Best Treatments For Sciatic Nerve Pain

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! Read more...

Sciatica SOS Summary


4.8 stars out of 25 votes

Contents: Ebook
Author: Glen Johnson
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Price: $37.00

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My Sciatica SOS Review

Highly Recommended

Of all books related to the topic, I love reading this e-book because of its well-planned flow of content. Even a beginner like me can easily gain huge amount of knowledge in a short period.

Overall my first impression of this book is good. I think it was sincerely written and looks to be very helpful.

Sciatica and Back Pain Self-Treatment

Sciatica and Back Pain Self- Treatment is a natural way of treating sciatica and back pain problem. It is based on the daily ingestion of special herbal concoction and a completely unique 3-minute routine consisting of 3 easy-to-assume static positions performed in bed or on the floor. During the period of that video, you will simply change your knee positions to influence your back muscles, nerves and spinal discs in a logical progression.The product is a quick fix that has been designed to help you get a cure for your Sciatica and Back Pain in 7 days. The methods employed in this product are natural ones that have been proven by many specialists. The system comes with bonus E-books- The Ultimate Anti-Aging Guide; Smoking Solutions: How to Maintain the Stop Smoking Pledge; Green Smoothie Lifestyle: Drink Your Way to A Slim, Energetic and Youthful Life; The Prevention and Treatment of Headaches.Living without back pain can give you a great day. However, its presence in the body can cause a great level of discomfort and even a lot of unbudgeted expenses. However, when you get a method to relieve this pain, it comes with a great number of benefits.The product is in various digital formats and has been created at a very affordable price. Read more...

Sciatica and Back Pain SelfTreatment Summary

Contents: Ebooks
Author: John McPherson
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Price: $39.00

Cure Sciatica By Steven Guo

Stop Sciatica In 8 Minutes is a comprehensive program that puts an end to the sciatica naturally without using any synthetic drugs surgery. Alternatively, physical therapy. Came from Tcm (Conventional Chinese Medicine), Stop Sciatica In 8 Minutes developed by Steven Guo, a Oriental all-natural therapy specialist is truly all-natural and 100 occasions a lot better than Chinese medication as well as other conventional remedies. This unique method, which came from traditional Chinese medicine, is simple, 100, fast, safe and effectivePercent natural. It can improve your life for your better. Stop Sciatica In 8 Minutes describes the technique in details. Inside this e-reserve, youll learn the various triggers, reasons and symptoms of sciatica. Youll also find out about basic therapies that are utilized to treat this ailment and the step-by-stage method that can cure sciatica in 7 days. Stop Sciatica in 8 minutes gives useful ways regarding how to solve issues speedily. It has several steps and one has to spend little time to learn them. Imperative features may also be learnt on them. It is actually a simple method of achieving aims quickly. Stop Sciatica in 8 minutes shows the simple and effective way because of its operations. This system works in relation to my experience and exact evidence. Read more...

Cure Sciatica Naturally In 7 Days Summary

Contents: EBook
Author: Dr. Steven Guo
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Price: $37.00

Microangiopathy Diabetes And The Peripheral Nervous System Experimental Studies

Neuropathy Peripheral Nervous System

Tuck and colleagues (22) initially reported that experimental diabetes of rats was associated with a decline of sciatic nerve blood flow and endoneurial hypoxia. Several other laboratories have reported similar findings and a variety of interventions have been reported to both correct nerve blood flow and diabetic electrophysiological abnormalities in tandem (see review 2 ). A large number of such studies through their findings have consequently implied that reductions in nerve blood flow initiate the changes of diabetic neuropathy. Although this body of work has undoubtedly provided evidence of a linkage, cause and effect has not been proven. A number of the reports have arisen from relatively few experimental laboratories (33,34,64-97). Similarly, the spectrum of agents reported to correct blood flow and conduction slowing has been very wide. As such, this range of apparently beneficial interventions raises the strong possibility that they exert parallel benefits on separate, but...

Therapies For Microvascular Insufficiency

Multiple studies using a specific PKC-P inhibitor, ruboxistaurin mesylate (LY333531), have shown improvements in diabetic neuropathy. One study in obese rats observed that ruboxistaurin increased resting nitric oxide concentration, and reduced nitric oxide by 15 , indicating that this action is a PKC-P dependent phenomenon (33). Ruboxistaurin has been shown to improve nitric oxide-dependent vascular and autonomic nerve dysfunction in diabetic mice (46). In addition to improving nitric oxide levels, ruboxis-taurin improves nerve function and blood flow. Ruboxistaurin corrected the diabetic reduction in sciatic endoneurial blood flow, sciatic motor, and saphenous sensory nerve conduction velocity in diabetic rats (40,43). In another study, the investigators measured sciatic nerve, superior cervical ganglion blood flow, and nerve conduction velocity in STZ treated rats. After 8 weeks, the authors observed that diabetes reduced sciatic nerve and superior cervical ganglion blood flow by 50...

Conclusion Linking Microvessels Diabetes And Neuropathy

Examples of sciatic nerves from nondiabetic (left) and diabetic (right) rats perfused with India ink to outline vasa nervorum in the distal nerve stump 2 weeks following transection. Note the large number of perfused vessels in epineurial area of the nondiabetics, but fewer in diabetics. (Bar 1 mm) (Reproduced with permission from ref. 134.)

Role For Vascular Vs Nonvascular Mechanisms

The neurochemical consequences of nerve ischemia in the peripheral nerve have not been studied in detail. Retinal response to ischemia involves a compensatory upregula-tion of several neurotrophic factors partially protecting retinal neurons from the lack of oxygen and nutrients (24). Correspondingly, administration of neurotrophic factors to rats with experimental PDN prevents nerve conduction slowing, without counteracting a decrease in NBF. This phenomenon has been observed with neurotrophin-3, brain-derived neurotrophic factor as well as prosaposin (16). Furthermore, the most recent study by Calcutt et al. (25) demonstrated that treatment of diabetic rats with a sonic hedgehog-IgG fusion protein (1) ameliorated retrograde transport of nerve growth factor (NGF) increased sciatic nerve concentrations of calcitonin-gene related product and neuropeptide Y, (2) restored normal MNCV and SNCV, and (3) maintained the axonal caliber of large myelinated fibers.

Sonic Hedgehog And Diabetic Neuropathy

Mechanism Diabetic Neuropathy

There is a clear disruption in the gene expression of hedgehog genes in the peripheral nervous system of diabetic animals. The mRNA encoding Dhh is reduced in the sciatic nerve of the diabetic rat (4). In addition, shh was downregulated in the dorsal root ganglion (DRG) neurons of diabetic animals at 8 weeks duration of diabetes (Burnand et al., unpublished observations). The mechanism by which treatment with Shh-IgG restores functional deficits in the nerve is unknown.

Preoperative Evaluation Of The Diabetic Patient

Patients with diabetic neuropathy may be at increased risk for developing a peripheral nerve injury during surgery. Diabetic nerves may be more susceptible to ischemia from stretch and compression, leading to permanent disability. The brachial plexus, ulnar nerve, and sciatic nerve are most commonly affected (31). Whether transient hyperglycemia increases the incidence of perioperative nerve injury is unknown.

Role For Nonenzymatic Glycation

Using the state-of-the art technique, i.e., liquid chromatography with tandem mass spectrometry (MS) detection, Karachalias et al. (66) produced evidence of accumulation of fructosyl-lysine and AGE in peripheral nerve of STZ-diabetic rats. In particular, sciatic nerve concentrations of NMcarboxymethyl -lysine and - carboxyethyl -lysine were markedly increased in diabetic rats in comparison with controls. Hydroimidazolone AGEs derived from glyoxal, nethylglyoxal, and deoxyglucosone were major AGEs quantitatively. The receptor for AGE (RAGE) was localized both in endothelial and Schwann cells of the peripheral nerve (67). Recently generated RAGE- - mice appeared partially protected from diabetes-associated pain perception loss, an indicator of long-standing diabetic neuropathy (68). Furthermore, in the same study, loss of pain perception was reversed in the diabetic wild-type mice treated with soluble RAGE. The new inhibitor of AGE and advanced lipoxidation end product (ALE) formation,...

Role For Downstream Effectors Of Ros Injury And Other Newly Discovered Mechanisms

Vasa nervorum, and DRG neurons of STZ-diabetic rats (8,26,27,93) as well as peripheral nerves of STZ-diabetic (94) and ob ob mice (58). Using endothelial and Schwann cell markers and double immunostaining (8), the author's group localized PARP activation in endothelial and Schwann cells of diabetic rat nerve. The group was first to develop the Western blot analysis of poly(ADP)-ribosylated proteins in rat sciatic nerve (27) using this approach, it was found that poly(ADP)-ribosylated protein abundance increased by 74 in rats with 4-weeks duration of STZ-diabetes in comparison with nondiabetic controls. Furthermore, accumulation of poly(ADP)-ribosylated proteins was found to develop very early, i.e., within about 12-24 hours of exposure of cultured human endothelial and Schwann cells to high glucose (27). PARP-1 protein abundance was not affected by high glucose or PARP inhibitor treatment in either cell type consistent with the current knowledge on PARP-1 as abundantly expressed...

Blood Flow Of Nerve Trunks And Ganglia

The characteristics of the blood flow in nerve trunks and ganglia are unique and are distinguished from those of the central nervous system. Nerve trunks are supplied upstream by arterial branches of major limb vessels that share their supply with other limb tissues. At some sites, the overlapping vascular supply from several parent vessels renders zones of susceptibility to ischemia, or watershed zones. In the rat, and probably human sciatic nerve, a watershed zone can be found in the proximal tibial nerve (3). In some nerve trunks, the centrofascicular portion of the nerve trunk might be the most vulnerable to ischemia, accounting for corresponding centrofascicular patterns of axon damage. However, ischemic damage of large multifascicular nerve trunks is more commonly multifocal, with irregular zones of axon damage that depend on specific features of their perfusion and the exact vessels that are involved in causing ischemia (4,5). In general, nerve trunks are well-perfused from...

Therapies For Nerve Regeneration

Neurotrophic factors are proteins that promote survival of neurons regulating gene expression through second messenger systems. These proteins may induce morphological changes, nerve differentiation, nerve cell proliferation, and induce neurotransmitter expression and release. Subsequently, reduction in levels of neurotrophic factors (97) can lead to neuronal loss, possibly through activation of apoptosis (98). Many proteins have properties and characteristics of neurotrophic factors, including cytokine-like growth factors, TGF-P, NT3, nerve growth factor (NGF), insulin-like growth factor (IGF)-1, and VEGF. Although only a few neurotrophic factors have been extensively investigated, there are number of proteins that have been identified as neurotrophic factors (31,99). Many of these proteins appear to have altered expression in nerves of patients with diabetes (77). For example, interleukin-6, a cytokine-like growth factor may play a role in cell proliferation (100). Although their...

Role For Oxidativenitrosative Stress

Numerous new studies reveal the important role of oxidative stress in nerve functional, metabolic, neurotrophic, and morphological abnormalities characteristic of PDN. The role for ROS in diabetes-associated nerve conduction and blood flow deficits has been demonstrated in studies with the universal antioxidant DL-a-lipoic acid (5,23,91), which is known to combine free radical and metal chelating properties with an ability (after conversion to dehydrolipoic acid) to regenerate levels of other antioxidants, i.e., GSH, ascorbate, a-tocopherol, catalase, and glutathione peroxidase. It has also been confirmed with other antioxidants including the potent hydroxyl radical scavenger dimethylthiourea (96), HESD (22,23), and the SOD mimetic M40403 (97). Furthermore, diabetes-induced MNCV and SNCV deficits were reversed by the perox-ynitrite decomposition catalyst FP15 treatment (94). Two groups produced experimental evidence of an important role for oxidative stress in diabetes-associated...

Thigh Pain

Inner thigh pain often stems from the sciatic nerve which is suffering pressure at the lower back. If this is so, chiropractic adjustments should help. The correct treatment, after killing bacteria electronically, is to clean up the entire kidney area using the kidney herb recipe.

Acute Nerve Ischemia

Some forms of focal diabetic nerve injury at nonentrapment sites might have an ischemic origin. For example, diabetic lumbosacral plexopathy is thought to be a consequence of focal plexus ischemia either from microangiopathy or superimposed vascular inflammation (55,56). As demonstrated in work by Nukada (57,58), experimental diabetic nerves rendered even mildly ischemic develop more severe axonal damage than nondia-betic nerve. Similar findings were encountered in nerve trunks exposed to the potent vasoconstrictor endothelin (5,59). Rat diabetic sciatic nerves exposed to topical endothelin experienced more prolonged and severe vasoconstriction leading to focal axon nerve conduction block followed by local axonal degeneration. Axonal damage in diabetic nerves exposed to epineurial topical endothelin also had a striking multifocal distribution, resembling changes in human diabetic sural nerve biopsies. Rises in serum endothelin levels have been reported in some human studies, but not...

The Polyol Pathway

Because it is easier to develop TG mice than KO mice, TG approach was first used to investigate the role of AR in diabetic neuropathy. The first reported mouse model utilized the major histocompatibility complex (MHC) promoter, which is active in all tissues, to drive the expression of human AR (hAR) complementary DNA (cDNA) in TG mice. Indeed all tissues from the MHC-hAR TG mice tested were found to express the hAR mRNA, including liver, skeletal muscle, heart, kidney, brain, and lung. Under normal rearing condition, these mice developed thrombi of the renal vessels, but no abnormality was evident in the brain, lung, heart, thymus, spleen, intestine, liver, muscle, spinal cord, and sciatic nerve when examined under light microscopy (15). Under nondiabetic condition, sorbitol and fructose contents in the sciatic nerve of the TG mice were similar to that of the wild-type (WT). When induced to become diabetic, sciatic nerve sorbitol and fructose levels in the TG mice were twice that of...

Autonomic Ganglia

Prominent physiological and less dramatic pathological changes are present in auto-nomic ganglia of DAN. There is a significant reduction in blood flow in autonomic ganglia such as superior cervical ganglion (32,33). This reduction by about 50 is present as early as 1 week and is persistent over 24 weeks (4). Glucose uptake was reduced to 30 of control values in superior cervical ganglion in rats with DAN. a-Lipoic acid supplementation had no effect on glucose uptake in normal nerves at any dose, but reversed the deficit in DAN, with a threshold between 10 and 25 mg kg. ATP, creatine phosphate, and lactate were measured in sciatic nerve and superior cervical ganglion. a-Lipoic acid prevented the reduction in autonomic ganglion creatine phosphate (34).

Parp Activation

The PARP-1 gene KO mice were used to determine if PARP contributes to diabetic neuropathy. These mice showed no obvious abnormality. Under normal rearing condition, the MNCV of their sciatic nerve, the SNCV of their digital nerve, and the morphology of their sciatic nerve all appeared normal (56). When the WT mice were induced to become diabetic by streptozotocin, their MNCV and SNCV decreased significantly. In the sciatic nerve of the diabetic WT mice there was significant increase in immunostaining of PAR, the product of PARP activity, indicating that hyperglycemia activates PARP. The PARP-1 null mice on the other hand, showed no reduction in MNCV and SNCV when induced to become diabetic. The blood glucose level in the diabetic PARP null mice was not different from that of the diabetic WT mice, indicating that PARP did not affect diabetes, but plays an important role in the diabetes-induced functional impairment in the peripheral nerves. When fed a high galactose diet, which...

Candidate Genes

Under normal conditions glucose is metabolized by three key pathways, primarily by a hexokinase-dependent phosphorylating pathway to form glucose 6-phosphate, which then enters the glycolytic pathway to form lactate, or the hexose monophosphate shunt to form pentose-phosphate. Second, glucose might be oxidized to gluconic acid through an NAD+-dependent glucose dehydrogenase. Finally, nonphosphorylated glucose might enter an accessory pathway of glucose metabolism known as the polyol pathway. Aldose reductase is the first and rate-limiting enzyme in the polyol pathway. It is widely distributed in human tissues including Schwann cells. Reduced glutathione synthesis, impaired nitric oxide synthesis, reduced Na+, K+-ATPase activity, increased protein kinase (PK)-C activity as well as a redox imbalance have all been identified as critical changes secondary to enhanced aldose reductase activity that precipitate the development of diabetic neuropathy (29-34). Aldose reductase inhibitors can...

Low Back Pain

We have been told that lower back pain originates in an inherited weakness of the spine at its base because we humans walk upright instead of on four legs. And we have been told that the bony hooks that keep the spine aligned are flatter in some families, making it harder for them to hold the spine together. We are also told that proper exercises could have kept this part of our bodies strong so lower back pain could be avoided. These theories become obsolete when, without surgery or exercise or change in posture, lower back pain can be made to disappear quickly and permanently. Acupressure massage and chiropractic can bring miraculous relief. The most severely crippled lower back pain sufferer can shuffle lamely into a chiropractor's office and walk out normally, without pain or painkiller after treatments. So al- Oxalic acid crystals are as sharp as broken glass. Use the kidney cleanse (page 549) to dissolve them and other stones. All lower back pain can be cured by removing the...


A line of TG mice that express a fusion protein, where the carboxyl terminus of heavy NF was replaced by P-galactosidase, was found to be completely devoid of peripheral axonal NF, as the fusion protein causes aggregates of NF to precipitate in the perikarya (65). Interestingly, there was no obvious abnormality in the NF-deficient mice except that the caliber of their axons was smaller. In the tibial nerve of these mice the number of fibers and fiber density were higher than that of the WT mice, whereas the axon diameter and axon area were smaller (66). Under normal condition there was no obvious degeneration of their neurons, but the NCV was slower and the amplitude of the nerve action potential was dramatically lower than that of the WT mice, presumably because of the smaller caliber axons. The reduction in SNCV was much more pronounced than the reduction in MNCV. These mice were of Swiss genetic background. When induced to become diabetic, the WT mice exhibited no significant...

Diabetic Neuropathy

Diabetic rats show reduction in sensory motor conduction velocities and nerve action potentials and reduction in peripheral nerve blood flow and all these abnormalities can be prevented by pretreatment with anti-AGE agents such as aminoguanidine (114,115). Pentosidine content was increased in cytoskeletal proteins of the sciatic nerve of streptozotocin induced diabetic rats and decreased after islet transplantation (111).


Increased oxidative stress has emerged as a leading candidate in the pathogenesis of experimental diabetic neuropathy, with a direct relationship between measures of oxida-tive stress and the development of nerve blood flow and nerve conduction deficits (146-148). In diabetic rodents, measures of oxidative stress, including increased nerve conjugated dienes (148) and reduced levels of nerve superoxide dismutase (146,149), glutathione peroxidase (150), glutathione (151), and norepinephine (152) are closely associated with the development of neuropathy. In concert, oxidative stress has also been implicated in the development of cardiomyopathy (120,153) and a contributing factor to endothelial dysfunction (154,155) and changes in acute phase reactants (156). Increases in reactive oxygen species can stimulate apoptosis in cardiac myocytes (157,158) potentially resulting in myocardial dysfunction (159). In the heart, chronic oxidative stress might also impair neurotrophism by depleting...

Growth Factors

Neurotrophins promote neuronal survival by inducing morphological differentiation, enhancing nerve regeneration, and stimulating neurotransmitter expression (81). Although the data implicating deranged neurotrophical support is compelling in animal models, in diabetic patients results are somewhat contradictory. Thus, although dermal NGF protein levels are reduced in patients with diabetes, sensory fiber dysfunction (82), skin mRNA NGF (83), and NT-3 (84) are increased and sciatic nerve ciliary neurotrophic factor levels remain unchanged (85). Furthermore, in situ hybridization studies demonstrate increased expression of TrkA (NGF-receptor) and trkC (NT-3 receptor) in the skin of patients with diabetes (86), whereas a phase II clinical trial of recombinant human nerve growth factor demonstrated a significant improvement in neuropathy (87), a phase III trial failed to demonstrate a significant benefit (88). More recently brain-derived neurotrophic factor has demonstrated no significant...

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