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Dear Biomch-L readers,
Today, I received a copy of Prof. James R. Gage MD's long-awaited monograph
Gait Analysis in Cerebral Palsy (xvi+208 pp., hard cover, ill.)
(McKeith Press, London 1991)
announced in short on this list on 19 October. The book has been published
in the Series Clinics in Developmental Medicine, with the support of The
Spastics Society, London, U.K.; it is distributed in the U.K. by Blackwell
Scientific Publishers Ltd in Oxford (ISBN 0 901260 90 8), and in the U.S.A.
by Cambridge University Press, New York (ISBN 0 521 41277 3).
Jim Gage has been one of the founding fathers of quantitative, clinical gait
analysis during his position at the Newington Children's Hospital in Newington,
CT/USA. Recently, he moved to the Gilette Children's Hospital at the Univer-
sity of Minnesota Medical School, Minneapolis/St.Paul, MN/USA where he became
the medical director and a professor of orthopaedic surgery.
Rather than providing a discussion of his book (it'll take some time to read
and digest it properly), I'll quote his Table of Contents and Epilogue in full.
Herman J. Woltring, Eindhoven/NL
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
TABLE OF CONTENTS
Foreword (B.G.R. Neville)
Preface
1. Introduction (with Barry S. Russman, M.D.)
2. Basic measurements
3. The neurological control system for normal gait
4. Normal gait
5. Pathlogical gait
6. Principles of treatment in cerebral palsy
7. Hemiplegia
8. Diplegia and quadriplegia
9. Postoperative care
10. Assessment of outcome
11. Epilogue
Index
Chapter 11 -- EPILOGUE (pp. 201-203)
In this short text I have attempted to discuss the nature of the cerebral
palsy lesion, the rationale for treatment, and the use of gait analysis in
the formulation and assessment of that treatment. Now it is time to switch
from the realm of science to the realm of philosophy -- to reflect upon the
road that we have traveled, and then to look forward to the ultimate desti-
nation.
Until the advent of clinical gait analysis laboratories, the treatment of
cerebral palsy was an art, not a science. Physicians tended to treat patients
the way they had been taught, without ever asking why. Beyond the clinical
examination there was seldom any attempt to define the pathology precisely,
very little thought about how the treatments would affect the dynamics of that
pathology in either the short or long term, and not much effort to assess the
outcome of the intervention. Since the priorities of normal gait were not
well understood, the treatments were not aimed at establishing these objec-
tives. There was little understanding about the importance of muscles as
prime movers in gait, or about bones as the levers upon which they act, and
little effort was made to define or preserve muscles which were functioning
as accelerators or to restore their lever arms. As a result, a burden of
iatrogenic injury was often added to the physiological disability inflicted
by the cerebral palsy, and the child was worse off after the intervention
than before. Our physical therapy colleagues recognized this and therefore
often argued long and hard against surgical treatment. Further damage
resulted from prolonged immobilization which left the child weak and stiff,
and frequent interventions converted childhood from a time to play to a
perpetual state of recovery.
Fortunately this is starting to change. Thanks to computerized motion
analysis, we now have a much better understanding of the physiology of gait,
and we are beginning to understand the neurophysiology of motor control.
Because of gait analysis, our treatments have changed a great deal over the
past decade. We have learned about the role of the two-joint muscles in
cerebral palsy and can now understand why they are more severely involved.
This led to the isolated lengthening of the gastrocnemius and the intra-
muscular lengthening of the psoas while sparing the soleus and the iliacus.
We found that we were doing too much weakening of the hip adductors, and
that hip mechanics could be improved and flexion contractures of the hip
reduced without sacrificing hip-flexor power if we did our derotational
osteotomies in the intertrochanteric region proximal to the insertion of
the iliopsoas. The transfers of the distal end of the rectus femoris and
the semitendinosis were introduced. The former has been proven to be very
effective in unlocking the knee in swing (Muik et al. 1990, Sutherland et
al 1990), but there are still some problems with the latter which need to
be worked out.
Through measurement of oxygen consumption and cost, we are beginning to
understand the high energy costs of cerebral palsy and how our surgery
affects those costs. We are starting to use software programs which will
give us an idea how and where this energy is being wasted. One such program
estimates segment energies based on their approximate mass, acceleration and
distance traveled per unit of time. Another looks at each joint as a torque
generator and estimates the net forces which are being produced as a result
of muscle action across the joint (~Ounpuu et al. 1991).
As gait analysis becomes more widely used in the future, orthopaedic sur-
gery will routinely be based on objective evidence of dysfunction and sound
hypotheses. Pattern recognition, which we are already using in the treatment
of hemiplegia (Winters et al. 1987), will be applied to diplegia as well.
Existing statistical pattern recognition techniques can be used to accomplish
this, but very large data bases will be necessary. There will have to be
cooperation between different treatment centers, with data pooling and common
software formats for retrieval. Once pattern recognition in diplegia has been
accomplished, computer software will be written to recognize the criteria of
each pattern so that the computer will be able to make a printout of the
specific pattern type of the involvement, along with the rest of the data.
Treatment protocols will then need to be developed for each of the subtypes.
Since the gait laboratory computers of smaller treatment centers which are
not actively involved in research can use these programs, it will enable
them to tap into this knowledge as well and to apply proven treatments to
each of the various subtypes of involvement. Computer simulation of treat-
ment, which was only a pipe dream 10 years ago, is already being used (Delp
et al. 1990). In retrospect it would appear that our generation and the
ones that preceded it were `the carpenters of orthopaedics'. But because
today's technology has opened up new opportunities, tomorrow's orthopaedists
will need to be true `bio-engineers' of the human frame if they wish to
treat their patients well.
Rapid progress is being made in other fields as well. Selective dorsal
rhizotomy is an exellent example of this, and for the first time we have a
method of preserving or improving function in an appropriately selected
patient, while permanently normalizing muscle tone. It is my personal
feeling that as we gain more knowledge about the neuropharmacology of the
brain, we may be able to develop drugs which will be specific enough to
reduce tone without interfering with other CNS functions. At this time we
are aware of more than 40 different neurotransmitter substances (Guyton
1991). Some of the best known are acetylcholine, norepinephrine, histamine,
GABA and glutamate. The Edinburgh neurologist Dr Keith Brown has estimated
that as many as 200 may exist (Brown 1987). There is no way of knowing the
precise number of neurotransmitters: but as these substances are discovered
and their actions understood, and as drugs are synthesised to block or mimic
them, we will have many powerful new agents at our disposal for treatment.
If this does prove to be the case, as I believe it will, cerebral palsy may
become a condition which is treated primarily by our neurologist colleagues.
We are living in a dynamic time of rapid progress. The science of cere-
bral palsy has progressed rapidly in the past 15 years. However, we have only
just embarked upon what is certain to be a long but exciting journey.
References
Brown, J.K. (1987) Personal Communication.
Delp, S.L., Loan, J.P., Hoy, M.G., Zajac, F.E., Topp, E.L., Rosen, J.M.
(1990) `An interactive graphics-based model of the lower extremity to
study orthopaedic surgical procedures.' IEEE Trans. on Biomedical
Engineering, 37, 757-767.
Guyton, A.C. (1991), `The nervous system'. In Wonsiewicz, M.J. (Ed.)
Textbook of Medical Physiology, 8th Edn, Philadelphia: W.B. Saunders,
p. 482.
Muik, E., ~Ounpuu, S., Gage, J.R., Deluca, P.A. (1990) `The effects of
rectus femoris transfer and release on the gait of children with
cerebral palsy.' Developmental Medicine and Child Neurology, 32
(Suppl. 62), 25.
~Ounpuu, S., Gage, J.R., Davis, R.B. (1991), `Three-dimensional lower
extremity joint kinetics in normal pediatric gait.' Journal of
Pediatric Orthopaedics, 10, 433-442.
Sutherland, D.H., Gage, J.R., Hicks, R. (1987) `Gait patterns in spastic
hemiplegia in children and young adults.' Journal of Bone and Joint
Surgery, 69A, 437-441.
Today, I received a copy of Prof. James R. Gage MD's long-awaited monograph
Gait Analysis in Cerebral Palsy (xvi+208 pp., hard cover, ill.)
(McKeith Press, London 1991)
announced in short on this list on 19 October. The book has been published
in the Series Clinics in Developmental Medicine, with the support of The
Spastics Society, London, U.K.; it is distributed in the U.K. by Blackwell
Scientific Publishers Ltd in Oxford (ISBN 0 901260 90 8), and in the U.S.A.
by Cambridge University Press, New York (ISBN 0 521 41277 3).
Jim Gage has been one of the founding fathers of quantitative, clinical gait
analysis during his position at the Newington Children's Hospital in Newington,
CT/USA. Recently, he moved to the Gilette Children's Hospital at the Univer-
sity of Minnesota Medical School, Minneapolis/St.Paul, MN/USA where he became
the medical director and a professor of orthopaedic surgery.
Rather than providing a discussion of his book (it'll take some time to read
and digest it properly), I'll quote his Table of Contents and Epilogue in full.
Herman J. Woltring, Eindhoven/NL
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
TABLE OF CONTENTS
Foreword (B.G.R. Neville)
Preface
1. Introduction (with Barry S. Russman, M.D.)
2. Basic measurements
3. The neurological control system for normal gait
4. Normal gait
5. Pathlogical gait
6. Principles of treatment in cerebral palsy
7. Hemiplegia
8. Diplegia and quadriplegia
9. Postoperative care
10. Assessment of outcome
11. Epilogue
Index
Chapter 11 -- EPILOGUE (pp. 201-203)
In this short text I have attempted to discuss the nature of the cerebral
palsy lesion, the rationale for treatment, and the use of gait analysis in
the formulation and assessment of that treatment. Now it is time to switch
from the realm of science to the realm of philosophy -- to reflect upon the
road that we have traveled, and then to look forward to the ultimate desti-
nation.
Until the advent of clinical gait analysis laboratories, the treatment of
cerebral palsy was an art, not a science. Physicians tended to treat patients
the way they had been taught, without ever asking why. Beyond the clinical
examination there was seldom any attempt to define the pathology precisely,
very little thought about how the treatments would affect the dynamics of that
pathology in either the short or long term, and not much effort to assess the
outcome of the intervention. Since the priorities of normal gait were not
well understood, the treatments were not aimed at establishing these objec-
tives. There was little understanding about the importance of muscles as
prime movers in gait, or about bones as the levers upon which they act, and
little effort was made to define or preserve muscles which were functioning
as accelerators or to restore their lever arms. As a result, a burden of
iatrogenic injury was often added to the physiological disability inflicted
by the cerebral palsy, and the child was worse off after the intervention
than before. Our physical therapy colleagues recognized this and therefore
often argued long and hard against surgical treatment. Further damage
resulted from prolonged immobilization which left the child weak and stiff,
and frequent interventions converted childhood from a time to play to a
perpetual state of recovery.
Fortunately this is starting to change. Thanks to computerized motion
analysis, we now have a much better understanding of the physiology of gait,
and we are beginning to understand the neurophysiology of motor control.
Because of gait analysis, our treatments have changed a great deal over the
past decade. We have learned about the role of the two-joint muscles in
cerebral palsy and can now understand why they are more severely involved.
This led to the isolated lengthening of the gastrocnemius and the intra-
muscular lengthening of the psoas while sparing the soleus and the iliacus.
We found that we were doing too much weakening of the hip adductors, and
that hip mechanics could be improved and flexion contractures of the hip
reduced without sacrificing hip-flexor power if we did our derotational
osteotomies in the intertrochanteric region proximal to the insertion of
the iliopsoas. The transfers of the distal end of the rectus femoris and
the semitendinosis were introduced. The former has been proven to be very
effective in unlocking the knee in swing (Muik et al. 1990, Sutherland et
al 1990), but there are still some problems with the latter which need to
be worked out.
Through measurement of oxygen consumption and cost, we are beginning to
understand the high energy costs of cerebral palsy and how our surgery
affects those costs. We are starting to use software programs which will
give us an idea how and where this energy is being wasted. One such program
estimates segment energies based on their approximate mass, acceleration and
distance traveled per unit of time. Another looks at each joint as a torque
generator and estimates the net forces which are being produced as a result
of muscle action across the joint (~Ounpuu et al. 1991).
As gait analysis becomes more widely used in the future, orthopaedic sur-
gery will routinely be based on objective evidence of dysfunction and sound
hypotheses. Pattern recognition, which we are already using in the treatment
of hemiplegia (Winters et al. 1987), will be applied to diplegia as well.
Existing statistical pattern recognition techniques can be used to accomplish
this, but very large data bases will be necessary. There will have to be
cooperation between different treatment centers, with data pooling and common
software formats for retrieval. Once pattern recognition in diplegia has been
accomplished, computer software will be written to recognize the criteria of
each pattern so that the computer will be able to make a printout of the
specific pattern type of the involvement, along with the rest of the data.
Treatment protocols will then need to be developed for each of the subtypes.
Since the gait laboratory computers of smaller treatment centers which are
not actively involved in research can use these programs, it will enable
them to tap into this knowledge as well and to apply proven treatments to
each of the various subtypes of involvement. Computer simulation of treat-
ment, which was only a pipe dream 10 years ago, is already being used (Delp
et al. 1990). In retrospect it would appear that our generation and the
ones that preceded it were `the carpenters of orthopaedics'. But because
today's technology has opened up new opportunities, tomorrow's orthopaedists
will need to be true `bio-engineers' of the human frame if they wish to
treat their patients well.
Rapid progress is being made in other fields as well. Selective dorsal
rhizotomy is an exellent example of this, and for the first time we have a
method of preserving or improving function in an appropriately selected
patient, while permanently normalizing muscle tone. It is my personal
feeling that as we gain more knowledge about the neuropharmacology of the
brain, we may be able to develop drugs which will be specific enough to
reduce tone without interfering with other CNS functions. At this time we
are aware of more than 40 different neurotransmitter substances (Guyton
1991). Some of the best known are acetylcholine, norepinephrine, histamine,
GABA and glutamate. The Edinburgh neurologist Dr Keith Brown has estimated
that as many as 200 may exist (Brown 1987). There is no way of knowing the
precise number of neurotransmitters: but as these substances are discovered
and their actions understood, and as drugs are synthesised to block or mimic
them, we will have many powerful new agents at our disposal for treatment.
If this does prove to be the case, as I believe it will, cerebral palsy may
become a condition which is treated primarily by our neurologist colleagues.
We are living in a dynamic time of rapid progress. The science of cere-
bral palsy has progressed rapidly in the past 15 years. However, we have only
just embarked upon what is certain to be a long but exciting journey.
References
Brown, J.K. (1987) Personal Communication.
Delp, S.L., Loan, J.P., Hoy, M.G., Zajac, F.E., Topp, E.L., Rosen, J.M.
(1990) `An interactive graphics-based model of the lower extremity to
study orthopaedic surgical procedures.' IEEE Trans. on Biomedical
Engineering, 37, 757-767.
Guyton, A.C. (1991), `The nervous system'. In Wonsiewicz, M.J. (Ed.)
Textbook of Medical Physiology, 8th Edn, Philadelphia: W.B. Saunders,
p. 482.
Muik, E., ~Ounpuu, S., Gage, J.R., Deluca, P.A. (1990) `The effects of
rectus femoris transfer and release on the gait of children with
cerebral palsy.' Developmental Medicine and Child Neurology, 32
(Suppl. 62), 25.
~Ounpuu, S., Gage, J.R., Davis, R.B. (1991), `Three-dimensional lower
extremity joint kinetics in normal pediatric gait.' Journal of
Pediatric Orthopaedics, 10, 433-442.
Sutherland, D.H., Gage, J.R., Hicks, R. (1987) `Gait patterns in spastic
hemiplegia in children and young adults.' Journal of Bone and Joint
Surgery, 69A, 437-441.