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Peripheral nerve blocks can be used routinely in an outpatient setting. The innervation of the face and the technique we use to perform nerve blocks are reviewed. We present four cases of skin cancer and one of rhinophyma in which nerve blocks were used to minimize the discomfort associated with local anesthesia.
Peripheral nerve regeneration is dependent on the ability of regenerating neurites to migrate through cellular debris and altered extracellular matrix at the injury site, grow along the residual distal nerve sheath conduit, and reinnervate synaptic targets. In cell culture, growth cones of regenerating axons secrete proteases, specifically plasminogen activators (PAs), which are believed to facilitate growth cone movement by digesting extracellular matrices and cell adhesions. In this study, the PA system was shown to be specifically activated in sensory neurons after sciatic nerve crush in adult mice. The number of sensory neurons expressing urokinase PA receptor (uPAR) mRNA levels increased above sham levels by 8 hr after crush, whereas the number of sensory neurons expressing uPA and tissue PA (tPA) mRNAs was significantly increased by 3 d after crush. PA mRNA levels were also increased at the crush site, with uPA mRNA elevated by 8 hr after crush and tPA and uPAR mRNA levels markedly increased by 7 d. PA-dependent enzymatic activity was significantly increased from 1 to 7 d after crush in nerves that had been crushed compared with uncrushed nerves. Immunohistochemistry showed that tPA was localized within regenerating axons of the sciatic nerve. There were no significant changes in plasminogen activator inhibitor 1 activity between crush and sham after the injury. These results clearly demonstrated that after injury the PA system was rapidly induced in sensory neurons, where it may play an important role in nerve regeneration in vivo.
Inadequate peripheral nerve regeneration as a result of trauma contributes greatly to the morbidity of surgical patients. Animals admitted as an emergency often have concurrent orthopaedic injuries that impair mobility and may mask peripheral nerve dysfunction if a thorough neurological examination is not performed. This article reviews the pertinent anatomy of the peripheral nervous system as well as the degenerative and regenerative responses that occur in traumatized nerves. Physical examination and electrodiagnostic techniques that characterize the extent of nerve impairment are described. The management of peripheral nerve lacerations for open and closed wounds is detailed, as well as the presenting clinical signs and prognosis for brachial plexus avulsions, sciatic nerve damage, and sacrococcygeal injury.
(1) Capsaicin solution was applied for 15 min around a 1 cm length of sciatic nerve in the mid upper leg of adult rats. (2) Electron microscopic examinations of the nerve in the treated region after 14 days shows no signs of degeneration of either myelinated or unmyelinated fibres attributable to the capsaicin. (3) Fluoride resistant acid phosphatase FRAP disappears from the central terminals of the treated nerve by 7 days. (4) 1.5 mM capsaicin is sufficient to product a complete reduction of FRAP in the spinal cord. (5) The peptides substance P and cholecystokinin (CCK) are markedly depleted in the region of spinal cord terminations of the treated nerve at 14 days. (6) Substance P and CCk are not affected in spinal cord regions other than in the unmyelinated afferent terminal zone. Similarly neurotensin and neurophysin which are not present in afferent fibres are not influenced by capsaicin treatment of the sciatic. (7) It is concluded that there are chemical changes in the spinal cord terminals of fine afferents after local peripheral capsaicin.
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BACKGROUND: Inguinal herniorrhaphy (IH) is a common outpatient procedure, yet postoperative pain and anesthetic side effects remain a problem. Paravertebral somatic nerve blocks (PVB) have the potential to offer unilateral abdominal wall anesthesia and long-lasting pain relief with minimal side effects. We compared PVB with peripheral neural blocks for outpatient IH. METHODS: Forty-six patients scheduled for IH were entered into this prospective, single-blind study. All patients underwent a standardized general anesthetic. Patients were randomly assigned to receive a PVB (levels T10-L2) preoperatively (n = 24) or an intraoperative peripheral block (PB) by the surgeon (n = 22), using 0.5% ropivacaine (40 mL). Opioid use, verbal analog pain scores, and side effects were documented for 72 hours. RESULTS: The use of opioids during surgery was less for the PVB group 162 +/- 70 mg than the PB group, 210 +/- 60 (P =.02). Need for opioids in PACU was less for the PVB group (39%) than the PB group (61%) (P =.002). Time until first pain after discharge was not different between groups, 312 +/- 446 minutes (PB) and 425 +/- 384 minutes (PVB) (P =.12). Of the PVB patients, 29% used no opioids at all compared with 18% of PB patients (P =.12). Mean time until first oxycodone use was similar between groups, 303 +/- 469 minutes (PB) and 295 +/- 225 minutes (PVB) (P =.18). Oxycodone use was also similar; 35 +/- 34 mg (PVB) versus 49 +/- 42 mg (PB) (P =.30). More patients in the PB group (50%) required antiemetic treatment in the postanesthesia care unit than the PVB group (21%) (P <.001). Side effects were similar at all other measurements. CONCLUSIONS: This study shows that PVB provides analgesia equivalent to extensive peripheral nerve block for inguinal herniorrhaphy, offering an alternative method of postoperative pain management and perhaps fewer side effects.
The use of non-neural conduits to bridge gaps in peripheral nerves has been noted in the literature for many years. A logical extension of this concept is the introduction of neurotrophic or growth promoting factors into the lumen. We present here an injectable nerve guide that allows percutaneous access to the microenvironment of the regenerating peripheral nerve within the guide's lumen. Hyaluronic acid, a compound associated with decreased scarring and improved fibrin matrix formation, is added sequentially to the regenerating peripheral rat sciatic nerve via this injectable nerve guide. Assessment of nerve regeneration and reinnervation shows better conduction velocity, higher axon counts, and a trend toward earlier myelination with hyaluronic acid compared with saline. This work not only implies hyaluronic acid's role as an agent that aids nerve growth but also describes a new tool that allows percutaneous access to the milieu of a regenerating nerve.
Transected ganglion cell axons from the adult retina are capable of reinnervating their central targets by growing into transplanted peripheral nerve (PN) segments. Injury of the optic nerve causes various metabolic and morphological changes in the retinal ganglion cell (RGC) perikarya and in the dendrites. The present work examined the dendritic trees of those ganglion cells surviving axotomy and of those whose served axons re-elongated in PN grafts to reach either the superior colliculus (SC), transplanted SC, or transplanted autologous thigh muscle. The elaboration of the dendritic trees was visualized by means of the strongly fluorescent carbocyanine dye DiI, which is taken up by axons and transported to the cell bodies and from there to the dendritic branches. Alternatively, retinofugal axons regrowing through PN grafts were anterogradely filled from the eye cup with rhodamine B-isothiocyanate. The transection of the optic nerve resulted in characteristic changes in the ganglion cell dendrites, particularly in the degeneration of most of the terminal and preterminal dendritic branches. This occurred within the first 1 to 2 weeks following axotomy. The different types of ganglion cells appear to vary in their sensitivity to axotomy, as reflected by a rapid degeneration of certain cell dendrites after severance of the optic nerve. The most vulnerable cells were those with small perikarya and small dendritic fields (type II), whereas larger cells with larger dendritic fields (type I and III) were slower to respond and less dramatically affected. Regrowth of the lesioned axons in peripheral nerve grafts and reconnection of the retina with various tissues did not result in a significant immediate recovery of ganglion cell dendrites, although it did prevent some axotomized cells from further progression toward posttraumatic cell death.
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Following peripheral nerve transection, reorganizational plasticity has been reported to occur in two phases, one immediate and one more protracted. GABA (gamma-aminobutyric acid) has been implicated in the immediate "unmasking" phase of reorganization. We have used quantitative autoradiography to assess potential changes in GABA(A) and GABA(B) receptor binding in primate somatosensory cortex following peripheral nerve injury. Here we report reductions in GABA(A) receptor binding in layer IV of primate somatosensory cortex deprived of its normal activating inputs for 2-5 h by peripheral nerve transection.
Ischiatic, femoral and tibial nerves are commonly utilized in the studies of peripheral nerve surgery in rats. The authors present a new nerve-muscle unit model in which the nerve is distal enough to minimize morbidity and the muscle is convenient for all electromyographic studies. Twenty-five Wistar-Albino rats were used. In the control group; normal electromyography and histology were demonstrated in the lateral tibial nerve (LTN) and in the flexor digiti quinti brevis (FDQB) muscle. In experimental group I; a 0.5 cm nerve gap was made in the LT nerve and the proximal end was buried in the muscle in order to prevent reinnervation. In experimental group II, the LTN was cut and repaired primarily. In both groups I and II, electromyographic and histologic studies were performed at 6 and 12 weeks. In study group I, atrophic and degenerative findings were observed and in study group II, only regenerative findings were observed. The authors concluded that the LT nerve-FDQB muscle unit is a convenient model for peripheral nerve studies, with the advantages of easy dissection, wide exposure, and minimal morbidity. This model is also convenient for electromyographic and histologic evaluation.
Peripheral nerve (PN) isografts provide a favourable environment for axon regeneration after peripheral and central nervous system (CNS) injury, but definitive information on the extent of cellular intermixing between donor and host tissues is lacking. We wished to compare migration patterns in fresh and predegenerate PN grafts, and also compare the extent of cell migration after transplantation to peripheral nervous system (PNS) versus CNS. To discern how host and donor cells interact after PN transplantation, sciatic nerve segments were transplanted from inbred adult mice into PN defects (PN-PN grafts) or into lesioned cerebral cortex of opposite gender siblings. Migrating male cells were identified using a Y-chromosome-specific probe and in situ hybridization methods, and characterized immunohistochemically. The extent of donor and host cellular intermixing was similar in fresh and predegenerate PN-PN isografts. There was substantial intermixing of donor and host cells by 8 days. Many host cells migrating into epineurial regions of grafts were immunopositive for F4/80 (macrophages). The endoneurium of grafted PN was also colonized by host cells; some were F4/80+ but many were immunostained with S-100 (Schwann cell marker). Donor S-100+ Schwann cells rapidly migrated out into proximal and distal host PN and by 12 weeks were found at least 2 mm from the grafts. Endoneurial microvessels in grafts were mostly donor-derived. By comparison, in male PN grafts to female CNS, even after 6 weeks few donor cells had migrated out into surrounding host cortex, despite the observation that almost all grafts contained regenerating axons and were thus attached to host CNS tissue.
Peripheral nerves are susceptible to develop multiple changes in their morphology and biochemical composition as consequences of diabetes mellitus. This review focuses on diabetes-induced alterations of the extracellular matrix of the peripheral nerves, and on the potential molecular mechanisms causing these changes. The interest towards the extracellular matrix of peripheral nerves of diabetic patients is highlighted by the fact that the extracellular matrix does not only mechanically support the cells which it surrounds, but it also regulates their behavior through specific interactions mediated via molecules on the cell surface, such as integrin receptors and cell surface proteoglycans. Thus, changes in the structure and composition of the extracellular matrix may alter cellular functions in multiple ways. At the ultrastructural level, these changes include e.g. thickening of vascular, perineurial and Schwann cell associated basement membranes; accumulation of microfibrillar material in the vicinity of perineurial cells; and increased diameter of endoneurial collagen fibrils. At the molecular level, the changes may be associated with altered metabolism of various collagen types, such as type I, III, IV and VI collagens.
Peripheral nerve injury secondary to injection of therapeutic agents is well-documented. Until recently, the precise mechanism of injury has been obscure; even today, the treatment of these nerve injection injuries remains controversial. The aim of this study was to determine the involvement of ischemia-reperfusion injury in the development of peripheral nerve injection injury. Wistar rats were randomized into three groups. Sciatic nerve was used as the standardized nerve injection injury model. Two commonly used agents, lidocaine HCl 1 percent and phenol 5 percent, were tested for their comparative effects on the sciatic nerve. Lidocaine and phenol were injected into the sciatic nerves of the rats in Groups 1 and 2, respectively. Physiologic saline was used in the controls (Group 3). All the agents were injected intrafascicularly. The effects of nerve injection injury were assessed by measuring thiobarbituric acid reactive substance (TBARS) levels and obtaining walking-track analyses (WTA). Nerve injection caused significant increases in TBARS levels, which were correlated with the severity of the injury. The TBARS levels were related to the severity of injury caused by the tested agents; TBARS levels in phenol-injected nerves were significantly higher than those of lidocaine-injected nerves. Patterns of alterations in TBARS levels also paralleled the changes in print-length factor. Injection of lidocaine and phenol resulted in near-normal walking tracks at 8 and 12 weeks, respectively, while saline injection caused only transient impairment in walking tracks. These findings indicate that reactive oxygen species are involved in the pathogenesis of experimental peripheral nerve injection injury. Indices of free oxygen radical damage correlate with the progression of functional alterations after nerve injection injury.
This is a relatively specialised technique aimed more at enhancing the skills of doctors regularly performing local anaesthetic blocks. It is a useful device for confirming the location of major nerves and plexuses proximally, but not necessary for most peripheral nerve blocks.
To determine whether the blood-nerve barrier of the rat peripheral nerve transports manganese(II) (Mn) by a saturable mechanism similar to that found at the blood-brain barrier, we measured the uptake of 54Mn from blood into desheathed sciatic nerve and into cerebral cortex of awake rats at different plasma concentrations of unlabeled Mn using an intravenous infusion technique. The unidirectional influx (Jin) of Mn into sciatic nerve was facilitated and saturable, when steady-state plasma Mn ranged from 4 to 4,312 ng/ml (0.073-78.4 microM), as was the unidirectional influx of Mn into the cerebral cortex. Michaelis-Menten constants (Km and Vmax) and the passive diffusion constant (Kd), determined by nonlinear least squares, were as follows: for the blood-nerve barrier (sciatic nerve) Km = 4.7 microM, Vmax = 0.56 x 10(-3) nmol.s-1.g wet wt-1, and Kd = 6.3 x 10(-6) ml.s-1.g wet wt-1; for the blood-brain barrier (cerebral cortex) Km = 1.0 microM, Vmax = 0.40 x 10(-3) nmol.s-1.g wet wt-1, and Kd = 0.3 x 10(-6) ml.s-1.g wet wt-1. The results demonstrate facilitated concentration-dependent mechanisms of transport of Mn at the blood-nerve and blood-brain barriers.
This article describes recent, significant scientific advances leading to the development of the bioartificial nerve graft. Schwann cells, which play an active role in the repair and function of peripheral nerves, are used to seed a synthetic, often resorbable conduit, which is then used to bridge and repair nerve gaps caused by injury or disease. By enhancing the rate and extent of regeneration, the bioartificial nerve graft holds great promise for improving recovery in the peripheral (and central) nervous system.