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PAIN MEDICINE

Gastrointestinal Symptoms Secondary to Implanted Spinal Cord Stimulators

Department of Anesthesiology, Baystate Medical Center, Springfield, Massachusetts

Address correspondence and reprint requests to Neil Roy Connelly, MD, Department of Anesthesiology, 759 Chestnut St., Springfield, MA 01199. Address e-mail to neil.roy.connely{at}bhs.org

	Abstract

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IMPLICATIONS: We report severe gastrointestinal symptoms in two patients who had implanted spinal cord stimulators. These side effects were severe enough to require cessation of the stimulation, even though the patients reported significantly improved analgesia. It is important for clinicians caring for patients with these devices to be aware of these potentially severe side effects.

	Introduction

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Spinal cord stimulation is used in patients for pain from a variety of origins. It was first introduced in 1967 by Norman Shealy et al (1). It is unusual to offer patients the option of a spinal stimulator until a variety of other less invasive treatment options have been exhausted. The placement of a spinal cord stimulator system is usually preceded by a successful trial of stimulation with lead placement and an external stimulator. This is usually followed by the placement of a permanent generator. Most of the reported complications, after successful stimulator placement, are because of lead malfunction, migration or breakage, and battery depletion (2,3). Spinal cord stimulation provides analgesic relief to patients with a number of pain etiologies (4–8). Some 30 different mechanisms of action of spinal cord stimulation have been postulated, but all remain more or less speculative (9). The gate control theory remains the best explanation for the success of spinal cord stimulation, although details remain controversial (10).

A spinal cord stimulator is a multiprogrammable implantable device. It delivers low intensity, pulsed electrical impulses to neural structures in the dorsal aspect of the spinal cord. It consists of an external radio frequency (RF) transmitter, an external antenna, a receiver (either implanted or external), and implanted leads. The RF transmitter provides controlled delivery of low-intensity signals to an attached antenna positioned on the patient’s skin directly over the receiver site. The receiver is a device that contains electronic circuitry that converts the RF signals into low-level electrical impulses. The electrical impulses then travel to the leads that are connected to the receiver and are delivered to the selected nerve fibers.

We report two patients in whom permanent generators have been implanted who experienced significant gastrointestinal side effects. These side effects were severe enough that the patients chose not to use the stimulators (despite these stimulators successfully providing pain relief).

	Case Reports

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A 38-yr-old woman (5'7"; 229 lbs.) was seen at our Pain Management Center for evaluation and consultation for management of complex regional pain syndrome Type II of the lower extremities. The patient’s symptoms began 3 yr before evaluation with the sudden onset of pain in the right lateral femoral cutaneous nerve distribution immediately after a laparotomy; this pain subsequently became bilateral. The patient had undergone multiple treatments at other facilities. These included right femoral cutaneous nerve blocks (with no relief) and right lumbar sympathetic blocks (with short term improvement). Bilateral chemical sympathetic neurolysis was performed at another institution 2 yr after the onset of symptoms. After a brief period of improvement after the neurolysis, the pain worsened with generalization of the symptoms to include both lower extremities. Diagnostic testing including a lumbosacral magnetic resonance image and electromyelogram (EMG) were nonconclusive. The patient subsequently underwent multiple trials of non-opioid medications without relief. The patient developed severe opioid-induced myositis when treated with an aggressive opioid-dosing regimen.

The patient’s physical examination was unremarkable except for allodynia in the right femoral cutaneous nerve distribution. Because the patient did not have pain relief with previous management, she was offered a trial of a spinal cord stimulation using percutaneously placed dual leads. The patient had successful treatment of depression with amitriptyline. Evaluation by a psychiatrist and psychologist was performed before implantation. The patient reported 100% coverage of her pain distribution with 75% improvement in her pain during the trial. The next week, a permanent stimulator receiver (Advanced Neuromodulation Systems Renew, Model 3416; ANS Inc, Plano, TX) was implanted, which provided the same coverage as the trial. Postoperatively, the stimulator was programmed with six programs that provided excellent pain coverage. There was no change in the patient’s medication after implantation. Approximately 1 mo after placement of the stimulator, the patient complained of severe nausea and diarrhea with stimulation. These symptoms began immediately after implant. Before the implant, she had a bowel movement every 4 days; after the implant, the stool frequency was up to eight times each day. Multiple treatments with antiemetic and antidiarrheal medications were unsuccessful in relieving these symptoms. These symptoms resolved completely after discontinuation of stimulation.

During a trial of intermittently using the stimulator three times a day over a period of 1 mo, the gastrointestinal symptoms persisted. Multiple attempts at reprogramming also failed to alleviate the side effects. Nausea and diarrhea appeared with the onset of stimulation and persisted with each trial of using the spinal cord stimulator; these symptoms resolved within a few hours after discontinuation of the stimulator. Because of the severity of the side effects, the patient currently does not use the stimulator.

The second patient, a 50-yr-old woman (5'3"; 205 lbs.) was seen at our pain management center for evaluation of intractable pain secondary to nerve root injury. The patient initially sustained a work related injury 7 years before presentation. She later underwent a L5-S1 fusion, which failed. She then required re-instrumentation that provided partial pain relief. She subsequently underwent a L1-2 fusion for degenerative disk disease. The patient had persistent lower back pain with EMG-documented L5 and S1 radiculopathy. She had been treated with multiple epidural steroid injections with minimal relief. Treatment with opioids and antidepressants did not improve her pain. She was intolerant (nausea and vomiting) to all opioids with the exception of hydrocodone (Vicodin), which provided minimal relief. The patient’s medical history included migraine headaches, sinusitis, and gastroesophageal reflux.

On initial presentation, the patient’s physical examination was remarkable for well-healed midline scars with diffuse lower lumbar tenderness. She demonstrated decreased pinprick sensation in the L5 and S1 distribution. Her motor examination was normal. The patient consistently rated her pain as 8 of 10 on each evaluation over a 1-yr period; this pain radiated down her back to both lower extremities. Because conservative therapy (including translaminal steroid injection, transforaminal steroid injection, caudal steroid injection, acupuncture, and pharmacological treatment with opioids and antidepressants) had failed to adequately treat her pain, a trial of a spinal cord stimulator using temporary leads was offered. Psychological evaluation was performed before the stimulator, and drug-seeking behavior was not present. The patient had complete coverage of her pain areas with 80% reduction in her pain during the trial. She was able to decrease her hydrocodone use by 80%, and she demonstrated improvement in her daily activities, including the ability to sit and stand for prolonged periods without an increase in pain. She underwent placement of a permanent spinal cord stimulator receiver with dual percutaneous leads (Advanced Neuromodulation Systems Octrode) 1 mo later. After permanent placement, she obtained the same pain improvement as was experienced during the trial. Two months after implantation, the patient returned complaining of worsening gastroesophageal reflux symptoms, flatulence, and diarrhea associated with stimulator use. These symptoms started immediately after the implant. The symptoms resolved several days after cessation of stimulation. On resumption of stimulation, the patient developed these gastrointestinal symptoms within 1 h. These symptoms were refractory to medical management prescribed by the patient’s gastroenterologist (including proton pump inhibitor and oral antacids). Multiple attempts at reprogramming also failed to alleviate the side effects. Five months after insertion, at the patient’s request, the spinal cord stimulator receiver and leads were explanted. Unfortunately, her pain returned to prestimulator levels. She continues to be treated with hydrocodone with limited relief.

	Discussion

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Evidence suggests that sympathectomy (with an unopposed parasympathetic state) occurs with spinal and epidural anesthetics (11). An unopposed parasympathetic state can lead to side effects including nausea, vomiting, diarrhea, and increased gastrointestinal motility. Until now, there have been no reports of these side effects in patients who have spinal cord stimulators.

Significantly disabling gastrointestinal symptoms have been reported in patients with spinal cord injury (12,13). These lifestyle-altering symptoms included constipation and abdominal pain. A tendency towards increased colonic transfer time and a resultant increase in the frequency of defecation was documented in paraplegic patients who had a sacral nerve root stimulator implanted (14). Loubser (15) reported urethral spasm in a spinal cord injury patient who had been treated with spinal cord stimulation. He was able to document that the functional urethral obstruction was related to stimulator use; the obstruction lasted for approximately three hours after deactivation of the stimulator.

Spinal cord stimulation may improve sensitized dorsal horn neurons by restoring a more normal balance between inhibitory and excitatory mechanisms (16). We propose that our patients had their autonomic balance altered too much, i.e., an increased parasympathetic state. These side effects were consistent with an increased parasympathetic tone (e.g., diarrhea). This is analogous to the previous reports in paraplegic patients who had stimulators implanted, which resulted in parasympathetic effects (increased bowel motility and urethral spasm) (14,15).

In conclusion, we report severe gastrointestinal symptoms in two patients who had implanted spinal cord stimulators. These side effects were severe enough to require cessation of the stimulation, even though the patients reported significantly improved analgesia. It is important for clinicians caring for patients with these devices to be aware of these potentially severe side effects.

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Thakkar, N. Articles by Vieira, P. Search for Related Content PubMed PubMed Citation Articles by Thakkar, N. Articles by Vieira, P. Related Collections Equipment Complications Pain