PERIPHERAL NEUROPATHIES PRESENTING AS CHRONIC PELVIC PAIN
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PERIPHERAL NEUROPATHIES PRESENTING AS CHRONIC PELVIC PAIN
By:C. Paul Perry, M.D.
C. Paul Perry Pelvic Pain Center
Brookwood Women?s Medical Center
2006 Brookwood Medical Center Drive
Birmingham, Al 35209
Office (205) 877-2954
Fax (205) 877-2973
cpperry@aol.com
Presented at the 27th Annual Meeting of the International Congress of
Gynecologic Endoscopy, November 11th, 1998, Atlanta, Ga. ?Management of
Pelvic Pain?
Precis
Peripheral somatic nerve pathology may produce neuropathic chronic
pelvic pain difficult to distinguish from chronic pelvic pain of
visceral origin.
Abstract
Chronic pelvic pain is usually assumed visceral in origin by patient and
physician alike. Because of the phenomenon of viscerosomatic
convergence, it may be impossible to distinguish the origin without a
meticulous history, physical exam and differential nerve blocks. Error
in diagnosis and treatment may lead to unhelpful surgery and poor
treatment results. Peripheral somatic neuropathies will often mimic
internal organ pathology. Likewise, visceral pathology can produce
changes in the peripheral somatic nerves that must also be addressed if
maximum pain relief is to be attained. Awareness of peripheral
neuropathies will favor a more effective treatment for these long
suffering patients.
Chronic pelvic pain (CPP) is usually assumed visceral in origin by
patients and physicians alike. It is not uncommon for patients with low
lateral pain to present with the chief complaints of ?my ovary hurts?,
or ?my endometriosis is back?. Unfortunately, many gynecologists will
reinforce these assumptions without a critical analysis of the history
or without ruling out a somatic pelvic pain etiology by physical exam.
Many complex pelvic pain patients will have suffered multiple pelvic
surgeries, including adnexectomy or hysterectomy, only to continue
experiencing the same pain for which she originally sought relief. These
patients may be experiencing neuropathic pain. This type pain can be
from visceral of somatic nerves. The somatic nerves are very
accessible. Their role can be screened by history, physical exam and
nerve blocks. An awareness of peripheral neuropathies as an etiology of
CPP may avoid inappropriate surgery. Even the most skilled endoscopist
may be doomed to failure if appropriate screening is neglected before
surgical treatment of CPP.
Careful abdominal wall examination to look for trigger points and areas
of abnormal skin sensation should be routinely performed before bimanual
examination. Trigger points will manifest as areas of discrete
hyperalgesia. When palpated with fingertip pressure, they illicit sharp
pain that can refer to distant dermatomes1. These isolated neuro-motor
units differ in presentation and etiology from peripheral neuropathy
that will involve the total distribution of the involved nerve. It is
important to recognize that many tissue layers will be palpated during
bimanual exam- both visceral and somatic. Tenderness on bimanual
doesn?t equate to visceral pathology.
Subjective discrimination of somatic and visceral pain is difficult
because of a neurophysiologic phenomenon known as ?convergence and
projection? or ?viscerosomatic convergence?2,3. This occurs at the
level of the dorsal horn of the spinal cord (figure 1). The peripheral
somatic nerves and the visceral nerves synapse at the same dorsal horn
transmission cell of the spinal cord. These transmission cells relay
the pain signal to the brain. The cortex projects the signal as coming
from the same dermatome level regardless of visceral or somatic origin.
This makes it impossible for patients to distinguish internal organ pain
from abdominal wall pain.
To complicate matters even further, chronic visceral pain can produce
peripheral neuropathies by antidromic (reverse flow stimulation) through
the spinal cord transmission cells2. This will result in both somatic
and visceral components of the CPP. The longer the stimulation occurs,
the more difficult is the goal of complete relief. The somatic nerve
dermatomes affected are determined by the site of origin of the visceral
pain.
Those transmission cells sharing somatic and visceral nerves of the
pelvis involve the dermatomes at the T12-L3 and S2-4 levels (Table 1).
This includes the iliohypogastric, the ilioinguinal, genitofemoral,
lateral femoral cutaneous, and the pudendal nerves. Except for the
Iliohypogastric and pudendal nerves, these nerves are afferent (sensory)
with no significant efferent (motor) component in females. The somatic
nerve emerges from the dorsal root ganglion and travels in the
retroperitoneal space around or through the pelvis (figure 2). Their
sensory innervation includes the skin, subcutaneous tissue, muscle and
parietal peritoneum. This comprises the dermatomes just below the
umbilicus to the upper thigh (figure 3).
Somatic neuropathic pain originating from these nerves can have multiple
etiologies. Nerve injury has been reported from: 1. Stretching, 2.
Blunt trauma, 3. Compression with hypoxia, 4. Fibrosis with
entrapment, or 5. Suture ligature4.
The pain will often have a burning quality. Some patients will complain
of shooting or lancinating pain. The pain will usually become constant
and more intense with time. It is usually aggravated by activity.
Menstruation may aggravate the pain due to peri-neural edema,
hormone-induced increased neurotransmitters, and dysmenorrhea producing
dorsal horn transmission cell sensitivity. Clinical diagnosis is
dependent on a high index of suspicion. Differential nerve blocks that
provide complete relief, albeit temporary, are the sine qua non for
establishing this diagnosis4.
General principles of treatment include alleviation of compression,
rehabilitation and the use of medications with demonstrated
effectiveness for neuropathic analgesia (Table 2). Transection of
sensory nerves should be performed only after exhausting all other
avenues of pain relief. Two complications may develop from nerve
transection that would make further improvement very difficult: 1.
Neuroma formation and 2.Pain from maladaptive neuronal plasticity.
Iliohypogastric neuropathy
The iliohypogastric nerve (T12-L1) is the highest branch of somatic
pelvic nerves and shares dorsal horn dermatomes with the ovary and
distal tube. It passes through the psoas muscle, extending diagonally
along the anterior surface of the quadratus lumborum. From there, it
continues through the transversus abdominis, extending between the
transversus and the internal oblique and continuing medially deep to the
aponeurosis of the internal oblique at the level of the anterosuperior
iliac crest. The nerve then divides into its anterior and lateral
cutaneous branches. The anterior branch extends horizontally below the
aponeurosis to the external oblique and becomes cutaneous in the
anterior abdominal wall approximately 1 cm superior to the superficial
inguinal ring and 2 cm medial to the anterosuperior iliac crest. This
nerve serves as motor innervation to the transversus abdominis and the
internal oblique muscles. Its sensory distribution is the groin and the
symphysis pubis region. This distribution is overlapping with the
ilioinguinal and genitofemoral nerves (figure 2& 3).
The most common injury occurs from abdominal and pelvic incisions with
suture ligature or fibrotic entrapment. Patients may describe a pulling
or a throbbing sensation, which can occur many years after the offending
surgery. Physical activity is limited due to the aggravation of this
pain.
The treatment of this CPP from iliohypogastric neuropathy should include
therapeutic/diagnostic blocks at the paravertebral and peripheral nerve
levels. A paravertebral block of T12,L1 would provide relief, while
differential blocks of the ilioinguinal and genitofemoral nerves will
provide no pain relief. Transection of the nerve in the posterior
retroperitoneal area can be performed if blocks and medications fail to
provide prolonged pain relief.
Ilioinguinal Neuropathy
The ilioinguinal nerve (L1-2 ) shares dorsal horn transmission cells
with the proximal fallopian tubes and uterine fundus. It enters the
inguinal canal about 2 cm medial to the anterior superior iliac spine
and then courses just beneath the anterior leaf of the inguinal canal.
Here it exits out the superficial inguinal ring or pierces at the ring
to become a sensory nerve to the overlying skin. It supplies sensory
innervation to the groin, mons, labia, and inner thigh (figures 2&3).
The most common injury is entrapment by suture ligature in the lateral
edges of Pfannenstiel?s incision or at the time of needle bladder
suspension. Typically, the diagnosis may be delayed while multiple
visceral etiologies are suspected and treated unsuccessfully. This
diagnosis is easily made by blocking the nerve with local anesthetic
injected 2.5 to 3 cm medial and inferior to the anterior superior iliac
crest (figure 4). It is important to reproduce the exact pain by
needling and to obtain complete relief after anesthetizing to be certain
of the diagnosis5. The treatment of multiple blocks for desensitization
and medical therapy should be tried before transection is done. No
laparoscopic treatment of this neuropathy has been reported.
Genitofemoral Neuropathy
The genitofemoral nerve (L1-2) shares dorsal horn transmission cells
with the proximal fallopian tube and uterine fundus. It runs through
the substance of the psoas muscle and emerges near its medial border
opposite the third and fourth lumbar vertebrae (figure 5). It descends
retroperitoneally and crosses behind the ureter. At a variable distance
above the inguinal ligament, the nerve divides into genital and femoral
branches. The genital branch crosses the lower end of the external
iliac artery and enters the inguinal canal through the deep inguinal
ring together with the round ligament. The femoral branch descends
lateral to the external iliac artery, behind the inguinal ligament, and
through the fascia lata into the femoral sheath. The genital branch
supplies the skin of the mons pubis and labium majus. The femoral
branch supplies the skin of the femoral triangle.
The most common injury is of the right genitofemoral nerve. It may
occur when appendectomy causes peri-neural fibrosis where the nerve
exits the psoas muscle. Hernia repair can produce neuropathy of either
side by suture or staple entrapment at the inguinal canal. These
patients will complain of burning paresthesias and pain in the groin,
labia, and medial thigh. Transection can be accomplished
laparoscopically either transabdominally or extraperitoneally if
conservative treatment is unsuccessful. The diagnosis is made by
differential blocks. Blocking the ilioinguinal nerve affords no relief,
but a trans-psoas genitofemoral block produces complete relief7.
Lateral Femoral Cutaneous Neuropathy
The lateral femoral cutaneous nerve (L2-3) shares dorsal horn
transmission cells with the uterine fundus and lower uterine segment. It
runs inferolaterally on the iliacus muscle. It traverses the
retroperitoneum lateral to the iliac vessels. The nerve passes under
the iliopubic tract and inguinal ligament. It may pass behind or
through the ligament making this area vulnerable to compression injury
(figure 6).
This neuropathy produces pain and numbness in the upper outer thigh. The
symptoms are often termed meralgia paraesthetica. Decompression at the
inguinal ligament will usually alleviate this pain. After anesthetic
blocks make the diagnosis, neurolysis is the treatment of choice if
conservative treatment fails8,9,10.
At least 80 different etiologies for this neuropathy have been
described. Some of the more common are pressure form tight or wide
belts, tight pants, postsurgical scars after abdominal surgery,
pregnancy, iliac bone graft harvest, ascites, obesity, abdominal/pelvic
mass, and metabolic neuropathies10.
Pudendal Neuropathy
The pudendal nerve (S2-4) shares the dorsal horn transmission cells with
the cervix, uterosacral, and vulvovaginal areas. The pudendal nerve is
a mixed sensory and motor nerve. The efferent (motor) neuropathic
symptoms will usually accompany the afferent neuropathy that manifests
as CPP. The sacral motor neuropathy produces abnormal bladder and bowel
function, but this will not be discussed here.
The pudendal nerve enters the pelvis through the lesser sciatic foramen
and then immediately wraps behind the ischial spine. It is accompanied
by the pudendal artery and vein. Once in the perineal area, it travels
in Alcock?s canal, which is the tunnel created by parietal fascia.
Sensory distributions include those areas bordered by the inferior pubic
ramus superiorly, the labiocrural folds laterally, and the inter gluteal
fold posteriorly (figure 7)3.
Nerve injury can be caused by prolonged compression or stretching as in
the second stage of labor. Surgical injuries have also been reported
with sacrospinous vaginal vault suspension, vaginal laceration repairs,
and various types of episiotomies. Other patients have developed
pudendal neuropathy after straddle injuries, prolonged motorcycle
riding, and laser treatment to the vulva and perineum. Diagnosis can be
easily made with pudendal nerve block.
The symptoms of this neuropathy range from constant burning to intense
lancinating pain. It can be unilateral or bilateral. This neuropathy
will often be accompanied by pelvic floor myalgia and spasm.
Because of the motor functions of this nerve, neurectomy is not an
option. Repeated pudendal blocks (with and without steroids),
cryo-neurolysis, and trans-cutaneous electrical stimulation have met
with mixed results. Sacral nerve stimulation with an implantable device
is being investigated. Neuro-magnetic therapy is also undergoing
clinical trials.
Neuroma Formation and Maladaptive Neuronal Plasticity
As stated earlier, the two most feared complications of peripheral nerve
transection are neuroma formation and maladaptive neuronal plasticity. A
neuroma is a bulbous, exquisitely sensitive terminal of a cut nerve.
These can be very painful if touched or can generate spontaneous action
potentials and recurrent neuropathic pain. We currently have no
reliable therapy for neuroma formation.
Maladaptive neuronal plasticity is the theory that interruption of a
nerve fiber may cause irreversible changes of hyperexcitability of the
dorsal horn transmission neurons. This results in continual neuropathic
pain in the distribution of the peripheral nerve, which has been
transected. Examples of this are phantom limb pain, continued pain
after dorsal rhizotomy, and deafferentation pain (e.g., after brachial
plexus injury).
Studies thus far have not established the incidence of neuroma formation
or maladaptive neuronal plasticity after neurectomy for the treatment of
chronic pelvic pain. However, our experience is limited and patients
should be aware of these potential risks11.
Overview
Clinicians responsible for the care of women must understand the
relationship between peripheral neuropathies and chronic pelvic pain.
Because of the phenomenon of viscerosomatic convergence, neuropathic
pain should be considered in all patients unresponsive to conventional
therapy. Knowledge of the innervation patterns and nerve block
techniques is necessary to properly diagnose and treat these
long-suffering women.
References
1. Travell JG, Simmons DG. Myofascial Pain and Dysfunction: The
Trigger Point Manual: The Lower Extremities. Baltimore, Williams and
Wilkins, 1983: 1; 1-4
2. Fields HL. Pain. New York, McGraw-Hill inc., 1987: 79-97
3. Rogers RM. Basic pelvic neuroanatomy. In Chronic Pelvic Pain: An
Integrated Approach. Edited by JF Steege, DA Metzger, and BS Levy.
Philadelphia, WB Saunders, 1998, pp 31-58
4. Kline DG, Hudson AR. Nerve Injuries. Philadelphia, WB Saunders
Co., 1995: 327-30
5. Monga M Ghoniem GM. Ilioinguinal nerve entrapment following needle
bladder suspension procedures. Urology 44(3): 447-50, 1993
6. Sippo WC, Burghardt A, Gomez AC. Nerve entrapment after
Pfannenstiel incision. Am J Obstet Gynecol 157: 420-1, 1987
7. Perry CP. Laparoscopic treatment of genitofemoral neuralgia. J
Amer Assoc Gynecol Laparosc 4(2): 231-4, 1997
8. Broin EO, Horner C, Mealy K, et al: Meralgia paraesthetica following
laparoscopic inguinal hernia repair. Surg Endosc 9: 76-8, 1995
9. Macinol MF, Thompson WF. Idiopathic meralgia paresthetica. Clin
Orthop 254 May: 270-4, 1999
10. Williams PH, Trzil KP. Management of meralgia paresthetica. J
Neurosurg 74: 76-80, 1991
11. Kennedy EM, Harms BA, Starling JR. Absence of maladaptive neuronal
plasticity after genitofemoral-ilioinguinal neurectomy. Surgery 116(4):
665-71, 1994
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