Thursday, May 31, 2012
The intent of this post is two-fold: 1) to discuss and explore a very relevant, critical, yet controversial subject of dicussion within Cerebral Palsy (CP) (and other disorders of movement and posture)...2) to link previous posts together with this one to shape a formulate the overall narrative. As always, my overall intention is not to discredit any particular school of thought, strategy, or central philosophy...rather to bring the realities of the mechanical challenegs (and consequences) that accompany CP to the forefront so that specific, goal-oriented strategies can be formulated. It should be clear that these strategies are case specific and therefore need to be evaluated with it´s own set of standards.
This first installment will focus on the direct effect of load-bearing (weight-bearing) on the bones. However, before any in-depth discussion begins, I should define what load-bearing means within the context of this post. To be very specific, load bearing is: exposing an architectural system to structural load or stress. Therefore, in the human organism this is very clearly achived in either a seated or standing position.
The benefits of load bearing or weight bearing in the healthy person are quite obvious and straightforward...the ground force reaction promotes to development of growing bones and contributes to the development of healthy bone density. Although this is very true, the fundamental mistake that is quite often made is that this statement is imported to the CP community. Why is this a mistake? This statement assumes that the transmission of ground force reaction is efficient and therefore travels to the relevant load bearing structures throughout the body...in disorders of movement and posture (CP, for example), force transmission is extremely disrupted and inefficient. This disruption leads to improper stress distribution, accessory and compensatory activation of skeletal muscle, overuse and fatigue syndromes, as well as structural deterioration. To be very clear: mechanical forces in the CP individual DO NOT travel in a manner that facilitates healthy growth and development.
I doubt any responsible professional would debate this fact...however, a fundamental question is therefore raised: if this is an understandable fact, why is there such a rush to implement "standing" protocols? This is a glaring contradiction that generally goes unseen, but certainly exists...and therefore needs to be addressed.
In order to address this delicate topic intelligently and responsibly, we need to dissect the effects of load bearing into some fundamental component parts: the effect on the bony skeleton itself and the effect on the soft tissue. The effects on the system as a whole are actually greater than the sum of the component parts, but far more complex...therefore a basic understanding of the component parts should give some clarity on the potential "biomechanical tax" that is paid when weight bearing is aggressively promoted.
MECHANOTRANSDUCTION IN BONES: If the term Mechanotransduction is new to you, i would refer you to my previous post titled "Mechanotransduction: Response to Manual Therapy". However, to summarize the concept, it is the cellular response to mechanical forces or loads. The precise mechanism in which bones sense mechanical stimulii is still largely being researched, however the concept of cellular mechanotransduction in the bones is widely accepted as a likely mechanism. With respect to the skeleton, there is an integration of the understanding of the connective tissue memebrane of the bone (periosteum), cellular tensegrity, and the effects of mechanotransduction on the nucleus of the osteoblast. Effectively, mechanical stress and deformation that is load-induced activates a change in the genetic program of the bone (gene transcription). Mechanical information is relayed from the bone to the gene by a succession of long-term deformation and changes in conformation. If the stresses applied to the bone are not distributed properly, skeletal growth and absorption are disrupted...which leads to eventual bony deformation and therefore impaired function.
Although this is a common understanding in the field of cellular biochemistry, it doesnt seem to reach the professional "masses" to be applied responsibly in rehabilitative protocols. Given this knowledge, it becomes clear that consistent, intensive, and aggressive strategies geared towards standing protocols (standers, for example) is potentially costly when you consider the "biomechanical tax" to be paid in the long-term. Although bony misalignment is a reality in the CP individual, load bearing and exposing an altered structural "scaffold" to loads exacerbates the deterioration of structural integrity.
Although significant, this is only part of the overall perspective. The effects of load bearing with respect to the soft-tissue will be the subject of the second load-bearing post. Hopefully both or either will stimulate some analytical thought on the subject and consequenty result in more informed and effective strategies.
Wednesday, May 23, 2012
Tuesday, May 22, 2012
Stretching is most commonly performed to achieve a specific end result: elongation of a particular muscle or group of muscles. This seems relatively intuitive and would make sense to any lay person. The part that is not so intuitive is that the muscles themselves are embedded within a connective tissue matrix...which is in turn blended with other differentiated connective tissue (tendon) that is continuous with the outer layer (periosteum) of the bone. From there, the periosteum continues and eventually blends once again and the kinematic chain continues.
Muscle is defined as a tissue composed of bundles of elongated cells capable of contraction and relaxation to produce movement. Connective Tissue can be descried as a tissue developed from the embryonic mesoderm that consists of collagen or elastic fibres, fibroblasts, fatty cells, etc., within a jelly-like extracellular matrix. It supports organs, fills the spaces between them, and forms tendons and ligaments. Knowing these basic facts and definitions, their respective functional appearances within the normal muscle and the spastic muscle (CP) need to be defined. They should be the same, right? This couldnt be further from the truth. This is what the current (and most popular)approach assumes...that muscle is muscle and fascia is fascia. I have attached a very interesting and informative study that was performed to identify the similarities / differences between spastic and normal muscle tissue, spastic and normal extracellular matrix, as well as the differences between individual cells and collective bundles of cells for both. I recommend that you take the time to read it, but I will summarize its contents here in an effort to expediate my point (it´s effectively the abstract of the article): 1) The difference between bundles and single cells was much greater in normal muscle tissue (16 times stronger) than in spastic muscle (2 times stronger). 2) Actual muscle fiber strength is greater in spastic muscle than in normal muscle. However..... 3) Extracellular matrix strength / Connective Tissue strength is 43.5 times weaker!! Therefore, the ¨inconvenient truth¨ is exposed and a fundamental question is raised: if the spastic muscle itself is stronger than normal muscle, and the connective tissue attachments are 43 times WEAKER...what is really happening when you attempt to stretch that particular muscle(s)? In my professional opinion, it seems only logical that the likely result is further weakening and de-stabilization of an already weak connective tissue system...however, I am more than willing to set that staunch opinion aside if ever there was a way to guarantee this wouldn´t happen. The current reality is that, at best, there is no definite way to determine if the attempts to relax spastic muscles via stretching will not potentially be of some detriment. Indeed, there are some cases where some relief has been attributed to active stretching...however, these responses are transient and were most likely done in a very mild form.
The article goes into more important details (muscle fiber size and area is smaller in spastic muscle, for example), so I will leave those for the more curious to digest. In summary, I do not belong to the extreme end of the continuum in saying that ¨all stretching is bad¨ and that it absolutely shouldnt be done. My main message is that proper consideration be made to the actual mechanical and physiological benefits / consequences of ANY therapeutic intervention. If, through careful thought, consideration, and analysis, stretching is indicated...then it is obviously worthy of implementation. The harsh reality is that many forms of stretching are dispensed without any constructive analysis...which is fundamentally dangerous. To put a final point on this topic...forget about absolute ¨black and white¨solutions. There is a whole lot of grey to choose from! Cheers! Inferior Mechanical Properties of Spastic Muscles Due to Compromised Extra Cellular Matrix Material