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13 Interventional Treatment for Chronic Pain

13 Interventional Treatment for Chronic Pain
The Massachusetts General Hospital Handbook of Pain Management

13
Interventional Treatment for Chronic Pain

Milan Stojanovic

Divinum est sedare dolorem—“It is divine to allay pain.”
—Galen (A.D. 129-199)

I. Spinal cord stimulation for chronic pain

1. Mechanism of action

2. Indications and patient selection

3. Stimulator trials

4. Choice of hardware

5. Implantation techniques

6. Troubleshooting and complications
II. Chronic intrathecal therapy for cancer and nonmalignant pain

1. Patient selection

2. Screening

3. Hardware selection

4. Medication selection and dosage

5. Complications and side effects
III. Discography

1. Brief overview of disc anatomy and pathophysiology

2. Discogenic low back pain: diagnostic studies

3. Technical aspects of lumbar discography

4. Discogenic low back pain: treatment options
IV. Intradiscal electrothermal therapy
V. Vertebroplasty
Selected Readings

In recent years, complex interventions for pain control have become part of everyday practice in pain clinics. Although interventions are more invasive than nerve blocks, many of them are not neurodestructive. Unlike nerve ablation, they may be reversible and therefore more appropriate for use in patients with nonmalignant pain. Their clinical efficacy has been widely documented. In carefully selected patients, these interventions can reduce pain and suffering, increase functional status, decrease oral medication intake, and facilitate an early return to work. In comparison with the more conservative measures for pain control, interventional treatments may appear costly, but when a good outcome is achieved, their overall cost can actually be lower (e.g., decreased cost of medications, fewer emergency room visits, less absence from work).
The implementation of these interventions should be integrated into a multidisciplinary team treatment plan. Patient benefit from these procedures can be achieved only by careful evaluation of scientific evidence, good clinical judgment, and excellent technical skills.
I. SPINAL CORD STIMULATION FOR CHRONIC PAIN
Electrical stimulation for treatment of pain was first documented in 600 B.C., utilizing electrical power from the torpedo fish. However, electrical treatment did not find a place in pain medicine until 1967, when spinal cord stimulation (SCS) was introduced by Shealy and associates. Their work was based on the “gate control” theory of pain proposed by Melzack and Wall and published just 2 years earlier. Initially, the SCS implantation involved open laminectomy, performed only by neurosurgeons. With recent advances in technology, the SCS has become a minimally invasive treatment and it is currently performed by physicians from various specialties. Further improvements in hardware design and patient selection criteria have enhanced the efficacy of SCS, and success rates of 50% to 70% have been recently reported. Besides SCS, peripheral nerve stimulation (PNS) can be performed in selected patients with localized neuropathic pain. Today, SCS presents a valuable tool for treatment of many chronic pain conditions.
1. Mechanism of action
The Melzak and Wall gate control theory of pain was a foundation for the first SCS trials. It was based on the idea that stimulation of A-beta fibers closes the dorsal horn “gate” and reduces the nociceptive input from the periphery. However, it seems that other mechanisms play a more significant role in the mechanism of SCS action.
One proposed mechanism involves increased dorsal horn inhibitory action of neurotransmitters, such as g-aminobutyric acid (GABA) and adenosine A-1, during SCS. The potential activation of descending analgesia pathways by serotonin and norepinephrine is another explanation for SCS action. In patients with peripheral ischemic pain, the SCS may act by a combination of two mechanisms: suppression of sympathetic activity and suppression of a calcitonin gene-related peptide (CGRP)–mediated mechanism. The probable mechanism for pain relief in ischemic heart disease is redistribution of the coronary blood flow from regions with normal perfusion to regions with impaired perfusion. Also, SCS may suppress the excitatory effects of myocardial ischemia on intrinsic cardiac neurons.
2. Indications and patient selection
Patients with complex regional pain syndrome (CRPS) or with neuropathic pain with upper and lower extremity involvement are the best candidates. Excellent long-term success rates (50% to 91% efficacy and a decrease in analgesic consumption by 50%) have been reported for SCS used in patients with CRPS.
However, the same does not apply to phantom limb pain, stump pain, or spinal cord injury pain. The most likely explanation is that central nervous system (CNS) remapping, which may be critical to the development of these pain syndromes, is not affected by SCS. Diabetic neuropathy may respond well to SCS, but the infection risks in these patients are higher than in the nondiabetic population. The use of SCS in postherpetic neuralgia is controversial.
Patients with failed back surgery syndrome (FBSS) may respond well to SCS. It has been documented that patients with FBSS respond better to SCS than to reoperation. This applies in particular to low back pain (LBP) with a radiating component to the leg. In these patients, the chance of long-term success with SCS varies from 12% to 88%, with an average efficacy of 59% as indicated by a systematic review of the literature. In addition, 25% of patients may return to work, 61% show an improvement in activities of daily living, and 40% to 84% decrease their consumption of analgesics. Opinions on axial LBP (pain limited only to the low back area) are divided. Some studies show that the dual-lead system provides better pain relief for axial LBP than single-lead stimulation, but others find the opposite.
Severe peripheral vascular disease is also an indication for SCS. Patients with advanced peripheral vascular disease who are not surgical candidates respond well to SCS, with reported efficacy rates ranging from 60% to 100%. Besides providing pain relief, SCS promotes ulcer healing and potentially contributes to limb salvage.
Ischemic heart disease refractory to pharmacologic and surgical treatments may respond well to SCS, with reported efficacy rates of 60% to 80% several years after implantation. These patients have demonstrated a reduction in anginal pain, decreased use of short-acting nitrates, and increased exercise capacity. SCS does not completely abolish anginal pain, but it raises the anginal threshold. Fear of a potential increase in myocardial damage does not seem to be justified.
New indications and techniques for PNS have emerged recently. Some patients with occipital neuralgia seem to respond well to PNS. In those cases, the SCS lead is placed subcutaneously around the C1-2 spinous process. In patients with pelvic pain (e.g., interstitial cystitis, pain of unknown origin), sacral placement of two to four SCS leads may provide adequate analgesia. Sacral placement can also be helpful in patients with impaired bladder control. Some cases of lumbar radiculopathy may respond better to SCS leads placed directly through neural foramina (retrograde lead placement).
Infection, drug abuse, and severe psychiatric disease are major contraindications for SCS implantation. Before SCS implantation, a psychological evaluation of patient is recommended.
3. Stimulator trials
Before proceeding with permanent SCS implantation, a stimulation trial is warranted. The trial allows patients to evaluate the SCS analgesic activity in their everyday surroundings. The criteria for a successful trial include at least a 50% pain reduction, a decrease in analgesic intake, and a significant functional improvement. The SCS trial is a minimally invasive procedure (similar to placing an epidural catheter), and it can positively predict a long-term outcome in 50% to 70% of cases.
There is no consensus on the length of an SCS trial. Minimal trial time should be 24 hours, although many centers perform 3- to 5-day trials. The trial begins in the hospital with proper SCS adjustment, after which the patient is discharged for several days of home trial. In cases of equivocal results, the trial time can be extended.
There are two technical approaches for an SCS trial. In the first approach, the SCS lead is placed percutaneously. This has the advantage of minimal invasiveness. At trial completion, the lead is removed, and a new lead and internal pulse generator (IPG) are placed (on a separate occasion). The other approach is to tunnel in and anchor the trial lead via a surgical incision. This approach simplifies the final procedure and ensures that stimulation coverage remains the same during both the trial period and the permanent implantation. The major disadvantage of the second approach is the need for a second visit to the operating room for lead removal in the case of an unsuccessful trial.
A percutaneous trial followed by lead placement via a laminotomy is another, less frequently utilized approach for SCS. In this case, a lead with wider electrodes is placed via laminotomy during permanent implantation. Wider electrodes might provide better coverage in certain patients, and they are less prone to migration than standard SCS leads.
4. Choice of hardware
The permanent SCS hardware consists of the SCS lead, an extension cable, a power source, and a pulse generator.
The number of electrodes in the lead varies from four (Medtronic and ANS) to eight (ANS). The distance between the electrodes and the length of the leads also can differ. It is not clear whether an increased number of electrodes provides better coverage, but it might be beneficial in case of lead migration. The leads with minimal space between electrodes (such as the Medtronic Quad compact lead) are better suited for localized pain (such as foot pain) or cases of isolated axial LBP. Many leads contain a removable stylet, which eases lead steering during implantation.
There are two types of pulse generators: (a) the completely implantable pulse generator containing a battery, and (b) an IPG supplied by external power through the radiofrequency antenna applied to the skin. The implanted pulse generator is more convenient to use and can be easily adjusted by the patient using a small telemetry device. Patients can turn the stimulator on and off, and they can control the stimulation amplitude, frequency, and pulse width. A separate external programmer allows more complex IPG reprogramming by the physician. In case of inadequate stimulation, the physician can change the polarity and the number of functioning electrodes to provide better stimulation coverage. The batteries have to be changed every 3 to 6 years, which requires a brief visit to the operating room. The battery life depends on the time the stimulator is used and the stimulation amplitude. The externally powered IPG, therefore, has an advantage over the implanted one in patients requiring higher amplitudes of stimulation, which deplete implanted batteries in a short time.
5. Implantation techniques
For lumbar lead placement, the patient is placed in the prone position, and for cervical placement both prone and lateral decubitus positions are used. The patient is prepared and draped in usual fashion. Both trial and permanent implantations are performed under local anesthesia with light intravenous (IV) sedation. The most common entry sites are the T12-L1 and L1–L2 spinal interspaces for the lumbar area and C7-T1 for the cervical area. These interspaces are first identified with fluoroscopic guidance, making sure to obtain a true anteroposterior (AP) view. The true AP view is achieved by C-arm rotation until the spinous process is placed on the midline in relation to the spinal pedicles.
For the percutaneous SCS trial, the Tuohy needle entry site is at the level of the spinous process below the desired interspace. It is important to achieve a shallow entry angle or to use the alternate Piles needle. The needle tip should stay close to midline during insertion. As the needle is advanced, lateral fluoroscopic view can be obtained to assess needle depth. Once adequate depth is achieved, the loss-of-resistance technique is used to identify the epidural space. At this point, the SCS lead is inserted into the epidural space under continuous fluoroscopic guidance. The curved stylet, or curved lead tip, allows lead steering. The lead tip during insertion and at final position should lie at the lateral border of the spinous process on the ipsilateral side of the pain.
Once adequate lead position is obtained, the trial stimulation is performed. It is important that stimulation paresthesias provide 70% to 80% overlap with the patient’s pain location. Adequate patient feedback during this stage is important. Maximal effort should be used to provide adequate pain coverage, since this optimizes the trial. Frequent lead repositioning might be needed during this stage. Once adequate coverage is achieved, the needle is removed under continuous fluoroscopy, ensuring no change in lead position. The lead is then taped to the skin.
Permanent stimulator placement technique is similar to the trial. Although the trial is usually done in the pain clinic setting, permanent SCS placement is performed in the operating room. Under local anesthesia and IV sedation, a skin incision is made along the cervical or lumbar insertion site. Tissue dissection is performed until lumbar fascia is encountered. At that point, the Tuohy needle and the stimulator lead are inserted as done in the SCS trial. Once adequate coverage is obtained, the Tuohy needle is removed under continuous fluoroscopic guidance and the SCS lead is anchored with sutures to the fascia and supraspinous ligament. The pocket for the IPG is made in the gluteal or abdominal area. The SCS lead is then connected to the IPG through an extension cable tunneled through the skin. The skin and subcutaneous tissues are closed in layers.
Patients should avoid any extreme activity for the first 6 to 8 weeks following permanent SCS implantation to prevent lead migration and allow for epidural scar tissue formation.
Lead positioning
The SCS topographic coverage depends on the spinal level at which the SCS lead tip is positioned. The following landmarks are for orientation only; the variance can be very high in individual patients. Careful intraoperative mapping is needed for optimal coverage (“sweet spot placement”).
Upper extremity: SCS tip at a level between C2 and C5. The shoulder area can be difficult to cover (Fig. 1).

Figure 1. Spinal cord stimulation (SCS) lead at the C2-3 level as seen on lateral fluoroscopic view (A) and anteroposterior (AP) view (B). Note the alignment of the SCS lead with a lateral margin of the odontoid process in the AP view.

Foot: SCS lead tip at a level between T11 and L1 (Fig. 2).

Figure 2. SCS lead placed at the thoracic spinal level as seen in lateral (A) and AP fluoroscopic view (B).

Lower extremity: SCS lead tip at the T9–10 level
Low back: SCS lead tip at a level between T8 and T10; two parallel leads can be used.
Chest: SCS lead tip at the T1–2 level.
Occipital neuralgia: SCS lead placed around C1–2 subcutaneously.
Pelvic pain: multiple SCS leads placed retrogradely within the sacrum or through foramina at S2 to S4.
6. Troubleshooting and complications
SCS Not Functioning or Inadequate Coverage

1.
Obtain AP and lateral fluoroscopic images of SCS lead tip to rule out lead migration.

2.
Image the IPG and all connections, and search for disconnection or breakage.

3.
Using programmer, check the batteries.

4.
Change amplitude and pulse width.

5.
Reverse electrode polarity, and change electrodes activated if there is no response to prior measures.

6.
If adequate pain coverage cannot be obtained, measure impedance of each electrode in relation to the IPG. Exactly the same impedance on two electrodes raises the possibility of a short circuit between the two electrodes. Some mechanical failures might require surgical revision and replacement of affected SCS components.
Progressive decrease in stimulation threshold
Consider intrathecal migration of the SCS lead. If it stays unnoticed, it can lead to serious complications such as spinal cord injury. Intrathecal migration is most common in patients with significant spinal canal stenosis. If this condition is suspected, a magnetic resonance imaging (MRI) scan of the targeted spinal level should be obtained before anticipated SCS placement.
SCS and pacemakers
The SCS can cause interference and inhibition of a cardiac pacemaker if they are used simultaneously. However, both devices can be used in the same patient if these guidelines are followed: (a) both devices should be programmed in bipolar mode, (b) the SCS frequency should be set at 20Hz, and (c) each SCS programming should be performed using continuous electrocardiographic (ECG) monitoring. A cardiology consult should be obtained in these patients, and the recommendations of the pacemaker’s manufacturer should be closely followed.
Other complications
The most common other complications of SCS are hardware failure, lead migration, infection, skin irritation at the IPG site, and failure to provide pain relief. Bleeding at the IPG site (subcutaneous hematoma) is usually self-limiting and gradually reabsorbs in a few weeks. If infection occurs at the IPG insertion site, make sure to aspirate the site before initiating antibiotic coverage and removing the hardware.
II. CHRONIC INTRATHECAL THERAPY FOR CANCER AND NONMALIGNANT PAIN
Intrathecal drug delivery has gained its popularity since the discovery of opioid receptors in the spinal cord. It provides targeted delivery of medications and avoids side effects encountered by systemic administration of drugs. Opioids are delivered to the intrathecal space via a surgically implanted subcutaneous pump containing a reservoir for the medication. The pump is easily refilled with medication every 2 to 4 months depending on the infusion rate.
Medications other than opioids have been used recently for intrathecal delivery. This includes local anesthetics, clonidine, and baclofen, given alone or in combination with opioids. Because numerous receptors involved in nociceptive transmission are located in the spinal cord, this approach seems to be very promising. The efficacy of intrathecal drug delivery has been shown in patients with malignant and nonmalignant pain.
The completely implanted intrathecal system has many advantages over the epidural drug delivery via an external catheter. The epidural route is more costly because of the maintenance needed for the external system, and it is frequently more inconvenient for the patient; therefore, it should be reserved for short-term use only (less than 3 months). The completely implanted intrathecal delivery is preferred when treatment is expected to last longer than 3 to 6 months. Patients with implanted intrathecal pumps may safely undergo an MRI procedure for other purposes.
1. Patient selection
Cancer pain responds well to intrathecal therapy in carefully selected patients. The following cancer patients might be considered for intrathecal trial:

Patients who have failed oral or IV opioids as a result of severe side effects (nausea, vomiting, sedation, constipation)

Patients who have a life expectancy of more than 3 months

Patients who have no obstruction in CSF flow

Patients who have neuropathic cancer pain that does not respond to oral regimen and nerve blocks.
The main contraindication for intrathecal therapy is infection.
Nonmalignant pain may respond to intrathecal therapy but it should be considered as a last resort. In general, patients with cancer pain tend to respond better to intrathecal therapy than patients with nonmalignant pain. Therefore, the selection criteria for intrathecal therapy for nonmalignant pain should be very strict. Only patients who have failed nerve blocks, oral medications, physical therapy, and cognitive-behavioral programs and who have passed psychological evaluation should be considered for intrathecal trial.
2. Screening
Before considering implantation of intrathecal hardware, patients should undergo a trial procedure to better assess the odds of a favorable outcome. The actual trial procedure varies, and no consensus has been made on the best procedure. Preceding the trial, oral opioids are either discontinued or decreased substantially. It is important to monitor the patient for signs of respiratory depression during the trial. The most common screening methods are the following:
An intrathecal trial is performed by implanting the temporary intrathecal catheter. Pediatric or standard epidural catheters can be used for this purpose. After intrathecal placement, the catheter is taped to the skin. The medication bolus is given first, followed by continuous infusion via an external infusion pump. The intrathecal opioid dose starts at 1/300th of the usual oral daily dose. The patient is kept in a hospital, for several days up to 3 weeks, during which time the infusion rate is gradually increased. The longer the trial time is, the smaller the likelihood of a placebo response. The patient pain intensity score, functional status, and use of medications for breakthrough pain are monitored during the trial period.
An epidural trial is performed in the same way as the intrathecal trial, except that the catheter is placed in the epidural space. The administered epidural opioid daily dose is higher than the intrathecal one, representing 1/30th of the usual daily oral dose.
A one-time bolus is the simplest screening method. The intrathecal bolus of medication is given and the patient is monitored for 24 hours. The patient pain intensity score, functional status, and use of medications for breakthrough pain are monitored. This method does not allow dose titration, as the other methods do, but it can provide information on patient response to intrathecal opioids.
A side-port catheter can be surgically implanted for a trial. Its advantages include the ease of adding an implanted infusion pump in case the trial is successful. However, the added risk of infection, and the need to surgically remove the catheter in the case of a failed trial, are disadvantages of using this approach.
3. Hardware selection
Two kinds of pumps exist: (a) battery powered externally programmable pumps and (b) nonprogrammable pumps, many of them gas driven. The amount of medication delivered by nonprogrammable pumps is dependent on drug concentration. Although externally programmable pumps offer the great advantage of an adjustable infusion rate, continuous-rate pumps can be used in patients requiring less frequent rate adjustments.
4. Medication selection and dosage
All intrathecally administered medications should be preservative free. The most commonly administered intrathecal medication is morphine. Other opioids include fentanyl, sufentanil, hydromorphone, and meperidine.
To convert intrathecal doses to other routes of administration, the following ratios are used: (a) intrathecal to epidural, 1:10; (b) intrathecal to IV, 1:100; (c) intrathecal to oral, 1:300. In opioidnaive patients, morphine should be started at 0.2 mg/day and gradually increased. In opioid-tolerant patients, the initial intrathecal dose should be less than the conversion dose, and oral opioids should be used for breakthrough pain. Gradually, the intrathecal dose should be increased and breakthrough pain medications discontinued.
The addition of local anesthetics to intrathecal opioids may be used for cancer and nonmalignant pain, with particular benefit to patients with a neuropathic component of pain. A typical bupivacaine dose range is from 2 to 30 mg/day, although dosages of over 100 mg/day have been reported. Alpha-adrenergic agonists (clonidine, epinephrine) can be used in conjunction with opioids. Clonidine is now approved by the U.S. Food and Drug Administration (FDA) for epidural administration, and its intrathecal-equivalent dosage is 50 to 900 µg/day. It should be carefully titrated since it can cause significant hypotension (most severe in dosage range of 400 to 570 µg/day).
Other investigational drugs are used intrathecally, and their use is supported by excellent results in clinical trials. Somatostatin seems to be particularly beneficial for the treatment of cancer pain. For neuropathic and nociceptive pain, the new investigational drugs include: calcium channel blockers (SNX-111), acetylcholinesterase (neostigmine), N-methyl-D-aspartate (NMDA) receptor antagonist (ketamine), GABA-A receptor agonists (midazolam), and GABA-B receptor agonist (baclofen). Many other intrathecally administered analgesics have proven their efficacy in animal research and await final testing in human clinical trials.
5. Complications and side effects
Medication-Related Complications
Medication-related side effects and complications of neuraxial opiates include respiratory depression, pruritus, nausea, vomiting, urinary retention, reduced libido, edema with weight gain, and constipation.
Respiratory depression can occur immediately after opioid administration or with several hours’ delay. It is much more frequent in opioid-naive patients. The factors increasing the risk for respiratory depression are advanced age, high opioid dose, and concomitant use of baclofen, benzodiazepines, and sedatives. Monitoring the vital signs and pulse oximetry is mandatory following initiation of an intrathecal opioid infusion.
The treatment of respiratory depression depends on its severity. The intrathecal infusion should be discontinued or reduced. If the patient cannot be aroused, IV naloxone should be administered. In severe cases, intrathecal naloxone can be administered in conjunction with airway protection and assisted ventilation.
Pruritus, nausea, and vomiting usually occur with initiation of intrathecal opioid bolus administration and can precede the onset of pain relief. These side effects can be prevented by more gradual opioid dose increase.
The incidence of urinary retention ranges from 40% to 80% and is not dose dependent. It occurs most often in men with an already-enlarged prostate. Cholinomimetic drugs (terazosin and carbachol) can be effective in treating urinary retention.
Hormonal abnormalities are reported with intrathecal opioid administration. Serum lipids, estrogens, androgens, insulin-like growth factor (IGF-1), and 24-hour urinary cortisol should be monitored in these patients. There is a 3% to 5% incidence of decreased libido in patients receiving intrathecal opioid therapy, because of hormonal abnormalities. Persistent decreased libido may require hormonal replacement. Approximately 5% to 10% of patients may experience weight gain and edema, which is not dose dependent.
Surgical complications
Infection at the pump insertion site may require complete hardware removal. Symptoms of infection are pain at the insertion site, local increase in temperature, and edema. Antibiotics should be started after wound cultures (by aspiration) are obtained. Seroma at the insertion site is usually benign and does not require revision. Necrosis and skin perforations can also occur and should be surgically treated.
Meningitis presents with stiff neck, fever, and meningeal signs. The CSF can be obtained from the pump for cultures and cell count.
Granuloma formation at the catheter tip is a very rare complication, potentially leading to cord compression. MRI of the spinal cord is indicated if neurologic symptoms occur in these patients.
Bleeding at the pump site usually spontaneously resolves, although it can increase the incidence of infection. Epidural hematoma can lead to spinal cord compression.
A CSF leak occurs after almost any intrathecal pump placement and if significant can lead to severe postdural puncture headache. If conservative therapy fails, headache can be treated with an epidural blood patch. However, the patch should be performed under fluoroscopic guidance to avoid risk of intrathecal catheter damage.
Hardware complications
Hardware complications usually involve the catheter and rarely the pump. Catheter kinking, disconnection, dislodgement, breaks, and migration can occur. Withdrawal symptoms and loss of analgesia are signs of inadequate drug delivery and warrant further investigation. Although the catheter is radiopaque and can be seen on fluoroscopy, it should be tested with a nonionic-contrast bolus. Before administering the bolus, medication should be aspirated from the catheter dead-space to avoid overdose. This can be accomplished through the pump side port. If the pump does not have a side port, it should be emptied, filled with radiolabeled tracer, and imaged.
Pump failures can also occur. Torsion of the pump within the pocket, and subsequent catheter kinking, can be prevented by adequate pump anchoring. The most serious technique-related complication is drug overdose caused by filling the pump through the side port. If this occurs, the CSF should be partially replaced with saline and the patient immediately transferred to the intensive care unit. Intrathecal naloxone should be administered.
Other mechanical pump failures include battery depletion and internal pump failure. The manufacturer’s recommendations and testing protocols should be followed meticulously to rule out internal pump failure.
III. DISCOGRAPHY
Discography is a diagnostic procedure and has no therapeutic value. It is best suited for diagnosis of discogenic low back pain caused by internal disc disruption. The term discogenic pain should not be confused with disc herniation or protrusion. The pathology of and treatment options in these two conditions differ significantly.
1. Brief overview of disc anatomy and pathophysiology
Each disc consists of a central mass, the nucleus pulposus, and an outer ring, the annulus fibrosus. The annulus fibrosus is connected by Sharpey’s fibers to the articular surface of vertebral bodies. The inner structure of the annulus is formed of concentric lamellae of collagen fibrils. There are 10 to 12 overlapping concentric lamellae in each annulus. The lamellae are thinner and less numerous at the posterior portion of the disc. Many studies suggest that the annulus is a well-innervated structure. Degenerated discs lose nuclear hydrostatic pressure, which leads to buckling of the annular lamellae. With progressive degeneration of the disc, the annulus undergoes delamination and develops fissures. “Microfractures” of the annular collagen fibrils have been demonstrated using electron microscopy. The annular nociceptors become sensitized with the decrease in their firing thresholds. The increased stimulation of the dorsal root ganglion by sensitized nociceptors may cause a referred pain pattern to the lower extremities. Furthermore, the damaged disc promotes the growth of nerve fibers along radial tears into the inner annulus.
2. Discogenic low back pain: diagnostic studies
Most patients with discogenic LBP have increased pain with prolonged sitting. The pain can be limited to the back area (axial pain), or it can radiate to one or both lower extremities. The physical exam, including the straight leg raising test, can be normal.
Normal diagnostic imaging findings (e.g., by MRI) do not rule out internal disc derangement pathology. However, certain MRI findings are highly suggestive of discogenic disease:

Decreased disc signal intensity on T2-weighted MRI images is suggestive of disc dehydration.

High T2-weighted signal intensity within the annulus of a disc has been termed the high intensity zone (HIZ) and is associated with annular tears. Patients with an HIZ are more likely to suffer from LBP than patients without it.

A “bulging” or “protruding” disc on MRI is more likely associated with disc disruption and pain than a “normal” disc.

Even a disc that is completely normal on MRI can be associated with discogenic pain. The decrease in disc height is often seen when internal disc derangement has taken place.
Provocation discography remains the gold standard for the diagnosis of discogenic pain. The key feature of discography is the reproduction of the patient’s pain. Discography is performed at three or four lumbar levels, using unaffected discs as controls. Morphologically, a normal disc presents as a unilocular, bilocular, spherical, or rectangular shape. A degenerated disc loses its water content and may have tears and fissures in the annulus fibrosus. The most common types of annular tears are concentric, radial, and transverse tears. Although the pattern of the spread of contrast material is important, the concordant pain with low pressure or low volume discography is the most important diagnostic finding.
3. Technical aspects of lumbar discography
The patient is placed in the prone position and the lower back area is adequately prepared and draped. An AP fluoroscopic image is obtained first, providing good visualization of the selected disc. The end plates of adjacent vertebral bodies are aligned. The C-arm is then rotated to the oblique view, maintaining alignment of the vertebral bodies. The optimal endpoint of the rotation angle is when the superior articular process (SAP) image reaches the midline of the corresponding vertebral end plate. At this point, the skin entry site is determined by the radiopaque pointer overlapping the SAP projection.
After anesthetizing the skin with 1% lidocaine, an 18-gauge, 3-inch needle is inserted in a “tunneled view” toward the SAP. The needle tip should be advanced approximately 2 inches. A 22-gauge, 6-inch needle with a slightly bent tip is then inserted through the 18-gauge needle. Under tunneled fluoroscopic guidance, the needle is steered just lateral to the SAP, making sure that it is approaching the disc at midline. A slightly caudally placed needle can help to avoid contact with the nerve root. Once the needle has entered into the disc, a “spongy” feeling is encountered. From that point, several AP and lateral fluoroscopic views should be obtained to ensure that the needle tip is in the center of the disc.
The L5-S1 disc level can be more difficult to approach because of the iliac crest. Maneuvering the needle bend at its distal tip around the iliac crest usually helps.
Discography is performed once the needles are placed at all desirable levels (Fig. 3). Nonionic contrast (Omnipaque-240) is appropriate for discography, and it should be mixed with 5 to 10 mg/cc of antibiotic such as cefazolin.

Figure 3. Appropriate needle position for lumbar discography at L4, L5, and S1 levels as seen in AP fluoroscopic view. Note contrast spread, down the annular fissure at the L4 level to the right.

The concordant pain is sought at less than 30 pounds per square inch above opening pressure, or with less than 1.25 mL of contrast material administered into the disc. The reproduced LBP (or pain referred to the lower extremity) under these conditions is considered to be discogenic in origin. Disc disruption and leakage of dye through an annular tear is usually seen with the onset of pain. Disc disruption alone, without reproduction of the patient’s pain, is an insufficient finding for the diagnosis of discogenic pain.
Postdiscography computed tomography (CT) is not an absolutely necessary diagnostic tool, but it can be helpful in planning further treatments. The CT should be performed within 2 hours of discography. The most serious complication of discography is discitis. Although rare, it is very resistant to treatment because of the limited blood supply to the disc. Intradiscal administration of antibiotic minimizes its occurrence. Discography has been shown to be a generally safe procedure and has not been found to produce damage to the disc.
4. Discogenic low back pain: treatment options
There are several treatment options in a patient presenting with discogenic pain. Conservative therapy such as McKenzie exercises or dynamic lumbar stabilization exercises can be helpful in some patients.
Radiofrequency (RF) denervation of the annulus appears to be of limited value since RF requires a fluid environment to adequately disperse RF energy. In the case of discogenic pain, disc and annular tissues are often dehydrated. Also, current RF probes seem to be too small to treat large surface areas of annular tissue. Alternatively, the technique of annular denervation can be used. For this purpose, the RF lesioning of gray rami has been used with mixed results. Intradiscal steroid injections have also been used but with mostly unsatisfactory results. Laser disc lesioning has a high risk of complications.
Surgical approaches (anterior and posterior lumbar fusion, titanium cages) are the most commonly used treatments for discogenic LBP, with success rates in the range of 50% to 85%. Drawbacks of surgery are its expense and potential complications. Surgery may be reserved for severe morphologic disc damage, when regeneration of annulus fibrosus is unlikely.
IV. INTRADISCAL ELECTROTHERMAL THERAPY
Intradiscal electrothermal therapy (IDET) is a new, minimally invasive approach for the treatment of discogenic LBP. Initial results with this treatment are encouraging, but more clinical studies are needed to prove its efficacy. It involves percutaneously threading a flexible catheter (SpineCath) into the disc tissue with fluoroscopic guidance. The catheter is composed of thermal-resistive coil, enabling heating its distal part to the desired temperature.
The technique for approaching the disc for the IDET procedure is similar to that of discography. After the skin is infiltrated with local anesthetic, a 17-gauge introducer needle is inserted in the disc tissue guided by oblique fluoroscopic imaging. Once appropriate needle position is established by AP and lateral fluoroscopic views, the catheter is inserted through the needle. The SpineCath is designed to be easily navigated through the disc tissue. The final position of the electrode is such that the end of the catheter is placed circumferentially around the inner surface of the posterior annulus (Fig. 4). The best approach to the disc is from the side opposite the symptoms; however, some patients require ipsilateral approach if catheter navigation from the opposite side fails. IV sedation can be administered, but IV anesthesia is contraindicated during IDET procedure to ensure appropriate patient feedback.

Figure 4. SpineCath placement for intradiscal electrothermal therapy (IDET) procedure at the L4 spinal level as seen on AP fluoroscopic view. The thermal-resistive coil is placed along the inner surface of the posterior disc annulus.

Once the catheter is in a satisfactory position, as confirmed by AP and lateral fluoroscopy, the distal part of the catheter is heated gradually with the ORATEC ElectroThermal Spine System Generator. Increments in temperature are achieved automatically, and the target temperature is 80° to 90°C, which must be maintained for 4 to 6 minutes to achieve optimal results. The actual annular tissue temperature is up to 15°C lower than the temperature of the catheter tip. Comprehensive patient and cadaver temperature-mapping studies have shown the safety of reaching this high target temperature as long as the catheter tip is located within the disc tissue. The simultaneous epidural space temperatures remain within the normal range, reaching a maximum of 39.3°C even if the catheter tip is heated to 90°C. A slight increase in concordant pain during heating is normal. Patients can be discharged home 1 hour after the procedure.
The putative mechanisms of IDET action are thermal modification of collagen fibers and destruction of sensitized nociceptors in the annular wall. Besides the usual risks such as infection and bleeding, a possible serious complication of IDET is catheter tip shearing due to forceful manipulation. Inappropriate catheter handling can result in more serious complications, such as nerve damage or cauda equina injury.
Patients with discogenic pain for more than 6 months who have failed conservative treatment are considered appropriate candidates for IDET. However, patients with severe radicular symptoms due to a herniated disc or those with severe spinal stenosis are not good candidates. Also, a severely collapsed disc (>50% of disc height) or a disrupted disc might not respond well to IDET. In patients over 50 years of age, there may be an adverse effect on the disc healing process and therefore lower success rates with treatment. Multilevel disc disease and a history of prior spinal fusion are not contraindications for IDET.
Considering its potential advantages over surgery, IDET might become the treatment of choice for discogenic pain. It could potentially fill the large gap between conservative treatment and surgical options.
V. VERTEBROPLASTY
Percutaneous vertebroplasty is a relatively new procedure consisting of percutaneously injecting polymethylmethacrylate cement into vertebral bodies destabilized by osseous lesions and causing intractable pain. By reinforcing vertebral lesions, injected cement provides analgesia in these patients. The major indications for vertebroplasty are osteoporotic vertebral compression fractures, vertebral angiomas, and osteoporotic vertebral tumors.
The procedure is performed under fluoroscopic or CT guidance. With the patient in the prone position and under local anesthesia, an 11-gauge bone marrow biopsy needle is directed through the transpedicular approach into the vertebral body. The depth of the needle is ensured in lateral fluoroscopic views. An intraosseous venogram is then performed to ensure that the needle tip is not within a blood vessel. The cement is than injected under continuous fluoroscopic guidance.
Recent clinical studies have shown good efficacy of vertebroplasty. Potential complications include leakage of cement into adjacent structures with neural damage caused by mechanical compression and thermal necrosis. Therefore, high technical expertise is needed to perform this procedure. Current research efforts are focused on designing improved bone cement that does not leak into unwanted areas and that minimizes tissue damage.
SELECTED READINGS

1.
Barr JD, Barr MS, Lemley TJ, McCann RM. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine 2000;25: 923–928.

2.
Carey C, Lee H, Schaff RA, eds. The Washington manual of medical therapeutics, 29th ed. New York: Lippincott Williams & Wilkins, 1998.

3.
Cousins M, Bridenbaugh P, eds. Neural blockade in clinical anesthesia and management of pain, 3rd ed. Philadelphia: Lippincott, 1998.

4.
Deer T, Winkelmuller W, Erdine S, et al. Intrathecal therapy for cancer and non-malignant pain: Patient selection and patient management. Neuromodulation 1999;2:55–66.

5.
Kay J, Findling JW, Ralf H. Epidural triamcinolone suppresses the pituitary-adrenal axis in human subjects. Anesth Analg 1994; 79:501–505.

6.
Kemler MA, Barendse GA, van Kleef M, et al. Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. N Engl J Med 2000;343:618–624.

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Krames E, Bucher E, Hassenbuch S, Levy R. Future trends in the development of local drug delivery systems: Intraspinal, intracerebral and intraparenchymal therapies. Neuromodulation 1999; 2:133–148.

8.
North RB, Kidd DH, Zahurak M, et al. Spinal cord stimulation for chronic intractable pain: Two decades’ experience. Neurosurgery 1993;32:384–395.

9.
Parry SW, Kenny RA. The management of vasovagal syncope. Q J Med 1999;92:697–705.

10.
Saal SS, Saal AS. Management of chronic discogenic low back pain with a thermal intradiscal catheter. Spine 2000;25:382–388.

11.
Stanton-Hicks M. Spinal cord stimulation for the management of complex regional pain syndromes. Neurostimulation 1999;2: 193–201.

12.
Stojanovic M. Stimulation methods for neuropathic pain control. Curr Pain Headache Rep (in press).

13.
Tehranzadeh J. Discography 2000. Radiol Clin North Am 1998; 36:463–495.

14.
Waldman SD, Winnie AP, eds. Interventional pain management. Philadelphia: WB Saunders, 1996.

15.
Weissberg D, Refaely Y. Pneumothorax. Chest 2000;117: 1279–1285.

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4 comments on “13 Interventional Treatment for Chronic Pain

  1. […] back pain options – Google Blog Search 13 Interventional Treatment for Chronic Pain | Free Medical Textbook Discogenic low back pain: diagnostic studies. 3. Technical aspects of lumbar discography. 4. Discogenic low back pain: treatment options. IV. Intradiscal electrothermal therapy. V. Vertebroplasty Selected Readings. In recent … more info… […]

  2. jacks
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  4. good material for revision and practice.
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    Dr Nankar

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