PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Injections, Spinal”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed1996

The opioid ketobemidone has a NMDA blocking effect.

There are clinical observations that neurogenic pain can respond well to the opioid ketobemidone, in contrast to pethidine and morphine. This has led us to the hypothesis that the analgesic effect of ketobemidone in neurogenic pain may be due to both opioid as well as additional non-opioid effects. The present study was therefore made to evaluate the effects of ketobemidone. The study consists of two parts. (1) Single unit recordings were made from dorsal horn neurones in the halothane-anaesthetised rat. Neurones were activated by transcutaneous electrical stimulation of their receptive fields at C-fibre strength and their responses quantified. The wind-up of the neurones, due to N-methyl-D-aspartate (NMDA) receptor activation, leading to marked increases in C-fibre responses and an associated post-discharge was also measured. Ketobemidone, applied to the spinal cord, equivalent to an intrathecal injection, dose-dependently and selectively reduced C-fibre evoked responses. Ketobemidone was also found to block wind-up more effectively than morphine at equieffective doses, but unlike morphine in a non-naloxone-reversible manner. (2) In a binding study ketobemidone was shown to inhibit [3H]MK-801 binding with a Ki value of 26 microM. Therefore, ketobemidone appears to possess both mu opioid agonist as well as NMDA blocking effects.

Analgesics, Opioid↗
PubMed1999

Intrathecal galanin alleviates allodynia-like behaviour in rats after partial peripheral nerve injury.

We have previously suggested that the neuropeptides galanin and galanin message-associated peptide (GMAP) may have an inhibitory role in spinal nociception. The present study examined the effects of intrathecal (i.t.) administration of these two peptides on allodynia-like behaviours in response to mechanical and cold stimulation in rats after photochemically induced ischaemic peripheral nerve injury. I.t. galanin significantly alleviated the mechanical- and cold-allodynia-like behaviours in nerve injured rats, and was not associated with motor impairment or sedation. I.t. GMAP relieved mechanical allodynia much less than galanin. I.t. M-35, a high-affinity galanin receptor antagonist, did not significantly alter the response of the rats to mechanical or cold stimulation. At 1 or 2 weeks postinjury, around 15% of dorsal root ganglion (DRG) neuron profiles showed galanin-like immunoreactivity. These profiles were mostly small sized. Although the number of galanin positive cells was thus increased in the DRG in the present model, the increase was substantially less than after complete sciatic nerve section, as previously shown. The present results showed that spinal administration of galanin inhibited some abnormal pain-like behaviours in rats after partial peripheral nerve injury. These results further support an inhibitory function for galanin in nociception. However, endogenous galanin may not play a significant role in suppressing nociceptive input after partial ischaemic peripheral nerve injury, as the upregulation of galanin is moderate.

Animals↗
PubMed2003

Could ultrasonography be used by an anaesthetist to identify a specified lumbar interspace before spinal anaesthesia?

BACKGROUND: Insertion of a needle into the lumbar subarachnoid space may cause damage to the spinal cord. Current techniques to identify a safe interspace have limitations. Ultrasound was investigated as a means to improve anatomical accuracy. METHODS: Seventeen patients attending for elective magnetic resonance imaging (MRI) of the spine were studied. Ultrasonic identification of the L3-4 interspace was attempted by an anaesthetist and a marker was placed. A radiologist identified the anatomical location of the marker on the MRI scan. RESULTS: Thirteen out of 17 markers were at the L3-4 interspace; four were at the L2-3 interspace. CONCLUSIONS: These results suggest that ultrasonography may be a useful adjunct to safe subarachnoid anaesthesia.

Adult↗
PubMed2007

Glial phosphorylated p38 MAP kinase mediates pain in a rat model of lumbar disc herniation and induces motor dysfunction in a rat model of lumbar spinal canal stenosis.

STUDY DESIGN: Immunohistochemical and behavioral study using rat models of lumbar disc herniation and cauda equina syndrome. OBJECTIVE: To investigate the expression of activated p38 mitogen-activated protein kinases (p38 MAP kinase; p38) in the spinal cord and to determine the effect of intrathecal administration of a specific p38 inhibitor on pain in a lumbar disc herniation model and on motor function and hypoalgesia in a spinal canal stenosis (SCS) model. SUMMARY OF BACKGROUND DATA: In pathologic lumbar disc herniation-induced neuropathic pain and compression of cauda equina-induced motor dysfunction and hypoalgesia caused by SCS, glia are activated and produce certain cytokines, including tumor necrosis factor-alpha (TNF-alpha) and interleukins, which play a crucial role in the pathogenesis of nerve degeneration. p38 is phosphorylated by these cytokines, suggesting that it may play an important role in pain transmission and nerve degeneration. Here we have examined the role of p38 in rat models of lumbar disc herniation and SCS. METHODS: Six-week-old male Sprague-Dawley rats were used. For the disc herniation model, autologous nucleus pulposus was applied to L5 nerve roots, which were then crushed. For the SCS model, a piece of silicon was placed under the lamina of the fourth lumbar vertebra. We assessed mechanical allodynia, hypoalgesia, and motor function using von Frey hairs, treadmill tests, and immunohistochemical localization of phosphorylated p38 (P-p38) in the cauda equina, dorsal root ganglion (DRG), and spinal cord, which were also double-stained with NeuN (neuronal marker), GFAP (astrocyte/Schwann cell marker), or isolectin B4 (IB4; microglia marker). We also examined the effects of intrathecal administration of a specific p38 inhibitor, FR167653, on nucleus pulposus-induced pain, hypoalgesia, and motor dysfunction following SCS. RESULTS: We demonstrated that activated P-p38-immunoreactive cells in the spinal cord and cauda equina were not observed before nerve injury but appeared in the cauda equina, DRG, and spinal dorsal horn in the disc herniation and SCS models. Double-labeling revealed that most P-p38-immunoreactive cells were isolectin B4-labeled microglia and GFAP-immunoreactive Schwann cells. Intrathecal administration of the p38 inhibitor FR167653 decreased mechanical allodynia in the disc herniation model and improved hypoalgesia and intermittent motor dysfunction in the SCS model. CONCLUSIONS: Our findings suggest that activated p38 may play an important role in the involvement of microglia in the pathophysiology of pain following lumbar disc herniation and mechanical hypoalgesia, and motor nerve dysfunction of cauda equina following SCS.

Animals↗
PubMed1985

Serum concentrations and urinary excretion of lidocaine and its two desethylated metabolites after spinal anaesthesia using lidocaine or lidocaine with phenylephrine.

In 13 patients undergoing transurethral prostatic resection under spinal anaesthesia with heavy lidocaine or with heavy lidocaine plus phenylephrine hydrochloride, the serum concentrations of lidocaine, monoethylglycinexylidide and glycinexylidide and their renal excretion were measured with a HPLC method. Seven patients were given lidocaine alone 1.25 mg/kg and six lidocaine 1.25 mg/kg mixed with phenylephrine hydrochloride 3 mg. There was no significant difference between the two groups either in the serum levels of lidocaine or in the renal excretion rate of lidocaine and its metabolites. This finding gives support to the opinion that phenylephrine in low doses has no prolonging effect on spinal anaesthesia performed with heavy lidocaine.

Aged↗
PubMed2004

Inhibition of N-type voltage-activated calcium channels in rat dorsal root ganglion neurons by P2Y receptors is a possible mechanism of ADP-induced analgesia.

Patch-clamp recordings from small-diameter rat dorsal root ganglion (DRG) neurons maintained in culture demonstrated preferential inhibition by ATP of high-voltage-activated, but not low-voltage-activated, Ca2+ currents (I(Ca)). The rank order of agonist potency was UTP > ADP > ATP. ATP depressed the omega-conotoxin GVIA-sensitive N-type current only. Pyridoxal-5-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) and 2'-deoxy-N6-methyladenosine 3',5'-bisphosphate tetraammonium, two P2Y1 receptor antagonists, almost abolished the ATP-induced inhibition. Both patch-clamp recordings and immunocytochemistry coupled with confocal laser microscopy indicated a colocalization of functional P2X3 and P2Y1 receptors on the same DRG neurons. Because the effect of ATP was inhibited by intracellular guanosine 5'-O-(2-thiodiphosphate) or by applying a strongly depolarizing prepulse, P2Y1 receptors appear to block I(Ca) by a pathway involving the betagamma subunit of a G(q/11) protein. Less efficient buffering of the intracellular Ca2+ concentration ([Ca2+]i) by reducing the intrapipette EGTA failed to interfere with the ATP effect. Fura-2 microfluorimetry suggested that ATP raised [Ca2+]i by a Galpha-mediated release from intracellular pools and simultaneously depressed the high external potassium concentration-induced increase of [Ca2+]i by inhibiting I(Ca) via Gbetagamma. Adenosine 5'-O-(2-thiodiphosphate) inhibited dorsal root-evoked polysynaptic population EPSPs in the hemisected rat spinal cord and prolonged the nociceptive threshold on intrathecal application in the tail-flick assay. These effects were not antagonized by PPADS. Hence, P2Y receptor activation by ADP, which is generated by enzymatic degradation of ATP, may decrease the release of glutamate from DRG terminals in the spinal cord and thereby partly counterbalance the algogenic effect of ATP.

Adenosine Diphosphate↗
PubMed2001

Two-tiered inhibition of axon regeneration at the dorsal root entry zone.

Glial-derived inhibitory molecules and a weak cell-body response prevent sensory axon regeneration into the spinal cord after dorsal root injury. Neurotrophic factors, particularly neurotrophin-3 (NT-3), may increase the regenerative capacity of sensory neurons after dorsal rhizotomy, allowing regeneration across the dorsal root entry zone (DREZ). Intrathecal NT-3, delivered at the time of injury, promoted an upregulation of the growth-associated protein GAP-43 primarily in large-diameter sensory profiles (which did not occur after rhizotomy alone), as well as regeneration of cholera toxin B-labeled sensory axons across the DREZ and deep into the dorsal horn. However, delaying treatment for 1 week compromised regeneration: although axons still penetrated the DREZ, growth within white matter was qualitatively and quantitatively restricted. This was not associated with an impaired cell-body response (GAP-43 upregulation was equivalent for both immediate and delayed treatments), or with astrogliosis at the DREZ, which begins almost immediately after rhizotomy, but with the delayed appearance of mature ED1-expressing phagocytes in the dorsal white matter between 1 and 2 weeks after lesion, marking the beginning of myelin breakdown. After rhizotomy with immediate NT-3 treatment, regeneration continues beyond 2 weeks, but in the dorsal gray matter rather than in the degenerating dorsal columns. The ability of NT-3 to promote regeneration across the DREZ, but not after the beginning of degeneration after delayed treatment reveals a hierarchy of inhibitory influences: the astrogliotic, but not the degenerative barrier is surmountable by NT-3 treatment.

Animals↗
PubMed2001

Leukemia inhibitory factor determines the growth status of injured adult sensory neurons.

Conditioning injury to adult mammalian sensory neurons enhances their regeneration potential. Here we show that leukemia inhibitory factor (LIF) is a fundamental component of the conditioning response. Conditioning injury in vivo significantly increases the intrinsic growth capacity of sensory neurons in vitro from LIF+/+ mice. This conditioning effect is significantly blunted in sensory neurons from LIF-/- mice. Enhanced growth is rescued in vitro in LIF-/- mice by the addition of exogenous LIF, and the effect blocked by human LIF-05, an LIF receptor antagonist. Furthermore, we demonstrate that LIF promotes elongating but not arborizing neurite outgrowth in vitro and is required for normal regeneration of injured adult sensory neurons in vivo. LIF is also functionally protective to peptidergic sensory neurons after nerve damage in vivo. Our results indicate that the alteration in intrinsic growth status of injured sensory neurons depends, at least in part, on LIF.

Animals↗
PubMed2001

[Low dose intrathecal morphine and postoperative pain relief in elderly patients].

Patient (ASA PS I-III, mean age 68 +/- 14 yr) who had undergone lower extremity surgery under spinal anesthesia were studied to determine the effect of intrathecal administration of morphine 0.1 mg on intra- and postoperative pain relief and its side effects. They were randomly divided into control (C) and intrathecal morphine (M) groups (n = 25, respectively) and received 10 mg tetracaine in 4 ml of a quarter saline with 7.5 micrograms epinephrine. Incidence of intraoperative tourniquet pain was significantly lower in M group (36.8%) than in C group (64.3%). Postoperative pain was examined in terms of the duration until the first supplemental analgesic within 24 hr. The mean duration was 7.0 +/- 4.3 hr in the control group, but 11 patients in the M group needed it within 24 hr (18.1 +/- 6.8 hr, excluding 6 patients who did not receive analgesic). Although incidences of postoperative nausea, vomiting, and itching were higher in M group than in C group, none required antiemetic or naloxone. Both groups showed no difference in postoperative respiratory depression measured by apnea monitor (Eden Trace II, Mallinkrodt Japan, Tokyo). The results suggest that a low dose of intrathecal morphine is effective on postoperative 24 hr pain relief in elderly patients and that its side effects are negligible.

Aged↗
PubMed2005

The posterior lumbar ramus: CT-anatomic correlation and propositions of new sites of infiltration.

BACKGROUND AND PURPOSE: Lumbar zypapophyseal joints are innervated by the medial branch of the posterior lumbar ramus. The aim of this work was to describe the precise course of the medial ramus on axial CT scans and to define a precise location for its selective infiltration. METHODS: Lumbar spines of two cadavers were first dissected to assess the route of the L1-L5 posterior ramus. Thirty lumbar spinal nerves of three cadavers were injected in the epineural space with a mixture of iodine contrast and stain to perform a correlation between anatomic gross sections and CT sections in the axial plane. A histologic study was also performed to ensure the neurologic nature of the structure identified. RESULTS: The fibroosseous canal located between the mamillary and the accessory processes was a constant pathway for the medial branch of the L1-L4 posterior ramus. This former was always located closer to the accessory process. The L5 posterior ramus and its divisions could also be identified into a groove bounded laterally by the ala of the sacrum and medially by the base of the superior articular process of S1. CONCLUSION: The accessory process and the groove bounded laterally by the ala of the sacrum and medially by the base of the superior articular process of S1 can be easily depicted on CT images and may allow a precise and selective infiltration of the medial branch of the posterior lumbar ramus.

Aged↗
PubMed1989

[Clinical aspects of spinal anesthesia administered using 0.5% isobar bupivacaine (Maracine) at the L2/L3 or L4/L5 level].

The effect of employing different interspaces for lumbar puncture during spinal anaesthesia was evaluated in 40 patients receiving 4 ml of 0.5% plain bupivacaine at level L2/L3 or L4/L5. No differences were observed in onset, spread or duration of analgesia. Furthermore, we found that only 80% of the patients, independently of the interspace used, had a cephalad spread to T8 and conclude that spinal anaesthesia using plain bupivacaine is not ideal for supraumbilical surgery.

Aged↗