Sciatica Pain Relief

Sciatica SOS

This ebook teaches you an often-ignored trick that the medical industry refuses to acknowledge to get rid of sciatica pains. This trick comes from the mountains of Nepal; it is natural remedy that gives you all of the pain relief that you need to feel better, just like you deserve. You don't have to succumb to the horrible pains that sciatica will bring you; you can instead feel the relief that comes to people who carefully follow this treatment plan. Your nerves are often too sensitive to put up with much pain or discomfort of any kind; now, you will be able to get rid of that pain and reclaim your manhood; you can do all of the things that you used to be able to do, but now you can do them without fearing that you are going to trigger horrible, debilitating pain in your body! More here...

Sciatica SOS Overview


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Author: Glen Johnson
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My Sciatica SOS Review

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Cure Sciatica By Steven Guo

Stop Sciatica In 8 Minutes is a guidebook revealing natural remedies and treatments for sciatica. The author of this comprehensive program is Steven Guo. He is a natural treatment researcher coming from Chinese. With Stop Sciatica In 8 Minutes, he has helped over 6,000 sciatica patients cure their sciatica successfully since 2008. This method is totally safe and so there wont be any damage to your back. There is no need for extreme surgical procedures or painful physiotherapy because they can worsen your back. You will learn about the current treatments and remedies for this condition, including: drugs, epidural steroid injection, surgery, physical therapy, chiropractic care, alternatives treatments. The author guarantees that the program will work for you as it did for more than 6,000 sciatica patients who successfully cured this condition. It is not necessary for you to take harmful drugs and You do not need to endure painful physiotherapy You dont have to perform this method at a special time or in a special place. You can do this any-time and anywhere you wish sitting, standing or even lying down. More here...

Cure Sciatica Naturally In 7 Days Overview

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Author: Dr. Steven Guo
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Popliteal Nerve Block Sciatic Nerve Block in Popliteal Region

The sciatic nerve is a bundle consisting of the tibial and common peroneal nerves contained in an epineural sheath. A popliteal nerve block will block components of the sciatic nerve (tibial and common peroneal) at the level of the popliteal fossa where the two branches typically diverge. The common peroneal nerve gives sensory innervation to the inferior portion of the knee joint and lateral and posterior portion of the upper calf. The tibial nerve is a branch of the sciatic nerve and provides sensation to the posterior portion of the calf, the medial plantar surface, and heel of the foot. The tibial nerve at the knee lies just below the popliteal fossa and runs between the two heads of the gastrocnemius muscle and then passes deep to the soleus muscle. It divides into the lateral and medial plantar nerves as it turns medially between the Achilles tendon and medial malleolus. Dermatome distribution of the lower extremity innervated by the popliteal nerve block is indicated in Table...

Sciatic Nerve Block Proximal

The sciatic nerve is the largest nerve in the human body. It is composed of the tibial and peroneal segments and is derived from L4-S3 anterior rami. The sciatic nerve runs through the greater sciatic foramen to the gluteal region deep to gluteus maximus muscle. Most of the conventional approaches for sciatic nerve blockade at this level are relatively deep and therefore not attractive for ultrasonography in much of the adult surgical population. Once the sciatic nerve enters the dorsal side of the thigh between the caudal border of the gluteus maximus and the biceps muscles, its position is more superficial, appears as an oval or flat hyperechoic structure, is more easily seen with current ultrasound technology, and is an easier block to perform under ultrasound guidance. Posterior cutaneous nerve of the thigh is in a medial position relative to the sciatic nerve at the subgluteal level. Distally, the sciatic nerve components (tibial and common peroneal) run between the...

Sciatic Nerve Block

Sciatic nerve originates from the lumbosacral plexus (L4, L5, S1, S2, and S3) and is the largest nerve of the lower extremity. The sciatic nerve innervates the lower extremity as indicated in Table 20.9. Table 20.9 Sciatic nerve innervation of the lower extremity. Table 20.9 Sciatic nerve innervation of the lower extremity. The patient lies in a lateral decubitus position with the side to be blocked non-dependent. The knee of the non-dependent leg is flexed 45-60 so as to rest the plantar portion of the foot or ankle on the knee of the dependent limb. Mark the palpable location of the GT, PSIS, and the SH. Then draw two lines, one connecting the PSIS to the GT and another connecting the SH to the GT. At the midpoint of the line between the PSIS and the GT, another 4-5 cm long perpendicular line is drawn which should approximate the line between the SH and the GT this point will serve as the block needle insertion site. Subsequent to aseptic precautions, a local anesthetic skin wheal...

Animal Models Of Neuropathic Pain

Unravelling the mechanisms involved in neuropathic pain requires the use of laboratory animal models that replicate as far as possible, with the above caveats, the different pathophysiological changes present in patients. For reasons of reproducibility and simplicity, most studies of neuropathic pain are based upon animal models of traumatic nerve injury, usually in the rat sciatic nerve (Figure 1.2).

Experimental evidence Adenosine receptors

Sciatic nerve blockade and compared this with that of bupivicaine. They found that amitriptyline, doxepin, and imipramine produced a longer complete sciatic nerve block than bupivicaine whereas trimipramine and desipramine produced a shorter block. Nortriptyline and maprotiline failed to produce any block. When the effect of topical application of amitriptyl-ine is compared with that of lidocaine, amitriptyline is seen to produce longer cutaneous analgesia than lidocaine.

Peripheral opioid receptors

One method for examining the location of opioid receptors is to use autoradiographic techniques. When this technique is used in rats in which the sciatic nerve is ligated, opioid receptors are found to accumulate proxi-mally and distally to the ligature in a time-dependent fashion suggesting that there is bidirectional axonal transport of these receptors. In another rodent model, non-inflamed paw tissue is known to contain some opioid receptors. When inflammation is induced by application of Freund's adjuvant to a paw, the density of opioid receptors increases in the paw massively. These opioid receptors are found in the cutaneous nerves and in immune cells infiltrating the surrounding tissue.

Neurotransmitter effects

A variety of neuropathic pain states. Schechtmann and colleagues8 studied the addition of clonidine at small (1-20 mg) subeffective doses in nerve-injured animals in which SCS failed to suppress tactile hypersensitivity. The combination of clonidine and SCS in these animals was synergistic and effectively decreased the hypersensitivity. In a nerve ligation model of neuropathic pain, depolarization-induced acetylcholine release was enhanced by clonidine only in nerve-injured animals, but not in the control animals. This implies that clonidine-induced acetylcholine release is important in analgesia, but first requires depolarization.9 Animal data led to a human study that examined the role of baclofen or adenosine phosphate as an adjunct to spinal stimulation. Forty-eight patients with peripheral neuropathic pain unresponsive to spinal stimulation were recruited, of whom 28 responded to drug bolus. Seven patients ultimately had both intra-thecal pumps and spinal stimulators implanted,...

Antioxidant Enzymes

Free radical defenses of peripheral nerve are reduced relative to brain and liver, especially involving glutathione (GSH)-containing enzymes (9). Cuprozinc superoxide dismutase (SOD) is reduced in sciatic nerve of experimental diabetic neuropathy, and this reduction is improved by insulin treatment (10). Glutathione peroxidase (GSH-Px) is reported to be further reduced in experimental diabetic neuropathy in alloxan diabetic mice 7-21 days after induction of diabetes, and enzyme activity inversely regresses with glucose level (11). We recently evaluated the gene expression of the antioxidant enzymes, GSH-Px, SOD (cuprozinc czSOD and manganese mnSOD separately), and cata-lase (CAT) in L4-L6 dorsal root ganglia (DRG) and superior cervical ganglion (SCG) of rats that had been diabetic for 3 and 12 months (Kishi et al unpublished data). cDNA fragments for rat GSH-Px, czSOD, mnSOD, CAT, and cyclophilin was obtained by reverse transcriptase polymerese chain reaction of rat DRG RNA using...

Glucose Uptake And Energy Metabolism

A-Lipoic acid has a number of actions in addition to its antioxidant properties. These include its effect on glucose uptake. We therefore evaluated glucose uptake, nerve energy metabolism, and the polyol pathway in EDN induced by streptozotocin. Control and diabetic rats received lipoic acid at various doses (0, 10, 25, 50, and 100 mg kg). Duration of diabetes was 1 month, and a-lipoic acid was administered intraperitoneally 5 times during the final week of the experiment. Nerve glucose uptake was reduced to 60 , 37 and 30 of control values in the sciatic nerve, L5 DRG, and superior cervical ganglion, respectively, in EDN. a-Lipoic acid supplementation had no effect on glucose uptake in normal nerves at any dose but reversed the deficit in EDN, with a threshold between 10 and 25 mg kg. Endoneurial glucose, fructose, sorbitol, and myo-inositol were measured in sciatic nerve and L5 DRG. ATP, creatine phosphate, and lactate were measured in sciatic nerve and superior cervical ganglion....

Neurotrophic Factors

NGF undergoes retrograde transport in sensory and sympathetic neurons in adult rats (22,23), and about 50 of adult lumbar sensory neurons can bind NGF with high affinity (24). BDNF and NT-3 also undergo retrograde transport from an injection site in the sciatic nerve to the dorsal root ganglia (DRG) and motor neurons of adult rats (25).

Neurotrophins In Diabetic Neuropathy

Decreased capture and retrograde transport of iodinated NGF in the sciatic nerve was observed in diabetic rats many years ago (34). Reduced retrograde transport of iodinated NGF in ileal mesenteric nerves has also been demonstrated (35). These observations imply that even in the absence of any deficit in production of NGF in diabetes, a deficit in the amount delivered to the cell body might be expected. In diabetic rats, there are reduced levels of NGF in the submandibular gland, superior cervical ganglion, and sciatic nerve (3638). NGF levels have also been shown to be decreased in the serum of diabetic patients with symptomatic peripheral neuropathy (39). Work in our laboratory has shown that with increasing duration of diabetes, progressive reductions in NGF mRNA appear in leg muscle and sciatic nerve followed by reductions in skin. There is a profound reduction in the retrograde transport of NGF in the sciatic nerve, which can be reversed by intensive insulin treatment, and...

Shu Ming Wang MSci MD Janet S Jedlicka PhD Otrl Anne M Haskins PhD OTRL and Jan E Stube PhD OTrl

Harris is a 45-year-old, otherwise healthy man suffering from lower back pain. He over exerted himself lifting a heavy box from the floor. He did not experience immediate pain until the following morning. He complained that his pain was very severe and had significantly affected his movement. He stated that he experienced sharp pain associated with every movement. The pain radiated downward over the buttocks and both legs. He had no other symptoms, and an MRI of his back was normal. The patient received several sessions of massage, but his symptoms and pain did not subside. As a result, he is here to receive acupuncture treatment.

Role For glaaata In The Treatment Of Diabetic Neuropathy

This is the first instance of a treatment that is capable of attenuating both electrophysiological and neurochemical deficits in the nerves of diabetic rats. The effect of the GLA V TA conjugate is also remarkable when related to the current effects of TA and previously reported effects of EPO. Approximate calculations suggest that the dose of GLA' TA used here could deliver about 14 mg kg day TA and 18 mg kg day GLA. TA must be given at doses of at least 50 mg kg day to influence nerve conduction (19), and in the present and in previous (20) studies had little effect on sciatic nerve NGF levels at 100 mg kg day. Assuming an approximate content of 10 GLA in EPO (83), a daily consumption of about 180 mg oil would be required to match the current dose of the conjugate. A previous study demonstrated no effect of EPO at about 3.5 g day per rat (equivalent to about 10 g kg day) on the deficit in sciatic nerve SP in diabetic rats (82). It is therefore clear that the properties of the...

Human clinical pain

Another commonly studied condition in which neuropathic pain is prominent is postherpetic neuralgia. Lidocaine appears to reduce both the pain and allodynia which characterize this condition. It has also been shown to reduce neuropathic pain of central origin, peripheral nerve injury, sciatica, and complex regional pain syndrome (type I). Both positive and negative results have been obtained when this treatment has been used in patients with spinal cord injury pain. Cahana and colleagues (2004) report their findings on positron emission tomography of a patient with central neuropathic pain who responded to IV lidocaine and in whom there was hypoactivity of the left posterolateral thalamus before treatment, which disappeared with therapy.

Role Of Oxidative Stress In Diabetic Neuropathy Clinical And Experimental Evidence

In experimental diabetic neuropathy, oxygen free radical activity in the sciatic nerve is increased (9). Treatment with a-lipoic acid, a potent lipophilic free radical scavenger (14), results in prevention of neurovascular abnormalities associated with experimental diabetic neuropathy (15). It has been demonstrated that reduced digital nerve conduction velocity (NCV), nerve blood flow, and glutathione levels in diabetic rats are normalized and in vitro lipid peroxidation of neural tissue reduced by a-lipoic acid in a dose-dependent manner (15,16), suggesting that the improvement in neurovascular changes were induced by improving oxygen free radical scavenging activity. One mechanism of reduced nerve blood flow is the inhibitory effect of superoxide anion on nitric oxide synthase. Because nitric oxide synthase is reduced in experimental diabetic neuropathy (17), a-lipoic acid might prevent this inhibition by reducing oxidative stress (15). A recent study has also demonstrated that...

Mechanism of effect of carnitine

A number of modes of action of carnitine in relationship to its antinociceptive effect have been proposed. One of these relates to the observation that in rats with induced diabetes the content of substance P, an important pain-related neurotransmitter, is reduced in the sciatic nerve and lumbar spinal cord and that this decrease found with the onset of diabetes can be prevented by carnitine pretreatment.

Femoral Nerve Block

Indications for an ultrasound femoral block include surgical procedures in the sensory distributions of the femoral, lateral femoral cutaneous, and anterior branch of the obturator nerve. A femoral nerve block together with a sciatic nerve block (described below) may provide anesthesia analgesia for surgical procedures of the majority of lower extremity surgeries. The ultrasound-guided femoral block is a simple technique, but good anatomical knowledge is necessary for optimal performance of this block. In many surgical indications, only a femoral nerve block is necessary and since the femoral nerve is a superficial structure just distal to the inguinal ligament, a high-frequency linear ultrasound probe (> 10 MHz) is adequate for optimal visualization.

Acute postamputation pain

Immediate postoperative residual limb pain can usually be successfully treated with conventional analgesics (paracetamol, nonsteroidal anti-inflammatory drugs (NSAIDs), opioids), perhaps in combination with various blocks (e.g. epidurals, and axillary, femoral, or sciatic nerve blocks).

Peripheral Nerve Blockade

When pain is refractory to pharmacologic treatment, peripheral nerve blockade may be an option (Raj 1996). Somatic nerve blocks are used in patients with intractable pain, generally from cancerous invasion of parts of the body, including the nervous system. At times, these blocks are employed in peripheral nerve pain, sciatica, and carpal tunnel syndrome. In addition, peripheral nerve blocks are employed to provide analgesia during localized surgery so that the patient can avoid general anesthesia.

Generic treatment options

A comprehensive understanding of the anatomy is essential to be able to diagnose specific nerve involvement and access the nerves in a safe manner. The sympathetic, parasympathetic and somatic nerves can be blocked separately. Using appropriate imaging and neurotracing techniques allows nerves to be identified sequentially. For instance, in the region of the piri-formis, the sciatic nerve, posterior femoral cutaneous nerve and its perineal nerve, inferior gluteal nerve, the nerve to obturator internus and the pudendal nerve can be separated out. A lot of attention has been paid to blocking these posterior nerves recently as well as the anterior nerves such as the ilio-inguinal, iliohypogastric and genitofemoral nerves. In our clinic, we now have to assess many more patients with nerve compression in the groin, buttock region and perineum than was done a few years ago. Some patients do gain long-term benefit from injections occasionally combined with pulsed radiofrequency...

Sopioid Receptors And Inflammatory Pain

And U50,488H, but not DTLET, was enhanced in arthritic rats 155 . The ICV administration of DAMGO, morphine, D-Ala2,Glu4 deltorphin, or SNC80 to rats made arthritic with complete Freund's adjuvant (CFA) demonstrated an enhanced antihyperalgesic response of these compounds 156 . Inflammation has been associated with an upregulation of spinal opioid peptides or of mRNA for the peptides 157,158 . Enhanced axonal transport of 5-opioid and A-opioid receptors to terminals of the sciatic nerve was demonstrated, indicating a mechanism for enhanced antinociception of centrally and systemi-cally administered 5-opioid and A-opioid agonists 159 . More recently, Hammond and colleagues demonstrated significant potentiation of the antinociceptive action of DAMGO or of D-Ala2,Glu4 -deltorphin administered into the RVM of rats with inflammation induced by CFA 160,161 . Moreover, based on observations that naltriben in the RVM alone enhanced hyperalgesia, and that Met5 enkephalin and Leu5 enkepha-lin...

Intraoperative irradiation

Intraoperative radiotherapy (IORT) involves a large single-dose irradiation at the time of surgical exploration and is used in conjunction with chemotherapy and postoperative external radiotherapy to treat tumors with high risk for local recurrence.70 Peripheral neuropathy is the dose-limiting toxicity of IORT. It develops in 30 of the patients 6-18 months after the treatment and involves nerves within the IORT field.71 A single dose of 20 Gy is considered a maximum tolerable dose for peripheral nerve injury but additional factors may enhance its toxic effect.71 Experimental animal studies of lumbosacral and sciatic nerve IORT-induced injury demonstrate loss of large myelinated fibers, endoneural fibrosis, and endo- and epineural vessel thickening70 as well as small-vessel necrosis, hyalinization, thrombosis and hemorrhage.70 Schwann cells and vasa nervosum have been implicated in the development of the observed changes.73

Clinical presentation of muscle spasm

Particular varieties of muscle spasm give rise to identifiable conditions. For example, spasm of the sternomastoid muscle gives rise to torticollis or rye neck where the head is held rotated to the side of the muscle spasm. A further example would be piriformis muscle spasm where pain is felt over the greater trochanter, sciatic notch, and sacral area. This pain is worse on abduction and external rotation of the leg on that side as well as on passage of a bowel motion. Neuropathic pain may also accompany the piriformis muscle spasm as the sciatic nerve is compressed as it passes with the piriformis muscle through the sciatic notch. The tender, tense piriformis muscle can be palpated on digital rectal examination because of the close proximity of the piriformis muscle to the rectum.

Gcp Ii Inhibitors Provide Analgesia

GCP II inhibitors were also examined as potential analgesics for neuropathic pain and peripheral neuropathy using a chronic constrictive injury (CCI) model.22 Briefly, one sciatic nerve was exposed by blunt dissection proximal to nerve trifurcation and four ligatures loosely tied. The other side was sham operated. After twelve days, thermal pain threshold (withdrawal latency) was assessed by means of the plantar test.23 The ligated and non-ligated hind limbs of the CCI rats were tested and a difference score for each animal was determined by subtracting the mean withdrawal latency of the non-ligated (sham-operated) leg from the mean withdrawal latency of the ligated leg.23 Negative values indicate a relative hyperalgesia on the operated side as compared to the sham side. The unoperated animals (untreated control) showed no difference between right and left leg withdrawal latencies. Vehicle-treated animals remained hyperalgesic over the period of testing as indicated by the negative...

Therapeutic Studies With Gcp Ii Inhibitors In Rodent Models

Repeated administration of 2-PMPA was also shown to be effective in enhancing recovery in an in vivo model of peripheral nerve injury. Four weeks of daily oral administration of a GCP II activity inhibitor was reported to improve nerve morphology, physiology and endurance in a walking test after sciatic nerve crush injury.56 Thus, evidence is accumulating that inhibition of catabolism of NAAG may have significant potential as a therapy for neuronal injury as well as for neurodegenerative disorders.

Streptozotocin Diabetic

There is ample evidence that markers of oxidative stress are increased in the most widely accepted rodent model of type 1 diabetes, the streptozotocin-diabetic rat. For example, plasma and liver lipid peroxides, as measured by the thiobarbituric acid reactive substances assay, are elevated in the streptozo-tocin-diabetic rat (35). In addition, recent evidence indicates that in this model of type 1 diabetes, sciatic nerve levels of reduced glutathione (GSH) are lower and the ratio of oxidized to reduced glutathione (GSSG GSH) is elevated compared with tissue from normoglycemic control animals (36). Chronic treatment with the antioxidant lipoic acid brings about a nearly complete normalization of the GSH and GSSG GSH profiles in sciatic nerve from the streptozotocin-diabetic rats and also significantly improves nerve blood flow and conduction velocity (36).

Pbpk Models For Four Classes Of Compounds

An early PBPK model was developed for the hexane metabolite 2,5-hexanedione in rats by Angelo and Bischoff (1982) for the purpose of reconstructing tissue concentration histories following long-term, high-dose exposures. This model was described as a flow-limited model having plasma, liver, kidney, sciatic nerve, spinal cord, brain, and lean tissue compartments with mass balance equations describing the flow between compartments. Fat tissue was included with lean tissue because there was no difference in partitioning for 2,5-hexanedione observed in these tissues. Tissue plasma partition coefficients were described as distribution ratios as the in vivo ratio of the respective concentrations during steady-state conditions following constant intravenous (i.v.) exposure. Metabolic and clearance rates were described by first-order terms calculated from i.v. infusion data. For intraperitoneal (i.p.) injection exposure data, the model simulation results were in very good agreement with...

Inhibitory and Excitatory Effects of Nociception at the Spinal Cord Level

Respiratory Depression

Melanocortins are a group of endogenous peptides that are derived from pro-opiomelanocortin. The melanocortins include adrenocortico-tropic hormone (ACTH), and the X- and 6-melanocyte stimulating hormone (MSH). Recent studies indicate that spinal melanocortin receptors (the MC4 subtype) are upregulated in animal models of neuropathic pain. Also, both (X-MSH and 6-MSH have been identified in areas of the spinal cord associated with nociception 34 . The MC4 melanocortin receptor agonists MTII and d-Tyr-MTII increase the sensitivity of rats to painful stimuli following sciatic nerve constriction. In contrast, the pain responses are attenuated following pretreatment with the melanocortin receptor antagonist SHU9119 34 . Cholecystokinin (CCK) belongs to a gastrin family of peptides. In the central nervous system it is widely distributed and predominantly exists as CCK-8, which binds to CCKs or CCKz receptors. In the periphery, the receptors that normally bind CCK are CCKA or CCK1. Axotomy...

Rodent models of neuropathy

The most commonly used nerve injury models are the chronic constriction injury (CCI) of sciatic nerve,7 the partial sciatic nerve ligation (PNL) model,8 the spinal nerve ligation (SNL) transection model (Figure 1.2),9 and the spared nerve injury (SNI) model.6 All models are associated with the development of hypersensitivity to thermal (heat and cold), and mechanical stimuli which are used experimentally as correlates of hyperalgesia and allodynia symptoms in neuropathic pain patients.10 However, the relevance of these measures to the human condition is questionable. The CCI model consists of the loose ligation of the sciatic nerve with chromic gut sutures. An inflammatory reaction develops and consequentially damage to most A-fibers and some C-fibers. It is likely that there is a significant inflammatory component in the development Figure 1.2 Rodent models of nerve injury. Many rodent models are based upon injury to the peripheral, usually sciatic, nerve. Schematic drawing of...

Popliteal Nerve Block Distal Sciatic

This is a peripheral nerve block of the sciatic nerve performed more distal in the leg proximal to the popliteal crease. With the patient in the supine or prone position, the ultrasound probe is placed to scan in the transverse plane on the posterior surface of the popliteal fossa 5 cm or more proximal to the popliteal flexion crease of the knee (Fig. 21.11a). Subtle inclination of the ultrasound probe in the caudad or cephalad direction may be needed to produce ideal visualization of the nearly round, hyperechoic sciatic nerve or sciatic nerve components (Fig. 21.11b) (within this proximity of the popliteal crease, the sciatic nerve will often take on the appearance of separate tibial and common peroneal nerve branches). The sciatic nerve is surrounded by a large amount of fat, and, laterally, the typical muscular pattern of the biceps femoris can be recognized with its medial surface concave toward the nerve. Medial to the nerve, the muscle tendon of the semimembranosus is...

Peripheral Nerve Blocks of the Lower Extremity

Nerves could be blocked from a single injection at the femoral crease. However, it has been demonstrated that the femoral and lateral femoral cutaneous nerves can be reliably blocked by a single injection, but the obturator nerve is often missed. The femoral nerve block is an ideal block for surgeries of the hip, knee, or anterior thigh and can be combined with a sciatic nerve block for near complete lower extremity analgesia. Complete analgesia of the leg can be achieved by adding an obturator nerve block. Sciatic nerve supplies motor and sensory innervation to the posterior aspect of the thigh as well as the entire lower leg (except for sensory to the medial leg below the knee, which is supplied by the saphenous nerve, a terminal branch of the femoral nerve). The sciatic nerve, formed from the ventral rami of spinal nerves L4-S3, forms most of the sacral plexus (L4-S4) and is the largest nerve in the human body. Since the sciatic nerve is so large, it can be blocked at several...

Sreekumar Kunnumpurath Mbbs Md Fcarcsi Frca Ffpmrca

Andrew is 75-year-old man who has been very active until about a year ago. He used to play golf twice a week. One year ago, he slowly started to get persistent lower back pain which gradually began to worsen. A few months later he noted that he was getting pain in his thigh and to his dismay his neck was becoming painful too. Finally, he had to stop playing golf altogether. He was seen by his PCP who after a careful examination made a diagnosis of non-specific back pain. Andrew was started on acetaminophen and ibuprofen, which reduced his back pain to such an extent that he could play some golf again. However, a few months later during a routine checkup his PCP noticed edema of his ankles. On further investigation, he was found to have elevated blood urea and crea-tinine. Ibuprofen was promptly stopped with resulting recurrence of back and neck pain. Andrew was then prescribed regular codeine phosphate and diazepam before bedtime for

B GABAb Receptor Agents

Baclofen is reported to be effective in reducing mechanical allodynia in an animal model of trigeminal pain whether it is administered during or after the development of the syndrome, suggesting no change in the sensitivity of the relevant GABAb receptors in this condition (Deseure et al., 2003). In contrast, the antinociceptive effects of baclofen in the sciatic nerve ligation model of neuropathic pain declines in the ipsilateral but not contralateral limb, indicating a change in responsiveness over time (Franek et al., 2004). These contradictory conclusions may arise from differences in the animal models or the route of administration of baclofen with constant infusion being employed in the trigeminal pain study and daily subcutaneous injections in the sciatic nerve model. The plasticity of the GABAB receptor system, which may contribute to variability in the response to GABAB receptor agonists and antagonists, is illustrated by studies aimed at examining the effects of pain and or...

Interactions Between Pmca And Phospholipid Nmethylation

PMCA is very sensitive to the phospholipid milieu in which it is situated. Activation of PMCA by acidic phospholipids has been found to increase both the Vmax and the affinity for Ca2+.33 Our continued interest in phospholipid methylation (PLM)-PMCA interactions derives from its enhancement by volatile and gaseous anesthetics, which may produce changes in the membrane lipid microenvironment of PMCA, with associated changes in PMCA pumping activity. PLM, a ubiquitous process occurring in cell membranes, utilizes two enzymes, phospholipid-N-meth-yltransferases I and II (PLMT I and II), which successively methylate phosphati-dylethanolamine (PE) to phosphatidyl-N-methylethanolamine (PME), phosphatidyl-N-dimethylethanolamine (PDE), and phosphatidylcholine (PC). PLMT I, located on the cytoplasmic surface, drives the first, rate-limiting, methylation step, producing PME. Associated with successive methylation is rapid translocation of the methylated product from the inner to the outer...

Case Scenario

A combined femoral and sciatic nerve block using catheters could be used. This technique can provide adequate acute pain relief. It has the advantage of being useful in providing adequate surgical anesthesia even during a limb salvage operation which Andreas might be undergoing.


A large epidemiological study in The Netherlands included data from a random sample of 161 general practitioners in 103 practices with a total population of 335,000 patients 9 . The registration period was from April 1987 to April 1988 using the ICPC classification. The incidence of low back pain was 28.0 episodes per 1000 persons per year. The reported incidence of low back pain with sciatica was 11.6 per 1000 per year. The incidence of low back pain was higher for men (32.0) than for women (23.2) and was highest for people between 25 and 64 years of age. Another epidemiological study from The Netherlands reported data collected by 59 general practitioners in 21 practices with a population of 41,000 patients 10 . The ICPC was used for classification. The incidence of low back pain (ICPC code L03) was 30 episodes per 1000 persons per year. The incidence of low back pain with sciatica (ICPC code L86, including herniated disk and diskopathy) was six episodes per 1000 persons per year....

LPA receptors

In agreement with the finding that LPA is a Schwann cell survival factor, an increased number of apoptotic Schwann cells are present in the sciatic nerve of LPA1-deficient mice (Contos et al. 2002a Weiner and Chun 1999). In contrast to Schwann cells derived from wild-type mice, Schwann cells from LPA1-deficient mice fail to undergo normal actin rearrangements in response to LPA treatment (Weiner et al. 2001). LPA1 was originally identified as a gene present in the ventricular zone of the cerebral cortex (Hecht et al. 1996). LPA treatment induces morphological changes and enhances the proliferation of neurob-lasts derived from this region (Contos et al. 2000 Fukushima et al. 2000). In response to LPA, cortical neuroblast cultures derived from LPA1-deficient mice fail to undergo LPA-dependent cell rounding and compaction and show slightly reduced proliferation compared to cultures derived from wild-type mice (Contos et al. 2000). Elegant experiments conducted using ex vivo cultured...


Neuropathological alterations in sciatic nerve have been modest in EDN. However, with more recent focus on nerve root, marked alterations in the spinal roots have been reported in long-standing streptozotocin-diabetic rats (16). We recently undertook a study addressing the status of vascular perfusion and neuropathology of DRG (17). Vascular perfusion and neuropathology evaluation of the lumbar spinal roots and DRG were studied in long-standing (duration of 12-18 months) streptozotocin-induced diabetic rats and age- and sex-matched control rats. We also undertook nerve conduction studies, including F wave recordings.


Neuropathy is a common complication of diabetes mellitus. Studies in patients and animal models have shown that endoneurial hypoxia, caused by impaired nerve blood flow, is a major factor in the etiology of diabetic neuropathy (l-4). Changes in vascular function, particularly of the endothelium, occur early after diabetes induction in experimental models, and in some preparations, this may even be partially mimicked by acute exposure to hyperglycemia (5,6). In streptozotocin-induced diabetic rats, sciatic nerve blood flow is reduced by approximately 50 within a week of diabetes induction (7,8), and this precedes changes in nerve conduction velocity (NCV). Large diameter sensory and motor fibers are particularly susceptible to endoneurial hypoxia in experimental diabetes (9,10).


NPY in the sciatic nerve may derive from mixed fiber populations some must be in sympathetic postganglionic fibers (88,89), but there may also be some in somatic sensory fibers. However, the level of expression in somatic afferents is low unless they are damaged, when it increases (90) after axo-tomy, this increased expression may be reduced by either NT-3 or NGF (91,92). Expression of NPY by the sympathetic phenotype is clearly stimulated by NGF (93), and NGF-responsive elements have been identified on the NPY promoter (94). Thus, the findings reported here might be most easily explained by the proposition that the NPY deficit in sciatic nerves of diabetic rats is also derived from reduced NGF neurotrophic support. However, our previous study showed that treatment of diabetic rats with NGF, although normalizing the SP levels in sciatic nerve, did not affect the NPY deficit (20). Thus, there may be control of NPY expression in these fibers by another neuro-trophin, and the NGF...

Animal pain models

The use of spinal nerve root ligation in rats is a conventional method for producing allodynia, a cardinal feature of neuropathic pain, and allows the efficacy of pharmacological entities to be assessed as potential antineuro-pathic pain agents. When lidocaine is systemically infused for a defined period of time in rats with surgically induced allodynia, paw-withdrawal thresholds, a measure of allodynia, are increased for the period of infusion when low doses of lidocaine are administered. When larger doses are given, the reduction in allodynia persists well beyond the period of infusion. It has been noted that in some animals a dramatic reduction in allodynia is observed while in others absolutely no effect is generated at all. This parallels human clinical practice closely. An alternative model involves the creation of neuromas in rat sciatic nerves. Electrophysiological measurements can then be made to quantify the amount of spontaneous electrical activity that emanates from the...

Treatment Strategy

Treatments with the lowest risk of adverse effects should be tried first. Evidence supporting conservative nonpharmacologic treatments (e.g., physiotherapy, exercise, transcutaneous electrical nerve stimulation, CBT, acupuncture) is limited however, given their presumed safety, nonpharmacologic treatments should be considered whenever appropriate. Simple analgesics (e.g., acetaminophen, NSAIDs) are usually ineffective in pure neuropathic pain but may help with a coexisting nociceptive condition (e.g., sciatica with musculoskeletal low back pain). Additionally, early referrals to a pain clinic for nerve blocks or other interventional therapy may be warranted in some cases to facilitate physiotherapy and pain rehabilitation.

Neuropathic Pain

It has been repeatedly demonstrated, in several animal models of nerve injury and clinically, that morphine is either ineffective or markedly attenuated against behavioral signs of neuropathic pain 185-192 . In addition, spinal morphine has been shown to be completely inactive against tactile hypersen-sitivity after L5 L6 spinal nerve ligation (SNL), even at doses that normally produce antinociception 187,188,193 . However, there are some inconsistencies in the literature moreover, the effects of peripheral nerve injuries on the antinociceptive activity opioid agonists other than morphine have not been resolved. For example, in one study, systemic morphine was shown to elevate vocalization thresholds in animals with chronic constriction injury (CCI) of the sciatic nerve 194 . Rats with CCI also demonstrated attenuation of mechanical nociception in response to IV DAMGO or to the putative 5-opioid agonist BUBU 195 . Similarly, systemic BUBUC or DTLET also produced equivalent...

Pain Models

In collaboration with Tatsuo Yamamoto from Chiba University (Yamamoto et al., 2004 Yamamoto et al., 2001) we examined the effects of peptidase inhibitors in two different pain models inflammatory pain (measurements of flinching responses after injection of dorsal surface of the right paw with 5 formalin) and neuropathic pain (measurements of pain responses using von Frey filaments after partial ligation of right sciatic nerve). Inhibitors of


Thione and other putative antioxidants such as taurine (38). The novel hypothesis that AR pathway activation produces mitochondrial dysfunction through osmotic stress is discussed in this volume. Mitochondrial dysfunction could impair antioxidative defense by diminishing ATP for the de novo synthesis of glutathione (39). AR pathway activation may also contribute to the activation of PKC reported in some (15,16) but not all tissues prone to diabetic complications (total PKC activity is reduced rather than increased by diabetes in rat sciatic nerve (40,41), but selective activation of specific isoforms in some tissue components has been described in diabetic kidney (42) and has not been excluded in diabetic PNS). Increased AR pathway activity could promote de novo DAG synthesis by diverting dihydroxyacetone phosphate toward formation of a-glycerophosphate or PKC activation through osmotic stimulation of the JNK-kinase cascade. PKC activation would further exacerbate reciprocal osmolyte...

Ankle Block

Innervations to the ankle involves five major nerve branches of the foot as indentified in Table 20.12. An ankle block is basically an infiltration block. Peripheral nerves blocked during an ankle blockade are derived from the terminal branches of the sciatic nerve (deep and superficial peroneal and sural nerves) and one from the distal branch of the femoral nerve (saphenous nerve). Motor blockade is not often needed for surgeries carried out under the influence of an ankle blockade. The deep peroneal nerve is derived from the common peroneal nerve that is a continuation of the sciatic nerve. The common peroneal nerve obtains fibers from the posterior branches of L4, L5, S1, and S2 nerve roots. It descends behind the head of the fibula and after crossing the fibula tunnel the nerve divides into the superficial and deep peroneal nerves. The deep peroneal nerve provides innervation to the space between the first and the second toes and the adjacent dorsal area.

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