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Showing posts with label injury management. Show all posts
Showing posts with label injury management. Show all posts

Wednesday, 8 August 2012

Biomechanics of joint manipulation


Manipulation can be distinguished from other manual therapy interventions such as joint mobilisation by its bio mechanics, both kinetics and kinematics.

Kinetics
Until recently, force-time histories measured during spinal manipulation were described as consisting of three distinct phases: the preload (or prethrust) phase, the thrust phase, and the resolution phase. Evans and Breen added a fourth ‘orientation’ phase to describe the period during which the patient is oriented into the appropriate position in preparation for the prethrust phase.
When individual peripheral synovial joints are manipulated, the distinct force-time phases that occur during spinal manipulation are not as evident. In particular, the rapid rate of change of force that occurs during the thrust phase when spinal joints are manipulated is not always necessary. Most studies to have measured forces used to manipulate peripheral joints, such as the metacarpophalangeal (MCP) joints, show no more than gradually increasing load. This is probably because there are many more tissues restraining a spinal motion segment than an independent MCP joint.

Kinematics
The kinematics of a complete spinal motion segment when one of its constituent spinal joints are manipulated are much more complex than the kinematics that occur during manipulation of an independent peripheral synovial joint. Even so, the motion that occurs between the articular surfaces of any individual synovial joint during manipulation should be very similar and is described below.
Early models describing the kinematics of an individual target joint during the various phases of manipulation (notably Sandoz 1976) were based on studies that investigated joint cracking in MCP joints. The cracking was elicited by pulling the proximal phalanx away from the metacarpal bone (to separate, or 'gap' the articular surfaces of the MCP joint) with gradually increasing force until a sharp resistance, caused by the cohesive properties of synovial fluid, was met and then broken. These studies were therefore never designed to form models of therapeutic manipulation, and the models formed were erroneous in that they described the target joint as being configured at the end range of a rotation movement, during the orientation phase. The model then predicted that this end range position was maintained during the prethrust phase until the thrust phase where it was moved beyond the 'physiologic barrier' created by synovial fluid resistance; conveniently within the limits of anatomical integrity provided by restraining tissues such as the joint capsule and ligaments. This model still dominates the literature. However, after re-examining the original studies on which the kinematic models of joint manipulation were based, Evans and Breen[2] argued that the optimal prethrust position is actually the equivalent of the neutral zone of the individual joint, which is the motion region of the joint where the passive osteoligamentous stability mechanisms exert little or no influence. This new model predicted that the physiologic barrier is only confronted when the articular surfaces of the joint are separated (gapped, rather than the rolling or sliding that usually occurs during physiological motion), and that it is more mechanically efficient to do this when the joint is near to its neutral configuration.

Cracking joints

Main article: Cracking joints
Joint manipulation is characteristically associated with the production of an audible 'clicking' or 'popping' sound. This sound is believed to be the result of a phenomenon known as cavitation occurring within the synovial fluid of the joint. When a manipulation is performed, the applied force separates the articular surfaces of a fully encapsulated synovial joint. This deforms the joint capsule and intra-articular tissues, which in turn creates a reduction in pressure within the joint cavity. In this low pressure environment, some of the gases that are dissolved in the synovial fluid (which are naturally found in all bodily fluids) leave solution creating a bubble or cavity, which rapidly collapses upon itself, resulting in a 'clicking' sound. The contents of this gas bubble are thought to be mainly carbon dioxide. The effects of this process will remain for a period of time termed the 'refractory period', which can range from a few minutes to more than an hour, while it is slowly reabsorbed back into the synovial fluid. There is some evidence that ligament laxity around the target joint is associated with an increased probability of cavitation.

Clinical effects and mechanisms of action
The clinical effects of joint manipulation have been shown to include:
   Temporary relief of musculoskeletal pain.
   Shortened time to recover from acute back sprains (Rand).
   Temporary increase in passive range of motion (ROM).
   Physiological effects upon the central nervous system.
   No alteration of the position of the sacroiliac joint.
Common side effects of spinal manipulative therapy (SMT) are characterised as mild to moderate and may include: local discomfort, headache, tiredness, or radiating discomfort.
Shekelle (1994) summarised the published theories for mechanism(s) of action for how joint manipulation may exert its clinical effects as the following:
   Release of entrapped synovial folds or plica
   Relaxation of hypertonic muscle
   Disruption of articular or particular adhesion
Unbuckling of motion segments that have undergone disproportionate displacement

Monday, 23 April 2012

Physiotherapy and clinical Pilates


Physiotherapy and clinical Pilates
The last decade has seen a growing body of research supporting proximal stabilisation for management of spinal injuries. Poor control and lack of endurance of trunk musculature are associated with low back pain. Researchers have developed a range of criteria for training "core control".
With the focus now on control of muscle rather than strength a "new" approach had to be taken to meet the criteria.
The Pilates (Pi-lart-ees) system of exercise been popular amongst performers for many years. With a basis of submaximal /variable resistance work in potentially unstable positions it had many of the right ingredients to satisfy stability training criteria. The exercises can encourage efficiency and submaximal muscle control by using variable (i.e. spring loaded) resistance and movement. To execute the exercises properly a stable, controlled pelvic and shoulder girdle is established with load facilitating both deep and global stability musculature.
Clinical Pilates description


The Clinical Pilates program has been developed by Australian physiotherapist Craig Phillips since 1990 to develop training of functional stability by progressing static stability into dynamic. Drawing on the original work of Joseph Pilates the program needed refinement to improve safety and highlight the components valid in stability training and injury diagnosis and management.
Developed specifically as a treatment tool for physiotherapists, Clinical Pilates is unique as a tool for establishing differential diagnoses, identification of radiological false positives / false negatives, establishment of outcome predictors  and  application of pathology specific exercise programs. 
DMA Clinical Pilates is the first to use real time ultrasound to determine if muscle activation patterns are being achieved. As a result changes had to be made to the traditional Pilates approach as a predominance of "bracing" activity was being consistently noted instead of appropriately sequenced, controlled tonic activity of the deep stabilisers.
Movement dysfunction often leads to pathology and vice versa. Low level Type 1 endurance musculature is the primary focus of stability training, and the aim is for early onset, at low loads, of both the local / deep stabilisers such as transversus abdominus and the deep multifidus and the more superficial global stabilisers such as the oblique / superficial multifidus, latdorsi etc. The difficulty in getting patients to activate stability musculature is because low % maximum voluntary contraction (MVC) required for stability and postural control is not as easy to "feel" as higher % MVC.
Therefore the exercises must facilitate and challenge those muscles irrespective of whether the patient is consciously aware of the muscle activity or not. If the muscle is to act as a background to movement it stands to reason that it should then be trained in the background and a "movement pattern" developed .Stability training must progress from the static to the dynamic and incorporate the connection between the shoulder and pelvic girdles. Static isolated muscle activity does not guarantee carry over into the dynamic situation. Load and movement are key factors in muscle activity so "if you want a muscle to do a job it must have a job to do" and it must be appropriate.
Injury management with clinical Pilates
An important issue in stability training is the effect of pathology. Pathologies are generally load sensitive as well as direction sensitive. Therefore if a pain producing pathology exists it must be determined if it has a direction preference. The neutral position required for ideal posture may in fact be provocative in the initial stages leading to pain, hence, muscle inhibition. Unloading the pathology in either flexion, extension or off center may well protect the pathology and allow muscle activity to occur. With progression, neutral is incorporated and eventually the provocative position used to determine the "threshold of function" of the injury.
As the research and knowledge develops in this area it is encouraging to know that the CLINICAL PILATES program can be "tuned" to both satisfy the guidelines of the researchers and meet the needs of the clinician.