PACIFIC UNIVERSITY School of Physical Therapy

DPT 631
Musculoskeletal Examination and Intervention for the Neck and Trunk
CLINICAL INSTABILITY AND LUMBOPELVIC CORE STABILIZATION
Peter Huijbregts, PT, OCS, FAAOMPT

ANATOMY

• Three subsystems are responsible for lumbar spine stability: passive, active, and neural
control subsystem (Richardson et al, 1999).
• Passive subsystem restrictions to motion are imposed by capsuloligamentous structures,
orientation and shape of joint surfaces, and the mechanical characteristics of joint cartilage.
• The active subsystem consists of the muscles and tendons exerting their forces and moments
in the lumbar region (Figure 1).
• The neural control subsystem is responsible for a coordinated activation of the active system
and consists of receptors in skin, muscle, tendon, joint capsule, etc. and the CNS.

Figure 1 Diagrammatic representation of muscles and tendons of the active

subsystem exerting forces to enhance spinal stability (McGill and
Cholewicki, 2001)

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• The active subsystem can be further subdivided in a local and a global stabilizing system
(Table 1).
• Activity in the LOCAL stabilizing system entails the following (Comerford and Mottram,
2001):
- deepest layer muscles that originate and insert segmentally
- control of neutral joint position
- activity is independent of direction of movement
- activity precedes motion and is continuous throughout movement
- proprioceptive input
• Activity in the GLOBAL stabilizing system includes the following (Comerford and Mottram,
2001):
- more superficial muscles that do not have segmental attachments
- activity is dependent upon direction of movement
- generate force to control range of motion
- ability to control “inner range” and “outer range” of muscle length
- ability to control range by decelerating momentum PRN

Local stabilizing system Global stabilizing system

• Intertransversarii • Longissimus thoracis pars thoracis
• Interspinales • Iliocostalis lumborum pars thoracis
• Multifidus • Quadratus lumborum, lateral fibers
• Longissimus thoracis pars lumborum • Rectus abdominis
• Iliocostalis lumborum pars lumborum • Obliquus externus abdominis
• Quadratus lumborum, medial fibers • Obliquus internus abdominis
• Transversus abdominis
• Obliquus internus abdominis (fibers attaching to
TLF)
Table 1: Local and global stabilizing system (Richardson et al, 1999)

• The thoracolumbar fascia (TLF) consists of three layers (Bogduk, 1997; Vleeming et al,
1997).
• The thin anterior layer is the ventral fascia of the quadratus lumborum muscle. Medially it
attaches to the lumbar transverse processes blending with the intertransverse ligaments.
• The middle layer of the TLF connects the transverse abdominis (and sometimes the internal
oblique) muscle to the tips of the transverse processes.
• The posterior layer attaches to the lumbar spinous processes, covers the lumbar muscles, and
blends with the middle layer lateral to the iliocostalis lumborum in the lateral raphe.
• Latissimus dorsi, gluteus maximus, gluteus medius, external oblique, trapezius, and serratus
posterior inferior muscles all attach to the posterior layer of the TLF; the biceps femoris
attaches indirectly to this layer of the TLF by way of its connection to the sacrotuberous
ligament (Vleeming et al, 1997).
• The lumbar multifidus is enclosed by the posterior layer of the TLF (Vleeming et al, 1997).
• The TLF and all muscles attaching to it could be included in the global stabilizing system of
both the lumbar and pelvic region.

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BIOMECHANICS

• The anteromedial portion of the superior articular facet limits the forward translation
accessory to spinal segmental flexion (Bogduk, 1997).
• The posterior portion of the superior facet is oriented in the sagittal plane. With rotation,
impaction occurs in the posterior portion of the contralateral zygapophyseal joint, limiting
rotation (Bogduk, 1997).
• Loss of the integrity of the collagen network in the zygapophyseal joint cartilage allows for
greater mobilization of water out of the cartilage with compression.
• Degenerative changes in the articular cartilage will allow for increased anterior translation
and axial rotation, especially when disk degradation has caused segmental narrowing and
capsuloligamentous laxity: “loss of packing material between vertebrae” (Bogduk, 1997;
Huijbregts, 2001).

• Passive subsystem deficiency can also occur congenitally, result from trauma, surgery etc.
• Spondylolisthesis is a forward (anterolisthesis) or backward (posterolisthesis) translaed
position of a superior on an inferior vertebra.
• Spondylolysis is a structural deficiency in the interarticular pars between superior and
inferior facet (can be the result of a fracture).
• Spondylolysis is only one of the possible causes for spondylolisthesis.
• Question: if a patient has a traumatic spondylolisthesis of L5-S1 with a fracture of the
interarticular pars of L5, where do you expect to see and palpate the step?
• Question: If a patient has a degenerative spondylolisthesis at L5-S1, where do you expect to
see and palpate the step deformity?

• NEUTRAL ZONE: that part of the range of physiological intervertebral motion, measured
from the neutral position, within which the spinal motion is produced with a minimal internal
resistance (Panjabi, 1992).
• Ligaments, capsules, joint geometry, and muscular contraction limit physiological motion at
the endranges.
• Muscles play a major role in stabilization of the spine around the neutral zone, i.e. in the
beginning and midrange.

• INSTABILITY: a significant decrease in the capacity of the stabilizing system of the spine to
maintain the intervertebral neutral zones within the physiological limits so that there is no
neurological dysfunction, no major deformity, and no incapacitating pain (Panjabi, 1992).
• Simulated contractions of the local stabilizing system decrease the neutral zone of the
lumbar spine segments despite increasingly severe injuries to the passive stabilizing systems
of the lumbar spine (Panjabi et al, 1989; Wilke et al, 1995).
• A fresh cadaveric spine devoid of muscles can carry an axial load of no more than 20N
before it buckles: muscles are needed to stabilize the spine (Panjabi et al, 1989).

• The transverse abdominis, multifidus, pelvic floor, and diaphragm muscles all contract with a
low-level, continuous, tonic contraction that precedes the contraction of the prime mover
during arm or leg movements that may jeopardize stability of the trunk (Richardson et al,
1999).

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• This activation is independent of the direction of movement or the possible resultant

disturbance of trunk stability: these muscles increase non-direction specific stiffness of the
lumbar spine, thereby increasing stability (Richardson et al, 1999).
• Contraction of the transverse abdominis and the oblique orientation of the TLF causes a
small extensor moment on the lumbar spine (2% of the maximal extensor moment). The
resultant segmental compression may increase stability (Bogduk, 1997).
• Contraction of the transverse abdominis, multifidus, pelvic floor, and diaphragm muscles
increases intra-abdominal pressure (IAP) without causing a flexion moment on the spine;
direct pressure of the abdominal contents against the ventral aspect of the spine may increase
spinal stability. Increased IAP increases the stiffness of the abdominal contents; this may also
contribute to lumbar stability (Richardson et al, 1999).

• Contraction of the latissimus dorsi, gluteus maximus, and biceps femoris muscles increases
the tension in the posterior layer of the TLF (Vleeming et al, 1997).
• Contraction of these “extremity” muscles increases compressive force over the lumbopelvic
region. This results in increased stability in the lumbar spine and pelvic joints. See “posterior
oblique sling” in Figure 2.

Figure 2 Posterior and anterior oblique slings that contribute to force closure of the
SIJ and stability of the lumbar spine. A = posterior oblique sling with (1)
latissimus dorsi, (2) thoracolumbar fascia, (3) gluteus maximus, (4)
iliotibial band. B = anterior oblique sling with (5) linea alba, (6) external
oblique muscle, (7) transverse abdominis muscle, (8) piriformis muscle,
(9) rectus abdominis muscle, (10) internal oblique, (11) inguinal ligament
(Pool- Goudzwaard et al., 1998).

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EXAMINATION

• Lumbar spine stability tests examine for deficiencies in the 3 subsystems responsible for
stability.
• There are three types of tests relevant to examination of lumbar spine stability: segmental
stability tests, tests for the local stabilizing system, and tests for the global stabilizing system.
• Meadows (1999) and Paris (1985) mentions the signs and symptoms listed in table 2 as
indicative of lumbar spine instability; these findings are obviously not sensitive, nor very
specific.

• Long-term non-acute LBP • Temporary relief from movement.

• Long-term morning stiffness • Complaints of “slipping out”.
• Short-term episodic pain • Reports of being able to “twist it back into position”.
• A history of ineffective treatments • “Giving way syndrome” with patient actually falling
• Posterior creases on observation to the ground.
• Full ROM, but abnormal movements: angulation, • A visible step in the lumbar spine.
hinging, deviation, walking up the thighs during return • A band of hypertrophied muscle at the level of this
from flexion (positive Gower’s sign). step.
• Ledge deformity on palpation. • Sudden shake, catch, or hitch on trunk flexion.
• Minimal provocation causing LBP. • Segmental sidebending during flexion.
• Incomplete recovery from trauma. • Uncoordinated muscle contraction during movement.
• A feeling of instability. • Transient neurological signs.
• A feeling of giving way.
• Consistent clunking or clicking noises.
• Inconsistent ability to perform tasks.
• Hypermobility on PPIVM tests.
• Instability on segmental stability tests.
• LBP on assuming a sitting or other static weightbearing
position.
Table 2: Signs and symptoms of lumbar instability

A. Segmental stability tests (Meadows, 1999)

• Segmental stability tests are (in general) passive accessory motion tests.
• Stability tests examine accessory motions that should not be possible in a normal segment.

Anterior shear test

• Patient position: sidelying on either side; spine

in a neutral position; hips flexed to 45 degrees for
testing L5-S1, hips flexed to 80 degrees for testing
T12-L1 to L4-L5; the patient’s knees are placed
between the therapist’s thighs.
• Therapist position: standing on the ventral side
of the patient.

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• Hand placement: one hand stabilizes the

superior vertebra of the segment tested; the
other hand palpates the spinous process of the
inferior vertebra of the segment tested.
• Test: the therapist applies a posterior
shear by axial compression with the knees
through the patient’s thighs.
• Positive test: shifting or linear
displacement indicates anterior instability.

Posterior shear test (demonstration only)

• Patient position: sitting with legs over the edge of the treatment table, forearms on the
therapist’s chest (use pillow as needed).
• Therapist position: standing in front of the patient.
• Hand placement: both hands stabilize the inferior vertebra of the segment to be tested; one
finger palpates the spinous process of the superior vertebra for motion.
• Test: using a scapular protraction motion the patient gently pushes in the therapist’s chest
creating a segmental posterior shear force.
• Positive test: backward slipping of the superior on the inferior vertebra indicates posterior
instability.

Torsion test

• Patient position: prone.

• Therapist position: standing by the side of
the treatment table.
• Hand position: with the distal hand the
therapist reaches around the patient to contact
the contralateral ASIS; the proximal hand is
placed with the hypothenar aspect over the
central and contralateral aspect of the superior
vertebra of the segment to be tested.

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• Test: the therapist pulls the ASIS perpendicular to the table, up towards the ceiling, inducing
pure axial rotation. Stabilization is started at T12, the test is repeated with stabilization at L1,
L2 through L5.
• Positive test: excessive axial rotation indicates rotational segmental instability.

B. Local stabilizing system tests (Richardson et al, 1999)

• Tests of the local stabilizing system examine the neuromuscular coordination of the
transverse abdominis and deep segmental multifidus muscles.
• The test can be modified to test neuromuscular endurance by having the patient perform 10
repetitions of 10 seconds duration.

Transverse abdominis test

• The first part of the test consists of patient education. Start with describing the action of the
transverse abdominis muscle; an anatomical drawing may be useful. Analogy of the
transverse abdominis muscle as the patient’s own internal corset. Clarify the difference
between abdominal drawing-in action and movement of the trunk. The therapist may need to
demonstrate abdominal drawing-in.
• The second part of the test is a simplified practice version. Start with the patient in the four
point kneeling position: gravity and the abdominal contents put the transverse abdominis
muscle in a more stretched position allowing for increased proprioceptive feedback. Have the
patient take a relaxed breath in and out and then, without breathing, draw the abdomen up
towards the spine. The contraction must be slow and controlled. The patient resumes
breathing and is asked to maintain the contraction for 10 seconds. The formal test follows the
educational and practice portion.
• Patient position: prone with the lower abdomen positioned on a pressure biofeedback unit
inflated to 70 mm Hg.
• Test: abdominal drawing-in action held for 10 seconds. Use the instructions listed in Table 3.
• Positive test: the patient is unable to reduce the pressure by 6 to 10 mm Hg for a period of 10
seconds indicating neuromuscular dyscoordination of the transverse abdominis muscle;
inability to repeat the test with good form for 10 repetitions indicates decreased
neuromuscular endurance.
• False negative test: the patient may attempt any of the substitutions listed in Table 4.

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Segmental lumbar multifidus test

• A palpatory assessment precedes the formal test. The therapist palpates the muscle at each
segment with the patient in a prone, relaxed position for loss of muscle consistency possibly
due to segmental multifidus inhibition.
• Patient position: prone.
• Therapist position: standing to the side of the treatment table.
• Hand placement: the therapist can use the thumb, index, or middle fingers of each hand, or
the the thumb and index fingers of one hand to palpate the segmental multifidus muscle
directly adjacent to the lumbar spinous processes. Fingers or thumb are gently sunk into the
muscle in preparation for the test.
• Test: patient breathes in and out, then holds breath while attempting to gently swell out the
muscles into the therapist’s fingers, and then resume normal breathing.
• Positive test: inability to perform (10 repetitions) of a 10 second duration slow, tonic hold.
• False negative tests: see Table 4.

Transverse abdominis muscle

• Slowly draw in your lower abdomen away from the
elastic in your pants.
• Slowly draw in your lower abdomen to support the
weight of the abdominal contents (prone).
• Slowly draw your navel up and in towards your
backbone.
• Slowly pull in your abdominal contents to gently
flatten your stomach below your navel (standing).

Multifidus muscle
• Gently swell out or contract your muscles against
my fingers.
Table 3: Examples of verbal instructions (Richardson
et al, 1999)

Aberrant movement
• Posterior pelvic tilt.
• Flexion of the thoracolumbar junction.
• Rib cage depression.
Countours of the abdominal wall
• No movement of the lower abdomen.
• Increased lateral diameter of the abdominal wall.
• Visible contraction of the obliquus abominis externus muscle fibers at their origin.
• Patient unable to voluntarily relax the abdominal wall.
Aberrant breathing patterns
• Inappropriate active oblique abdominal during breathing cycle.
• Patient unable to perform diaphragmatic breathing pattern.
Unwanted activity of the back extensors
• Co-activation of the thoracic portions of the erector spinae.

Table 4: Physical signs of unwanted global muscle activity (Richardson et al, 1999)

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C. Global stabilizing system tests

• May include tests for strength, endurance, and coordination of all muscles of the global
stabilizing system.

DIAGNOSIS

• Diagnosis is based on an extrapolation of (patho)anatomical and (patho)biomechanical

knowledge (Huijbregts, 2001; Meadows, 1999).
• Minimal research support is available for the validity of segmental stability tests (Tilscher et
al, 1994).
• Some research support for validity of transverse abdominis and multifidus tests (Richardson
et al, 1999).

A. Ligamentous instability

• Caused by increased length and/or decreased mechanical stiffness of zygapophyseal and

other ligamentous structures.
• May allow for hypermobility on both physiological and accessory motions.
• Increased mobility with a soft capsular endfeel or normal mobility with a muscular endfeel
(protective reaction due to painful hypermobility) on PPIVM (passive physiological
intervertebral motion) and PAIVM (passive accessory intervertebral motion) tests.
• Positive segmental stability tests.
• Only becomes symptomatic when active and neural control subsystem are failing: therefore,
positive ligamentous instability will likely have positive local and/or global stabilizing
system deficiencies.

B. Segmental instability

• Caused by disk degradation and zygapophysial joint surface degeneration.

• May increase translatory or accessory movements (Weiler et al, 1990).
• Segmental narrowing as a result of disk degradation increases the contact between the tips of
the articular facets and the lamina of the vertebra below or the interarticular pars of the
vertebra above. This will likely decrease physiological range of motion in extension (and
sidebending) (Burton et al, 1996; Dunlop et al, 1984).
• Zygapophysial joint surface degeneration may allow for increased segmental axial rotation
(Bogduk, 1997)
• Active ROM tests are likely to be restricted in extension and sidebending with a hard endfeel
on overpressure.
• PPIVM tests are restricted in extension and sidebending with a hard endfeel indicating bony
impaction (Huijbregts, 2001).
• PAIVM tests may reveal decreased accessory motion. They may show excessive translatory
motion, but are less likely to be positive than segmental stability tests (Tilscher et al, 1994).
• Segmental mobilization aimed at increasing extension and sidebending is contraindicated
(Huijbregts, 2001).

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• Only becomes symptomatic when active and neural control subsystem are failing: therefore,
positive segmental instability will likely have positive local and/or global stabilizing system
deficiencies.

C. Active and neural control subsystem deficiency

• May be a combination of local and global stabilizing system deficiency.

• Local stabilizing system deficiency appears to be related to neuromuscular coordination and
inhibition rather than loss of strength and endurance:
1. In patients with chronic LBP, the transverse abdominis muscle contraction no
longer precedes the contraction of the prime mover. It is delayed by 50 to 450 ms
in arm movements and follows the contraction of the prime mover in leg
movements with up to several 100 ms. Innervation of the transverse abdominis by
T7 to L1 excludes monosegmental inhibition as a cause for changes activity and
implicates changes in motor control strategies (neuromuscular coordination)
(Richardson et al, 1999).
2. In acute LBP patients monosegmental unilateral decreases in cross-sectional
multifidus area occur sometimes within 24 hours implicating inhibition (Hides et
al, Richardson et al, 1999).
• Global stabilizing system deficiencies also involve insufficient strength and endurance.
• Positive local and global stabilizing system tests.

C. Mixed subsystem deficiency

• Active and/or neural control subsystem deficiencies can cause symptoms without passive
subsystem deficiencies (ligamentous or segmental instability).
• Passive subsystem deficiencies only become symptomatic if the other two subsystems can no
longer compensate.

TREATMENT

A. Passive subsystem deficiency

• If passive subsystem deficiency (ligamentous instability) is acute and traumatic, we can

attempt to create optimal circumstances for healing by applying the appropriate modalities
and limiting/ slowly reintroducing the stresses that may maintain the instability.
• In an existing chronic ligamentous or segmental instability we can minimize the stresses to
the segment by ergonomic adaptations, lumbar belts, mobilization of possibly hypomobile
adjacent segments, or by addressing dysfunctions in the lower extremity that may
inappropriately focus stress through the segment.
• Segmental instability can be mistaken for segmental hypomobility. However, attempts at
mobilizing especially segmental extension and sidebending are contra-indicated and will
increase LBP. Careful diagnosis is important.
• Passive subsystem deficiencies only become symptomatic when the active and neural control
subsystems are failing: treatment always needs to include appropriate stabilization
(Huijbregts, 2001).

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B. Active and neural control subsystem deficiency

• Stabilization training consists of three stages (Richardson et al, 1999):

1. Formal motor skill training of the deep muscles.
2. Incorporation of the skills into light formal tasks.
3. Progression to heavier functional tasks.

• FORMAL SKILL TRAINING

• Aimed at increasing deep muscle (multifidus, transverse abdominis, pelvic floor, and
diaphragm) function.
• Aimed at decreasing global muscle substitution strategies (see examination).
• Training of the motor skill is similar to the tests of multifidus and transverse abdominis
function described above.
• Discuss with the patient the goal of a tonic rather than phasic, long-duration versus short-
duration, low-level (10 to 15% maximum effort) versus maximal effort.
• Tactile clues may be given at the segmental multifidus or anterior and inferior to the ASIS,
lateral to the rectus abdominis for the transverse abdominis.
• Use a variety of positions (sidelying, supine crook lying, standing, sitting, four point
kneeling, standing or sitting leaning forwards with weight supported through the arms) to
find the best position for the patient. The position needs to be painfree. Supported positions
tend to decrease global muscle activity. The position chosen needs to allow for relaxed
breathing.
• Facilitation of the desired contraction can occur by way of:
1. Asking the patient to co-activate lumbar multifidus and transverse abdominis.
2. Asking the patient to co-contract the pelvic floor.
3. Increase the expiratory effort.
4. Verbal feedback by the therapist.
5. Visual feedback with real-time ultrasound imaging.
6. Visual feedback through a mirror placed obliquely at the side of the patient.
7. Self-palpation by the patient.
• Inhibition of global system overactivity can be done through:
1. EMG activity monitoring of the global system to avoid co-activation.
2. Training of diaphragmatic breathing patterns.
3. Facilitated elevation and expansion of the lower rib cage against the hands of the
therapist to decrease external oblique activity.
4. Deep inhibitory massage of overactive muscles.

• INCORPORATION INTO LIGHT TASKS

• This stage of stabilization aims to train deep muscle co-contraction with the added challenge
of light loads.
• Supine leg and arm loading exercises with the pressure biofeedback unit under the lumbar
spine.
• Trunk inclination exercises: small (5-10-15 degrees) trunk inclination motions (waiter’s bow)
while maintaining co-contraction first in sitting, then in standing.
• Deep muscle co-contraction during ADL motions (walking, sitting, yard work). Be careful
not to overly fatigue muscles and fall into substitution patterns. Can be a powerful stimulus
for patients: painfree with contraction in a previously painful position!

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• INCORPORATION INTO HEAVIER FUNCTIONAL TASKS

• This stage is needed to ensure that deep muscle co-contraction can be maintained during
heavier tasks.
• Make use of different patient positions (prone, supine, sidelying, sitting, standing, tall
kneeling, half kneeling, etc.).
• Use different support surfaces (gym ball, wobble board, foam mat, small ball, etc.).
• Use eyes open versus closed.
• Use different dimensions of the base of support (feet together, heel-to-toe, etc.).
• Vary speed of movement, resistance used (manual, elastic, pulley, dumbells), direction of
resistance, point where resistance is applied (proximal versus distal), number of repetitions,
load used, type of contraction used, etc.
• Limitless possibilities.
• Maintain deep muscle co-contraction throughout.

• Question: use all variables mentioned above to develop exercises for this stage of
rehabilitation in the following positions: bridging position, quadruped position, side lying,
sitting, half kneeling, standing, sitting.

• Final stage is rehabilitation of those activities relevant to occupation and sport of the patient.
• Perform a needs analysis of the activity to be trained and develop a specific exercise routine.
• Needs analysis answers questions such as:
1. Which muscles are used?
2. What type of contraction do these muscles perform?
3. How long or how often does this contraction need to be performed?
4. What external loads need to be displaced?
5. At what speed do these loads need to be moved?
6. What energy system is responsible for fueling the activity?
7. What is the movement structure of a movement?
• The therapist should be able to get all this information during history taking.
• A specific exercise routine uses exercises aimed at slowly incorporating all parameters of the
movement to be improved while taking into account the limitations imposed by the patient’s
pathology, impairment, and disability (Huijbregts and Clarijs, 1995).
• This approach is also used to address the global subsystem deficiencies in strength,
endurance, and coordination identified during your examination.

• Question: develop a final stage training program for a basketball player with active and
neural control subsystem deficiency; the function you wish to improve involves vertical
jumping; you found a decrease in strength in the right quadriceps muscle (in addition to the
subsystem deficiency).

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REFERENCES

• Bogduk, N. Clinical Anatomy of the Lumbar Spine and Sacrum, 3rd ed. Edinburgh, Scotland:
Churchill Livingstone; 1997.
• Burton AK, Battie MC, Gibbons L, Videman T, Tillotson KM. Lumbar disc degeneration
and sagittal flexibility. J Spinal Disord 1996; 9: 418-24.
• Comerford MJ, Mottram SL. Movement and stability dysfunction – contemporary
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• Dunlop RB, Adams MA, Hutton WC. Disc space narrowing and the lumbar facet joints. J
Bone Joint Surg 1984; 66B; 706-10.
• Hides JA, Richardson CA, Jull GA. Multifidus muscle recovery is not automatic after
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• Huijbregts PA. HSC 11.2.4. Lumbopelvic Region: Aging, Disease, Examination, Diagnosis,
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2001.
• Huijbregts PA, Clarijs JP. Krachttraining in Revalidatie en Sport. Utrecht, The Netherlands:
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• McGill SM, Cholewicki J. Biomechanical basis for stability: an explanation to enhance
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Patient. In: Wadsworth C, ed. HSC 9.3. Management of Lumbar Spine Dysfunction.
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• Richardson C, Jull G, Hodges P, Hides J. Therapeutic Exercise for Spinal Segmental
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in vivo. Spine 1990; 15: 1300-6.
• Wilke HJ, Wolf S, Claes LE, Arand M, Wiesend A. Stability increase of the lumbar spine
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