Guide
to Pudendal Neuralgia and PNE from Ava
The Core Group would like to extend its gratitude to Ava for writing
this in-depth analysis which covers a broad spectrum of topics related to
Pudenal Neuralgia and PNE. Our
membership will find this document to be a great asset as they attempt to sort
out many of the nuances of this baffling medical problem.
We would like to point out that all of the posts on this forum are for
informational purposes only and the information contained in this “Guide to
Pudendal Neuralgia and PNE from Ava” has come directly from Ava and not from
The Core Group.
As always, we advise our members to rely on the advice of their doctors
before making any decisions regarding information they have gleaned from any
website.
Once again, we would like to express our deepest thanks to Ava for the
time and the solid research that she has put into preparing this document and
for sharing all of her ideas with us, both on the forum and in this document.
The Core Group
Table of
Contents
A. The application of
logic to PNE issues
B. On opinions given on
the forum
C. Assisting others by
sharing information
II. On PNE
A. Mechanisms of nerve
injury
B. Path of the pudendal
nerve and sites of possible entrapment
III. On
pudendal neuralgia following vaginal or abdominal hysterectomy
IV. On reasons for failed pudendal
decompression surgery
V. On diagnostic testing
A. Practical guide
B. PNMLT
1.
neurophysiology
2. analogy
3.
sensitivity and specificity
4. validity
of intra-operative and post-operative PNMLT
5. reasons
for PNMLT despite concerns over validity
5. Botox and
the PNMLT
6. nerve
testing of the penis
C. MR neurography
D. Nerve blocks
E. Botox (diagnostic)
VI. On the processes involved in pain
A. The mechanism of
central sensitization
B. Activation of opiate
receptors following surgical event
C. Nociceptive versus
neuropathic pain
D. The four horsemen of
pain
VII. On
pharmaceuticals
A. Valium and other
benzodiazepams
B. Indocid suppositories
and NSAIDs
C. Narcotic analgesics
D. Neurontin
E. Cymbalta
F. AV411
G. PARP-1
H. minocin
I. Quinamm
J. Tylenol
K. Effectiveness of current medications for
neuropathic pain
L. On the pharmaceutical industry
VIII. On the use of medications in combination to
address neuropathic pain
IX. On
acupuncture
X. On spinal cord stimulators
XI. On
lumbar disc herniation
XII. On MRI, CT and discography for lumbar disc
diagnosis
XIII. On alternative medicine
XIV. On prolotherapy and SIJD
XV. On a proposal to evaluate responses to
neuropathic analgesics
A. The application of logic to PNE issues
Several have
written that it is difficult for the non-science trained individual to
understand the basis for some of these arguments. Yet in order for us to apply
logic to PNE, it is important that the process begins. Otherwise it is like the
Japanese film Rashomon, where the same event is viewed from diametrically
different positions, thus the interpretations from the varying position is
wildly disparate. So I would like for those who want not only to understand but
to participate to begin with the anatomy of the nerve. Take your hand and
palpate your sacrum. Imagine the sacral plexus originating from the cord,
forming on the other side of the bone you are touching. Imagine the nerve as it
courses along the inside of the gluteus maximum muscle...feel the muscle,
imagine the course of the nerve. Trace the course of the nerve a little further
each day, rehearsing three or four times what you know. There are many books
and drawings to guide you, but none more powerful than your own imagination of
the nerve in your own body. In 30 days or less you will know the nerve and all
adjacent anatomical structures, and you will find confidence in this knowledge.
Not only that, you will have begun to penetrate the layers and layers of
mundane that science requires in order to begin a pursuit of the profound.
While the value of this forum is already immeasurable, suppose we were to link
in series the processing capabilities of all 780 or so minds, these being all
well informed, and then perhaps produce the single original thought that would
turn the tide. Yes, we have talked about the paucity of diagnostic modalities
and their limitations, and the doubts that arise because such modalities are
used in a way that conflicts with science, but I believe we can do better than
that. It is important to realize that the law of diminishing returns applies to
doubts as well.
We have talked about the frailties of the PNMLT, the neuropathological basis
for those frailties, and the fact that a post op or intra-operative PNMLT
cannot be valid. But what would be the solution... those are the questions we
should be debating. Since the degeneration regeneration process compromises
velocity and latency in post release testing, what means, theoretical or
otherwise, might be devised. In terms of nerve testing, the one which gave the
most desirable clinical information would be that test which measured what the
dendrite was saying to the cord. Is the cord being told that pain is present or
not? We can now measure the quantity, osmolality, osmolarity, and particulate
size of a liquid passing through a tube without actually sampling the tube. Is
it possible to do the same in terms of measuring impulse propagation along the
axon? Or perhaps we can find greater reliability in measuring velocity and
latency
in unmyelinated axons in the pudendal nerve. This has not been discussed for
obvious reasons, but the pudendal nerve, like all peripheral nerves, has axons
that are mylenated to different degrees as well as axons that have not been
myelinated at all. Again, since the thicker, heavier myelinated axons are what
transmit the impulse quickest, they are the axons carrying the impulse that is
measured in the PNMLT. When damaged, they transmit slower. Neuropathy shows us
why, and that these changes persist. But suppose we were able to subject the
pudendal nerve to a test of unmyelinated axons only, or if we devise an impulse
that would not transmit in the myelin sheath but instead be transmitted in the
same manner that unmyelinated axons transmit.
If we look at the mechanics of entrapment, then apply the same physics to the
cellular level, one sees why injury occurs initially to the sheath of
myelinated axons within the nerve. A force applied to a structure of many
consistencies will first affect those parts of the structure that provide the
least resistance, unless the architecture of the structure is designed to
diffuse such as force. It was never necessary for such an architectural
modification in peripheral nerves...protection came from location and outside
structures... the nerve never had to evolve a mechanism to protect itself from
compression.
This gives rise to the possibility of another means of testing for PNE, one
that would give correct data (excluding the uncertainty principle) either
pre-op or post-op as to persistent entrapment.... peripheral nerve impedance
testing. In the time before telephones were owned by customers, but were
instead rented from the phone company, electrical tests were developed to
monitor if phones had been added illegally to your service. The phone company
would dial your number and measure impedance on your line. One phone ringing
gave a certain impedance, 2 phones another level, 3 phones more, and so on. If
you were paying for 2 phones, but impedance testing revealed three, then your
bill would be adjusted. Customers could defeat impedance testing by clipping
the wires to the ringer, but most did not have that savvy. If equipment of
exquisite sensitivity could be developed, we would not have to apply a stimulus
to the rectum. Instead we would measure the response of the nerve to a
carefully measured stimulus applied proximally. If the nerve was firing above
baseline (there would always be some level of activity, but this could be
quantified and standardized in animal and human models), this would suggest
entrapment. It is possible that if the sensitivity of the readings was great,
the degree of impedance could correlate in a linear or sigmoid fashion, again
carefully quantified, with degree of entrapment. Impedance would not be a
measure of velocity or latency and therefore unaffected by the state of the
myelin sheath. A person still symptomatic but with baseline impedance would not
have persistent PNE, but rather the pain would have to come from either the
cord or cortex level. A post release but still symptomatic patient whose
impedance was elevated into the levels associated with entrapment could have
persistent PNE, but then again, other sources of stimuli to the nerve (other
pathological processes) would have to be ruled out.
But we should never be satisfied with nerve testing alone, even if we reach the
point where velocity, latency and impedance could be measured with a high
degree of sensitivity and specificity, and that correlation to entrapment was
impeachable. We need to be able to see the nerve in much the same manner that a
cardiologist can visualize the coronary anatomy via catheterization. We are not
far from the point that magnetic resonance imaging could measure the
configuration of the pudendal nerve at each millimeter along its path. Then in
most cases of true PNE the exact anatomical location of entrapment could be
pinpointed. At present this is more a software problem than a hardware one. In
my opinion Bill and Melinda Gates are an extraordinary couple, and I certainly
do not wish PNE upon them. But I am willing to bet my husband's every last
nickel that if one or the other of them had developed PNE a year or so ago,
reliable nerve testing would now be available to us, and software would have
been developed that allowed precise visualization of the pudendal and other
nerves. Such diagnostic modalities might seem far-fetched to our doubters , but
these modalities are far more realistic than an MRI scan or lithotripsy was two
decades ago.
But while we can look to the future, we live in the present, and many patients
with PNE still have pain. Again, I contend that if one can be cured, something
has to be responsible for dismal results in those still suffering. Do we simply
accept these treatment failures as a part of doing business, or do we figure
out why they happened and what can be done, both to prevent future failures and
to give relief to those who live with that failure every day. To do so we have
to look at what we are doing and the basis for doing it. Take diagnostic blocks
for instance. When your phone goes out of service and a repairman is summoned,
he does not check the cable closest to the central office first. He goes to the
protector outside your home, and checks to see if there is a dial tone. If not,
he goes to the pedestal where the drop to your house connects to the residential
cable, and then works his way back to the switching equipment.
If there is a dial tone at the pedestal, then the problem is in the wire
overhead or buried underground to your individual dwelling. You may be tempted
to argue that when an electrician comes to your house to check out a faulty
outlet, he first goes to the electrical panel. There are both therapeutic and
diagnostic implications for this exception. First, the electrician does not
wish to be electrocuted, so he turns off power to the outlet before repair.
Second, he does not trace the pathway of power in a logical sense, at least not
initially, because he does not have to go back to his truck, drive three miles,
climb a pole and sort through hundreds of cable pairs to find yours in order to
do so. To the telephone repairman it is much more efficient, time and energy
wise, to apply logic to the problem presented than it is to do so to the
electrician's problem. One will generally find logic applied to those
activities where substantial resources can be saved through its application,
but will not necessarily find logic applied where its application will make no
difference. With nerve testing, it seems logical to test at every point
possible. A positive block at Colles' fascia says that a decompression
procedure only to Alcock's canal will not help that patient. The more
information that is available prior to surgery, especially given the pitfalls
of current testing, and very especially given that re-operation entails
difficulties of its own, is the only responsible manner in which to approach
PNE.
B. On opinions given on the forum
In a recent
edition of the Bay City Journal, a
Because one sits in the bleachers and catches the home run ball does not
automatically make that individual a professional batting coach. Because one
has been so fortunate as to recover completely following pudendal decompression
does not qualify that person to teach neurosurgery. Such behavior in and of
itself does not concern me. What does concern me is that the innocent, truly
searching human who, in the midst of the misery of pudendal neuropathy, will
grasp at anything, perhaps even suppositions found here but grounded in neither
reason nor fact. This site seeks to do much, but what it does not seek to do is
mislead. Those who contribute have a duty to qualify remarks, especially when
remarks are submitted in quantity.
Let's look at two examples of misleading information. The first is rather
harmless, the second potentially less so. In the same post in which she calls
me “patronizing”, one member writes: “You also say that vaginal birth injures
tissues and the only issue is to what degree. I know plenty of women who had no
tearing, no pain afterwards, and no dysfunction. So I further disagree that
injury always happens.”
While we should appreciate disagreement, such dispute should be substantive.
Granted the member may not have immediate access to an obstetrical textbook,
but the internet lists more than 54,000 sites in which pelvic floor dysfunction
and pelvic injury following normal labor is discussed. One such site is: http://www.cmaj.ca/cgi/content/full/166/3/337.
That injury occurs during normal uncomplicated labor is not a subject of debate
among obstetricians, so one wonders why it should be debated here. Yes, we all
know women who show no flagrant signs of postpartum injury. I was one, and
fortunately so are most women. But this does not diminish the credibility of
the science, nor does it require the imposition of reverse logic. Instead, it
is most logical to propose that woman cannot go through all the tremendous
physiological changes that occur during pregnancy and delivery without some
injury to supporting structures, mucous membranes, pelvic muscles, or the
cervix. That one might recover quickly and without noticeable residual effect
is not only a testament to God’s creation of woman, but it is also the result
of a process of healing that has evolved a maturity and serenity over time.
When we tell our men folk of the terrible pain that accompanies labor and
delivery, and when we laugh in comparing this pain to everyday agonies that
accompany the exercise of manhood, are we honest with them? Is the pain of
labor and delivery that severe? If so, as we often say it is, what do you think
our axons were telling us with all that afferent sensory stimulation.... does
this pain come to celebrate the expectant birth? Doesn't it seem much more
logical that our sensory apparatus throughout the pelvis is screaming
"injury" to the cord?
The other example is this. A member wrote: “Scans such as MRI don't show
nerves, so it is not surprising that you had the experience that you did.” I
found this quote particularly interesting since today I was examining a L4/5
nerve root on an MRI scan. The neurosurgical resident standing beside me
remarked: "Interesting the displacement...more posterior than lateral.
Should be easier to get at". "Nonsense", I rebutted. "That
nerve is only in your imagination. It can't be seen on scan." I had
learned this medical fact on the forum.
What if a guest had read her statement of fact, decided against an MRI on the
basis of that post, and died 8 months later from an osteoblastic malignancy
that would have been picked up by scan? The same with our new mother. What if
her pelvic pain was from a deep perineal abcess that resulted from fecal
contamination of the deep wound that occurred during delivery. At 5 weeks an
undiagnosed abcess is low on the index of suspicion, but it still ranks far
above PNE. Every bout of short term perineal and pelvic pain is not going to be
PNE, nor is it going to be readily amendable to PT. Given the brief interval
between delivery and pain, it is the obstetrician who should determine the
merits of a PT evaluation.
More importantly, this young lady's doctor has had 10 - 11 months to get to
know his patient well, maybe even longer. We have 2 or 3 paragraphs. What makes
better sense... to let the doctor give guidance, or some far away internet
user.
C. Assisting others by sharing
information
Karen's last post
is not just thoughtful and sincere, but it is filled with the elegance of
wisdom and experience. One must do exactly as she suggests if they are to
expect even a small measure of satisfaction from a visit to their physician.
For if the symptom complex is outside of that physician's level of expertise
and knowledge, even if the symptoms appear to be due to a process within that
physician's specialty, it is highly doubtful that physician will take the time
that evening to search for answers. Karen knows as well as I that this is not
the way it should be, and I would wage large sums that it is not the manner in
which she confronts puzzling issues in her own patients. But we all know, that
for the most part, this is the way it is when most patients go to doctors. The
posts I am honored to add to this forum are done with the intent of teaching, but
also to explore the many sides of pudendal neuropathy. The more energy and
effort each of us puts into thought brings us closer to answers that make
sense. These answers then provide patients with information with which to make
choices about diagnostic modalities and treatments in the search for relief
from a terrible pain. Those who use this forum for information are lucky to
have insightful members like Karen and Les and Celeste and Greg and Callie and
Marianne and all the other ones (who also deserve individual mention) who are
constantly monitoring and offering helpful comments. They are lucky as well to
have the occasional antagonist, like L.G., whose experiences are invaluable in
relating the not-so-good sides of current care. If anything, this forum is
fair, giving credibility to all sides. As for me, it led me to
II. On PNE
A. Mechanism of nerve injury
Nerves can be
damaged in any number of scenarios, by compression, entrapment, or disruption
of their usual anatomic pathway. Also by toxins, by viruses (herpes zoster), by
trauma, by surgery, by autoimmune disease, by diabetes (diabetic peripheral
neuropathy), even by vitamin deficiency (B-12). But while the number of disease
processes that can affect the nervous system in some way is large, the types of
pathology that can affect an individual nerve alone is limited. This not only
narrows the probabilities with respect to injury in PNE, but it is extremely
helpful in understanding the cellular mechanisms involved. By doing so, one can
make appropriate decisions regarding the efficacy of different treatment
strategies, and thereby one's willingness to undertake them. If a strategy
makes sense on a biochemical and cellular physiology level, then it is far more
likely to be successful. Conversely, if such strategy fails to meet that
criteria, while it may be advocated strongly by some, and there may be isolated
cases of success (which may or may not have anything to do with the applied
treatment), it is doubtful such strategies will measure up when compared to
placebo. Just like football, the basics of tackling and blocking, while hardly
glamorous, are usually what eventually determine outcome. As one who, like
others, suffered for years, it is outcome and outcome and outcome that
interests me most. When one considers the possible etiologies of individual or
paired neuropathy, they may at the outset eliminate severance, which elicits an
entirely different response at the cellular level than one will find in PNE.
Yet in numerous places in the forum axonal re-growth is discussed and projected
as a mechanism to explain delayed response. Again, severance is not the injury
in PNE and axonal re-growth not the cellular response. In severance, the
partially or completely interrupted axon has to first seal its interrupted cell
membrane, but this occurs in the first hours following injury. Then the repair
process is initiated and supervised from the nucleus residing in the cell body.
The problem with the now linearly expanding axon is that while the DNA can
direct every tiny facet of axonal restructuring within the cell, it has almost
no information on how to proceed outside the cell, so that usually in the case
of total severance the nerve really does not know where to go or what
structures, synapses or receptors to innervate. The re-growth of axons of a non
completely severed nerve have the luxury of following the course of those not
severed, so the chance of re-innervation is far greater. But the forum
addressed notion of measured millimeters per week of axonal re-growth has
little applicability to the neuropathology involved in PNE. Besides severance,
individual or paired neuropathy can result from blunt trauma, or from
structural abnormalities, usually acquired. It is this we will focus on.....
B. Path of Pudendal Nerve and
sites of possible entrapment
When the pudendal
nerve leaves the sacral plexus, it travels posterior to the coccygeus muscle
and sacrospinus ligament, and anterior to the gluteus maximus muscle and the
sacrotuberous ligament. It then continues inferior-medially, remaining
posterior-lateral to the levator ani muscle, but generally before entering
Alcock's canal gives off the inferior rectal nerve. The clinical implications here
have importance. Since my surgery involved division of the sacrotuberous
ligaments bilaterally, and much of my pain was rectal in the beginning, careful
dissection prior to Alcock's canal would play a role in recovery. Alcock's
canal is basically composed of an extension of the obturator internus fascia,
again clinically important. Fascia, like other collagen vasular tissues, can
undergo pathologic change, and in doing so, adhere, entrap, compress or
otherwise compromise the transiting nerve. Shortly after exiting Alcock's canal
the pudendal nerve gives off the perineal nerve which must pass through the
superficial perineal fascia (except for a single rectal branch) before reaching
its area of responsibility. Whereas the transit through Alcock's canal is
parallel to fascia, the transit of the perineal nerve through Colles' fascia is
perpendicular, giving rise to an additional consideration of restriction. The
pudendal nerve itself must also pass through Colles' fascia, enter the
urogenital diaphragm and become renamed (dorsal nerve of the penis in the male,
labial nerve in the female). Even as the pudendal nerve becomes another there
is ample opportunity for restriction. While I do not know the step by step
moves of the surgical procedures involved in PNE surgery, I am aware of those
descriptions, and especially the fact that visual exposure is very limited. I
am unsure of dissection to the level of Colles' fascia, but I do intend to
review operative notes to study the extent of dissection. If one were to compare
this to a hundred pair telephone cable, with each set of wires leading off to
homes of Family A, the Family B, then Family C, and so on and so on until the
last pair of ten or so wires went to the homes of Families Y and Z.
If the main cable is disrupted somewhere between the switching equipment in the
central office but before the first wires are given off to Family A, then all
the wires will be affected and no family would have phone service. But if the
cable is disrupted after giving off service to Families A-J, but before service
to Families K and after, then only Families K through Z will be out of service.
Given the many variations in human bodies, the different courses an artery or
vein might take, even the fact that the appendix can generally be found in one
of four positions, or especially the different but complex relationships of the
cystic artery, the right hepatic artery and the cystic duct in different
individuals, one can reasonably suppose that branches from the pudendal nerve
come off in different places in different individuals, and while these branches
usually innervate the same structures, the courses to those structures is also
variable. More than supposition, anatomical dissection shows this to be true in
the case of every nerve. Also, it is not reasonable to suppose that every true
case of PNE is due to compression, entrapment, stretching, or irritation at the
same location along the pudendal nerve's course. All of this has strong
clinical implications in answering such questions as to relief of some symptoms
and not others, partial relief of all symptoms but not complete relief, as well
as the one we pray for, relief of all symptoms. Nor is it necessarily
reasonable to assume that restriction and damage, if caused by displacement,
hypertrophy, inflammation or otherwise, cannot be the result of two sites or
more, especially given that the processes involved may be regional, involving
an area the size of a tennis ball, rather than an area the size of a marble. If
the nerve is then freed at one point but not the other, especially if the freed
point is the proximal one, then one would expect relief in the posterior
perineum but not the anterior one.
III. On
pudendal neuralgia following vaginal or abdominal hysterectomy
1.
Vaginal
hysterectomy involves the cutting and ligature of the uterosacral and cardinal
ligaments, as well as freeing the uterus from its close attachment to the
levator ani muscle, but the surgical field should never reach as far as the
sacrotuberous ligaments. These should remain unharmed by surgery, with
exceptions. Those being the development of scarring and adhesions, or
post-operative infection moving laterally to involve these structures. With
hysterectomy, by whatever approach, there is some residual weakening of the
pelvic floor musculature, but usually this can be minimized by careful
operative technique and post op strengthening therapies. Pelvic pain can come
from so many sources, and the symptoms might seem to be pudendal in
distribution. Because there is a great deal of nerve overlap, and because
sympathetic fibers also play a role in sensory innervation to this area, and
because of the radiating nature of pain along sensory dermatomes, it is
imperative that consideration be given to the myriad pelvic pain pathologies
that are not PNE. For those interested in a more technical description, or at
the least, a partial listing of the possibilities, try this link: http://www.foamix.co.il/eMedicine.htm
2.
Here I've quoted,
and wonder which of the three procedures you had:
"The 3 common vaginal procedures to suspend the prolapsed vaginal apex are
sacrospinous ligament fixation, modified McCall culdoplasty, and iliococcygeus
fascia suspension. As originally described by Amreich and modified by Richter
and Nichols, sacrospinous ligament fixation is usually performed on the
patient's right side to avoid the rectosigmoid (Nichols, 1982). The vaginal
apex is attached, using permanent sutures, to the sacrospinous ligament. A
thorough knowledge of pelvic anatomy is critical in order to avoid
complications. [b][u]Take care to place the sutures 1-2 cm medial to the
ischial spine to avoid injury to the pudendal bundle and the inferior gluteal
vessels. [/u][/b]Place the suture through—rather than around—the ligament.
Excellent results have been reported for correcting vaginal vault prolapse
using fixation to the sacrospinous ligament. However, in 1992, Shull and
colleagues reported a predisposition for recurrence of anterior vaginal wall
relaxation after sacrospinous ligament fixation.
The McCall culdoplasty may be used to correct apical descent or as prophylaxis
against future prolapse (McCall, 1957). This procedure uses the uterosacral
ligaments, which, if strong, are shortened and reattached to the vaginal cuff
after completion of the vaginal hysterectomy. In the authors' opinion,
attaching the prolapsed vagina to stretched prolapsed uterosacral ligaments is
of little value. The surgeon must be bold enough to grasp the uterosacrals near
the sacrum, where they are usually strong and undetached, but careful enough to
respect and avoid the neighboring ureters. Intraoperative cystourethroscopy is
therefore essential to be sure the ureters have not been ligated or kinked.
The iliococcygeus fascia suspension provides effective cuff suspension, since
it attaches the apex to the obturator internus fascia and iliococcygeus fascia
with less risk of neurovascular damage than does the sacrospinous ligament
fixation (Shull et al, 1993). Alternatively, the authors have described placing
the suture through the iliococcygeus and the periosteum at the ischial spine,
where it is attached (Scotti et al, 1998)."
How did Nates determine that you had axonal loss and demyelination in all
branches of the pudendal? Without cadaver dissection and study, that would be a
remarkable feat. And such is not done in other peripheral neuropathies.
Here you go under the knife without past history of pudendal pain, only to
waken with symptoms. Either the dorsal lithotomy position of your body during
surgery caused pudendal damage, which is possible but would hardly persist, or
a branch of your pudendal caught a suture during the procedure. As eloquently
as you write and as well as your posts indicate you think you must realize
nerve entrapment from an ill-placed suture to be by far the most likely
explanation for your neuropathy. Nerve tissue has almost no structure, with
less resistance to pressure than does jello. It is extremely fragile, and for that
reason as we were created it was done in such a fashion so as to afford nerves
and the nervous system the finest protections available to a body. Even the
endings of axons that branch up to the skin surfaces do not run along the
surface where they could suffer insult. Instead they course deep, then turn
towards the surface they innervate. Larger nerves are hidden behind bone and
cartilage at every site possible, or tucked deep behind muscle. A nerve has
absolutely no defense against a suture.The PNMLT does not measure conduction
through individual branches. The peroneal branch could not be accessed through
the rectum, nor the dorsal nerve of the clitorus. The inferior rectal branch,
which comes off the pudendal prior to its passage through Alcock's canal, is
the tract along which the electrical impulses from PNMLT tranverse. If you were
told that the PNMLT measured individual branches, and that a determination
could be made based on PNMLT that each of these branches were diseased in some
way, then you were misled.
Then you were told that the pudendal nerve, on its exploration, "the
fibers appeared in shreds". Unless the surgeon opened the epineurium of
the nerve, which I greatly doubt he did, because it would serve no utility and
increase the possibility of both trauma to the nerve as well as vascular
injury, then he could not see the nerve bundles. Since axons are microscopic,
he could not have legitimately referred to those. And since nerve bundles of
axons are then lumped together and covered with epineurium, he could not see
those either.
The wonderful vibes from the tribal group are fine, Amanada. I would join with
the Cherokee every night for ritualistic dance if it would work. Your best
interests may be paramount, but knowledge and skill must accompany. Ketamine
put you at risk with zero possibility of lasting difference. Intrathecal drugs
the same. If the purpose was to aid in diagnosis then such modalities can be
justified. But when the theory says "no" in fifteen different ways,
its not going to work. Just like it didn't. Bedside manners are much
appreciated by patients, as well as the caring and concern from staff. But
neither of these factor into outcomes when the pathology is real.
No one looked at your pudendal and saw a nerve in shreds. No one tested each
individual branch of the pudendal. Your entrapment neuropathy is most likely
far distal to Alcock's, has not been seen, and has not been helped.
3.
Not the pudendal,
but some of its tributaries are very close to the wound margins. That's the
point with Amanda. Most likely her entrapment is far distal to Alcock's canal.
That is why surgery failed her, but also why nerve blocks and other modalities
proximal to the entrapment have achieved some short term results. I have
previously noted four sites of possible entrapment along the course of the
pudendal and its branches, and the arrangement of the entrapment structure in
relation to nerve. So while the PT is right... we do not always follow Gray's
anatomy... neuropathic pain from distal pudendal nerve branch injury is quite
possible with vaginal hysterectomies, and in fact, probably occurs more
frequently than thought.
IV. On reasons
for failed pudendal decompression surgery
1.
Like others who
have commented, I am sympathetic to your continuing symptoms and pray you can
find relief. I am fairly confident based on your aggressive approach (early
diagnosis and prompt decision to travel for surgery) that you are still
searching for help. The information I am providing is based on common sense and
after thorough review of other neuropathic conditions and the results of
procedures to remedy those maladies. In addition, I have recently had PNE
surgery in
2.
My words are not
intended to supply "sweet comfort", but rather to apply analytical
logic to the question of PNE, and to do so in such a way that others can make
informed choices. Where there are pitfalls I have made an effort to note them...
such as the sensitivity and specificity of the PNMLT. Yes, in theory it should
supply accurate data each and every time, but the fact that it does not does
not relegate it to worthlessness. When this series of posts began I noted that
I also have an MD son who has done hundreds of nerve decompression procedures.
I am somewhat surprised that no one has latched onto this. But the role that it
played in my decision to undergo surgery was large, and that reason is solely
about outcome. During a multi-year period of time in the 1980s he performed 365
carpal tunnel release procedures, and then staff carefully studied the short
and long term results. As many of you know, CTS supposedly involves entrapment
of the median nerve at the wrist from hyperplasia of the flexor retinaculum,
which is due to numerous etiologies, from thyroid disease to occupational ones.
The median nerve is much like the pudendal, and like the sciatic... the same
things I wrote about before... arrangement of axons, sensory and motor components,
etc. In fact, the median is a tad larger, and while they have not been actually
counted, there are probably more sensory receptors in the distal digits than in
the perineum (which doesn't seem true but makes sense from an evolutionary
standpoint). At 1, 4, and 8 years not a single patient had recurrence of
symptoms. At 2 weeks following each of 365 releases not a single patient had
pain. How can such results be explained? First, apply logic to the
neuropathologies involved in true entrapment, and one can see that if a single
patient can be cured, then (if the diagnosis is correct) it follows that all
patients can be cured. The rate limiting factor is simply the extent and
fastidiousness of the dissection. In this, I must boast, there was probably none
better... in religious and sometimes extreme preparation, in focused dissection
far more proximal and distal (even to the mid-metacarpals) than was customary.
The approach was clear... initial exploration provides clear planes of
dissection (virgin tissue), and most likely it is this one single occasion in
which cure will be the outcome...so make the very most of it. Granted this was
in a decade when there was little issue with such things as compensation
neurosis and the long term use of narcotics to address chronic pain. Such
iatrogenic addictions take from many patients the ability to determine for
themselves if pain is still real. My decision to travel to
When it is not, I refer back to past comments. I would like to say that in a
previous description of the course of the pudendal nerve I wrote of its
perpendicular penetration of Colles's fascia, another site of possible
entrapment. The body's response to dissection at this point would be much like
the response of the tympanic membrance to myringotomy, it would attempt to
rapidly seal (over 4-5 weeks). That is why all children undergoing
myringotomies also get tubes. Tubes are nothing fancy, just cm long tubes of plastic
perhaps 3 to 4 mm in diameter. They are quickly placed in the surgical
laceration in the tympanic membrane in order to keep the TM from healing itself
and sealing. A very similar tube could be used to protect the pudendal nerve at
Colles' fascia... the only adjustment would have to be for size and perhaps
length, and to also make a slit down the length of the tube so that it could be
easily fitted around the nerve. I also see in the next 5 years the development
of much more minute endoscopic equipment that could be used for more distal
dissection in PNE and other entrapment syndromes such as the anterior cutaneous
nerve entrapment syndrome. It would probably be preferable to combine an open
procedure with an endoscopic one which would allow dissection to be carried
into places now perhaps unreachable.
V. On
diagnostic testing
A. Practical guide
1.
Yesterday I suggested that millimeter by millimeter visualization of the
pudendal nerve, and thereby the likely probability of pinpointing entrapment,
might be possible in the near future with enhanced MRI software. This morning I
discovered (by way of the forum), that in three places in the
the specific anatomical slicing presented by imaging. I read the latest article
prepared by those who promote the current technology, and you may find this at:
http://www.neurography.com/images/NeurolClinics-Neurography.pdf.
I also reviewed the 2005 American Medical Association's medical policy and
technology assessment committee on Magnetic Resonance Neurography, which says:
"MR neurography refers to modifications of MRI using special software and
hardware upgrades, which have been proposed for the diagnosis of peripheral
nerve disorders. The development of MR neurography enables direct high
resolution longitudinal and cross-sectional images of peripheral nerves such
that the morphology of the nerve can be visualized. Published literature
regarding MR neurography primarily consists of small case series of
heterogeneous patients. There is inadequate data regarding the diagnostic
performance of MR neurography, in terms of defining the normal range of
morphologies, the sensitivity and specificity of identification of
abnormalities in comparison to other diagnostic tests, and the impact on the
management of the patient." As this modality becomes more refined and
tested it will become an important tool in both the diagnosis and pre and post
surgical management of the PNE patient.
But for many considering surgery, and for those post surgical patients who have
not found freedom from pain as the outcome, modalities that are down the road
have little importance on May 8, 2006. There seems no clear cut guide of how to
proceed for the symptomatic but undiagnosed. And the post surgical patient with
pain is faced with an even more vexing puzzle.
Here I would like to present a modest guideline for the patient with suspected
PNE to follow before surgery is entertained, leaving it for each of you to
agree, disagree or add, all of which should contribute to our understanding.
1. You must first rule out those conditions, local, regional or systemic, which
would mimic PNE but which would not be remedied by a decompression procedure:
a. the following labs:
CBC, sedimentation rate,
C-reactive protein, Thyroid Stimulating
Hormone assay (TSH), Prostatic
Specific Antigen assay (if male),
Anti-Nuclear Antibody Assay
(ANA), CMP (complete metabolic
panel) Rheumatoid factor,
Fasting blood sugars for three successive days,
Urinalysis, CEA
b. the following imaging studies:
X-rays of the pelvis and
lumboscaral spine
CT scan of the pelvis
MRI of the lumbosacral spine
c. a complete physical exam, including a detailed neurological exam
2. If this testing is all normal, then consider each of the modalities which
are useful in varying degrees to diagnose entrapment of the pudendal nerve:
a. The PNMLT has a low level of specificity but a moderate level of sensitivity
in the diagnosis of entrapment. The test measures a function of nerve velocity
called latency. Entrapped nerves conduct an nerve impulse slower than a normal
nerve. The purpose of the test is to measure impulse conduction along the nerve
in order to compare latency to standard. In balance, there is considerable
controversy concerning the reliability of this test, but it is this member's
opinion that testing is worthwhile.
b. Magnetic resonance neurography is considered "investigational/not
medically necessary" by the American Medical Association, but the
literature suggests that improvements in both imaging and interpretation are
being made on a regular basis. Information for patients can be viewed at www.neurography.com.
It is this member's opinion that current testing is valuable in that there is a
greater than 50-50 probability results might provide significant information to
the neurosurgeon. In addition, since it is doubtful diagnostic modalities will
be developed because of concern over PNE alone, participation in developing
technologies will increase both the credibility of PNE as a syndrome as well as
expand the knowledge base upon which future PNE patients might rely.
c. CT guided injections are diagnostic blocks of the pudendal nerve at specific
locations which help determine the location of pathology. They are not specific
for PNE, but their sensitivity for pathology is high. It is possible to be even
more selective and block at each anatomically conceivable area of entrapment.
The development of this capability would be straight-forward and highly
recommended. Also recommended is a practice of careful sensory testing
following diagnostic blocks. Far more information could be obtained from
vibratory testing and two point discrimination, then carefully documented, than
the current practice of checking results by phone. The applicability of such
information in determining other sites of possible entrapment after failed
procedures could be significant.
3. If such testing suggests PNE, then the decision for surgery should be well
informed. Many physicians are skillful, but it is the wise physician who
appreciates the partnership with their patient that knowledge will bring. You
will have reached this point only because you have suffered much. To guide you
out of entrapment your surgeon will need both wisdom and skill. Make your
choices well informed ones. Speaking for many others in this forum, we wish you
the very best.
4. If pain is totally relieved from Botox, then the pain is not neuropathic
from pudendal entrapment at Alcock's. The pelvic floor muscles innervated by
the pudendal can spasm and thus place compressive forces on pudendal branches
feeding them. If this persisted to such a point that the nerve branch was
injured, the pain would be neuropathic, but again, the site of injury would not
be at Alcocks. The sole mechanism of action of Botox is at the neuromuscular
junction, the site at which the nerve passes on to muscle instructions that
have been received from the cord. The action of Botox at this site is quite
well understood, blocking the transfer of information from the nerve to the
muscle, resulting in muscle paralysis. The paralysis is flaccid, not rigid. The
muscle becomes totally relaxed, unable to contract without orders from the
cord. Only if the pudendal passed though a muscle that was in a state of
constant or almost constant contraction, which it does not, could muscle be
held liable for neuropathy (except for tiny branches, which could be liable).
If pain is relieved from Botox, then PT is not only advisable, it is necessary
in order to prepare the pelvis for the time when the effects of Botox have worn
off. Only when Botox affords no relief, and PT causes additional pudendal
distribution symptoms, is PT inadvisable.
While Botox works at the junction between muscle and nerve, it does not affect
sensory afferents coming from muscle, or from areas surrounding muscle. A
pathological process affecting the pelvis in the area infiltrated with Botox
would nonetheless generate transduction forces that would be interpreted and
recognized as pain. A nerve block, however, defeats transmission in the area of
administration, so that any nociception, whether nociceptive or neuropathic,
whether from laceration, fracture, tumor, or nerve entrapment, regardless of
etiology, would not reach the cord or brain.
I believe this allows us to suggest the following: do not entertain PNE
decompression until you have undergone a trail of Botox therapy. If your pain
is musculoskeletal, and relieved by Botox, you will not find relief from
surgical decompression at Alcock's. Instead, all efforts.... PT, medication
(including Botox) ... should be focused on achieving muscle relaxation on
command. This needs to be added to the recommendations to the patient with PNE
symptoms.
2.
This is in
response to your request for information on the utility of the above specified
laboratory tests in eliminating pathology that might mimic true pudendal nerve
entrapment. Your question involved the context of pathology that would not
otherwise be revealed by scanning modalities. In another thread you patiently
explained to me the difficulties involved in deciphering medical terminology.
Unfortunately, as I explained later, it is only possible to dissect this
terminology but so far. Here I will attempt to do just that. But keep in mind
that at 75 this mind is approaching senility, and could lapse into much too
technical a discourse. If that happens, please query me on a single item or
two, and I will explain more carefully.
Some of the testing recommended could reveal disease both in lab results and on
imaging studies as well as on either alone. For example, carcinoma of the
prostate that was metastatic both to bone as well as adjacent tissue would most
likely result in an elevated PSA, an elevated alkaline phosphatase on the
metabolic panel, as well as bony lesions on X-rays of the pelvis, and soft
tissue masses on pelvic CT. Still, the PSA could be elevated in the absence of
other findings, and while elevations do not necessarily mean cancer, they would
demand thoughtful evaluation of the prostate. Since the prostate is located in
an area that has sensory innervation by the pudendal, PNE would have to take
second place until significant prostatic pathology was eliminated as the source
of pain. Likewise, I think that it is important for all clinicians to realize,
especially those who diagnose and treat PNE, that the presence of disease such
as prostatic carcinoma does not totally exclude the possibility, however
remote, that the patient with unresolved pain could also be suffering from a
disease such as PNE.
You are aware that disease affecting peripheral nerves can be intrinsic to the
nerve, extrinsic to the nerve, or both. Even more confusing, within the nerve
disease can be either intrinsic or extrinsic to the axons. There are many
diseases that will affect the nerve either at its origin, down its path, or
within its own cellular processes, and do so in such a way that the result is
pain. The acronym TITMEND, though not all-inclusive, is useful as a guide to
etiologic categorization: toxic, infectious, traumatic, metabolic,
endocrinologic, neoplastic, or degenerative. Within one or the other of these
categories can one find the cause of most disease, and in each of these
categories one can find disease processes that would affect the pudendal nerve.
But for example of the utility of lab testing for disease that would not be
evidenced by scanning, let us consider the case of diabetic peripheral
neuropathy. It is quite well recognized in medical communities that most folks
with type two diabetes are actually diabetic for 4 to 7 years before diagnosis,
and 5 million is the figure generally given for the number of undiagnosed
diabetics in our population. In addition, almost 10% of these undiagnosed
diabetics are felt to already have neuropathies due to their diabetes before
they are diagnosed. That means that 500,000 Americans have peripheral
neuropathies due to a condition yet undiagnosed. Even this does not fully
portray the possibilities for non entrapment pudendal neuropathy due to
diabetes. People whose fasting blood sugars run between 100 and 125 are
considered pre-diabetic, and studies show this group of Americans to be at risk
for neuropathy as well. The lab test... fasting blood sugars times 3...is given
as a recommendation because diabetes and pre-diabetes is prevalent in our
society, it is often asymptomatic, and the statistical probabilities of it
producing neuropathy is far greater than entrapment. Granted that long standing
sitting pain should have led to an earlier work-up to exclude such a
possibility, but it is this member’s contention that all avenues should be
explored and re-explored before the commitment to surgery.
Several members with recognized diabetes have written about suspected PNE. For
them diagnostic testing in the form of nerve blocks and PNMLT have little
promise. Blocking the pudendal would temporarily relieve the distress of almost
any illness affecting it, including a neuropathy due to diabetes. Studies on
the validity of PNMLT in the diabetic, to my knowledge, are unavailable if
performed. And if so, they most likely represent such small numbers that little
confidence can be found in their results. The known diabetic with sitting pain
has to rely solely on the wisdom of the recommendation of his/her physician, but
so often this is insufficient.
3.
In chess one
weighs the statistical probabilities of every move in anticipation of your
opponents. Yes, diabetic neuropathy usually affects the distal extremities
first, and a research article I gave web directions to above partially explains
why. But diabetic neuropathy affecting the extremities first is not always the
case. Given the large numbers of people with undiagnosed diabetes, the fact
that they may not be having the typical symptoms of fatique, urinary frequency
and nocturia et al, there is still a greater likelihood that isolated pudendal
area pain could be diabetic neuropathy than it could be PNE. Before this forum
I knew of no patients with PNE, but I knew several with isolated diabetic
pudendal neuropathy. For the cost saver a FBS can at times be free.... the
health department, the knowledgeable diabetic neighbor with a glucometer, and
sometimes the local pharmacy does free glucose testing.
As far as using the CEA to rule in or out an occult malignancy before
entertaining PNE surgery, there are certainly no double-blind studies to
support it. Yet if one were to accept the premise of ruling out all disease
that has a greater statistical probability of causing pudendal pain than PNE,
this test would have efficacy. Perhaps not to some, but to the clinician who is
a grandmaster at clinical thought and diagnosis, this is the way they would
proceed.
I have argued that it is necessary to take the disease and all its diagnostic
and therapeutic remedies to the cellular and biochemical level in order to
prove or disprove utility. But to do so in a discussion of proposed testing
would require an investment of time for explanation that I anticipate most
members would neither appreciate or understand.
B. PNMLT
1. Neurophysiology
There remain many
unanswered questions in the field of peripheral nerve injury and nerve
regeneration. Yet some assumptions can be made with a good degree of medical
certainty. These assumptions rest on an understanding of latency and the current
state of knowledge with respect to neuronal healing. Although this may not be
new information or helpful to you, I am going to assume otherwise, and give the
basis for my answer to your question. Any peripheral nerve, the pudendal nerve
included, is comprised of axons of varying diameters. As you well know, the
nerve cell has many structures, but is divided into three parts... the cell
body, (which contains the nucleus, mitochondria, golgi apparatus and ribosomes)
the dendritic process, and the axon. The axon in the pudendal nerve is part of
the single nerve cell whose cell body resides in the spinal cord. Multiple
axons from multiple cells form a nerve bundle, and many bundles make up the
pudendal nerve. Injury to axons within the pudendal nerve results in a dropout
of the total number of axons stimulated by the PNMLT and thus you have a
decrease in the amplitude of the evoked electrical response, called the
compound motor action potential. What nerve latency is, in essence, is a
reflection of the pattern of activation of the separate axons that make up the
pudendal nerve. The axons in the nerve that are myelenated the heaviest are the
axons that deliver the compound action potential the fastest, thus it are these
fibers that determine the nerve velocity and also the latency. Nerves transmit
via their myelin sheaths, and the thicker the myelin the faster the
transmission. Latencies that are prolonged have occurred because faster
myelinated axons have dropped out (due to injury such as compression), and thus
what is recorded are slower velocities because most of the nerves now have
reduced myelin and thus slower velocities of conduction.
That is why, in general, higher numbers in the PNMLT reflect more significant
disease in the nerve. Very interesting, recent work has shown that chronic
nerve compression injury does not produce immediate axonal pathology but in
fact is a Schwann cell mediated disease, and chronic nerve compression induces
both Schwann cell proliferation and apoptosis before the onset of axonal
degeneration. Since PNE is usually longstanding, it is important to evaluate
what happens to the nerve after Schwann cell proliferation, and indeed, these
are the changes that produce the abnormal PNMLT. Evaluation of the thickness of
myelin and the diameter of axons in chronic compression indicate an alteration
in the myelin structure, specifically a dramatic increase in the number of
axons with thin myelin sheaths. Measurement of the myelin thickness shows not
only a greater than 600% increase in the number of axons that are thin (less
than 5 nm thickness) but also a proportionate decrease in the number of axons
with thick myelin sheaths so characteristic of a normal pudendal nerve. This
takes us to the critical point in the answer. A nerve chronically compressed
has many axons that have undergone a process of demyelination and then
remyelination at the site of injury, and the remyelination is not nearly as
thick as prior to compression. Therefore, with respect to a followup PNMLT
following initial surgery, one would expect persistent latency and abnormal
numbers, even though the compression has been either relieved, partially
relieved, or unrelieved.
The degree of remyelination, however, should have little to no impact on
residual pain.
2. Analogy
Like the PNMLT, in car racing the fastest time is the one that wins the prize.
There are many different cars (axons) on the racetrack (the peripheral nerve).
Generally speaking, some cars and drivers are more capable than others, and
these are the ones that can be predicted to win.
Suppose that a substance had been invented that could coat the cars, making
them less resistant to air, the result being faster times. Also suppose that
only a percentage of car owners could afford this substance, so that some of
the cars in the race were coated and some were not. There would be a far
greater likelihood that one of these coated cars would cross the finish line
first, and in fact, that coated cars would win every race. Coated nerves
(myelinated ones) transmit impulses faster than unmyelinated ones, and win the
race in PNMLT. It is the winning time that is recorded, not the average time
from each of the contestants. The winning time is then compared to what the
usual winning time should be (in a normal pudendal nerve). We know that rain
affects the condition of the racetrack so that slower times can be predicted.
Similarly we know that some conditions affect conduction in normal nerves,
these being such things as age, temperature, even whether or not the nerve is
located in the upper or lower extremity
(http://jnnp.bmjjournals.com/cgi/content/full/70/3/372).
What the PNMLT measures is the fastest time from the winning car and then
compares this number to what is expected of winning times in usual and normal
races on the pudendal nerve. If there has been a terrorist event (pudendal
neuropathy is sort of like long standing nerve terrorism) at the race track,
where an explosion or other insult caused debris to be thrown onto the track,
or perhaps displaced the wall surrounding the track so that the space available
for driving was limited in this area, then the race cars would have to slow
down when they approached this area, and the winning time from the race
affected by terrorism would be slower than a race that had not been affected
(normal race).
The race cars that have been coated to make them less resistant to air and thus
faster are the cars that win the race. Therefore these are the cars that
determine the value of the PNMLT. But these are not the race cars that carry
the pain impulse around the tract. Coated cars carry instructions to muscle.
The uncoated cars are carrying pain stimuli. We assume, and probably rightfully
so, that the terrorist event affects all cars on the race track, so measuring
the speed of the fastest cars against what is normal allows us to suppose that
uncoated cars are likewise affected. You can find far more detailed information
at: http://www.uphs.upenn.edu/ortho/oj/1999/html/oj12sp99p45.html.
3. Sensitivity and
specificity
Sensitivity and specificity are two critical measures in determining the
utility of any diagnostic procedure. In the case of nerve electrophysiologic
studies like the PNMLT, sensitivity refers the procedure’s ability to detect
the presence of sensory abnormalities in a group of patients. If the patients
being tested are at high risk for neuropathy, such as patients with advanced
diabetes, then the sensitivity would be expected to be high. Testing a group of
randomly selected diabetic children, however, would naturally include some that
have not yet developed neuropathy and yield a correspondingly lower level of
detection sensitivity.
A test that is “too” sensitive, however, can result in false positive measures
that wrongly identify a healthy patient as having an abnormality.
Specificity is the statistic that expresses the ability of a diagnostic
procedure to correctly identify healthy (control) subjects. A specificity of
100% means that there were no false positive measures in the healthy group.
Diagnostic tests balance sensitivity against specificity, so that the maximum
number of abnormalities are detected with the fewest number of false positives.
The following table presents sensitivity and specificity measures drawn from
eight different studies. With the exception of Study #4, each study used
randomly selected patients for whom a clinical finding of sensory impairment
was not a selection criterion. As a consequence, the sensitivities will vary
depending upon the patient population selected. Statistical analyses presented
in these cited studies all revealed statistically significant differences
between patients and control subjects.
Sensitivity 94% Specificity 100% n = 33 diabetic patients and 54 controls
Sensitivity 77% Specificity 100% n= 29 dialysis patients and 137 controls
Sensitivity 84% Specificity 88% n = 70 radiculopathy patients *
Sensitivity 23% Specificity 100% n = 92 diabetic children and 80 controls
Sensitivity 50% Specificity 95% n = 16 Fabry’s disease patients and 50 controls
Sensitivity 54% Specificity 95% n = 2360 diabetic patients *
Sensitivity 60% Specificity 95% n = 73 diabetic patients and 47 controls
Sensitivity 93% Specificity 100% n = 10 syringomyelia patients and 15 controls
Statistical Analyses of CPT vs NCV Sensitivity
1. Ro, L.S., Chen, S.T., Tang, L.M., Hsu, W.C., Chang, H.S., Huang, C.C.
Current Perception Threshold Testing in Fabry’s Disease. Muscle & Nerve,
Volume 22: 1531-1537, 1999. Appendix E., Reference 15.
A chi-square SPSS statistical analysis was conducted to compare the detection
sensitivity of neuropathy by sNCT/CPT and NCV tests in this study. The CPT
detected neuropathy in 50% of the patients. The NCV detected neuropathy in 0%
of the patients. There was a significant superiority of the detection
sensitivity of the sNCT/CPT electrodiagnostic test over the NCV test in this
study (p<0.001, df=1).
2. Katims, J.J., Rouvelas, P., Sadler, B.T.,
A chi-square SPSS statistical analysis was conducted to compare the detection
of neuropathy by sNCT/CPT measure and NCV measures in the median nerve and in
the peroneal nerve. The tests were equally sensitive in their detection
sensitivity for neuropathy (p<0.193, df =1, median nerve and p<0.707, df
= 1, peroneal nerve).
3.
A chi-square SPSS statistical analysis was conducted to compare the detection
of neuropathy by sNCT/CPT measure and NCV measures in the median nerve and in
the peroneal nerve. The tests were equally sensitive in their detection
sensitivity for neuropathy (p<0.119, median nerve and p<0.701, peroneal
nerve).
4. Kurozawa, Y., Nasu, Y. Current Perception Thresholds in Vibration-Induced
Neuropathy. Archives of Environmental Health, Volume 56(3):254-256, 2001.
A. A chi-square SPSS statistical analysis was conducted to compare the
detection of stage 3 vibration neuropathy by sNCT/CPT measure and NCV measures.
The tests were equally sensitive in their detection sensitivity for this stage
of vibration neuropathy (p<0.308, df = 1).
B. A chi-square SPSS statistical analysis was conducted to compare the
detection of stage 2 vibration neuropathy by sNCT/CPT measure and NCV measures.
There was a significant superiority of the detection sensitivity of the
sNCT/CPT electrodiagnostic test over the NCV test in the detection of this
stage of neuropathy(p<0.000, df=1).
5. Rendell, M.S., Katims, J.J., Richter, R., Rowland, F. A comparison of nerve
conduction velocities and current perception thresholds as correlates of
clinical severity of diabetic sensory neuropathy. Journal of Neurology,
Neurosurgery and Psychiatry, Volume 52:502-511, 1989. Appendix E., Reference 5.
A. Among the diabetic subjects in this study classified by both Physical Score
and Symptom Score as normal, the 5 Hz CPT measures were the most “effective
discriminator” of these “normal” patients in comparison with the NCV and other
measures in the study (p<0.05, Tables 6 and 7). This finding is a indication
of the specificity of the CPT evaluation based on clinical findings.
B. Lower extremity sensory NCV measures were unable to discriminate between the
normal and abnormal subjects as classified by both Physical Score and Symptom
Score. All three frequency CPT measures were able to discriminate between these
same two groups of subjects. The significance of these observations ranged from
p<0.01 (5 Hz and 250 Hz) to p<0.05 (2 kHz). This finding demonstrates
that the CPT evaluation is a more effective discriminator than the sensory NCV.
See Table 7.
C. A strong correlation is defined as a correlation coefficient > 0.5.
Correlations of the upper and lower extremity Physical and Symptom Scores with
the CPT and sensory NCV measures were significant, with p values ranging from
0.001 to 0.05. The strongest correlation was observed with physical evaluation
and the 250 Hz CPT from the lower extremity (Spearman correlation coefficient =
0.57, p<0.001). The sensory NCV from the same extremity showed a very weak
correlation (Spearman correlation coef. = 0.15, p<0.05). See Tables 4 and 5.
D. When the electrodiagnostic measures were further divided into “Relatively
Abnormal” and “Very Abnormal Groups”, the sensory NCV was unable to
discriminate between the normal and relatively abnormal groups Physical or
Symptom scores in either the upper or the lower extremity. In contrast, the CPT
measures were able to discriminate between the normal and relatively abnormal
groups Physical or Symptom scores in either extremity (p<0.01). These
findings indicate that the sensory NCV is not effective for discriminating
moderate neuropathy, but is effective for discriminating severe neuropathy. In
contrast the CPT measures are effective for discriminating both moderate
neuropathy, and severe neuropathy.
6. Masson, E.A., Veves, A., Fernando, D., Boulton, A.J.M. Current perception
thresholds: a new, quick, and reproducible method for the assessment of
peripheral neuropathy in diabetes mellitus. Diabetologia, Volume 32:724-728,
1989.Appendix E., Reference 7.
A. This publication does not permit a direct comparison of the detection
sensitivities of the sNCT/CPT and the NCV measures.
B. A significant correlation between the 2000 Hz CPT measures and the
NCVmeasures (Spearman correlation coefficient -0.66, p<0.005) was reported
inTable 2.
C. A significant correlation between the 5 Hz CPT measures and the
thermalmeasures (Spearman correlation coef .34, p<0.005) was reported in
Table 2.
D. No significant correlation was observed between the NCV and the thermal
endorgan sensory threshold test as reported in Table 2. This was expected as
the NCV is a large fiber test and thermal end-organ stimulation is conducted by
the small fibers. As neuropathies can selectively effect the large or small
diameter nerve fibers the ability of the sNCT evaluation to test the function
of both sub-populations of nerve fibers makes this test a more effective tool
for the evaluation of neuropathy than the NCV test.
Based on the above publications the sensitivity of the sensory nerve conduction
velocity testing for the detection of polyneuropathy is between 0% and 79%.
One must also take into account these studies were undertaken in world class
electrophysiologic laboratories and performed by highly skilled technicians
under strict quality assurance standards and supervision.
This data confirms conclusions drawn in posts previously presented. The PNMLT
is a modality we have, and gives information which must be viewed in light of
results from the remaining arms of the diagnostic triad. Alone it has little
value. Intra-operatively and post-operatively it has no value. To answer the
question of a patient with a normal PNMLT yet with severe pain having a greater
likelihood of poor outcome from surgical decompression versus a patient with an
abnormal PNMLT, this type of conclusion cannot be reached. It cannot be reached
based upon theoretical approach, and there are no controlled studies which
would allow one to dispute such theory. In fact, such a statement is contrary
to theory. Let me explain. High numbers on the PNMLT should reflect disease
involvement of an increasing number of heavily myelinated axons, while normal
numbers reflect such axons are as yet uninvolved in the compression neuropathy
(or there is no neuropathy). Differentiation of pain into categories like
severe does not reflect on transduction forces nor on transmission, but instead
is a very poor indication of disease severity because it involves some
modulation but is mostly a matter of perception. Several considerations must be
made in the patient with a normal PNMLT and in severe pudendal distribution
pain. If the CT guided (where we can reasonably assume the analgesic has
reached the pudendal) nerve block gives the patient immediate relief of pain,
and the duration of such analgesia is consistent with the labeled duration of
effect of the analgesic, then it can be concluded with a reasonable degree of
certainty that the pudendal nerve is indeed responsible for delivering
nociceptive input to the spinal cord. This conclusion can be made whether the
PNMLT is normal or not.
A second CT guided block (and indeed, a third or fourth) should achieve the
same results as the first. If not, one of the following must apply: (1) for
whatever reason, the analgesic did not reach the pudendal nerve, (2) the
analgesic was mislabeled, thus no analgesic reached the nerve, (3) the response
to the first injection was a placebo one, (4) the neuropathy has extended
proximally to involve the nerve between the site of the first injection and the
spinal cord, (5) since the time of the first injection another disease process
has involved the pudendal nerve proximal to the site of the initial injection.
It has been alleged that degree of PNMLT abnormality correlates with prognosis
and well as severity of compression. There are no controlled studies to support
this view. Moreover, carefully designed, placebo controlled studies of
commonplace compression neuropathies generally find no correlation between
degree of entrapment as visualized on MRI with severity of symptoms,
probability of analgesia following decompression, or degree of abnormality on
electrophysiologic testing. Given the limitations of PNML testing, it is not
reasonable to offer the results of this test as a prognostic indicator of
surgical decompression.
4.
Validity of intra- operative and post operative PNMLT
The axons injured
by compression or some other structural reason do not form new axons. The ones
you have at birth are with you all through life, and the very same axons that
formed the pudendal nerve when you were seventeen and seemingly indestructible
are still there... in bundles that form the pudendal nerve. The myelin sheath
that coats each axon degenerates and then regenerates once injured. There may
be several episodes of degeneration and regeneration, but in almost all cases
the regenerated myelin sheath is thin, unlike the sheath of a healthy nerve.
Since thickness of the sheath determines velocity of conduction of the nerve
impulse, a thin sheath conducts slower than a thick one. It is likely, and
appears to be so both in research and cadaver dissections, that the axon will
never regain its original myelin thickness. Therefore, yes, Greg, you are
right. Dr. Ansell's belief is more than that. It is correct based upon fairly
extensive neurophysiologic studies. Latency will not change during surgical
decompression, and I'm certain that it is easy for you to see this given the
nature of latency as previously described and the cellular changes that are
responsible for delayed conduction. The severity of pain during my illness made
it clear that hyperbole and subjectivity is not the way to approach PNE.
Providers and patients need to make decisions based on the most current
evidence-based, non-biased science, and such science is generally repetitive,
for researchers as well as those who depend on research find comfort when
results are reproducible. It is important to realize, as I wrote before...
demyelination with insufficient remyelination does not account for persistent
symptoms in supposedly decompressed patients. Once again I allege the only
reasonable probabilities for this: incorrect diagnosis, insufficient
decompression, or established central pathways at the cord or cortex level that
take time to resolve despite the absence of stimuli. The latter would explain
progressive improvement in a subset of post-operative patients, and I am aware
of several medications that would speed this along.
5. Reasons for PNMLT
despite concerns over validity
As I have written
before, the sensitivity of the diagnostic triad leaves much to be desired. The
same is true of its specificity. But suppose we were to dismiss the PNMLT
altogether. This would be much like dismissing the upper GI series, which
misses 65% of endoscopically proven gastric ulcers, or even the CXR, which
misses most bronchogenic carcinoma until the tumor has had 5 years to double
and spread to regional nodes. Or we could dismiss the PSA, since levels of 4 to
8 are gray and may or may not suggest disease, or could be the result of
tobacco dependence. No, what we do is take the modalities that are available to
us and constantly refine them, improving technical skills as well as
technology, until new modalities become available. Just like baking a cake,
sometimes it is easier and more efficient to adjust a recipe than to start from
scratch. What is known to each of us is that resources for PNE are few and far
between. We have no lobby of Hollywood stars pleading with Congress for
research monies, as did the sufferers of AIDS. Our numbers are relatively few
and hardly spark the interests of a pharmaceutical industry whose focus is the
bottom line. Although my state has huge, reputable medical centers, I, like
others, have had to travel out of state to see a physician who has even heard
of PNE. So while PNMLT is not a panacea, it is a modality we have. The future
may bring new technologies that are far more reliable, but these will be only
as good as their operators. Colonoscopy misses 5% of colorectal tumors, but in
the hand of others, and on a good day, the miss rate is zero. If a technology
and its results can be correlated with gross and microscopic pathology, then it
is much more likely to be successful in diagnosis, as well as in monitoring
improvement. Nerve conduction technology should improve dramatically in the next
decade.
Intervertebral disc herniation should be ruled out before PNE surgery is
contemplated, and an MRI is the most reliable method to do so. In addition,
pelvic pathology that could produce a pudendal neuralgia, either from
compression or invasion of the nerve, should also be ruled out, and a pelvic CT
scan should suffice. I had both before making the first trip to Houston. At 75,
most of my discs were bulging (discs dehydrate with age and uniformly bulge),
but there was no encroachment on the neural canal.
In fact, we could pull 100 asymptomatic folks out of the isles of Walmart, do
MRIs of their lumbosacral spine, and more than 30% would have significant disc
disease. Like PNMLT, MRIs are not a panacea for diagnosis.
But I promised to write about nerve injury, those "damaged" and those
compressed. For the sake of an intellectual exercise I will write about the
sciatic nerve rather than the pudendal. Both are peripheral nerves, with the
same configurations, same arrangement of axons, same location of cell bodies
within the cord, same type of synapses both dendritic and axonal. Except for
size, location, areas innervated, and location of cord synapses, they are the
same. We do ourselves and others disservice by thinking somehow the pudendal
nerve is subject to a disease process that affects that nerve alone. All
peripheral nerves can suffer compression and are subject to disease. While the
structure or lesion precipitating compression may be different, the changes
that take place in the nerve are the same. The same is true of systemic
diseases affecting peripheral nerves. But since polyneuropathy is essentially
ruled out in most of our cases, especially given the duration of symptoms, I
will avoid a discussion of those injuries and the neuropatholgies involved.
Rather I will focus, or attempt to do so, on disease and how it affects a
single sciatic nerve. In essence, that is what has happened to us.
6. Botox and the
PNMLT
Botox should not
affect the PNMLT. Botox affects the neuromuscular junction at the efferent
nerve ending, working to block any impulse from the brain from reaching the
muscle. In theory this blocks all the impulses flowing from the cord to muscle
while the cord is in a hyper-excitable state from chronic pain.
The PNMLT measures impulse conduction along afferent axons. The neuromuscular
junction is not involved in this measurement, nor any synapse.... therefore
Botox will not affect it.
7. Nerve testing of
penis
Electrophysiologic
testing of the penis, with either positive or negative results, have about as
much efficacy in ruling in or out pudendal neuropathy (of whatever cause) as
does measuring the growth of one's eyebrows.
This test (see: http://www.hawaii.edu/hivandaids/Innervation_of_the_Human_Glans_Penis.pdf#search='nerve%20conduction%20studies%20in%20penis'
)
measures conduction through a very short length of nerve (dorsal nerve of the
penis). Pudendal neuropathy does not arise from entrapment along the dorsal
nerve of the penis. PNE could be present while such a test was positive or
negative. PNE could be absent while such a test was positive or negative. There
is no validity of such a test to PNE. Surely your doctor did not intend to rule
out PNE with nerve testing of the penis ???
C. MR Neurography
Does MR
neurography have application to PNE, either for pre-operative determination of
location and degree of entrapment, or for post-operative determination of
successful decompression? In another post I have written:
"Magnetic resonance neurography is considered "investigational/not
medically necessary" by the American Medical Association, but the
literature suggests that improvements in both imaging and interpretation are
being made on a regular basis. Information for patients can be viewed at www.neurography.com.
It is this member's opinion that current testing is valuable in that there is a
greater than 50-50 probability results might provide significant information to
the neurosurgeon. In addition, since it is doubtful diagnostic modalities will
be developed because of concern over PNE alone, participation in developing
technologies will increase both the credibility of PNE as a syndrome as well as
expand the knowledge base upon which future PNE patients might rely."
Yet this dismisses other considerations, each of which suggests less
reliability, but which in fairness must also be presented.
1. If the CAUSATIVE MECHANISMS involved in PNE are consistent with those of
nearly all other cases of nerve entrapment syndromes in the human body, and are
also consistent with the vision of injury expressed to me by Dr. Renney during
my original visit to Houston, then the mechanism and thus the injury will most
likely not be seen on MR neurography. I have previously written that the
causative mechanism is most likely as follows: "at least one side of the
compressive surface is mobile, so that chronic injury to the pudendal involves
either a repetitive slapping insult, or a
sliding-rubbing-against-sharp-or-tight-edges type of insult"., neither of
which would likely be demonstrated with current MR neurography technology. This
is not to say that as software is further refined, so that the nerve could be
actually visualized during movement, and thus a more reliable indication of
pathology would result.
2. Visualization of pudendal nerve injury might be solely positional
(POSITIONAL ENTRAPMENT), in which case the above described software modifications
might help. And also answer for us the question of whether or not the constant
pain that is the hallmark of long standing and unresolved pudendal neuropathy
represents central sensitization with continuing but intermittent injury or
rather a progression to continuous injury. In such case where injury is solely
positional, then only a procedure performed with the patient in that position
would demonstrate an abnormality in the nerve.
3. While those who have reason to seek neurography for failed lumbar spine
surgery number in the hundreds of thousands, the number of patients seeking MR
neurography for pudendal neuropathy would be few. As such, the repetition of
study that gives boost to improvement in clinical skills in both analysis and
interpretation of results is not going to be present at any of the three
centers where this software is available in the US. Moreover, the length of
nerve that must be examined in failed lumbar procedure is short. In contrast,
the pudendal courses over a wide area, and as I have written before, there are
four possible sites of entrapment.
4. Finally, the demonstration of a compressed segment of pudendal nerve on MR
neurography might be meaningless unless studies had shown in a statistically
significant number of patients that such a lesion corresponded to anatomical
findings at the time of surgery and surgical decompression of this MR
neurography demonstrated segment resulted in relief of pain. Given the usual
duration of symptoms in PNE and the role of central sensitization in
perpetuating pain long after the injury to the nerve has been removed, it is
doubtful that such rigorous scrutiny could ever be applied to PNE and MR
neurography.
D. Nerve blocks
1.
Karen is correct
in that the duration of analgesia from a nerve block should be equal to the
expected duration of effect of the analgesic, but no longer. If the analgesic
is marcaine, the analgesia may last several days. If the analgesic is
xylocaine, the concentration of drug selected can be varied, but the effect
should last no longer than 12 hours at the extreme.
Several studies have demonstrated that the prolonged and very occasional
permanent effect of a nerve block to the median nerve was not due to the
anti-inflammatory nature of the attendant corticosteroid but was rather due to
a reduction in constriction of the nerve.
Apparently steroids injected locally help break down adipose tissue (fat). In
these studies it was shown that a reduction in the amount of fat beneath the
transverse carpal ligament (which was entrapping the median nerve) relieved the
entrapment to such an extent that neuropathy resolved. Generally speaking,
steroids have no effect on scar or fibrotic tissue, unless that fibrous tissue
is acutely inflamed, such as an acute tendonitis, or a active collagen vascular
disease process. Since there is very little fat, if at all, in Alcock's,
combinations of local anesthetics with corticosteroids injected into this area
will have no consequence other than the transient analgesia expected of the
anesthetic.
If pain is totally relieved from Botox, then the pain is not neuropathic from
pudendal entrapment at Alcock's. The pelvic floor muscles innervated by the
pudendal can spasm and thus place compressive forces on pudendal branches
feeding them. If this persisted to such a point that the nerve branch was
injured, the pain would be neuropathic, but again, the site of injury would not
be at Alcocks. The sole mechanism of action of Botox is at the neuromuscular
junction, the site at which the nerve passes on to muscle instructions that
have been received from the cord. The action of Botox at this site is quite
well understood, blocking the transfer of information from the nerve to the
muscle, resulting in muscle paralysis. The paralysis is flaccid, not rigid. The
muscle becomes totally relaxed, unable to contract without orders from the
cord. Only if the pudendal passed though a muscle that was in a state of
constant or almost constant contraction, which it does not, could muscle be
held liable for neuropathy (except for tiny branches, which could be liable).
If pain is relieved from Botox, then PT is not only advisable, it is necessary
in order to prepare the pelvis for the time when the effects of Botox have worn
off. Only when Botox affords no relief, and PT causes additional pudendal
distribution symptoms, is PT inadvisable.
While Botox works at the junction between muscle and nerve, it does not affect
sensory afferents coming from muscle, or from areas surrounding muscle. A
pathological process affecting the pelvis in the area infiltrated with Botox
would nonetheless generate transduction forces that would be interpreted and
recognized as pain. A nerve block, however, defeats transmission in the area of
administration, so that any nociception, whether nociceptive or neuropathic,
whether from laceration, fracture, tumor, or nerve entrapment, regardless of
etiology, would not reach the cord or brain.
I believe this allows us to suggest the following: do not entertain PNE
decompression until you have undergone a trial of Botox therapy. If your pain
is musculoskeletal, and relieved by Botox, you will not find relief from
surgical decompression at Alcock's. Instead, all efforts.... PT, medication
(including Botox) ... should be focused on achieving muscle relaxation on
command. This needs to be added to the recommendations to the patient with PNE
symptoms.
2.
I want to run some
things by you. Since your son has had both an MRI and a CT, and I presume were
normal, I would also like to presume that work up included blood tests to rule
out systemic disease.
You've seen a urologist, so testicular malignancy, the most common cancer in a
male that age, has been ruled out. To me that is a critical determination. You
write that you were given a diagnosis of prostatitis. Since antibiotics were
prescribed, I presume the diagnosis was bacterial prostatitis. I also presume
that the urinalysis showed leukocytes, and a positive result was received on
urine culture. These are essential for such a diagnosis. The urine specimen
should have included premassage and postmassage of the prostate. This test is
known as the 2-glass test. If the 2 glass test was positive, the culture of
prostatic fluid positive, then the diagnosis of prostatitis was not false. If
these tests were negative, or worse... not done... then the diagnosis is
suspect, and could certainly be false.
Then the visit to the neurologist, and on to Dr. Antolak. You are certainly
putting in the effort, and I admire that. You were told to be patient
"that the effects of the injection may not be noticable for 5-6
weeks". First, the failure to obtain immediate and complete though
temporary analgesia after the injection of 6 cc of marcaine is a major red
flag, and lowers the index of suspicion with respect to PNE. Second, much of
what Dr. Antolak told you is suspect. The literature does not support his
contention that the effects of steroid injection may not be noticable for 5-6
weeks, nor does clinical practice in other areas of nerve entrapment. Placebo
has a response rate of 47%, so a response rate as given by Dr. Antolak (15-70%)
could easily be placebo. In fact, symptomatic improvement as measured in 5 or
10 minute intervals of sitting is no reasonable measure of treatment efficacy.
You were told your son "has damaged a nerve that will require many months
to heal". Just the simple fact that there was no immediate analgesia with
a potent nerve block should give pause to such a remark. You have a normal
PNMLT, a negative response to nerve block, and yet the doctor is telling you
the problem is neuropathy. "pain under his stomach" is a little
difficult for me to locate, but from reading your posts in total it is not
apparent the distribution of symptoms is predominantly pudendal. And you were
told there is a cumulative effect over time, but there is nothing in the
literature, clinical studies or pathology models, to support such a statement.
You've heard the saying: two heads are better than one. The most effective way
to address a chronic pain state is with an interdisciplinary team approach. A
psychiatric evaluation should be a part of any such team effort. Chronic pain
is both influenced by emotions and precipitates emotions, some of them
destructive. Someone needs to explore work history, social history, drug
history, school history, for all of these histories might give important clues.
The team approach needs to be guided by what movements the physical therapist
says he can and cannot make. It needs to be guided by response to medication
that target specific generators of pain, whether nociceptive or neuropathic,
for that response, or lack of response, also gives clues. It might be helpful
to bring in an occupational therapist as well. You need a physician to head
such a team that is willing to listen, to search the literature, and to make
sense. When a physician tells a patient that they need look no further (but
offers no results that would stand up to scruity) and advises that you bide
your time (although his treatments to date have resulted in essentially zero
response), that patient needs to take a hard look at what is going on.
3.
Across many topics
on the forum the issue of nerve blocks is raised. Some members wonder about
side effects, others the probability of cure. Questions abound, and responses
usually reflect what physicians have said to patients or family members. It is
apparent that there is a lot of false information out there, giving false hope,
which, when deflated, then causes suspicion of other modalities which might be
effective.
Karen has made it clear, and I totally agree, that the nerve block should be
considered a diagnostic tool only. Patients should not go into the test
expecting anything other. If the nerve block gives permanent analgesia from
pudendal pain, then you can bless the heavens, for you did not have PNE in the
first place.
But answering this question about nerve blocks generates many others. Greg
writes that he knows people who have improved following nerve block.
What is the length of action of steroids, and are they washed away by
increasing the blood flow during physical therapy? These are just two of a
myriad of questions surrounding a pudendal block.
In my opinion the two most important questions are these: Aside from the use of
a local anesthetic to determine if the persisting pain is carried to the cord
via the pudendal nerve, thereby possibly indicating the pudendal itself as the
instigator (although again, any structure or tissue innervated by the pudendal
past the point of block could also be giving rise to these pain messages), what
does the added steroid tell us? Could the ste