Introduction

The complexity of chronic abdominal pain requires an understanding of its associated physical and psychosocial features as it may cause severe disruptions in functional capacity and quality of life (QOL) ( ). Complexity of chronic abdominal pain is costly to society, causing frequent doctor visits, diagnostic imaging, and surgery interventions that may not result in expected pain relief ( ). Chronic visceral pain is frequently poorly localized and referred to somatic structures, sometimes confusing the clinical picture and delaying definitive diagnosis ( ). Moreover, only 50%–70% of patients with abdominal pain have established definitive etiology of their pain ( ). The research helps in understanding visceral pain pathways and the dorsal column’s (of the spinal cord) role in transmission and amplification of chronic abdominal pain. Exciting data in both animal models and human subjects suggest greater therapeutic role of spinal cord stimulation (SCS) to maintain profound analgesia and improved functional capacity when used for complexity of chronic abdominal pain.

Mechanisms of Abdominal Pain

Complexity of chronic abdominal pain pathophysiology includes physical, emotional, and perceptual integration that no longer serves proper adaptive and protective roles. Hyperalgesia and allodynia may result from such maladaptive neuroplastic changes involving peripheral and central sensitization. A bidirectional neural circuit, referred as “Brain-gut axis,” integrates peripheral (sensory, motor, and autonomic) and central nervous system (CNS) (spinal cord as well as midbrain and cortex) input to end organs (GI mucosa, glands, muscles,etc.) and dictates normal gastrointestinal (GI) physiology ( ). Imbalance of brain-gut axis may be linked to both, functional GI disorders, as well as chronic visceral pain ( ). Despite historical assumptions that chronic visceral pain is of nociceptive origin, current evidence implies a neuropathic pain source ( ).

Polymodal visceral nociceptors, unevenly distributed in the abdomen, respond to either mechanical, thermal, and chemical stimuli ( ). Autonomic and spinal nociceptors project mainly on unmyelinated C-, or Aδ-fibers. On their path to the dorsal horn (DH) of the spinal cord, visceral spinal afferents project collaterals to both prevertebral and paravertebral ganglia allowing for modulation of autonomic response to sensory stimuli. Convergent input somewhat explains frequent referral to somatic structures ( ). In animal studies, repeated colonic distension results in the enlargement and convergence of visceral afferent receptive fields, demonstrating the CNS involvement in visceral hypersensitivity ( ) and generation of chronic visceral pain ( ).

Dorsal columns (DCs) transmit and modulate (amplify) visceral pain ( ). Long-standing chronic stimulation and/or inflammation of peripheral visceral nerves results in plastic changes of signal transduction of postsynaptic DC neurons ( ).

The role of DCs in processing of visceral information seems to be excitatory and central to pain processing, where, in turn, surgical lesions of the DC provides significant improvements in cancer-related abdominal and pelvic pain ( ). Consequently, less invasive treatment options would benefit a larger patient population with benign pain etiologies.

Causes of Chronic Non-Malignant Abdominal Pain

Prevalence of the complexity of chronic abdominal pain does not differ with age, ethnicity, or geographic regions; however, gender seems to play an important role as more women have abdominal pain than men. Inflammatory bowel disease (IBD), mainly in form of Crohn’s disease and ulcerous colitis, is a disease of young adults with a peak incidence from 15 to 35 years of age, while few patients acquire disease between the ages of 50–60 ( ). Risk factors for IBD-associated complexity of chronic abdominal pain include preexisting psychiatric illness, female gender, smoking, and longer duration of disease ( ). SCS may be an interesting therapeutic option for this patient population, but only for the treatment of persistent complexity of chronic abdominal pain during clinical remission from disease. The main reason is the possibility for SCS to conceal an acute inflammatory event, including bowel perforation, or ileus. SCS may be a very useful therapeutic alternative to continued use of stronger opioids during the clinical remission of IBD that is seen in about 20% of the patients ( ). Another neuromodulation therapy for IBD includes vagal nerve stimulation. See Chapter 126 , Chapter 127 .

Chronic pancreatitis is a frequent cause of the complexity of chronic abdominal pain. Moreover, chronic or intermittent pain is present in about 80%–90% of chronic pancreatitis patients, with the most significant chronic opioid use among all of the complexity of chronic abdominal pain syndromes ( ). Postsurgical adhesions are a known cause of the complexity of chronic abdominal pain with an incidence of between 45% and 90% of the patients undergoing abdominal surgical procedures. Risk factors for development of chronic pain related to intraabdominal adhesions include open procedures, use of implants (i.e., mesh), and the presence of a contaminated surgical field. Surgical procedures with high incidence of postsurgical complexity of chronic abdominal pain are cholecystectomy, herniorrhaphy, and adhesiolysis. Preexisting psychiatric illness, female gender, and younger age provide higher risk for complexity of chronic abdominal pain after abdominal surgery ( ).

Approximately 10%–30% of the complexity of chronic abdominal pain originates from the abdominal wall. Chronic abdominal wall pain (CAWP) is defined as pain in a fixed location less than 2.5 cm of diameter lasting more than a month. Entrapment of the cutaneous abdominal nerve branches (ACNES) seems to be most frequent cause and is usually the direct result of surgical trauma. CAWP is frequent in patients with chronic visceral disease ( ).

Establishing a Diagnosis

Careful history and complete physical examinations help guide diagnostic testing. Clinical presentations may vary. Excluding correctable organic diseases is essential, but many times repetitive diagnostic testing is unnecessary to confirm a functional disorder. In general, nerve blocks may be of diagnostic, therapeutic, or even of prognostic value. The cause of the complexity of chronic abdominal pain often remains elusive in a significant group of patients despite extensive work-ups to determine the source of the abdominal pain. In such cases, various nerve blocks may have both diagnostic and therapeutic values. There are two types of blocks that are commonly performed for abdominal pain. Sympathetic nerve blocks are used to block the splanchnic nerves, celiac plexus, superior hypogastric nerve plexus, or ganglion of Impar. Somatic nerve blocks used for the complexity of chronic abdominal pain include paravertebral nerve block, intercostal nerve block, Transversus Abdominis Plane (TAP) block, rectus abdominis sheath block, and blocks of the ilioinguinal, iliohypogastric, and genitofemoral nerves. These blocks may help determine visceral versus somatic pain and guide treatments ( ).

Inspection of the abdomen may provide a first clue on the possible chronic pain source. For example, surgical scars from previous laparotomies might be present. When associated with localized allodynia and/or hyperalgesia, one should consider possible nerve damage and/or neuroma. CAWP is best diagnosed based on patient’s history and physical examination. The pain is usually well localized with point tenderness on palpation. On the contrary, visceral pain is usually poorly localized. Carnett’s test ¹

1 Carnett’s test is a simple clinical test in which abdominal tenderness is evaluated while the patient tenses the abdominal muscles. It is useful for differentiating abdominal wall pain from intraabdominal pain.

Psychosocial assessment is an essential component of the diagnostic process. Psychometric tests such as depression inventories are useful tools. In addition to history and physical examinations, many physicians suggest ordering additional tests on the basis of objective findings rather than pain severity. Diagnostic procedures are often required to establish appropriate diagnosis ( ).

Differential retrograde epidural block (DREB) may be used to help differentiate visceral from nonvisceral sources of pain. Studies suggest that responses to DREB may be a useful predictor of treatment responses ( ). The diagnostic value of DREB relies on the sensitivity of various nerve fibers to local anesthetics. Sympathetic fibers and visceral afferent nerves have a higher C to Aδ fiber ratio (10:1) and are more sensitive to local anesthetic blockade than somatic nociceptive fibers. A local anesthetic (usually 2% 3-chlorprocaine or 1% lidocaine 10–30 cc) serves to differentiate between predominantly visceral, somatosensory, or central chronic pain, while saline injections may help differentiate placebo effects, malingering, and sometimes psychogenic source of pain. However, the validity of DREB remains to be established and if combined with other clinical information, may be only suggestive of visceral, somatic, or central source of pain ( ).

TAP block is a newer diagnostic and therapeutic technique for somatic abdominal pain. TAP provides analgesia to the entire anterolateral abdominal wall between the costal margin and the inguinal ligament and establishes diagnosis of abdominal wall pain ( ).

Spinal Cord Stimulation for Chronic Abdominal Pain

SCS has been used for years to treat numerous chronic pain syndromes (see Table 115.1 ), but currently approved indications in the United States exclude the use of SCS for the complexity of chronic abdominal pain. The mechanism of SCS neuromodulation resulting in pain relief for complexity of chronic abdominal pain is not completely understood; however, a number of hypotheses have been proposed ( ). Activation of supraspinal pain modulatory pathways by SCS could account for its analgesic effects ( ). It is possible that the SCS modulates the afferent signal in the DH by “closing the spinal gate” by activating large, myelinated fibers that inhibit small nociceptive fibers ( ) or by the release of inhibitory neuromodulators, such as gamma-aminobutyric acid ( ). Alternatively, SCS could provide a blockade of nerve conduction ( ), possibly by antidromic activation. Neurosurgical data (discussed earlier) suggests that lesioning the postsynaptic DC pathway via midline myelotomy interferes with the generation and maintenance of chronic visceral pain by removing the ascending limb of a facilitatory pain loop. It is possible that the electrical field from SCS also interrupts this ascending limb without physical lesioning of the pathway. Another possible mechanism for SCS is downregulation of intersegmental or supraspinal sympathetic outflow ( ). Regardless of the exact mechanism of SCS, the resultant neuromodulation in the DH provides great potential for the treatment of the complexity of chronic abdominal pain Fig. 115.1 .

Basic Science

SCS has been studied in rats with and without postinflammatory visceral hypersensitivity during colonic distention. The visceromotor response (VMR) elicited by colonic distention is suppressed by SCS in both normal and sensitized rats ( ). In addition, the authors of this study reported that the effect of SCS on VMR continues to be observed for a prolonged duration, even after SCS is discontinued. These data are consistent with previous SCS data for the treatment of refractory angina pectoris ( ) and suggests that SCS may result in persistent, complex alterations of neural activity and neurotransmitter release. SCS electrodes placed in either cervical or lumbar regions have been shown to inhibit lumbosacral neural responses to colonic distention in rats ( ). These data lead the authors to hypothesize that SCS may cause antidromic activation of peripheral sensory fibers, negating the afferent input ( ).

Clinical Evidence in Humans

At this time, there is very compelling yet limited data on decreased pain intensity and improved functional capacity in patients with a wide variety of chronic, visceral pain syndromes. Numerous case reports and case series document positive treatment outcomes of SCS for chronic visceral syndromes including mesenteric ischemic pain ( ), esophageal dysmotility ( ), gastroparesis ( ), irritable bowel syndrome (IBS) ( ), chronic pancreatitis ( ), familial Mediterranean fever ( ), posttraumatic splenectomy ( ), generalized complexity of chronic abdominal pain ( ), painful abdominal visceral adhesions ( ), and various other dysmotility syndromes ( ). While these studies provide encouraging results, the full significance of their findings needs to be validated by higher levels of evidence including randomized, placebo-controlled trials (RCTs).

The first reported use of SCS for refractory abdominal pain was in patient with chronic mesenteric ischemia. Leads were placed in the epidural space at T6 spinal level and the patient received long-term, almost complete, relief of the pain ( ). Several case studies for esophageal dysmotility ( ) and larger case series including patients with gastroparesis ( ) suggest that, in addition to providing visceral pain relief, SCS may improve dysmotility (function) of functional GI disorders. This was supported by a small cross-over study assessing effectiveness of SCS for the pain from IBS. In that study, longevity of pain control was well documented, as well as an improvement in number of diarrheal episodes in the few patients who received SCS ( ).

Improvements in chronic abdominal pain (CAP) scores were best documented in patients with chronic pancreatitis ( ). See Table 115.1 . Those patients report a significant pain relief with a mean visual analog score (VAS) decrease of 4–6, requiring less than half the narcotics when compared to prior to initiation of SCS.

Table 115.1

Published Studies on Use of Spinal Cord Stimulation for Treatment of Chronic Abdominal Pain

Origin of Chronic Abdominal Pain by Reported Diagnosis	Study/Case Series/Case Report	Number of Patients Studied
Mesenteric ischemia	(46)	1
Esophageal dysmotility	(47)	1
Irritable bowel syndrome	(49)	1
Chronic pancreatitis	(52)	5
Familial Mediterranean fever	(55)	2
Gastroparesis	(48)	2
Chronic pancreatitis	(51)	1
Chronic pancreatitis	(53)	1
Chronic pancreatitis, abdominal adhesions, gastroparesis, mesenteric ischemia, postgastric bypass pain	(50)	35
Chronic pancreatitis, post-surgical intraabdominal adhesion, gastroparesis	(57)	76
Chronic pancreatitis	(56)	30
Chronic pancreatitis, post-surgical, inflammatory bowel disease	(54)	26
Irritable bowel syndrome	(58)	9

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