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At least 199 records · Page 11Linked to original sources
PubMed2000

Effective gene transfer into regenerating sciatic nerves by adenoviral vectors: potentials for gene therapy of peripheral nerve injury.

Replication defective adenoviral vectors have been demonstrated as an effective method for delivering genes into a variety of cell types and tissues both in vivo and in vitro. Transfecting genes into neuronal cells has proven to be difficult because of their lack of cell division. Since the major problem in neurological disease is the degeneration of the terminally differentiated neuronal cells, the adenoviral vector's ability to transfer genes into differentiated post-mitotic cells makes them advantageous for a gene delivery system for the nervous system. Here we showed that a replication defective recombinant adenovirus carrying the lacZ gene could infect the neuronal stem cells and even the differentiated neuronal cells derived from the central nervous system. The lacZ gene delivered into the neuronal cells was expressed efficiently. In addition, the recombinant virus also infected Schwann cells in intact and injured nerves in vivo. The expression of the lacZ gene lasted for 5 weeks, within which nerve regeneration is accomplished in the rat. Adenoviral vectors might thus be used to modulate Schwann cell gene expression for treating peripheral nerve injury or peripheral neuropathy.

Adenoviridae↗
PubMed2005

Behavioral and pharmacological characterization of a distal peripheral nerve injury in the rat.

Previous rat neuropathic pain models have utilized peripheral nerve injuries that damage a significant proportion of large nerves such as the sciatic nerve or its divisions. Injuries that lead to neuropathic pain in humans may involve the peripheral extremities. The current study evaluated the behavioral effects of injury to the plantar nerves in the rat (distal nerve injury-DNI). A delayed onset of hypersensitivity to an innocuous mechanical stimulus was observed following cutting of the left plantar nerves, whereas mechanical hypersensitivity developed more rapidly in rats with either an injury near the sciatic nerve trunk (chronic constriction injury (CCI), spared nerve injury (SNI)) or a spinal nerve root (spinal nerve ligation (SNL). Similar to other nerve injury pain models, rats with injured plantar nerves also developed an early onset and persistent sensitivity to a cooling stimulus. The effects of morphine, gabapentin and imipramine on mechanical and cold hypersensitivity were evaluated in rats with a DNI, CCI and SNI. In all three models, morphine dose-dependently suppressed mechanical and cold hypersensitivity, whereas gabapentin only suppressed mechanical hypersensitivity. Imipramine had no effect on either cold or mechanical hypersensitivity in any of the nerve-injured rats. The pharmacological data suggest that the underlying basis of neuropathic pain may be similar irrespective of the site of nerve injury.

Amines↗
PubMed1997

Loss of GABA-immunoreactivity in the spinal dorsal horn of rats with peripheral nerve injury and promotion of recovery by adrenal medullary grafts.

Abnormal pain-related behaviour that accompanies peripheral nerve injury may be the result of altered spinal neuronal function. The long-term loss of inhibitory function by GABA neurons in particular may be a mechanism by which abnormal neural hyperactivity occurs, leading to exaggerated sensory processing following nerve injury. In order to assess this, changes in spinal GABA immunoreactivity at several time points following constriction nerve injury were quantified in parallel with behavioural assessments of abnormal sensory responses to noxious and innocuous stimuli. In addition, the effects of spinal adrenal medullary transplants were determined since previous findings have demonstrated alleviation of behavioural pain symptoms by such transplants. In response to unilateral sciatic nerve injury, GABAergic profiles normally found in lumbar dorsal horn laminae I-III significantly decreased. The decrease was apparent three days following ligation, particularly on the side ipsilateral to the nerve injury. By two weeks, no GABAergic profiles could be seen, with the deficit appearing in the spinal dorsal horn both ipsilateral and contralateral to the unilateral peripheral nerve injury. Marked decreases in GABA-immunoreactive profiles persisted for at least up to five weeks post-injury, with partial restoration occurring by seven weeks. However, even at seven weeks, losses in GABA-immunoreactive profiles persisted in the dorsal horn ipsilateral to peripheral nerve injury. These findings were comparable in animals receiving control striated muscle transplants. In contrast, adrenal medullary transplants markedly reduced the loss in GABA-immunoreactive profiles at all time-points examined. In addition, GABA-immunoreactive profile levels were normalized near that of intact animals by five to seven weeks following nerve injury in animals with adrenal medullary transplants. Parallel improvements in sensory responses to innocuous and noxious stimuli were also observed in these animals. The results of this study indicate that peripheral nerve injury can result in severe losses in spinal inhibitory mechanisms, possibly leading to exaggerated sensory processes in persistent pain states. In addition, adrenal medullary transplants may provide a neuroprotective function in promoting recovery and improving long-term survival of GABAergic neurons in the spinal dorsal horn which have been damaged by excitotoxic injury.

Adrenal Medulla↗
PubMed2001

Gait analysis in rats with peripheral nerve injury.

Rats are commonly used to study peripheral nerve repair and grafting. The traditional footprint method to assess functional recovery is messy, indirect, and not useful when contractures develop in the animal model. The aim of the present study was to establish an accurate, reproducible, but simple, method to assess dynamic limb function. The basic quantitative aspects of a normal gait were characterized from 59 recorded walks in 23 rats. The video was digitized and analyzed frame by frame on a personal computer. Seven parameters of the gait were assessed: (1) walking speed; (2) stance phase, swing phase and right to left stance/swing ratio; (3) step length and step length ratio; (4) ankle angles at terminal stance and midswing; (5) tail height; (6) midline deviation; and (7) tail deviation. These gait parameters were then applied to groups of animals with sciatic (group S), tibial (group T), and peroneal (group P) nerve injuries. A discriminant analysis was performed to analyze each parameter and to compute a functional score. We found that the video gait analysis was superior to the footprint method and believe it will be very useful in future studies on peripheral nerve injury.

Animals↗
PubMed2000

Peripheral nerve injury from intravenous cannulation: a case report.

The following is a case report of a patient who had an intravenous (i.v.) catheter inserted into her cephalic vein and thereafter sustained an injury to the superficial branch of the radial nerve. When an i.v. catheter penetrates a nerve, it can cause temporary or permanent damage. After sustaining an injury, a nerve will regenerate in an attempt to reconnect with the fibers it once innervated. Recovery from nerve damage may take only weeks or a year or more. Some patients, however, may sustain lifelong damage depending on the severity of the needle stick to the nerve. To avoid injury to peripheral nerves when inserting i.v. catheters, a few recommendations should be followed. First, if inserting an i.v. catheter in the cephalic vein, be conscious of the proximity of the superficial peripheral nerves. Second, if a paresthesia is elicited when inserting an i.v. catheter, withdraw the catheter immediately. Third, if a patient complains of paresthesias or numbness near the i.v. site, remove the i.v. catheter immediately. Fourth, limit the amount of probing after inserting the catheter into the skin. Finally, if nerve damage is suspected from a peripheral i.v. cannulation, consult a hand specialist promptly.

Catheterization, Peripheral↗
PubMed2006

Delayed acetyl-L-carnitine administration and its effect on sensory neuronal rescue after peripheral nerve injury.

Protection of sensory neurons after peripheral nerve injury is clinically crucial since inadequate sensory recovery is seriously affected by the death of up to 40% of sensory neurons. Immediate acetyl-L-carnitine (ALCAR) treatment eliminates this cell loss, but may not always be clinically feasible, hence we studied the effect of delaying the initiation of ALCAR treatment. Five groups of rats (n=5 per group) underwent unilateral sciatic nerve axotomy. ALCAR treatment (50 mg/kg/day) was initiated immediately, or after delays of 6 h, 24 h or 7 days after injury. A sham-treated group served as control. L4 and L5 dorsal root ganglia were harvested bilaterally 2 weeks after injury and stereological sensory neuron counts were obtained. Immediate sham treatment provided no neuroprotection (25% loss). Cell loss was eliminated when ALCAR was commenced within<or=24 h of axotomy. No statistically significant neuroprotective effect (18% loss) was evident compared to sham when ALCAR administration was initiated 7 days post-axotomy. When commenced within a clinically applicable time frame ALCAR treatment remains highly neuroprotective, potentially improving clinical outcome following peripheral nerve trauma.

Acetylcarnitine↗
PubMed1987

Is it possible to predict the outcome of peripheral nerve injuries? A probability model based on prospects for regenerating neurites.

The long term functional consequences of peripheral nerve injuries are notoriously unpredictable. We hypothesized that considering the individual regrowth of the elementary components of a nerve (the neurites) rather than the global regeneration of the organ could lead to a better understanding of the mechanisms of nerve repair. Our basic assumptions were that regrowth was random and regrowth of any individual neurite could be defined in terms of its influence on recovery; this influence could be either valid, neutral or invalid. We designed a probability model describing the prospects of regrowth for nerves composed of several types of fibers. Our goal was to propose a general explanation of nerve healing rather than to predict the outcome in individual situations. The results suggested that this model satisfactorily described the events taking place in a healing nerve.

Animals↗
PubMed2004

Clinical application of axonal repair technique for treatment of peripheral nerve injury.

OBJECTIVE: To evaluate the efficacy of axonal repair technique for treatment of peripheral nerve injury clinically. METHODS: In 1998, the authors applied axonal repair technique to treat peripheral nerve injuries in 12 patients with 13 nerves. It consists of four steps, ie, stumps of the nerve being soaked in a modified Collins fluid, freezed, trimmed, and coapted with glue, making the injured nerve repaired at the axonal level. RESULTS: The patients were followed up for an average of 13 months. Results showed that in 4 cases of first-stage contralateral C7 transfer, regenerating axons reached to the sternoclavicular joint or axilla at 4 to 7 months, offering the timing for performing the second-stage contralateral C7 transfer. In 5 cases of accessory nerve transferred to the suprascapular nerve, the abduction of the shoulder was 40 degree on average. In the other 3 patients with four different nerves repaired, results were also satisfactory. CONCLUSIONS: This technique is promising in the treatment of peripheral nerve injury.

Adult↗
PubMed2003

The electrodiagnostic examination with peripheral nerve injuries.

The EDX examination can be of considerable use to the clinician in the evaluation of focal peripheral nerve injuries. It can confirm the presence ofsuch lesions and help determine their location, severity, and prognosis. The major reason why it is capable of doing so is because it discloses the pathophysiology of focal neuropathies, at least in regard to large myelinated nerve fiber damage.

Action Potentials↗
PubMed1996

Changes of Schwann cell antigenic profile after peripheral nerve injury.

Axons and Schwann cells (SC) in the peripheral nerve (PN) are in permanent interaction. Both myelin-forming SC (MSC) and nonmyelin-forming SC (NMSC) have a defined antigenic phenotype. Four weeks after PN transection, the proliferating SC in the distal stump lose some of their antigens, they start to display antigenic profile of NMSC and, in addition, to reexpress nerve growth factor receptor (NGF-rec) and growth associated protein (GAP-43), two antigens of their precursor cells. It can be assumed that migrating SC may differ in their antigenic profile in regard to resident proliferated SC in denervated distal nerve stump. We found that many SC specific antigens (S-100 protein, glial fibrilary acidic protein-GFAP, NGF-rec, GAP-43) are down-regulated in migrating SC as compared to SC proliferating in situ in the absence of axons.

Animals↗
PubMed1981

Rehabilitation of peripheral nerve injuries.

Rehabilitation of the patient with a peripheral nerve injury requires knowledge, understanding, and cooperation between the patient, the physician, and the therapist. Careful documentation of the patient's status prior to beginning rehabilitation and periodic follow-up assessments are of utmost importance. We have presented a detailed scheme for initial and follow-up evaluation. Prevention of unnecessary stiffness, swelling, and contractures is emphasized. Education of the patient to prevent the individual from doing further damage to the anesthetic area is important. Proper splinting techniques, from the postoperative splint and cast to splints that prevent deformities as well as overcome established contractures and improve function, will aid in the patient's recovery. Desensitization is an important aspect of sensory recovery, and sensory reeducation will aid in recovery of sensibility. Early tendon transfers are found to be particularly advantageous for high radial and median nerve palsies to gain functional recovery earlier and to allow the patient to become brace-free sooner.

Edema↗
PubMed1995

Changes in the spinal terminal pattern of the superficial radial nerve after a peripheral nerve injury. An anatomical study in cats.

The occurrence of changes within the spinal cord over a long period after a peripheral nerve injury was investigated in adult cats. The lateral superficial branch of the radial nerve was exposed and transsected unilaterally. In one group the nerve endings were re-approximated with epineural sutures and in the other group the proximal nerve stump was enclosed to prevent regeneration. After a survival period of 4-17 months the same nerve on both sides was exposed to an intra-axonal nerve tracer, lectin-conjugated horseradish peroxidase, to label the nerve terminals within the spinal gray matter by transganglionic transport. The general distribution of the terminal field was almost the same after suturing as after encapsulation of the transsected nerve, except for a slightly more cranial location of the terminal area after suturing compared with the control side. The terminal area comprised laminae I-IV of the fifth cervical to the first thoracic spinal segment, concentrated towards the sixth to eighth cervical segments. This distribution was the same as on the control side, but the experimental and control sides differed in intensity of terminals. There was a loss of terminals throughout the terminal field in both operated groups, but after nerve suture there was some recovery of terminal intensity between 4 and 17 months after the injury.

Animals↗
PubMed2004

Mitchell's influence on European studies of peripheral nerve injuries during World War I.

OBJECTIVE: Describe the influence of S. Weir Mitchell's (1829-1914) work, and in particular his ideas on causalgia, on European physicians who treated peripheral nerve injuries during World War I (WWI). BACKGROUND: During the American Civil War (1861-1865), Mitchell studied peripheral nerve injuries with colleagues George Read Morehouse and William Williams Keen. Three monographs resulted from this work. All were important landmarks in the evolution of knowledge of peripheral nerve injuries. A subsequent occasion to improve knowledge came in WWI. METHODS: The most important European monographs or series on peripheral nerve injuries from WWI were studied with special interest in references to causalgia and Mitchell's works on peripheral nerve injuries. We included works by Tinel, Athanassio-Benisty, Purves-Stewart & Evans and Carter, Foerster and Oppenheim. RESULTS: Tinel and Athanassio-Benisty provided the most detailed information on peripheral nerve injuries and causalgia and often referred to Mitchell. Both mentioned a possible sympathetic origin. Athanassio-Benisty described tremor and other movement disorders in relation to causalgia. Purves-Stewart and Evans mentioned Mitchell and causalgia in the second edition of their book. They advocated the term "thermalgia." Carter, who had access to data of many cases, concentrated his work on causalgia, referring to Mitchell. Foerster provided data of a great number of peripheral nerve injuries, but did not refer to Mitchell. However, he described the symptoms of causalgia cursorily, applying the term Reflexschmerz (reflexpain). Oppenheim was particularly interested in muscle innervation and referred to Mitchell with respect to hypertrichosis and glossy skin. Oppenheim did not use the term causalgia, although he described the syndrome in some of his patients. It wasn't until around 1920 that German physicians devoted significant attention to causalgia and began using the term. CONCLUSION: Knowledge of peripheral nerve injuries was greatly advanced during and after WWI. Mitchell's influence was mainly found in the French medical literature, where his findings provided the basis for further research on the origin of causalgia. In England, Mitchell and causalgia were also well-known. We found evidence to suggest that some of the English knowledge came from French physicians. German physicians described the symptoms of causalgia, but did not use the term, nor did they refer to Mitchell. This variation in Mitchell's influence by country probably reflects the fact that Mitchell's Injuries of nerves and their consequences was translated into French but not German.

Biomedical Research↗