Cure for Sciatica Discovered

Stop Sciatica In 8 Minutes

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. In addition to natural herbs to cure sciatica, Steven also reveals exercises as an important part in reducing pain related to sciatica. The exercises are not hard to perform but they require you to practice right and combine doing exercises with taking rest to get rid of sciatica pain effectively. Exercises introduced by Steven also help increase blood circulation that help sciatica patients maintain the correct posture to fight sciatica pain and help them flexible bodies. This Program is a 100% legit product that will get you the results you need, but you should be patient and be dedicated for it to work. Sciatica sufferers blindly look for one and the other product, in order to get relieve from the intense pain they have to endure. In their rush, they are often misguided. More here...

Cure Sciatica Naturally In 7 Days Summary


4.7 stars out of 12 votes

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Author: Dr. Steven Guo
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Stop Sciatica in 8 Minutes Review

Highly Recommended

The author presents a well detailed summery of the major headings. As a professional in this field, I must say that the points shared in this ebook are precise.

As a whole, this manual contains everything you need to know about this subject. I would recommend it as a guide for beginners as well as experts and everyone in between.

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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. More here...

Sciatica and Back Pain SelfTreatment Summary

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Author: John McPherson
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Local Influences of Myelin on Axon Cytoskeleton

Myelin Electron Microscopic Image

Electron microscopic images of Trembler peripheral nerves in cross-section typically show many axons undergoing active demyelination or lacking myelin. Axons were smaller and thinner than normal (Ayers and Anderson, 1976). Remarkably, this reduction in axonal caliber was a local phenomenon (Aguayo et al., 1977 de Waegh and Brady, 1991 de Waegh et al., 1992). When sciatic nerve segments from Trembler mice are grafted into wild-type sciatic nerve and axons are allowed to regenerate, axon regions in the Trembler graft have a Trembler phenotype, demyelinated axons, and reduced axonal caliber in graft regions (Aguayo et al., 1977 de Waegh and Brady, 1991). In these nerves, axons proximal and distal to the graft had normal compact myelin and axon caliber. The reverse graft experiment (normal sciatic nerve segment grafted in Trembler sciatic nerve) had normal myelin and axonal caliber in the graft, but Trembler phenotype proximal and distal to the graft (Aguayo et al., 1977 de Waegh and...

F I Consequences of Demyelination

Studies on axons demyelinated in vivo provided more details. Hall and Gregson (1971) introduced a method for focal demyelination that reproduces many aspects of inflammatory demyelinating disease and can be used in amphibian and mammalian species. A small amount of lysolecithin (1 pl, 1 in adult sciatic nerve) is injected surgically directly into a nerve trunk and the animal is allowed to recover. The drug vesiculates the outmost layers of myelin, which initiates an inflammatory response, with macrophages entering the lesion from the blood and removing myelin debris by phagocytosis. Affected internodes are completely stripped of myelin, a process that is completed by 1 week postinjection. At this time, if the nerve is dissected and teased, axons can be found that are devoid of all glial membranes and are surrounded only by a disrupted basal lamina. If the animal is allowed to recover for longer periods, Schwann cells proliferate and begin the process of remyelination (Shrager and...

Na Channel Subtypes Involved in Generating Persistent Na Current in Myelinated Nerve

These properties of NaV1.6 contribute to the spontaneous and burst-firing of cerebellar Purkinje neurons (Kahliq et al., 2003). NaV1.6, when transfected and expressed in NaV1.8 null neurons, may well generate a persistent current over a wider potential range than NaV1.7 (data presented by Herzog et al. 2003a). Baker and Bostock (1997, 1998) found a low-threshold, persistent TTX-s Na+ current in large diameter DRG neurons in the rat, and Kiernan et al. (2003) found a similar current in about one third of small (< 25 im, apparent diameter) neurons. This current also exhibited resurgence in large neurons (unpublished observation). NaV1.6 appears to be the predominant Na+ channel at peripheral nodes of Ranvier and in optic nerve (Caldwell et al., 2000). It is also found in unmyelinated axons in the retina and the parallel fibers of the cerebellum (Caldwell et al., 2000 Schaller and Caldwell, 2003). Black et al. (2002) have provided evidence that NaV1.6 is present in unmyelinated corneal...

Lumbar Clinical Experience

While there is no doubt that the z-joint can contribute to low back pain, there are no unique identifying features in the history, physical examination, and imaging of these patients (36) and therefore the existence of a primary facet syndrome or zygapophyseal joint syndrome is dubious (37). Nevertheless a prospective randomized trial was performed to try and elucidate clinical characteristics that support the z-joint as a primary or significant nociceptor. Although there is no specific syndrome that discriminates between lower back pain caused by z-joint and other etiologies, there were several predictors identified. The factors of age above 65 years and pain that was not exacerbated by coughing, not worsened by hyperextension, not worsened by forward flexion, not worsened when rising from flexion, not exacerbated by extension-rotation, and relieved by recumbent positioning were found to be five clinical characteristics indicating pain related to the z-joint (38). This investigation...

Schwann Cell Differentiation

MRNAs (Martini and Schachner, 1986 Trapp et a ., 1981 Winter et a ., 1982). P0 and MBP accumulation and the levels of their respective mRNAs parallel the rate of myelin formation during development. Removal of axons by transection (Trapp et a ., 1988b) or cellular dissociation (Brockes et a ., 1980 Mirsky et a ., 1980) results in rapid decreases in myelin protein gene expression. Following nerve transection, sciatic nerve axons regenerate among distal stump Schwann cells, these Schwann cells re-express myelin protein genes and myelinate, whether they come from previously myelinated or unmyelinated nerves (Aguayo et a ., 1976a, 1976b Politis et a ., 1982).

Axonal Support by Nonmyelinforming Schwann Cells

Support of axons is not restricted to the intimate relationship with myelinating Schwann cells. Some sensory and all postganglionic sympathetic axons have diameters below 1 im and are unmyelinated (Type C fibers). These axons assemble in Remak bundles and are engulfed as groups of axons by nonmyelinating Schwann cells. In one study, axoglial signaling was specifically ablated for these non-myelinating Schwann cells by transgenic overexpression of a dominant-negative ErbB4 receptor (Chen et al., 2003). Mutant mice develop a progressive neuropathy, including apoptosis and proliferation of nonmyelinating Schwann cells. Of importance, there was secondary degeneration of sensory C fibers and subsequent apoptosis of DRG neurons. These results indicate bidirectional interactions and signaling also between small-diameter axons and their associated (nonmyelinating) Schwann cells in the Remak bundle. The molecular mechanism of glial support was suggested to involve neurotrophic factors, as GDNF...

Antibodies as Neuroelectric Blocking Factors

Antibodies against GM1 gangliosides may alter axonal conduction by altering sodium channel activity. High titers of antibodies against GM1 ganglioside have been found in many patients with GBS, as well as in patients with lower motor neuron disease and motor neuropathy (Kornberg et al., 1994). Anti-GM1 antibodies exhibited a complement-dependent inhibition of sodium currents in rabbit sciatic nerve (Takigawa et al., 1995), identifying for the first time a specific antibody that inhibited a crucial component of axonal conduction. This result was especially intriguing because GM1 may be localized at the node of Ranvier where sodium channels are clustered along axons (Corbo et al., 1993), suggesting that anti-GM1 antibodies might bind at nodal membrane, where they could block sodium channels and disrupt axonal conduction. A study of conduction in rat ventral roots, however, failed to confirm that anti-GM1 antibody could block nerve conduction or sodium channels (Hirota et al., 1997),...

Stimulus strength times threshold

FIGURE 3.3 Recruitment curves for single twitch contractions at various stimulus intensity levels, measured as force normalized to the maximal twitch for 100 recruitment of the muscle. A. Comparison of recruitment of cat medial gastrocnemius by nerve cuff electrodes (open circles) and nerve hook electrodes (open diamonds) on the common sciatic nerve, as opposed to intramuscular electrodes configured as in the BION (solid circles) for acutely implanted (solid lines) and chronically implanted (dashed lines) electrodes (adapted from Singh et al., in press). B. Recruitment of cat posterior biceps muscle by a BION1 implanted acutely in a proximal or distal location in the muscle belly, with stimulus intensity (abscissa) normalized to the threshold for a just palpable twitch at each of two pulse widths (adapted from Cameron et al., 1997). The plateau effects at less than 100 recruitment represent stimulus current levels at which compliance voltage limits were reached for an earlier version...

Structural and Cellular Changes

Figure I Early structural changes during wwallerian degeneration (A) Twelve hours after transection of the sciatic nerve of an adult rat shows one of the earliest structural changes that take place during wwallerian degeneration, accumulation or organelles, including mitochondria (arrows) (original magnification x 10,000.) (B) Within 24 hours of the transection, granular disintegration of the cytoskeleton takes place. Notice that in panel A and B, the axons are swollen as evidenced by the decrease in g-ratio (ratio of the myelin thickness to the whole fiber diameter) (original magnification x 10,000). (C) At 7 days after transection of the nerve, Schwann cell proliferation, macrophage infiltration, and myelin degradation are all well underway (original magnification x 2,000). Figure I Early structural changes during wwallerian degeneration (A) Twelve hours after transection of the sciatic nerve of an adult rat shows one of the earliest structural changes that take place during...

Wallerian Degeneration Is an Active Process

Waller's initial observation, more than 150 years ago, that the distal stumps of transected nerve fibers degenerate (Waller, 1850), and subsequent findings that most proteins in the axon are synthesized in the cell body and transported down the axons using specialized transport mechanisms led to the attractive hypothesis that degeneration of the distal stump of a transected axon occurs because of lack of necessary proteins and other materials. However, slowed waller-ian degeneration observed in a strain of mice (C57Bl Ola, now called Wlds for wallerian-like degeneration slow) changed that perception dramatically (Lunn et al., 1989 Perry et al., 1990 Glass and Griffin, 1991). In this spontaneously generated strain, degeneration of the transected axons is slowed significantly (Fig. 2). In a wild-type animal, transection of the sciatic nerve results in loss of electrical conductivity in the distal portion within a day or two, followed by dissolution of the axoplasm. In contrast, a...

Demyelination and Wallerian Degeneration

One potential mechanism by which demyelination can lead to axonal degeneration is disruption of axonal transport through demyelinated segments (Rao et al., 1981 Guy et al., 1989 Munoz-Martinez et al., 1994 Kirkpatrick et al., 2001). This is more apparent in the optic nerve system where local injections of very small quantities of anti-Gal-C antibody can lead to focal demyelination and abnormal axonal cytoskeleton and axonal transport through the demyelinated segment (Zhu et al., 1999). Similarly, in animal models of experimental allergic neuritis, there are axonal transport deficits in the optic nerve (Rao etal., 1981 Guy et al., 1989). The issue is less clear in the PNS demyelination in the sciatic nerve induced by focal injection of a neurotoxin from K. humboldtiana causes slowed fast axonal transport (Munoz-Martinez et al., 1994), but demyelination induced by intraneural injection of antigalac-tocerebroside does not have any effect on fast axonal transport (Armstrong et al., 1987).

Posterior Tibial Nerve Ss2

This nerve also arises from the division of the sciatic nerve in the popliteal fossa and descends behind the tibia, terminating in the medial and lateral plantar nerves which innervate the small muscles of the foot. The sensory branch contributes to the sural nerve. Damaged by

Peripheral And Cranial Nerve Injury

Another consideration in the repair of peripheral nerves is the determination of whether an epineurial or fascicular repair is more appropriate. Several experimental 8 and clinical 9 studies have addressed the issue of whether epineurial or fascicular repair is more effective, with no conclusive evidence suggesting the superiority of one over the other 2 . Studies examining the specificity of muscle reinnervation of rat sciatic nerve have demonstrated that fascicular repair resulted in more accurate regeneration as compared to epineurial repair 10,11 .

Neurotoxic Effects in Experimental Animals

MeHg fed to rodents in high dosages caused posterior paralysis and sensory neuropathy, characterized by cerebral and cerebellar necrosis and degeneration of dorsal root ganglionic nerves and sciatic nerve 236-238 . At the ultrastructural level, deposition has been shown to occur within lysosomes of target glial cells.

Last Observation Carried Forward

Last observation carried forward (LOCF) is probably the most widely used technique in drug trials and has gained the seal of approval from the Food and Drug Administration. The name says it all when a person drops out of a study, the last recorded value is carried forward to fill in the blanks. The logic is that this is conservative, operating against the hypothesis that people will get better over time, and so it supposedly underestimates the degree of improvement. The advantages of LOCF are that it is easy to do and that we do not lose subjects. However, there are some problems with this technique. The first is the assumption that no change occurs aside from the effect of the intervention. This may indeed be a conservative assumption for the experimental group but is actually quite liberal with regard to the control or comparison group. It ignores the fact that the natural history of many disorders, ranging from depression to lower back pain, is improvement over time, even in the...

Piriformis Syndrome Description

Radiating Pain

The piriformis syndrome is characterized by nondisco-genic, extrapelvic, sciatic nerve compression in the area of the greater sciatic notch. The symptoms include pain and dysesthesias isolated to the buttock region, radiating to the hip or posterior thigh, and or occurring distally as radicular pain.42 The symptoms of piriformis syndrome are thought to be caused by entrapment of one or more divisions of the sciatic nerve by the piriformis muscle.43,44 The original description of this condition dates back to 1928 when Yeoman45 first described the possibility of a pathologic relationship between the sciatic nerve and the piriformis mus cle. Edwards46 described it as neuritis of branches of the sciatic nerve, caused by pressure of an injured or irritated piriformis muscle. Freiberg and Vinke43 were the first to describe the classic findings of Lasegue's sign and tenderness at the sciatic notch over the piriformis muscle. The common peroneal division of the sciatic nerve is thought to be...

Dictums On Hip Arthroscopy

Femoral Nailing Arm Position

The operative hip is positioned in extension and approximately 25 degrees of abduction. Slight flexion might relax the capsule and facilitate distraction, but this also causes tension on the sciatic nerve, which could increase the risk of traction neuropraxia. Neutral rotation of the extremity during portal placement is important for proper orientation, but freedom of rotation of the footplate during the procedure facilitates visualization of the femoral head.

Kv1 Channel Localization and Function in Demyelinated and Remyelinating Axons

Kv1 channel localization after demyelination and during remyelination was described using the lysolecithin model of peripheral demyelination (Rasband et al., 1998). In these experiments, lysolecithin was injected directly into the sciatic nerve, resulting in activation of macrophages, and the disruption and eventual phagocytosis of myelin. In this model, complete, focal demyelination occurs at the site of injection within about 1 week. After demyelination, Schwann cells proliferate and are able to remyelinate the injured region. However, the structure of remyelinated axons is different than before the drug injection there are fewer layers of myelin, and the internodal length is decreased to about one-fourth the length found in uninjured animals. As a result, new nodes of Ranvier form in regions that were formerly internodal with low densities of ion channels. Finally, it is relatively easy to isolate the sciatic nerve and record action potentials in the demyelinated remyelinating...

Diagnostic Round And Anatomy Of The Peripheral Hip Joint Cavity

Patient Positioning And Draping

Access to the posterior area can be achieved by moving the scope straight posteriorly between the zona or-bicularis and the lateral synovial fold. After insertion of the 70-degree lens, the posterolateral and lateral part of the labrum, head, and neck and the posterior syn-ovium can be inspected (see Figure 11.8H). The lateral and the posterior areas are more difficult to inspect compared with the anterior and medial areas. Hypertrophy of the synovium and tight joints (e.g., osteoarthritic hip joints with capsular fibrosis) can significantly decrease orientation and mobility for passing the arthroscope to the lateral and posterior areas. In addition, the posterior area is the smallest because the posterior wall and labrum cover most of the head in extension and the attachment of the joint capsule is 2 to 3 cm proximal to the intertrochanteric crest, thus more proximal than on the anterior sur-face.53 If the arthroscope cannot be brought in this part of the joint without traction,...

Molecular Axon Components

Wallerian Degeneration Axons

Figure 3 The remarkable phenotype of the Wlds mouse (Lunn et al., 1989). Central panel (B) illustrates the appearance of the normal sciatic nerve in a 1- m semithin section stained with toluidine blue. Panel (C) illustrates the appearance of the distal nerve of a wild-type mouse nerve undergoing wallerian degeneration 7 days after transection. Panel (A) shows the remarkable preservation of the distal axon segment 7 days after sciatic nerve transection in the Wlds mouse. Figure 3 The remarkable phenotype of the Wlds mouse (Lunn et al., 1989). Central panel (B) illustrates the appearance of the normal sciatic nerve in a 1- m semithin section stained with toluidine blue. Panel (C) illustrates the appearance of the distal nerve of a wild-type mouse nerve undergoing wallerian degeneration 7 days after transection. Panel (A) shows the remarkable preservation of the distal axon segment 7 days after sciatic nerve transection in the Wlds mouse.

Posterolateral Portal

Sciatic Nerve Pathway

It is facilitated by direct visualization through the arthroscope from the anterolateral portal. Maintaining direct visualization is of greater importance because the posterolateral portal gets closer to major structures, specifically the sciatic nerve. The posterolateral portal penetrates both the glu-teus medius and minimus before entering the lateral capsule at its posterior margin (Figure 7.9). Its course is superior and anterior to the piriformis tendon (Figure 7.10). It lies closest to the sciatic nerve at the level of the capsule. The distance to the lateral edge of the nerve averages 2.9 cm. Several technical errors or alterations in technique during arthroscopy can place the sciatic nerve at greater risk. First, although hip flexion may relax the capsule, easing distraction, it may potentially draw the FIGURE 7.9. Posterolateral portal pathway relationship to sciatic nerve and superior gluteal nerve. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.) FIGURE 7.9....

Participation of Opioid Mechanisms in Cannabinoid Antinociception

Of the paw (31), sciatic nerve (30), or tooth (32). Electrophysiological studies have largely confirmed these antinociceptive properties of cannabinoids (33). Cannabinoid agonists also induce antinociception in inflammatory models of pain, such as hyperalgesia induced by carrageenan (34), capsaicin (35), formalin (36-38), and Freund's adjuvant (39). Doses of cannabinoid agonists required to induce antinociception in inflammatory processes are usually lower than those required in other nociceptive models (35), in agreement with the anti-inflammatory properties of cannabinoid agonists (22). Cannabinoid agonists are also effective in visceral models of pain, such as the bladder wall inflammation induced by turpentine administration (38), and neuropathic models, such as the painful mono-neuropathy induced by loose ligation of sciatic nerve (40-42). In contrast with opioid responses, antinociceptive effects of cannabinoids in neuropathic pain are not decreased after repeated administration...

Neurovascular Structures

Lateral Femoral Circumflex Artery

The superior gluteal nerve and artery are the most superior of 10 neurovascular structures that exit through the sciatic notch (Figure 6.7). They course transversely in a posterior to anterior direction between the deep surface of the gluteus medius and the superficial surface of the gluteus minimus, innervating and supplying blood to both. The sciatic nerve exits the notch under the piriformis tendon and then lies posterior to the other short external rotators in a vertical direction as it courses distally (see Figure 6.7).

Direct Trauma To Neurovascular Structures

Injury to the sciatic nerve or femoral nerve or vessels is a disastrous complication of hip arthroscopy. Evidence from anatomic studies suggests that the structures are at a safe distance when proper technique in portal placement is observed.7 The reported clinical experiences also suggest that this is a relatively safe technique. However, one femoral nerve palsy has been reported.2 This author is also aware of one anecdotal case of laceration of the femoral nerve associated with arthroscopy of the hip. This further emphasizes that those embarking on this technique should know the anatomy and landmarks and be versed in proper portal placement. Although the femoral neurovascular structures and the sciatic nerve should be safely away from the operative field, the lateral femoral cutaneous nerve (LFCN) warrants special mention. The LFCN is always vulnerable to injury from the anterior portal.7 One of its branches will invariably lie close to the portal. It cannot be predictably avoided...

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.

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...

Indications and Contraindications for 224RaCl Therapy in Ankylosing Spondylitis

The decision for treatment with 224RaCl always should be made in close collaboration of the nuclear medicine specialist and the rheumatologist. Diagnosis of AS and a failure of conservative pharmacotherapy with both nonsteroidal anti-inflammatories and analgesics, or the presence of specific contraindications against these drugs are a prerequisite. The patients frequently complain of lower back pain, severe morning stiffness in the back and spine, and of breathing impairment owing to progressive inflammation and stiffening of their chests.

Compartments of the Peripheral Nerve

Compartments of the peripheral nerve. a Cross section of the sciatic nerve of the rat with four fascicles each surrounded by the perineurium (pn), epineurium (ep) with adipose tissue (ac), epidural vessels with arteriole (a) and venule (v) bar 500 m. b Higher magnification of the perineurium (pn) with its slender cytoplasmic lamellae separating endoneurium (en) and epineurium (ep). Endoneurial small arteriole (a). Semithin section, bar 10 m. c Endothelial cells with junctional complexes (arrows), pericyte (p) and macrophage (ma) of the endoneurium. Capillary (c). Electron micrograph, bar 1 m. d Junctional complexes (arrows) between single perineurial cells. Note the membrane vesiculation. Fine collagen fibrils (cf) occur regularly between the perineural lamellae, endoneurium (en), epineurium (ep). Electron micrograph, bar 1 m.

Schmidtlanterman Incisures

Paranodes and their total number within individual internodes increases with myelin sheath thickness and internodal length. The largest fibers in rat sciatic nerve have approximately 25 incisures. They are present during early stages of myelination and in remyeli-nated internodes. Their existence as a normal feature of the PNS internode or as a byproduct of poor Wxation or mechanical stress sheering defect was initially debated (Peters et a ., 1991). However, electron microscopy established ultrastructural criteria for their identification as Schwann cell cytoplasmic channels that are confluent with the cytoplasm of the outer and inner margins of the internode (Robertson, 1958). When examined ultrastructurally in longitudinal orientation, Schmidt-Lanterman incisures appear as a series of cytoplasmic openings of the compact myelin that are in register with each other (Robertson, 1958 also see Ghabriel and Allt, 1981 Hall and Williams, 1970 Peters et a ., 1991) (Fig. 1.10B). Because...

Experimental Models of Neurological Disorders

Into two rate components fast (100- to 400-mm day) and slow (0.1-3-mm day). Warita and colleagues (1999) have investigated whether fast axonal components are modified in ligated sciatic nerves of SOD1 transgenic mice and how they are altered developmentally from an early preclinical stage. Defects in fast anterograde transport machinery (decreased accumulation of the microtubule activated ATPase kinesin after ligation of the sciatic nerve) were observed, and led the authors to hypothesize that this impairment may contribute to selective motor neuron death.

Developmental Antigens

Slits, semaphorins and netrins are families of axonal guidance molecules which are expressed in the developing nervous system throughout the animal kingdom. More than 30 semaphorins have been cloned in mammals. Vertebrate semaphorins are secreted (class 3) or membrane bound (classes 4-7), and have a dual role acting as chemoattractants and chemorepellents in axonal growth 15 . The receptors neuropilin-1 and -2 (NP-1, NP-2), cell adhesion molecule L1 and axonal plexin-A3 transmit the axonal guidance effects of class 3 semaphorins in the developing nervous system. NP-2 deficient mice suffer from developmental defects in axonal pathfinding in the CNS and PNS. In the adult nervous system it was shown that NP-1, NP-2, semaphorin-3F and to a lesser extent semaphorin-3A mRNA levels are increased particularly distal to a crush injury of sciatic nerve in rat. The results suggested that a concentration gradient of semaphorin-3F which results in the injured tissue may serve as guidance in axonal...

Neurovascular Traction Injury

Neuropraxia due to traction has been reported, most commonly involving the sciatic nerve. Glick was the first to report four such cases, which he attributed to his early technique for performing the procedure.3 Later, Sampson reported on a larger series from this same center, observing that all neuropraxias were associated with prolonged traction times.6 He advocates that the traction time should be kept under 2 hours Transient sciatic nerve neuropraxia (4) All reported traction neuropraxias were transient and the recovery was complete. However, this author is anecdotally aware of two cases by different surgeons in which the patients demonstrated evidence of sciatic nerve damage that only partially recovered. In both cases, the traction time was well under 2 hours, indicating that other factors may be involved in addition to the duration of traction. Sufficient traction force is necessary to ensure adequate joint space separation. Otherwise, there is greater risk of damage from the...

Distribution of Ion Channels in Myelinated Axons

Axons can be substantially altered by a redistribution of Na+ and K+ channels. Impulse conduction can be restored by an increase in the number of Na+ channels expressed in the normally electrically unexcitable internode (Bostock and Sears, 1978), allowing continuous conduction and thus the restoration of function (Fig. 1), albeit with prolonged conduction times. The same authors (Sherratt et al., 1980 Bostock et al., 1981) also showed that blockade of axonal fast K+ channels exposed by myelin withdrawal, using the channel blocker 4-aminopyridine, could help overcome conduction failure after demyelination. This provided a clinical strategy for the symptomatic treatment of MS that has met with some success (e.g., Schwid et al., 1997, and Sheean et al., 1998), although it is limited by the nonspecific effects of K+ channel blockers on nervous system function. Craner et al. (2003) reported that in allergic encephalomyelitis, apparently demyelinated optic nerve axons express NaV1.6 and...

Physiological Effects

Initially, two separate studies showed that intraneural injections, in rats, of human anti-GM1 antibodies caused acute conduction block (Santoro et al., 1992 Uncini et al., 1993), but this finding was not confirmed by another group that used immunoglobulin fractions with IgG or IgM anti-GM1 reactivity purified from patients with GBS or multifocal motor neuropathy (Harvey et al., 1995). The basis for these discrepant findings has not been resolved, but it could reflect factors that were not strictly matched (1) anti-GM1 antibody properties such as fine specificity and or affinity, (2) whole serum versus purified immunoglobulins and anti-GM1 titers, and (3) source and activity of the exogenous complement. This issue of anti-ganglioside antibody-mediated conduction failure is rekindled by a recent report indicating that, in a rabbit model of AMAN associated with anti-GM1 antibodies, conduction abnormalities were noted in myelinated fibers in the spinal roots (Susuki et al., 2003). To...

B K Channel Therapy

Besides acute effects on excitability, K channel blockage may lead to changes in axoglial relationship potentially resulting in long-lasting changes in nerve excitability. One reason is that glial cells express K channels, and blocking glial K channels affect glial cell mitosis and myelinogenesis (Chiu and Wilson, 1989 MacFarlane and Sontheimer, 2000a, 2000b). A novel question raised by these studies is whether normal myelinogenesis requires normal expression of glial K channels. Several provocative studies have shed light on this issue. Genetic ablation of K channels has produced hypomyelination in certain transgenic mouse models. A striking example is genetic ablation of a Kir channel (Kir4.1), which causes severe hypomyelination in the CNS axons (Neusch et al., 2001). Kir4.1 is expressed in oligodendrocytes and deleting Kir4.1 channels from oligodendrocytes results in a depolarized resting membrane potential and immature morphology in these cells (Neusch et al., 2001). Global...

Mechanisms Of Action

It is now generally accepted that epidural steroids give relief by their anti-inflammatory effects. Green et al. noted that inflammation of the involved spinal nerves has often been documented at surgery (26), and there is strong evidence of inflammation in lumbar radiculopathy and disc degeneration. In fact, McCarron et al. observed an intense inflammatory reaction after injection of autologous disc material into the epidural spaces of dogs and a rapid onset of fibrosis (27). Franson et al. demonstrated high levels of phospholipase A2 (PLA2) around symptomatic disc herniations and painful discs. Subsequently, they engendered an inflammatory response by injecting PLA2 into mouse paws (28). PLA2 exerts its effect by liberating arachidonic acid from cell membranes, causing an intense inflammatory reaction in adjacent tissues (4). The inhibition of PLA2 activity is one of the anti-inflammatory actions of corticosteroids (29,30).


The pelvis is innervated by the sacral and coccygeal plexi. The sacral plexus lies on the anterior surface of the piriformis muscle just beneath the sacroiliac joint. It gives rise to the sciatic and pudendal nerves. The sciatic nerve leaves the pelvis through the greater sciatic foramen and enters the posterior thigh lateral to the ischial tuberosity. The pudendal nerve also leaves the pelvis through the greater sciatic foramen between the piriformis and coccygeus muscles, hooks around the ischial spine and sacrospinous ligament and enters the perineum via the lesser sciatic foramen.


Symptoms of posterior wall weakness typically entail pelvic and perineal pressure, a vaginal bulge, and associated lower back pain. Many women need to digitally reduce or splint the posterior vaginal bulge or the perineum to initiate or complete a bowel movement. Accumulation of stool within the rectocele reservoir leads to increasing degrees of perineal pressure and obstructive defecation. In the absence of digital reduction, women will note incomplete emptying, which leads to a high degree of frustration. A vicious cycle of increasing pelvic pressure, need for

Historical Aspect

In 1984, the Veterans Administration (VA) funded the initial animal studies at the Togus VA Medical Center (Augusta, Maine). These were aimed at determining what changes would be required to use a modified cochlear implant with a maximum pulse output of 4.3 mA and 0.4-ms pulse width, to be suitable for FES use in humans. An initial decision was taken to utilize epineurally placed electrodes (2.5 mm diameter platinum disks) in preference to epimysial or intramuscular electrodes because it was known that the stimulation currents would be lower and that there would be less movement of the electrodes. To determine exactly how low the stimulation currents would be and to determine the stimulation sites, initial anesthetized rabbits studies were conducted 9 . The threshold found for each branch of the split sciatic nerves of was 0.1 to 0.2 mA at 0.2 ms with 50 pps frequency. Maximal stimulation was achieved usually between 0.5 and 1.0 mA. Simultaneous dorsiflexion of both paws as well as...

Figure 210

Axons differentially regulated myelin gene expression in the PNS (A-E) and CNS (F-H). Following transection of peripheral nerves, myelin protein mRNA levels rapidly (by 5 days) decrease to undetectable levels in Schwann cells undergoing Wallerian degeneration. Panels A through D compare P0 (A, B) and MBP (C, D) mRNA distributions determined by in situ hybridization in intact (A, C) and 5d transected (B, D) sciatic nerves. QuantiWed by slot blot hybridization (E), both mRNAs are undetectable by 5d post-transection. In contrast, oligodendrocytes continue to express myelin protein mRNAs 40d after axonal degeneration. Panels F and G show in situ hybridization distributions of PLP (F) and MBP (G) mRNAs in spinal cord dorsal columns with intact axons (right of dotted line) and 40d after contralateral axon transection (left). As quantified by Northern blots (H), oligodendrocytes in axon-free optic nerves express signiWcant myelin protein mRNA levels. Reproduced from Trapp et al, 1988b (A...

Figure 212

Martini, R., and Schachner, M. (1986). Immunoelectron microscopic localization of neural cell adhesion molecules (L1, N-CAM, and MAG) and their shared carbohydrate epitope and myelin basic protein in developing sciatic nerve. J. Cell Biol. 103, 2439-2448. Webster, H. d. (1971). The geometry of peripheral myelin sheaths during their formation and growth in rat sciatic nerves. J. Cell Biol. 48, 348-367.

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


This assessment will normally allow the patient to be placed into one of three loose diagnostic categories back pain with evidence of nerve root induced sciatica, mechanical back pain from posterior spinal structures (e.g. facet joint syndrome) or non-specific back pain not referable to any particular anatomical structure.

General Technique

Smith And Nephew Offset Gauge

The relationship of the major neurovascular structures to the three standard portals. The femoral artery and nerve lie well medial to the anterior portal. The sciatic nerve lies posterior to the posterolateral portal. Small branches of the lateral femoral cutaneous nerve lie close to the anterior portal. Injury to these is avoided by using proper technique in portal placement. The anterolateral portal is established first because it lies most centrally in the safe zone for arthroscopy. FIGURE 10.11. The relationship of the major neurovascular structures to the three standard portals. The femoral artery and nerve lie well medial to the anterior portal. The sciatic nerve lies posterior to the posterolateral portal. Small branches of the lateral femoral cutaneous nerve lie close to the anterior portal. Injury to these is avoided by using proper technique in portal placement. The anterolateral portal is established first because it lies most centrally in the safe zone for...

Subjective Data

A few characteristic features may clue the examiner to suspect an intraarticular hip problem. These hallmarks include complaints of anterior, inguinal, or medial thigh pain. Complaints of lateral hip pain or posterior or buttock symptoms are more commonly caused by extraarticular sources such as trochanteric bursitis, abductor muscle injury, or sciatica. A history of catching or popping of the hip may be related to intraarticular pathology, but these symptoms can also occur with disorders outside the joint. Extraarticular sources of hip pain can be the lumbar spine, sacroiliac joint, or sciatic nerve. Strains of certain muscles, such as the hip adductors or flexors, can also imitate hip joint symptoms. When deep tendinous involvement occurs, such as from the piriformis or iliopsoas tendon, it may be difficult to differentiate these symptoms from mechanical hip symptoms. Although uncommon, a femoral hernia also produces groin pain.

Optical Stimulation

Optical Stimulation

The basis of this work is that delivery of pulsed laser light can be used for contact-free, damage-free, artifact-free stimulation of discrete populations of neural fibers. We have previously shown that a pulsed, low-energy laser beam elicits compound nerve and muscle action potentials, with resultant muscle contraction, which is indistinguishable from responses obtained with conventional bipolar, electrical stimulation of the rat sciatic nerve in vivo (Wells et al., 2005a). The stimulation threshold (0.3 to 0.4 J cm2) at optimal wavelengths in the infrared (1.87, 2.1, 4.0 im) is at least two times less than the threshold at which any histological tissue damage occurs (0.8 to 1.0 J cm2). Optical nerve stimulation has three fundamental advantages over electrical stimulation (Wells et al., 2005b) that make it ideal for a number of procedures that currently employ electrical means as the standard of care FIGURE 21.1 Typical experimental setup for optical stimulation and recording in the...

Figure 23

In contrast to normal development, MAG and P0 protein co-localize in the same membrane in the dysmyelinating mouse mutants Trembler J (Heath et a ., 1991) and Quaking (Trapp, 1988). These mice have deficits in converting mesaxon membranes to compact myelin. Several observations concerning these studies are worth noting. First, the deficits in converting mesaxon membranes to compact myelin occur in the setting of remyelination and not during initial myelination. Second, the deficits occur in a proximal to distal gradient in the peripheral nervous system with ventral roots more severely affected than sciatic nerves. Third, the deficits are caused by mutations in the genes for PMP-22 (trembler mouse) (Suter et a ., 1992) and Quaking (Ebersole et a ., 1996 Hardy et a ., 1996), indicating that neither P0 nor MAG is directly affected. Fourth, while the defects that prevent mesaxon membrane conversion to compact myelin in Trembler J and Quaking differ, both appear to involve the failure to...


MTs can be disassembled by a variety of methods, including MT depolymerizing drugs (colchicine, colcemid, nocodazole), low temperature, and hypertonic shock. In one study, the MT depolymerizing drug colchicine was used to reversibly depolymerize myelinating Schwann cell MTs in rat sciatic nerve (Trapp et a ., 1995). Two distinct but overlapping functions for MTs during myelination were identified. As described in other cells (Lee et a ., 1989 Rogalski and Singer, 1984 Terasaki et a ., 1986), Schwann cell MT disassembly disrupted the organization of Golgi membranes, endoplasmic reticulum (ER) and intermediate filaments (Fig. 2.6). Although the organization of RER and Golgi membranes was disrupted, these organelles continued to synthesize P0, MAG and laminin. These proteins accumulated in the Schwann cell perinuclear cytoplasm (Fig. 2.7), indicating that MTs are essential for their transport to sites along the myelin internode. MTs, therefore, organize the distribution of the major...

Sacral Plexus

The plexus is located on the posterior wall of the pelvis. The five roots of the plexus divide into anterior and posterior divisions. The L4L S,S2 divisions form the common peroneal nerve. The L4L5S1S2S3 anterior divisions form the tibial nerve. Both these nerves fuse to form the sciatic nerve. Sciatic nerve L4L5S1S2S3 Sciatic nerve The common peroneal and tibial nerves (sciatic nerve) leave the pelvis by the greater sciatic foramen. In the popliteal fossa the sciatic nerve splits into its constituent nerves.

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