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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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