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Peripheral Nerve Injury

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6461. Intrathecal lidocaine reverses tactile allodynia caused by nerve injuries and potentiates the antiallodynic effect of the COX inhibitor ketorolac. (PubMed)

Intrathecal lidocaine reverses tactile allodynia caused by nerve injuries and potentiates the antiallodynic effect of the COX inhibitor ketorolac. Systemic lidocaine and other local anesthetics reduce hypersensitivity states induced by both acute inflammation and peripheral nerve injury in animals and produce analgesia in some patients with chronic pain. The mechanisms underlying the antiallodynic effect of systemic lidocaine are unclear, although most focus is on peripheral mechanisms. Central (...) mechanisms, particularly at the spinal dorsal horn level, are less known. In this study, the authors aimed to determine whether intrathecal lidocaine has an antiallodynic effect on established mechanical allodynia in two well-characterized neuropathic pain rat models: partial sciatic nerve ligation (PSNL) and spinal nerve ligation (SNL).Lidocaine (100-300 micro g) was intrathecally injected in PSNL and SNL rats. The withdrawal threshold of both hind paws in response to mechanical stimulation was measured

2003 Anesthesiology

6462. Painful nerve injury decreases resting cytosolic calcium concentrations in sensory neurons of rats. (PubMed)

Painful nerve injury decreases resting cytosolic calcium concentrations in sensory neurons of rats. Neuropathic pain is difficult to treat and poorly understood at the cellular level. Although cytoplasmic calcium ([Ca]c) critically regulates neuronal function, the effects of peripheral nerve injury on resting sensory neuronal [Ca]c are unknown.Resting [Ca]c was determined by microfluorometry in Fura-2 AM-loaded neurons dissociated from dorsal root ganglia of animals with hyperalgesia (...) the proportion of neurons sensitive to capsaicin in the L5 group but increased the proportion in the L4 group.Painful SNL nerve injury depresses resting [Ca]c in sensory neurons. This is most marked in axotomized neurons, especially the large and capsaicin-insensitive neurons presumed to transmit non-nociceptive sensory information.

2005 Anesthesiology

6463. Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. (PubMed)

Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. Neuropathic pain is inadequately treated and poorly understood at the cellular level. Because intracellular Ca signaling critically regulates diverse neuronal functions, the authors examined effects of peripheral nerve injury on the Ca transient that follows neuronal activation.Cytoplasmic Ca levels were recorded by digital microfluorometry from dissociated dorsal root ganglion neurons (...) of hyperalgesic animals after ligation of the fifth lumbar spinal nerve and control animals. Neurons were activated by field stimulation or by K depolarization.Transients in presumptively nociceptive, small, capsaicin-sensitive neurons were diminished after axotomy, whereas transient amplitude increased in axotomized nonnociceptive neurons. Axotomy diminished the upward shift in resting calcium after transient recovery. In contrast, nociceptive neurons adjacent to axotomy acquired increased duration

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2007 Anesthesiology

6464. Contribution of injured and uninjured dorsal root ganglion neurons to pain behavior and the changes in gene expression following chronic constriction injury of the sciatic nerve in rats. (PubMed)

Contribution of injured and uninjured dorsal root ganglion neurons to pain behavior and the changes in gene expression following chronic constriction injury of the sciatic nerve in rats. Neuropathic pain models, such as the chronic constriction injury (CCI) model, are partial nerve injury models where there exist both intact and injured peripheral axons. Recent studies suggested that dorsal root ganglion (DRG) neurons with intact axons also show the alteration of excitability and gene (...) neurons decreased in the ipsilateral DRG and GABA(A)-R- and ATF3-labeled neurons rarely overlapped. These changes in molecular phenotype in intact and injured primary afferents may be involved in the pathophysiological mechanisms of neuropathic pain produced by partial nerve injury.

2003 Pain

6465. Oral donepezil reduces hypersensitivity after nerve injury by a spinal muscarinic receptor mechanism. (PubMed)

Oral donepezil reduces hypersensitivity after nerve injury by a spinal muscarinic receptor mechanism. Cholinesterase inhibitors which reach the central nervous system produce pain relief but are poorly tolerated because of gastrointestinal side effects. Here, the authors tested whether donepezil, a central nervous system penetrant cholinesterase inhibitor with a low incidence of gastrointestinal side effects, would relieve hypersensitivity in an animal model of neuropathic pain.Male rats were (...) anesthetized, and the L5 and L6 spinal nerves were ligated unilaterally. Hypersensitivity was measured by withdrawal threshold to von Frey filament application to the hind paw after oral donepezil, and antagonists administered centrally and peripherally. Efficacy of chronic oral donepezil to relieve hypersensitivity was tested, and activation of G proteins by M(2) muscarinic receptors was determined by carbachol-stimulated [(35)S]guanosine triphosphate (gamma)S autoradiography in brain and spinal

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2007 Anesthesiology

6466. Tramadol and several anticonvulsants synergize in attenuating nerve injury-induced allodynia. (PubMed)

Tramadol and several anticonvulsants synergize in attenuating nerve injury-induced allodynia. Neuropathic pain results from injury or dysfunction of the central or peripheral nervous system. The treatment of neuropathic pain is challenging, in part because of its multiple etiologies. The present study explores combinations of the analgesic tramadol and each of four anticonvulsants in the treatment of surgically induced (ligation of the L5 spinal nerve) allodynia in rats. Each of the five drugs

2007 Pain

6467. GW406381, a novel COX-2 inhibitor, attenuates spontaneous ectopic discharge in sural nerves of rats following chronic constriction injury. (PubMed)

GW406381, a novel COX-2 inhibitor, attenuates spontaneous ectopic discharge in sural nerves of rats following chronic constriction injury. There are several lines of evidence to suggest that cyclooxygenase-2 (COX-2) plays an important role in the generation and maintenance of neuropathic pain states following peripheral nerve injury. However, COX-2 inhibitors are generally ineffective in reversing mechanical allodynia and hyperalgesia in models of neuropathic hypersensitivity. Here, we have (...) investigated the effects of GW406381, a novel COX-2 inhibitor, on mechanical allodynia, hyperalgesia and generation of spontaneous ectopic discharge in rats following chronic constriction injury (CCI) of the sciatic nerve and compared it with rofecoxib. GW406381 (5mg/kg, 5 days of treatment) significantly reversed the CCI-induced decrease in paw withdrawal thresholds (PWTs), assessed using both von Frey hair and paw pressure tests, whereas an equi-effective dose of rofecoxib (5mg/kg, 5 days of treatment

2007 Pain

6468. Age-dependent responses to nerve injury-induced mechanical allodynia. (PubMed)

Age-dependent responses to nerve injury-induced mechanical allodynia. Developmental differences in responses to acute and chronic nerve injury have received minimal attention. This study examines developmental differences in behavioral responses to a proximal (closer to the spinal cord) (L5 and L6 spinal nerve root ligation) or to a more distal (closer to peripheral innervation) (partial sciatic nerve ligation) nerve injury in rats paralleling the infant to young adult human.Withdrawal (...) < 0.05). In the 2-week-old animals, distal injury partial sciatic nerve ligation did not cause a reduction in withdrawal threshold from baseline. This was different from the spinal nerve root ligation group and the older animals in the partial sciatic nerve ligation group. However, when compared with age-matched control animals, both nerve injuries resulted in reduced withdrawal thresholds (P < 0.05). The resolution of hypersensitivity to mechanical stimulation, as measured by return of threshold

2006 Anesthesiology

6469. Nerve puncture and apparent intraneural injection during ultrasound-guided axillary block does not invariably result in neurologic injury. (PubMed)

Nerve puncture and apparent intraneural injection during ultrasound-guided axillary block does not invariably result in neurologic injury. Nerve puncture by the block needle and intraneural injection of local anesthetic are thought to be major risk factors leading to neurologic injury after peripheral nerve blocks. In this study, the author sought to determine the needle-nerve relation and location of the injectate during ultrasound-guided axillary plexus block.Using ultrasound-guided axillary (...) examined for any neurologic deficit.Twenty-two of 26 patients had nerve puncture of at least one nerve, and 21 of 26 patients had intraneural injection of at least one nerve. In the entire cohort, 72 of a total of 104 nerves had intraneural injection. Sensory and motor testing before and 6 months after the nerve injections were unchanged.Under the conditions of this study, puncturing of the peripheral nerves and apparent intraneural injection during axillary plexus block did not lead to a neurologic

2006 Anesthesiology

6470. Perioperative administration of the alpha2-adrenoceptor agonist clonidine at the site of nerve injury reduces the development of mechanical hypersensitivity and modulates local cytokine expression. (PubMed)

blocked by BRL44408. We conclude that peri-neural administration of clonidine at the site and time of injury reduces the degree of hypersensitivity in part by altering the balance of pro- and anti-inflammatory cytokines through activation of alpha2A-adrenoceptors. These results support testing of whether clonidine, as an adjuvant in continuous peripheral nerve blocks in settings of known major nerve injury, such as limb amputation, might prevent the development of chronic pain. (...) Perioperative administration of the alpha2-adrenoceptor agonist clonidine at the site of nerve injury reduces the development of mechanical hypersensitivity and modulates local cytokine expression. The development of chronic pain after surgery is not rare. Nerve injury from complete or partial nerve section during surgery leads to macrophage recruitment and release of pro-inflammatory cytokines, leading in turn to sensitization. Macrophages also express alpha2-adrenoceptors, and we previously

2003 Pain

6471. Upregulation of spinal cannabinoid-1-receptors following nerve injury enhances the effects of Win 55,212-2 on neuropathic pain behaviors in rats. (PubMed)

Upregulation of spinal cannabinoid-1-receptors following nerve injury enhances the effects of Win 55,212-2 on neuropathic pain behaviors in rats. Exogenous cannabinoids are effective in attenuating neuropathic pain behaviors induced by peripheral nerve injury, but the mechanisms of their effectiveness remain unclear. Here we examined the expression of spinal cannabinoid-1-receptors (CB1Rs) following chronic constriction sciatic nerve injury (CCI) and its relation to the effects of a CBR agonist (...) in a significant reduction of the effects of Win 55,212-2 in CCI rats. These results indicate that upregulation of spinal CB1Rs following peripheral nerve injury may contribute to the therapeutic effects of exogenous cannabinoids on neuropathic pain.

2003 Pain

6472. Assessment and analysis of mechanical allodynia-like behavior induced by spared nerve injury (SNI) in the mouse. (PubMed)

Assessment and analysis of mechanical allodynia-like behavior induced by spared nerve injury (SNI) in the mouse. Experimental models of peripheral nerve injury have been developed to study mechanisms of neuropathic pain. In the spared nerve injury (SNI) model in rats, the common peroneal and tibial nerves are injured, producing consistent and reproducible pain hypersensitivity in the territory of the spared sural nerve. In this study, we investigated whether SNI in mice is also a valid model (...) system for neuropathic pain. SNI results in a significant decrease in withdrawal threshold in SNI-operated mice. The effect is very consistent between animals and persists for the four weeks of the study. We also determined the relative frequency of paw withdrawal for each of a series of 11 von Frey hairs. Analysis of response frequency using a mixed-effects model that integrates all variables (nerve injury, paw, gender, and time) shows a very stable effect of SNI over time and also reveals subtle

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2006 Pain

6473. Modulation of P2X receptors via adrenergic pathways in rat dorsal root ganglion neurons after sciatic nerve injury. (PubMed)

to G(q) protein, perhaps dominantly alpha(1b) adrenergic receptors, in DRG neurons after sciatic nerve injury. This may account for a nociceptive pathway in response to noradrenergic sprouting after peripheral nerve injury. (...) Modulation of P2X receptors via adrenergic pathways in rat dorsal root ganglion neurons after sciatic nerve injury. The present study examined noradrenaline-induced modulation of ATP-evoked currents in dorsal root ganglion (DRG) neurons after sciatic nerve injury (transection). ATP (10 microM) generated fast/mixed type of whole-cell membrane currents, possibly as mediated via P2X(3)/P2X(3)-like receptors, and slow type of the currents, possibly as mediated via P2X(2/3) receptors, in acutely

2006 Pain

6474. Downregulation of spinal glutamate transporter EAAC1 following nerve injury is regulated by central glucocorticoid receptors in rats. (PubMed)

Downregulation of spinal glutamate transporter EAAC1 following nerve injury is regulated by central glucocorticoid receptors in rats. Previous studies have shown that glucocorticoid receptors (GR) were upregulated, whereas glutamate transporters were downregulated, within the spinal cord dorsal horn after peripheral nerve injury. However, the relationship between the expression of spinal GR and glutamate transporter after nerve injury remains unknown. In the present study, we examined (...) shown to regulate the expression of those cellular elements linked to inflammation and tissue injury and its activity can be negatively regulated by GR activation, these results suggest that spinal GR through NF-kappaB may play a significant role in the regulation of EAAC1 expression after peripheral nerve injury, a cellular pathway that may contribute to the development of neuropathic pain behaviors in rats.

2006 Pain

6475. Genetic impairment of interleukin-1 signaling attenuates neuropathic pain, autotomy, and spontaneous ectopic neuronal activity, following nerve injury in mice. (PubMed)

Genetic impairment of interleukin-1 signaling attenuates neuropathic pain, autotomy, and spontaneous ectopic neuronal activity, following nerve injury in mice. Peripheral nerve injury may lead to neuropathic pain, which is often associated with mechanical and thermal allodynia, ectopic discharge of from injured nerves and from the dorsal root ganglion neurons, and elevated levels of proinflammatory cytokines, particularly interleukin-1 (IL-1). In the present study, we tested the role of IL-1 (...) in neuropathic pain models using two mouse strains impaired in IL-1 signaling: Deletion of the IL-1 receptor type I (IL-1rKO) and transgenic over-expression of the IL-1 receptor antagonist (IL-1raTG). Neuropathy was induced by cutting the L5 spinal nerve on one side, following which mechanical and thermal pain sensitivity was measured. Wild-type (WT) mice and the parent strains developed significant allodynia and hyperalgesia in the hind-paw ipsilateral to the injury compared with the contralateral hind-paw

2006 Pain

6476. Assessment of sensibility after nerve injury and repair: a systematic review of evidence for validity, reliability and responsiveness of tests. (PubMed)

Assessment of sensibility after nerve injury and repair: a systematic review of evidence for validity, reliability and responsiveness of tests. Recovery of sensibility after peripheral nerve injury and repair needs to be assessed using psychometrically robust measures. In this study the literature was reviewed to identify what tests are available to quantify sensibility and to assess their validity, reliability and responsiveness. The databases Medline, CINAHL, Embase and AMED were searched (...) for studies reporting the psychometric properties of sensibility tests. While there is a plethora of tests and studies reporting the outcomes after peripheral nerve suture only a few of the tests have evidence of validity, reliability and responsiveness. Currently the touch threshold test using monofilaments such as the Weinstein Enhanced Sensory Test (WEST) or Semmes-Weinstein Monofilament Test (SWMT) and the shape-texture identification (STI) test for tactile gnosis are the only tests which meet

2005 Journal of hand surgery (Edinburgh, Scotland)

6477. Increase in inflammatory cytokines in median nerves in a rat model of repetitive motion injury (PubMed)

, increases in all 5 cytokines by week 5. This response was transient as all cytokines returned to control levels by 8 weeks of performance of a high repetition negligible force task. Cytokine sources included Schwann cells, fibroblasts and phagocytic macrophages (ED1-immunopositive). These findings suggest that cytokines are involved in the pathophysiology of repetitive motion injuries in peripheral nerves. (...) Increase in inflammatory cytokines in median nerves in a rat model of repetitive motion injury We examined cytokines in rat median nerves following performance of a high repetition reaching and grasping task at a rate of 8 reaches/min for up to 8 weeks. IL-1alpha, IL-1beta, TNF-alpha, IL-6 and IL-10 were analyzed by immunohistochemistry. Double-labeling immunohistochemistry for ED1, a marker of phagocytic macrophages, was also performed. We found increased immunoexpression of IL-6 by week 3

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2005 Journal of Neuroimmunology

6478. Ischemic preconditioning prevents skeletal muscle tissue injury, but not nerve lesion upon tourniquet-induced ischemia. (PubMed)

the peripheral nerve suffers from prolonged ischemia time and mechanical deterioration on IPC.In anesthetized rats, hind limb ischemia was induced by tourniquet for 3 hours followed by 24 hours of reperfusion. In an additional series of experiments, IPC (three cycles of 10 minutes I/10 minutes R) preceded hind limb ischemia. Sham-operated animals without ischemia served as controls. Skeletal muscle tissue injury was assessed with respect to microcirculation, inflammatory cell response, and cell integrity (...) susceptibility of the peripheral nerve to compression-induced ischemic injury disproves IPC in its clinical application for surgical procedures requiring prolonged tourniquet ischemia.

2007 Journal of Trauma

6479. Measuring the strength of the intrinsic muscles of the hand in patients with ulnar and median nerve injuries: reliability of the Rotterdam Intrinsic Hand Myometer (RIHM). (PubMed)

Measuring the strength of the intrinsic muscles of the hand in patients with ulnar and median nerve injuries: reliability of the Rotterdam Intrinsic Hand Myometer (RIHM). To determine the reliability and measurement error of measurements of intrinsic muscle strength of a new hand-held dynamometer (the Rotterdam Intrinsic Hand Myometer [RIHM]).With the RIHM we obtained repeated measurements of the intrinsic muscle strength of the hand in 27 patients with peripheral nerve injury of the ulnar (...) and/or median nerve in different stages of rehabilitation. The average time period after injury was 4.4 years (range, 99 days-11 years).Differences between 2 measurements greater than 6.3 N were interpreted as a real change in assessing the strength of the abduction of the little and index finger; for the median innervated muscles of the thumb this value was 16 N.In patients with nerve injuries the muscle strength is usually assessed with manual muscle strength testing and grip- and pinch-strength

2004 Journal of Hand Surgery - American

6480. Radial nerve injuries associated with humeral fractures. (PubMed)

Radial nerve injuries associated with humeral fractures. A radial nerve injury associated with a humeral shaft fracture is an important injury pattern among trauma patients. It is the most common peripheral nerve injury associated with this fracture. Although treatment for this injury pattern is a controversial subject among upper-extremity surgeons, certain principles of management need to be applied in all cases. As our understanding of the pathoanatomy of the humerus and surrounding

2006 Journal of Hand Surgery - American

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