Peripheral neuropathies causing chronic pelvic pain

Peripheral neuropathies causing chronic pelvic pain

May 2000, Vd. 7, No. 2 The Journal of the American Association of Gynecologic Laparoscopists Peripheral Neuropathies Causing Chronic Pelvic Pain C. ...

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May 2000, Vd. 7, No. 2

The Journal of the American Association of Gynecologic Laparoscopists

Peripheral Neuropathies Causing Chronic Pelvic Pain C. Paul Perry, M.D.

Abstract

Chronic pelvic pain is usually assumed to be visceral in origin by both patients and physicians. Because of the phenomenon of viscerosomatic convergence, it may be impossible to distinguish the origin without a meticulous hislory, physical examination, and nerve blocks. Error in diagnosis and treatment may lead to unhelpful surgery and poor results. Peripheral somatic neuropathies often mimic internal organ pathology. Similarly, visceral pathology can produce changes in peripheral somatic nerves that must also be addressed if maximum pain relief is to be attained. Awareness of peripheral neuropathies will favor more effective treatment for these patients. (] Am Assoc Gynecol Laparosc 7(2):281-287, 2000)

Patients and physicians generally consider chronic pelvic pain (CPP) to be visceral. It is not uncommon for women with low lateral pain to complain, "my ovary hurts," or "my endometriosis is back." Unfortunately, many gynecologists reinforce these assumptions without critical analysis of the history or without ruling out a somatic etiology by physical examination. Many patients with complex pelvic pain undergo several pelvic surgeries, including adnexectomy or hysterectomy, only to continue experiencing the same pain. These women may be experiencing neuropathic pain, which can be from visceral or somatic nerves. Somatic nerves are very accessible and their role can be assessed by history, physical examination, and nerve blocks. Awareness of peripheral neuropathies as an etiology of CPP may avoid inappropriate surgery. Before bimanual examination, careful abdominal wall examination should be performed routinely to look for trigger points and areas of abnormal skin sensation. Trigger points manifest as areas of discrete hyperalgesia. When palpated with fingertip pressure, they cause sharp pain that can refer to distant der-

matomes.~ These isolated neuromotor units differ in etiology from peripheral neuropathy that involve total distribution of the nerve. It is important to recognize that many tissue layers are palpated during bimanual examination, both visceral and somatic, and tenderness does not equate with visceral pathology. S u bj ective discrimination of somatic and visceral pain is difficult because of a neurophysiologic phenomenon known as convergence and projection, or viscerosomatic convergence. 2'3 It occurs at the level of the dorsal horn of the spinal cord (Figure 1). Peripheral somatic nerves and 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 further, chronic visceral pain can produce peripheral neuropathies by antidromic (reverse flow stimulation) through spinal cord

From the C. Paul Perry Pelvic Pain Center, Brookwood Women's Medical Center, Birmingham, Alabama. Address reprint requests to C. Paul Perry, M.D., C. Paul Perry Pelvic Pain Center, Brookwood Women's Medical Center, 2006 Brookwood Medical Center Drive, Birmingham, AL 35209; fax 205 877 2973. Prcsented at the 27tta annual meeting of the American Association of Gynecologic Laparoscopists, Atlanta, Georgia, November 11-15, 1998. Accepted for publication December 11, 1999.

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Peripheral Neuropathies Causing Chronic Pelvic Pain Perry

Somatic

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space around or through the pelvis (Figure 2). Sensory innervation includes skin, subcutaneous tissue, muscle, and parietal peritoneum, as well as dermatomes just below the umbilicus to the upper thigh (Figure 3). Somatic neuropathic pain originating from these nerves may have several etiologies. Nerve injury has been reported from stretching, blunt trauma, compression with hypoxia, fibrosis with entrapment, and suture ligature. 4 The pain often has a burning quality and in some patients may be shooting or lancinating. It usually becomes constant and more intense with time. It is usually aggravated by activity. Menstruation may aggravate it due to perineural edema, hormone-induced increased neurotransmitters, and dysmenorrhea producing dorsal horn transmission cell sensitivity. Clinical diagnosis is dependent on a high index of suspicion. Nerve blocks that provide complete, albeit temporary, relief are the sine qua non for establishing the diagnosis. 4 General principles of treatment include alleviation of compression, rehabilitation, and drugs with demonstrated effectiveness for neuropathic analgesia (Table 2). Transection of sensory nerves should be performed only after exhausting all other avenues of relief. Two complications may develop from nerve

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Visceral Viseero-Somatie Convergenees FIGURE 1. Convergence-projection, or viscerosomatic convergence. transmission cells. 2 This results in both somatic and visceral components of CPR The longer the stimulation lasts, the more difficult it is to achieve complete relief. Somatic nerve dermatomes affected are determined by the site of origin of visceral pain (Table 1). Transmission cells sharing somatic and visceral nerves of the pelvis involve the dermatomes at the T 1 2 - L 3 and $2-4 levels. This includes iliohypogastric, ilioinguinal, genitofemoral, lateral femoral cutaneous, and pudendal nerves. Except for iliohypogastric and pudendal nerves, these nerves are afferent (sensory) with no significant efferent (motor) component in women. The somatic nerve emerges from the dorsal root ganglion and travels in the retroperitoneal TABLE 1. Peripheral Somatic Sensory Nerve Dermatomes

with Corresponding Visceral Sensory Nerve ConvergenceProjection Fields Somatic Nerve

Dermatome

Visceral Field

lliohypogastric

T12-L1

Ovary, distal fallopian tube Proximal tube, uterine fundus Proximal tube, uterine fundus Fundus, lower uterine segment Lower uterine segment, cervix, bladder, distal ureter, upper vagina, rectum

l[ioinguinal

L1-2

Genitofemoral

L1 2

Lateral femoral cutaneous Pudendal

L2-3 $2 4

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llioinguinal / Iliohypogastric I Nerve" ] ..........................................

FIGURE 2. Peripheral somatic nerves of the pelvis.

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borum. From there it continues through the transversus abdominis, extending between the transversus and internal oblique muscles and continuing medially deep to the aponeurosis of the internal oblique at the level of the anterosuperior iliac crest. The nerve then divides into 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 internal oblique muscles, its sensory distribution is the groin and symphysis pubis region. This distribution overlaps with ilioinguinal and genitofemoral nerves (Figures 2 and 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 aggravation of this pain. Treatment of CPP from iliohypogastric neuropathy should include therapeutic-diagnostic blocks at paravertebral and peripheral nerve levels. A paravertebral block of T12-L1 would provide relief, whereas differential blocks of the ilioinguinal and genitofemoral nerves would not. Transection of the nerve in the posterior retroperitoneal area can be performed if blocks and drugs fail to provide prolonged relief.

1

FIGURE 3. Dermatome distribution of peripheral somatic nerves,

TABLE 2. Drugs and Dosages for Neuropathic Pain

Dosage

Drug

Amitriptyline Carbamazepine Doxepin Gabapentin Lamotrigine Mexiletine HCI Nortriptyline Phenytoin Topiramate Trazodone

10-75 mg at bedtime 200 mg b.i.d. (titrate with blood levels) 50 150 mg at bedtime 100 400 mg t.i.d. 20 mg every other day x 2 wks, then/day 200 mg t.i.d. 25 mg t.i.d.-q.i.d. 100 mg t.i.d. (titrate with blood levels) 2 5 - 2 0 0 mg b.i.d. 5 0 - 1 0 0 mg at bedtime

Ilioinguinal Neuropathy The ilioinguinal nerve (LI-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 anterosuperior iliac spine and courses just beneath the anterior leaf of the inguinal canal. Here it exits out of the superficial inguinal ring or pierces at the ring to become a sensory nerve to overlying skin. It supplies sensory innervation to the groin, mons, labia, and inner thigh. The most common injury is entrapment by suture ligature in the lateral edges of Pfannenstiel incision or at the time of needle bladder suspension. Typically, the diagnosis may be delayed while visceral etiologies are suspected and treated unsuccessfully. The 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

transection that would make further improvement very difficult: neuroma formation and 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 lum-

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Peripheral Neuropathies Causing Chronic Pelvic Pain Perry

lliohypogasiric Nerve llioinguinal Nerve l,atcral Femoral Cutaneous Nerve t,emoralRa rlllis o f (;enitofc'moral Nerve

Anterior lliacCrestSuperim"

FIGURE 4. I l i o h y p o g a s t r i c - i l i o i n g u i n a l n e r v e block.

reproduce the exact pain by needling and to obtain complete relief after anesthetizing to be certain of the diagnosis. 5 Treatment of several blocks for desensitization and medical therapy should be tried before transection is done. No laparoscopic treatment of this neuropathy has been reported.

lliohypogastric /

Genitofemoral Neuropathy

//Psoas Muscle

Ilioinguinal Nerve~---

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

N e r v e ( ;)~ ~f " ~ enitofemoral Femoral -Si ~ GenitalBranch u .........

Genitofemoral Nerve Anatomy FIGURE 5. Location of g e n i t o f e m o r a l nerve.

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mons pubis and labium 1-najus. The femoral branch supplies the skin of the femoral triangle. The most common injury is to the right genitofemoral nerve. It may occur when appendectomy causes perineural 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 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 blocks. Blocking the ilioinguinal nerve affords no relief, but a trans-psoas genitofemoral block produces complete relief. 6

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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 and traverses the retroperitoneum lateral to 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. Symptoms are often called meralgia paraesthetica. Decompression at the inguinal ligament usually alleviates this pain. After anesthetic blocks make the diagnosis, neurolysis is the treatment of choice if conservative treatment fails. 7 9 At least 80 etiologies for this neuropathy have been described. Some of the more common are pressure from tight or wide belts, tight pants, postsurgical scars after abdominal surgery, pregnancy, iliac bone graft harvest, ascites, obesity, abdominopelvic mass, and metabolic neuropathies. 9

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Cutaneous Nerve J

FIGURE 6. Route and sites of possible compression of the lateral femoral cutaneous nerve. The nerve usually courses deep to the lateral end of the inguinal ligament, superficial to the sartorius muscle. The nerve may (1) overlie the anterior lilac wing, (2) pass between two slips of the inguinal ligament, or (3) pass deep to or (4) through the sartorius muscle, and (5) may be compressed distally when it passes through deep fascia.

behind the ischial spine (Figure 7). 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 areas bordered by the inferior pubic ramus superiorly, labiocrural folds laterally, and intergluteal fold posteriorly (Figure 8). 3 Nerve injury can be caused by prolonged compression or stretching as in the second stage of labor. Surgical injuries have been reported with sacrospinous vaginal vault suspension, vaginal laceration repairs, and various types of episiotomies. Other patients developed pudendal neuropathy after straddle injuries, prolonged motorcycle riding, and laser treatment to the vulva and perineum. Diagnosis can be made easily with pudendal nerve block. Symptoms of this neuropathy range from constant burning to intense lancinating pain that can be unilateral or bilateral. The neuropathy is often accompanied by pelvic floor myalgia and spasm.

Pudendal Neuropathy The pudendal nerve ($2-4) shares the dorsal horn transmission cells with the cervix, uterosacral, and vulvovaginal areas. It is a mixed sensory and motor nerve. Efferent (motor) neuropathic symptoms usually accompany the afferent neuropathy that manifests as CPR Sacral motor neuropathy causes abnormal bladder and bowel function, but this is not discussed here. The pudendal nerve enters the pelvis through the lesser sciatic foramen and then immediately wraps

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Peripheral Neuropathies Causing Chronic Pelvic Pain Perry

N e u r o m a F o r m a t i o n and M a l a d a p t i v e N e u r o n a l Plasticity As stated, these are the two most feared complications of peripheral nerve transection. A neuroma is a bulbous, exquisitely sensitive terminal of a cut nerve. It can be very painful if touched or can generate spontaneous action potentials and recurrent neuropathic pain. Currently, no reliable therapy is available for neuromas. Maladaptive neuronal plasticity is based on 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 that was transected. Examples 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 frequency of either disorder after neurectomy for treatment of CPP. Experience is limited, and patients should be aware of these potential conditions. J0

Ischlal Spine - -

Pudendal

Artery

Levator Ani M u s c l t ' (cut edge)

/ Pudendal i Nerve Anatomy ] FIGURE 7. Pudendal nerve.

Conclusion

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Clinicians responsible for the care of women must understand the relationship between peripheral neuropathies and CPR Because of viscerosomatic convergence, neuropathic pain should be considered in all patients who are unresponsive to conventional therapy. Knowledge of innervation patterns and nerve block techniques is necessary to diagnose and treat these long-suffering women.

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References [.

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1. Travell JG, Simmons DG: Myofascial Pain and Dysfunction: The Trigger Point Manual: The Lower Extremities. Baltimore, Williams & Wilkins, 1983, pp 1-4

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I Sacral Nerve LDistribution

2. Fields HL: Pain. New York, McGraw-Hill, 1987, pp 79-97

FIGURE 8. Approximate dermatomes of perineum, S2-4. Because of motor functions of this nerve, neurectomy is not an option. Repeated pudendal blocks (with and without steroids), cryoneurolysis, and transcutaneous electrical stimulation yield mixed results. Sacral nerve stimulation with an implantable device is being investigated. Neuromagnetic therapy is also undergoing clinical trials.

. Rogers RM: Basic pelvic neuroanatomy. In Chronic Pelvic Pain: An Integrated Approach. Edited by JF Steege, DA Metzger, BS Levy. Philadelphia, WB Saunders, 1998, pp 31-58

4. Kline DG, Hudson AR: Nerve Injuries. Philadelphia, WB Saunders, 1995, pp 327-330

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5. Monga M, Ghoniem GM: Ilioinguinal nerve entrapment following needle bladder suspension procedures. Urology 44(3):447-450, 1993

8. Macinol ME Thompson WF: Idiopathic meralgia paresthetica. Clin Orthop 254:270 274, 1999

6. Perry CP: Laparoscopic treatment of genitofemoral neuralgia. J Am Assoc Gynecol Laparosc 4(2):231-234, 1997

9. Williams PH, Trzil KP: Management of meralgia paresthetica. J Neurosurg 74:76-80, 1991

7. Broin EO, Homer C, Mealy K, et al: Meralgia paraesthetica following laparoscopic inguinal hernia repair. Surg Endosc 9:76-78, 1995

t0. Kennedy EM, Harms BA, Starling JR: Absence of maladaptive neuronal plasticity after genitofemoralilioinguinal neurectomy. Surgery 116(4):665-671, 1994

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