Teach-in '99 on Control of Standing: What people said...

Hi Dr. Kirtley and List members,

This is very interesting issue.
But I am somewhat against the idea -passive spring stiffness" concept for
control of standing.

I do not think we should be conscious and have 150-250 ms to control the
ankle muscle for standing. I think our movement including standing and
walking is not done by only continuous control of CNS but many
spinal -monosynaptic or polysynaptic- reflex and other extrapyramidal
systems. About monosynaptic reflex, H-reflex, as we know, has only 30 ms
duration from sensory stimulation on lower leg to spinal cord then return to
gastrocnemius. I do not think that your graph has enough resolution to see
this amount of time relation. Would you improve the time resolution up to 10
msec level? You may have 100 Hz kinematic data.

I do agree that some component of passive stiffness would contribute to
standing control but it is not the sole mechanism, I am sure. We can see
many patients with sensory deficit but with strong motor nerve and muscle
can not stand still - sensory ataxia.

I am perfectly willing to be proved wrong, too.

Sun G Chung

Dear Sun and others,

Sorry - I didn't mean to suggest that the time delay was necessarily due
to conscious control, although in this experiment volition must have
been involved to a large extent, I think. I was deliberately introducing
volition to make any time delay as large as possible.

As I understand it, the Waterloo group are distinguishing between
passive spring-like control, in which only very fast short-range
(mono-segmental) spinal reflexes are involved, and active control via
higher levels. I presume that's what they mean! In any case, I am, as I
say, sceptical that such information could be gleaned from the CoP.

Sorry for my confusing terms. I have also replotted the data at a higher
time scale - you can see it at:
/teach-in/sway/zoom.gif

Chris Kirtley
The Hong Kong Polytechnic University

Dear Sun,

My congratulations! I think you caught the main point that the
postural control of quiet stance is rather sensory than motor
problem. However,  postural control of quiet stance is more difficult
problem that you imagine. Hopefully, paper listed below wil be
helpful to you.

 Gatev, P., Thomas, S., Kepple, T. and Hallett M. (1999) Feedforward
 ankle strategy of balance during quiet stance. Journal of Physiology
 (London) v. 514: 915-928.

Sincerely Yours,
Assoc. Prof. Plamen Gatev MD, PhD
Institute of Physiology,
Bulgarian Academy of Sciences
Acad. G. Bontchev St. Bl. 23
1113 Sofia, BULGARIA 


Dear all,

I've been notified of the following rebuttal of the stiffness control of
standing hypothesis by Morasso & Schieppati (Genova, Italy) in Journal
of Neurophysiology (1999) 82: 1622-1626. Here's the abstract:

Can Muscle Stiffness Alone Stabilize Upright Standing? A stiffness
control model for the stabilization of sway has been proposed recently.
This paper discusses two inadequacies of the model: modeling and empiric
consistency. First, we show that the in-phase relation between the
trajectories of the center of pressure and the center of mass is
determined by physics, not by control patterns. Second, we show that
physiological values of stiffness of the ankle muscles are insufficient
to stabilize the body "inverted pendulum." The evidence of active
mechanisms of sway stabilization is reviewed, pointing out the
potentially crucial role of foot skin and muscle
receptors. <http://jn.physiology.org/cgi/content/abstract/82/3/1622>

I guess that just about says it all...

Chris
--
Dr. Chris Kirtley
Dept. of Rehabilitation Sciences
The Hong Kong Polytechnic University


Dear readers,

Just an addition to the discussion:

As I read the present topic, I remembered the experiment in Winter's
textbook (Biomechanics and Motor Control of Human Movement, 2nd ed.,
1990, p93), which probably serves as the origin triggering the
alternative approach by Patla and others. (Sorry, I haven't read their
paper yet.)

Winter explains that in a back and forth sway experiment the CNS senses
the shift of the CoG and as a compensation the CoP is modified by
(de)activating the plantarflexors. This would suggest that there should
be a delay. The larger amplitude of the CoP compared to that of the CoG
might reflect that the CNS is trying to catch up by rushing the CoP
after the CoG and overshooting a bit in order to slow it down.

It is fascinating that others re-addressed the topic looking at the
delay and found none.

Gabor

--
Dr Gabor Barton MD
Manager, Gait Analysis Laboratory
Alder Hey Children's Hospital        tel: +44 (0)151 252 5949
Eaton Road, Liverpool, L12 2AP, UK   fax: +44 (0)151 252 5846


The experiment on phase relation of CoP and CoM is quite interesting. In
my opinion the biological significance of phase lag result may be
two-fold, if the volunteer is self-conscious on his motion during quiet
standing, it seems there should exist some lag because of the conduction
delay from CNS; otherwise his behavior may be controlled by CPG, a
biologically plausible, preprogrammed pattern organ most probabaly
located in spinal cord, in this case the lag may be trivial. I've
noticed that on experiment page, Dr. Chris wrote that "the motion is
consciously generated by the subject", so I'm wondering if it will make
any difference by adopting two volunteers separately in the way that
telling one to think and behave while keeping the other free standing?

Zhijun Yang

COPPE
Federal Univ. of Rio de Janeiro
Brazil


Hi all,

It may not be that simple, in that there are really a number of
"stiffnesses" associated with muscle, depending on the measurement technique
and relevant time interval of stiffness.  While I've read only the abstract,
if they are using the contractile force-length relation as their "stiffness"
or a "stiffness" based on multi-second time intervals, which they probably
are knowing the history of Morasso's group, it's certainly true that there's
no way the intrinsic muscles can provide the mathematical stiffness
necessary for the inverted pendulum (I noted this about 9 yrs ago).
However, the initial transient stiffness due to perturbation or drift is due
more to the series elasticity, which with just a bit of muscle tone DOES
have adequate stiffness.  As shoun by George Zahalak's students in the late
70's and Peter Rack's group in the early 70's, this "short range" (weakly
grounded) series stiffness is the dominant component for much spring-mass
behavior (e.g., limb oscillations).  There is also, of course,
reflex-induced "stiffness" that unlike SE is not instantaneous (but
complementary).   The SE sets the upper limit on transient stiffness
(muscles and tendons are not rigid pipes) and the tension-length relation is
roughly the lower limit -- what actually transpires depends on many things,
and just thinking of muscles as force generators is a big mistake.  Jerry
Loeb's preflex concept (and stuff by me, but I never used such a cool
name), discusses the reality of a proactive multi-part response (combo of
intrinsic mechanics and feedback/feedforward control) that's has a lot of
the properties of a "stiffness" -- though really part of neuromuscular
system in which the upper brain needn't worry about the relative
contribution of mechanical and neural factors (which can change for a
nonlinear system).

My only point is that muscle mechanics (and the various forms of stiffness
that unfold) does matter, and that if muscle were replaced by DC motors,
being a biped would be more scary. Check out the humbling of the walking
robots community -- in the early and mid 80's, I head many talks suggesting
that robust walking systems were around the corner -- as was routine FES
walking.  Hasn't happened.  Perhaps because those robots weren't using
intrinsicly spring-like actuators (with several types of springs), that if
nothing else can help slow down a catrostrophic fall by providing some sort
of postural impedance field as a first line of defense.  Sensors (muscle,
foot, ...) are also clear part of an integrated approach -- but from my
perspective, any theory on sway needs to seriously consider actuator
mechanics.

Jack

Jack Winters, Ph.D.,  Professor and Chair,
Dept. of Biomedical Engineering, Pangborn 131
Catholic University of America
Cardinal Station   (or 620 Michigan Ave NE)
Washington, DC 20064
202-319-5843,  -4499 fax,
http://www.ee.cua.edu/~winters,
see also http://www.hctr.be.cua.edu/ 


As part of my dissertation back in 1989 I constructed a four link model of
a 1.7m, 72.6kg standing human so as to analyze the mechanics induced by
translatory postural perturbations.  The model was constructed of plywood,
hinges, and paired springs.  It had a foot, lower extremity, trunk, and
head segments  which were connected with strap hinges.  Each segment was
weighted with lead bricks to approximate segment weights and COMs.  Spring
tensions were set to a level which would keep the model from falling if
leaning +/- 4 deg.
        The model was then tested on the perturbation platform.  Kinematic data
were recorded using a Selspot system.  Force plate data were not available
at that time so I did not describe COP.
        When perturbed the model segments began moving in an ascending order.
They then began to oscillate for over 1 min.  I was careful not to give the
model too big of a perturbation, so in all cases it eventually returned to
an upright position.
        Interestingly, in agreement with Jack Winter's comments, immediately
following the perturbation the model's movements closely resembled those of
a human subject, in the ascending delay before the superimposed segment
moved, the general sine wave shape of the movements, and the correction of
the perturbation (reversal of movement) prior to the onset of an EMG
response -- the EMG was only recorded from the human subjects  :)    The
amplitude of this initial movement did not change over the series of trials
(almost no trial to trial variance).  And neither the model or the human
behaved like a rigid inverted pendulum.
        At approximate time of the muscle response the model and human behavior
diverged sharply.  The model continued to oscillate while the human
movement was dampened.   The slight reductions in the EMGs did not reflect
the changes seen in the movement amplitudes.
        The muscle responses following the perturbations occurred after the
movement had reversed directions and the subject was regaining an upright
position.  Based on these data I would agree that the "preflex" muscle
properties were the primary means of correcting perturbations to balance.
These properties, in conjunction with the muscle responses, functioned to
dampen the ongoing effects of the perturbations, not to keep the subject
upright.

Paul H.

Hansen, P.D. An examination of the responses in humans to postural
perturbations, 1989. Ph.D., University of Oregon. (182pp 2f $8.00) PH 1123
        Available from Microform Publications  http://darkwing.uoregon.edu/~micropub/

* * * * * * * * * * * * * * * * * * * * *
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


Dear all,
This is really an interesting discussion. I have not yet read the
Winter and Morasso papers, this e-mail thing requests immediate but
unripe reactions. I may thus well duplicate arguments from one of
the papers.
My point is that for purely mechanical reasons there will NEVER be a
phase delay between CoP and CoM (at least as long as a single
inverted pendulum model is valid.)
Winter himself (Gait and Posture 3:193-214, 1995) has given the
relation between positions  of CoM and CoP, xp and xg,
respectively, in such a model (Eq 2):

        xp - xg = K.d2 .g/dt2

And this is just what nicely can be seen in on our Website: when CoM
deviates for/aft from the midposition, CoP is always in front of it,
it "drives it back to the midposition".
The electrical engineers among us (and they are many) may appreciate
the transfer function in Laplace form of the above differential
equation:

H(s) = xg/xp(s) = 1/ 1-Ks2

As s2 equals - 2pf, this means that the transfer function is real
for all frequencies (and low-pass). This may seem a bit unusual, but
it is a reflection of the unstable character of an inverted pendulum.
The control of such an instable system  requires a controller
WITHOUT DELAY. To compensate for the unavoidable delays in muscle
force generation etc. the controller should thus be predictive, it
should anticipate the unbalance. Again this is what we see: the CoP
is always "in front of" the CoM to bring it back to the midposition.
Try to balance a broomstick on your hand, and you see it before your
eyes.
The example on the website, by the way, shows a purposive to-and-fro
movement, not really posture control at work. But to this argument,
it makes no difference.
A completely different point: what is regulated in standing balance?
CoM position seems me very hard to sense. Maybe head angular
velocity (semicircular canals) or acceleration (otoliths). Or maybe
just the CoP, sensed by foot pressure?
In all movements there are also a feed-forward actions to keep
balance.

Best wishes,

At Hof
Department of Medical Physiology &
Laboratory of Human Movement Analysis AZG
University of Groningen
Bloemsingel 10
NL-9712 KZ GRONINGEN
THE NETHERLANDS
Tel:   (31) 50 3632645
Fax:   (31) 50 3632751


Dear At and others,

I have read the Morasso & Schieppati paper, and I must say it is a very
good read - extremely well-written and insightful. You might also be
interested to know, At, that one of your publications is cited in it!

In fact, your recent email could be said to be a nice summary of the
paper. Their own model has the following equation:

COM acceleration = g(COM - COP)/h + z

where h is the height of the COM and z is a noise term. They also derive
the Laplace equation, and point out that it is unstable unless ankle
stiffness were of the order of 1835 Nm/deg. Referring to your (Hof &
Berg) estimate of ankle stiffness around 250-400 Nm/deg, they conclude
that the physiological values reported are much too small to maintain
stability.

Incidentally, they do admit that the values quoted from your paper were
not measured during standing, and in fact (and I find this a stunning
comment) say that ankle stiffness during standing has NEVER been
reported!

This is like a red rag to me.. can anybody suggest a method whereby we
might measure ankle stiffness during quiet standing?

Chris
--
Dr. Chris Kirtley
Dept. of Rehabilitation Sciences
The Hong Kong Polytechnic University

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