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Epidural injections

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    Epidural injections

    Epidural injections for neuropain? anyone have any luck? experience?
    cauda equina

  • #2
    i'll let u know in about a month. got 2 scheduled coming in the next couple weeks. would like to see other input on it too. cool u asked first.

    Un désir ardent de coeur à sentir, guéri par seulement l'amour.


      The following are some abstracts describing nerve blocks as a means of treating pain. Hildebrandt (2001) points out some of the assumptions and difficulties of ensuring adequate therapies. Several recent studies have reported the epidural analgesia may prevent development of neuropathic pain after amputation (Fainsinger, et al., 2000).

      Much depends on what is being injected epidurally. Epidural steroid injections which is commonly used to reduce inflammation induced pain may actually contribute to neuropathic pain (Field, et al., 2000). Eisenach, et al. (2000) compared intrathecal and epidural clonidine, showing that intrathecal is >6x more potent than epidural. Takahashi, et al. (1998) described the beneficial effects of low-dose epidural ketamine. Intrathecal glycine (an inhibitory neurotransmitter) reduces neuropathic pain in rats (Simpson, et al., 1996). Epidural opioids may also be effective (Bedder, 1996; Collins, et al. 1996). Intrathecal morphine may also be effective for malignant pain (Wen, et al. 1996). Glynn & O'Sullivan (1996) compared epidural clonidine, lignocaine, and combination clonidine and lignocaine.


      • Hildebrandt J (2001). [Relevance of nerve blocks in treating and diagnosing low back pain--is the quality decisive?]. Schmerz. 15: 474-83. Schwerpunkt Algesiologie, Zentrum Anasthesiologie, Rettungs- und Intensivmedizin, Georg-August-Universitat Gottingen. Diagnostic nerve blocks: The popularity of neural blockade as a diagnostic tool in painful conditions, especially in the spine, is due to features like the unspecific character of spinal pain, the irrelevance of radiological findings and the purely subjective character of pain. It is said that apart from specific causes of pain and clear radicular involvement with obvious neurological deficits and corresponding findings of a prolapsed disc in MRI or CT pictures, a diagnosis of the anatomical cause of the pain can only be established if invasive tests are used [5]. These include zygapophyseal joint blocks, sacroiliacal joint blocks, disc stimulation and nerve root blocks. Under controlled conditions, it has been shown that among patients with chronic nonradicular low back pain, some 10-15% have zygapophyseal joint pain [58], some 15-20% have sacroiliacal joint pain [36, 59] and 40% have pain from internal disc disruption [60]. The diagnostic use of neural blockade rests on three premises. First, pathology causing pain is located in an exact peripheral location, and impulses from this site travel via a unique and consistent neural root. Second, injection of local aneasthetic totally abolishes sensory function of intended nerves and does not affect other nerves. Third, relief of pain after local anaesthetic block is attributable solely to block of the target afferent neural pathway. The validity of these assumptions is limited by complexities of anatomy, physiology, and psychology of pain perception and the effect of local anaesthetics on impulse conduction [28]. Facet joints: The prevalence of zygapophyseal joint pain among patients with low back pain seems to be between 15% and 40% [62], but apparently only 7% of patients have pure facet pain [8, 29]. Facet blockade is achieved either by injection of local anaesthetic into the joint space or around the medial branches of the posterior medial rami of the spinal nerves that innervate the joint. There are several problems with intraarticular facet injections, mainly failure to enter the joint capsule and rupture of the capsule during the injection [11]. There is no physiological means to test the adaequacy of medial nerve block, because the lower branches have no cutaneous innervation. Medial ramus blocks (for one joint two nerves have to be infiltrated) are as effective as intraarticular joint blocks [37]. Reproducibility of the test is not high, the specifity is only 65% [61]. For diagnosis of facet pain fluoroscopic control is always necessary as in the other diagnostic blocks. Sacroiliacal joint: Definitely the sacroiliacal joint can be the source of low back pain. Stimulation of the joint by injection in subjects without pain produces pain in the buttock, in the posterior thigh and the knee. There are many clinical tests which confirm the diagnosis, but the interrater reliability is moderate [53]. Intraarticular injection can be achieved in the lower part of the joint with fluoroscopic guidance only, but an accurate intraarticular injection, which is confirmed by contrast medium, even at this place is often difficult. It is not clear whether intraarticular spread is necessary to achieve efficacy. Discography: Two primary syndromes concerning the ventral compartment have been described: anular fissures of the disc and instability of the motion segment. In the syndrome of anular tear, leakage of nucleus pulposus material into the anulus fibrosus is considered to be the source of pain. The studies of Vaharanta [71] and Moneta [41] show a clear and significant correlation between disc pain and grade 3 fissures of the anulus fibrosus. intervertebral discs are difficult to anaesthetize. Intradiskal injections of local anaesthetics may succeed in relieving the patient's pain, but such injections are liable to yield false negative results if the injected agent fails to adequately infiltrate the nerve endings in the outer anulus fibrosus that mediate the patient's pain. In the majority of cases MRI provide adaequate information, but discography may be superior in early stages of anular tear and in clarifying the relation between imaging data and pain [71]. Selective spinal nerve injection: In patients with complicated radiculopathy, the contribution of root inflammation to pain may not be certain, or the level of pathology may be unclear. Diagnostic root blocks are indicated in the following situations: atypical topography of radicular pain, disc prolapses or central spinal stenosis at more than one level and monoradicular pain, lateral spinal stenosis, postnucleotomysyndrome. Injection of individual spinal nerves by paravertebral approach has to be used to elucidate the mechanism and source of pain in this unclear situations. The premise is that needle contact will identify the nerve that produces the patient's characteristic pain and that local anaesthetic delivered to the pathogenic nerve will be uniquely analgesic. Often, this method is used for surgical planning, such as determining the site of foraminotomy. All diagnostic nerve root blocks have to be done under fluoroscopic guidance. Pain relief with blockade of a spinal nerve cannot distinguish between pathology of the proximal nerve in the intervertebral foramen or pain transmitted from distal sites by that nerve. Besides, the tissue injury in the nerve's distribution and neuropathic pain (for instance as a result of root injury) likewise would be relieved by a proximal block of the nerve. Satisfactory needle placement could not be achieved in 10% of patient's at L4, 15% at L5 and 30% at S1 [28]. The positive predictive value of indicated radiculopathy confirmed by surgery ranged between 87-100% [14, 22]. The negative predictive value is poorly studied, because few patients in the negative test group had surgery. Negative predictive values were 27% and 38% of the small number of patients operated on despite a negative test. Only one prospective study was published, which showed a positive predictive value of 95% and an untested negative predictive value [66]. Some studies repeatedly demonstrated that pain relief by nerve root block does not predict success by neuroablative procedures, neither by dorsal rhyzotomy nor by dorsal gangliectomy [46]. Therapeutic nerve blocks - facet joints: Intraarticular injection of steroids offer no greater benefit than injections of normal saline [8, 15] and long lasting success is lacking. In this case, a denervation of the medial branches can be considered. To date three randomized controlled studies of radiofrequency facet denervation have been published. One study [20] reported only modest outcomes and its results remained inconclusive, another study [72] with a double blind controlled design showed some effects in a small selected group of patients (adjusted odds ratio 4.8) 3, 6 and 12 months after treatment, concerning not only reduction of pain but alleviating functional disability also. The third study (34a) showed no effect 3 months after treatment. Discogenic pain: Intradiscal radiofrequency lesions, intradiscal injections of steroids and phenol have been advocated, but there are no well controlled studies. Just recently, intradiscal lesion and denervation of the anulus has been described with promising results, but a randomized controlled study is lacking up to now [31, 55]. Epidural Steroids: Steroids relieve pain by reducing inflammation and by blocking transmission of nociceptive C-fiber input. Koes et al. [33] reviewed the randomized trials of epidural steroids: To date, 15 trials have been performed to evaluate the efficacy, 11 of which showed method scores of 50 points (from 100) ore more. The trials showed inconsistent results of epidural injections. Of the 15 trials, 8 reported positive results and 7 others reported negative results. Consequently the efficacy of epidural steroid injections has not yet been established. The benefits of epidural steroid injections seem to be of short duration only. Future efficacy studies, which are clearly needed, should take into account the apparent methological shortcomings. Furthermore, it is unclear which patients benefit from these injections. In our hands the injection technique can be much improved by fluoroscopic guidance of the needle, with a prone position of the patient, and lateral injection at the relevant level and with a small volume (1-2 ml) and low dose of corticosteroid (20 mg triamcinolone in the case of a monoradicular pain, for example). In the case of epidural adhesions in postoperative radicular pain [50], the study of Heafner showed that the additional effect of hyaloronidase and hypertonic saline to steroids was minimal. In our hands there was no effect in chronic radicular pain 3 months after the injection.

      • Fainsinger RL, de Gara C and Perez GA (2000). Amputation and the prevention of phantom pain. J Pain Symptom Manage. 20: 308-12. Division of Palliative Medicine, Department of Oncology, University of Alberta, Edmonton, Alberta, Canada. Although it has been proposed that preoperative analgesia with epidural administration of analgesics may prevent long-term phantom pain, published results to date have been contradictory and controversial. In this case report, we describe a 41-year-old man with local recurrence of squamous cell carcinoma of the anus who underwent a hemipelvectomy. Preoperatively he had a significant neuropathic pain syndrome requiring oxycodone 60 mg every 4 hours. An epidural infusion of morphine and bupivacaine was started 24 hours preoperatively and discontinued on the third postoperative day. Over the next 10 days the oxycodone was gradually decreased and eventually discontinued prior to discharge. A review of the literature reveals conflicting reports on the benefit of preoperative epidural pain management in the prevention of postoperative pain syndromes. Conflicting research and conclusions of commentators leaves unanswered questions for clinicians. Nevertheless, we do know that we need to provide the best pain relief for patients both before and after amputation. This may require a combination of the oral, subcutaneous or intravenous, and epidural routes.

      • Field J, Rathmell JP, Stephenson JH and Katz NP (2000). Neuropathic pain following cervical epidural steroid injection. Anesthesiology. 93: 885-8. Department of Anesthesiology, University of Vermont College of Medicine, Burlington, Vermont, USA.

      • Eisenach JC, Hood DD and Curry R (2000). Relative potency of epidural to intrathecal clonidine differs between acute thermal pain and capsaicin-induced allodynia. Pain. 84: 57-64. Department of Anesthesiology, Wake Forest University Medical Center, Winston-Salem, NC 27157-1009, USA. Clonidine is approved in the US for epidural administration in the treatment of intractable neuropathic cancer pain, but is also administered intrathecally for this indication and both epidurally and intrathecally in the treatment of acute, postoperative pain. The purpose of the current study was to estimate the relative potency of clonidine by epidural and intrathecal routes in the treatment of capsaicin-induced hyperalgesia and allodynia as a model of central hypersensitivity and of noxious heat as a model of acute pain. Twenty-four healthy volunteers were randomized to receive either intrathecal clonidine (75, 150, or 300 micrograms) or epidural clonidine (150, 300, or 600 micrograms) and rated pain from a Peltier-controlled thermode at a lumbar, thoracic, and cervical dermatomal site before and after drug administration. In addition, they rated pain from intradermal capsaicin injections at a lumbar dermatome before and 60 min after clonidine injection and described areas of hyperalgesia and allodynia to mechanical stimuli. Clonidine's effect differed with route of administration and modality of sensory testing. For acute thermal pain, intrathecal clonidine produced a dose-dependent analgesia with a lumbar>thoracic>cervical gradient, whereas only one dose of epidural clonidine reduced thermal pain and this was at the thoracic testing site. In contrast, the potency of clonidine to reduce capsaicin-induced allodynia was similar between the two routes of injection, and for hyperalgesia, clonidine was only slightly more potent after intrathecal than epidural injection. These data support clinical studies from non-comparative trials and suggest there is a >6-fold potency ratio of intrathecal:epidural administration of clonidine for acute pain, but a <2-fold potency ratio for these routes for mechanical hypersensitivity.

      • Simpson RK, Jr., Gondo M, Robertson CS and Goodman JC (1996). Reduction in the mechanonociceptive response by intrathecal administration of glycine and related compounds. Neurochem Res. 21: 1221-6. Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA. We have previously reported that enhanced glycine release is produced by epidural spinal cord stimulation, a clinical method for treating neuropathic pain. Our current hypothesis is that glycine administered intrathecally reduces neuropathic pain as measured by the Randall-Selitto method. Neuropathic rats created by unilateral partial ligation of the sciatic nerve were treated with intrathecal infusion of glycine, strychnine, MK-801, or 5,7-DKA at 0.1 mumol, or artificial CSF for 2 hours at a rate of 10 microliters/min. Force required to produce the pain response was significantly increased after glycine administration and reduced using strychnine, a specific glycine receptor (Gly l) antagonist. Strychnine blocked the response to glycine when infused together. Administration of the non-specific NMDA receptor MK-801 antagonist and 5,7-DKA, a specific glycine-NMDA receptor (Gly 2) antagonist, however, failed to block the response to glycine. Our results provide evidence for the use of glycine and related compounds to treat neuropathic pain.

      • Bedder MD (1996). Epidural opioid therapy for chronic nonmalignant pain: critique of current experience. J Pain Symptom Manage. 11: 353-6. Advanced Pain Management Group, Inc., Portland, Oregon 97225, USA. The current use of epidural catheter techniques for nonmalignant pain follows directly from its successful use of treating intractable malignant pain states. Long-term studies are confirming the safety of epidural infusions of morphine and local anesthetics. Limitations of this technique related to technical catheter considerations, neuropathic pain states, and cost considerations are being reevaluated as more information is developed. Epidural infusions in nonmalignant pain may prove their value in prolonged treatments for conditions that may resolve in time. They are also being utilized increasingly as screening tools prior to implanting permanent infusion pump systems.

      • Collins JJ, Grier HE, Sethna NF, Wilder RT and Berde CB (1996). Regional anesthesia for pain associated with terminal pediatric malignancy. Pain. 65: 63-9. Department of Anesthesia, Children's Hospital, Boston, MA 02115, USA. The objectives of this study were to identify the characteristics of children who required regional anesthesia for pain associated with terminal malignancy and to identify the safety, tolerability and effectiveness of regional anesthesia as an analgesic modality in terminal pediatric malignancy. A retrospective examination was made of the medical records of children who died of malignancy following treatment at the Dana-Farber Cancer Institute and Children's Hospital, Boston, Massachusetts and who required either epidural or subarachnoid infusions, or neurolytic blockade for pain management (June, 1986--April, 1994) during the terminal phase of their illness. Eleven patients were identified, with a duration of epidural or subarachnoid infusions ranging from 3 days to 7 weeks. Indications for this intervention included limiting side effects of opioids, neuropathic pain unresponsive to either rapid escalation of opioids or massive opioid infusions, analgesia for thoracocenteses for the drainage of malignant pleural effusions and instillation of intrapleural chemotherapy. Pain was localized to one area in ll patients. Analgesia was judged to be satisfactory in all cases after regional anesthesia was instituted and remained satisfactory in all cases throughout the treatment course. Complications associated with regional anesthesia included dural puncture headache and mild respiratory depression. Five patients were nursed at home with either epidural or subarachnoid infusions.

      • Wen YR, Hou WY, Chen YA, Hsieh CY and Sun WZ (1996). Intrathecal morphine for neuropathic pain in a pregnant cancer patient. J Formos Med Assoc. 95: 252-4. Department of Anesthesiology, Chayi Provinicial Hospital, Taipei. Although they have been documented, opioid treatments in obstetrics are mostly limited to methadone maintenance treatment in pregnant addicts or analgesia/anesthesia for labor. A literature search revealed no previous studies describing analgesic techniques for relief of severe cancer pain in pregnant patients. As response to morphine is dose-dependent, its conventional use can be problematic in pregnant women suffering from severe cancer pain because it is important to prevent opioid intoxication of the fetus. Furthermore, long-term exposure to morphine may result in physical dependence on the drug by the fetus, causing acute withdrawal syndrome and growth retardation after delivery. We report our experience in treating a 35-year-old pregnant female, in her 32nd gestational week, suffering from neuropathic pain due to advanced ovarian cancer. Using a microcatheter technique, we administered small doses of morphine intrathecally and successfully controlled the pain before delivery without complications in the mother and fetus. Treatment options of systemic vs spinal and epidural vs intrathecal opioids under such unique circumstances are discussed.

      • Glynn C and O'Sullivan K (1996). A double-blind randomised comparison of the effects of epidural clonidine, lignocaine and the combination of clonidine and lignocaine in patients with chronic pain. Pain. 64: 337-43. Oxford Regional Pain Relief Unit, Nuffield Department of Anaesthetics, Churchill Hospital, University of Oxford, UK. Twenty patients with chronic pain who previously had obtained analgesia from epidural clonidine and lignocaine agreed to participate in a double-blind crossover study of lumbar epidural clonidine (150 micrograms), lignocaine (40 mg) and the combination of clonidine (150 microgram) and lignocaine (40 mg), all drugs were given in a volume of 3 ml. There were 11 women and 9 men with a mean age 53 years (range: 23-78 years); 9 patients had low back and leg pain, 9 had neuropathic pain, 1 had pelvic pain and 1 Wegner's granulomatosis. Pain intensity and pain relief, as well as sensory and motor blockade, were assessed for 3 h following each injection. The combination was reported as the best pain relief by 12 of the 17 patients who completed all three arms of the study; 4 patients reported that clonidine was the best, 1 patient reported that none of the injections provided any analgesia and no patient reported that lignocaine was the best. SPID analysis revealed a significant difference between the combination and lignocaine (P < 0.05) but no other significant difference. TOTPAR analysis revealed no significant difference between any of the injections. All 3 injections produced evidence of neurological blockade; clonidine produced sensory blockade in 3 patients and motor blockade in 3 patients. Lignocaine produced sensory blockade in 6 patients and motor in 8 patients, while the combination produced evidence of neurological blockade in all 17 patients, sensory in 6 and motor in 11 patients. Overall there was no relationship between neurological blockade and analgesia. The reported side effects appeared to be related to clonidine. These data indicate that in these patients with chronic pain epidural clonidine had a supra-additive effect and behaved more like a co-analgesic than a pure analgesic.


        Dear Dr. Young,

        Thank you for that very interesting review of nerve blocks. There is obviously a great deal of controversy. I approached a neuroradiologist with some of it and he said doing medial branch of posterior dorsal root OR nerve blocks around the foramina should always be done under CT fluoroscopy for two reasons:

        1) the new software permits about 1/10th the rads of conventional CT
        2) precision of placement increases results.

        He was not concerned about rupture of the facet joint, which has capacity of 1.5 ml. He injects 3.0 ml routinely, since he had some feelings that rupture actually helps the pain, eventually (hurts initially). There is also controversy whether bupivicaine(short acting) or marcaine (long acting) should be used. This is different from the anesthesiologist in Kansas City, who totally opposes rupture of the facet joint, as does the radiologist down in New Orleans. Maybe when the joint ruptures, it just means there is more medicine around. Who knows.

        This neuroradiologist feels ablation fails after about a year since new nerves grow in, but it is worth it because it diagnoses the source of pain, and avoids surgery when surgery won't help. He also uses the little wire with a coil to insert into the disc, (so far only lumbar) which heats and eliminates a little of the nucleus. He says no one really knows what is going on, but the heat may be causing collagen to form an internal ring which supports the disc, or removal of a little nucleus causes less pressure on the bulging disc.

        It is all pretty scary, especially if you have neck pain, which I do in spades. The part about epidural steroids CAUSING neuropathic pain is REALLY troubling.

        I have always thought in terms of pain in the spine=pain in the disc, but this "new" stuff is pretty confusing, if only 40% of pain is due to disc, even in spinal stenosis.

        Thank you for your very helpful review. It is very much appreciated. I wonder why they chose intrathecal glycine instead of intrathecal GABA. One scientist thinks glycine more active in brain and GABA more active in cord, so I wonder what the results you cite, prove.

        For general consumption:

        The nerves which exit the spine, do so through an opening created by the way the vertebrae above articulates with the vertebrae below. This hole is known as the foramina. As the nerve comes out it bifurcates and the posterior branch bifurcates again. The deep branch innervates the facet, a roundish structure which represents the posterior bony articulation of one vertebra with the one above. The joint slopes down about 45 degrees with the superior vertebrae articulation in back, lower in front. Think of it as like two dinner plates close to each other (the joint between them being the zygapophyseal joint). The medial branch of the dorsal root of the spinal nerve (one comes out at each vertebral level) supplies the zygapophyseal joint (the vertical line of which on either side is called the articular pillar) and then branches around on the lamina, or bone running horizontally and posteriorly toward the midline in back of the spine, where they meet the spinous process, which is what you feel as the bump in the midline of your back. These lamina form the back of a triangular space, which is called the spinal canal, in which is the cord. The front of the space behind the vertebral bodies is formed by a ligament going vertically which rests against the bodies of the vertebrae. The front of the space at disc levels is formed by the posterior longitudinal ligament(shaped like a vertical row of connected diamonds) and the back of the disc annulus, against which the ligament rides, being actually attached only at the sides, in the front of the foraminal opening.

        I will just add that the work on the nerve which loops back into the canal is very poorly done, with Bogduk in New Zealand considered by many the ONLY person whose work is to be trusted. His work on the recurrent nerve which comes back onto the spinal canal from the white ramus outside the foramina is the ONLY study on point. That is the nerve they sometimes try to block at the foramina, but injections there are dangerous, because they might get into the anterior spinal artery, causing vasospasm, seizures, brain damage. There is also a risk at C5-7 that a little artery from outside the canal which shoots back through the foramina to help supply the cord will be injected.

        As to the medial branch of the p.dorsal ramus, it supposedly supplies ONLY the multifidis muscle. However, there are other anatomists who claim the dorsal root contributes to all the deep neck muscle groups. This is annoying to read, since it is something the anatomists should have worked out years ago. The spinal musculature is definitely the stepchild of anatomy. I wish I were still well enough to work. Yet, when I was well, I was as neglectful as everyone else because it didn't matter to me then. Not only in amputations, but everywhere in the body, injection of analgesic prior to cutting markedly reduces postoperative pain. I worked with the person who invented the modern laparoscope and he injected demerol before cutting and the patients had virtually no postoperative pain, so that is why I am shocked steroids CAUSE neuropathic pain.

        I am starting to think no one really knows how these medications work. Their mechanism of action is boldly declared, but I suspect almost anything can be linked to glutamate and NMDA and GABA, but I don't know if that is really explaining the mechanism.

        [This message was edited by dejerine on 01-15-04 at 01:22 AM.]


          thanks, when its time for me , i will have good informantion to ask the doctor. and try and get the beter medicatations for neural pain
          cauda equina


            Does this mean injections might help my upper back pain, or not (forget the rest of me for now?)


            "Was it over when the Germans bombed Pearl Harbor?"

            Proofread carefully to see if you any words out.


              Alan, it might be worth a try. But the question is what to use. Wise.