The Sarah Key ‘working hypothesis’ offers an explanation for; non-specific low
back pain of unknown aetiology; and the progressive breakdown of a lumbar
motion segment.
Sarah Key postulates that the breakdown of a lumbar motion segment and
subsequent production of pain occurs in sequence and runs through 5 stages.
These are;
Stage 1:
Stiff spinal segment or External disc dysfunction
Stage 2:
Facet joint arthropathy
Stage 3:
Acute locked back
Stage 4:
Prolapsed Intervertebral disc
Stage 5:
Unstable spinal segment
As long ago as 1970, Nachemson postulated, “a deficiency of nutrient supply to
the disc may be a contributing factor in disc degeneration”. Sarah Key says a
reduced nutrient supply to the disc results in a stiff spinal segment (stage one of
the Sarah Key 5 stages of spinal breakdown).
Decreased proteoglycan content within the nucleus pulposis results in a
decreased osmotic gradient (Adams et al., 2006).
The resultant effect is a
decrease in water content within the nucleus pulposis, the disc begins to ‘deflate’
and bulge, a bit like a car tyre. The outer wall of the annulus fibrosis is structured
to resist torsional stress (Urban et al., 1981), but with decreased water content
within the nucleus pulposis the outer wall of the annulus fibrosis becomes load
bearing (Bernick et al., 1991).
As the outer layers of the annulus fibrosis start to bear increased load they stiffen
and thicken in response. This has a number of problematic effects. Ishihara and
Urban (1999) state that discs receive nutrition via 3 mechanisms of transport.
Small molecular weight solutes (glucose and oxygen) travel by diffusion and
osmosis and larger molecular weight solutes (pro-inflammatory cytokines) travel
mainly by convection. A thickened posterior disc wall also means that there is a
greater distance to travel for water being enticed via osmosis or diffusion into the
nucleus pulposis.
A greater distance to travel results in decreased fluid
exchange which obviously leads to further decrease in water content within the
nucleus pulposis and results in further thickening of the posterior disc wall,
annulus fibrosis (Adams et al., 1996).
A second problematic effect of a tight and thick posterior disc wall is that it
inhibits or restricts stretch of the posterior disc wall. If the posterior disc wall is
thickened, stiff and resistant to stretch it means it cannot drive its convection
‘pump’ effectively (Ishihara et al., 1995). This again results in a reduction in fluid
exchange between the external and internal disc environment, leading to
decreased water content within the nucleus pulposis, further stiffening of the
posterior disc wall and decreasing proteoglycan synthesis and decreased
proteoglycan content within the nucleus pulposis (Ishihara et al. 1995).
Coppes et al., (1997) state that degenerate discs have more extensive nerve
innervation. Kuslich et al., (1991) state, “by far the most common painful tissue
(of the back) is the outer layer of the annulus and the posterior longitudinal
ligament”. Bogduk (1991) also agrees stating,
“Compression injuries of the disc are initially asymptomatic but may
set in train a degradative process that, in time, leads to internal disc
disruption, which becomes symptomatic as a result of chemical or
mechanical irritation of nociceptors in the outer annulus fibrosis”.
Sarah Key believes to overcome this problem you must stretch the posterior disc
wall and encourage fluid back into the nucleus though mild traction and
increasing the convection pump.
By stretching the posterior disc wall she
believes you can reduce scarring and reduce the thickness of the disc wall
making fluid exchange easier.
This will help restore disc health and disc
nutrition. With mild traction a negative pressure is produced within the disc which
helps attract water to the nucleus pulposis via the lateral and anterior aspects of
the disc wall, as well as through the end plates and of course through the
posterior disc wall. The resultant effect is a plumper, healthier disc. With a
plumper, healthier disc there is less irritation or sensitisation of the mechanoreceptors and chemo-receptors.
A lumbar intervertebral disc has a number of roles. As well providing shock
absorption for a lumbar motion segment a disc also acts as a spacer for the
posterior section of the motion segment, the facet joints. Sarah Key’s second
stage of spinal breakdown is facet joint arthropathy. She postulates that facet
arthropathy is secondary to a stiff spinal segment. Dunlop et al., (1984) support
Sarah Key’s postulation stating, when a disc loses height the facets over-ride,
increasing load baring through the facet surface by up to 70%, they should only
bear approximately 16% of load.
To fix this problem Sarah Key believes one must work in reverse. Unload the
facet joints and stiff spinal segment. By ‘plumping up’ the stiff spinal segment the
overall effect will be decreased load bearing through the facets.
Sarah Key’s third stage of spinal breakdown is an acute locked back. Sarah
postulates the acute facet locking is a hiccup in the spines coordinated control
which results in minute subluxation of a facet (Sarah Key Masterclass, level one
notes). Adams et al., (1996) demonstrated that multifidus fibres blend with the
facet joint capsule and help to uplift one facet on another in flexion. Ng et al.
(2003) demonstrated that fatigue could delay the reaction time of multifidus in
response to load so that injury to the spine may occur. They also said that overreaction of muscles can follow delayed reaction of multifidus resulting in
excessive compressive forces.
Adams et al. (1996) state that a stiff spinal
segment predisposes to acute facet locking because the disc is flatter and the
upper vertebrae in the spinal motion segment is poorly spring loaded to flexion.
After you have reduced the presenting symptoms of muscular spasm and
movement dysfunction Sarah Key says, fix the reduction in disc height and you
will reduce the incidence of acute lock-ups. If you increase the disc height (by
encouraging fluid into the disc) the motion segment is primed / spring loaded,
ready to bend with its surrounding muscles at optimal length tension relationship.
Stage four of the five stages of spinal breakdown is a prolapsed intervertebral
disc. Sarah Key believes disc prolapse is rare and predated by degeneration
(stiff spinal segment) which lowers intra discal pressure and renders the nucleus
‘expressible’. Bogduk agrees that a prolapsed intervertebral disc starts off as a
stiff spinal segment. Bogduk (1991) states, “Disc prolapse is but one possible
end stage of internal disc disruption and represents the culmination of a series of
destructive processes affecting the disc”. Mooney (1987) also supports Sarah
Key’s postulation and found epidemiologically, disc prolapse accounts for fewer
than 5% of presentations of low back pain. Once again, after the ‘acute phase’ of
disc prolapse is over (medication and bed rest) one should move towards dealing
with the core of the problem. If you can increase the proteoglycan content of the
disc you can assist in restoring its health. This is done by reducing compressive
muscle spasm in the lumbar erectors, normalising pressure in a stiff motion
segment and decreasing a thick scarred posterior disc wall so fluid exchange is
optimised with a follow on effect of increased disc health.
Stage five is an unstable spinal segment.
Sarah Key’s proposition is that a
segment becomes unstable when the two main stabilising structures degenerate
(the discs and facets). Twomey et al., (1985) support this notion. For the same
reason this stage behaves very much like an acute lock up. The major difference
is there is radiographic evidence with this stage which is not often present with
an acute lock up. The disc has ‘deflated’ so much that it allows anterior shear of
the motion segment.
The body tries to stabilise and the resultant effect is
‘traction spurs’ of the vertebral bodies as they try to meet and facet trophism,
again as they look to provide bony support.
With the loss of the passive
subsystem (Panjabi, 1992) the therapists job is to assist in stabilising through the
active and control systems to prevent increased segmental shear. Lotz et al.,
(2006) sum it up well stating, ‘loss of nuclear volume (and, consequently,
pressure) is a common trigger for tissue remodelling and anatomical change
consistent with disc degeneration in humans’.
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