[Study of malignant neoplasms of the peripheral spinal nerves; sarcoma of the sciatic nerve].
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We have shown that diabetes-induced reduction in endoneurial blood flow (EBF) and impaired endothelium-dependent vascular relaxation precede slowing of motor nerve conduction velocity (MNCV) and decreased sciatic nerve Na(+)/K(+) ATPase activity. Furthermore, vascular dysfunction was accompanied by an accumulation of superoxide in arterioles that provide circulation to the sciatic nerve. In the present study, we examined the effect that treatment of streptozotocin-induced diabetic rats with antioxidants has on vascular and neural function. Diabetic rats were treated with 0.5% alpha-lipoic acid as a diet supplement or with hydroxyethyl starch deferoxamine (HES-DFO) by weekly intravenous injections at a dose of 75 mg/kg. The treatments significantly improved diabetes-induced decrease in EBF, acetylcholine-mediated vascular relaxation in arterioles that provide circulation to the region of the sciatic nerve, and MNCV. The treatments also reduced the production of superoxide by the aorta and superoxide and peroxynitrite by arterioles that provide circulation to the region of the sciatic nerve. Treating diabetic rats with alpha-lipoic acid prevented the diabetes-induced increase in thiobarbituric acid-reactive substances in serum and significantly improved lens glutathione levels. In contrast, treating diabetic rats with HES-DFO did not prevent diabetes-induced changes of either of these markers of oxidative stress. Diabetes-induced increase in sciatic nerve conjugated diene levels was not improved by treatment with either alpha-lipoic acid or HES-DFO. Treating diabetic rats with alpha-lipoic acid but not HES-DFO partially improved sciatic nerve Na(+)/K(+) ATPase activity and myo-inositol content. The increase in sciatic nerve sorbitol levels in diabetic rats was unchanged by either treatment. These studies suggest that diabetes-induced oxidative stress and the generation of superoxide may be partially responsible for the development of diabetic vascular and neural complications.
Regeneration of the sciatic nerve was studied in rats pretreated in a pulsed electromagnetic field (PEMF). The rats were exposed between a pair of Helmholtz coils at a pulse repetition rate of 2 pps at a field density of 60 or 300 microT. The PEMF treatment was then discontinued. After an interval of recovery, regeneration of the sciatic nerve was initiated by a crush lesion. Regeneration of sensory fibers was measured by the "pinch test" after an additional 3-6 days. A variety of PEMF pretreatments including 4 h/day for 1-4 days or exposure for 15 min/day during 2 days resulted in an increased regeneration distance, measured 3 days after the crush lesion. This effect could be demonstrated even after a 14-day recovery period. In contrast, pretreatment for 4 h/day for 2 days at 60 microT did not affect the regeneration distance. The results showed that PEMF pretreatment conditioned the rat sciatic nerve in a manner similar to that which occurs after a crush lesion, which indicates that PEMF affects the neuronal cell body. However, the mechanism of this effect remains obscure.
Transganglionic labelling of the saphenous nerve in rats with WGA-HRP revealed the central distribution of its terminals in the lumbar dorsal horn. The terminal field was clearly defined and consistent in rats aged between day 6 and day 90. If, however, the sciatic nerve was sectioned on day 1 of postnatal life, the saphenous terminal field expanded to occupy twice the normal area (measured between the L2 and L4 boundaries). The spread was caudal, medial, and lateral into areas normally occupied by sciatic nerve terminals. This sprouting was very weak if the sciatic nerve was sectioned later in postnatal life, on day 5, and nonexistent if sectioning took place on day 10. Crushing the sciatic nerve on day 1 also triggered the effect but the spread of the terminal field was less than that produced by section of the sciatic nerve. There was no evidence of sprouting from the contralateral intact sciatic nerve. The results demonstrate the necessity of intact afferent input during a critical period of neonatal life in order to maintain the precise somatotopic termination pattern of dorsal root afferents.
Schwannoma is a benign tumor generally observed on peripheral nerves. A sciatic localization is rare, observed in 1% of the patients. Multiple localizations have been reported in exceptional cases. We report the case of a bifocal schwannoma observed at the bifurcation of the sciatic nerve in a high-level athlete. The misleading clinical presentation of this localization causes a delay in diagnosis.
The amount of nerve growth factor (NGF) in the L5, L6, and cervical dorsal root ganglia of rats was examined from 1 to 30 days after a unilateral crush lesion of the sciatic nerve and adjacent branches of the lumbar plexus at the level of the sciatic notch. Unilateral nerve crush produced increases in NGF content of lumbar ganglia at 1, 4, and 7-8 days after injury, with increased NGF mRNA at 4 and 7-8 days. Increases in NGF at 1 and 4 days were most pronounced on the unlesioned side while increases at days 7 and 8 were most pronounced on the lesioned side. NGF content increased in cervical ganglia of nerve-lesioned animals at 3 and 7 days after injury and in lumbar and cervical ganglia of sham-operated animals 3-5 days after surgery, with no comparable changes in NGF mRNA. Elevations of ganglionic NGF coincide temporally with some of the alterations in metabolism and morphology which occur in dorsal root ganglion neurons after sciatic nerve crush. However, the bilateral nature of increases in NGF demonstrates that the factor(s) producing the response is not restricted to ganglia axotomized by the injury. The data suggest that ganglionic NGF may be regulated by systemic factors, produced during stress or trauma, as well as by factors from the denervated target tissue and/or regenerating axons.
UNLABELLED: The sciatic nerve (SN) originates from the L4-S3 roots in the form of two nerve trunks: the tibial nerve (TN) and the common peroneal nerve (CPN). The TN and CPN are encompassed by a single epineural sheath and eventually separate (divide) in the popliteal fossa. This division of the SN occurs at a variable level above the knee and may account for frequent failures reported with the popliteal block. We studied the level of division of the SN in the popliteal fossa and its relationship to the common epineural sheath of the SN. The level of division of the SN sheath into TN and CPN above the knee was measured in 28 cadaver leg specimens. The SN was invariably formed of independent trunks (TN and CPN) encompassed in one common epineural sheath. The SN divided at a mean distance of 60.5 +/- 27.0 mm (range 0 to 115 mm) above the popliteal fossa crease. We conclude that the TN and CPN leave the common SN sheath at variable distances from the popliteal crease. This finding and the relationship of the TN and CPN sheaths may have significant implications for popliteal block. IMPLICATIONS: When performing popliteal block, insertion of the needle at 100 mm above the popliteal crease is more likely to result in placement of the needle proximal to the division of the sciatic nerve than placement at 50 or 70 mm, according to the classical teaching.
Rat sciatic nerve was crushed at mid thigh level. 30 minutes up to 24 hours after the lesion, the nerve was excised, fixed, stained for acid phosphatase activity, and embedded in araldite. The nerve was cut lengthwise over a distance of 6 mm proximally and distally to the lesion and examined by electron microscopy. Not more than 30 minutes after damage fundamental changes were found to take place, with little difference between the proximal and the distal "stump". Changes affect the axon itself, the axolemma and the Schwann cell. In the axoplasm, structures not existent in normal axons became visible during the first hour. Acid phosphatase activity appeared in the endoplasmatic reticulum, vesicles and cisterns, along the axolemma, and in the Schwann cell. Enzyme filled vesicles were released from the Schwann cell into the axoplasm. Mitochondria were found in increasing numbers in the axoplasm next to the lesion, being mainly small and round in shape and prominent where various organelles and enzymes had accumulated. It is concluded that the axon itself is capable of enzyme activation and organelle production, and that there is a complex interaction between the Schwann cell and the axoplasm after nerve crush.
In rat sciatic nerves, the effect of Wallerian degeneration on the rate of transperineurial passage of sodium between the endoneurium and the epineurial extracellular space was investigated. In nerves transected and ligated at the sciatic notch, an in situ technique was used to measure the permeability coefficient-surface area product (PS) of the mid-thigh portion of the perineurium to 22Na. Sampling times ranged from one day to sixteen weeks after the lesion. Additionally, endoneurial water content (an indicator of nerve edema) was also measured in transected, degenerating nerves at the same sampling times. Endoneurial water content increased significantly by the fourth day after transection, peaked at four weeks, and then remained elevated through 16 weeks of post-lesion measurement. The PS of the perineurium to 22Na on the 4th day after transection was significantly greater than that of control animals. This increase then declined to normal levels through the 2nd week, and finally increased to values that were 3-fold to 4-fold of control values for the remainder of the observation period. The earlier, short lasting increase in perineurial PS is probably associated with the inflammatory response to nerve section, and proliferation of perineurial layers and cells. The later increase in perineurial permeability is proposed to play a role in the dissipation of endoneurial hydrostatic pressure and clearance of myelin debris from the endoneurium. In view of the complex changes in perineurial permeability described herein, it would seem inappropriate to consider these phenomena merely as passive breakdowns of the barrier properties of the perineurium.
The effects of levocarnitine acetyl were investigated on both peripheral nerve regeneration and neuromuscular remodelling in male Sprague-Dawley rats, three months of age, following crush of their left sciatic nerve. Levocarnitine acetyl, 150 mg/kg/day in drinking water, was given from one week before to 5, 15, 20, and 60 days after nerve crush. The sciatic nerve was examined morphologically at all given times and morphometrically at 15, 20, and 60 days after the lesion. Morphology, at 5, 15, and 60 days, and morphometry, at 60 days after the nerve crush, were also performed on the neuromuscular junction in the soleus and extensor digitorum longus muscles. Five days after nerve crush, complete axonal degeneration was observed in both control and treated rats. At 15 and 20 days, recovery from injury in treated animals was better than in controls, as shown by a significantly higher increase in the number of regenerating axons. At the same times, denervated endplates were present in both groups. At 60 days, axonal regeneration restored the number of axons to normal values in all injured animals, while their size maturation was greater in treated rats than in controls. A markedly lower number of degenerating elements was found in treated animals. In the neuromuscular junctions of the soleus and extensor digitorum longus muscles, nerve terminal branch points were reduced in the lesioned rats in comparison with uninjured ones. However, morphometric analysis revealed a greater endplate complexity in treated animals in which, at 60 days after nerve crush, nerve terminal branching and sprouting index values were significantly higher than in controls. It is concluded that levocarnitine acetyl exerts a beneficial effect on nerve regeneration processes and synaptic remodelling in crush-induced neuropathies.
Our aim was to objectively evaluate the efficacy of obturator nerve anesthesia after a parasacral block. Patients scheduled for knee surgery had a baseline adductor strength evaluation. After a parasacral block with 30 mL 0.75% ropivacaine, sensory deficit in the sciatic distribution (temperature discrimination) and adductor strength were assessed at 5-min intervals. Patients with an incomplete sensory block (defined as a temperature discrimination score of less than 2 in the 3 cutaneous distributions of the sciatic nerve tested) 30 min after the parasacral block were excluded from the study. Subsequently, a selective obturator block was performed with 7 mL 0.75% ropivacaine and adductor strength was reassessed at 5 min intervals for 15 min. Finally, a femoral block was performed using 10 mL 0.75% ropivacaine. Patient discomfort level during each block was assessed using a visual analog scale (VAS). Thirty-one patients completed the study. Five patients were excluded as a result of inadequate sensory block in the sciatic distribution 30 min after the parasacral block (success rate of 89%). Thirty min after the parasacral block, adductor strength decreased by 11.3% +/- 7% compared with baseline (85 +/- 24 versus 97 +/- 28 mm Hg, P = 0.002). Fifteen min after the obturator nerve block, adductor muscle strength decreased by an additional 69% +/- 7% (16.6 +/- 15 versus 85 +/- 24 mm Hg, P < 0.0001). VAS scores were similar for all blocks (26 +/- 19, 28 +/- 24, and 27 +/- 19 mm for parasacral, obturator, and femoral respectively). Four parasacral blocks were simulated in 2 fresh cadavers using 30 mL of colored latex solution. The spread of the die in relation to the obturator nerve was assessed. Injection of 30 mL colored latex into cadavers resulted in spread of the injectate restricted to the sacral plexus. These findings demonstrate the unreliability of parasacral block to achieve anesthesia of the obturator nerve. A selective obturator block should be considered in the clinical setting when this is desirable.
Regeneration of the sciatic nerve in transplanted nerve grafts in which laminin was inactivated was examined electron microscopically. Nerve grafts for transplantation were obtained from close cloned donor Wistar rats; 1-cm nerve segments of the sciatic nerve were frozen and thawed to kill the Schwann cells. Control recipient rats received grafts treated with normal rabbit serum to repair the artificially-made complete defect of the right sciatic nerve, and the experimental group of rats received grafts doubly treated with normal serum and rabbit anti-laminin antiserum. In the control grafts regenerating axons grew almost completely through the inside of the basal lamina scaffolds (92%) and adhered to the structure, while in the anti-laminin antiserum treated grafts the axons were present outside (52%) and inside (48%) the scaffolds simultaneously. In this case, the adhesion of axons to the scaffolds was obscure. Axons were associated with and without Schwann cells both inside and outside the basal lamina scaffolds. No unassociated Schwann cells were observed. The maximal number of axons in a 2 mm portion of the antiserum-treated grafts was approximately 250 axons per 100 x 100 microns square and 520 in the control at 15 days. At 30 days, almost the same number of axons was found at the distal (8 mm) portion of both groups. The growth in the former was delayed for 3 days. These results indicate that regenerating peripheral nerve axons may enter the basal lamina scaffolds and grow well because of the neurotrophic function of laminin present at the inner side of Schwann cell basal lamina.
The sciatic nerve was crushed in the right hindlimb in newborn (3-8 h old) rats. Two to four months later, electromyographic activity was recorded from both the control and reinnervated ankle extensor muscles soleus or lateral gastrocnemius and from the ankle flexor muscle tibialis anterior. Tonic postural activity was present in the extensor muscles on both sides during quiet stance. The control flexor muscles were usually silent in this situation, but the reinnervated flexors exhibited abnormal sustained activity. During locomotion, the control extensors were activated during the stance phase and their mean burst made up 61.5% of the step cycle. The control tibialis anterior muscle fired only during the swing phase, with the burst lasting 18.1% of the step cycle. In the reinnervated extensor muscles, the mean burst duration was decreased (46% of the cycle) but the basic locomotor pattern was not impaired. The reinnervated tibialis muscle, however, was activated abnormally, with one appropriate flexor burst during the swing phase and an "extensor-like" burst during the stance phase of the step. Reflex responses to stretch were weak or absent on the operated side. Histological examination showed that the reinnervated soleus and tibialis muscles were almost devoid of muscle spindles. The motor unit mean firing rates in the reinnervated soleus (22 imp/s) and lateral gastrocnemius (45 imp/s) matched those of the control muscles (25 and 42 imp/s, respectively). In contrast to the phasic, high-frequency firing (52-80 imp/s) in the control tibialis, the reinnervated tibialis motor units fired at significantly lower rates (22-56 imp/s).(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: To investigate the effect of pyrroloquinoline quinone (PQQ) on nerve regeneration of transected sciatic nerve in animal models. METHODS: Forty SD rats weighing 220-240 g were randomized into a PQQ group (n = 20) and a control group (n = 20). Each animal underwent sciatic nerve transection operation. After the operation, PQQ 0.5 ml (250 microg/Kg) was injected at the operation site in the PQQ group, while the same volume of normal saline was delivered in the control group. Nerve functional evaluation, electrophysiological index recording were carried out according to the experimental design. Newly generated nerve specimens were harvested 12 weeks postoperatively for morphological studies. RESULTS: In the PQQ group there was a good nerve regeneration and the sciatic nerve function, sciatic nerve function index, electrophysiological index and morphological appearance were superior to the control group (P < 0.05). CONCLUSIONS: PQQ has a remarkable effect in enhancing nerve regeneration of transected peripheral nerve.
After sciatic transection a strong decrease in immunoreactivity occurred, starting at 2 days. After 6, 10, 14, and 20 days survival only 5% of the sciatic motoneurons were strongly labeled for GluR2/3 against 80% in the control situation. From Day 20, GluR2/3 labeling started to increase again, reaching near normal levels at Day 80 after sciatic transection. In contrast, after sciatic crush, the decrease in GluR2/3 labeling in motoneurons was less pronounced and returned to normal in 30 days. In all animals, the GluR1 and GluR4 labeling of motoneurons remained unchanged after sciatic transection or crush. It is concluded that sciatic nerve injury leads to a strong, time-dependent decrease in the expression of GluR2 and 3 subunits in the corresponding motoneurons. As a consequence, AMPA receptors with a different subunit composition may be assembled, leading to a change in the functional properties of these receptors. Moreover, if they lack the GluR2 subunit, they may become calcium permeable.
Adult rat sciatic nerves were subjected to a crush lesion and allowed to survive during 2 weeks-11 months. Segments of regenerated nerve were removed from exsanguinated animals and subjected to physiological analysis and light microscopic examination of teased fibres. Application of the potassium channel blocking agent 4-aminopyridine (4-AP) to regenerated nerve segments had marked effects on action potential waveform and recovery properties. When applied to normal control nerves 4-AP had minimal effects. Examination of teased preparations from the same nerves revealed the presence of two classes of internodes along regenerated nerve fibres. A majority of conventional regenerated internodes exhibited lengths (L) of at least 150 microns. Maximal L reached about 350 microns after one month survival and 550 microns 10 months later. In the individual nerve the maximal L-values tended to increase with fibre size. Most convential regenerated internodes had L-values of 200-400 microns. In addition, scattered unusually short sheaths, with L-values of 10-150 microns, were found intercalated between conventional internodes. Some intercalated sheaths had a wrinkled irregular configuration and some lacked a light-microscopically distinct myelin layer. We suggest that the occurrence of unusually short and partly distorted sheaths along regenerated fibres reflects a nodal-internodal remodelling in response to longitudinal crowding. These sites might represent foci with aberrant functional properties, possibly accounting for the 4-AP sensitivity of regenerated nerve.
The rostrocaudal distribution of saphenous nerve inputs into the lumbar dorsal horn from L2 to L6 has been investigated in urethane anaesthetized rats whose left sciatic nerve was cut and ligated at birth. In normal cord, electrical stimulation of the saphenous nerve evoked dorsal horn spikes in L2 to caudal L4. Few or no spikes were evoked in L5. After neonatal sciatic nerve section, saphenous nerve stimulation evoked spikes throughout segments L2 to L6. Dorsal horn cell receptive fields were also altered following neonatal sciatic nerve section. A somatotopic map of the lumbar enlargement in normal rats was constructed from the receptive fields (RFs) of adjacent dorsal horn cells. Cells with RFs in the saphenous skin region were concentrated in L3 and rostral L4 and very few were found in L5. After neonatal sciatic nerve section, however, a substantial number of cells with low threshold saphenous skin RFs were also found in caudal L4 and throughout L5. These results show that the central saphenous nerve terminal sprouts that grow into the sciatic terminal region following neonatal sciatic nerve section (Fitzgerald, 1985, J. Comp. Neurol., 240, 414-422; Fitzgerald et al., 1990, J. Comp. Neurol., 300, 370-385) form functional connections. This results in dorsal horn cells that are not normally influenced by saphenous nerve inputs developing substantial low threshold RFs in saphenous nerve skin regions.
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