CGA FAQ: The Spinal Engine

I would like to have some comments about the theory of the " spinal engine " (
Gracovetsky 1988 ).  Are the legs following pelvic motion or other wise. What
is the role of the sacroiliac joint during gait ??
                          Just wondering .....
                                  Vesa ( Physiotherapist near from polar
Thanks Craig  and  Howard (   Vleeming ´s book is very
interesting ).
 I´m working in public healthcare system and I´m dealing a lot with patients
having promblems in their  lower extremity kinetic chain system.
In Finland we have  many different point of views or schools in treating
patient with lower extremity problems ( orthopedic, podiatric, manual therapy,
orthotic etc ).
 ( Manual therapist is especially convinced on importance of SIJ, podiatrist is
dealinig only with foot etc.)
 I personally believe that combination of all these elements will  give best
 Usually there is a problem of finding the basic backround of the symptoms.For
example:   Is the foot hyperpronation  causing the SIJ problem or the other
wise.  If we ask the manual therapist , he believes that the origin of the problem
is in the  movement of SIJ or somewhere else in  pelvic / low back area. The
podiatric side is  treating the problem from the foot.
 In my point of  view this is not a problem in therapeutic means, because I try
to deal with the whole locomotion system by using different methods (
physiotherapy, othotics etc.)
I just curious to hear your comments about the pathomechanics and methods of
treating  patients with lower extremity problem.

                                   Many Thanks !! Vesa


        Another approach that was not mentioned in your email is to approach
locomotion from the neurological perspective.  It is well described in the
neurological literature that the primary afferent information for
triggering the gait cycle arises from a stretch of the hip flexors
(primarily the iliopsoas).  This does not arise from the hip joint
afferents.  As the iliopsoas cross the hip, SI, and lumbar spine
limitations in any of these joints will constrain / limit the excursion of
the iliopsoas so the stretch will be minimized.  Furthermore, as the muscle
group cross all of the articulations, increasing the extension range at any
of the articulations would have the effect of increasing the stretch on the
iliopsoas -  a finding that clinically validates the theories any of the
hip, SI, or lumbar spine therapists.
        A second important afferent signal arises from the stretch and tension
receptors in the triceps surae (gastroc and soleus).  During terminal
stance, the unweighting of the triceps facilitates the initiation of the
swing phase (facilitates flexors and inhibits extensors); during mid stance
the loading of the limb facilitates extensors and inhibits flexors.  (Note
the wonderful reversal of the effects of triceps stretch.)
        If the stretch of the posterior calf muscles is decreased then this
facilitation of flexion during terminal stance or of extension during mid
stance is reduced.  Specifically, if during mid stance the calcaneus is
allowed to plantarflex, then the stretch of the triceps is decreased.  This
calcaneal plantar flexion occurs if the longitudinal arch is allowed to
fall.   In terminal stance, if the calcaneus is allowed to maintain its
plantar flexion, the stretch on the triceps remains for a longer time
period which could delay the facilitation of the swing phase.
        Viewing locomotion from a neurological control perspective helps to
synthesize the manual therapist and podiatric perspectives.  I need to
emphasize that the primary, locomotion-triggering input arises from the
stretch of the hip flexors -- not from the triceps.  While this has been
shown in animal research, it is also clinically apparent when working with
bilateral lower extremity amputees who can walk and run (<11 sec for 100m).
 This does not negate the importance of the afference from the lower leg,
rather it ranks their relative values -- Primary is hip flexor stretch,
next is the variable stretch of the triceps, and then finally "other"
        Perhaps, a patient who is unable to gain enough afference from one source
(either hip or triceps), may compensate by trying to increase the afference
from the other source.  If this could be shown, then hip/SI/lumbar
articular problems could give rise to an "over-use" problems of the foot
(and the opposite should hold true as well).
        For an in depth discussion of the neurology of locomotion I would
recommend the excellent reviews by Whelan (1996) and Pearson (1995).

Paul H.

Paul D. Hansen, Ph.D., P.T.
  Fircrest Physical Therapy
  1105 Regents Blvd., Suite C
  Fircrest, WA  98466

Voice:  253.565.7796
Fax:    253.565.7836

Pearson KG  1995  Proprioceptive regulation of locomotion.  Current Opinion
in Neurobiology 5:786-791.

Whelan, PJ 1996 Control of locomotion in the decerebrate cat. Progress in
Neurobiology 49:481-515.   (This is my favorite review paper on the
neuroanatomy of locomotion)

Thank you all for your comments !!!Here are few  questions , which i hope that you could throw some light on ( especially Howard D. ).
First about the subtalar joint : in your opinion.
1.  What is  the " normal " neutral STJ position ( Root   versus Astrom & Arvidson ) & ROM and the RCSP in
urbanized population ??
2.  Is it, in general,  possible to  estimate  STJ ´s ability to be  shock absorption  mechanism / rigid " push off "
platform for example by measuring calcaneal inversion / everson , naviculare drop test etc?
3. STJ hyperpronation, is it as common problem as  is given to understand ?  Could it be possible  that
the hypermobile forefoot (  MTJ , 1 -ray ) is causing the same patomechanics as STJ  hyperpronation  when
STJ itself is hypomobile and MTJ and 1 -ray are a compensation for  STJ`s lack of shock absorption ability  ??
M. Peroneus Longus dysfunction.
 For me it seems to be quite common phenomenon... is it ?
 The connection : peroneus - biceps - lig. sacrotuberale - SI  force closure  has been presented by Vleeming &
5.   Would it be possible  that  SI - dysfuction could cause peronel dysfunction   or  the other way round ??
Functional hallux limitus.
 6. Could it be possible that peroneus  longus dysfunction  during terminal stance - preswing is causing "
automatical  contact or weight baring avoidance " on forefoot / first metatarsal " because the first ray is unstable
and  maybe in dorsiflex position, (  all this happens before the Windlass is active  or it is weak ).
So there is no hallux dorsiflexion, because the whole gait phase is been avoided because of forefoot balance
problems  ( and lack of first ray plantarflexion / windlass ) caused by peroneus longus dysfunction which is
cause by ......??
 I hope that you have  enough time and patience  to comment my thoughts ,as odd as they may seem like.
                                                        Regards Vesa

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