Mohammad Alkhazim Alghamdi, MS,
PT
Queen's University
Kingston, ON K7M 2W8
Canada
Tel (613) 544 9531
I will take the yea side (with caveats) in regards to the existence
of
locomotor CPG in humans.
First, the evidence for CPGs for locomotion in animals from fish
through
primates is very strong. To my knowledge, there is no
direct evidence of
their existence in humans; the evidence is only by inference.
As in my
previous posting, I point to the paper by Whelen (1996) who
reviewed the
cat locomotor work. CPGs for locomotion in higher animals
do not appear to
be comprised of a discrete set of neurons, such as observed in the
stomatogastric ganglion's control of peristalsis, rather the network
is
distributed through several levels of the cord. Furthermore,
CPGs are
modifiable and are very low in the locomotion hierarchy.
Locomotion does
have a very well defined hierarchically organized circuitry which utilizes
the spinal cord CPGs to produce the agonist-antagonist muscle activity
which results in the swing-stance limb movements.
The medullary reticular
formation locomotor region has been described as
the 'head ganglion' of locomotion -- a region where descending commands
converge before traveling to the cord. The mesencephalic locomotor
region
perhaps has the greatest control over locomotion, as progressively
more
stimulation can induce the animal to walk, walk faster, then transition
to
trotting, then galloping. The cerebral cortex appears
to play a minimal
role in locomotion, since decorticated animals locomote with minimal,
if
any difficulty (locomotor behavior has been described in anencephalic
children). There are other identified regions involved in locomotor
circuitry but these are a few of the critical domains.
I feel that the most dramatic
human evidence for a constrained neural
network that controls normal locomotion comes from the 1998 paper by
Visintin et al. In that paper the results of a randomized
study of 100
rehabilitation patients with cerebral cortex strokes were presented.
Half
of the patients were treated with traditional PT and half were treated
with
body weight support gait training done over a treadmill.
As expected, the traditionally
treated patients improved during the six
weeks of rehab from a walking speed of 0.17 m/s to 0.25 m/s.
The BWS
trained patients improved significantly more from 0.18 m/s to 0.34
m/s.
The most dramatic effect was when the patients were re-evaluated three
months after discharge -- after three months of not having therapy.
The
traditionally trained patients were walking 0.30 m/s while the BWS
trained
patients improved to 0.52 m/s ! (For US therapists, like myself,
those
numbers translate to final walking speeds of 0.7 mph for the traditionally
trained and 1.2 mph for the BWS trained, this is not a small difference,
it
is a HUGE improvement.)
It is my position that when
gait training patients with stroke using
traditional PT the focus is on teaching the patient cortical means
of
locomotion, bypassing the normal brainstem control mechanisms. Cortical
control constrains locomotion to slower speeds, perhaps by requiring
enough
time for afference to reach the cortex. Cortical control
also increases
the attentional demands for locomotion. I would posit that by
using PWB
gait training the patients were allowed to re-activate (for lack of
a
better term) the normal brainstem mechanisms of locomotion. In
these
patients the brainstem was not damaged so more normal locomotion could
be
recovered.
Hesse et al's work
(1994 ) supported this finding in a paper that used a
similar training paradigm for patients who were an average of three
months
post stroke, who, after three weeks of traditional PT were non-ambulatory
(they required the assistance of two PTs to walk). In the
three patients
reported, after only three weeks of body weight support gait training
their gait improved to where they needed only intermittent physical
support
or only verbal cues. Such a rapid effect would not have been
expected
unless the body weight support gait training was able to recruit a
mechanism that was not utilized by traditional PT -- perhaps a mechanism
already present for locomotion which was undamaged by their cortical
injury.
Other work which supports
the presence of a CPGs in humans includes the
body wight support treatments for walking following spinal cord
injury, the
pharmacological stimulation of locomotion, and the sensory
electrical
stimulation paradigms.
In wrapping up, I think that
the presence of spinal CPGs for locomotion
will be found in humans, in some form. Although CPGs may be present,
they
are very low in the hierarchical control of locomotion. Furthermore,
while
there is central neural control of locomotion, those control mechanisms
do
utilize sensory afference to modulate locomotor output. Furthermore,
locomotion is constrained or augmented by the mechanics of the total
system, including intrinsic factors, such as muscle strength
or limb
length, and extrinsic factors, such as the coefficient of friction
of the
locomotor surface.
Paul H.
Hesse S, Bertelt C, Schaffrin A, Malezic M, Mauritz KH. Restoration
of gait
in nonambulatory hemiparetic patients by treadmill training with partial
body-weight support. Arch Phys Med Rehabil 1994; 75:1087-1093.
Visintin M, Barbeau H, Korner-Bitensky N, Mayo NE. A new approach to
retrain gait in stroke patients through body weight support and treadmill
stimulation. Stroke 1998; 29: 1122-1128.
Whelan, PJ 1996 Control of locomotion in the decerebrate cat. Progress
in
Neurobiology 49:481-515. (This is presently my favorite
review paper on
the neurology of locomotion)
Paul D. Hansen, Ph.D., P.T.
Fircrest Physical Therapy
1105 Regents Blvd., Suite C
Fircrest, WA 98466
Voice: 253.565.7796
Fax: 253.565.7836
Email: FircrestPT@att.net
It's nice to read Dr. Hansen's post, surely I take the yea side also,
to the
existence of the mechanism of CPGs. There are quite a few significant
contributions on vertebrate locomotion, including human locomotion,
governed
by locomotor CPGs, such as:
Grillner, S., "Locomotion in vertebrates: central mechanisms and reflex
interaction", Physiol. Rev., 55: 247-304, 1975.
Grillner, S., "Neurobiological bases of rhythmic motor acts in vertebrates",
Science, 228: 143-149, 1985.
Pearson, K.G., "Common principles of motor control in vertebrates and
invertebrates", Annu. Rev. Neurosci., 16: 265-297, 1993.
Just as Dr. Golubitsky et al. argued, although current neurophysiological
techniques are unable to isolate such circuitry (CPGs) among the intricate
neural connections of complex animals, but the indirect experimental
evidence
for their existence is strong. His group developed a very interesting,
mathematically strict, general modular network for retrieval the mechanism
of
CPGs underlying legged locomotion, see:
Golubitsky, M., Stewart, I., Buono, P.L., and Collins, J.J., "A modular
network
for legged locomotion", Physica D, 115: 73-86, 1998.
COPPE SISTEMAS UFRJ
Caixa Postal 68511
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Rio de Janeiro - RJ
Brazil
This discussion has tweeked my interest, largely because of a paper
I just finished reading. The paper was published in the J.
Exp. Biol. just 2 days ago by Robert Full and Daniel Koditschek and
outlines a "neuromechanical hypothesis" to legged
locomotion. As someone who initially trained as a biomechanist,
and who has subsequently become quite interested in motor
control, this paper addresses several issues which I have believed
for a long time, but have seen little discussion of in the
scientific literature.
Traditionally, there have been two approaches to studying locomotion:
(1) neurophysiology, and (2) engineering and
biomechanics. These approaches, however, have only rarely (if at all)
crossed paths. However, locomotion is a behavior that is
expressed by a whole organism, which means that in order to fully understand
the behavior that is being expressed, one must
consider BOTH the neurophysiological structures AND the mechanical
structures of the animal. Full and Koditschek quote
another paper by Mark Raibert and Jessica Hodgins (1993) as follows:
Many researchers in neural motor control think of the nervous system as a source of commands that are issued to the body as direct orders. We believe that the mechanical system has a mind of its own, governed by the physical structure and laws of physics. Rather than issuing commands, the nervous system can only make suggestions which are reconciled with the physics of the system and the task [at hand].
Full and Koditschek then go on to give several examples from the literature, and conclude that:
During slow, variable-frequency locomotion tasks requiring precise stepping, the nervous system probably dominates control by way of continuous feedback... [However,] the dynamics of the mechanical system most probably begins to dominate at intermediate and fast speeds.
In my own research (currently submitted for publication), we found that
diabetic
patients with severe peripheral neuropathy were able to maintain stable
walking patterns (for at least 10 minutes continuously). Our results demonstrated
that peripheral sensory feedback is not ESSENTIAL for producing stable
locomotion in humans. Most likely, this result occurred because these patients
were able to substitute information from other sensory sources (i.e. vision),
or because locomotion at
self-selected speeds is largely a mechanical behavior as Full and Koditschek
suggest, or both. My bet is on both.
Jim Collins (and others as well) developed some very nice coupled-oscillator
models of CPG output that provide insight into
gait transition mechanisms (at least in quadrupedals), but these
CPG models still do not produce robust and adaptive locomotor behavior.
On the opposite end of the spectrum, passive dynamic walking machines (Garcia
et al., 1998) have been constructed which produce stable locomotor behavior
with NO actuators or nervous system at all. Gentaro Taga, on the
other hand, was able to produce robust locomotor behavior by coupling some
form of CPG model to a mechanical model of a walking human.
My point in bringing this up is that I believe there is indeed a substantial
amount of literature supporting the evidence of CPGs in
quadrupeds and there are likely CPGs of some sort in humans as well.
However, these neural circuits are intimately
inter-connected within a mechanical system that must obey the laws
of mechanics, regardless of what the CNS may or may not
WANT it to do. Thus, if we want to understand how locomotor patterns
are generated and controlled, we must think both
mechanically as well as neurophysiologically.
REFERENCES:
Collins, J.J. and I.N. Stewart, Coupled Nonlinear Oscillators and The
Symmetries Of Animal Gaits. Journal of Nonlinear
Science, 1993. 3: 349-392.
Collins, J.J. and S.A. Richmond, Hard-Wired Central Pattern Generators
For Quadrupedal Locomotion. Biological
Cybernetics, 1994. 71: 375-385.
Full, R.J. and D.E. Koditschek, Templates and Anchors: Neuromechanical
Hypothesis of Legged Locomotion. Journal of
Experimental Biology, 1999. 202(23): 3325-3332.
Garcia, M., A. Chatterjee, A. Ruina, and M. Coleman, The Simplest Walking
Model: Stability, Complexity, and Scaling.
Journal of Biomechanical Engineering, 1998. 120(2): 281-288.
Golubitsky, M., I. Stewart, P.-L. Buono, and J.J. Collins, A Modular
Network for Legged Locomotion. Physica D, 1998.
115: 56-72.
Taga, G., A Model of the Neuro-Musculo-Skeletal System for Human Locomotion
I: Emergence of Basic Gait. Biological
Cybernetics, 1995. 73(2): 97-111.
Taga, G., A Model of the Neuro-Musculo-Skeletal System for Human Locomotion
II: Real-Time Adaptability Under Various
Constraints. Biological Cybernetics, 1995. 73(2): 97-111.
Taga, G., A Model of the Neuro-Musculo-Skeletal System for Anticipatory
Adjustment of Human Locomotion During
Obstacle Avoidance. Biological Cybernetics, 1998. 78(1): 9-17.
Jonathan
Dingwell, Ph.D.
Postdoctoral Research Associate
Rehabilitation Institute
of Chicago
345 East Superior, room
1401
Chicago, Illinois, 60611
Phone:
(312) 238-1233 *** NOTE: NEW PHONE
# ***
FAX:
(312) 908-2208
Web:
http://manip.smpp.nwu.edu/dingwell/
It sounds like you have already made up your mind and you are just looking
for information to support your view that humans do not have a locomotor
CPG.
But if you are open-minded about the idea, I suggest that you read the
following article, which to my mind, provides the best evidence
yet for a
locomotor CPG in man: Calancie B, Needham-Shropshire B, Jacobs
P, Willer
K, Zych G, Green BA. Involuntary stepping after chronic spinal
cord
injury. Evidence for a central rhythm generator for locomotion in
man.
Brain. 1994; 117(Pt 5):1143-59.
Clearly, it is difficult to obtain evidence of CPG-related locomotor
activity in humans (and primates) with complete SCI. But to my
mind this
does mean it's not there, it simply has more to do with the inhibitory
mechanisms that have evolved in higher animals that make it
difficult to
elicit this activity (See: Fedirchuk B, Nielsen J, Petersen N, Hultborn
H.
Pharmacologically evoked fictive motor patterns in the acutely spinalized
marmoset monkey (Callithrix jacchus). Exp Brain Res. 1998
Oct;
122(3):351-61)
For further reading I would refer you to the following articles:
Pinter MM, et al; Gait after spinal cord injury and the central pattern
generator for locomotion. (Spinal Cord, 1999 Aug)
Dimitrijevic MR, et al; Evidence for a spinal central pattern generator
in
humans. (Ann N Y Acad Sci, 1998 Nov 16)
McKay WB, et al; Assessment of corticospinal function in spinal cord
injury using transcranial motor cortex stimulation: a review. (J
Neurotrauma, 1997 Aug)
Dimitrijevic MR, et al; Motor control physiology below spinal cord injury:
residual volitional control of motor units in paretic and paralyzed
muscles. (Adv Neurol, 1997)
Regards,
Edelle
Edelle "Edee" Field-Fote, PhD, PT
University of Miami School of Medicine, Division of Physical Therapy
5915 Ponce de Leon Blvd, 5th FL; Miami, FL 33146
& The Miami Project to Cure Paralysis
M-W-F: 305-585-7970 (The Miami Project)
T-Th: 305-284-4535 (Division of PT)
FAX: 305-284-6128
They make a clear distinction between Human gait and Locomotion. Human
mature gait is plantigrade and characterised uniquely by a marked
heel
strike in front of the body with toe in the air, followed by toe contact
and heel lift with toe still in contact. Moreover there is a marked
knee
flexion-extension in the swing phase. There is a secondary locomotor
pattern which can be termed infant stepping where there is no
ankle
extension at the end of the stance and flexion-extension at the knee
is not
present.
Forssberg reports of anencephalic infants able to produce similar
patterns
of infant stepping; moreover, the stepping movement patterns are already
present as spontanous coordinated kicking movements in supine infants.
All
of these postulate that CPG are present at a very low level in the
spinal
cord, are innate, but they can generate only stepping locomotion.
From Parkinsonians and hemiplegic patients some evidence has been
acquired
that alterated sensory feed-back produce alterated locomotion (e.g.
toe
walking), which suggests that brain stem CPG can be largely modified.
Their picture is that CPG in the brain stem have been acquired
phylogenically, and are genetically hardwired in the
brain stem ciruits.
These are the patterns which are used by lower vertebrates for locomotion.
In Humans a higher form of locomotion developed late epigenetically,
over a
larger set of motor structures.
I would very much like to see the video of the patients of Dr. Hansen
after
recovery and see their re-acquired locomotion pattern
Best regards.
N. Alberto Borghese
Laboratory of Human Motion Study and Virtual Reality
Istituto Neuroscienze e Bioimmagini, CNR
LITA, via Fratelli Cervi, 93 - 20090 Segrate (Milano) - Italy
Tel. +39-02-21717.544 office Fax +39-02-21717.558
http://www.inb.mi.cnr.it/Borghese/Borghese_page.html
Also, I would like to second Alberto Borghese's recommendation of the
Forssberg group's papers; they are excellent discussions of locomotor
neurology.
Hesse S, Bertelt C, Schaffrin A, Malezic M, Mauritz KH. Restoration
of gait
in nonambulatory hemiparetic patients by treadmill training with partial
body-weight support. Arch Phys Med Rehabil 1994; 75:1087-1093.
Visintin M, Barbeau H. The effects of body weight support on the locomotor
pattern of spastic paretic patients. Can J Neurol Sci 1989; 16:315-325.
Visintin M, Barbeau H. The effect of parallel bars, body weight support
and
speed on the modulation of the locomotor pattern of spastic paretic
gait. A
preliminary communication. Paraplegia 1994; 32:540-553.
Paul H.
Paul D. Hansen, Ph.D., P.T.
Fircrest Physical Therapy
1105 Regents Blvd., Suite C
Fircrest, WA 98466
Voice: 253.565.7796
Fax: 253.565.7836