DERMATOMAL SOMATOSENSORY EVOKED POTENTIAL DEMONSTRATION OF NERVE ROOT DECOMPRESSION AFTER VAX-D THERAPY
William K. Naguszewski, Robert K. Naguszewski, and Earl E. Gose *
Department of Neurology, Coosa Medical Group, Rome, Georgia, USA
*Department of Bioengineering, University of Illinois at Chicago, Chicago,
IL, USA
ABSTRACT
Reductions in low back pain and referred leg pain associated with a
diagnosis of herniated disc,
degenerative disc disease or facet syndrome have previously been reported
after treatment with a VAX-D
table, which intermittently distracts the spine. The object of this
study was to use dermatomal
somatosensory evoked potentials (DSSEPs) to demonstrate lumbar root
decompression following
VAX-D therapy. Seven consecutive patients with a diagnosis of low back
pain and unilateral or bilateral
L5 or S1 radiculopathy were studied at our center. Disc herniation
at the L5-S1 level was documented by
MRI or CT in all patients. All patients were studied bilaterally by
DSSEPs at L5 and S1 before and after
VAX-D therapy. All patients had at least 50% improvement in radicular
symptoms and low back pain and
three of them experienced complete resolution of all symptoms. The
average pain reduction was 77%.
The number of treatment sessions varied from 12 to 35. DSSEPs were
considered to show improvement
if triphasic characteristics returned or a 50% or greater increase
in the P1-P2 amplitude was seen. All
patients showed improvement in DSSEPs after VAX-D therapy either ipsilateral
or contralateral to the
symptomatic leg. Two patients showed deterioration in DSSEPs in the
symptomatic leg despite clinically
significant improvement in pain and radicular symptoms. Overall, 28
nerve roots were studied before and
after VAX-D therapy. Seventeen nerve root responses were improved,
eight remained unchanged and
three deteriorated. The significance of DSSEP improvement contralateral
to the symptomatic leg is
emphasized. Direct compression of a nerve root by a disc herniation
is probably not the sole explanation
for referred leg pain. (Neurol Res 2001; 23:706-714)
Key words: lumbar radiculopathy vertebral decompression dermatomal somatosensory
evoked
potentials low back pain VAX-D therapy
INTRODUCTION
Improvements in low back and referred leg pain associated with a diagnosis
of herniated disc,
degenerative disc disease or facet syndrome have previously been reported
after VAX-D therapy (1). In
71% of the 778 cases, the pain was reduced to 0 or 1 on a 0 to 5 scale.
Improvements in mobility and
activities of daily living were also noted. The average decrease in
pain, plus or minus the standard error
of the estimate, was 2.88 +/-0.05 units on a scale of 0-5, and a paired
two-sample t-test shows that this
pain decrease was at least 2.68 units with p<0.00005. The average
increase in mobility was 1.17 +/- 0.03
on a 0-3 scale, and this value was at least 1.04 units with p<0.00005.
Similarly, the average increase in
the activity score was 0.96+/-0.04 units on a 0-3 scale, and this average
improvement was at least 0.83
with p<0.00005. The coefficient of linear correlation (2) between
mobility and pain scores was 0.72 and
between pain and activity it was 0.60. The clinical improvement in
pain, mobility and activities of daily
living argues strongly that nerve root decompression can reasonably
be expected to follow VAX-D
therapy.
Lumbar disc decompression is clearly possible non-surgically through
the application of effective lumber
distraction tensions. Gupta and Ramarao (3) treated 14 patients with
prolapsed intervertebral disc
syndrome with continuous traction and showed complete or partial resolution
of the defects on
epidurogram. Mathews (4) likewise showed reductions in disc herniations
in two patients by
epidurography accompanied by vertebral body separation of 2mm per disc
space. Ramos and Martin (5)
measured intradiscal pressure by connecting a cannula inserted into
the patient’s L4-5 disc space to a
pressure transducer. Tensions applied by the VAX-D table were observed
to decompress the nucleus
pulposus significantly, to below –100 mm Hg.
Dermatomal somatosensory evoked potentials (DSSEPs) are an established
and effective physiologic
tool for assessing single nerve root function pre- and post- operatively
(6,7,8,9,10,11) and are useful as
well for monitoring potential acute nerve root injury during surgical
procedures using intrapedicular fixation
of the lumbosacral spine (12).
Dvonch et al (13) studied the root specificity of DSSEPs using myelograms
and surgical findings as the
standards and found the accuracy of DSSEPs to be 85.7% for lumbar radiculopathy
when compared to
myelograms and 87.5% when compared to surgery. Sensitivity was 0.93
and specificity was 0.86. Chi
square analysis was applied and accuracy was defined as the ratio of
all correct results to the total
number of nerve root pairs tested. Bilateral DSSEPs were performed
on each patient at L5 and S1.
Each nerve root was compared to the contralateral root and differences
in latency of more than 3 msec or
amplitude differences of more than 75% were considered significant.
Overall, DSSEPs were shown to
have an 86% accuracy in root specific diagnosis. The authors also concluded
that since pain is a frequent
accompaniment of root entrapment, DSSEP findings can provide information
in addition to the structural
abnormalities demonstrated by myelograms by offering a physiologic
way of monitoring the sensory side
of the nervous system. DSSEPs should thus be a useful adjunct in the
selection of patients undergoing
lumbar spine surgery.
PAIN LEVEL (0 to 10 scale)
| PATIENT | BEFORE | AFTER | # OF TREATMENTS |
| VAX-D | VAX-D | ||
| 1 | 5 | 0 | 12 |
| 2 | 8 | 0-0.5 | 35 |
| 3 | 7-8 | 4 | 13 |
| 4 | 3 | 0 | 10 |
| 5 | 5 | 1 | 10 |
| 6 | 5-6 | 2 | 20 |
| 7 | 6-7 | 2 | 20 |
Figure 1. Pain levels and number of treatments for the seven patients.
| Scarff et al (14) performed DSSEPs on 38
consecutive patients with suspected disc herniation. These patients subsequently underwent myelography and surgery with verification of nerve root entrapment by disc herniation. For each patient, comparisons were made regarding latency and amplitude of the DSSEPs from the involved and uninvolved leg. Differences in latency of more than 3 msec measured from the peak positive wave or an amplitude reduction of 75% were considered significant. Of the 38 patients, 35 had abnormal evoked potentials for the specific root involved. One patient had abnormalities for the contra-lateral root and 2 patients with bulging discs had normal DSSEPs. Similarly, Larson (15) utilized somatosensory
|
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MATERIALS AND METHODS
DSSEPs were conducted at our center on seven consecutive patients suffering
from mechanical low
back pain with referred leg pain in either an L5 or S1 distribution
or both. Clinically, patients with L5
radiculopathy experience pain in the back of the thigh, lateral calf
and dorsum of the foot. Patients with S1
radiculopathy experience pain in the back of the thigh, back of the
calf and lateral foot (17). Two patients
had bilateral symptoms. All seven patients had disc bulging or disc
herniation on MRI or CT at the L5-S1
level. Two of these patients had disc herniations at L4-5 and one patient
(patient #2) had multilevel disc
herniations with symptoms referring into the left S1 distribution only.
The initial pain levels and numbers of
treatments are shown in Figure 1.
Each patient underwent bilateral lower extremity DDSEPs at L5 and S1
immediately before and within two
weeks after the completion of VAX-D therapy. Data was obtained using
a Nihon-Kohden Neuro Pack #4
instrument. All patients were studied at our center by a certified
technologist from Rasmussen
Diagnostics, Woodstock, Georgia. The number of treatment sessions per
patient varied from 10 to 35.
Dermatomal stimulation at L5 was done medial to the extensor hallicus
tendon on each side with the
ground reference over the anterior ankle. For S1, stimulation was done
at the lateral aspect of the fifth
metatarsal with the ground electrode over the ankle, as shown in Figure
2. Cortical electrodes were
placed 3 cm anterior and posterior to Cz. Filter settings were set
at 10 Hz to 250Hz. The rate of
stimulation was 3 per second delivered as a square wave pulse of 0.2msec
duration with intensities of 2.2
to 7.6 mA. Stimulation intensity varied somewhat between patients and
was determined by beginning at a
low level of stimulation and increased until the patient perceived
a strong but not painful, tapping
sensation. Two trials were performed on each root to verify that the
waveform was reproducible. The
number of stimulations per trial ranged from 150 to 300. The two trials
were then averaged and the final
waveform was smoothed using a 9-point running average. Each patient
was studied consistently each
time either supine or in a recliner. Room temperature remained constant
at 72 degrees Fahrenheit and
wakefulness was assured.

The authors theorized that the morphology of the waveforms would be
distorted or suppressed prior to
VAX-D therapy given that the duration of clinical symptoms ranged from
8 weeks to 60 months for the
patients in this study. Treatment sessions were given Monday through
Friday with patients under
treatment from 2 to 7 weeks. This amount of time may have allowed nerve
root functional recovery while
the patient was receiving VAX-D therapy. Our study is in contrast to
previous studies in the literature
which eliminated patients with poorly reproducible waveforms before
surgery. Intra-operative studies have
focused on latency delays or a sudden loss of the first component of
the waveform as a sign of acute nerve
root injury. Because VAX-D therapy is a treatment which may have cumulative
benefit over time (1), the
authors assumed that as nerve roots were decompressed, electrical transmission
would improve but not
necessarily return the DSSEP to a truly normal waveform. We thus placed
emphasis on the reconstitution
of the waveform and its overall morphology, while evaluating DSSEPs
generated in this study using
latency and amplitude parameters consistent with the literature as
well. Additionally, the literature has
emphasized side to side comparisons at each nerve root level. This
study compares each nerve root
before and after VAX-D therapy.
Several quantitative measures of waveform quality were considered, including
the amplitudes of the
P1-P2 and P2-P3 portions of the waveform, their post-stimulus times
of occurrence, and the presence or
absence of P1, P2, and P3 “peaks” (positive or negative) in the waveform.
However, for some
waveforms it was not possible to distinguish with certainty between
true peaks and noise artifacts. In this
circumstance, the authors felt that it was more practical to consider
the waveform as a whole, and decide
if its quality increased or decreased significantly. The quality depends
on the amplitudes, the presence or
absence of P1, P2, and P3 peaks, and the ability to distinguish the
waveform from the noise. The
measure is subjective, so all the waveforms are shown in Figure 4,
and are labeled as “better”, “worse”, or
“same”. These decisions were made separately by the three authors and
the technician, all of whom
agree with this labeling.
RESULTS
All the DSSEPs, before and after VAX-D therapy, are shown in Figure
4. Clinically, all patients in our
study were symptomatic before VAX-D therapy. Low back and referred
leg pain were reduced by over
50% in each patient after VAX-D therapy and three were essentially
pain free. The average pain
reduction was 77%. Before VAX-D therapy, DSSEP waveform morphology
was often abnormal, with
absence of the first peak (P1) being most typically seen. This is not
an unexpected finding since temporal
dispersion of axonal volleys will affect early cortical DSSEP peaks,
resulting in their
diminution or loss without the loss of later peaks. It has been postulated
that the resiliency of later peaks is
due to the cerebral cortex functioning as an integrator, resynchronizing
the incoming inputs (18). For
those DSSEPs in which P1 was present before and after VAX-D therapy,
a P1 latency was measured as
well as a P1-P2 amplitude. Following the criteria of Scarff et al (14)
for latency and Larson (15) for
amplitude, a difference in latency of 3 msec or greater or an amplitude
change of 50% or greater was
considered significant. No significant changes were seen on average
in either latency or amplitude in our
study for those DSSEPs possessing a distinct P1 before and after VAX-D
therapy.
If there were no intrinsic difference between the data before treatment
and the data after treatment, then
the probability that the DSSEP response would improve would be equal
to the probability that it would get
worse. There would also be some probability that the quality of the
response would neither increase nor
decrease but would remain the same, within the limits of our ability
to estimate the quality of these
waveforms.

In Figure 5, eight of the 28 responses did not change significantly,
17 improved, and three were worse
after treatment. The probability that results this good would be obtained
by chance is less than 0.0013, i.e.
p< 0.0013, according to the cumulative binomial distribution, as
shown below. If it were true that, for the
20 responses that changed, a change for the better (B) were as likely
as a change for the worse (W), then
P (17 of the 20 are B ) = 20!/ (17! 3! 220 ) = 0.001087189
P (18 of the 20 are B ) = 20!/ (18! 2! 220 ) = 0.000181198
P (19 of the 20 are B ) = 20!/ (19! 1! 220 ) = 0.000019073
P (all 20 are B ) = 20!/ (20! 0! 2 20 ) = 0.000000954
Sum 0.001288414
The sum of these gives the probability that 17 or more of the 20 would
be better by chance: P (17 or more
are B ) = 0.001288414 . So p < 0.0013 that results as favorable
as those found in this study would
occur by chance. Statistically, these results are very
significant.
CASE REPORTS
Patient #1
A 48 year old male with a five-month history of chronic low back and
left leg pain predominantly in an S1
distribution. Lumbar MRI revealed a moderate left paramedian herniated
nucleus pulposis compressing
the S1 nerve root. The patient received 12 VAX-D treatments and experienced
complete resolution of low
back and left leg pain.
Patient #2
A 54 year old county school psychologist with an eight week history
of low back pain and left S1
radiculopathy. He had a previous episode of left leg sciatica several
years before which resolved with bed
rest and medication. Lumbar CT revealed a large left paracentral herniated
nucleus pulposis at L5-S1
compressing the left S1 root. Additionally, a moderate central herniated
disc was seen at L4-5 resulting in
moderate spinal stenosis and a small left paracentral disc herniation
was seen at L3-4. He underwent a
total of 35 VAX-D treatments and experienced a greater than 90% reduction
of his low back and left leg
pain.
Patient #3
A 31 year old female with a 2 year history of chronic low back pain
and intermittent left leg pain following
an L5 and S1 distribution. Lumbar CT showed a contained central annular
bulging of the L3-4 and L4-5
discs with no significant underlying neural compromise, as well as
a small to moderate midline herniation
at L5-S1 causing some effacement of the underlying thecal sac. She
completed 13 VAX-D sessions with
a 50% reduction in pain and experienced a subjective increase in mobility.
Patient #4
A 48 year old male with a 60 month history of chronic low back pain
and right leg pain in an S1
distribution. Lumbar MRI showed desiccation and degenerative changes
of the L5-S1 disc with a right
sided herniation causing effacement of the right S1 root. Minimal bulging
of the L3-4 and L4-5 discs was
noted as well. After ten VAX-D treatments all pain was eliminated.
Patient #5
A 56 year old female with a 9 month history of chronic low back pain
and occasional episodes of right
sided sciatica in an L5 distribution. Lumbar MRI showed degenerative
disc disease at L4-5 and L5-S1
with a mild diffuse disc bulge at L4-5 encroaching upon the right L5
root. The patient experienced an 80%
reduction of pain after her tenth VAX-D treatment.
Patient #6
A 23 year old male with a 10 month history of low back pain after a
lifting injury at work. Pain and
numbness were present intermittently in both legs in an L5 and S1 distribution
but more severely affected
the left leg. Lumbar MRI scan showed degenerative disc disease at L4-5
and L5-S1 with a left sided
herniated disc at L5-S1. After twenty VAX-D treatments he no longer
experienced any numbness in his
legs and his pain was reduced by 50%. He elected to stop further treatments
in favor of returning to work.
Patient #7
A 33 year old EMT with a 38 month history of low back pain associated
with periods of either right, left or
bilateral leg pain and numbness in an L5 and S1 distribution. Predominantly
the right leg was most
symptomatic at the time she underwent VAX-D therapy. A lumbar MRI before
treatment showed a
degenerated L4-5 disc with a left paracentral herniation indenting
the thecal sac. At L5-S1 the disc was
degenerated with a small left paracentral herniation without nerve
root compromise. The patient
underwent 20 VAX-D treatments with complete resolution of leg numbness
and a 70% reduction in low
back and leg pain.
DISCUSSION
We know that VAX-D is a safe and generally successful treatment of low
back pain associated with
lumbar disc herniation, degenerative disc disease, or facet syndrome.
VAX-D was designed with a
primary purpose to relieve low back pain with or without radiculopathy.
Surgery, oftentimes, is focused
primarily on nerve root decompression to relieve radicular pain and
any improvement in back pain follows
as a secondary benefit. This secondary benefit occurs despite the fact
that discectomy and laminectomy
involve further disc and spine disruption. The literature is clear
that not all patients benefit by surgical
nerve root decompression and also that surgical patients on average
fare no better long term than patients
who are managed conservatively (20,21,22,23 24).
The present study used DSSEPs to provide an objective means of measuring
a physiologic cortical
manifestation of nerve root decompression. In 1994 using disc manometrics,
Ramos provided clear
documentation that negative intradiscal pressure changes down to –150
mm Hg were achieved with
VAX-D treatment. Tilaro and Miskovich (25), using a CPT neurometer,
showed that peripheral peroneal
and sural nerve distribution sensation were improved in 27% or returned
to normal in 67% of 17 patients
with radiculopathy symptoms after VAX-D treatment. They used the CPT
Neurometer to deliver a
sinusoidal electrical stimulus. The threshold of perception was defined
as the minimal amount of stimulus
required to evoke a sensation at least 50% of the times it was presented.
Results were taken three times
at each site and were reliable, i.e., statistically they could not
have been fabricated by a patient. Tilaro
and Miskovich reasoned that improvement with VAX-D must have reflected
nerve root decompression
because no other change in function of the peroneal and sural nerves,
spinal cord, brainstem or cerebral
cortex would be expected. Neurometer measurements rely on the patient’s
subjective experience
(perception) of sensory stimulation. Perception involves cortical activation
and integration. It is a
conscious subjective response.
Somatosensory testing, in general, assesses the electrophysiology of
the pathway to the brain’s cortex as
a consequence of a sensory experience such as vision, hearing, or extremity
sensation. Scalp electrodes
pick up cortical activity which is then signal averaged to create a
waveform. Our results extend the work of
Ramos and Tilaro. We chose DSSEPs to isolate L5 and S1 root function
by dermatomal stimulation.
Further, results were taken bilaterally such that each patient in essence
served as his or her own control.
Four roots were monitored for all patients. Restored waveforms had
a triphasic appearance which is
normal and expected for the method of recording we used. DSSEP’s are
used widely for monitoring
potential spinal cord or nerve root injury during spinal surgery, particularly
when there is a concern about
injuring nerve roots.
In this study, we found that multiple nerve roots appear to be decompressed
in most of the patients, which
fits nicely with the data of Tilaro and Miskovich. Their neurometer
measurements were taken over the
peroneal and sural nerves, which are relatively large. Although these
nerves derive from a limited number
of nerve roots, they are not pure. Stimulation of the peroneal nerve
sends impulses through L4 and L5
roots. Likewise, stimulation of the sural nerve sends impulses through
L5 and S1. It may be that multiple
nerve root decompression was responsible for the large improvements
in the perception thresholds
measured by Tilaro and Miskovich.
Clinical implications that can be derived may have importance as to
how we view the low back and what
we may think is the main source of pain for a particular patient. Patient
clinical histories and examinations
suggest that nerve roots are not involved in isolation but that adjacent
nerve roots and even contralateral
changes may exist to account for symptoms that overlap dermatomes or
are bilateral despite a unilateral
lesion. The DSSEPs reviewed here provide physiologic evidence that
this possibility not only exists but
is likely.
The best surgical outcome to be expected occurs when spine imaging is
consistent with symptoms and
clinical findings. These patients tend to do well with surgery and
therefore one might conclude that nerve
root decompression has something to do with why leg pain in particular
responds. Other patients do less
well, particularly when symptoms and clinical findings are inconsistent
with the results of diagnostic
imaging. Possible explanations relate to irreversible nerve root injury
from a ruptured disc, epidural
fibrosis and other poorly understood reasons.
The remarkable improvements following VAX-D therapy (71%) for a variety
of pathologies (1) suggests
some possibilities for these “otherwise poorly understood reasons.”
Our study suggests that VAX-D
exerts its benefit at more than one level ipsilateral and contralateral
to the direction of disc herniation.
Evidence is provided that multiple root abnormalities by DSSEP may
be present despite one structural
lesion by MRI. Although clinicians assume that the consequences of
such structural pathology is an
important source of pain, our present results raise the possibility
that such pathology may not be the main
cause of pain but may allow consequent or subsequent changes to become
the primary source of pain for
an individual patient. Tsai et al (26) studied 33 patients with intraoperative
DSSEPs undergoing
micro-decompression for single level, unilateral lumbosacral radiculopathy.
Nineteen patients had
acceptable DSSEPs at baseline with 13 of these19 patients having an
abnormal DSSEP for the
symptomatic nerve root defined as a side-to- side latency asymmetry
of greater than 5% before surgery.
Four patients had DSSEP side-to-side latencies within 5% at each nerve
root level and 2 patients had
poorly reproducible evoked responses on the symptomatic side. All latency
asymmetries resolved and
improved waveforms were seen in the 2 patients with poor evoked responses
before surgery. Despite
apparently successful nerve root decompression, clinical outcome at
3 months was good to excellent in 13
patients, fair in 4 patients and poor in 2 patients. This may at first
seem surprising but do we really know
what is the most important source of pain and whether it relates to
the primary event such as a disc
herniation or does it follow as a consequence? In our study, all patients
were clinically improved but only
one showed contralateral improvement by DSSEP. The authors wonder what
the outcome would have
been if the patient had been operated on ipsilaterally. With the above
analysis, we now have an
explanation for overlapping dermatomal complaints, bilateral symptoms,
and sometimes pain going down
“the wrong leg”- meaning that the MRI shows a disc herniation directed
opposite to the symptomatic leg.
We suggest that VAX-D therapy effectively manages mechanical low back
pain with or without referred
leg pain through spine segment mobilization. Spine segment motion integrity
is a crucial concept and
probably best explains the correlation previously found between reduced
pain and improved gross spine
mobility subsequent to VAX-D therapy (1). A spine motion segment consists
of two vertebral bodies with
an intervening disc and all attached and enclosed structures (27).
Segment motion normally is dynamic
with flexion, extension, torsion, and tilting often combined simultaneously
allowing pain-free movement in a
normal spine. This occurs normally without nerve root impingement despite
even extreme spine flexion
and extension seen in gymnasts and contortionists. Furthermore, it
is known that the spinal cord can
adapt to length changes of the spinal canal because the cord itself
is folded when the spine is in a neutral
position and will unfold during flexion and can fold further during
spine extension. The nerve roots follow
the spinal cord but do not fold and unfold (27). It is the ability
of the vertebra to translate and rotate upon
each other that provides slack to the nerve roots. Impairments here
stymie functional compensations to
reduce “the pressure on nerve roots” as the spine is loaded by weight-
bearing activities. VAX-D therapy
helps to restore mobility and allows for a return of dynamic functional
compensation. A natural
consequence of disc injury is to accelerate “natural” fusion of the
segment. If the segment “fuses” in a
position that allows enough room in the lateral recess, central canal,
and neural foramina –then there may
be no pain. If however, such fusion is less harmonious there will be
pain plus lost motion. VAX-D is
unique in its position to alter the reactive process leading to symptomatic
bony fusion whereby osteophytic
changes are seen on the anterior and posterior aspects of the vertebral
endplates. Again Gose,
Naguszewski and Naguszewski (1) showed a clear and strong correlation
between increased mobility and
decreased pain reported after VAX-D therapy. This dynamic compensation
is presumed to be the result
of spinal reflexes that function specifically to maintain proper alignment
of stacked spine motion
segments. These spinal reflexes are protective against nerve root injury
and can be acted upon by higher
centers to facilitate smooth, safe and effective voluntary movement.
We know that the erector spinae
muscles are “ratcheted” on the spine like shingles on the roof of a
house to allow accordion-like motion.
The transversospinal muscles span one, two, three or more segments
(28). Spinal reflexes are in place to
coordinate all of these muscles to allow full range of motion without
nerve root impingement. With acute
lumbar injuries, the spinal reflexes may induce sustained muscular
contraction resulting in radiographic
straightening of the lumbar spine and immobilization of one or more
lumbar motion segments. Sustained
muscular contraction for weeks may lead to adhesive capsulitis of the
facets, perpetuating motion
segment immobility despite eventual resolution of muscular spasm. Additionally,
the persistence of
contracted musculature may eventuate into contracture reducing mobility
of the affected lumbar motion
segment. Such focal contracture so to speak, is myofascial fusion.
We argue that VAX-D therapy is best
suited to release such contracture.
With degenerative disc disease there is a loss of disc height. Disc
height is crucial in determining neural
foraminal vertical height. Ligamentum flavum hypertrophy may develop
and encroach upon the nerve roots
posteriorly. End plate changes and facet changes can also encroach
on the neural foramina anteriorly and
posteriorly respectively. All these changes limit the extent to which
neuro-protective spinal reflexes can
relieve pressure on nerve roots. The spine motion segment loses dynamic
range and the small “shingled”
muscles cannot act to cause a dynamic translation of the segment and
reduce pressure on the
neuro-vascular bundle. At this point axial loading of the motion segment
is poorly tolerated because there
is no dynamic reserve to allow minute translation, rotation or tilting
of the neural foramen. The neural
foramen is fixed in anterior and posterior diameter with further narrowing
occurring vertically as the disc
fatigues and bulges under axial loading. Disc fatigue is probably time
dependent under sustained axial
loading and accounts for the clinical presentation of patient complaints
that they cannot stand or sit for
more than a minute or two (static loading) before worsening radicular
symptoms occur. Walking relieves
symptoms at least initially by providing external dynamic weight shifting
across the affected lumbar motion
segment.
Typically, patients with mechanical back pain experience an increase
in their low back pain and radicular
symptoms during times when their spine is asked to support body weight
such as during prolonged sitting
or standing. The pain generators for these patients may be a herniated
disc, reduced neuroforaminal size
secondary to degenerative disc disease or facet syndrome. It has been
shown that lumbar traction can
produce a “distraction” or increased separation of 1 to 2 mm between
each pair of lumbar vertebra (4) as
well as reduce the size of disc herniations (3,4). Furthermore,
Twoney (29) studied the effects of traction on the lumbar spines of
cadavers stripped of the paraspinal
musculature and found residual lengthening of the lumbar spine after
release from sustained traction. This
residual lengthening was seen in those spines in which degenerative
disc changes were prominent and
may relate to disc rehydration since the spines were continuously bathed
in normal saline throughout the
experiment. In-vivo, we do not know whether “traction” physically results
in sustained lengthening of the
spine segment after a distraction tension has been released but we
do know that lengthening of the
lumbar spine segments does occur during applied traction. Lumbar distraction
may improve facet joint
mobility by releasing an entrapped interarticular meniscus or fold
of the capsule or synovial membrane
(30) and may restore spine segment mobility by stretching and releasing
erector spinae muscles
contracted by sustained spasm.
The VAX-D table represents a technological advance in the application
of effective lumbar distraction
tensions with improved patient tolerability and satisfaction compared
to previous lumbar traction devices
requiring thoracic corsets or the application of heavy static weights
(1). VAX-D therapy has been shown
to decompress the nucleus pulposis significantly, to below –100 mm
Hg (5). The intervertebral discs
separate the vertebra with the annulus fibrosis containing the nucleus
pulposis by its attachment to the
vertebral margins. The negative intradiscal pressures generated by
VAX-D suggests that an increased
separation of the vertebra occurs during VAX-D therapy, as it did with
older lumbar traction devices.
Traditionally, the term “decompression” as applied to the spine has
referred to nerve root decompression.
Surgery for decompression has been directed at the radiographic sites
of nerve root entrapment including
the removal of herniated disc material or osteophytes at the lateral
recess or neural foramen. This study,
however, has demonstrated that most of the patients suffering from
chronic low back pain and
radiculopathy had multiple nerve root abnormalities based on abnormal
DSSEPs, many of which would
not be predicted radiographically. Successful treatment by VAX-D therapy
resulted in clinical reduction in
pain and improved DSSEP waveforms suggesting that nerve root decompression
is occurring at multiple
levels. With VAX-D therapy, the concept of “decompression” can now
be broadened to include the lumbar
spine motion segment itself, with decompression not only of the nerve
roots, but also the disc, facet joints
and potentially, the paraspinal musculature as it is stretched and
muscular spasm resolves.
An acute disc injury and discogenic pain may often be the primary process
leading to low back pain and
lumbar radiculopathy. Biochemical and inflammatory changes within the
disc contribute to the patient’s
pain. The negative intradiscal pressures generated by Vax- D therapy
may promote healing as nutrients,
oxygen and water are transfused into the disc which is otherwise an
avascular structure, dependent
predominantly upon a diffusion gradient as the main mechanism of transport
of these vital substances into
the disc (31). However, chronic low back pain is often accompanied
by lost mobility and secondary
consequences such as nerve root dysfunction above and contralateral
to the disc herniation, as indicated
by this study.
For any given patient with low back and referred leg pain, we cannot
predict with certainty which cause
has assumed primacy. Therefore surgery, by being directed at root decompression
at the site of the
herniation alone, may not be effective if secondary causes of pain
have become predominant. Vax- D
therapy however addresses both primary and secondary causes of low
back and referred leg pain. We
thus submit that VAX-D therapy should be considered first, before the
patient undergoes a surgical
procedure which permanently alters the anatomy and function of the
affected lumbar spine segment.
REFERENCES
1. Gose EE, Naguszewski WK, Naguszewski RK, Vertebral axial decompression
therapy for pain
associated with herniated or degenerated discs or facet syndrome: An
outcome study. Neurological
Research, 1998, Volume 20, April pp. 186-190.
2. Gose EE, Johnsonbaugh R, Jost S. Pattern Recognition and Image Analysis,
Upper Saddle River, NJ:
Prentice Hall PTR,1996: pp.1- 484.
3. Gupta RC, Romarao SV. Epidurography in the reduction of lumbar disc
prolapse by traction. Arch
Phys Med Rehabilitation 1978; 59: 322-327.
4. Matthews JA. Dynamic discography: A study of lumbar traction. Ann Phys Med 1968; IV: 275-279.
5. Ramos G, Martin W. Effects of vertebral axial decompression on intradiscal
pressure. J. Neurosurg
1994; 81: 350-353.
6. Aminoff MJ, Goodin DS, Parry GJ, Barbaro NM, Weinstein PR, Rosenblum
ML. Electrophysiologic
evaluation of lumbosacral radiculopathies: electromyography, late responses
and somatosensory evoked
potentials. Neurology 1985; 35: 1514-8.
7. Eisen A, Hoirch M, Moll A. Evaluation of radiculopathies by segmental
stimulation and somatosensory
evoked potentials. Can J Neurol Sci 1983; 10: 178-182.
8. Cohen BA, Huizenga BA. Dermatomal monitoring for surgical correction
of spondylolisthesis. Spine
1988; 13: 1125-8.
9. Katifi HA, Sedgewick EM. Somatosensory evoked potentials from posterior
tibial nerve and
lumbo-sacral dermatomes. Electroencephalogr Clin Neurophysiol 1986;
65: 249-59.
10. Herron LD, Trippi AC, Gonyeau M. Intraoperative use of dermatomal
somatosensory-evoked
potentials in lumbar stenosis surgery. Spine 1987; 12: 379-83.
11. Machida M, Asai T, Sato K, Toriyama S, Yamada T. New approach for
diagnosis in herniated
lumbosacral disc: Dermatomal somatosensory evoked potentials (DSSEPs)
Spine 1986; 11: 380-4.
12. Toleikis JR, Carlvin AO, Shapiro DE, Schafer MF. The use of dermatomal
evoked responses during
surgical procedures that use intrapedicular fixation of the lumbosacral
spine. Spine 1993; 18: Number
16: 2401-2407.
13. Dvonch V, Scarff T, Bunch WH, Smith D, Boscardin J, Lebarge H, Ibraham
K. Dermatomal
somatosensory evoked potentials: Their use in lumbar radiculopathy.
Spine 1984; 9: No 3: 291-293.
14. Scarff TB, Dallman D, Toleikis JR, Bunch WH. Dermatomal somatosensory
evoked potentials in the
diagnosis of lumbar root entrapment. Surgical Forum 1981; 32: 439-291.
15. Larson SJ. Somatosensory evoked potentials in lumbar stenosis. Surgery,
Gynecology and
Obstetrics 1983; 157: 191-196.
16. Scarff TB, Toleikis JR, Bunch WH, et. al,: Dermatomal somatosensory
evoked potentials in children
with myelomeningocele. Z Kinderchar Grenzgeb 28: 384-387, 1979.
17. Patten J. Neurologic Differential Diagnosis. New York: Springer-Verlag, 1987: p.210-211.
18. Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle: Principles
and Practice. Edition 2.
Philadelphia: F.A. Davis Company, 1989: p.375-414.
19. Larson SJ, Sances A, Christenson PC. Evoked somatosensory potentials
in man. Arch Neurol 1966:
15: 88-93.
20. Weber H. Lumbar disc herniation. A controlled prospective study
with ten years of observation. Spine
1983: 2: 131-9.
21. Hakelius A. Prognosis in sciatica. Act Orthop Scand (Suppl)1970; 129: 1-76.
22. Saal JA, Saal JS, Herzog R. The natural history of lumbar intervertebral
disc extrusions treated
non-operatively. Spine 1990; 683-86.
23. Saal JA, Saal JS. Non-operative treatment of herniated lumbar intervertebral
disc with radiculopathy.
An outcome study. Spine 1989; 14:43 1-37.
24. Bush K, Cowen N, Kaatz D, Gishen P. The natural history of sciatica
associated with disc pathology.
Spine 1992; 17: 1205-1212.
25. Tilaro F, Miskovich D. The effects of vertebral axial decompression
on sensory nerve dysfunction.
Canadian Journal of Clinical Medicine 1999; Vol 6 No 1: 2-7.
26. Tsai RY, Yang RS, Nuwer MR, Kanim LE, Delamarter RB, Dawson EG.
Intraoperative dermatomal
evoked potential monitoring fails to predict outcome from lumbar decompression
surgery. Spine 1997
Sep 1; 22 (17): 1970-5.
27. Anderson GBJ, McNeill TW. Lumbar Spine Syndromes Evaluation and
Treatment. New York:
Springer-Verlog Wien, 1989: p 5-15.
28. Kirkaldy-Willis WH, Burton CV. Managing Low Back Pain. 3rd Edition.
New York: Churchill
Livingstone, 1992 p21-22.
29. Twoney LT. Sustained lumbar traction: An experimental study of long
spine segments. Spine 1985;
10: 146-149.
30. Kos J, Wolf J: Inter-vertebral menisci and their possible role in
vertebral blockages. Chartered
Society Physiotherapy Newsletter 4-5, 1972.
31. Ballard WT, Weinstein JN. Biochemistry of the intervertebral disc.
In: Kirkaldy-Willis WH, Burton CV,
eds. Managing Low Back Pain, New York: Churchill Livingston, 1992:
p. 39-48.