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PubMed1992

Conditioning effect induced by chronic nerve compression. An experimental study of the sciatic and tibial nerves of rats.

To find out if chronic nerve compression could affect the peripheral nerve by acting as a "conditioning lesion", silicone tubes (internal diameter 0.8-1.6 mm) were placed round the sciatic or tibial nerves of adult rats for different time periods. After the period of compression the tubes were removed and a test crush lesion was made on the sciatic nerve in the thigh. Regeneration distances of the sensory nerve fibres were analysed by the pinch reflex test after a further three or six days. Compression of sciatic or tibial nerves induced a significant increase in outgrowth length compared with nerves subjected to mobilisation and crush lesion alone. All the tubes tested had a conditioning effect, but only tubes with a small internal diameter seemed to induce nerve fibre degeneration as assessed by immunocytochemistry. The results showed that chronic compression induced a regenerative response in the peripheral nerve. The mechanism by which this was accomplished remains obscure but it may involve both the neurons and the non-neuronal cells.

Animals↗
PubMed1993

Acute nerve compression at low pressures has a conditioning lesion effect on rat sciatic nerves.

Effects of acute compression for 2 hours around the sciatic nerve trunk at 30 or 80 mmHg on the regeneration potential in rat sciatic nerves were studied. Sham compression or mobilization was performed contralaterally. A week later a crush injury was inflicted proximal to the compressed segment. After another 3 or 6 days the length of axonal outgrowth was measured, using the pinch test technique. We found that compression at either level caused an increased length of axonal outgrowth compared to the mobilized or sham-compressed nerves. The results show that an acute compression at low pressures does have a conditioning lesion effect on peripheral nerves.

Animals↗
PubMed2004

Pathophysiology of peripheral nerve injury: a brief review.

Clinicians caring for patients with brachial plexus and other nerve injuries must possess a clear understanding of the peripheral nervous system's response to trauma. In this article, the authors briefly review peripheral nerve injury (PNI) types, discuss the common injury classification schemes, and describe the dynamic processes of degeneration and reinnervation that characterize the PNI response.

Axons↗
PubMed1992

Nerve transfer in brachial plexus traction injuries.

Brachial plexus palsy due to traction injury, especially spinal nerve-root avulsion, represents a severe handicap for the patient. Despite recent progress in diagnosis and microsurgical repair, the prognosis in such cases remains unfavorable. Nerve transfer is the only possibility for repair in cases of spinal nerve-root avulsion. This technique was analyzed in 37 patients with 64 reinnervation procedures of the musculocutaneous and/or axillary nerve using upper intercostal, spinal accessory, and regional nerves as donors. The most favorable results, with an 83.8% overall rate of useful functional recovery, were obtained in patients with upper brachial plexus palsy in which regional donor nerves, such as the medial pectoral, thoracodorsal, long thoracic, and subscapular nerves, had been used. The overall rates of recovery for the spinal accessory and upper intercostal nerves were 64.3% and 55.5%, respectively, which are significantly lower. The authors evaluate the results of nerve transfer and analyze different donor nerves as factors influencing the prognosis of surgical repair.

Accessory Nerve↗
PubMed1995

Lower number and thinner myelin of large myelinated fibers in human cervical compression radiculopathy.

The authors conducted a morphometric investigation of the histopathological alterations in myelinated fibers (MFs) of the nerve roots of C-6, which showed macroscopic indentation, presumably due to cervical spondylotic radiculopathy. In six cadavers, designated as the radiculopathy group, in which the nerve roots of C-6 showed indentation due to compression on one side (indented side) and the remaining nerve roots (normal side) showed a normal appearance macroscopically, morphometric findings of the nerve roots and the MFs on both the indented and normal sides were evaluated and subjected to blind comparison. Seven cadavers with normal-appearing C-6 nerve roots served as controls. In the control group, there were no differences in the morphometric parameters: that is, total transverse fascicular area, total number of small and large MFs, and relationship between myelin thickness and the radius of the axon between the right and left sides in either the ventral or dorsal roots. There was no evidence found of axonal degeneration, ongoing demyelination, or loss of MFs in either the ventral or dorsal roots in the radiculopathy group on the indented side. However, there were significantly lower numbers of large MFs per root and significantly thinner myelin sheaths relative to axon size on the indented side compared with those on the normal side in both the ventral and dorsal roots. These findings are characteristic alterations of the MFs produced by chronic low-grade compression.

Aged↗
PubMed2002

Mechanism of trigeminal neuralgia: an ultrastructural analysis of trigeminal root specimens obtained during microvascular decompression surgery.

OBJECT: Recent progress in the understanding of abnormal electrical behavior in injured sensory neurons motivated an examination, at the ultrastructural level, of trigeminal roots of patients with trigeminal neuralgia (TN). METHODS: In 12 patients biopsy specimens of trigeminal root were obtained during surgery for microvascular decompression. Pathological changes in tissue included axonopathy and axonal loss, demyelination, a range of less severe myelin abnormalities (dysmyelination), residual myelin debris, and the presence of excess collagen, including condensed collagen masses in two cases. Within zones of demyelination, groups of axons were often closely apposed without an intervening glial process. Pathological characteristics of nerve fibers were clearly graded with the degrees of root compression noted at operation. Pain also occurred, however, in some patients who did not appear to have a severe compressive injury. CONCLUSIONS: Findings were consistent with the ignition hypothesis of TN. This model can be used to explain the major positive and negative symptoms of TN by axonopathy-induced changes in the electrical excitability of afferent axons in the trigeminal root and of neuronal somata in the trigeminal ganglion. The key pathophysiological changes include ectopic impulse discharge, spontaneous and triggered afterdischarge, and crossexcitation among neighboring afferents.

Adult↗
PubMed2002

Temporal pattern of cochlear nerve degeneration following compression injury: a quantitative experimental observation.

OBJECT: It has been empirically recognized that the cochlear nerve is highly vulnerable to traumatic stress resulting from surgical procedures; therefore, careful manipulation of the cochlear nerve is mandatory in preventing trauma-induced hearing loss during cerebellopontine angle (CPA) surgery. There is, however, no precise knowledge about the temporal pattern of cochlear nerve degeneration following trauma. This study was performed to determine the temporal pattern of injury that occurs after cochlear nerve trauma, knowledge of which is indispensable not only to neurosurgeons but also to all those who manage lesions involving the cochlear nerve. METHODS: Right suboccipital craniectomies were performed in groups of rats with the aid of a surgical microscope, and the seventh and eighth cranial nerve trunks were identified at the internal auditory meatus. The cochlear nerve was quantifiably compressed while compound action potentials of the cochlear nerve were monitored and recorded. Following injury, one group of rats was killed for histological examination at the end of each week for 4 weeks. Data from this study disclosed that the degeneration of the compressed cochlear nerve progressed in a relatively rapid manner and was complete within 1 week after the insult. The main pathophysiological mechanisms responsible for cochlear neuronal death in this experimental setting appeared to be necrosis, and an apoptotic mechanism seemed to play a subsidiary role. CONCLUSIONS: Accurate knowledge about the temporal profile of trauma-induced cochlear nerve degeneration is closely linked with the problem of the therapeutic time window. The results of the present study indicated that any measures to ameliorate cochlear nerve degeneration following trauma should be started as early as possible (within 1 week) after an injury.

Animals↗
PubMed2006

Surgical treatment and outcomes in 15 patients with anterior interosseous nerve entrapments and injuries.

OBJECT: The authors present data obtained in 15 surgically treated patients with anterior interosseous nerve (AIN) entrapments and injuries. METHODS: Fifteen patients with AIN entrapments and injuries underwent surgery between 1967 and 1997 at Louisiana State University Health Sciences Center (LSUHSC) or Stanford University Medical Center. Patient charts were reviewed retrospectively. The LSUHSC grading system was used to evaluate the function of muscles supplied by the AIN. Nontraumatic injuries included seven AIN compressions by bone or soft tissue. Traumatic injury mechanisms consisted of stretch or contusion (six patients), injection (one patient), and burn scar (one patient). Presentations included weakness in the flexor digitorum profundus (FDP) muscle to the index finger, FDP muscle to the middle finger, pronator quadratus muscle, and flexion of the distal phalanx of the thumb. Preoperative evaluations included electromyography and nerve conduction studies as well as elbow and forearm plain radiographs. On surgery, lesions in continuity involved seven compressions, four stretch or contusion injuries, and one injection injury, all of which demonstrated nerve action potentials (NAPs) and were treated with neurolysis. Among the seven compression and four stretch or contusion injury cases, six and three patients, respectively, had LSUHSC Grade 3 or better functional recoveries postoperatively. Two stretch or contusion injuries involved lesions in continuity but demonstrated negative NAPs at surgery. Thus, each was treated using a graft repair after resection of a neuroma. There was one burn scar injury, which was treated via an end-to-end suture anastomosis, leading to a functional recovery better than Grade 3. CONCLUSIONS: Fifteen AIN entrapments or injuries responded favorably to nerve release and/or repair.

Action Potentials↗
PubMed2006

Surgical treatment and outcomes in 45 cases of posterior interosseous nerve entrapments and injuries.

OBJECT: The authors report data in 45 surgically treated posterior interosseous nerve (PIN) entrapments or injuries. METHODS: Forty-five PIN entrapments or injuries were managed surgically between 1967 and 2004 at Louisiana State University Health Sciences Center (LSUHSC) or Stanford University Medical Center. Patient charts were reviewed retrospectively. The LSUHSC grading system was used to assess PIN-innervated muscle function. Injuries were caused by nontraumatic (21 PIN entrapments and four tumors) and traumatic (nine lacerations, eight fractures, and three contusions) mechanisms. Presentations included weakness in the extensor carpi ulnaris muscle, causing compromised wrist extension and radial drift; extensor digitorum, indicis, and digiti minimi muscles with paretic finger extension; extensor pollicis brevis and longus muscles with weak thumb extension; and abductor pollicis longus muscle with rare decreased thumb abduction due to substitutions of the median nerve-innervated abductor pollicis brevis muscle and, at 90 degrees, the extensor pollicis brevis and longus muscles. Preoperative evaluations consisted of electromyography and nerve conduction studies, elbow and forearm plain x-ray films, and magnetic resonance imaging for tumor detection. At surgery, in continuity lesions were found in 21 entrapments and three fracture-related and three contusion injuries; all transmitted nerve action potentials (NAPs) and were treated with neurolysis. Five fracture-related PIN injuries, one of which was a lacerating injury, were in continuity and transmitted no NAPs; graft repairs were performed in all of these cases. Among nine lacerations, three PINs appeared in continuity, although intraoperative NAPs were absent. Two of these nerves were treated with secondary end-to-end suture anastomosis repair and one with secondary graft repair. There were six transected lacerations: three were treated with primary suture anastomosis repair, two with secondary suture anastomosis, and one with graft repair. Four tumors involving the PIN were resected. Most muscles innervated by 45 PINs had LSUHSC Grade 3 or better functional outcomes. CONCLUSIONS: Forty-five PIN entrapments or injuries responded well to PIN release and/or repair.

Action Potentials↗
PubMed2003

[Effect of Yiqi Huayu Recipe on regeneration process after L5 nerve root compression in rats].

OBJECTIVE: To study the effect of Yiqi Huayu Recipe on neurons in neuromuscular junction after L5 nerve root compression in rats. METHODS: By using immunohistochemistry, confocal laser scanning techniques and protein gene product 9.5 as a neuronal marker, the motor endplates were visualized with fluorescein-conjugated alpha-BTX. The effect of Yiqi Huayu Recipe on nerve terminals of neuromuscular junction at 10, 20, 30, 60 days after L5 nerve root compression was observed in rat soleus muscles during regeneration. The overlap areas of terminals and endplates were measured with NIH image technique. RESULTS: As for the aggregates, sprouts, extension of nerve terminal during regeneration, the connecting speed and range of nerve terminal with endplates, as well as the reformation of neuromuscular junctions during regeneration, Yiqi Huayu Recipe group was better than that of the control group. CONCLUSION: Yiqi Huayu Recipe can promote the hyperplasia of neurons and enhance the regeneration function. It also can accelerate the neuromuscular junction reformation and shorten the process of regeneration.

Animals↗
PubMed2006

[Effects of Yiqi Huayu Recipe on neural cell adhesion molecule in rats with lumbar nerve root compression].

OBJECTIVE: To study the effects of Yiqi Huayu Recipe on neural cell adhesion molecule (N-CAM) in neuromuscular junctions during nerve regeneration in rats with lumbar nerve root compression. METHODS: The rats with lumbar nerve root compression were given Yiqi Huayu Recipe for 10, 20 and 30 days respectively. The distribution of N-CAM in neuromuscular junctions of soleus muscle in rats was examined with immunohistochemical method and confocal laser scanning microscopy technique. The acetylcholine receptor (AChR) was visualized with fluorescein-conjugated alpha-bungarotoxin (alpha-BTX). The overlap areas of N-CAM and AChR sites were measured with NIH image technique. RESULTS: The aggregates, sprouts and extensions of N-CAM in the neuromuscular junctions and the overlap areas of N-CAM and AChR sites in the Yiqi Huayu Recipe-treated group were all better improved than those in the untreated group. CONCLUSION: The expression of N-CAM is regulated according to the state of innervation for muscles. Yiqi Huayu Recipe may accelerate this nerve regeneration process.

Animals↗
PubMed1994

Corticosteroid Injections: Their Use and Abuse.

Local injections of corticosteroids are commonly used in orthopaedic practice on the assumption that they will diminish the pain of inflammation and accelerate healing. Less often considered is the possibility that their use may delay the normal repair response. Among the multitude of conditions treated with corticosteroids are acute athletic injuries, overuse syndromes, nerve compression, bone cysts, and osteoarthritis. Unfortunately, there is a paucity of well-controlled studies that provide definitive recommendations for nonrheumatologic use of corticosteroids. Also troubling are the significant potential complications that can occur with their use. The authors believe that use of corticosteroids should be limited to the few conditions that have been proved to be positively influenced by them. Their use must be accompanied by a well-orchestrated treatment plan including close follow-up, physical therapy, and limitation of activities.

Journal Article↗
PubMedDate not supplied

A modified technique for Morton's neuroma. Decompression with relocation.

Interdigital nerve decompression with relocation was performed on 82 feet in 78 patients. The primary indication for surgery was chronic neuritic symptoms that did not resolve with conservative treatment. All but four patients (95%) achieved complete resolution of preoperative symptoms within an average of 7 days following surgery, with full sensation restored at an average of 5 weeks. All of the patients could tolerate a shoe with a wide toe box within 8 days postoperatively. Interdigital nerve decompression with relocation provides for rapid resolution of neuritic symptoms and early return to normal activities. It is also a relatively easy surgical technique. As such, nerve decompression with relocation should be the procedure of choice for the treatment of Morton's neuroma or interdigital nerve compression syndrome.

Adult↗
PubMed1998

[Effect of crushing of sciatic nerve on neuron of lumbar spinal cord].

In order to investigate the effect of nerve compression on neurons, the commonly used model of chronic nerve compression was produced in 48 SD rats. The rats were sacrificed in 1, 2, 3, 4, 5 and 6 months after compression, respectively. The number of neuron and ultrashruchure of alpha-motor neurons and ganglion cells of the corresponding spinal segment were examined. The results showed as following: After the sciatic nerve were crushed, the number of neuron and ultrastructure of alpha-motor neurons and ganglion cells might undergo ultrastructural changes, and even the death might occur. These changes might be aggravated as the time of crushing was prolonged and the compression force was increased. It was concluded that for nerve compression, decompression should be done as early as possible in order to avoid or minimize the ultructural changes of the neuron.

Animals↗
PubMedDate not supplied

Sensory potential can be preserved in severe common peroneal neuropathy.

Neuropathy of Common Peroneal Nerve (CPN) is a frequent clinical condition, generally caused by compression at the fibula head. Three neurophysiological patterns were described: 1) segmental demyelination with conduction block; 2) axonal damage with loss of motor units and sensory potential; 3) a mixed pattern. We report 5 patients with foot drop in whom CPN neuropathy was identified. In 3 in spite of impressive abnormalities in various motor branches and fascicles of the nerve, the peroneus nerve sensory potential remained well preserved. Focal neuropathies can be remarkably selective in terms of motor and sensory deficits, the reason can rely on a different location of the fibres or be related to a distinct histological-biochemical constitution. A preserved SPSP should not exclude a CPN neuropathy.

Action Potentials↗
PubMed2000

Molecular mechanisms of tumor-bone interactions in osteolytic metastases.

In patients with advanced disease, several cancer types frequently metastasize to the skeleton, where they cause bone destruction. Osteolytic metastases are incurable and cause pain, hypercalcemia, fracture, and nerve compression syndromes. It was proposed over a century ago that certain cancers, such as that of the breast, preferentially metastasize to the favorable microenvironment provided by bone. Bone matrix is a rich store of immobilized growth factors that are released during bone resorption. Histological analysis of osteolytic bone metastases indicates that the bone destruction is mediated by the osteoclast rather than directly by the tumor cells. These observations suggest a vicious cycle driving the formation of osteolytic metastases: tumor cells secrete factors stimulating osteoclasts through adjacent bone marrow stromal cells; osteoclastic resorption in turn releases growth factors from the bone matrix; finally, locally released growth factors activate the tumor cells. This vicious cycle model has now been confirmed at the molecular level. In particular, transforming growth factor beta (TGF3beta) is abundant in bone matrix and released as a consequence of osteoclastic bone resorption. Bone-derived TGFbeta plays an integral role in promoting the development and progression of osteolytic bone metastases by inducing tumor production of parathyroid hormone-related protein (PTHrP), a known stimulator of osteoclastic bone resorption. In breast cancer cells TGFbeta appears to stimulate PTHrP secretion by a posttranscriptional mechanism through both Smad and p38 mitogen activated protein (MAP) kinase signaling pathways. Osteolytic metastases can be suppressed in vivo by inhibition of bone resorption, blockade of TGFbeta signaling in tumor cells, and by neutralization of PTHrP. Other factors released from bone matrix may also act on tumor cells in bone, which in turn may produce other factors that stimulate bone resorption, following the vicious cycle paradigm established for TGFbeta and PTHrP. An understanding at the molecular level of the mechanisms of osteolytic metastasis will result in more effective therapies for this devastating complication of cancer.

Bone Neoplasms↗