Hi

Its hard to know where to start with this one, but for me, the way that 'Psoas Syndrome' is
mentioned with such unwaivering confidence as to its existence with no inclination of doubt as to
the processes involved is the one thing I could not let go without a mention. Psoas holds such a
fascination for Osteopathy and is one of the areas where there is actually a lot of research
concerning both its function and the changes it undergoes in patients with pain (hip or low
back). Unfortunately the evidence does not really support what I understand Psoas Syndrome to
be (a tightening or shortening of the muscle causing lumbar spine restriction and some kind of hip
flexion contracture or reduced range of extension, with secondary postural changes). Please
correct me if I'm wrong.

So, even ignoring the lack of a satisfactory assessment of psoas as described in the methods;
"Psoas syndrome was diagnosed by finding a psoas muscle tender point upon palpation in
conjunction with suspected imbalance of the psoas muscles as determined by restriction during a
sweeping motion of the hip capsule." If we look from a biomechanical/anatomy perspective, as
the authors supposedly are, the evidence is quite contradictory to their assumptions of the
influence psoas may have, which for me renders the experiment they conduct to treat this
'syndome' irrelevant.

the fascicle lenght of the muscle fibres of psoas are very short (much like multifidus) and
suggest it serves more of a stabilising role than a prime mover, which would need long
fascicles to generate sufficient changes in total muscle length (Regev et al 2011).
the structure of psoas and its attachement points in the lumbar spine mean it is unlikely to be
able to move the lumbar spine, only compress it as a stabilieser would (Bogduk 1992), it
would therfore be unable to influence spinal posture or position even if it did shorten or
tighten.
as well as having similair fascicle length, cross sectional area and biomechnical properties to
multifidus, psoas also operates on the opposite side of the length tension curve to
multifidus, meaning both muscles become more efficient as the lumbar spine flexes and
therefore requires more stabilisation.
during unilateral hip flexion, psoas is the only muscle classed as a hip flexor to contract
bilaterally, again supporting its role as a spinal stabiliser (Hue et al 2011).
the optimal length of the sarcomeres in psoas for hip flexion are not reached until 120 degrees
hip flexion, psoas would therefore be a weak or ineffecient hip flexor in the normal
functional range of hip flexion (Regev et al 2011).
psoas does however generate significant pressure on the anterior aspect of the femoral head
between 0-15 degrees flexion, thereby preventing anterior femoral head translation. This
suggests it serves more as a hip stabiliser during functional ranges of hip movement, i.e.
gait (Yoshio et al 2002).
in the presence of back pain or pathology such as following a discectomy, psoas has been
shown to have increased levels of fatty infiltrate and/or a reduced cross sectional area, both
suggesting atrophy and weakness. Similair findings are also observed in multifidus
(Dangaria and Naesh 1998, Barker et al 2004, Bouche et al 2011).
it is also thought that underactivity of the psoas muscle contributes to hip instability and the
resultant pain and damage this may produce (Comerford and Mottram 2013).
My interpretation of the research I have read is that psoas functions more importantly as a spine
and hip stabiliser and is not structured to provide efficient hip flexion in a functional range. It is
also weakend and atrophied in the presence of spinal pathology and shows no evidence of
shortening or reduced extensibility. I would be intersted to hear how (or even if) psoas syndome is
diagnosed and treated in clinic and any supporting evidence for such a diagnosis and approach.
Thanks

Dan

Barker KL, Shamley DR, Jackson D 2004 Change in cross sectional area of multifidus and psoas in patients
with unilateral back pain. Spine 29:515-519

Bogduk NM, Pearcy M, Hadfield G 1992 Anatomy and biomechanics of psoas major. Clinical Biomechanics
7:109-119

Bouche KGW, Vanovermeire O, Stevens VK, Coorevits PL, Caemaert JJ, Cambier DC, Verstraete K,
Vanderstraeten GC, Danneels LA 2011 Computed tomography analysis of the quality of trunk muscles in
asymptomatic and symptomatic lumbar discectomy patients. BMC Musculoskeletal Disorders 12:65-73

Comerford MJ, Mottram SL (2013) Kinetic Control PTY4028 [Manual]. Motor Control. Keele University,
School of health and Rehabilitation 4-8th Jan.

Dangaria TR, Naesh O 1998 Changes in the cross sectional area of psoas major muscle in unilateral sciatica
caused by disc herniation. Spine 23:928-31

Hu H, Meijer OG, van Dieen JH, Hodges PW, Bruijn SM, Strijers RL, Nanayakkara PWB, van Royen BJ, Wu
WH, Xia Chun 2011 Is the psoas a hip flexor in the active straight leg raise? European Spine Journal 20:759-
765

Regev GJ, Kim CW, Tomiya A, Lee YP, Ghofrani H, Garfin SR, Lieber RL, Ward SR 2011 Psoas muscle architectural
design, in vivo sarcomere length range, and passive tensile properties support its role as a lumbar spine
stabiliser. Spine 36(26):1666-1674

Yoshio M, Murakami G, Sato T, Sato S, Noriyasu S 2002 The function of psoas major muscle: passive kinetics and
morphological studies using donated cadavers. Journal of Orthopaedic Science 7:199-207