions.
While these studies showed that the locomotor pattern in cats is generated at the spinal level, other work
showed that the locomotor pattern is also generated
centrally. This concept of spinal central-pattern generation (CPG) for locomotion [9f, originally derived from
work in invertebrates and low vertebrates, operationally defines an ensemble of spinal neurons whose membrane, synaptic, and network properties are capable of
generating, in the absence of peripheral or descending
inputs, a detailed motor pattern such as locomotion.
In cats, evidence for such central-spinal generation of
locomotion has been obtained by recording the activity
in motor nerves or motoneurons after neuromuscular
blockade (the so-called “fictive” locomotion), which
prevents the locomotor movements themselves and
therefore, all movement-related phasic afferent feedback and after spinal cord transection, which abolishes
all descending influences. Although evidence of central-spinal rhythms was sometimes obtained without
any drugs in paralyzed semi-chronic spinal cats, these
locomotor rhythms are usually triggered by noradrenergic drugs such as the precursor L-dopa administered
intravenously or an alpha-2 noradrenergic agonist such
as clonidine. In chronic spinal cats which have regained
the ability to walk on a treadmill, clonidine can markedly increase the step length and decrease the cutaneous excitability 17, 81.
How relevant is this work in cats to SCI patients?
Are there CPGs in primates? In humans? Some earlier
work with monkeys indicated that such “fictive” patterns could not be generated by the means usually employed to trigger these patterns in cats. Recent evidence, however, suggests that L-dopa can trigger
“fictive” locomotion in the spinal marmoset, a low-level
primate {lo). A 1994 paper by Calancie and associates
[11] describes how involuntary rhythmic movements
of the legs were generated in one exceptional patient
when the patient laid down with his hips extended.
These movements were abolished by flexing the hips
or by standing. By decreasing the weight with a harness, however, the locomotor-like pattern could be
triggered again. This patient provides solid evidence
that an involuntary well organized locomotor pattern
can be generated in humans, in nervous structures that
have yet to be defined. The findings are also consistent
with our own observations and with those of Wernig
and Muller [4],who described patients who could not
make isolated voluntary movements when asked to do
so (complete functional paralysis), but yet could generate involuntary well coordinated locomotor patterns on
a treadmill. Thus, although these patterns may or may
not be generated in part by a spinal central-pattern
generator, they represent low-level involuntary coordinated locomotor movements that could be used as part
of locomotor rehabilitation if we can learn to trigger
and improve the patterns by various means (e.g., drugs,
functional electrical stimulation, and training).
We have investigated in complete SCI patients the potential for locomotor improvement using noradrenergic
agonists, serotonergic antagonists, and locomotor training with external weight-support control over a treadmill, as well as functional electrical stimulation. So far,
our results suggest that two experimental drugs, clonidine and cyproheptadine, can improve the locomotor
Copyright 0 1995 by the American Neurological Association
555
pattern in SCI patients IS, 121 when compared to a placebo in incomplete SCI patients. Preliminary results
from a Canadian multicenter trial I61 are consistent with
previous studies showing modulation of locomotor patterns with clonidine and cyproheptadine, and the results
suggest that, as in the cat, noradrenergic and serotonergic substances have a modulating effect on locomotor
pattern I 131. Two other rehabilitation approachesinteractive locomotor training using a treadmill and progressive weight support, and locomotor training using
functional electrical stimulation (FES)-have
shown
great potenrial to improve locomotor recovery in incomplete SCI patients (reviewed in 17, 81).
The results that Dietz and colleagues reported in the
incomplete paraplegics are consistent with these earlier
findings; the results reported in the complete paraplegics
are intriguing and more difficult to evaluate. It is regrettable that a more complete description of the
amount and type of assistance provided by the therapists during locomotion is not given. It is impossible
to assess the active contributions of the patients and
the passive contributions of the therapists to the kinematics and electromyographic (EMG) patterns observed. In an almost identical experimental situation in
1991, Stewart and colleagues I121 showed that when
therapists moved limbs alternately on a treadmill and
weight support was provided by a harness a pattern of
rhythmical EMG activity due to the rhythmic stretches of
the muscles was induced. When this assistance ceased,
the rhythmic EMG pattern also ceased. Thus, rhythmic
muscle stretch can be sufficient to induce activity in
these muscles and create the impression that the muscles are rhythmically activated.
Experiments with intrathecal injections of neurotransmitters are needed to activate potential spinalresidual functions, and it is again unfortunate that we
have so few details and about only one patient. If the
activity reported by Dietz and colleagues I 11 results
largely from muscle stretch, then clonidine will markedly decrease the observed activity, as Stewart and associates [12] clearly showed, during therapist-assisted
locomotor movements as well as during passive stretch
in the seated position. in contrast, norepinephrine acting on alpha-1 and -2 receptors may exert a more
prominent overall excitatory effect on reflexes.
Spinal learning is also a phenomenon of great interest given recent evidence of spinal learning in primates.
That there are small changes in EMG amplitude after
five months of training is most probable; the suggestion
that this is due to spinal learning, however, appears
premature. Should all changes in amplitude occurring
over time in SCI patients be considered learning?
These patients began their five months training five to
six weeks after the lesion; what would have been the
normal evolution of EMG amplitude in a matched population without training (controls)?
It is clear that knowledge about the generating
556 Annals of Neurology Vol 37 No 5
May 1995
mechanisms of locomotion in animals has now reached
a stage where it can be cautiously extrapolated to locomotor rehabilitation in SCI patients and provide a
sound basis for complementary approaches (e.g., locomotor pharmacology, interactive locomotor training,
and FES). Given the hopes generated, it is important,
however, to increase the number of patients (especially
to document reliable drug effects), provide control series, and be critical and conservative in the interpretation of results. The quest for locomotion improvement
in SCI patients has been progressive, and we should
maintain this secure pace to insure that sound knowledge is accumulated and integrated eventually to meet
the enormous needs and expectations of SCI patients
with debilitating locomotor deficiencies.
Serge Rossignol, M D , PhD
Hugues Barbeau, PT, PhD
Centre for Research in Neurological Sciences
University of Montreal, Faculty of Medicine
Montreal, Quebec, Canada
References
1. Dietz V, Colombo G, Jensen DM, Baumgartner L. Locomotor
capacity of spinal cord in paraplegic patients. Ann Neurol 1995;
37:574-582
2. Fung J, Stewart JE, Barbeau H . The combined effects of clonidine and cyproheptadine with interactive training on the modulation of locomotion in spinal cord injured subjects. J Neurol
Sci 1990;100:85-93
3. Barbeau H, Dannakas M, Arsenault B. The effects of locomotor
training in spinal cord injured subjects: a preliminary study.
Restorative Neurol and Neurosci 1992;1293-96
4. Wernig A, Muller S. Laufband locomotion with body weight
support improved walking in persons with severe spinal cord
injuries. Paraplegia 1992;30:229-238
5. Wainberg M, Barbeau H, Gauthier S. The effects of cyproheptadine on locomotion and on spasticity in patients with spinal cord
injuries. J Neurol Neurosug Psych 1990;53:754-763
6. Norman KE, Barbeau H. Comparison of cyproheptadine, clonidine and baclofen on the modulation of gait pattern in subjects
with spinal cord injury. In: Thilmann A, Burke D, Rymer 2 ,
eds. Spasticity. New York: Springer-Verlag. 1992:410-425
7. Rossignol S, Barbeau H. Pharmacology of locomotion: an account of studies in spinal cats and spinal cord injured subjects.
J Amer Parapleg SOC1993;16:190-196
8. Barbeau H , Rossignol S. Spinal cord injury: enhancement of
locomotor recovery. Curr Opin Neurol 1994;7:5 17-524
9. Rossignol S, Dubuc R. Spinal pattern generation. Curr Opin
Neurobiol 1994;4:894-902
10. Hultborn H , Petersen N, Brownstone R, Nielsen J. Evidence
of fictive spinal locomotion in the marmoset (Callithrixjacchus).
Soc Neurosci Abstr 1993;19:539 (no. 225.1)
11. Calancie B, Needhan-Shropshire B, Jacobs P, et al. Involuntary
stepping after chronic spinal cord injury. Evidence for a central
rhythm generator for locomotion in man. Brain 1994;117:
1143-1 159
12. Stewart-JE. Barbeau H, Gauthier S. Modulation of locomotor
patterns and spasticity in spinal cord injured patients. Can J
Neurol Sci 1991;18:321-332
13. Barbeau H, Rossignol S. Initiation and modulation of the locomotor pattern in the adult chronic spinal cat by noradrenergic, serotonergic and dopaminergic drugs. Brain Res 1991;546:250-260
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spina, approach, cord, locomotor, rehabilitation, injury, new
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