Dr. Jesse Jutkowitz
Member |
What everyone seems to miss, because they did not post it, was my answer to
Dr. Rob Ward.
What he states is based on the preliminary data in ADVERSE MECHANICAL TENSION
ON THE CENTRAL NERVOUS SYSTEM. Ward did not bother to get SKULL TRACTION AND
CERVICAL CORD INJURY which was published 11 years later (1989) and included a
further decade of research.
There, the further case studies are well documented and the further
conclusions are drawn. Rob Ward's comments were on incomplete researching of the
data.
He got very quiet when I posted the exact quotes from SKULL
TRACTION... |
GWDC
Member | not to defend JJ, but rather to further understanding...I
am glad that you posted the post you did. Perhaps it should
be included under Gary's post.
Do you really believe that the errector spinae transmit forces the way the
article's author suggests???
If so could you please provide me with EMG documentation of the same?
So it would appear that the critic uses unsubstantiated claims to slam a
fellow DC.
After reading both of David Butler's books, don't you feel that the neural
tension model is viable???
Would not a more mature statement be " an alternative explanation to neural
tension, might be the transmission of tension in the erector spinae muscles"?
Isn't this a case of the kettle calling the pot black?
What is Soto-Hall's maneuver?? Flexing the neck re-producing lower body
pain....by what?? Dural tension! The concept has been around for years.
In our rush to be right, do we fail to consider that we may not have all the
knowledge needed to understand the concept?
Neitche (sp?) said it best...there is no bird's eye view....everything is
looked at from one perspective...our own!!!
BTW1:I was particularly un-impressed by Dr. Wards lack of refs to back up his
OPINIONS
------------------
BTW2: DM you have read Butler's books...If my
reading of Butler is correct it seems to contradict Ward's assumptions of the
mechanisms of dural tension....see the "slump test" Butler's first book...It's
been a while am I
incorrect??? |
GWDC
Member | Just a follow-up to Rob Ward's opinions...
"However, the simple experiment that Dr. Jutkowitz proposes you perform will
in fact demonstrate to you that due to the overlapping nature of the erector
spinae, you will become aware of greater tension on the cervical musculature
with head flexion in a squatting posture.
>>>> It is doubtful that this phenomenon is related to spinal
cord stretching, >>>> which doesn't become apparent to most people
until you flex the entire spine, flex the hip, extend the knee, and possibly add
dorsiflexion of the ankle."
Is this correct???
1: J Orthop Sports Phys Ther 1997 Dec;26(6):310-7
The slump test: the effects of head and lower extremity position on
knee
extension.
Johnson EK, Chiarello CM
Physical Medicine and Rehabilitation Center, Englewood, NJ, USA.
Maitland's slump test is a widely used neural tissue tension test. During
slump testing, terminal knee extension is assessed for signs of restricted range
of motion (ROM), which may indicate impaired neural tissue mobility. A number of
refinements that modify hip and ankle position has been added to the basic slump
test procedure, but no research to date has measured the effects of ankle and
hip position on knee extension ROM during testing. The purpose of this study was
to examine the effect of neural tension-producing movements of the cervical
spine and lower extremity on knee extension ROM during the slump test.
Thirty-four males with no significant history of low back pain were
tested in the slump position with the cervical spine flexed and extended in each
of three lower extremity test positions: neutral hip rotation with the ankle in
a position of subject comfort (neutral), neutral hip rotation with ankle
dorsiflexion (ankle dorsiflexion), and medial hip rotation with ankle
dorsiflexion. >>>>>>
Results showed significant decreases in active knee extension ROM (F1,198 =
29.53, p < 0.0001) in the cervical flexion compared with the cervical
extension conditions.
Subjects also exhibited significant decreases in active knee extension
ROM (F2,198 = 56.76, p < 0.0001) as they were progressed from neutral to the
ankle dorsiflexion to the medial hip rotation with ankle dorsiflexion positions
of the lower extremity. The results of our study indicate that limitations in
terminal knee extension ROM may be considered a normal response to the inclusion
of cervical flexion, ankle dorsiflexion, or medial hip rotation in the slump
test in young, healthy, adult males. In addition, the presence of a cumulative
effect on knee extension ROM with the simultaneous application of these motions
is noted. These findings may assist clinicians when assessing knee extension ROM
during slump testing.
|
This is part of a discussion from a MD message board.
I am a 45 year old pediatrician who was given a diagnosis
of multiple sclerosis due to progressive neurologic signs
and symptoms. I wish to publicly thank my neurosurgical colleagues
who determined that the correct diagnosis was congenital and
acquired cervical spinal stenosis. Although clinically I had
classic "MS", my MRIs revealed no plaques. I underwent
a laminoplasty from C3 to C7 and have now fully recovered.
A bonus is that it also cured a lifelong history of severe
neurocardiogenic syncope with prolonged episodes of asystole
and resting bradycardia - the sympathetic tracts were also
compromised. My cardiologist was amazed at my recovery! He
no longer recommends a pacemaker. Perhaps there are many others
with such misdiagnoses.
=================================
Response -
MS without plaques on MRI? MS should be more than simply
cord problems--even transverse myelitis usually appears on
MRI. Did you have eye problems or other brain problems in
your "Classic MS"?
I have seen patients with both MS and cervical stenosis, but
if the only symptoms are related to the neck I wouldn't think
MS.
===================================
Response -
Did the LP show Oligoclonal Banding?
===================================
Response -
: Hail fellow! You have been so fortunate in having such
astute physicians investigating your problems. I assume that
a complete workup including all the necessary studies to r/o
MS and that other causes thus were investigated. Do not be
skeptical. You have been essentially cured and have made an
astonishing recovery. The proof is in the pudding. God Bless!
================================
(Supe again)...Now, I'm no great believer in Jesse's proprietary
technique, but maybe ol' Breig was onto something... I would
say that perhaps certain pathologies that irritate or put
tension on the spinal cord produce clinical presentations
that are clinically indistinguishable from classic MS.
More from the original discussion:
Supe,
did any of the MDs on the board jump all over this doc and
talk about how it's just an anecdotal story...and then suggest
that the recovery was merely placebo???
I didn't think so!!!
The big question is: can any manipulative procedure performed
by DC's have any effect on a stenotic canal? I say again:
an atomically stenotic canal?
Mirtzy
---------------
Dr. Mirtz,
perhaps this should go under scanners anecdotal evidence...
Patient getting left arm numbness down into fingers, burning
sensation into neck and face.
Worse at night.
Cardiologist wanted to do a catheterization. Your old
boy in the burgh does some neuro-othopedic tests and can reproduce
the patient symptoms...
I say MRI c spine...cardiologist says cath lab.
Before the patient could get the catheterization...she
gets the MRI...DC wins cervical stenosis...patient refused
cath....
long story short....chiropractic reduces cord compression
enough that the patient has not had S & S in several years
(I see her 2-3X per years as follow-up).
As for lumbar spinal stenosis....I've treated literally
100s...had 1 go onto surgery.
BTW: interesting that the surgeons (some) feel that cervical
spondylitic myelopathy results more from tension in the dentate
ligament on the cord than from compression from stenosis.....yikes
this supports JJ (Dr. Jutkowitz's) ideas!!!!
I'll get the ref soon.
------------------
1: J Spinal Disord 1991 Sep;4(3):286-95
Cervical laminectomy and dentate ligament section for
cervical spondylitic
myelopathy.
Benzel EC, Lancon J, Kesterson L, Hadden T
Division of Neurosurgery, University of New Mexico School
of Medicine,
Albuquerque 87131.
Seventy-five patients who underwent surgical treatment
for cervical spondylotic
myelopathy were evaluated with respect to the operative procedure
performed and
their outcome. Forty patients underwent a laminectomy plus
dentate ligament
section (DLS), 18 underwent laminectomy alone, and 17 underwent
an anterior
cervical decompression and fusion (ACDF). The patients were
evaluated
postoperatively for both stability and for neurologic outcome
using a
modification of the Japanese Orthopaedic Association Assessment
Scale.
Functional improvement occurred in all but one patient in
the laminectomy plus
DLS group. The average improvement was 3.1 +/- 1.5 points
in this group; whereas
the average improvement in the laminectomy and the ACDF groups
was 2.7 +/- 2.0
and 3.0 +/- 2.0 points respectively. All of the patients who
improved
substantially (greater than or equal to 6 points) in the laminectomy
plus DLS
and the laminectomy alone groups had normal cervical spine
contours (lordosis).
The remainder had either a normal lordosis or no curve (no
kyphosis or
lordosis). All patients in the ACDF group had either a straight
spine or a
cervical kyphosis. These factors implicate spine curvature,
in addition to
choice of operation, as factors which are important in outcome
determination. No
problems with instability occurred in either the laminectomy
or the laminectomy
plus DLS group. Two patients incurred problems with stability
in the ACDF group.
Both required reoperation. In addition, four patients in this
group who
initially improved, subsequently deteriorated. Six patients
in the laminectomy
plus DLS group had a several day febrile episode related to
an aseptic
meningitis process. Laminectomy plus DLS is a safe and efficacious
alternative
to laminectomy for the treatment of cervical spondylotic myelopathy.
The data
presented here suggests that myelopathic patients with a cervical
kyphosis are
best treated with an ACDF and that patients with a normal
cervical lordosis are
best treated with a posterior approach. Although some selected
patients may
benefit from DLS, no criteria are available which differentiate
this small
subset of patients.
PMID: 1802159
1: J Neurol Neurosurg Psychiatry 1997 Apr;62(4):334-40
Pathogenesis of cervical spondylotic myelopathy.
Levine DN
Department of Neurology, New York University Medical Center,
New York, NY 10016,
USA.
OBJECTIVE: To determine whether either of two mechanical
theories predicts the
topographic pattern of neuropathology in cervical spondylitic
myelopathy (CSM).
The compression theory states that the spinal cord is compressed
between a
spondylitic bar anteriorly and the ligamentum flava posteriorly.
The dentate
tension theory states that the spinal cord is pulled laterally
by the dentate
ligaments, which are tensed by an anterior spondylitic bar.
METHODS: The spinal
cord cross section, at the level of a spondylitic bar, is
modeled as a circular
disc subject to forces applied at its circumference. These
forces differ for the
two theories. From the pattern of forces at the circumference
the distribution
of shear stresses in the interior of the disc-that is, over
the transverse
section of the spinal cord-is calculated. With the assumption
that highly
stressed areas are most subject to damage, the stress pattern
predicted by each
theory can be compared to the topographic neuropathology of
CSM. RESULTS: The
predicted stress pattern of the dentate tension theory corresponds
to the
reported neuropathology, whereas the predicted stress pattern
of the compression
theory does not. CONCLUSIONS: The results strongly favor the
theory that CSM is
caused by tensile stresses transmitted to the spinal cord
from the dura via the
dentate ligaments. A spondylotic bar can increase dentate
tension by displacing
the spinal cord dorsally, while the dural attachments of the
dentate, anchored
by the dural root sleeves and dural ligaments, are displaced
less. The
spondylotic bar may also increase dentate tension by interfering
locally with
dural stretch during neck flexion, the resultant increase
in dural stress being
transmitted to the spinal cord via the dentate ligaments.
Flexion of the neck
increases dural tension and should be avoided in the conservative
treatment of
CSM. Both anterior and posterior extradural surgical operations
can diminish
dentate tension, which may explain their usefulness in CSM.
The generality of
these results must be tempered by the simplifying assumptions
required for the
mathematical model.
top
|
