Spinal Cord Stimulation for Chronic Abdominal Pain

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 ( ).