(1/234) Ropivacaine or 2% mepivacaine for lower limb peripheral nerve blocks. Study Group on Orthopedic Anesthesia of the Italian Society of Anesthesia, Analgesia, and Intensive Care.

BACKGROUND: Intra- and postoperative clinical properties of sciatic-femoral nerve block performed with either ropivacaine at different concentrations or mepivacaine have been evaluated in a multicenter, randomized, blinded study. METHODS: Adult patients scheduled for foot and ankle surgery were randomized to receive combined sciatic-femoral nerve block with 225 mg of either 0.5% (n = 83), 0.75% (n = 87), or 1% (n = 86) ropivacaine, or with 500 mg of 2% mepivacaine (n = 84). A thigh tourniquet was used in all patients. Onset time, adequacy of surgical anesthesia, time to offset of nerve block, and time until first postoperative requirement for pain medication were evaluated by a blinded observer. RESULTS: The adequacy of nerve block was similar in the four treatment groups (the ratios between adequate:inadequate: failed blocks were 74:9:0 with 0.5% ropivacaine, 74:13:0 with 0.75% ropivacaine, 78:8:0 with 1% ropivacaine, and 72:12:0 with 2% mepivacaine). The onset of the block was slower with 0.5% ropivacaine than with other anesthetic solutions (P < 0.001). Regardless of the concentration, ropivacaine produced a longer motor blockade (10.5+/-3.8 h, 10.3+/-4.3 h, and 10.2+/-5.1 h with 0.5%, 0.75%, and 1% ropivacaine, respectively) than with mepivacaine (4.3+/-2.6 h; P < 0.001). The duration of postoperative analgesia was shorter after mepivacaine (5.1+/-2.7 h) than after ropivacaine (12.2+/-4.1 h, 14.3+/-5 h, and 14.5+/-3.4 h, with 0.5%, 0.75%, or 1% ropivacaine, respectively; P < 0.001). Pain relief after 0.5% ropivacaine was 14% shorter than 0.75% or 1% ropivacaine (P < 0.05). During the first 24 h after surgery, 30-37% of patients receiving ropivacaine required no analgesics compared with 10% of those receiving mepivacaine (P < 0.001). CONCLUSIONS: This study suggests that 0.75% ropivacaine is the most suitable choice of local anesthetic for combined sciatic-femoral nerve block, providing an onset similar to mepivacaine and prolonged postoperative analgesia.  (+info)

(2/234) Motor neuropathy in porphobilinogen deaminase-deficient mice imitates the peripheral neuropathy of human acute porphyria.

Acute porphyrias are inherited disorders caused by partial deficiency of specific heme biosynthesis enzymes. Clinically, porphyrias are manifested by a neuropsychiatric syndrome that includes peripheral neuropathy. Although much is known about the porphyrias' enzyme defects and their biochemical consequences, the cause of the neurological manifestations remains unresolved. We have studied porphyric neuropathy in mice with a partial deficiency of porphobilinogen deaminase (PBGD). PBGD-deficient mice (PBGD-/-) imitate acute porphyria through massive induction of hepatic delta-aminolevulinic acid synthase by drugs such as phenobarbital. Here we show that PBGD-/- mice develop impairment of motor coordination and muscle weakness. Histologically femoral nerves of PBGD-/- mice exhibit a marked decrease in large-caliber (>8 microm) axons and ultrastructural changes consistent with primary motor axon degeneration, secondary Schwann cell reactions, and axonal regeneration. These findings resemble those found in studies of affected nerves of patients with acute porphyria and thus provide strong evidence that PBGD deficiency causes degeneration of motor axons without signs of primary demyelination, thereby resolving a long-standing controversy. Interestingly, the neuropathy in PBGD-/- mice developed chronically and progressively and in the presence of normal or only slightly (twofold) increased plasma and urinary levels of the putative neurotoxic heme precursor delta-aminolevulinic acid. These data suggest that heme deficiency and consequent dysfunction of hemeproteins can cause porphyric neuropathy.  (+info)

(3/234) Loss of distal axons and sensory Merkel cells and features indicative of muscle denervation in hindlimbs of P0-deficient mice.

Mice lacking the major Schwann cell myelin component P0 show a severe dysmyelination with pathological features reminiscent of the Dejerine-Sottas syndrome in humans. Previous morphological and electrophysiological studies on these mice did not only demonstrate a compromised myelination and myelin maintenance, but were suggestive of an impairment of axons as well. Here, we studied the axonal pathology in P0-deficient mice by quantitative electron microscopy. In addition, we investigated epidermal receptor end organs by immunocytochemistry and muscle pathology by histochemistry. In proximal sections of facial and femoral nerves, axon calibers were significantly reduced, whereas the number of myelin-competent axons was not diminished in 5- and 17-month-old P0-deficient mice. However, in distal branches of the femoral and sciatic nerve (digital nerves innervating the skin of the first toe) the numbers of myelin-competent axons were reduced by 70% in 6-month-old P0-deficient mice. Immunolabeling of foot pads revealed a corresponding loss of Merkel cells by 75%, suggesting that survival of these cells is dependent on the presence or maintenance of their innervating myelinated axons. In addition, quadriceps and gastrocnemius muscles showed pathological features indicative of denervation and axonal sprouting. These findings demonstrate that loss of an important myelin component can initiate degenerative mechanisms not only in the Schwann cell but also in the distal portions of myelinated axons, leading to the degeneration of specialized receptor end organs and impairment of muscle innervation.  (+info)

(4/234) Changes in transmission in the pathway of heteronymous spinal recurrent inhibition from soleus to quadriceps motor neurons during movement in man.

H reflexes were induced in the human quadriceps muscle by electrical stimulation of the femoral nerve. The reflexes were conditioned by prior stimulation of the inferior soleus nerve. The conditioning stimulus produced an inhibition of long duration (>20 ms). The threshold of this inhibition was at zero soleus motor discharge and the inhibition scaled with soleus motor discharge. It was concluded that the inhibition was a heteronymous recurrent inhibition of quadriceps motor neurons mediated by Renshaw cells which had been activated by soleus motor neuron discharge. This recurrent inhibition declined during voluntary tonic contraction of the quadriceps, falling to zero at around one-third of maximum voluntary contraction. Antagonist contraction and weak co-contraction of the quadriceps and its antagonists did not lead to any significant change in recurrent inhibition. It is concluded that motor commands descending from the brain reduce heteronymous recurrent inhibition during isolated quadriceps muscle contraction, but to a much lesser extent during co-contraction. No evidence was obtained for any descending facilitation of heteronymous recurrent inhibition.  (+info)

(5/234) Mechanoreceptors in collateral knee ligaments: an animal experiment.

The mechanoreceptors in the collateral ligaments of the knee joint in rat hindlimbs were studied. In group II (n=10) the femoral and obturator nerves were sectioned. In both groups III and V (n=20) the sciatic nerve was sectioned. In group V (n=10) the sectioned sciatic nerve was sutured 4 weeks after sectioning. In group IV (n=10) all three nerves were sectioned. Group I (n=10) served as control. After 4 months all animals were killed. The ligaments of the knee joint were preserved and stained with gold chloride, paraffin-embedded and cut in sagittal serial sections. The results showed that 4 months after partial or total denervation of the limb, there was necrosis and a decrease in the number of mechanoreceptors, which was dependent upon the severity and site of the lesion. After suture of the sciatic nerve the increase in mechanoreceptors suggested a regenerative process.  (+info)

(6/234) Overexpression of nerve growth factor in skin selectively affects the survival and functional properties of nociceptors.

Mice that overexpress nerve growth factor (NGF-OE) in the skin have double the normal number of cutaneous sensory neurons, have increased innervation of the skin and spinal cord, and are hyperalgesic. Here, we have asked whether the increased cutaneous NGF level results in a selective survival of only certain functional types of neurons and whether it changes the properties of cutaneous neurons. Using electron microscopy, we show that the number of both myelinated and unmyelinated nociceptors increases substantially in NGF-OE mice by a factor of 3.3 and 1.5, respectively. Using extracellular recordings from single units, we demonstrate that large myelinated (Abeta) fibers are unchanged in prevalence and receptive properties. In contrast, among thin myelinated (Adelta) fibers, the percentage of nociceptors increased from a normal 65 to 97%, consistent with a selective survival of nociceptors during embryogenesis. These afferents showed a twofold increase in their mechanical responsiveness, but their heat responsiveness remained normal. Among unmyelinated (C) fibers, there was a profound increase in the percentage of heat responsive neurons from a normal 42 to 96%. This change cannot be accounted for by a selective survival of heat-sensitive neurons. Unmyelinated nociceptors increased fourfold in their thermal responsiveness but decreased in mechanical responsiveness. Therefore, target-derived NGF selectively rescues nociceptors during the period of programmed cell death with different efficacy for thin myelinated or unmyelinated fibers. NGF also affects the response to noxious heat or mechanical stimuli in each group differently, implying specific regulations of transduction processes rather than general changes of excitability.  (+info)

(7/234) A search for the factors responsible for absence of recovery of the normal vascular response to oxytocin following sympathetic nerve injury.

In dogs following crush injury to the lumbar sympathetic trunk, reflex vasoconstriction reappears in 4-6 months but the normal vasodilator response to oxytocin does not return even 12 months after crush. Histochemical examination of the walls of the blood vessels shows that division or crush of the lumbar sympathetic trunk or removal of terminal ganglia leads to decentralization, not denervation of the blood vessels. True denervation follows division or crush of the sciatic and femoral nerves. Following recovery from sciatic or femoral crush the pattern of peripheral innervation appears histochemically normal. However, there is no return of the normal vasodilator response to oxytocin. It is concluded that a normal response to oxytocin does not return even after long-term recovery from sympathetic injury, nor does its effect depend on a normal pattern of peripheral adrenergic innervation, but on an unknown more central activity of the sympathetic nervous system.  (+info)

(8/234) Nerve palsy after leg lengthening in total replacement arthroplasty for developmental dysplasia of the hip.

We reviewed 508 consecutive total hip replacements in 370 patients with old developmental dysplasia of the hip, to relate the amount of leg lengthening to the incidence of nerve palsies after operation. There were eight nerve palsies (two femoral, six sciatic), two complete and six incomplete. We found no statistical correlation between the amount of lengthening and the incidence of nerve damage (p = 0.47), but in seven of the eight hips, the surgeon had rated the intervention as difficult because of previous surgery, severe deformity, a defect of the acetabular roof, or considerable flexion deformity. The correlation between difficulty and nerve palsy was significant (p = 0.041). We conclude that nerve injury is most commonly caused by direct or indirect mechanical trauma and not by limb lengthening on its own.  (+info)