Jodi Coffee, LMT, NMT
Four components of joint function-SI Joint (Diane Lee, physiotherapist)
The Integrated Model of Function (Lee & Vleeming) addresses 4 separate components which are essential for optimal function. The primary functional requirement of the pelvis is to transfer load between the trunk and the lower extremities. The first component is called "form closure". This term was coined by Andry Vleeming and Chris Snijders."

"Form closure addresses how a joint's shape and its ligaments contribute to stability. In other words, how does the integrity of the joint help to prevent shearing and excessive translation between the two joint surfaces when under load. At the SIJ, vertical forces must be controlled during walking, sitting and prolonged standing while forward and backward forces (anteroposterior translation) must be controlled during forward bending activities such as vacuuming, making beds or putting on your shoes."

"The second component of our model is called Force closure - another term coined by Vleeming and Snijders. This component addresses how and what extra forces are necessary to control translation between two joint surfaces when load is applied. The necessary force for controlling shear at the SIJ is compression. Compression is provided by the deep stabilizing muscles of the low back and pelvis which are transversus abdominis, multifidus and the pelvic floor. Collectively, these muscles have been referred to as the core muscles."

"The third component of our model is motor control. Motor control addresses the nervous system and is about the co-ordination or co-activation of these deep stabilizers. One of the world's leading research teams from the University of Queensland (Richardson, Jull, Hodges & Hides) have investigated the timing of these muscles in low back pain patients. They found that normally, these deep stabilizers should contract before load reaches the low back and pelvis so as to prepare the system for the impending force. They found that in dysfunction, there is a timing delay or absence of contraction of these muscles and consequently the system is not stabilized prior to loading. They also found that recovery is not spontaneous, in other words - the pain may go away but the dysfunction persists."

"The fourth component of our model addresses the role that our emotional state has on our ability to motor control effectively. It is well known that stress, anxiety, fear and pain all impact our emotional state and we now know that this state impacts our ability to motor control. Several studies are currently underway to specifically look at the impact of attention deficit, stress, fear etc on the core muscles. Holstege has shown that the emotional state is critical to health and recovery since it is through the muscle system that the mind ultimately expresses itself."

Vleeming A, Stoeckart R, Volkers A C W, Snijders C J 1990a Relation between form and function in the sacroiliac joint. 1: Clinical anatomical aspects. Spine 15(2): 130-132.

Vleeming A, Volkers A C W, Snijders C J, Stoeckart R 1990b Relation between form and function in the sacroiliac joint. 2: Biomechanical aspects. Spine 15(2): 133-136.

Hides J A, Stokes M J, Saide M, Jull G A, Cooper D H 1994 Evidence of lumbar multifidus muscles wasting ipsilateral to symptoms in patients with acute/subacute low back pain. Spine 19(2): 165-177.

Hides J A, Richardson C A, Jull G A 1996 Multifidus recovery is not automatic following resolution of acute first episode low back pain. Spine 21(23): 2763-2769.

Hodges P W, Richardson C A 1996 Inefficient muscular stabilization of the lumbar spine associated with low back pain. A motor control evaluation of transversus abdominis. Spine 21(22): 2640-2650.

Holstege G, Bandler R, Saper C B 1996 The emotional motor system. Elsevier Science.
Joint hypermobility syndrome
Joint hypermobility syndrome in 2004

Rodney Grahame MD, Hypermobility Clinic, Centre for Rheumatology, University College London Hospitals, London, UK

The original concept of the joint hypermobility syndrome (JHS) as a largely trivial complaint, whereby loose hypermobile joints give rise to aches, pains, strains, dislocations, and occasionally, osteoarthritis is now obsolete and should be abandoned. The last two decades have seen a major shift in opinion, all new evidence now pointing to a multi-system heritable disorder of connective tissue (HDCT) with clinical features that overlap with those of other HDCTs such as the Marfan and Ehlers-Danlos syndromes (EDS) [ 1 ]. These features include marfanoid habitus, thin stretchy skin with impaired scar formation, a tendency to osteopenia, and an autosomal dominant pattern of inheritance [ 2 ].

The (9-point) Beighton score [ 3 ], useful as an initial screen, can no longer be considered the gold standard for recognizing hypermobility syndrome in clinical or epidemiological practice. It is an arbitrary all-or-none test that does not take into account the degree of laxity and in some individuals the score diminishes with advancing age, perhaps even reaching zero. Moreover, it samples only five sites, although studies have now shown that pauciarticular hypermobility is more common than polyarticular [ 4 , 5 ]. The revised 1998 Brighton criteria for the (Benign) Joint Hypermobility Syndrome, published in July 2000, take all of these characteristics into consideration in addition to the symptomatic aspect and the multi-systemic involvement [ 6 ].

New research has identified associated neurophysiological abnormalities resulting in chronic pain [ 7 ], joint proprioceptive impairment [ 8 , 9 ], resistance to the local anaesthetic effects of lignocaine [ 10 ], autonomic dysfunction [ 11 ], and psychological distress [ 12 ]. The latter, combined with a wide array of musculoskeletal and visceral problems may result in a serious reduction in quality of life [ 13 ]. This complex constellation of problems presents health providers with major challenges, yet rheumatologists remain largely unaware of the significance of hypermobility and its impact [ 14 ]. The clinical prevalence of the JHS phenotype, as judged by the Brighton Criteria, has recently been estimated to be as high as one in three in both males and females among unselected consecutive new adult referrals to a community hospital rheumatology service in London. In the case of non-Caucasian females the figure rises to 58% [ 15 ].
The Stabilizing System of the Spine-Manohar M. Panjabi
The Stabilizing System of the Spine. Part I. Function, Dysfunction, Adaptation, and Enhancement-Manohar M. Panjabi

The spinal stabilizing system consists ofthree subsystems. The vertebrae, discs, and ligaments
constitute the passive subsystem. All muscles and tendons surrounding the spinal
column that can apply forces to the spinal column constitute the active subsystem.
The nerves and central nervous system comprise the neural subsystem, which
determines the requirements for spinal stability by monitoring the various trans-
ducer signals, and directs the active subsystem to provide the needed stability.

A dysfunction of a component of any one of the subsystems may lead to one or more
of the following three possibilities: (a) an immediate response from other subsys-
tems to successfully compensate, (b) a long-term adaptation response of one or
more subsystems, and (c) an injury to one or more components of any subsystem.

It is conceptualized that the first response results in normal function, the second
results in normal function but with an altered spinal stabilizing system, and the
third leads to overall system dysfunction, producing, for example, low back pain.
In situations where additional loads or complex postures are anticipated, the
neural control unit may alter the muscle recruitment strategy, with the temporary
goal of enhancing the spine stability beyond the normal requirements.