Abstract
Nerve pain is more often than not a cause of pelvic pain. This is particularly true in patients in whom pain started after pelvic trauma, surgery, or vaginal delivery. Unfortunately, most of gynecologists who are often physicians of primary contact for mesh patients are not trained in recognizing and treating patients with nerve injury pain. Patients with nerve injury pain can almost always pinpoint the moment when the pain started. It is often unilateral and neuropathic in nature. Patients have a burning, tingling sensation often associated with increased sensitivity to stimuli analogous to skin pain after sunburn. Pain is often exacerbated by body movements and certain body positions. It is very important for the first provider who sees patients with pelvic pain that pain may be related to nerve injury because expeditious treatment increases the chances of recovery. It is also important to instruct patients to avoid activity that started the pain in the first place and minimize activity that exacerbates the pain. Trial of muscle relaxants, gabapentin, or pregabalin may be appropriate first treatment; however, prompt referral to physical therapy, neurology, or a specialized pelvic pain center is often necessary.
Editor’s Introduction
Nerve pain is more often than not a cause of pelvic pain. This is particularly true in patients in whom pain started after pelvic trauma, surgery, or vaginal delivery. Unfortunately, most of gynecologists who are often physicians of primary contact for pelvic pain patients are not trained in recognizing and treating patients with nerve injury pain. Patients with nerve injury pain can almost always pinpoint the moment when the pain started. It is often unilateral and neuropathic in nature. Patients have a burning, tingling sensation often associated with increased sensitivity to stimuli analogous to skin pain after sunburn. Pain is often exacerbated by body movements and certain body positions. It is very important for the first provider who sees patients with pelvic pain that pain may be related to nerve injury because expeditious treatment increases the chances of recovery. It is also important to instruct patients to avoid activity that started the pain in the first place and minimize activity that exacerbates the pain. Trial of muscle relaxants, gabapentin, or pregabalin may be appropriate first treatment; however, prompt referral to physical therapy, neurology, or a specialized pelvic pain center is often necessary.
Introduction
Chronic pain is defined by the International Academy for the Study of Pain as “pain without apparent biological value that has persisted beyond the normal tissue healing time (usually taken to be 3 months)” [1]. It has been estimated that more than 30% of Americans suffer from chronic pain. According to the 2011 Institute of Medicine Report “Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research,” pain is a significant problem costing US society at least $560 to $635 billion annually [2]. Although repeat estimates have not been published, the rates of chronic pain and accompanying opioid abuse have only been increasing. The understanding of the pathophysiology of pain is constantly evolving and this chapter attempts to summarize our current knowledge.
Pertinent Anatomy
Abdominal and pelvic pain can originate from the gynecological, urological, gastrointestinal, neurological, or musculoskeletal systems. Often pain may stem from multiple systems simultaneously. To understand the complex interplay between these systems and structures, one must understand the neuroanatomy involved. Abdominal and pelvic pain can stem from the somatic system (T12–S5) or the visceral system (T10–S5). Somatic pain arises from skin, muscles, joints, and the pleural and peritoneal lining. Visceral pain arises from the hollow organs of the abdominopelvic cavity including the bladder, bowel, uterus, and fallopian tubes. The complexity of pelvic pain is in part related to the interactions between these two systems. Of importance, the visceral nerves converge on the same somatic levels in the thoracic, lumbar, and sacral spinal cord. This is termed viscerosomatic convergence and can result in visceral pain being perceived in somatic regions. With time, muscles innervated by the stimulated somatic nerves can develop trigger points leading to worsening somatic pain. Viscerovisceral convergence can also occur, leading to referred symptoms in other organs. This neural convergence can also be useful therapeutically to treat pain.
Somatic Pain
Peripheral neuropathic pain typically has a very specific localization along nerve distributions. Nerve injury can occur through a variety of mechanisms such as trauma, stretch, compression, fibrosis, or entrapment. Understanding neuroanatomical relationships, especially within the pelvis, is vital to both diagnosis and treatment.
The abdominal wall is innervated by the thoracoabdominal intercostal nerves (T6–T12) along with the iliohypogastric and ilioinguinal nerves. The intercostal nerves travel between the transversus abdominis and internal oblique muscles within the transversus abdominis plane (TAP). At the midaxillary line, perforating branches diverge to innervate the lateral abdominal wall. The segmental nerves of T6–T9 perforate the abdominal wall along the path of the anterior costal margin. The remaining intercostal nerves perforate the rectus abdominis sheath, providing sensation to the anterior abdominal wall. Near the anterior superior iliac spine (ASIS) the ilioinguinal and iliohypogastric nerves, which previously ran within the TAP, transition to travel between the internal and external oblique muscles.
The iliohypogastric nerve arises from the T12–L1 spinal segments. It travels through the psoas and transversus abdominis muscle, coursing medially below the internal oblique. It splits into two branches, with the anterior branch piercing the external oblique muscle at the level of the ASIS to provide cutaneous sensation to the mons pubis and the lateral branch to the posterolateral gluteal region. This nerve converges on the dorsal horn structures shared by the distal fallopian tube and ovary.
The ilioinguinal nerve arises from L1–L2 spinal segments. It follows a course similar to that of the iliohypogastric nerve but enters the inguinal canal 2 cm medial to the ASIS. It exits the superficial inguinal ring to provide sensation to the groin, labia majora, and the medial aspect of the thigh. It converges with the neurons of the proximal fallopian tube and uterine fundus.
The genitofemoral nerve also arises from the L1–L2 spinal segments and converges with neurons from the proximal fallopian tube and uterine fundus. It courses through the psoas muscle, exiting along its medial border at the L4 vertebral level, where it divides into a genital and femoral branch. The genital branch supplies the mons pubis and labia majora while the femoral branch supplies the skin of the femoral triangle. It can commonly be injured as a result of post-appendectomy fibrosis or hernia repair.
The obturator nerve arises from L2–L4 spinal segments and travels along the pelvic sidewall, exiting the pelvis through a tunnel in the pubic ramus, and then divides into two branches. The anterior branch sends motor fibers to the adductor longus, adductor brevis, and gracilis and sensory fibers to the distal medial two thirds of the thigh. The posterior branch sends motor fibers to the adductor magnus and sensory fibers to the knee joint.
The lateral femoral cutaneous nerve arises from L2–L3. It courses over the iliacus muscle, passing under the inguinal ligament to provide sensory fibers to the upper outer thigh. Although it does not innervate any structures in the pelvis, it converges with neurons from the uterus in the dorsal horn.
The pudendal nerve arises from S2–S4. It carries motor, sensory, and autonomic fibers. The sensory component of the nerve innervates the clitoris, labia, distal one third of the vagina, perineum, and rectum. The motor component innervates the external urethral sphincter, perineal muscles, and external anal sphincter. After exiting the sacrum, it travels inferiorly and laterally on the anterior surface of the piriformis muscle. Once it enters the gluteal region it joins the pudendal artery and vein, which accompany the nerve through its course. It briefly exits the pelvis through the greater sciatic foramen and reenters through the lesser sciatic foramen, where it passes between the sacrospinous and sacrotuberous ligaments approximately 1 cm medial to the ischial spine. In this location the nerve is the most dorsal structure. It then travels through the aponeurosis of the obturator internus muscle, an area referred to as Alcock’s canal. On exiting the canal, it divides into the inferior rectal nerve, the perineal nerve, and the dorsal clitoral (penile) nerve. The pudendal nerve converges in the dorsal horn on neurons from the cervix, uterosacral ligaments, and vulvovaginal region. Reference Chapter 15 for further detailed information about the pudendal nerve and its involvement in chronic pelvic pain.
The nerve to the levator ani is separate from the pudendal nerve. This nerve arises from S3–S5 and travels along the superior surface of the coccygeal muscle and innervates the coccygeus, iliococcygeus, pubococcygeus, and puborectalis [3]. The nerves to the levator ani and the pudendal nerve run approximately 5–6 mm from one another at the level of the ischial spine; therefore, a pudendal nerve block often results in a block of both.
Visceral Pain
Visceral pain is mediated through the autonomic nervous system via the sympathetic and parasympathetic divisions. The autonomic innervation of the pelvis is via the superior and inferior hypogastric plexi. The superior hypogastric plexus overlies the L4–S1 vertebrae along the sacral promontory. It contains sympathetic fibers from the lumbar sympathetic chains and the aortic plexus. The inferior hypogastric plexus is formed by the hypogastric nerves carrying sympathetic fibers from the superior hypogastric plexus and parasympathetic fibers from the pelvic splanchnic nerves. Sympathetic fibers inhibit peristalsis of organs and stimulate muscle contraction during orgasm. Parasympathetic fibers stimulate peristalsis of the bladder and rectum to facilitate urination and defecation as well as erectile function.
The ganglion impar is a singular structure located retroperitoneally at the level of the sacrococcygeal junction. It is the terminal fusion of the two sacral sympathetic chains, and it provides nociceptive and sympathetic input to the perineum, distal rectum, urethra, and vagina. Blocks of the ganglion impar are used to treat intractable perineal pain, poorly localized visceral pelvic pain, and coccydynia.
Acute Pain Processing
To understand chronic pain, it is first important to understand the physiology of acute, nociceptive pain processing. Pain processing involves multiple steps: transduction, transmission, perception, and modulation. Any insult or injury to tissue activates nociceptors. These are free nerve endings that serve as sensory receptors to detect damage or threat of damage to tissue. The ability to sense pain is a protective biological mechanism. Nociceptors are found in the dermis, muscles, connective tissues, synovia, parietal pleura, and peritoneal membranes. Nociceptive activation occurs from stimulation of either visceral or somatic structures. Different classes of nociceptors respond to different stimuli such as mechanical, thermal, or inflammatory trauma. Aδ fibers are small myelinated fibers that sense temperature and sharp pain and conduct at a rate of 5–30 m/s [4]. Aβ fibers sense nonpainful touch. C-fibers are small-diameter unmyelinated axons that respond to multiple types of stimuli such as dull pain, temperature, and itch. They conduct signals at a rate of 0.4–1.4 m/s and represent about 70% of all nociceptive fibers in the body. Somatosensory nociceptors have a single process emanating from the cell body in the dorsal root ganglion (DRG) that bifurcates, sending one axon to the peripheral tissue and another to synapses on second-order neurons within the dorsal horn of the spinal cord [5]. This functions to reduce the risk of conduction failure.
Initial injury leads to localized tissue damage that produces neurogenic inflammation and release of histamine, prostaglandins, bradykinin, and substance P at the site of injury. These peptides are sensed at the free nerve ending and transduced into an electrical signal that is then transmitted to the dorsal horn. Nociceptors are excitatory neurons and release glutamate as a primary neurotransmitter along with other peptides such as substance P, calcitonin gene-related peptide (CGRP), and somatostatin [5]. The second-order neuron in the spinal cord is then activated within the anterolateral system. The anterolateral system has both a direct pathway, in which Aδ fibers run within the spinothalamic tract, and an indirect pathway, in which C-fibers run within the spinoreticular tract [6]. The Aδ fiber second-order neurons cross over to the contralateral spinothalamic tract and transmit the information to the thalamus, where pain is perceived. They then synapse onto a third-order neuron that relays the signal to the somatosensory cortex for localization. The C-fiber first-order neurons first synapse onto interneurons. These interneurons then synapse on second-order neurons within the ipsilateral and contralateral spinoreticular tracts that convey information into the reticular formation in the brainstem. Impulses from the reticular formation are then relayed bilaterally to the thalamus, where they are perceived as well as relayed to the primary somatosensory cortex, hypothalamus, and limbic system.
Noxious stimuli or injury to tissue induces physiological processes meant to signal a problem and protect us from further injury. Following tissue damage, locally noxious substances are released leading to a decrease in the threshold of C-fibers for activation and pain perception. This is termed primary hyperalgesia. This process occurs by upregulation of existing receptors that results in an increased response to the same concentration of neurotransmitters or mechanical stimulus. There is also an increase in the number of receptors in response to nerve growth factor. This combination results in primary hyperalgesia of the injured area. The area surrounding the injury is termed the “zone of flare,” which becomes increasingly sensitive to mechanical stimuli (secondary hyperalgesia) as well as exhibiting pain in response to innocuous stimuli (allodynia) [7]. This process is termed peripheral sensitization and evolutionarily served as a protective process to allow us to heal. For example, if you burn your hand, the injured tissue releases various noxious chemicals, which leads to neurogenic inflammation and a primary zone of injury. Surrounding uninjured tissue becomes further sensitized as a protective mechanism to keep you from grabbing things with your hand and potentially injuring it further. This eventually resolves because of plasticity in the nervous system. Once healing takes place, the system can and typically does revert back to its preinjured state.
The experience of pain is much more than the detection of noxious stimuli. Emotions have a significant effect on our experience of pain. According to the International Association for the Study of Pain (IASP), pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage [8]. The perception of pain is influenced by mood, past experiences, and expectations and in short, it is the affective component that makes pain painful. While the somatosensory cortex determines characteristics such as location and duration, the anterior cingulate cortex (ACC) and insula, part of the limbic system, are responsible for the emotional aspects of pain perception. Our understanding of this aspect of pain sensation is more limited. A number of studies have found that even observing another individual in pain can activate some of these same areas of the brain in the observer. This can result in “priming” of the brain and effect the subject’s subsequent experience of the same noxious stimulus [9].
Lastly, pain can undergo modulation by descending inhibitory pathways. Pain modulation involves several regions of the central nervous system (CNS), including the prefrontal cortex, ACC, insula, and periaqueductal gray (PAG). These regions modulate pain by either inhibiting or facilitating transmission of nociceptive input at the synapse of the first- and second-order neurons within the dorsal horn [10]. Serotonin, norepinephrine, and dopamine are the primary neurotransmitters involved in this inhibition. Modulation can be disrupted with the development of chronic pain.
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