Education
The following articles are copyrighted work products of Rafael Miguel, M.D.. These are intended for the use of education by Dr. Miguel’s patients. Others reviewing the site are welcome to do so but are reminded that no copying or any unauthorized use in part or in whole is permitted.
Articles by Rafael Miguel, M.D.
Non-Opioid Medical Management of Chronic Pain
Introduction
The World Health Organization has developed a 3-step ladder to treat pain based on mild, moderate, or severe pain (Figure). For mild pain, acetaminophen (Tylenol), aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and adjuvants (e.g., muscle relaxants, antidepressants, antiseizure drugs, Physical Therapy, etc…) are recommended. Acetaminophen combinations, tramadol (Ultram), and adjuvants are used for mild to moderate pain. Severe pain usually requires morphine, hydromorphone (Dilaudid), methadone, fentanyl (Duragesic patch, Actiq lozenge, Fentora effervescent lozenge) oxycodone, plus adjuvants. Even when chronic pain is well-controlled, it is usually characterized by two components: persistent pain and breakthrough pain.
Persistent and Breakthrough Pain
In 1990, Portenoy and Hagen1 developed definitions for persistent pain and breakthrough pain in patients with cancer. These definitions have become the standards for many clinical investigators when designing and comparing studies of breakthrough pain. Persistent pain is moderate-to-severe and present most of the time, day and night.2 Portenoy and Hagen defined persistent pain as that “reported by the patient as the average pain intensity experienced for 12 or more hours during the 24 hours prior to the interview.” Persistent pain is also called chronic or baseline pain. Breakthrough pain is a flare of pain that may occur even when persistent pain is well-controlled. Breakthrough pain is commonly defined as “a transient increase in pain over the baseline pain”. Breakthrough pain should be distinguished from uncontrolled pain, in which even the persistent pain is escalating and severe. Persistent pain and breakthrough pain require different management. Persistent pain is managed with medications dosed regularly around-the-clock (ATC), with the goal of alleviating pain until the patient reports no more than a mild-to-moderate “daily average” of pain. It is generally accepted that the combination of long acting to treat baseline pain and short acting medications to treat breakthrough pain should be delivered in a 80% to 20% ratio, respectively. Breakthrough pain is best managed with medications that have actions directed toward the source of the breakthrough pain with rapid onsets and short to intermediate duration. Breakthrough pain does not necessarily mean that ATC analgesia has failed. Pain is an unstable phenomenon that may vary with numerous factors, including disease progression, activity level, specific body movements, or stress level. Most patients experience numerous peaks and valleys of pain daily. Optimal pain management requires an understanding of the variable nature of pain and how different medications affect this variability. There are several different types of breakthrough pain. Incident pain is associated with movement or activity, such as walking, rising, defecating, or coughing. Incident pain traditionally has been difficult to manage, with lower chances of obtaining adequate pain control. Although end-of-dose failure is often listed as a type of breakthrough pain, this is not considered true breakthrough pain, as it typically results from drug blood levels falling below the analgesic threshold rather than from increased pain stimuli. End-of-dose failure is best managed by adjusting the dose of the ATC medication, either by increasing the dose or shortening the dosing interval.
Acetaminophen
Acetaminophen (paracetamol, APAP) is the most widely used analgesic and antipyretic in the world. The mechanism of action of APAP is not known but may involve nitric oxide, NMDA, Substance P, and COX-2 pathways. Acetaminophen is used for mild-to-moderate pain and has efficacy superior to placebo and inferior to NSAIDs in osteoarthritic conditions3. It is commonly combined with other analgesics for increased pain relief. Acetaminophen has few adverse effects, but hepatic toxicity is possible at doses greater than 4 g/d or less (90mg/kg in children) with chronic alcohol abuse, dehydration or malnutrition (e.g., anorexia nervosa). It is the most common cause of acute liver failure in the US and is the second leading cause of liver transplantation (1st in UK).
NSAIDs
NSAIDs attenuate prostaglandin production by inhibiting cyclooxygenase-1 (COX-1) and COX-2 enzymes. Analgesic, antipyretic, and anti-inflammatory effects are produced because of decreased prostaglandin production. NSAIDs are frequently prescribed for mild-to-moderate pain. Constipation, confusion, and headaches are mild adverse effects associated with NSAIDs. Serious adverse effects include gastrointestinal (GI) and renal toxicity and should be avoided in high-risk patients with congestive heart failure, coronary artery disease, hypertension, or previous liver or renal disease. Hypertension may certainly be worsened by the concomitant use of NSAIDs, but not all share the same potential to worsen blood pressure. Aspirin and sulindac have been reported to have no effect and piroxicam, naproxen and indomethacin have the most worsening of blood pressure.4 Elderly patients should also avoid NSAIDs. NSAIDs may interact with -blockers, angiotensin-converting enzyme (ACE) inhibitors, loop diuretics, and anticoagulants.
Combination analgesics are useful in the treatment of pain for several reasons. Multiple pain pathways can be targeted by using agents with different sites of action. Combination analgesics also provide the opportunity for complementary pharmacokinetic activity and potentially synergistic analgesia. A reduced adverse event profile with comparable efficacy is the goal of combination therapy.
Muscle Relaxants
The use of skeletal muscle relaxants is commonly used to assist in the management of osteoarthritic and intervertebral disc related painful conditions, especially acute low back pain and strain. Neural compression/irritation may manifest itself as skeletal muscle spasm. The use of many muscle relaxants has been limited due to their dose related sedation and in some cases (e.g., carisoprodol [Soma], prodrug of meprobamate [Miltown]) a high abuse potential and attractive street value. Nonetheless, the use of centrally acting muscle relaxants have evidence backing their benefit independent of their sedating properties. The use of botulinum toxin as a local muscle relaxant has demonstrated efficacy in double-blinded studies of low back pain, particularly with paravertebral trigger points in disc herniations, most commonly on the contralateral side.5
Antidepressants
There has been well-documented efficacy and safety of antidepressants in major chronic pain conditions; namely, neuropathic pain, headaches, low back pain, fibromyalgia, irritable bowel syndrome (IBS) and cancer pain. The beneficial use of antidepressants in chronic pain has been primarily limited to the use of tricyclic antidepressants. Pasternak first made this observation in 1983.6 While the newer noradrenergic and serotonin reuptake inhibitors have less supporting evidence in their use in chronic pain, they can be recommended in neuropathic pain, migraines and fibromyalgia.7 The beneficial effect of SSRIs appears to be in an improved feeling of “well-being” and not in an actual decrease in pain.7
Anticonvulsants
Anticonvulsant drugs are most effective for relieving neuropathic pain most commonly caused by damage to nerves or spinal cord (e.g., injury or disease) or neural compression (e.g., intervertebral disc herniation). Examples of documented benefit are neuropathic pain, e.g., postherpetic neuralgia and painful diabetic neuropathy. Approximately two-thirds of patients who take either carbamazepine, gabapentin or pregabalin can be expected to achieve good pain relief. More recent studies have documented beneficial effects of gabapentin in radiculopathy associated with low back pain8 and perioperative pain.9 While gabapentin is increasingly being used for neuropathic pain the evidence would suggest that it is not superior to carbamazepine.10
Summary
The discovery of a wide variety of non-opioid receptors and the identification of their role in pain modulation, has led to a literal explosion in a combination pharmacotherapeutic approach to pain management. In mild to moderate pain, effective pain control may be able to be achieved without the use of opioids. Furthermore, the more widespread availability of non-medical techniques such as acupuncture, transcutaneous nerve stimulation (i.e., TENS), physical therapy, chiropractic care and complementary strategies that assist in coping mechanisms make achieving pain relief without opioids a real option.
References
1. Portenoy RK, Hagen NA. Breakthrough pain: definition, prevalence and characteristics. Pain. 41:273-281, 1990.
2. Mercadante S, Maddaloni S, Roccella S, Salvaggio L. Predictive factors in advanced cancer pain treated only by analgesics. Pain. 50:151-155, 1992.
3. Towheed et al. Acetaminophen for osteoarthritis. Cochrane Database Syst Rev. Jan 25;(1):CD004257, 2006
4. J Clin Hypertension 2:319-323, 2000
5. Foster et al. Botulinum toxin A and chronic low back pain: a randomized, double-blind study. Neurology 56(10):1290-3, 2001
6. Spiegel K, Kalb R, Pasternak G. Analgesic activity of tricyclic antidepressants. Ann Neurol. 13(4):462-465, 1983
7. Verdu et al. Antidepressants in the treatment of chronic pain. Drugs 68(18) 2611-2632, 2008
8. Chou et. al. Medications for acute and chronic low back pain: a review of the evidence for an American Pain Society/American College of Physicians clinical practice
guideline. Ann Intern Med. 2007 Oct 2;147(7):505-14
9. Tippanna et. al. Do surgical patients benefit from perioperative gabapentin/pregabalin? A systematic review of efficacy and safety. Anesth Analg. 2007 Jun;104(6):1545-56
10. Wiffen et. al. Anticonvulsant drugs for acute and chronic pain. Cochrane Database of Systematic Reviews 2005, Issue 2. Art. No.: CD001133. DOI: 10.1002/14651858.CD001133.pub2
![]()
Introduction
The World Health Organization has developed a 3-step ladder to treat pain based on mild, moderate, or severe pain (Figure). For mild pain, acetaminophen (Tylenol), aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and adjuvants (e.g., muscle relaxants, antidepressants, antiseizure drugs, Physical Therapy, etc…) are recommended. Acetaminophen combinations, tramadol (Ultram), and adjuvants are used for mild to moderate pain. Severe pain usually requires morphine, hydromorphone (Dilaudid), methadone, fentanyl (Duragesic patch, Actiq lozenge, Fentora effervescent lozenge) oxycodone, plus adjuvants. Even when chronic pain is well-controlled, it is usually characterized by two components: persistent pain and breakthrough pain.
Persistent and Breakthrough Pain
In 1990, Portenoy and Hagen1 developed definitions for persistent pain and breakthrough pain in patients with cancer. These definitions have become the standards for many clinical investigators when designing and comparing studies of breakthrough pain. Persistent pain is moderate-to-severe and present most of the time, day and night.2 Portenoy and Hagen defined persistent pain as that “reported by the patient as the average pain intensity experienced for 12 or more hours during the 24 hours prior to the interview.” Persistent pain is also called chronic or baseline pain. Breakthrough pain is a flare of pain that may occur even when persistent pain is well-controlled. Breakthrough pain is commonly defined as “a transient increase in pain over the baseline pain”. Breakthrough pain should be distinguished from uncontrolled pain, in which even the persistent pain is escalating and severe. Persistent pain and breakthrough pain require different management. Persistent pain is managed with medications dosed regularly around-the-clock (ATC), with the goal of alleviating pain until the patient reports no more than a mild-to-moderate “daily average” of pain. It is generally accepted that the combination of long acting to treat baseline pain and short acting medications to treat breakthrough pain should be delivered in a 80% to 20% ratio, respectively. Breakthrough pain is best managed with medications that have actions directed toward the source of the breakthrough pain with rapid onsets and short to intermediate duration. Breakthrough pain does not necessarily mean that ATC analgesia has failed. Pain is an unstable phenomenon that may vary with numerous factors, including disease progression, activity level, specific body movements, or stress level. Most patients experience numerous peaks and valleys of pain daily. Optimal pain management requires an understanding of the variable nature of pain and how different medications affect this variability. There are several different types of breakthrough pain. Incident pain is associated with movement or activity, such as walking, rising, defecating, or coughing. Incident pain traditionally has been difficult to manage, with lower chances of obtaining adequate pain control. Although end-of-dose failure is often listed as a type of breakthrough pain, this is not considered true breakthrough pain, as it typically results from drug blood levels falling below the analgesic threshold rather than from increased pain stimuli. End-of-dose failure is best managed by adjusting the dose of the ATC medication, either by increasing the dose or shortening the dosing interval.
Acetaminophen
Acetaminophen (paracetamol, APAP) is the most widely used analgesic and antipyretic in the world. The mechanism of action of APAP is not known but may involve nitric oxide, NMDA, Substance P, and COX-2 pathways. Acetaminophen is used for mild-to-moderate pain and has efficacy superior to placebo and inferior to NSAIDs in osteoarthritic conditions3. It is commonly combined with other analgesics for increased pain relief. Acetaminophen has few adverse effects, but hepatic toxicity is possible at doses greater than 4 g/d or less (90mg/kg in children) with chronic alcohol abuse, dehydration or malnutrition (e.g., anorexia nervosa). It is the most common cause of acute liver failure in the US and is the second leading cause of liver transplantation (1st in UK).
NSAIDs
NSAIDs attenuate prostaglandin production by inhibiting cyclooxygenase-1 (COX-1) and COX-2 enzymes. Analgesic, antipyretic, and anti-inflammatory effects are produced because of decreased prostaglandin production. NSAIDs are frequently prescribed for mild-to-moderate pain. Constipation, confusion, and headaches are mild adverse effects associated with NSAIDs. Serious adverse effects include gastrointestinal (GI) and renal toxicity and should be avoided in high-risk patients with congestive heart failure, coronary artery disease, hypertension, or previous liver or renal disease. Hypertension may certainly be worsened by the concomitant use of NSAIDs, but not all share the same potential to worsen blood pressure. Aspirin and sulindac have been reported to have no effect and piroxicam, naproxen and indomethacin have the most worsening of blood pressure.4 Elderly patients should also avoid NSAIDs. NSAIDs may interact with -blockers, angiotensin-converting enzyme (ACE) inhibitors, loop diuretics, and anticoagulants.
Combination analgesics are useful in the treatment of pain for several reasons. Multiple pain pathways can be targeted by using agents with different sites of action. Combination analgesics also provide the opportunity for complementary pharmacokinetic activity and potentially synergistic analgesia. A reduced adverse event profile with comparable efficacy is the goal of combination therapy.
Muscle Relaxants
The use of skeletal muscle relaxants is commonly used to assist in the management of osteoarthritic and intervertebral disc related painful conditions, especially acute low back pain and strain. Neural compression/irritation may manifest itself as skeletal muscle spasm. The use of many muscle relaxants has been limited due to their dose related sedation and in some cases (e.g., carisoprodol [Soma], prodrug of meprobamate [Miltown]) a high abuse potential and attractive street value. Nonetheless, the use of centrally acting muscle relaxants have evidence backing their benefit independent of their sedating properties. The use of botulinum toxin as a local muscle relaxant has demonstrated efficacy in double-blinded studies of low back pain, particularly with paravertebral trigger points in disc herniations, most commonly on the contralateral side.5
Antidepressants
There has been well-documented efficacy and safety of antidepressants in major chronic pain conditions; namely, neuropathic pain, headaches, low back pain, fibromyalgia, irritable bowel syndrome (IBS) and cancer pain. The beneficial use of antidepressants in chronic pain has been primarily limited to the use of tricyclic antidepressants. Pasternak first made this observation in 1983.6 While the newer noradrenergic and serotonin reuptake inhibitors have less supporting evidence in their use in chronic pain, they can be recommended in neuropathic pain, migraines and fibromyalgia.7 The beneficial effect of SSRIs appears to be in an improved feeling of “well-being” and not in an actual decrease in pain.7
Anticonvulsants
Anticonvulsant drugs are most effective for relieving neuropathic pain most commonly caused by damage to nerves or spinal cord (e.g., injury or disease) or neural compression (e.g., intervertebral disc herniation). Examples of documented benefit are neuropathic pain, e.g., postherpetic neuralgia and painful diabetic neuropathy. Approximately two-thirds of patients who take either carbamazepine, gabapentin or pregabalin can be expected to achieve good pain relief. More recent studies have documented beneficial effects of gabapentin in radiculopathy associated with low back pain8 and perioperative pain.9 While gabapentin is increasingly being used for neuropathic pain the evidence would suggest that it is not superior to carbamazepine.10
Summary
The discovery of a wide variety of non-opioid receptors and the identification of their role in pain modulation, has led to a literal explosion in a combination pharmacotherapeutic approach to pain management. In mild to moderate pain, effective pain control may be able to be achieved without the use of opioids. Furthermore, the more widespread availability of non-medical techniques such as acupuncture, transcutaneous nerve stimulation (i.e., TENS), physical therapy, chiropractic care and complementary strategies that assist in coping mechanisms make achieving pain relief without opioids a real option.
References
1. Portenoy RK, Hagen NA. Breakthrough pain: definition, prevalence and characteristics. Pain. 41:273-281, 1990.
2. Mercadante S, Maddaloni S, Roccella S, Salvaggio L. Predictive factors in advanced cancer pain treated only by analgesics. Pain. 50:151-155, 1992.
3. Towheed et al. Acetaminophen for osteoarthritis. Cochrane Database Syst Rev. Jan 25;(1):CD004257, 2006
4. J Clin Hypertension 2:319-323, 2000
5. Foster et al. Botulinum toxin A and chronic low back pain: a randomized, double-blind study. Neurology 56(10):1290-3, 2001
6. Spiegel K, Kalb R, Pasternak G. Analgesic activity of tricyclic antidepressants. Ann Neurol. 13(4):462-465, 1983
7. Verdu et al. Antidepressants in the treatment of chronic pain. Drugs 68(18) 2611-2632, 2008
8. Chou et. al. Medications for acute and chronic low back pain: a review of the evidence for an American Pain Society/American College of Physicians clinical practice
guideline. Ann Intern Med. 2007 Oct 2;147(7):505-14
9. Tippanna et. al. Do surgical patients benefit from perioperative gabapentin/pregabalin? A systematic review of efficacy and safety. Anesth Analg. 2007 Jun;104(6):1545-56
10. Wiffen et. al. Anticonvulsant drugs for acute and chronic pain. Cochrane Database of Systematic Reviews 2005, Issue 2. Art. No.: CD001133. DOI: 10.1002/14651858.CD001133.pub2
Minimally Invasive Treatment of Disc Herniation
Introduction
Since the most common reason for low back pain is a musculo-ligamentous sprain or strain, generally speaking, patients will improve over a 6-week period, with or without treatment. However, this is not to say that all back pains will respond in like manner. Asides from the patient with arthritis which is the most common reason for resistant to therapy low back pain, patients with documented herniated nucleous pulposus (HNP) with radiatin to their legs should be treated in a step-wise progressive manner of increasing interventionality. Many may benefit from conservative measures such as medications (e.g., short course of oral steroids, NSAID’s, muscle relaxants, low dose antineuropathic meds, etc) and physical therapy. Epidural steroid injections are now commonly used in this early conservative regimen. Physical therapy may be put off for a week or two until the patient is able to fully participate. Epidural steroid injections may provide symptomatic improvement to allow for effective physical therapy to ensue. There appears to be no benefit from bed rest in these patients complaining of radicular (referred pain down ams or legs) disease.6 There may be a role for massage therapy in the acute phase of back pain, but further research is needed in this regard.7
If a patient does not demonstrate significant improvement after 4-6 weeks of the aforementioned conservative regimen and lower extremity pain is a primary complaint, then considerations for needle based, outpatient PDD (Percutaneous Disc Decompression) prior to surgery should be considered. Surgical indications remain with extruded discs, free disc fragments and acute neurologic emergencies (e.g., cauda equina syndrome). For patients with persistent neurologic symptoms despite conservative measures after 4-6 weeks, PDD is a reasonable alternative to open surgical disc decompression.
Types of PDD
Intradiscal Electrothermy (IDET) IDET technology uses temperature controlled heat imbedded in a thin catheter placed into the disc under fluoroscopic guidance. The heat is controlled by a microprocessor to generate disc wall temperatures ranging from 60-70°C. This temperature range should cauterize the small nerve fibers imbedded in the disc wall, the small blood vessels that have grown into the disc, and shrink the collagen protein material that makes up the disc wall. Collagen shrinkage should improve disc function and the cauterization of the nerve fibers should relieve pain. Shah and cols. proposed that rather than denervation, collagen denaturation and coalescence causes the beneficial effects of IDET on disc disease.8 Its utility in discogenic back pain has been questioned with one retrospective study reporting a 50% patient dissatisfaction rate, although 45% of all patients studied used no or less medication than before IDET and 53% said they would have the procedure again.9
Intradiscal Coblation® therapy (Nucleoplasty®) Nucleoplasty percutaneous disc decompression utilizes Coblation® technology for ablating and coagulating soft tissue. Coblation technology removes tissue by using low-energy radiofrequency waves to create an ionic plasma field from sodium atoms within the nucleus. This low-temperature plasma field removes tissue from the treatment area via a molecular dissociation process that converts the tissue into gases which exit the treatment site. Coblation does not rely on heat energy to remove tissue, so thermal damage and tissue necrosis may be minimized. Chen and collaborators performed a microscopic study on cadaver pigs that had undergone disc decompression with nucleoplasty and found clear evidence of coblation channels with no evidence of damage to surrounding tissue.10 More recently, Nau and Diederich measured 26 temperature points around the disc after nucleoplasty.11 While they also found a narrow area of coagulation, transient peaks of 80-90°C with temperatures of 60-65°C measured 3-4mm from the introducer. Due to the channels of destruction, nucleoplasty has proven to dramatically decrease intradiscal pressures in non-degenerated discs and may have a negligible effect in degenerated ones.12 Lumbar (channels of disc destruction) and cervical (“scoop” lesions) probes are available for use.
Mechanical disc removal (DeKompressor®) The DeKompressor device is an independent handheld system in which the probe rotates creating suction and removal of nucleus pulposus through the cannula using Archimede’s screw pump principle. The thixotropic nature of the nucleus pulposus (a fluid gel that becomes less viscous when in motion) facilitates transport through the probe’s pump mechanism. Older, degenerated discs generally remove less disc material as they are less hydrated and removal may be facilitated by the addition of a small amount of saline. Lumbar (17 gauge) and cervical (19 gauge) probes are available for use.
Laser disc decompression Lasers destroy tissue by generation of localized heat. In testing various lasers (CO2 lasers in continuous wave and pulse mode; erbium:YAG; Nd:YAG 1318 m and 1064 m; argon; Ho:YAG; excimer), Choy found greatest efficiency with CO2 laser in continuous wave and pulse mode and the lowest efficiency with the argon laser. Data on the Ho:YAG were unreliable, likely because of the early generation of laser tested. Sherk et.al. found that the CO2 laser produced the best cutting and ablating effects among the infrared lasers.13 Contact Nd:YAG and Ho:YAG (LASE®) lasers were nearly as satisfactory, offering the additional advantage of fiberoptic capability and the ability to be used in saline. The LASE® system also offers the ability to endoscopically view the area to be treated. The free-beam Nd:YAG laser and coagulation mode electrosurgical device produced unacceptably severe thermal change.
Back to Top
Skip to:
Introduction
Since the most common reason for low back pain is a musculo-ligamentous sprain or strain, generally speaking, patients will improve over a 6-week period, with or without treatment. However, this is not to say that all back pains will respond in like manner. Asides from the patient with arthritis which is the most common reason for resistant to therapy low back pain, patients with documented herniated nucleous pulposus (HNP) with radiatin to their legs should be treated in a step-wise progressive manner of increasing interventionality. Many may benefit from conservative measures such as medications (e.g., short course of oral steroids, NSAID’s, muscle relaxants, low dose antineuropathic meds, etc) and physical therapy. Epidural steroid injections are now commonly used in this early conservative regimen. Physical therapy may be put off for a week or two until the patient is able to fully participate. Epidural steroid injections may provide symptomatic improvement to allow for effective physical therapy to ensue. There appears to be no benefit from bed rest in these patients complaining of radicular (referred pain down ams or legs) disease.6 There may be a role for massage therapy in the acute phase of back pain, but further research is needed in this regard.7
If a patient does not demonstrate significant improvement after 4-6 weeks of the aforementioned conservative regimen and lower extremity pain is a primary complaint, then considerations for needle based, outpatient PDD (Percutaneous Disc Decompression) prior to surgery should be considered. Surgical indications remain with extruded discs, free disc fragments and acute neurologic emergencies (e.g., cauda equina syndrome). For patients with persistent neurologic symptoms despite conservative measures after 4-6 weeks, PDD is a reasonable alternative to open surgical disc decompression.
Types of PDD
Intradiscal Electrothermy (IDET) IDET technology uses temperature controlled heat imbedded in a thin catheter placed into the disc under fluoroscopic guidance. The heat is controlled by a microprocessor to generate disc wall temperatures ranging from 60-70°C. This temperature range should cauterize the small nerve fibers imbedded in the disc wall, the small blood vessels that have grown into the disc, and shrink the collagen protein material that makes up the disc wall. Collagen shrinkage should improve disc function and the cauterization of the nerve fibers should relieve pain. Shah and cols. proposed that rather than denervation, collagen denaturation and coalescence causes the beneficial effects of IDET on disc disease.8 Its utility in discogenic back pain has been questioned with one retrospective study reporting a 50% patient dissatisfaction rate, although 45% of all patients studied used no or less medication than before IDET and 53% said they would have the procedure again.9
Intradiscal Coblation® therapy (Nucleoplasty®) Nucleoplasty percutaneous disc decompression utilizes Coblation® technology for ablating and coagulating soft tissue. Coblation technology removes tissue by using low-energy radiofrequency waves to create an ionic plasma field from sodium atoms within the nucleus. This low-temperature plasma field removes tissue from the treatment area via a molecular dissociation process that converts the tissue into gases which exit the treatment site. Coblation does not rely on heat energy to remove tissue, so thermal damage and tissue necrosis may be minimized. Chen and collaborators performed a microscopic study on cadaver pigs that had undergone disc decompression with nucleoplasty and found clear evidence of coblation channels with no evidence of damage to surrounding tissue.10 More recently, Nau and Diederich measured 26 temperature points around the disc after nucleoplasty.11 While they also found a narrow area of coagulation, transient peaks of 80-90°C with temperatures of 60-65°C measured 3-4mm from the introducer. Due to the channels of destruction, nucleoplasty has proven to dramatically decrease intradiscal pressures in non-degenerated discs and may have a negligible effect in degenerated ones.12 Lumbar (channels of disc destruction) and cervical (“scoop” lesions) probes are available for use.
Mechanical disc removal (DeKompressor®) The DeKompressor device is an independent handheld system in which the probe rotates creating suction and removal of nucleus pulposus through the cannula using Archimede’s screw pump principle. The thixotropic nature of the nucleus pulposus (a fluid gel that becomes less viscous when in motion) facilitates transport through the probe’s pump mechanism. Older, degenerated discs generally remove less disc material as they are less hydrated and removal may be facilitated by the addition of a small amount of saline. Lumbar (17 gauge) and cervical (19 gauge) probes are available for use.
Laser disc decompression Lasers destroy tissue by generation of localized heat. In testing various lasers (CO2 lasers in continuous wave and pulse mode; erbium:YAG; Nd:YAG 1318 m and 1064 m; argon; Ho:YAG; excimer), Choy found greatest efficiency with CO2 laser in continuous wave and pulse mode and the lowest efficiency with the argon laser. Data on the Ho:YAG were unreliable, likely because of the early generation of laser tested. Sherk et.al. found that the CO2 laser produced the best cutting and ablating effects among the infrared lasers.13 Contact Nd:YAG and Ho:YAG (LASE®) lasers were nearly as satisfactory, offering the additional advantage of fiberoptic capability and the ability to be used in saline. The LASE® system also offers the ability to endoscopically view the area to be treated. The free-beam Nd:YAG laser and coagulation mode electrosurgical device produced unacceptably severe thermal change.