Spinal Cord Stimulation for Visceral Abdominal Pain

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Chapter 12 Spinal Cord Stimulation for Visceral Abdominal Pain

Leonardo Kapural

Chapter Overview

Chapter Synopsis: Visceral abdominal pain is among the many pain states that can be improved by electrical stimulation of the spinal cord (SCS). This chapter examines how SCS works to alleviate visceral pain, including considerations of the unique features of visceral pain transmission, which differ from somatic pain sensations. Spinal afferents from the viscera convey predominantly nociceptive (noxious) information, whereas vagal afferents carry information about the physiological state. Visceral pain is generally poorly localized and referred to somatic areas, although painful responses arising from different visceral organs vary. As in other indications, SCS is thought to relieve chronic visceral pain in several ways. Spinal gating of pain signals from small-fiber afferents may be decreased by continued stimulation of large-fiber, nonnociceptive afferents. Suppression of sympathetic efferents may also reduce the conditions leading to painful states, particularly ischemia. Because the underlying pathophysiology of visceral pain can vary dramatically among patients, it is crucial to determine proper electrode lead placement for implantation specific to the condition. Patient selection is of particular importance in treating visceral abdominal pain with SCS, and the treatment should be incorporated into a multidisciplinary plan.

Important Points:

Proper patient selection seems to provide better outcome of SCS for visceral abdominal pain.

Appropriately long trial of SCS is required to objectively assess patient’s improvements in pain and function.

Psychological evaluation and interdisciplinary committee for implantable devices assessment are now frequently required before conducting an SCS trial and are an essential part of the patient selection process.

Collaboration and consultation with the referring physician (frequently gastroenterologist) and continued exchange of information on implantation techniques should advance our understanding of mechanisms and refine this novel technique of SCS for abdominal visceral pain.

Clinical Pearls:

In most patients SCS leads are positioned with their tips at the level of the T5 vertebral body.

Midline position of the leads is most frequently used, and the number of leads used for trialing is not related to the success of the trial.

Retrograde differential epidural block can assist in proper selection of patients by identifying those who have predominantly visceral abdominal chronic pain.

Clinical Pitfalls:

On the basis of the currently available data, SCS for abdominal pain may be an exciting therapeutic option for patients with severe visceral pain. Food and Drug Administration (FDA) approval of the new indication for SCS is still required; that process should be initiated as soon as possible in the form of a randomized, prospective clinical trial.

Patients who require repeated magnetic resonance imaging (MRI) for ongoing monitoring of the disease process should not have SCS leads implanted.

Although there is no evidence that recurrent inflammatory acute pancreatitis episodes could be concealed with use of SCS, those painful episodes seem to respond poorly to such treatment.

Introduction

Abdominal pain is one of the most frequent complaints to a primary care physician, accounting for nearly 2.5 million office visits a year.¹ In many patients who present with abdominal pain, a definitive diagnosis can be made, but in 35% to 51% of patients, no identifiable cause is found.² There are approximately 2 million patients in the United States who currently experience severe abdominal pain. Most of them undergo a multitude of imaging studies and consultations with gastroenterology and surgery before being referred to a chronic pain specialist.^3,⁴ Despite adequate evaluations by multiple physicians, the etiology of some abdominal pain remains unknown.

Characteristics of visceral pain have been described extensively in literature as poorly localized, referred to somatic structures, and not evoked by all viscera.⁵ Visceral nociceptors are capable of responding to a variety of noxious stimuli such as mechanical and chemical stimuli. However, pain is not necessarily evoked from all of the viscera or from visceral injury. Some internal organs lack nociceptors and can be damaged without the individual perceiving pain. Spinal and vagal afferent fibers convey sensory information from the upper gastrointestinal tract to the central nervous system. Vagal afferents transmit predominantly physiological information, whereas spinal afferents transmit noxious information.⁶ The dorsal root ganglia of the spinal nerves contain cell bodies of both vagal and spinal afferents. Vagal afferents enter the brainstem, whereas spinal afferents enter the spinal cord, making synaptic connections with second-order neurons, thereby conveying visceral information to the central nervous system. The ascending spinal pathways project to the thalamic nuclei. Afferent fibers with visceral and somatic information converge onto spinothalamic and spinoreticular pathways.

The role of the dorsal column pathway in transmission/amplification of visceral pain has been described more recently by Palacek and Willis ⁷ and Palacek,⁸ and its role as participating in the neuromodulation of visceral painful information by spinal cord stimulation (SCS) has been hypothesized.⁹ Still the spinothalamic tracts are considered to be the major pathways for visceral nociception.¹⁰

Spinal sensitization process following tissue injury is characterized as a leftward shift in pain sensation/behavior (hyperalgesia) and enlargement of receptive fields within cutaneous areas able to activate the dorsal horn neuron (allodynia). This pattern is analogous to the change in functional bowel disorders, where a leftward shift in the stimulation-pain curve and enlargement of the somatic referral area occur.¹¹ The expansion of convergent cutaneous fields after repetitive distension of a viscus indicates the presence of a central mechanism contributing to the alteration of excitability of central neurons.¹² Brain-gut axis abnormalities can manifest as gastrointestinal motility and functional disorders. Because the neural activity plays a major role in these disorders, interventions aiming to modulate these processes can possibly improve the symptoms.