Cerebral Palsy Treatment: Past, Present, Future: A Clinical Perspective with New Scientific Insights
Author:Mark J. Barna PT
Abstract: This article presents a short summary of the impressions and experiences of a Pediatric Physical Therapist who practices Integrative Manual Therapy, with a focus on Cerebral Palsy. This paper highlights the past, present, and future treatment philosophies and techniques available to children with a diagnosis of Cerebral Palsy.
Key Words: Cerebral Palsy, Pediatric, Biomechanics, NDT (Neurodevelopmental Technique), Bobath
Introduction
The purpose of this paper is to present a short summary of my impressions, experiences, and understanding of the past, present, and possible future treatment philosophies and techniques available to children with a diagnosis of cerebral palsy. I do not intend to go into detail regarding all the possible surgical interventions that have been performed in the past or present. The various surgical procedures are too numerous to mention and are not the main focus of this paper. This paper instead will focus on my personal experiences along with the experiences of many other therapists. These observations may differ significantly from other practitioners working in the field of pediatrics.
I am writing this paper in a free flowing format. I am focusing on my answer to the question, "why do severe biomechanical problems continue to occur in the children that we treat?" I am sure that many people will disagree with some of my thoughts and assumptions. However one of the goals for writing this paper is to possibly provoke additional thought and improvement in the area of treatment of children.
I have been a pediatric physical therapist for the past twenty-one years, treating children with a wide variety of disabilities. A high percentage of the children have had a diagnosis of cerebral palsy, and I have also treated children with spina bifida, Downs syndrome and central hypotonia. I have an extensive background in neuro-developmental treatment techniques. I took my basic eight week course seventeen years ago, along with numerous short and advanced courses in neuro-developmental treatment techniques through the years. I also benefitted greatly from having the wonderful opportunity of sharing common office and treatment space with two Neuro-Developmental Treatment certified instructors for twelve years.
By the old definition, the term cerebral palsy reflects a static non-progressive "disorder to movement and posture due to defect or lesion of the immature brain" (1) usually caused by a lack of oxygen to the brain right before birth, during the birth process, or immediately after birth. I purposely stated "by the old definition" because I will discuss later how I believe modern science has started to present us with enough new information that the definition and ideas about the cause of cerebral palsy is changing, which in my mind means that our treatment philosophies should change accordingly.
When I first graduated from physical therapy school in 1979 and for approximately the next four years, the common medical opinion was that when any type of surgical intervention was necessary for a child with cerebral palsy it was expressed as a negative event. The accepted major medical and therapeutic goal or conception was an attempt to avoid any surgical intervention. The major reason for any surgical intervention during that time period was to prevent any further deterioration of mobility, function, range, and status. At that time, it was the common belief or perception, that any specific orthopedic surgical procedure would only need to be performed once during a child's life. The normal standard orthopedic protocol was to initially perform soft tissue muscle tendon lengthening. If that did not correct the decreasing range and mobility along with the increasing deformities, then more invasive and complicated bone surgery would be performed. Unfortunately it was my experience, along with many other orthopedists and therapists, that soft tissue orthopedic surgery was not maintaining the functional range of motion and mobility that was initially gained right after the operation. In our experiences, it has now become the norm, that tendon lengthening surgical procedures will need to be redone as the child grows and will even need to be repeated during adulthood.
The same scenario has now also occurred with children that required bilateral derotational osteotomies. Initially the belief was that children would only require this surgical intervention once during their lifetime, but it has now become relatively common for children to have repeated bilateral derotational osteotomies before they reach adulthood. Another surgical procedure that seems to be on the rise is tibial derotational osteotomies in an attempt to correct the severe biomechanical mal-alignment of the knee due to severe tibial torsion.
After approximately my first five years of working in pediatrics, (from 1984 to the present), I also had the enlightening opportunity to develop a close working relationship with an excellent pediatric orthopedic surgeon and pediatric neurologist; we started to look at surgical intervention as a positive means to increase mobility, range, function, and status. The earlier we could correct the biomechanical dysfunctions in the child, the sooner we could get them upright (sitting, standing, and ambulating), and the better they would function over time. Using this concept during the past sixteen years has resulted in many positive success stories in terms of children achieving functional independence. The use of the selective dorsal root rhizotomy along with orthopedic intervention has also led to many positive results. The recent introduction (approximately five years ago) of threshold electrical stimulation (TES) has also increased the functional status of children that have used the stimulator consistently as designed in their individualized treatment protocols. In our limited experiences with botulinum A toxin injections, we have only seen some short term positive results and have not seen any long term functional positive results or gains. Unfortunately, I have heard of more complications from the use of intrathecal baclofen therapy than positive results.
Another purpose of this paper is to discuss the fact that despite the development and use of past and currently available medical, neurological, and orthopedic philosophies and techniques, the children that we treat still have many serious physical problems. These serious physical problems start with severe biomechanical dysfunctions and continue to increase with age. One of the major problem areas observed by myself and many other physical therapists, is the development of a debilitating pelvic obliquity. Despite all of our advanced neurological, orthopedic, and therapeutic interventions the majority of children that I have treated and observed, with a diagnosis of cerebral palsy, have a developing pelvic obliquity starting with elevated or depressed pubes, inflares or outflares of the ilium, upslip or downslip of the ischium, and an anterior or posterior innominate. (2)
One of the frustrating questions that I have had through the years is that despite all that we are attempting to do from a neurological, orthopedic, and therapeutic perspective, why do our children still have a great number of physical dysfunctions and asymmetries. Another confusing and frustrating issue deals with the question of why do orthopedic surgical procedures need to be repeated and what factors are taking place that cause this process to occur. In the past, it was expressed that growth along with the pull and force of spasticity would cause muscles to become tight again and require repeated orthopedic surgical lengthening procedures. But why then do children who have undergone selective dorsal root rhizotomies still require repeated orthopedic surgical lengthening procedures when their lower extremity spasticity has been taken away? Furthermore, why do all children who have undergone selective dorsal root rhizotomies develop biomechanical problems, such as a pelvic obliquity, severe lumbar lordosis, kyphosis, and scoliosis?
Presently, an orthopedist, who has performed hundreds of bilateral derotational osteotomies is stating that all children that have bilateral derotational osteotomies will have an increased lordotic curve due to the pelvis (ilium) rotating anteriorly right after surgery. (He has taken numerous X-rays's pre-op and post-op bilateral derotational osteotomies, supporting this claim, showing the increase in the anterior rotation of the iliums bilaterally. I believe that he is attributing this pull into an anterior pelvic tilt and an increased lumbar lordosis as a purely common biomechanical phenomena. Our philosophy and intention of bilateral derotational osteotomies is correction of the severe femoral anteversion along with achieving a pelvic tilt more to the posterior direction or rotation. In most of our ambulatory children, (with or without aids), we initially achieved our desired results, (correction of femoral anteversion and pelvic rotation more towards a posterior tilt), but the pelvic obliquity immediately increased post surgically. As stated earlier, the severe problem in children that are post operative bilateral derotational osteometries is their severe developing pelvic obliquity and lumbar lordosis. Since this tendency now appears to be a relatively common occurrence in children with a diagnosis of cerebral palsy, is it possible that this phenomena may be caused by something other than a purely biomechanical reason? Could these severe postural asymmetries be somehow related to other areas of dysfunction? Could it be that all of the hip and lower extremity flexion, adduction and internal rotation are there for a reason and not just spasticity resulting from damage to the internal capsule, motor cortex or pathways? Why do even the minimally involved spastic diplegics have elevated shoulder girdles, protracted shoulders, and internal rotation of their upper extremities along with slightly pronated forearms?
Before I start addressing some of these questions I would first like to go back to the "old definition" of cerebral palsy. What I am about to present is just a very small sampling of the available research literature, which is extensive, in terms of maternal infection and its relationship to cerebral palsy. Modern science and medicine, using many advanced immunochemistry techniques dealing with infection and toxin blood markers, has been recently presenting a great deal of information stating that maternal infection continues to be identified as an important reason for the development of brain damage of the fetus and newborn infant. The maternal infection may be silent (no symptoms), so neither the mother nor physician are aware of it, or the infection can be evident with fever and signs of poor health, often including kidney or bladder infection. In either case, the placenta, the placental membranes and/or the umbilical cord may show signs of infection. The fetal and newborn brain are very susceptible to the toxins produced by infectious agents and to the dysfunction of an infected placenta and umbilical cord. (3)
Other studies, "show that babies of normal birth weight who were exposed to infection in the womb had nine times the normal risk of developing cerebral palsy". (4) Still "other recent studies have linked prenatal infection to premature birth". (5) And more studies report that "interruption of the oxygen supply during birth contributes approximately 6% of spastic cerebral palsy". (6) I have found all of this information extremely enlightening and thought provoking, especially the last group of studies reporting that the "interruption of the oxygen supply during birth contributes approximately 6% of spastic cerebral palsy". (7) Isn't this an almost complete contradiction to the "old definition of cerebral palsy" being caused by problems during labor and delivery causing a lack of oxygen to the brain? (8) Could it be possible that if our past assumptions of the causative factors of cerebral palsy were incorrect, can we also assume that some of our past and present treatment philosophies and techniques may not be giving us our expected and desired results because we are missing some important pieces to the puzzle? As I have been writing this paper I have come across an interesting quote in one Dr. Karen Pape's papers stating that "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." (Orville Wright, 1871-1948, Aviation Pioneer) (9) This quote resonated with me because so much of this new scientific information challenges many assumptions and beliefs that we have all taken to be absolute facts. These are assumptions and beliefs that we use as a basis for our treatment philosophies. Obviously the medical community has made tremendous strides in the treatment of children with cerebral palsy, but does this new scientific information offer possible new and more efficient means for treatment?
Berta and Karel Bobath stated that the "child with cerebral palsy also develops, but at a slower rate. His development, however, is not only retarded, but follows an abnormal course." (10) The Bobaths also stated that "spasticity initially presents itself in the neck, shoulder girdle, and upper extremities and then gradually develops through the hips and lower extremities." (11) Connor, Williamson, and Siepp also state that "the head, neck, and trunk may show hypertonicity before it is apparent in the limbs". (12) They also state that "full rotation between shoulder and pelvis cannot develop when spasticity is present". (13) The Bobaths further state that the sequential acquisition of skill (normal motor development skills) depends upon the higher centers of the brain gradually imposing inhibitory control over responses from the lower centers. However, if something occurs that interferes with this dynamic process, the course of development will proceed along very different lines. Damage to the brain before birth or in earliest childhood may prevent sensory messages from reaching or becoming fully integrated at the higher levels of the central nervous system. Instead, these messages are short-circuited to lower portions of the nervous system, and the responses that emerge are appropriate to responses from those lower levels. Since the lesion has occurred in an immature brain, before development has been completed, the highest centers of the brain may never get a chance to evolve full control over the lower centers. The movement responses that are deprived of higher-level control are manifested as motor patterns that are stereotyped, atypical, and usually associated with an abnormal quality of muscle tone (Bobath, 1966). (14)
The Bobaths also stated that this abnormal postural tone and spasticity blocks the development and refinement of all the righting and equilibrium reactions which are manifested at higher brain level centers. (15)
The medical and scientific communities have both demonstrated some of the extremely complicated and complex compensatory and protective mechanisms within our bodies. These protective mechanisms are extensive, multi-system, and too numerous to mention here. A small sampling of these compensatory and protective mechanisms include many different automatic reactions to fight infection as well as compensations which protect our spinal cord and nervous system when pressure is put on a nerve root. These compensatory and protective mechanisms are life supporting, sustaining, and saving mechanisms that allow us to function in our everyday life.
Relatively new scientific research has stated that heart attacks may be due to cardiac ruptures. The body's natural protective mechanism responds to the rupture by scarring down in that area, sealing the rupture. In doing so, the scarring can cause a blockage in a coronary artery which will cause a heart attack. (16) Further research also indicates that the cardiac rupture may actually be due to an infection in the coronary arteries. (17) This is a possible example of a life saving protective mechanism in our bodies that if it accidently over corrects a problem, or stays in the compensatory or protective mode too long, the results can be more harmful then beneficial, even to the point of ending life instead of sustaining life.
The field of "Integrated Manual Therapy"SM (18) has uncovered and presented a tremendous amount of anatomical, physiological, pathophysiological, and neurological information regarding the body's natural protective and compensatory mechanisms that help sustain life. With all of this new scientific information regarding compensatory and protective mechanisms available to us, is it possible to apply the concepts to other breakdowns within different systems in our body?
When you start to analyze all of the new scientific literature dealing with the possible causative factors of cerebral palsy, maternal infection is coming to the forefront as an important and major factor. Keeping this new scientific information in mind, is it possible that spasticity may be the result or a combination of an automatic protective mechanism from infection, and not solely an internal capsule issue caused by lack of oxygen to the brain?
Before further considering the effect of maternal infection, I would like to include a quick review of prenatal circulation in which umbilical vein supplying nutrients and oxygenated blood, in which a moderate amount first passes through the liver and the ductus venosus into the inferior vena cava and then most of this blood entering the right atrium is directed in a straight pathway across the posterior aspect of the right atrium and thence through the foramen ovale directly into the left atrium of the fetus. Thus, the well-oxygenated blood from the placenta enters the left side of the heart rather than the right side and is pumped by the left ventricle mainly into the vessels of the head and forelimbs. The blood entering the right atrium from the superior vena cava is directed downward through the tricuspid value into the right ventricle. This blood is mainly deoxygenated blood from the head region of the fetus, and it is pumped by the right ventricle into the pulmonary artery, then mainly through the ductus arteriosus into the descending aorta and through the two umbilical arteries into the placenta. Thus, the deoxygenated blood becomes oxygenated. (19)
Is it conceivable and possible that due to an infection or toxic process within the mother, that the fetus must find a way to contain this process or suffer life threatening consequences? It has been previously stated that "the fetal and newborn brain are very susceptible to the toxins produced by infectious agents and to the dysfunction of an infected placenta and umbilical cord." (20) Therefore, is it conceivable and possible that the fetus has some type of protective mechanism that attempts to contain or control this infection or toxic process? Hypothetically speaking, one would also expect to find this protective mechanism, that attempts to control an infection or toxic process, in an area of the fetus close to where it receives maternal blood before the infection or toxic process can circulate throughout the body. I find it extremely interesting that the body of the fetus is designed in such a way that a moderate amount of oxygenated blood from the placenta will first pass through the primary detoxification system (liver of fetus) before it is circulated throughout the rest of the body. Could this be designed as a possible first line of defense for any toxins or infections that pass through the placenta? In other words, with this understanding of prenatal circulation, and knowledge that the immature liver of a fetus does not have the ability and capacity for full detoxification as we know it, is it possible to assume that the next area of protection in order to prevent the infection or toxic process from circulating throughout the body might be in the heart and lungs of the fetus? These could be the next major line of defense of the fetus in order to fight, contain, or isolate the infection or toxin process before it is circulated throughout the body of the fetus. I find this hypothetical process very intriguing and thought provoking. As I mentioned earlier, when discussing most children with a diagnosis of cerebral palsy, "the Bobaths' also stated that spasticity initially presents itself in the neck, shoulder girdle, and upper extremities and then gradually develops through the hips and lower extremities." (21) Connor, Williamson, and Siepp also state that "the head, neck, and trunk may show hypertonicity before it is apparent in the limbs". (22) To continue with the hypothesis, it is possible that the spasticity that initially develops in the neck, shoulder girdle, and upper extremities is there as part of a protective mechanism that is attempting to fight, control, isolate, or contain the infection or toxic process in the fetus? As one studies the anatomy of the circulatory system especially around the heart and the path up to the brain, one starts to develop a tremendous appreciation of the extremely complex structural anatomy of the area. The system includes but is not limited to the inferior and superior vena cava, pulmonary arteries and veins, pulmonary trunk, aorta, arch of aorta, subclavian arteries, brachiocephalic trunk, common carotid arteries, external and internal carotid arteries, vertebral arteries, basilar artery, posterior cerebral arteries, middle cerebral arteries, and anterior cerebral arteries. It is conceivable that such a highly complex structural area would have it own self protective mechanisms. This intricate circulatory structural area is also located in the area where spasticity is first observed in all the children with a diagnosis of cerebral palsy.
This invites us to ask many questions. Is it just a coincidence that this is the initial area that spasticity presents itself, or is primary damage only in the area of the internal capsule and motor cortex, or is it part of an extremely complex and intricate protective mechanism within the body of the fetus that has been activated due to an infection or toxic process that has passed through the placenta blood barrier, or is it some form of combination of all the above factors?
It appears to me that modern science, using many advanced immunochemistry techniques, is presenting a tremendous amount of research supporting a major correlation and link between maternal infection and cerebral palsy. I feel that this relatively new scientific research data presents a new basis and foundation of information in terms of treatment philosophies and techniques that are used in treatment of children with cerebral palsy.
In the forward of Integrative Manual TherapySM for the Autonomic Nervous System, Dr. Mary Lynch briefly states that:
The autonomic nervous system is the normally involuntary or unconscious division of the peripheral nervous system. Its' efferent stimulation of all smooth muscles from blood vessels, lymphatic vessels, organs and glands as well as the resting muscle tone that allows us to sit up is a function of this autonomic nervous system. The autonomic nervous system has two divisions, the sympathetic and theparasympathetic. The parasympathetic system regulates the functions necessary for long term survival. Everything from salivation and digestion to heart rate, respiratory rate, pancreatic function, liver and gallbladder function, and urine excretion hrough thet kidneys, ureters and bladder, are only a few of the things that fall under autonomic control. The sympathetic system meets all crises; it spares no expense. The parasympathetics pick up after the sympathetics, replenishing, restoring and replacing, preparing for a rainy day. And when the parasympathetics can no longer keep up all life becomes a crisis and the overload escalates more and more with less and less provocation. All cells have sympathetic innervation, including blood vessels which when hypertonic, decrease distribution of oxygen even to the brain in crisis. The impact of this is reduced healing, increased hypertension, facilitated segments, changes in endocrine function impacting metabolism, brain function and ultimately all homeostatic mechanisms. (23)
As stated above, since "efferent stimulation of all smooth muscles from blood vessels, lymphatic vessels, organs and glands as well as the resting muscle tone that allows us to sit up is a function of this autonomic nervous system," (24) it is easy to see how this system, when facilitated, will use protective muscle spasm as a means of protection. It is conceivable, therefore, that the abnormal posturing and spasticity that children with cerebral palsy demonstrate, is also part of a major protective or containment mechanism of the body in order to prevent further damage to the brain, heart, aorta, subclavian arteries, carotid arteries, vertebral arteries, iliac arteries, femoral arteries, lungs, or any other organ or tissues due to an infection or toxic process. I feel that it is very conceivable and probable, for example, that when performing bilateral derotational osteotomies, and any additional elongation to the muscles, especially the adductors and hamstrings, along with the external rotation gained from the osteotomy, puts additional stress on the body's autonomic protective mechanism which causes it to actually increase or amp up its protective mode. Since the derotational osteotomies and subsequent muscle lengthening have put additional stress on the circulatory system, (aortic kinetic chain) the body's natural autonomic protective response is to further compress or constrict the vessels or organs that it is attempting to protect. This natural protective mechanism may be at the root of the cause of the pelvic obliquity and severe lumbar lordosis in our post-operative bilateral derotational osteotomy and tendon lengthening children. Since the protective mechanism of the artery, vein, nerve, myofascial, muscle, and lymph tissue has been further disrupted by the surgery, the body may actually be forced into a higher protective mode. This higher protective mode may then manifest itself by further restricting the movement of the components of the circulatory system (aortic kinetic chain) which is associated with the spine and pelvis. It is well documented that, "many spinal and pelvic asymmetries are the result of a protective mode of the body for protection of the circulatory system." (25)
I feel that it is necessary to give a brief summary of Integrated Manual Therapy'sSM hypothetical model of the body's natural hierarchy of protection because it's underlying philosophy gives a tremendous insight into new treatment philosophies and techniques for children with cerebral palsy, especially with all of the new scientific research information supporting an extremely strong correlation and link between maternal infection and cerebral palsy. Integrative Manual TherapySM, developed by Sharon Weiselfish-Giammatteo, Ph.D.,P.T., has given us a hypothetical model of the body's natural hierarchy of protection.
When the body's protection lasts after the tissue heals, this is the result of sustained neuro-reflexogenic protective modes. Regarding these sustained Neuro-reflexogenic protective modes: - the body has the inherent ability to provide protection, this ability is at least as profound as the body's ability to self-correct and self-heal
- the body's innate mechanisms of self- protection are reflexogenic, autonomic, and automatic
- the body's self-protection mode is initially a secondary problem, it is able to be transformed into a primary problem, the initial primary problem which required protection may or may not heal.
Some types of sustained neuro-reflexogenic protection modes include:
- compression syndromes (multiple system contractions)
- contractures, and
- contractions.
Some problems which commonly require protection are:
- arterial perfusion
- venous toxicity (CO2 toxicity)
- neural tissue tension
- disruptions of membranes of visceral tissue
- lymph derangement
- bone bruises
- infections, and
- toxins.
The sequence of hierarchy of significance of problems which require protection is as follows: arteries, veins, neural tissue, visceral tissue and finally lymphatic tissue. The significance of the above sequence of hierarchy of significance of problems which require protection is as follows:
- visceral tissue protects neural tissue, veins, and
arteries;
- neural tissue protects veins and arteries
- veins protect arteries
- arteries require maximalprotection
- all connective tissue which is meant to protect, protects arteries, veins, neural tissue and visceral tissue
- lymphatic tissue which is meant to protect, protects visceral tissue, neural tissue, veins, arteries, and other connective tissue problems.
Some possible results from these protective modes are muscle spasm, neural tissue contraction, ligament contraction, tendon spasm and connective tissue tension. Some possible initiating etiologies which cause protective modes are infection, inflammation, disruption of membrane integrity, and toxicity. In order to protect the deeper tissues, the superficial tissues also protect and must be treated for primary protective muscle spasm, which includes protective muscle spasm, muscle spasm of tissues innervated by the autonomic nervous tissue, fascial dysfunction, and biomechanical dysfunction with quantum disturbance of the intra-articular space. (26)
Almost all the past and present treatment philosophies and techniques for children with cerebral palsy deal with treating the signs and symptoms that were assumed to be a direct result of brain damage caused by lack of oxygen to the brain. Most philosophies and techniques, ranging from orthopedic surgery, neuro-surgery, botox, neuro-developmental techniques, threshold electric stimulation, etc., deal with attempting to influence, decrease, or change the abnormal muscle tone and spasticity that is always associated as being the primary problem or issue. In most cases, we have treated and continue to treat the muscle (spasticity) as the primary problem, mainly because it has become the primary problem, while we know that the majority of our children's problems are neurologically based. In an oversimplification of the traditional treatment process, we are attempting to change or influence the dysfunctional internal structures (brain and central nervous system) from input from the outside or the periphery (peripheral nervous system). We are constantly attempting to influence or change the child's abnormal muscle tone and spasticity, while at the same time, we are attempting to facilitate more functional movement patterns. I always found it very interesting, that early on, NDT was severely criticized for being a non-functional treatment approach and in reality the basis of NDT is to improve function through movement.
The majority of traditional treatment philosophies and techniques used in the treatment of children with cerebral palsy place their main emphasis on improving function. Scientific research has taught us that function influences structure and that structure dictates function. (27) When we apply this concept to our treatment philosophies and techniques we can begin to understand how, sometimes we fall short of our goals to improve functional independence despite our best intentions. If we are specifically working on function without having proper biomechanical balance in the specific joints that we are working on, along with proper biomechanical balance throughout the body, that child will be forced to use many compensations in order to improve the functional piece. I believe, that some early criticism of NDT was initiated because some people incorrectly assumed that NDT stated that you could not allow a child to move using their spasticity. This misconception could not be further from the truth, because early NDT simultaneously involved many techniques used to inhibit spasticity, along with many techniques used to facilitate a more normal movement pattern that would allow for improved function. The NDT treatment process was also attempting to improve gross biomechanical integrity of the body in order to facilitate more functional normal skills. A brief explanation of the neurophysiological piece of NDT, is that as the child experienced a more normal movement pattern, it would facilitate this pattern to be repeated by the child, possibly using different undamaged pathways or cortex areas. The NDT approach "utilizes an in-depth analysis of the intricacies of movement and how the details relate to the whole to allow for functional movement in a wide variety of environments". (28) The NDT philosophy also is based on the, "belief that control of movement is based on a complex interaction of many body systems which are plastic and adaptable, as well as on the tasks presented and the environments in which the tasks are performed. Therefore, function can be altered by changing any one or all of the elements." (29)
Since it was believed that damage to the brain at birth may prevent sensory messages from reaching or becoming fully integrated at the higher levels of the central nervous system, if we could facilitate and put in more appropriate normal sensory and motor movements, the child will eventually start to integrate these more normal sensory and motor patterns. But, in regard to any treatment philosophy and technique, one of the major underlying facts remain, that structure dictates function. I do not mean simply the gross biomechanical structure, because gross biomechanical structure is determined by the underlying anatomy, patho-anatomy, neuro-anatomy, physiology and patho-physiology of the child. For example, I found it noteworthy that Carl DeRosa, PT, PhD, in his lecture at last years APTA's Annual Conference, the John HP Maley Lecture which focuses on an evolving physical therapy environment, discussed how he, "came to appreciate the complexity and absolutely critical interactions between all essential elements (referring to different systems of the body). Very simply, parts are often linked albeit mechanically or neurologically, to allow the human body to function in the marvelous way that it does. Everything is connected to everything." (30)
This is where the field of Integrative Manual TherapySM plays such an essential and important role. Integrative Manual TherapySM attempts to uncover and address the root or initial source or sources of the dysfunctional tissues as well as all the compensations that have occurred in the body in order for the child to attempt to function in their environment. Integrative Manual TherapySM encompasses a multitude, and continually expanding repertoire, of innovative diagnostic and treatment techniques. All body systems can be addressed within the
Integrated Systems ApproachSM for Integrative Manual TherapySM. Some techniques include but are not limited to: Myofascial Release, Myofascial MappingC, Strain and Counterstrain, Advanced Strain and Counterstrain, Muscle Energy and 'Beyond' Technique, Neural Tissue Tension Techniques, Compression Syndromes, Visceral Mobilization, Lymphatic Congestion Therapy, and Neurofascial ProcessC. Since structure dictates function, and function influences structure, we must find the means to address and correct the underlying structure and/or body system requiring facilitated assistance in order to improve functional outcomes. The two go hand in hand, one cannot successfully address one without the other. Despite all of our intensive efforts, however, it seems that we continue to attempt to work on functional goals while the child still has a great deal of dysfunctional structural and biomechanical problems and compensations. It has become entirely evident that this process does not allow us to reach our desired or expected results. The new scientific research dealing with maternal infection and its relationship to cerebral palsy just further emphasizes the need to attempt to get to the root or source of the problem. In this case, the question remains, is the abnormal tone and spasticity also part of a higher level autonomic and automatic protective mechanism? Recently, with the advancement of MRIs, reports from pediatric neurologists have ranged from stating that based upon the child's normal MRI, he cannot understand why the child has such severe motor deficits, to reports stating that based upon the child's severely abnormal MRI, he cannot believe how functional and what few motor deficits the child demonstrates. This information is no longer as confusing, when an in-depth knowledge of anatomy, patho-anatomy, neurology, physiology, pathophysiology, and embryology, along with the understanding and knowledge of how all of these systems are interrelated and interact with each other. Rather, as Conner, Williamson, and Siepp has stated earlier, in reference to the child with cerebral palsy, "instead, these messages are short-circuited to lower portions of the nervous system, and the responses that emerge are appropriate to responses from those lower levels. Since the lesion has occurred in an immature brain, before development has been completed, the highest centers of the brain may never get a chance to evolve full control over the lower centers." (31)
This statement is harmonious with the concepts that in "normal child development" the brain does not fully develop and come completely on-line until approximately the age of eight, especially the cerebellum. Furthermore, we have the words of Dr. Karen Pape:
" the cerebellum is one of the later developing areas of the brain and cerebellar neuroblasts migrate until approximately two years of age. Then they begin to differentiate and between 4 and 6 years, they connect up to the rest of the brain. In the human, the cerebellum is in charge of rapid sequenced movement. A good layman's description is that this is the center of coordination. The cerebellum is also intimately involved with the corticospinal system, modifying and augmenting the basic movements." (32)
With all of this new scientific information and new facts in regards to the neural placidity of the brain and it's potential for regeneration, the continuing question is, why is it that our children with cerebral palsy, despite all of our interventions, continue to have severe physical and functional problems as they grow? Science has given us considerable evidence, and even with regeneration and new brain tissue growth, if a child's brainstem protective mechanism has been facilitated into operation for life sustaining purposes, the higher centers of the brain, despite their capacity and potential for growth and regeneration, will not be able to develop control over lower centers of the body. Therefore, the child with cerebral palsy continues to function on a brainstem level, with "the movement responses that are deprived of higher-level control are manifested as motor patterns that are stereotyped, atypical, and usually associated with an abnormal quality of muscle tone (Bobath, 1966)". (33) This process continues to occur and be re-enforced in our children due to the severity of the neuro-reflexogenic self-protection mode.
In summary, using a variety of these treatment approaches has obviously made tremendous strides and improvements in the treatment of children with cerebral palsy, but most of our children still have many major physical issues, problems and challenges. We have been treating spasticity as the initial and primary problem. In retrospect, however, when analyzing all the new scientific information dealing with maternal infection, and some of the basic underlying principles of Integrated Manual TherapySM, we can reasonably hypothesize that the abnormal spasticity was initially the body's natural, autonomic, and automatic means of protection that has now become the primary problem. The initial problem seems to be the maternal infection, toxin, or autoimmune response that passes through the placenta blood barrier and facilitates the fetus' self-protective modes. Since this infection, toxin, or autoimmune piece is in the circulatory system of the fetus, near the heart and lungs, we would only expect to see the highest degree of protection, which is supported by the Integrative Manual TherapySM hierarchy of self-protection. Due to the extremely high level of sensitivity and importance of this circulatory area around the heart, lungs, and leading up to the brain of the fetus, we can fully understand how a protective mode in this area could easily become hyper-facilitated and self-perpetuating. We could also expect that this process would become even more hyper-facilitated and dysfunctional if the infection, inflammatory, or toxin process reaches the internal capsule. This process will result in exacerbating a protective mode or mechanism into a primary debilitating problem. As stated earlier, normal motor development, "depends upon the higher centers of the brain gradually imposing inhibitory control over responses from the lower centers. However, if something occurs that interferes with this dynamic process, the course of development will proceed along very different lines." (34)
These brainstem neuro-reflexogenic protective modes may prevent information from reaching or becoming fully integrated at the higher levels of the central nervous system. Instead, these messages are short-circuited at the brainstem level, "and the responses that emerge are appropriate to responses from those lower levels. Since the lesion has occurred in an immature brain, before development has been completed, the highest centers of the brain may never get a chance to evolve full control over the lower centers." (35)
It is due to this process along with the role of the body's natural neuro-reflexogenic protective mechanisms, that despite the development and use all of our advanced and intensive medical, surgical, neurological, orthopedic, and therapeutic interventions, philosophies, and techniques, that the children we treat continue to have many serious physical, functional, and biomechanical dysfunctions and problems.
I have found that the field of Integrative Manual TherapySM will allow the children that we treat the opportunity to reach their fullest independent functional potential. As stated previously, many past and present day treatment interventions, philosophies, and techniques for children with cerebral palsy continue to be limited by severe underlying structural and biomechanical problems, and they can only bring a child to the point that their underlying physical structure will allow. Integrative Manual TherapySM gives the therapist the opportunity to address, treat, and correct core dysfunctional structural and biomechanical areas, as well as all the compensations that have occurred in the body, that are directly hindering functional outcomes. It gives the therapist the opportunity to be extremely specific in terms of why certain components of movement have not yet been achieved, or why certain severe postural asymmetries remain and continue to increase, in addition to greatly limiting a child's functional abilities. Integrative Manual TherapySM, which is based upon an in-depth knowledge of the underlying anatomy, patho-anatomy, biomechanics, neuro-anatomy, physiology and patho-physiology of the body, allows the therapist to treat the underlying primary and secondary dysfunctional structural and biomechanical tissues that are impeding function. As the underlying dysfunctional structural and biomechanical issues are addressed and corrected, function can be tremendously improved. Integrative Manual TherapySM opens the window of opportunity for improved potential and functional outcomes for each and every child.
We presently live in a very exciting time period in the field of pediatric rehabilitation. Modern science is giving us a much deeper understanding of all the intricate anatomical, biomechanical, neurological, and physiological inter-relationships within our bodies. We are standing at the threshold of limitless potential and possibilities for rehabilitation and restoration. There continues to be growing scientific evidence that the capacity and potential for central nervous system plasticity, regeneration, reorganization, and recovery is far greater than previously imagined. It is with the advent and growth of this new information that we can start to address some of these issues in order to more efficiently and successfully treat our children.
Works Cited
1 Green, Jones, Mac Keith, Bax, Scrutton, Thimpson, Denhff, Bleck, Sharrard, Evens, Banaks, Goldner, Perry, Hoffer, Samilson. Orthopaedic Aspects Of Cerebral Palsy. London: Heinemann Medical Books, 1975.
2 Weiselfish, S.; Manual Therapy with Muscle Energy Technique For the Pelvis, Sacrum, Cervical, Thoracic and Lumbar Spine. West Hartford, Conn: ANA Publishing, 1994.
3 Grether, J.K. Nelson, K.B. "Maternal Infection and Cerebral Palsy in Infants of Normal Birth Weight." JAMA, July, 16, 1997;278:3.
4 Grether, J.K.; Nelson, K.B. "Maternal Infection and Cerebral Palsy in Infants of Normal Birth Weight." JAMA, July, 16, 1997;278:3.
5 Dammann O, Leviton A. "Maternal Intrauterine Infection, Cytokines, and Brain Damage in the Preterm NewBorn." Pediatric Res July 1997; 42(1):1-8.
6 Nelson, K.B. Grether J.K.. "Causes of Cerebral Palsy." Current Opinion Perdiatrics, Dec. 1999; 11(6):487-91.
7 Nelson, K.B. Grether J.K.. "Causes of Cerebral Palsy." Current Opinion Perdiatrics, Dec. 1999; 11(6):487-91.
8 United Cerebral Palsy Research and Educational Foundation; "Some Thoughts on the Prevention of Cerebral Palsy." Jan. 1997.
9 Wright, Orville.
10 Bobath, B., Bobath, K.. Motor Development in the Different Types of Cerebral Palsy. London: Heinemann Medical Books, 1975.
11 Bobath, B., Bobath, K.. Motor Development in the Different Types of Cerebral Palsy. London: Heinemann Medical Books, 1975.
12 Connor F., Williamson G., Siepp J.. Program Guide for Infants and Toddlers With Neuromotor and Other Developmental Disabilities. New York: Teachers College Press, 1978.
13 Connor F., Williamson G., Siepp J.. Program Guide for Infants and Toddlers With Neuromotor and Other Developmental Disabilities. New York: Teachers College Press, 1978.
14 Connor F., Williamson G., Siepp J.. Program Guide for Infants and Toddlers With Neuromotor and Other Developmental Disabilities. New York: Teachers College Press, 1978.
15 Bobath, K., Bobath, B.. "Cerebral Palsy." Physical Therapy Services in the Developmental Disabilities. P.H. Pearson and C. E. Williams, Eds. Springfield, Ill.: Thomas 1972.
16 Oliva, P. "Cardiac Rupture." Science and Medicine. November/December 1998; Volume 5, Number 6.
17 Muhlestein, J.. "Chronic Infection and Coronary Artery Disease." Science and Medicine, November/December 1998;Volume 5,Number 6.
18 Giammatteo, T. Weiselfish-Giammatteo, S., Dialogues in Contemporary Rehabilitation.
19 Guyton, A.. Basic Human Physiology: Normal Function and Mechanisms of Disease. Philadelphia, PA: W.B. Saunders Company.
20 Grether, J.K. Nelson, K.B.. "Maternal Infection and Cerebral Palsy in Infants of Normal Birth Weight." JAMA, July, 16, 1997;278:3.
21 Bobath, B., Bobath, K.. Motor Development in the Different Types of Cerebral Palsy. London: Heinemann Medical Books, 1975.
22 Connor F., Williamson G., Siepp J.,; Program Guide for Infants and Toddlers With Neuromotor and Other Developmental Disabilities. New York: Teachers College Press, 1978.
23 Lynch, M.; Foreward in Integrative Manual TherapySM for the Autonomic Nervous System; Giammatteo, T. Weiselfish-Giammatteo, S.. Berkeley, CA: North Atlantic Books, 1997.
24 Lynch, M.; Foreward in Integrative Manual TherapySM for the Autonomic Nervous System; Giammatteo, T. Weiselfish-Giammatteo, S.. Berkeley, CA: North Atlantic Books, 1997.
25 Giammatteo, T. Weiselfish-Giammatteo, S.. Dialogues in Contemporary Rehabilitation.
26 Giammatteo, T. Weiselfish-Giammatteo, S.. Dialogues in Contemporary Rehabilitation.
27 Giammatteo, T. Weiselfish-Giammatteo, S.. Dialogues in Contemporary Rehabilitation.
28 The Basis of NDT and Current Concepts; "NDTA Progress In Motion"; Neuro-Developmental Treatment Association, Inc. March 2000.
29 The Basis of NDT and Current Concepts; "NDTA Progress In Motion"; Neuro-Developmental Treatment Association, Inc. March 2000.
30 DeRosa, C.. "Innovation In Physical Therapy Practice." PT Magazine. 2000 Feb.;8(2):40-6.
31 Connor F., Williamson G., Siepp J.. Program Guide for Infants and Toddlers With Neuromotor and Other Developmental Disablilities. New York: Teachers College Press, 1978.
32 Pape, K. "Get To Know Your Brain." TASC NetLetter. 2000 Jan/Feb.;2(1):1
33 Connor F., Williamson G., Siepp J.. Program Guide for Infants and Toddlers With Neuromotor and Other Developmental Disablilities. New York: Teachers College Press, 1978.
34 Connor F., Williamson G., Siepp J.. Program Guide for Infants and Toddlers With Neuromotor and Other Developmental Disablilities. New York: Teachers College Press, 1978.
35 Connor F., Williamson G., Siepp J.. Program Guide for Infants and Toddlers With Neuromotor and Other Developmental Disablilities. New York: Teachers College Press, 1978.
Bibliography
Baud, O., Emilie, D., Pelletier, E., Lacaze-Masmonteil, T., Zuoan, V., Fernandez, H., Dehan, M., Frydman, R., Ville, Y., "Amniotic Fluid Concentrations of Interleukin-1beta,Interleukin-6 and TNF-alpha In Chorioamnionitis Before 32 Weeks of Gestation: Histological Assocaitions and Neonatal Outcome." Br. Journal Obstet. Gynecologists. 1999 Jan;106(1):72-7.
Beintema, D.J. A Neurological Study of Newborn Infants (Clinics in Developmental Medicine, No.28). London: Heinemann Medical Books, 1968.
Bobath, B., Bobath, K.; Motor Development in the Different Types of Cerebral Palsy. London: Heinemann Medical Books, 1975.
Bobath, B., "The Very Early Treatment of Cerebral Palsy." Developmental Mecicine and Child Neurology, 1967,9.
Bobath, B.. Abnormal Postural Reflex Activity Caused By Brain Lesions, (2nd ed.) London: Heinemann Medical Books, 1971.
Bobath, K., Bobath, B.. Cerebral Palsy. In P.H. Pearson and C. E. Williams (Eds.), Physical Therapy Services in the Developmental Disabilities. Springfield, Ill.: Thomas 1972.
Bobath, K. The Motor Deficit In Patients With Cerebral Palsy, (Clinics in Developmental Medicine, No. 23). London: Heinemann Medical Books, 1966.
Connor F., Williamson G., Siepp J.,; Program Guide for Infants and Toddlers With Neuromotor and Other Developmental Disablilities. New York: Teachers College Press, 1978.
Dammann, O., Leviton, A. "Brain Damage In Preterm Newborns: Might Enhancement of Developing Regulated Endogenous Protection Open a Door For Prevention?" Pediatrics 1999 Sept;104(# Pt 1):541-5.
Dammann, O., Leviton, A. "Infection Remote From the Brain, Neonatal White matter Damage, and Cerebral Palsy In the Preterm Infant." Semin Pediatric Neurology 1998 Sept;5(3):190-201.
Dammann, O., Leviton, A. "Maternal Intrauterine Infection, Cytokines, and Brain Damage in the Preterm Newborn." Pediatric Res 1997 July;42(1):1-8.
DeRosa, C. "Innovation In Physical Therapy Practice." PT Magazine 2000 Feb.;8(2):40-6.
Dommergues, M.A., Patkai, J., Renauld, J.C., Evrard, P., Gressens, P., "Proinflammatory Cytokines and Interleukin-9 Exacerbate Excitotoxic Lesions of the Newborn Murine Neopallium." Ann. Neurol 2000 Jan.;47(1):54-63.
Dudley, D.J., Trautman, M.S., Edwin, S.S., Lundin-Schiller, S.,Mitchell, M.D., "Biosynthesis of Interleukin-6 By Cultured Human Chorion Laeve Cells: Regulation By Cytokines." Journal Clin. Endocrinol Metab. 1992 Oct;75(4):1081-6.
Ellis, W.G., Goetzman, B.W., Lindenberg, J.A., "Neuropathologic Documentation of Prenatal Brain Damage." Am. Journal Dis. Child 1988 Aug;(8):858-66.
Eschenbach, D.A., "Amniotic Fluid Infection and Cerebral Palsy. Focus on the Fetus." JAMA, July, 16,1997;278(3):247-248.
Giammatteo, T. Weiselfish-Giammatteo, S. Integrative Manual TherapySM for the Autonomic Nervous System. Berkeley, CA: North Atlantic Books, 1997
Giammatteo, T. Weiselfish-Giammatteo, S. Dialogues in Contemporary Rehabilitation.
Green, Jones, Mac Keith, Bax, Scrutton, Thimpson, Denhff, Bleck, Sharrard, Evens, Banaks, Goldner, Perry, Hoffer, Samilson. Orthopaedic Aspects Of Cerebral Palsy. London: Heinemann Medical Books, 1975.
Grether, J.K. Nelson, K.B.; "Maternal Infection and Cerebral Palsy in Infants of Normal Birth Weight." JAMA, July, 16, 1997;278:3.
Grether, J.K.; Nelson, K.B.. "Maternal Infection and Cerebral Palsy in Infants of Normal Birth Weight." JAMA, July, 16, 1997;278:3.
Gomez, R., Romero R., Ghezzi, F., Yoon, B.H., Mazor, M., Berry, S.M. "The FetalInflam matory Response Syndrome." Am. Journal Obstet. Gynecol. 1998 July;179(1):194-202.
Guyton, A. Basic Human Physiology: Normal Function and Mechanisms of Disease. Philadelphia,Pa: W.B. Saunders Company.
Keelan, J.A., Marvin, K.W., Sato, T.A., Coleman, M., McCowan, L.M., Mitchell, M.D., "Cytokine Abundance In Placental Tissues; Evidence of Inflammatory Activation In Gestational Membranes With Term and Preterm Parturition." Am. Journal Obstet. Gynecol. 1999 Dec.;181(6):1530-6.
Kim, J.N., Namgung, R., Chang, W., Oh, C.H., Shin, J.C., Park, E.S., Park, C.I.., Park, M.S., Park, K.I., Lee, C., Han, D.G. "Prospective Evaluation of Perinatal Risk Faactors for Cerebral Palsy and Delayed Development In High Risk Infants.", Yonse Med. J. 1999 Aug;40(4):363-70.
Larson, N.; Study Ties Cerebral Palsy to Inflammation and Blood-Clotting Abnormalities. News Release; National Institute of Neurological Disorders and Stroke, October 1, 1998.
Lieberman, E., Lang. J., Richardson, DK., Frigoletto FD., Heffner, LJ., Cohen, A. "Inatrapartum Maternal Fever and Neonatal Outcome." Pediatrics 2000 Jan;105(1Pt):8-13
Luheshi, G., Rothwell, N. "Cytokines and Fever." Int. Arch. Allergy Immunol. 1996 April;109(4):301-7.
Lynch, M.; Foreward in Integrative Manual Therapy for the Autonomic Nervous System; Giammatteo, T. Weiselfish-Giammatteo, S.. Berkeley, CA: North Atlantic Books, 1997
Martius, J.A., Roos, T., Gora, B., Oehler, M.K., Schrod, L., Papadopoulos, T., Gross, U., "Risk Factors Associated With Early- Onset Sepsis In Premature Infants." Eur. Journal Obstet. Gynecol. Reprod. Biol. 1999 Aug.;85(2):151-8.
Muhlestein, J. "Chronic Infection and Coronary Artery Disease." Science and Medicine, Nov/Dec 1998;Volume 5,Number 6
Murphy, D.J., Johnson, A. "Placental Infection and Risk of Cerebral Palsy in Very Low Birth Weight Infants." Journal of Pediatrics, Nov. 1996;129(5):776-8.
Nelson, K.B.; Dambrosia, J.M.; Grether, J.K.; and Phillips, T.M. "Neonatal Cytokines and Coagulation factors in Children with Cerebral Palsy." Annals of Neurology, October 1998, Vol. 4 No.4, pp 665-667.
Nelson, K.B., Ellenberg, J.H. "The Asymptomatic Newborn and Risk of Cerebral Palsy." Am. Journal Dis. Child 1987 Dec;141(12):1333-5.
Nelson, K.B. Grether J.K.; Causes of Cerebral Palsy. Current Opinion Pediatrics, Dec. 1999; 11(6):487-91.
Nelson, K.B., Grether, J.K.. "Potentially Asphyxiating Conditions and Spastic Cerebral palsy In Infants of Normal Birth Weight." Am. Journal Obstet. Gynecol. 1998 Aug;(179(2):507- 13.
NDTA. "NDTA Progress In Motion." The Basis of NDT and Current Concepts. Neuro-Developmental Treatment Association, Inc: March 2000.
Oliva, P. "Cardiac Rupture." Science and Medicine, November/December 1998; Volume 5, Number 6.
O'Shea, T.M., Klinepeter, K.L., Dillard, R.G.. "Prenatal Events and the Risk of Cerebral Palsy in Very Low Birth Weight Infants." Am. Journal Epidemiol 1998 Feb. 15;147(4):362-9.
O'Shea, T.M., Klinepeter, K.L., Meis, P.J., Dillard R.G.. "Intrauterine Infection and the Risk of Cerebral Palsy In Very Low-birthweight Infants." Paediatric Perinat Epidemiol Jan.; 12(1):72-83.
Pape, K., "Get To Know Your Brain", TASC NetLetter, 2000 Jan/Feb.;2(1):1
Perlman, J.M., "Maternal Fever and Neonatal Depression: Preliminary Observations." Clinical Pediatrics (Phila) 1999 May;38(5):287-91
Redline, R.W., Wilson-Costello, D., Borawski, E. Fanaroff, A.A., Hack, M. "Placental Lesions Associated With Neurologic Impairment and Cerebral Palsy In very Low-Birth-Weight Infants." Arch. Pathol. Lab. Med., 1998, Dec;122(12):1091- 8.
Spinillo, A., Cappuzzo, E., Orcesi, S., Stronati, M., Di Mario, M., Fazzi, E., "Antenatal and Delivery Risk Factors Simultaneously Associated With Neonatal Death and Cerebral Palsy in Preterm Infants." Early Human Development 1997 April 25;48(1-2):81-91.
United Cerebral Palsy Research and Educational Foundation; Some Thoughts on the Prevention of Cerebral Palsy, Jan. 1997.
Uvebrant, P., Hagberg, G., "Intrauterine Growth In Children With Cerebral Palsy." Acta Pediatric 1992 May;81(5):407-12.
Weiselfish, S. Manual Therapy with Muscle Energy Technique For the Pelvis, Sacrum, Cervical, Thoracic and Lumbar Spine. West Hartford, CT: ANA Publishing, 1994.
Yoon, B.H., Romero, R., Jun, J.K., Park, J.D., Ghezzi, F., Kim, B.I.. "Amniotic Fluid Cytokines (Interleukin-6, Tumor Necrosis Factor-alpha, Interleukin-1 Beta, and Interleukin- 8) and the Risk For the Development of Brochopulmonary Dysplasia." Am. Journal of Obstet. Gynecol. 1997 Oct.;177(4):825-30.
Yoon, B.H., Jun, J.K., Romero, R., Jun, K.H., Gomez, R., Choi, J.H., Kim, I.O. "Amniotic Fluid Inflammatory Cytokines (Interleukin-6, Interleukin-1 Beta, and Tumor Necrosis Factor-alpha) Neonatal Brain White Matter Lesions, and Cerebral Palsy." Am. Journal of Obstet. Gynecol.1997 July;177(1):10-26.
Yoon, B.H., Romero, R., Yang, S.H., Jun, J.K., Kim, I.O., Choi, J.H., Syn, H.C. "Interleukin-6 Concentrations In Umbilical Cord Plasma Are Elevated In Neonates With White Matter Lesions Associated With Periventricular Leukomalacia." Am. Journal Obstet. Gynecol 1996 May;174(5):1433-40.
Yudkin, P.L., Johnson, A., Clover, L.M., Murphy, K.W. "Assessing the Contribution of Birth Asphyxia to Cerebral Palsy In Term Singletons." Pediatric Perinat. Epidemiol 1995 April;9(2):156-70.