- Email: [email protected]
Efficacy of spinal cord stimulators in treating peripheral neuropathy: a case series
Journal of Clinical Anesthesia (2015) xx, xxx–xxx
Original contribution
Efficacy of spinal cord stimulators in treating peripheral neuropathy: a case series Alaa Abd-Elsayed MD, MPH (Assistant Professor)a,b,⁎, Nick Schiavoni MS c , Harsh Sachdeva MD (Assistant Professor)a a
Anesthesiology, University of Cincinnati, Cincinnati, OH, USA Anesthesiology, University of Wisconsin School of Medicine and Public Health, Madison WI, USA c Medical School, University of Cincinnati, Cincinnati, OH, USA b
Received 27 December 2014; revised 4 April 2015; accepted 10 August 2015
Keywords: Spinal cord stimulator; Peripheral neuropathy; Diabetes mellitus; Chemotherapy; Human immunodeficiency virus
Abstract Introduction: Peripheral neuropathy is a common cause of pain, and it is increasing in prevalence. Peripheral neuropathic pain is very hard to treat and can be resistant to multiple pain management modalities. Our series aimed at testing the efficacy of spinal cord stimulators (SCSs) in treating resistant painful peripheral neuropathy. Case Presentations: Case 1: A 79-year-old man presented to our clinic with long-standing history of painful peripheral diabetic neuropathy resistant to conservative management. After failure of all possible modalities, we offered the patient an SCS trial that was very successful, and we proceeded with the permanent implant that continued to help with his pain and allowed the patient to wean down his medications. Case 2: A 60-year-old man presented with chronic peripheral neuropathy secondary to HIV, patient failed all conservative and procedural management. Patient then had an SCS trial that relieved his pain significantly. Unfortunately, we did not proceed with the implant due to deterioration of the patient general health. Case 3: A 39-year-old woman presented with painful peripheral neuropathy secondary to chemotherapy for breast cancer. After failure of medication management and procedures, patient had a SCS trial that improved her pain and we then proceeded with performing the permanent implant that controlled her pain. Conclusion: We presented 3 cases with chronic painful peripheral neuropathy secondary to HIV, diabetes mellitus, and chemotherapy that was resistant to conservative pain management and procedures that was successfully treated with neurostimulation. © 2015 Elsevier Inc. All rights reserved.
1. Introduction Peripheral neuropathy can be a debilitating condition that results from peripheral nerve damage. Peripheral neuropathy ⁎ Corresponding author at: Department of Anesthesiology, University of Wisconsin School of Medicine and Public Health, B6/319 CSC, 600 Highland Ave, Madison, WI 53792-3272. Tel.: +1 608 263 8106; fax: +1 608 263 8111. E-mail address: [email protected] (A. Abd-Elsayed). http://dx.doi.org/10.1016/j.jclinane.2015.08.011 0952-8180/© 2015 Elsevier Inc. All rights reserved.
has an extremely diverse presentation that depends on the type (sensory, motor, and autonomic) and location of the affected nerve. Long nerves, such as the sensory nerves that extend to the toes, are most susceptible to neuropathic pain. The pain is often described as burning, sharp, jabbing, tingling, and/or electrical and can have a severe impact on a patient's quality of life [1]. Peripheral neuropathies are most prevalent in Western cultures. It has been estimated that more than 15 million people in the United States and Europe have some degree
2 of neuropathic pain and approximately 2 of every 100 individuals have peripheral neuropathy [2]. Approximately 8% of primary care patients aged 55 years or older have a polyneuropathy [3]. The incidence and prevalence of peripheral neuropathy are on the rise. Two major contributing factors are: the obesity/diabetes mellitus (DM) epidemic of Western society and the aging of our population as a whole. The most common cause of peripheral neuropathy is DM [4]. Researchers project that the number of Americans with DM will increase 165% over the next 50 years. These estimations predict that the prevalence of DM will grow from 11 million in 2000 (4.0%) to 29 million in 2050 (7.2%) [5]. Furthermore, the overall incidence of peripheral neuropathy increases with age. In 1950, the elderly population (age N 65 years) represented 8.1% of the total US population. By 2009, this group represented 12.8% of the population and is projected to reach 20.2% in 2050 [6]. As our nation's demographic shifts to a more elderly population with higher rates of DM, more people will inevitably develop painful peripheral neuropathy. More than 100 different causes of peripheral neuropathy have been identified [7]. These causative agents are highly diverse and include metabolic, infectious, and pharmacologic sources [8]. The most common cause of peripheral neuropathy is DM, with approximately 50% of diabetic patients developing a neuropathy within their lifetime [4]. Different studies have determined that HIV-related painful distal sensory polyneuropathy may affect 1/3 of HIV patients being treated with highly active antiretroviral therapy and 1/3 of all AIDS patients [9]. The most common medications that induce peripheral neuropathy are the chemotherapeutic agents such as the vinca alkaloids (vincristine), taxols (taxane, taxol, and docetaxel), platinum compounds (cisplatin, carboplatin, and oxaliplatin), and suramin [10]. Regardless of the cause, neuropathic pain is usually not successfully managed with pharmaceutical treatment. Recommended first-line medications include antidepressants, calcium-channel ligands (gabapentin and pregabalin), and topical lidocaine [11]. Other commonly used medications are opioid analgesics, tramadol, and antiepileptics. Randomized controlled trials have proven that these medications are not overwhelmingly effective. A systematic review of evidence-based recommendations for pharmaceutical management of neuropathic pain determined medications only provide 40% to 60% of patients with partial pain relief [11]. For this reason, it is time to consider a more lasting and efficacious treatment such as SCS. Literature about SCS is focusing mostly on using it for the treatment of failed back surgery syndrome (FBSS), complex regional pain syndrome, and radicular pain. This case series is unique in that it illustrates SCS ability to successfully manage 3 extremely diverse etiologies of neuropathic pain: DM, HIV, and chemotherapy. An informed consent was obtained from all patients for publishing this case series.
A. Abd-Elsayed et al.
2. Case presentation 2.1. Case 1 A 79-year-old man presented with lumbar and bilateral lower extremity pain for 11 years secondary to diabetic peripheral neuropathy. In addition to DM type II, the patient had a significant medical history for coronary artery disease, hypertension, and multiple failed back surgeries. His pain was not well controlled with medications (Neurontin, Robaxin, Tramadol, and Naproxen), physical therapy, epidural steroid injections, or transcutaneous electrical nerve stimulation. Upon initial presentation, the patient was mostly concerned with the pain in his feet, which he reported to be 9/10 on the visual analog scale for pain (VAS). He described this pain as nonradiating, constant, sharp, burning, and tingling in nature. The patient opted for an SCS trial that was performed and was associated with decreased pain scores down to 3/10 with improvement in the ability to perform daily activities. The SCS trial was performed using 2 octad leads to provide bilateral coverage and was performed for 1 week. We decided to proceed with the permanent implant. The SCS implantation leads were threaded under fluoroscopic guidance to T7 vertebral body, resulting in stimulation coverage of all painful areas. At 1-month postoperation, the patient was very happy with the 60% overall reduction in pain and a VAS score of 2/10. His oral pain medications were successfully weaned down, and he no longer needed breakthrough pain medications. Patient also reported increase in his ability to perform his daily activities as walking and grocery shopping and marked improvement in his sleep. Patient had the SCS 3 years ago and continues to do well.
2.2. Case 2 A 60-year-old man had been seen in our pain center for HIV-induced peripheral neuropathy for 15 years. He has a significant medical history of coronary artery disease, aseptic necrosis of the hip, cytomegalovirus colitis, pancreatitis, seizures, HIV, and herpes zooster virus infection of the lower extremities. He presented with a 15-year history of bilateral lower extremity pain that had a strong temporal correlation with his diagnosis of HIV in 1990. His HIV is currently treated with darunavir, emtricitabine-tenofovir, and ritonavir. He described his lower extremity pain as burning, stinging, and stabbing with a VAS pain score of 9/10. The pain was affecting his sleep at night (self-reported 4 hours per night) and his ability to ambulate without a walker. He had tried numerous pain medications with minimal success: methadone, morphine, hydromorphone, fentanyl, dilaudid, baclofen, ziconitide, gabapentin, pregabalin, amytryptyline, and duloxetine. An intrathecal drug delivery system implanted in 2005 provided variable relief with VAS scores ranging from 4/10 to 10/10. The patient failed many attempts to wean off his narcotic pain medications, and just before the SCS trial in 2013, he was heavily medicated with amitriptyline, buproprion,
3 duloxetine, gabapentin, lorazepam, oral morphine, oral oxycodone, and dilaudid via intrathecal drug delivery system. His SCS trial was performed using 2 octad leads to provide bilateral coverage, and it lasted for 1 week. The SCS trial proved to be highly effective with 95% pain relief. He could sleep better during the trial period, which he had not been able to do in a while because of severe pain in the legs; the patient said “I was unable to sleep like this for years.” Unfortunately, shortly after the trial, the patient's health has declined. He has elected to postpone permanent SCS implantation until his other health matters are resolved.
2.3. Case 3 A 39-year-old woman presented to our clinic with a long-standing bilateral lower extremity peripheral neuropathy for 3 years secondary to chemotherapy. The patient had a medical history of breast cancer that was treated with a lumpectomy in 2010 followed by 6 months of chemotherapy. She described her pain as nonradiating, constant, sharp, burning, and stabbing in nature with a VAS rating of 8/10. The pain was primarily below her knees, resulting in a significant negative impact on her ability to ambulate as well as other activities of daily living. Over the next 6 months, her pain was successfully managed with medications (Nortryptyline, Lyrica, and Percocet) and bilateral lumbar sympathetic block. After a while, the lumbar sympathetic block stopped working, and her pain increased to an unacceptable level. At this point, the patient agreed to an SCS trial for 1 week, which resulted in 95% pain relief. We used 2 octad leads for the trial to provide bilateral coverage for all the painful areas. We then proceeded with implantation of an SCS with lead placement at the T10-T11 area resulting in stimulation coverage of all painful areas. Three months later, the patient continued to have excellent pain relief; marked improvement in her ability to perform her daily activities, which made her less dependent on others to help; improvement in her sleep pattern, and she was successfully weaned off some of her pain medications. Patient had the SCS implant 2 years ago and continues to report improvement to date.
3. Discussion There are few pharmacological agents that have been proven to be consistently effective in relieving peripheral neuropathic pain. For example, there are only 2 Food and Drug Administration–approved medications for DM-induced peripheral neuropathy: pregabalin and duloxetine [12]. Typical first- and second-line medications for neuropathic pain include antidepressants, anticonvulsants, and opiate analgesics, all of which result in significant side effects, unconvincing efficacies, and a substantial financial burden [13]. The sale of opioid analgesics has quadripled between the years 1999 and 2010 with the United States consuming 80%
of the world's oxycodone and 99% of the hydrocodone [14]. It is not surprising that as the US prescription and consumption of opioid analgesics have increased so has its abuse. The data published in 2005 by The National Survey on Drug Use and Health reported that 2.4% (6.4 million people) of the US population 12 years and older have used prescription-type psychotherapeutic drugs nonmedically in the past month [15]. Our nation continues to grow more dependent on pharmaceutical agents that are often ineffective and potentially harmful. Utilization of SCS has the potential to hinder and perhaps reverse this trend of pharmaceutical dependence. SCS trial and implantation are typically performed in an outpatient setting. The procedure is minimally invasive. Real-time radiographs are used to confirm correct placement of the stimulator leads corresponding to the dorsal horn of the spinal cord at the appropriate vertebral level. The SCS trial is done in an outpatient setting for a period of 1 week. SCS trial is deemed successful if the patient has 50% or more pain reduction during the trial period along with improvement in activity. Permanent implantation involves placing the SCS leads through a surgically created incision in the back followed by attachment of the leads to a generator battery in the pocket created in the buttock area. The exact mechanism of SCS is still under debate. The first and most accepted theory suggests that stimulation of the dorsal horn via SCS suppresses the transmission of noxious stimuli from the peripheral nerves [16]. Currently, there are only a few indications for SCS with adequate support. One such indication is chronic spinal pain and/or FBSS. A recently published comprehensive review consisting of 10 different studies each with at least 50 subjects found that 48% to 77% of the participants in each study achieved greater than 12 months of pain relief from SCS. These data warranted level II-1 or II-2 evidence (US Preventative Services Task Force criteria) for SCS treatment of neuropathic pain of failed back surgery syndrome [17]. Recommendations assembled by a Cochrane Review and The American Society of Interventional Pain Physicians support the use of SCS for select patients with FBSS and complex regional pain syndrome due to its effectiveness in providing both short- and long-term pain relief [18]. There have been some published case reports in which SCS has successfully managed and/or eliminated various painful peripheral neuropathies such as meralgia paresthetica [19], Lyme disease [20], postherpetic neuralgia [21], postthoracotomy pain syndrome [22], pelvic visceral pain and chronic abdominal pain [23], angina pectoris [24], chemotherapy-induced neuropathy [25], diabetic neuropathy, ischemic heart disease, and peripheral vascular disease [26]. However, for these indications, as well as the cases presented in this series, further clinical trials are needed to prove the efficacy of SCS therapy. A recent study completed in the Netherlands analyzed the effects of SCS on 15 patients with painful diabetic peripheral neuropathy. Pain relief, quality of life, and amount of sleep were measured at ½, 3, 6, and 12 months. After 12 months of
4 SCS treatment, two-thirds of the patients continued to experience clinically significant pain relief, increased sleep, and improved quality of life [27]. This study not only displays the efficacy of SCS but also recognizes the importance of sleep and quality of life. Another recently published retrospective study analyzed the long-term effects of cervical spinal cord stimulation for treatment of various upper extremity peripheral neuropathies. Eighteen patients were interviewed 5.8 years (mean) after SCS implantation, and pain scores were 50% lower than the scores reported before the procedure. This demonstrates SCS's ability to serve as a long-term treatment for a variety of peripheral neuropathy subtypes, regardless of its origin [28]. In conclusion, the demand for a safe and efficacious long-term therapy for peripheral neuropathy grows stronger. This case series illustrates SCS's ability to effectively manage diverse forms of painful peripheral neuropathy. SCS has the potential to revolutionize peripheral neuropathy treatment, but the current clinical evidence is too sparse for mainstream application. Therefore, more extensive clinical trials are needed to verify its success.
References [1] National Institute of Neurologic Disorders and Stroke. http://www.ninds. nih.gov/disorders/peripheralneuropathy/detail_peripheralneuropathy. htm. [Accessed at 4/4/2014]. [2] Azhary H, Farooq MU, Bhanushali M, Majid A, Kassab MY. Peripheral neuropathy: differential diagnosis and management. Am Fam Physician 2010;81(7):887-92. [3] Beghi E, Monticelli MI, Amoruso L, et al. Chronic symmetrical polyneuropathy in the elderly—a field screening investigation in 2 Italian regions. Prevalence and general characteristics of the sample. Neurology 1995;45(10):1832-6. [4] Dyck PJ, Kratz KM, Karnes JL, Litchy WJ, Klein R, Pach JM, et al. The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: the Rochester Diabetic Neuropathy Study. Neurology 1993; 43:817-24. [5] Boyle JP, Honeycutt AA, Narayan KMV, Hoerger TJ, Geiss LS, Chen H, et al. Projection of Diabetes Burden Through 2050, impact of changing demography and disease prevalence in the U.S. Diabetes Care 2001;24(11):1936-40. [6] Shrestha LB, Heisler EJ. The changing demographic profile of the United States. Congressional Research Service; 2009 [http://www. aging.senate.gov/crs/aging4.pdf. accessed at 3/12/2014]. [7] The Neuropathy Association. http://www.neuropathy.org/site/PageServer?pagename=About_Facts. [Accessed at 4/2/2014].
A. Abd-Elsayed et al. [8] England JD, Asbury AK. Peripheral neuropathy. Lancet 2004; 363(9427):2151-61. [9] Smith HS. Treatment considerations in painful HIV-related neuropathy. Pain Physician 2011;14:E505-24. [10] Quasthoff S, Hartung HP. Chemotherapy-induced peripheral neuropathy. J Neurol 2002;249:9-17. [11] Dworkin RH, O’Connor AB, Backonja M, Farrar JT, Finnerup NB, Jensen TS, et al. Pharmacologic management of neuropathic pain: evidence-based recommendations. Pain 2007;132:237-51. [12] Sheth NU, Tata AL. Diabetes-induced peripheral neuropathy: a treatment review. Formulary 2012;47(4):142-6 [150-153]. [13] Trivedi JR, Silvestri NJ, Wolfe GI. Peripheral neuropathies treatment of painful peripheral neuropathy. Neurol Clin 2013;31(2):377-403. [14] Manchikanti L, Helm S II, Fellows B, Janata JW, Pampati V, Grider JS, et al. Opioid epidemic in the United States. Pain Physician 2012; 15:ES9-S38. [15] Substance Abuse and Mental Health Services Administration. Results from the 2005 National Survey on Drug Use and Health: National Findings. Office of Applied Studies, NSDUH Series H-30, DHHS Publication No. SMA 06-4194; 2006[Rockville, MD. www.oas. samhsa.gov/nsduh/2k5nsduh/2k5Results.pdf. Accessed at 3/23/2014]. [16] Melzack R, Wall P. Pain mechanism: a. new theory. Science 1965;150: 951-79. [17] Manchikanti L, Boswell MV, Datta S, Fellows B, Abdi S, Singh V, et al. Comprehensive review of therapeutic interventions in managing chronic spinal pain. Pain Physician 2009;12:E123-98. [18] Boswell MV, Trescot AM, Datta S, Schultz DM, Hansen HC, Abdi S, et al. Interventional techniques: evidence-based practice guidelines in the management of chronic spinal pain. Pain Physician 2007;10(1):7-111. [19] Barna SA, Hu MM, Buxo C, Trella J, Cosgrove GR. Spinal cord stimulation for treatment of meralgia paresthetica. Pain Physician 2005;8:315-8. [20] Shui Y, Tao W, Huang D, Li Y, Fan B. Spinal cord stimulation for chronic pain originating from Lyme disease. Pain Physician 2012;15:511-4. [21] Cameron T. Safety and efficacy of spinal cord stimulation for the treatment of chronic pain: a 20-year literature review. J Neurosurg 2004;100:254-67. [22] Graybill J, Conermann T, Kabazie J, Chandy S. Spinal cord stimulation for treatment of pain in a patient with post thoracotomy pain syndrome. Pain Physician 2011;14:441-5. [23] Kim CH, Issa MA. Spinal cord stimulation for the treatment of chronic renal pain secondary to uretero-pelvic junction obstruction. Pain Physician 2011;14:55-9. [24] Deer TR, Raso LJ. Spinal cord stimulation for refractory angina pectoris and peripheral vascular disease. Pain Physician 2006;9:347-52. [25] Cata JP, Cordella JV, Burton AW, Hassenbusch SJ, Weng HR, Dougherty PM. Spinal cord stimulation relieves chemotherapy-induced pain: a clinical case report. J Pain Symptom Manag 2004;27(1):72-8. [26] Stojanovic MP. Stimulation methods for neuropathic pain control. Curr Pain Headache Rep 2001;5:130-7. [27] Pluijms WA, Slangen R, Bakkers M, Faber CG, Merkies ISG, Kessels AG, et al. Pain relief and quality-of-life improvement after spinal cord stimulation in painful diabetic polyneuropathy: a pilot study. Br J Anaesth 2012;109(4):623-9. [28] Wolter T, Kieselbach K. Cervical spinal cord stimulation: an analysis of 23 patients with long-term follow-up. Pain Physician 2012;15:203-12.
Original contribution
Efficacy of spinal cord stimulators in treating peripheral neuropathy: a case series Alaa Abd-Elsayed MD, MPH (Assistant Professor)a,b,⁎, Nick Schiavoni MS c , Harsh Sachdeva MD (Assistant Professor)a a
Anesthesiology, University of Cincinnati, Cincinnati, OH, USA Anesthesiology, University of Wisconsin School of Medicine and Public Health, Madison WI, USA c Medical School, University of Cincinnati, Cincinnati, OH, USA b
Received 27 December 2014; revised 4 April 2015; accepted 10 August 2015
Keywords: Spinal cord stimulator; Peripheral neuropathy; Diabetes mellitus; Chemotherapy; Human immunodeficiency virus
Abstract Introduction: Peripheral neuropathy is a common cause of pain, and it is increasing in prevalence. Peripheral neuropathic pain is very hard to treat and can be resistant to multiple pain management modalities. Our series aimed at testing the efficacy of spinal cord stimulators (SCSs) in treating resistant painful peripheral neuropathy. Case Presentations: Case 1: A 79-year-old man presented to our clinic with long-standing history of painful peripheral diabetic neuropathy resistant to conservative management. After failure of all possible modalities, we offered the patient an SCS trial that was very successful, and we proceeded with the permanent implant that continued to help with his pain and allowed the patient to wean down his medications. Case 2: A 60-year-old man presented with chronic peripheral neuropathy secondary to HIV, patient failed all conservative and procedural management. Patient then had an SCS trial that relieved his pain significantly. Unfortunately, we did not proceed with the implant due to deterioration of the patient general health. Case 3: A 39-year-old woman presented with painful peripheral neuropathy secondary to chemotherapy for breast cancer. After failure of medication management and procedures, patient had a SCS trial that improved her pain and we then proceeded with performing the permanent implant that controlled her pain. Conclusion: We presented 3 cases with chronic painful peripheral neuropathy secondary to HIV, diabetes mellitus, and chemotherapy that was resistant to conservative pain management and procedures that was successfully treated with neurostimulation. © 2015 Elsevier Inc. All rights reserved.
1. Introduction Peripheral neuropathy can be a debilitating condition that results from peripheral nerve damage. Peripheral neuropathy ⁎ Corresponding author at: Department of Anesthesiology, University of Wisconsin School of Medicine and Public Health, B6/319 CSC, 600 Highland Ave, Madison, WI 53792-3272. Tel.: +1 608 263 8106; fax: +1 608 263 8111. E-mail address: [email protected] (A. Abd-Elsayed). http://dx.doi.org/10.1016/j.jclinane.2015.08.011 0952-8180/© 2015 Elsevier Inc. All rights reserved.
has an extremely diverse presentation that depends on the type (sensory, motor, and autonomic) and location of the affected nerve. Long nerves, such as the sensory nerves that extend to the toes, are most susceptible to neuropathic pain. The pain is often described as burning, sharp, jabbing, tingling, and/or electrical and can have a severe impact on a patient's quality of life [1]. Peripheral neuropathies are most prevalent in Western cultures. It has been estimated that more than 15 million people in the United States and Europe have some degree
2 of neuropathic pain and approximately 2 of every 100 individuals have peripheral neuropathy [2]. Approximately 8% of primary care patients aged 55 years or older have a polyneuropathy [3]. The incidence and prevalence of peripheral neuropathy are on the rise. Two major contributing factors are: the obesity/diabetes mellitus (DM) epidemic of Western society and the aging of our population as a whole. The most common cause of peripheral neuropathy is DM [4]. Researchers project that the number of Americans with DM will increase 165% over the next 50 years. These estimations predict that the prevalence of DM will grow from 11 million in 2000 (4.0%) to 29 million in 2050 (7.2%) [5]. Furthermore, the overall incidence of peripheral neuropathy increases with age. In 1950, the elderly population (age N 65 years) represented 8.1% of the total US population. By 2009, this group represented 12.8% of the population and is projected to reach 20.2% in 2050 [6]. As our nation's demographic shifts to a more elderly population with higher rates of DM, more people will inevitably develop painful peripheral neuropathy. More than 100 different causes of peripheral neuropathy have been identified [7]. These causative agents are highly diverse and include metabolic, infectious, and pharmacologic sources [8]. The most common cause of peripheral neuropathy is DM, with approximately 50% of diabetic patients developing a neuropathy within their lifetime [4]. Different studies have determined that HIV-related painful distal sensory polyneuropathy may affect 1/3 of HIV patients being treated with highly active antiretroviral therapy and 1/3 of all AIDS patients [9]. The most common medications that induce peripheral neuropathy are the chemotherapeutic agents such as the vinca alkaloids (vincristine), taxols (taxane, taxol, and docetaxel), platinum compounds (cisplatin, carboplatin, and oxaliplatin), and suramin [10]. Regardless of the cause, neuropathic pain is usually not successfully managed with pharmaceutical treatment. Recommended first-line medications include antidepressants, calcium-channel ligands (gabapentin and pregabalin), and topical lidocaine [11]. Other commonly used medications are opioid analgesics, tramadol, and antiepileptics. Randomized controlled trials have proven that these medications are not overwhelmingly effective. A systematic review of evidence-based recommendations for pharmaceutical management of neuropathic pain determined medications only provide 40% to 60% of patients with partial pain relief [11]. For this reason, it is time to consider a more lasting and efficacious treatment such as SCS. Literature about SCS is focusing mostly on using it for the treatment of failed back surgery syndrome (FBSS), complex regional pain syndrome, and radicular pain. This case series is unique in that it illustrates SCS ability to successfully manage 3 extremely diverse etiologies of neuropathic pain: DM, HIV, and chemotherapy. An informed consent was obtained from all patients for publishing this case series.
A. Abd-Elsayed et al.
2. Case presentation 2.1. Case 1 A 79-year-old man presented with lumbar and bilateral lower extremity pain for 11 years secondary to diabetic peripheral neuropathy. In addition to DM type II, the patient had a significant medical history for coronary artery disease, hypertension, and multiple failed back surgeries. His pain was not well controlled with medications (Neurontin, Robaxin, Tramadol, and Naproxen), physical therapy, epidural steroid injections, or transcutaneous electrical nerve stimulation. Upon initial presentation, the patient was mostly concerned with the pain in his feet, which he reported to be 9/10 on the visual analog scale for pain (VAS). He described this pain as nonradiating, constant, sharp, burning, and tingling in nature. The patient opted for an SCS trial that was performed and was associated with decreased pain scores down to 3/10 with improvement in the ability to perform daily activities. The SCS trial was performed using 2 octad leads to provide bilateral coverage and was performed for 1 week. We decided to proceed with the permanent implant. The SCS implantation leads were threaded under fluoroscopic guidance to T7 vertebral body, resulting in stimulation coverage of all painful areas. At 1-month postoperation, the patient was very happy with the 60% overall reduction in pain and a VAS score of 2/10. His oral pain medications were successfully weaned down, and he no longer needed breakthrough pain medications. Patient also reported increase in his ability to perform his daily activities as walking and grocery shopping and marked improvement in his sleep. Patient had the SCS 3 years ago and continues to do well.
2.2. Case 2 A 60-year-old man had been seen in our pain center for HIV-induced peripheral neuropathy for 15 years. He has a significant medical history of coronary artery disease, aseptic necrosis of the hip, cytomegalovirus colitis, pancreatitis, seizures, HIV, and herpes zooster virus infection of the lower extremities. He presented with a 15-year history of bilateral lower extremity pain that had a strong temporal correlation with his diagnosis of HIV in 1990. His HIV is currently treated with darunavir, emtricitabine-tenofovir, and ritonavir. He described his lower extremity pain as burning, stinging, and stabbing with a VAS pain score of 9/10. The pain was affecting his sleep at night (self-reported 4 hours per night) and his ability to ambulate without a walker. He had tried numerous pain medications with minimal success: methadone, morphine, hydromorphone, fentanyl, dilaudid, baclofen, ziconitide, gabapentin, pregabalin, amytryptyline, and duloxetine. An intrathecal drug delivery system implanted in 2005 provided variable relief with VAS scores ranging from 4/10 to 10/10. The patient failed many attempts to wean off his narcotic pain medications, and just before the SCS trial in 2013, he was heavily medicated with amitriptyline, buproprion,
3 duloxetine, gabapentin, lorazepam, oral morphine, oral oxycodone, and dilaudid via intrathecal drug delivery system. His SCS trial was performed using 2 octad leads to provide bilateral coverage, and it lasted for 1 week. The SCS trial proved to be highly effective with 95% pain relief. He could sleep better during the trial period, which he had not been able to do in a while because of severe pain in the legs; the patient said “I was unable to sleep like this for years.” Unfortunately, shortly after the trial, the patient's health has declined. He has elected to postpone permanent SCS implantation until his other health matters are resolved.
2.3. Case 3 A 39-year-old woman presented to our clinic with a long-standing bilateral lower extremity peripheral neuropathy for 3 years secondary to chemotherapy. The patient had a medical history of breast cancer that was treated with a lumpectomy in 2010 followed by 6 months of chemotherapy. She described her pain as nonradiating, constant, sharp, burning, and stabbing in nature with a VAS rating of 8/10. The pain was primarily below her knees, resulting in a significant negative impact on her ability to ambulate as well as other activities of daily living. Over the next 6 months, her pain was successfully managed with medications (Nortryptyline, Lyrica, and Percocet) and bilateral lumbar sympathetic block. After a while, the lumbar sympathetic block stopped working, and her pain increased to an unacceptable level. At this point, the patient agreed to an SCS trial for 1 week, which resulted in 95% pain relief. We used 2 octad leads for the trial to provide bilateral coverage for all the painful areas. We then proceeded with implantation of an SCS with lead placement at the T10-T11 area resulting in stimulation coverage of all painful areas. Three months later, the patient continued to have excellent pain relief; marked improvement in her ability to perform her daily activities, which made her less dependent on others to help; improvement in her sleep pattern, and she was successfully weaned off some of her pain medications. Patient had the SCS implant 2 years ago and continues to report improvement to date.
3. Discussion There are few pharmacological agents that have been proven to be consistently effective in relieving peripheral neuropathic pain. For example, there are only 2 Food and Drug Administration–approved medications for DM-induced peripheral neuropathy: pregabalin and duloxetine [12]. Typical first- and second-line medications for neuropathic pain include antidepressants, anticonvulsants, and opiate analgesics, all of which result in significant side effects, unconvincing efficacies, and a substantial financial burden [13]. The sale of opioid analgesics has quadripled between the years 1999 and 2010 with the United States consuming 80%
of the world's oxycodone and 99% of the hydrocodone [14]. It is not surprising that as the US prescription and consumption of opioid analgesics have increased so has its abuse. The data published in 2005 by The National Survey on Drug Use and Health reported that 2.4% (6.4 million people) of the US population 12 years and older have used prescription-type psychotherapeutic drugs nonmedically in the past month [15]. Our nation continues to grow more dependent on pharmaceutical agents that are often ineffective and potentially harmful. Utilization of SCS has the potential to hinder and perhaps reverse this trend of pharmaceutical dependence. SCS trial and implantation are typically performed in an outpatient setting. The procedure is minimally invasive. Real-time radiographs are used to confirm correct placement of the stimulator leads corresponding to the dorsal horn of the spinal cord at the appropriate vertebral level. The SCS trial is done in an outpatient setting for a period of 1 week. SCS trial is deemed successful if the patient has 50% or more pain reduction during the trial period along with improvement in activity. Permanent implantation involves placing the SCS leads through a surgically created incision in the back followed by attachment of the leads to a generator battery in the pocket created in the buttock area. The exact mechanism of SCS is still under debate. The first and most accepted theory suggests that stimulation of the dorsal horn via SCS suppresses the transmission of noxious stimuli from the peripheral nerves [16]. Currently, there are only a few indications for SCS with adequate support. One such indication is chronic spinal pain and/or FBSS. A recently published comprehensive review consisting of 10 different studies each with at least 50 subjects found that 48% to 77% of the participants in each study achieved greater than 12 months of pain relief from SCS. These data warranted level II-1 or II-2 evidence (US Preventative Services Task Force criteria) for SCS treatment of neuropathic pain of failed back surgery syndrome [17]. Recommendations assembled by a Cochrane Review and The American Society of Interventional Pain Physicians support the use of SCS for select patients with FBSS and complex regional pain syndrome due to its effectiveness in providing both short- and long-term pain relief [18]. There have been some published case reports in which SCS has successfully managed and/or eliminated various painful peripheral neuropathies such as meralgia paresthetica [19], Lyme disease [20], postherpetic neuralgia [21], postthoracotomy pain syndrome [22], pelvic visceral pain and chronic abdominal pain [23], angina pectoris [24], chemotherapy-induced neuropathy [25], diabetic neuropathy, ischemic heart disease, and peripheral vascular disease [26]. However, for these indications, as well as the cases presented in this series, further clinical trials are needed to prove the efficacy of SCS therapy. A recent study completed in the Netherlands analyzed the effects of SCS on 15 patients with painful diabetic peripheral neuropathy. Pain relief, quality of life, and amount of sleep were measured at ½, 3, 6, and 12 months. After 12 months of
4 SCS treatment, two-thirds of the patients continued to experience clinically significant pain relief, increased sleep, and improved quality of life [27]. This study not only displays the efficacy of SCS but also recognizes the importance of sleep and quality of life. Another recently published retrospective study analyzed the long-term effects of cervical spinal cord stimulation for treatment of various upper extremity peripheral neuropathies. Eighteen patients were interviewed 5.8 years (mean) after SCS implantation, and pain scores were 50% lower than the scores reported before the procedure. This demonstrates SCS's ability to serve as a long-term treatment for a variety of peripheral neuropathy subtypes, regardless of its origin [28]. In conclusion, the demand for a safe and efficacious long-term therapy for peripheral neuropathy grows stronger. This case series illustrates SCS's ability to effectively manage diverse forms of painful peripheral neuropathy. SCS has the potential to revolutionize peripheral neuropathy treatment, but the current clinical evidence is too sparse for mainstream application. Therefore, more extensive clinical trials are needed to verify its success.
References [1] National Institute of Neurologic Disorders and Stroke. http://www.ninds. nih.gov/disorders/peripheralneuropathy/detail_peripheralneuropathy. htm. [Accessed at 4/4/2014]. [2] Azhary H, Farooq MU, Bhanushali M, Majid A, Kassab MY. Peripheral neuropathy: differential diagnosis and management. Am Fam Physician 2010;81(7):887-92. [3] Beghi E, Monticelli MI, Amoruso L, et al. Chronic symmetrical polyneuropathy in the elderly—a field screening investigation in 2 Italian regions. Prevalence and general characteristics of the sample. Neurology 1995;45(10):1832-6. [4] Dyck PJ, Kratz KM, Karnes JL, Litchy WJ, Klein R, Pach JM, et al. The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: the Rochester Diabetic Neuropathy Study. Neurology 1993; 43:817-24. [5] Boyle JP, Honeycutt AA, Narayan KMV, Hoerger TJ, Geiss LS, Chen H, et al. Projection of Diabetes Burden Through 2050, impact of changing demography and disease prevalence in the U.S. Diabetes Care 2001;24(11):1936-40. [6] Shrestha LB, Heisler EJ. The changing demographic profile of the United States. Congressional Research Service; 2009 [http://www. aging.senate.gov/crs/aging4.pdf. accessed at 3/12/2014]. [7] The Neuropathy Association. http://www.neuropathy.org/site/PageServer?pagename=About_Facts. [Accessed at 4/2/2014].
A. Abd-Elsayed et al. [8] England JD, Asbury AK. Peripheral neuropathy. Lancet 2004; 363(9427):2151-61. [9] Smith HS. Treatment considerations in painful HIV-related neuropathy. Pain Physician 2011;14:E505-24. [10] Quasthoff S, Hartung HP. Chemotherapy-induced peripheral neuropathy. J Neurol 2002;249:9-17. [11] Dworkin RH, O’Connor AB, Backonja M, Farrar JT, Finnerup NB, Jensen TS, et al. Pharmacologic management of neuropathic pain: evidence-based recommendations. Pain 2007;132:237-51. [12] Sheth NU, Tata AL. Diabetes-induced peripheral neuropathy: a treatment review. Formulary 2012;47(4):142-6 [150-153]. [13] Trivedi JR, Silvestri NJ, Wolfe GI. Peripheral neuropathies treatment of painful peripheral neuropathy. Neurol Clin 2013;31(2):377-403. [14] Manchikanti L, Helm S II, Fellows B, Janata JW, Pampati V, Grider JS, et al. Opioid epidemic in the United States. Pain Physician 2012; 15:ES9-S38. [15] Substance Abuse and Mental Health Services Administration. Results from the 2005 National Survey on Drug Use and Health: National Findings. Office of Applied Studies, NSDUH Series H-30, DHHS Publication No. SMA 06-4194; 2006[Rockville, MD. www.oas. samhsa.gov/nsduh/2k5nsduh/2k5Results.pdf. Accessed at 3/23/2014]. [16] Melzack R, Wall P. Pain mechanism: a. new theory. Science 1965;150: 951-79. [17] Manchikanti L, Boswell MV, Datta S, Fellows B, Abdi S, Singh V, et al. Comprehensive review of therapeutic interventions in managing chronic spinal pain. Pain Physician 2009;12:E123-98. [18] Boswell MV, Trescot AM, Datta S, Schultz DM, Hansen HC, Abdi S, et al. Interventional techniques: evidence-based practice guidelines in the management of chronic spinal pain. Pain Physician 2007;10(1):7-111. [19] Barna SA, Hu MM, Buxo C, Trella J, Cosgrove GR. Spinal cord stimulation for treatment of meralgia paresthetica. Pain Physician 2005;8:315-8. [20] Shui Y, Tao W, Huang D, Li Y, Fan B. Spinal cord stimulation for chronic pain originating from Lyme disease. Pain Physician 2012;15:511-4. [21] Cameron T. Safety and efficacy of spinal cord stimulation for the treatment of chronic pain: a 20-year literature review. J Neurosurg 2004;100:254-67. [22] Graybill J, Conermann T, Kabazie J, Chandy S. Spinal cord stimulation for treatment of pain in a patient with post thoracotomy pain syndrome. Pain Physician 2011;14:441-5. [23] Kim CH, Issa MA. Spinal cord stimulation for the treatment of chronic renal pain secondary to uretero-pelvic junction obstruction. Pain Physician 2011;14:55-9. [24] Deer TR, Raso LJ. Spinal cord stimulation for refractory angina pectoris and peripheral vascular disease. Pain Physician 2006;9:347-52. [25] Cata JP, Cordella JV, Burton AW, Hassenbusch SJ, Weng HR, Dougherty PM. Spinal cord stimulation relieves chemotherapy-induced pain: a clinical case report. J Pain Symptom Manag 2004;27(1):72-8. [26] Stojanovic MP. Stimulation methods for neuropathic pain control. Curr Pain Headache Rep 2001;5:130-7. [27] Pluijms WA, Slangen R, Bakkers M, Faber CG, Merkies ISG, Kessels AG, et al. Pain relief and quality-of-life improvement after spinal cord stimulation in painful diabetic polyneuropathy: a pilot study. Br J Anaesth 2012;109(4):623-9. [28] Wolter T, Kieselbach K. Cervical spinal cord stimulation: an analysis of 23 patients with long-term follow-up. Pain Physician 2012;15:203-12.