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Dear Biomch-L members:
Following are all the replies to my original questions concerning
the adaptability of motor patterns in human locomotion. Thanks to all
those who replied.
Wen Liu
----------------------------------------
Original questions
----------------------------------------
Dear Biomch-L members:
It have been long observed and documented in certain degree that
the central neural system have the capability of adapting to compensate
for the loss of function in the pathological human locomotion. Even
though these adaptions lead to the abnormal kinematics and kinetics in the
locomotion, they should not be considered as pathological (D.A. Winter,
et al., 1990). Following are my questions:
1) How many such adaptions have been well defined in the human
walking and running gait?
2) How many such adaptions have been well defined in the upper
limbs and whole body related activities?
3) How can we always be able to distinguish the adaption from the
pathological change? As we all know, the patients with ankle instability
tend to move their hip more in order to keep their posture and balance.
If we observe the excessive motion in their hip joint during balance
exercise, can we simply ignore the possibility of overuse injury on their
hip joint soft tissues? This kind of injury may be a secondary injury
comparing to the primary injury. Is it possible for us to draw a limit
for the adaption?
I will post the summary as usual. Thank you in advance.
Wen Liu
Institute of Biomedical Engineering
Drexel University
**************************************************
Dear Liu,
You may be interested in the findings of my doctoral research
evaluating changes in motor control of the trunk muscles in low back
pain. We evaluated the behaviour of the trunk muscles in response to
rapid limb movement paradigm. One of the interesting findings from
the studies of people without low back pain was that transversus
abdominis was always the first trunk muscle active, preceding the
onset of EMG of the agonist upper limb muscle. Furthermore, unlike
the other trunk muscles investigated (RA, EO, IO, ES) the contraction
of transversus abdominis was not influenced by the direction of
movement of the limb. By manipulation of the movement preparation we
were able to demonstarte the organisational strategy used by the CNS
to control contraction of transversus abdominis was different ot the
other trunk muscles.
When we looked at people with a history of recurrent low back pain we
identified several changes in the motor control of the trunk muscles.
The most interesting were that TrA was delayed by 50-450 ms, occuring
after the onset of deltoid. The temporal parameters of the
contraction of this muscle were now dependent on the direction of
movement and the control strategy used by the CNS for control of TrA
was significantly altered.
In summary the results provide evidence of change in the control of the
muscles of the trunk associated with pathology. Whether this change
is an adaptation to low back pain (which is unlikely considering the
biomechanics and action of this muscle) or perhaps a predisposing
factor is as yet not confirmed.
The major low back pain study has been accepted for publication in
'Spine' and will be out later this year. Please let me know if I can
help further.
Paul Hodges
----------------------------------------------------------------------
Paul Hodges
Department of Physiotherapy Ph: +61 7 3365 4524
The University of Queensland Fax: +61 7 3365 2775
St Lucia QLD 4072 Australia Email: hodges@physio.therapies.uq.oz.au
----------------------------------------------------------------------
************************************************** *****************
I draw your attention to the following reference:
Mizrahi, J. Adaptation phenomena and compensatory mechanisms in
normal and pathological locomotion. In: Sensorimotor Plasticity,
Theoretical, Experimental and Clinical Aspects, eds. S. Ron, R. Schmid
and M. Jeannerod, INSERM, Vol 140, Paris, pp 343-366, 1986.
=====================================
Prof. Joseph Mizrahi , D.Sc.
Dept. of Biomedical Eng. Technion, Israel Institute of Technology
Haifa 32000, Israel
Phone: +972-4-8294128 Fax: +972-4-8234131
e-mail: jm@biomed.technion.ac.il
************************************************** *****************
liu wen,
-one particular set of gait adaptations has been observed in fully
rehabilitated acl-injured individuals. essentially, the adpatations
are a reduced mechanical output (torque and power) at the knee and
increased output at the hip and ankle. these results have been
observed in walking, running, sideways cutting, and stair climbing.
not all these adaptations have been observed in each sample of acl-
injured subjects but they each have been seen in various samples.
-these results were in agreement with emg analyses which have shown
reduced quadricep and increased hamstring activations.
-also, these results were observed in both acl-deficient and acl-
reconstructed individuals but, possibly, to different extents. some
deficient subjects have completely eliminated the midstance, knee
extensor torque, while reconstructed subjects had an extensor torque
at the knee but much reduced compared to healthy individuals.
-partial list of refs:
1. berchuck et al. 1990. j bone & joint surg. 871-877.
2. devita et al. 1992. med sci sports & exer. 797-806.
3. lass et al. 1991. acta orthop scand. 9-14.
4. limbird et al. 1988. j orthop res. 630-638.
5. timoney et al. 1993. amer j sports med. 887-889.
-sincerely,
paul devita
biomechanics lab
east carolina university
************************************************** ********
Dear Wen Liu,
I am interested in walking strategies as a result of constraints at the foot
and ankle. In response to your first question, the following are a number
of references which implicitly or explicitly describe walking strategies in
various patient populations;
Mueller MJ, Minor SD, Sahrmann SA, Schaaf JA, Strube MJ.
Differences in the gait characteristics of patients with
diabetes and peripheral neuropathy compared with age-matched
controls. Phys Ther 1994;74:299-308.
Winter DA, Patla AE, Frank JS, Walt SE: Biomechanical
walking pattern changes in the fit and healthy elderly. Phys
Ther 1990;70:340-347.
Winter DA, Sienko SE: Biomechanics of below-knee amputee
gait. J Biomechanics 1988;21:361-367.
Olney SJ, MacPhail HE. Hedden DM, Boyce WF: Work and power
in hemiplegic cerebral palsy gait. Phys Ther. 1990;70:431-
438.
Mueller MJ, Sinacore DR, Hoogstrate S, Daly L: Effect of
hip and ankle walking strategies on peak plantar pressures:
Implicaitons for neuropathic ulceration. Arch Phys Med Rehab
1994;75:1196-1200
Michael J. Mueller, PhD, PT
Program in Physical Therapy
Washington University School of Medicine
4444 Forest Park Blvd
Box 8502
St. Louis, MO 63108
Phone: 314/ 286-1400
FAX: 314/ 286-1410
Email: muellerm@medicine.wustl.edu
Following are all the replies to my original questions concerning
the adaptability of motor patterns in human locomotion. Thanks to all
those who replied.
Wen Liu
----------------------------------------
Original questions
----------------------------------------
Dear Biomch-L members:
It have been long observed and documented in certain degree that
the central neural system have the capability of adapting to compensate
for the loss of function in the pathological human locomotion. Even
though these adaptions lead to the abnormal kinematics and kinetics in the
locomotion, they should not be considered as pathological (D.A. Winter,
et al., 1990). Following are my questions:
1) How many such adaptions have been well defined in the human
walking and running gait?
2) How many such adaptions have been well defined in the upper
limbs and whole body related activities?
3) How can we always be able to distinguish the adaption from the
pathological change? As we all know, the patients with ankle instability
tend to move their hip more in order to keep their posture and balance.
If we observe the excessive motion in their hip joint during balance
exercise, can we simply ignore the possibility of overuse injury on their
hip joint soft tissues? This kind of injury may be a secondary injury
comparing to the primary injury. Is it possible for us to draw a limit
for the adaption?
I will post the summary as usual. Thank you in advance.
Wen Liu
Institute of Biomedical Engineering
Drexel University
**************************************************
Dear Liu,
You may be interested in the findings of my doctoral research
evaluating changes in motor control of the trunk muscles in low back
pain. We evaluated the behaviour of the trunk muscles in response to
rapid limb movement paradigm. One of the interesting findings from
the studies of people without low back pain was that transversus
abdominis was always the first trunk muscle active, preceding the
onset of EMG of the agonist upper limb muscle. Furthermore, unlike
the other trunk muscles investigated (RA, EO, IO, ES) the contraction
of transversus abdominis was not influenced by the direction of
movement of the limb. By manipulation of the movement preparation we
were able to demonstarte the organisational strategy used by the CNS
to control contraction of transversus abdominis was different ot the
other trunk muscles.
When we looked at people with a history of recurrent low back pain we
identified several changes in the motor control of the trunk muscles.
The most interesting were that TrA was delayed by 50-450 ms, occuring
after the onset of deltoid. The temporal parameters of the
contraction of this muscle were now dependent on the direction of
movement and the control strategy used by the CNS for control of TrA
was significantly altered.
In summary the results provide evidence of change in the control of the
muscles of the trunk associated with pathology. Whether this change
is an adaptation to low back pain (which is unlikely considering the
biomechanics and action of this muscle) or perhaps a predisposing
factor is as yet not confirmed.
The major low back pain study has been accepted for publication in
'Spine' and will be out later this year. Please let me know if I can
help further.
Paul Hodges
----------------------------------------------------------------------
Paul Hodges
Department of Physiotherapy Ph: +61 7 3365 4524
The University of Queensland Fax: +61 7 3365 2775
St Lucia QLD 4072 Australia Email: hodges@physio.therapies.uq.oz.au
----------------------------------------------------------------------
************************************************** *****************
I draw your attention to the following reference:
Mizrahi, J. Adaptation phenomena and compensatory mechanisms in
normal and pathological locomotion. In: Sensorimotor Plasticity,
Theoretical, Experimental and Clinical Aspects, eds. S. Ron, R. Schmid
and M. Jeannerod, INSERM, Vol 140, Paris, pp 343-366, 1986.
=====================================
Prof. Joseph Mizrahi , D.Sc.
Dept. of Biomedical Eng. Technion, Israel Institute of Technology
Haifa 32000, Israel
Phone: +972-4-8294128 Fax: +972-4-8234131
e-mail: jm@biomed.technion.ac.il
************************************************** *****************
liu wen,
-one particular set of gait adaptations has been observed in fully
rehabilitated acl-injured individuals. essentially, the adpatations
are a reduced mechanical output (torque and power) at the knee and
increased output at the hip and ankle. these results have been
observed in walking, running, sideways cutting, and stair climbing.
not all these adaptations have been observed in each sample of acl-
injured subjects but they each have been seen in various samples.
-these results were in agreement with emg analyses which have shown
reduced quadricep and increased hamstring activations.
-also, these results were observed in both acl-deficient and acl-
reconstructed individuals but, possibly, to different extents. some
deficient subjects have completely eliminated the midstance, knee
extensor torque, while reconstructed subjects had an extensor torque
at the knee but much reduced compared to healthy individuals.
-partial list of refs:
1. berchuck et al. 1990. j bone & joint surg. 871-877.
2. devita et al. 1992. med sci sports & exer. 797-806.
3. lass et al. 1991. acta orthop scand. 9-14.
4. limbird et al. 1988. j orthop res. 630-638.
5. timoney et al. 1993. amer j sports med. 887-889.
-sincerely,
paul devita
biomechanics lab
east carolina university
************************************************** ********
Dear Wen Liu,
I am interested in walking strategies as a result of constraints at the foot
and ankle. In response to your first question, the following are a number
of references which implicitly or explicitly describe walking strategies in
various patient populations;
Mueller MJ, Minor SD, Sahrmann SA, Schaaf JA, Strube MJ.
Differences in the gait characteristics of patients with
diabetes and peripheral neuropathy compared with age-matched
controls. Phys Ther 1994;74:299-308.
Winter DA, Patla AE, Frank JS, Walt SE: Biomechanical
walking pattern changes in the fit and healthy elderly. Phys
Ther 1990;70:340-347.
Winter DA, Sienko SE: Biomechanics of below-knee amputee
gait. J Biomechanics 1988;21:361-367.
Olney SJ, MacPhail HE. Hedden DM, Boyce WF: Work and power
in hemiplegic cerebral palsy gait. Phys Ther. 1990;70:431-
438.
Mueller MJ, Sinacore DR, Hoogstrate S, Daly L: Effect of
hip and ankle walking strategies on peak plantar pressures:
Implicaitons for neuropathic ulceration. Arch Phys Med Rehab
1994;75:1196-1200
Michael J. Mueller, PhD, PT
Program in Physical Therapy
Washington University School of Medicine
4444 Forest Park Blvd
Box 8502
St. Louis, MO 63108
Phone: 314/ 286-1400
FAX: 314/ 286-1410
Email: muellerm@medicine.wustl.edu