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At least 523 records · Page 29Linked to original sources
PubMed2005

Formalin injection causes a coordinated spinal cord CO/NO-cGMP signaling system response.

BACKGROUND: The CO/NO-cGMP signalling system participates in the regulation of many physiological processes. The roles this system plays in spinal cord nociceptive signalling are particularly important. While individual components have been examined in isolation, little study has been dedicated to understanding the regulation and functioning of the system as a whole. RESULTS: In these studies we examined the time course of expression of 13 genes coding for components of this system including isoforms of the heme oxygenase (HO), nitric oxide synthase (NOS), soluble guanylate cyclase (sGC), cGMP dependent protein kinase (PKG) and phosphodiesterase (PDE) enzyme systems. Of the 13 genes studied, 11 had spinal cord mRNA levels elevated at one or more time points up to 48 hours after hindpaw formalin injection. Of the 11 with elevated mRNA, 8 had elevated protein levels 48 hours after formalin injection when mechanical allodynia was maximal. No component had an increased protein level which did not have an increased mRNA level at one or more time points. Injection of morphine 10 mg/kg prior to formalin completely abolished the acute nociceptive behaviours, but did not alter the degree of sensitivity which developed in the formalin treated hind paws during the subsequent 48 hours. Morphine treatment did, however, eliminate formalin induced increases in enzyme protein levels. CONCLUSION: Our results indicate that the expression of the components of the CO/NO-cGMP signalling system seems to be coordinated in such a way that a generalized multi-level enhancement rather than a tightly limited step specific response occurs with noxious stimulation. Furthermore, the analgesic morphine administered prior to noxious stimulation can prevent long-term changes in gene expression though not necessarily nociceptive sensitisation.

Animals↗
PubMed1978

Spinal cord necrosis after intrathecal injection of methylene blue.

A 59 year old man had 6 ml of unbuffered methylene blue injected into the lumbar theca in an attempt to localise the source of cerebrospinal fluid rhinorrhoea. After injection of the dye he became shocked, and within the next few days he developed a mild paraparesis which subsequently progressed to a total paraplegia. The distribution of the spinal cord damage found at necropsy, eight and a half years after injection of the dye, is described and its relationship to the clinical picture discussed.

Cerebrospinal Fluid Otorrhea↗
PubMed1994

Transmission in a locomotor-related group Ib pathway from hindlimb extensor muscles in the cat.

It has been previously shown that phasic stimulation of group I afferents from ankle and knee extensor muscles may entrain and/or reset the intrinsic locomotor rhythm; these afferents are thus acting on motoneurones through the spinal rhythm generators. It was also concluded that the major part of these effects originates from Golgi tendon organ Ib afferents. Transmission in this pathway to lumbar motoneurones has now been investigated during fictive locomotion in spinal cats injected with nialamide and L-DOPA, and in decerebrate cats with stimulation of the mesencephalic locomotor region. In spinal cats injected with nialamide and L-DOPA, it was possible to evoke long-latency, long-lasting reflexes upon stimulation of high threshold afferents before spontaneous fictive locomotion commenced. During that period, stimulation of ankle and knee extensor group I afferents evoked oligosynaptic excitation of extensor motoneurones, rather than the "classical" Ib inhibition. Furthermore, a premotoneuronal convergence (spatial facilitation) between this group I excitation and the crossed extensor reflex was established. During fictive locomotion, in both preparations, the transmissions in these groups I pathway was phasically modulated within the step cycle. During the flexor phase, the group I input cut the depolarised (active) phase in flexor motoneurones and evoked EPSPs in extensor motoneurones; during the extensor phase the group I input evoked smaller EPSPs in extensor motoneurones and had virtually no effect on flexor motoneurones. The above results suggest that the group I input from extensor muscles is transmitted through the spinal rhythm generator and more particularly, through the extensor "half-centre". The locomotor-related group I excitation had a central latency of 3.5-4.0 ms. The excitation from ankle extensors to ankle extensors remained after a spinal transection at the caudal part of L6 segment; the interneurones must therefore be located in the L7 and S1 spinal segments. Candidate interneurones for mediating these actions were recorded extracellularly in lamina VII of the 7th lumbar segment. Responses to different peripheral nerve stimulation (high threshold afferents and group I afferents bilaterally) were in concordance with the convergence studies in motoneurones. The interneurones were rhythmically active in the appropriate phases of the fictive locomotor cycle, as predicted by their response patterns. The synaptic input to, and the projection of these candidate interneurones must be fully identified before their possible role as components of the spinal locomotor network can be evaluated.

Animals↗
PubMed2002

Steroid injections: effect on pain of spinal origin.

Pain originating from the spine is a common clinical problem that is often difficult to manage. This chapter considers the evidence supporting the use of corticosteroid injections for pain of spinal origin. Clinical problems considered in this review are radicular pain, zygapophyseal joint pain, discogenic pain and non-specific pain from the cervical, lumbar and thoracic spine. Issues of efficacy and adverse events are considered. No useful data were found concerning the treatment of any type of thoracic pain with corticosteroid injections. In the lumbar spine, there is evidence to support the use of transforaminal injections for radicular pain. Intradiscal and intra-articular injections in both lumbar and cervical spines have not been shown to be effective. Sacroiliitis responds well to intra-articular corticosteroids. There is insufficient evidence to support the use of atlanto-axial or atlanto-occipital joint injections.

Adrenal Cortex Hormones↗
PubMed1983

The distribution of substance P-containing neurons in the cat Edinger-Westphal nucleus: relationship to efferent projection systems.

The light microscopic localization of substance P-like immunoreactivity (SPLI) was examined in the cat Edinger--Westphal complex using the peroxidase--antiperoxidase method. A high density of cell bodies and processes staining for SPLI were found in the caudal part of the Edinger--Westphal complex (EWc) capping the somatic divisions of the oculomotor nucleus. This distribution continued rostrally into the anteromedian nucleus (AM). Cells labeled with SPLI were also found arranged in a thin layer dorsally capping the oculomotor nucleus, and scattered cells were found in the periaqueductal gray region at the same level. This distribution of SPLI-positive cells was then compared with the distribution of cells in EWc and AM that are retrogradely labeled by horseradish peroxidase or Nuclear Yellow injections into spinal cord, cerebellum, or ciliary ganglion. Injections of horseradish peroxidase into both cervical and lumbar cord labeled a large number of cells throughout the length of EWc and the more rostral AM. A similar pattern of labeling was seen following injections of Nuclear Yellow into the deep cerebellar nuclei. In contrast, cells innervating the ciliary ganglion were found predominantly outside of the Edinger--Westphal complex in AM, the rostral periaqueductal region, and the tegmentum ventral to the oculomotor complex. The distribution of cells projecting to spinal cord or cerebellum and the pattern of SPLI staining was found to closely overlap, evidence that substance P may be contained in cells that give rise to the central projections of the Edinger--Westphal complex.

Animals↗
PubMedDate not supplied

[Use of combined lidocaine and bupivacaine spinal-epidural anesthesia in vascular surgery of lower limbs].

The efficacy of combined spinal epidural anesthesia (CSEA) for femoral to distal artery bypass surgery is assessed. Thirty-eight patients were divided into 3 groups. CSE block was performed at L3-L4 (26G pensil-point spinal needle and 18G catheter). In group I (n = 14) blocking was induced with 20 mg of 1% lidocaine and maintained with 2% lidocaine through an epidural catheter. Group II (n = 15) received spinal plain 20 mg of 0.5% bupivacaine. In group III (n = 9) the initial dose of plain 0.5% bupivacaine was 3 ml (15 mg); 5 min after the first bolus the incremental dose of plain bupivacaine 3 ml (15 mg) was injected and spinal needle was withdrawn. Epidural 0.5% bupivacaine was injected as needed. Sensory blockade was assessed by the pinprick test. Two patients in group I (18.2%) were in need of general anesthesia (GA) (inadequate dissemination of solution in 1 case and catheter kinking in the other). In group II GA had to be performed in 1 case because surgery was longer than planned. In group III anesthesia was effective in all cases. The mean level of sensory block in group I was T11.2 +/- 0.4, in group II T9.4 +/- 0.5, and in group III T8.6 +/- 0.55 (p > 0.05). The mean dose of bupivacaine per segment in groups II and III was 1.47 +/- 0.08 and 2.08 +/- 0.01, respectively (p < 0.05), use of epidural catheter during surgery 40 and 11%, respectively (p < 0.05). Arterial pressure drop was 10.8, 14.1, and 11.6% in groups I, II, and III, respectively. The mean total dose was 735 +/- 89 mg (172 +/- 14 mg/h) in the lidocaine group, in group II 38.5 +/- 6.4 mg (10.25 +/- 1.15 mg/h), and in group III 32.8 +/- 2.8 mg (7.46 +/- 1.67 mg/h) (p < 0.05). No neurological problems or PDPH were observed in any of the patients and no vasoactive drugs were needed. CSEA is fit for anesthesia for peripheral vascular surgery. CSEA with double spinal injection is preferable, for it provides a longer anesthesia and hemodynamic stability.

Adult↗
PubMed1990

Differentiation of spinal and supraspinal opioid receptors by morphine tolerance.

Mice treated for 72 hrs with morphine (subcutaneously implanted pellets) were tested with a variety of opioid receptor agonists to examine the development of tolerance and cross-tolerance to their analgesic action. The development of spinal and supraspinal tolerance following morphine treatment was evaluated by administering compounds systemically (sc), intrathecally (IT) and intracerebroventricularly (ICV). Following morphine treatment, tolerance to morphine analgesia was observed following IT, ICV and sc administration. Chronic morphine treatment also produced cross-tolerance to the analgesic effects of the selective delta opioid receptor agonist [D-Pen2, D-Pen5]enkephalin (DPDPE) following IT and ICV administration. However, morphine treatment selectively produced cross-tolerance to ICV [D-Ala2, NMePhe4, Gly-ol5]enkephalin (DAGO) (mu receptor agonist) analgesia, without altering IT DAGO analgesia. These results suggest that brain and spinal cord receptors mediating the effects of DAGO differ in terms of the development of cross-tolerance to morphine; and suggest that tolerance to systemic morphine may be due to changes in spinal delta and brain mu and delta receptor mechanisms.

Animals↗
PubMed1988

Differential effects of subcutaneous and intrathecal morphine administration on blood glucose in mice: comparison with intracerebroventricular administration.

The s.c. administration of morphine (2.5-80 mg/kg) produced a dose-dependent hyperglycemia, whereas morphine (12.5-50 micrograms) given i.t. in the lumbar region caused a dose-dependent hypoglycemia in unanesthetized mice. Both effects on blood glucose were antagonized by s.c. naloxone, although inhibition of i.t. morphine required a higher naloxone dose. Naloxone pretreatment with 2 mg/kg, but not 1 mg/kg s.c., potentiated a hyperglycemic response to i.t. saline. High i.t. doses of morphine caused an early (within 2 min) scratching behavior that was not inhibited by naloxone or glucose loading and a later (greater than 20 min) tonic convulsive behavior (opisthotonus). Lethality was partially inhibited by glucose loading which delayed, but did not prevent, the hypoglycemic effect of i.t. morphine. The hypoglycemic effect of i.t. morphine was also delayed in streptozotocin-diabetic ICR mice and diabetic (db/db) C57BL/KsJ mice, but the latter were more sensitive to lethality, which occurred without hypoglycemia or seizures. All these effects of i.t. morphine were completely blocked by acute spinal transection of T10-T11, but the nociceptive, hypoglycemic and opisthotonic effects were not mimicked by i.c.v. morphine (6.25-50 micrograms) in ICR mice, which showed a bell-shaped hyperglycemic dose-response relationship and a brief explosive motor behavior at the higher doses (25-50 micrograms). It is concluded that the effects of morphine on blood glucose and on behavior are dependent upon the route of administration, and that the convulsive effect of i.t. morphine may be facilitated by the production of a profound hypoglycemia, which involves a spinal, rather than supraspinal or systemic, action of morphine.

Animals↗
PubMedDate not supplied

Sensory block extension during combined spinal and epidural.

BACKGROUND AND OBJECTIVES: During a combined spinal and epidural technique, extension of sensory block by epidural injection of saline or bupivacaine has been demonstrated and attributed to a volume effect or to the combination of a volume effect with a local anesthetic effect. This two-part study was designed to evaluate the time dependency of the volume effect and the local anesthetic effect on the mechanism of spinal block extension. METHODS: We performed two prospective studies. Thirty patients were randomized in each study. A combined spinal and epidural was performed in a sitting position in all groups. The patients in the first study received 15 mg hyperbaric bupivacaine intrathecally and were placed supine 2 minutes after spinal injection. They received 10 mL epidural saline either 5 minutes after spinal (group A) or 20 minutes after spinal (group B) compared to a control group (group C). The patients in the second study received 12.5 mg hyperbaric bupivacaine intrathecally and were placed supine 5 minutes after spinal injection. They then received epidurally either 10 mL saline 7 minutes after spinal (group D) or 10 mL bupivacaine 7 minutes after spinal (group E) or nothing (group F). Sensory block levels were assessed by a loss of sensation to cold using ether. RESULTS: In the first portion of this study, in group A, area under the curve of sensory block levels by time from 10 to 40 minutes after spinal injection, and maximum sensory block levels were significantly higher (P < .05) compared to groups B and C. In the second portion of the study, sensory block levels were comparable at all times in the three groups. CONCLUSIONS: During a combined spinal and epidural technique with the use of hyperbaric bupivacaine, the volume effect is time dependent and is seen when epidural top up is done soon after spinal injection. This volume effect is abolished when patients are left seated for 5 minutes after spinal injection. The local anesthetic effect is not demonstrated when high sensory block levels are achieved by spinal injection.

Adult↗
PubMed1987

Investigation of tolerance to chronic intrathecal morphine infusion in the rat.

Rats received chronic subcutaneous or intrathecal infusions of either saline or 25 micrograms/microliter/hr or 50 micrograms/microliter/hr of morphine sulfate. During five days of infusion individual groups of rats were assessed on either the nociceptive tail flick or hot plate test. After the infusions, the analgesic effects of either subcutaneous or intrathecal morphine test doses were evaluated. Tolerance developed to the analgesic effect of both subcutaneous and intrathecal morphine infusions on the tail flick test. Subcutaneously infused rats were also tolerant to a subcutaneous morphine challenge on this test. However, intrathecally infused rats were not tolerant to either the subcutaneous or intrathecal challenge. In contrast to these results, rats tested on the hot plate were not analgesic in response to either subcutaneous or intrathecal morphine infusions. However, these rats were tolerant when challenged with either subcutaneous or intrathecal morphine. The results are discussed in terms of the relative contribution of spinal and supraspinal sites to opiate tolerance, and the possibility that tolerance does not develop to the antinociceptive effect of spinal morphine on spinally mediated reflexes.

Animals↗
PubMed2002

The effect of introducer gauge, design and bevel direction on the deflection of spinal needles.

This study was performed to determine how the use of an introducer affects the extent to which a needle deflects during a spinal or combined spinal-epidural injection. A polystyrene block was used to simulate the paraspinal area of the back. A line was drawn perpendicular to the edge of the block to use as a guide and to measure the deflection. The use of an introducer needle decreased the deflection in all the bevelled needles (p < 0.001). Depending on the direction of both the bevels, the deflection decreased as the introducer bevel was changed from the same direction, to right-angles to bevel direction and then to a direction opposite to that of the spinal needle (p < 0.05). Deflection was decreased when a thick introducer was used (p < 0.001). The use of an introducer increased the deflection of the pencil-point needle only in the deflection direction of the introducer (p < 0.001). The 18-gauge Tuohy needle with a "backhole" deflected more than the corresponding needle without a backhole (p < 0.001), and the spinal needle inserted through the Tuohy needle with a backhole deflected more (p = 0.002). Besides the tip type and gauge, the deflection of a spinal needle depends upon the use of introducer, its gauge and bevel direction. The deflection of a Tuohy needle depends upon its design, gauge and the presence of a backhole.

Anesthesia, Epidural↗
PubMed2004

Spinal interneurons infected by renal injection of pseudorabies virus in the rat.

The potency of spinal sympathetic reflexes is increased after spinal injury, and these reflexes may result in life-threatening hypertensive crises in humans. Few, if any, primary afferents project directly to sympathetic preganglionic neurons (SPN). Therefore, spinal sympathetic interneurons (IN) must play a major role in generating dysfunctional sympathetic activity after spinal cord injury. Furthermore, these IN are potentially aberrant targets, either for ascending and descending axons that may sprout after spinal cord injury or for axons that regenerate after spinal cord injury. We identified IN via the transsynaptic retrograde transport of pseudorabies virus (PRV) injected into the kidneys of rats. The proportion of infected IN ranged from approximately 1/3 to approximately 2/3 of the number of infected SPN. IN were heavily concentrated among the SPN in spinal lamina VII. However, IN were located in all lamina of the dorsal horn. The longitudinal distribution of infected IN was closely correlated with the longitudinal distribution of infected SPN. Few infected IN were found rostral or caudal to the longitudinal range of infected SPN. Infected IN were heterogeneous in both their sizes and the extent of their dendritic trees. The strong correlation between longitudinal distributions of infected IN and SPN supports physiological data demonstrating a segmental organization of spinal sympathetic reflexes. The paucity of infected IN in segments distant from SPN suggests that multisegmental sympathetic reflexes are mediated by projections onto IN rather than onto SPN themselves. The morphological heterogeneity of IN probably manifests the variety of systems that affect spinal sympathetic regulation.

Animals↗
PubMed1982

Studies on the location and release of cholecystokinin and vasoactive intestinal peptide in rat and cat spinal cord.

By radioimmunoassay vasoactive intestinal peptide (VIP) and cholecystokinin (CCK) are found in the cat lumbar spinal ganglion and spinal cord with levels in dorsal greater than ventral horn. Unilateral rhizotomy, but not cervical hemisection produced a significant but incomplete depletion of CCK and VIP immunoreactivity in dorsal, but not ventral horn. Intrathecal capsaicin (0.5 mg) had no effect on the levels of spinal VIP or CCK. Intrathecal colchicine (0.5 mg)produced a significant increase in the levels of VIP in the dorsal and ventral horn but had no effect on the levels of CCK. The present experiments, using a preparation which permits in situ superfusion of the spinal cord, demonstrated in the chloralose-urethanized cat and rat the presence of measurable levels of VIP and CCK. In rats, the addition of potassium (40 mM in excess) resulted in a 138% and 46% increase in the levels of CCK and VIP, respectively above resting levels (3.7 +/- 1.2 fmol/ml/10 min and 1.7 +/- 0.5 fmol/ml/10 min, respectively). The deletion of calcium and substitution of cobalt (2 mM) resulted in a significant reduction in the potassium-evoked release. Intrathecal picrotoxin doubled the levels of CCK, but had no effect on the levels of VIP in the spinal superfusates. Capsaicin (3 X 10(-4) M) had no effect on the levels of either peptide in rat spinal superfusate. In cats, bilateral electrical stimulation of the sciatic nerve at high, but not low intensity, resulted in a 218% and 132% increase above prestimulation baseline in the levels of CCK and VIP, respectively. Separation of immunoreactivity on a Sephadex G-50 superfine column of the spinal superfusates and the extracted material from cat spinal cord, revealed that the immunoreactive CCK species in tissue co-migrated with the 8 and 33 amino acid peptide fragments. In the release samples, however, all the radioimmunoassayable activity migrated with the peak corresponding with CCK. No other peaks were detected. Column separation of spinal cord and the superfusate obtained during basal and evoked release, revealed that all activity in both the tissue and perfusate samples, travelled in a single peak which co-migrated with authentic VIP.

Animals↗