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 361 records · Page 20Linked to original sources

Ventral root axonopathy and its relation to the neurofibrillary degeneration of lower motor neurons in aluminum-induced encephalomyelopathy.

The injection of metallic aluminum (Al) into the cerebrospinal fluid of adult rabbits induces neurofibrillary degeneration of lower motor neurons. We studied the ventral roots and the corresponding motor neurons of Al-treated animals to clarify the modality and extent of reaction of the axon in relation to the severity of perikaryonal involvement. Moreover, the involvement of dorsal root ganglion cells was compared to that of lower motor neurons. Rabbits received 0.15 ml of a 1% Al slurry intracisternally and were perfused through the heart with aldehydes at 14-62 days after injection. Spinal cords and roots were embedded in Epon and examined morphologically and by morphometric techniques. An axonopathy was observed in the ventral roots, characterized by neurofilamentous axonal swellings and myelin attenuation in several size classes of axons. Results obtained from axons traced in serial sections indicate that there may be a unifocal or a multifocal axonopathy. Dorsal root ganglion cells showed milder changes by comparison with motor neurons and their axons in the ventral roots. The most severe axonopathy was associated both with an incidence of 66-81% of motor neurons showing neurofibrillary degeneration and with a rapidly progressing motor weakness. These findings are related in the discussion section to the pathological expression of human neurological disorders in which the lower motor neurons are selective targets.

Aluminum↗

Low back pain in older adults: are we utilizing healthcare resources wisely?

OBJECTIVES: 1) To examine recent change in prevalence and Medicare-associated charges for non-invasive/minimally invasive evaluation and treatment of nonspecific low back pain (LBP); and 2) to examine magnetic resonance imaging (MRI) utilization appropriateness in older adults with chronic low back pain (CLBP). DESIGN: Two cross-sectional surveys of 1) national (1991-2002) and Pennsylvania (2000-2002) Medicare data; and 2) patients aged >or= 65 years with CLBP. SETTING: Outpatient data. PARTICIPANTS: Patients aged >or= 65 years with LBP. MEASUREMENTS: Study 1: Outpatient national and Pennsylvania Part A Medicare data were examined for number of patients and charges for all patients, and for those with nonspecific LBP. Total number of visits and charges for imaging studies, physical therapy (PT), and spinal injections was also examined for Pennsylvania. Study 2: 111 older adults with CLBP were interviewed regarding presence of red flags necessitating imaging and history of having a lumbar MRI, neurogenic claudication (NC), and back surgery. RESULTS: Study 1: Between 1991 and 2002, there was a 42.5% increase in total Medicare patients, 131.7% increase in LBP patients, 310% increase in total charges, and 387.2% increase in LBP charges. In Pennsylvania (2000-2002), there was a 5.5% increase in LBP patients and 33.2% increase in charges (0.2% for PT, 59.4% for injections, 41.9% for MRI/CT, and 19.3% for X rays). Study 2: None of the 111 participants had red flags and 61% had undergone MRIs (29% with NC, 24% with failed back surgery syndrome). CONCLUSION: LBP documentation and diagnostic studies are increasing in Medicare beneficiaries, and evidence suggests that MRIs may often be ordered unnecessarily. Injection procedures appear to account for a significant proportion of LBP-associated costs. More studies are needed to examine the appropriateness with which imaging procedures and non-invasive/minimally invasive treatments are utilized, and their effect on patient outcomes.

Age Distribution↗

Antinociceptive effects and central nervous system depression caused by oxycodone and morphine in rats.

Antinociception and central nervous system depression (CNSD) caused by intraperitoneal, intrathecal and subcutaneous administration of oxycodone or morphine were studied in a randomized and blind, saline controlled study in rats. Antinociception was assessed with the tail-flick and hot plate tests. CNSD was assessed by testing the corneal, placing and righting reflexes and with a 4-point catalepsy score. Intraperitoneally and subcutaneously administered oxycodone and morphine were given in doses of 2.5-10 and 5-20 mg kg-1 respectively. The intrathecal doses were 12.5 micrograms and 100 micrograms of oxycodone and 6.25 micrograms and 50 micrograms of morphine. In both nociceptive tests subcutaneously and intraperitoneally administered oxycodone was 2-4 times more potent than morphine, while intrathecal morphine was over 14 times more potent. CNSD was more profound with oxycodone than with morphine after intraperitoneal and subcutaneous administration, but was not observed after intratechal administration of either drug. Differences in opioid receptor affinities, liposolubilities and metabolism are discussed as possible explanations.

Analgesics↗

LiCl attenuates M(1)AChR-mediated intrathecal pilocarpine-induced reciprocal hindlimb scratching in mice.

Pretreatment of mice with a subcutaneous (s.c.) injection of LiCl (1, 3, 10 mmol/kg) 18 h prior to testing produced dose-related attenuation of the reciprocal hindlimb scratching (RHS) response induced by intrathecal (i.t.) administration of pilocarpine. LiCl (10 mmol/kg, 424 mg/kg) pretreatment shifted the pilocarpine (2 microg)-induced RHS dose-response curve about 5-fold to the right compared to vehicle-injected controls (ED(50) = 2.97 and 0.56 microg, respectively). Coadministration of inositol-1,4,5-trisphosphate (IP(3); 5, 10, 20 microg), but not inositol hexaphosphate (0.03-3 microg), myo-inositol (10 microg) or EDTA (1.33 microg), produced dose-related reversal of the LiCl effect. IP(3) administration alone neither produced RHS nor enhanced the pilocarpine-induced RHS in animals not pretreated with LiCl. These findings provide in vivo evidence for a possible link between RHS and a LiCl-sensitive, possibly phosphoinositide-related, effector pathway.

Animals↗

In vivo biological activity of antioxidative aminothiazole derivatives.

For the development of novel antioxidants having therapeutic utility, a new series of condensed 4- and 5-aminothiazole derivatives has been synthesized using simple methods. Condensed 4-aminothiazoles were prepared by the reaction of alpha-bromolactams with thioamides in ethanol and 5-aminothiazole derivatives were obtained by the treatment of 3-(acylamino)lactams with a thiating agent such as phosphorous pentasulfide and Lawesson's reagent in pyridine. In vitro assay of the condensed 5-aminothiazole derivatives showed them to be potent inhibitors of lipid peroxidation. In order to evaluate these compounds in an in vivo system, we devised a simple and reproducible method in which the inhibition of characteristic behaviors induced by spinal injection of FeCl2 was expressed numerically. Compounds having strong in vitro activity protected the central nervous system form injury caused by iron-dependent lipid peroxidation. The results suggest that the in vivo assay developed in this study should be useful as a screening method for antioxidants and also that condensed 5-aminothiazole derivatives are promising candidates for the treatment of traumatic and ischemic injury of the central nervous system.

Animals↗

Disability of development of tolerance to morphine and U-50,488H, a selective kappa-opioid receptor agonist, in neuropathic pain model mice.

We examined the analgesic and anti-allodynic effects of morphine and U-50,488H (trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]-cyclohexyl)-benzeneacetamide methanesulfonate salt), a selective kappa-opioid receptor agonist, and the development of tolerance to their effects in neuropathic pain model mice induced by sciatic nerve ligation (SNL). In the tail-pinch method, morphine at 10 mg/kg, s.c. produced a weak analgesic effect in SNL mice; however, U-50,488H at 5 mg/kg, s.c. produced an analgesic effect equipotent to that in normal mice. In contrast, morphine produced an adequate analgesic effect when given either intracerebroventricularly (i.c.v.) or intrathecally (i.t.), but U-50,488H only produced analgesia when given i.t. Repeated administration of morphine (either i.c.v. or i.t.) or U-50,488H (either s.c. or i.t.), did not induce tolerance to the effect. In the static allodynia test with an application of von Frey filaments, both compounds given s.c. suppressed the allodynic effect, but in the dynamic allodynia test involving lightly stroking the plantar surface with a cotton bud, only U-50,488H produced an anti-allodynic effect. Repeated administrations of both compounds did not develop tolerance to these anti-allodynic effects. Thus, U-50,488H was found to be a highly effective at blocking hyperalgesia and allodynia in nerve injury, and these findings suggest that kappa-opioid receptor agonists are attractive pharmacological targets for the control of patients with neuropathic pain.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Intrathecal morphine after cardiac surgery.

OBJECTIVE: To assess whether intrathecal (IT) analgesia facilitates early extubation and provides superior pain control after cardiac surgery compared with patient-controlled analgesia (PCA) or nurse-administered SC injections. METHODS: Sixty-two patients undergoing elective cardiac surgery participated in this prospective, randomized, partly-blinded study. Perioperative care was standardized, and patients were assigned to receive IT morphine (ITM group) followed by PCA, IT placebo (ITP group) followed by PCA, or SC injections of morphine every 4 hours as needed (SC group). Rating scales and questionnaires were used to assess clinical outcomes. RESULTS: ITM did not favor earlier extubation, and there was even a tendency for longer extubation times in the ITM group compared with the ITP and SC groups. Pain scores, adverse effects, postoperative recovery, and patient satisfaction were also comparable in the 3 groups. CONCLUSIONS: Considering that the administration of IT morphine is more costly and can be riskier than conventional analgesic regimens, we conclude that its use is not indicated in patients undergoing cardiac surgery if early extubation is planned.

Analgesia, Patient-Controlled↗

An assessment of vascular pain using the flexor reflex in anesthetized rats.

This study assessed the flexor reflex induced by intraarterial algogenic drugs in anesthetized rats. The experiments were performed on male Sprague Dawley rats weighing 290-350 g. The animals were anesthetized with urethane (1.3 g/kg i.p.) and an arterial cannula was inserted to the level of the bifurcation of the femoral artery. The magnitude of the flexor reflex was examined by recording the electromyograph from the posterior biceps femoris/semitendinous muscles. Results showed that the flexor reflex evoked by intra-arterial injection of capsaicin (0.05-0.5 microg) was dose-dependent. A similar reflex resulted from pinching the toe of the hindlimb. These responses were inhibited by morphine (5 mg/kg s.c.) and restored with naloxone (1.5 mg/kg s.c.). Intraarterial preinjection of procaine (2%, 200 microl) and capsazepine (20 microg), which is a selective vanilloid receptor antagonist, inhibited the capsaicin-evoked response, but not that of pinching. These results indicate that the flexor reflex is a useful tool for assessing vascular pain in anesthetized animals.

Animals↗

Direct insulin signaling of neurons reverses diabetic neuropathy.

Diabetic polyneuropathy is the most common acquired diffuse disorder of the peripheral nervous system. It is generally assumed that insulin benefits human and experimental diabetic neuropathy indirectly by lowering glucose levels. Insulin also provides potent direct support of neurons and axons, and there is a possibility that abnormalities in direct insulin signaling on peripheral neurons relate to the development of this disorder. Here we report that direct neuronal (intrathecal) delivery of low doses of insulin (0.1-0.2 IU daily), insufficient to reduce glycemia or equimolar IGF-I but not intrathecal saline or subcutaneous insulin, improved and reversed slowing of motor and sensory conduction velocity in rats rendered diabetic using streptozotocin. Moreover, insulin and IGF-I similarly reversed atrophy in myelinated sensory axons in the sural nerve. That intrathecal insulin had the capability of signaling sensory neurons was confirmed by observing that fluorescein isothiocyanate-labeled insulin given intrathecally accessed and labeled individual lumbar dorsal root ganglion neurons. Moreover, we confirmed that such neurons express the insulin receptor, as previously suggested by Sugimoto et al. Finally, we sequestered intrathecal insulin in nondiabetic rats using an anti-insulin antibody. Conduction slowing and axonal atrophy resembling the changes in diabetes were generated by anti-insulin but not by an anti-rat albumin antibody infusion. Defective direct signaling of insulin on peripheral neurons through routes that include the cerebrospinal fluid may relate to the development of diabetic peripheral neuropathy.

Animals↗

Cryptococcal meningitis: complications due to intrathecal treatment.

A 50-year-old woman with cryptococcal meningitis was treated with amphotericin B intrathecally through a Rickham reservoir and intravenously, together with flucytosine orally. After 4 months of treatment cryptococci and cryptococcal antigen were still present in cerebrospinal fluid from time to time. After removal of the Rickham reservoir the patient recovered completely within 6 weeks. The persistent infection was thus found to be due to the presence of the Rickham reservoir, a complication to intrathecal therapy which has not been reported before.

Amphotericin B↗

Intrathecal labor analgesia using levobupivacaine 2.5 mg with fentanyl 25 microg--would half the dose suffice?

BACKGROUND: This randomized, double-blinded, controlled trial of 40 patients in early labor was conducted to determine whether a reduction in the total amount of intrathecal levobupivacaine and fentanyl would reduce the incidence of motor blockade and pruritus, respectively. MATERIAL/METHODS: Combined spinal epidural (CSE) analgesia was instituted. Group A (n=20) received 2.5 mg levobupivacaine with 25 microg fentanyl intrathecally while group B (n=20) received half that dose. RESULTS: The duration and quality of spinal analgesia were comparable in the 2 groups. There was a reduced incidence of motor blockade in patients from Group B (P<0.01). This was apparent 5 minutes after the spinal injection and persisted throughout the next 30 minutes. However, there were also 2 parturients from this group who required epidural supplementation as a result of partial analgesia. Other side effects were not different between the 2 groups. CONCLUSIONS: A reduction in the intrathecal dose of 2.5 mg levobupivacaine with 25 microg fentanyl by half is an option for CSE in labor because it can reduce the incidence of motor impairment. Although the reduced dose does not differ significantly from the full dose with respect to onset, duration, and quality of analgesia for the majority of parturients, it must be highlighted that insufficient labor analgesia may occur in certain individuals. In this respect, further studies related to dosage of intrathecal levobupivacaine in obstetric labor analgesia will be beneficial in substantiating this point.

Adult↗

[Animal experiment studies on the neurohumoral control of female puberty].

To study the mode of action of oestrogen in female sexual maturation, prepubertal female rats were treated in different ways with oestradiol benzoate (OB). Using an improved implantation method, former findings on a hypophysial site of oestrogen action in the positive feedback (Hohlweg effect) were confirmed. A single s.c. injection or intrahypophysial implantation of OB at 25 or 26 days of age induced precocious vaginal opening (VO) and one ovulation, but the subsequent ovarian cycle was significantly prolonged, so that the first spontaneous ovulation occurred only at the normal time of the onset of puberty. Further studies demonstrated that the sensitivity to the ovulation-inducing effect of oestrogen increases as the rats approach the age of puberty, and that the first pubertal ovulation can be suppressed by intrahypophysial, but not by intrahypothalamic implantation of progestereone. The conclusion is drawn that the precocious induction of one ovulation via the Hohlweg effect is not tantamount to an advancement of puberty. The results furthermore suggest that the positive oestrogen feedback forms the basis for the first pubertal ovulation as it does with regard to later cyclic ovulations. True acceleration of sexual maturation was achieved by daily injections of 0,05 microgram OB/100 g b.w. from 5 days of age to VO. In contrast to findings obtained by other authors in Sprague-Dawley rats, a shortened OB treatment from 26 days of age to VO was not effective in advancing the onset of puberty unless the rats had additionally been injected with OB from 5 to 10 days of age. A final experiment demonstrated that the first ovarian cycle was not prolonged after neonatal ovariectomy and implantation of ovaries at 24, 28 or 32 days of age. Thus, maturation of the neurohormonal mechanisms that are responsible for the cyclic ovarian function continues during the prepubertal development in the absence of ovarian steroids.

Age Factors↗

Analgesic effect of tramadol in the rat.

The analgesic effect of tramadol was studied in the rat using tail flick and hot plate tests following intrathecal and subcutaneous administrations. Tramadol had only a short-lasting analgesic effect (20 min) on intrathecal administration which may be due to rapid removal from the subarachnoid space. Its analgesic effects were antagonized by pretreatment with naloxone. It seems that the opiate system may involve in the analgesic effect of tramadol, while the noradrenergic, serotonergic and cholinergic systems may play a modulating role.

Analgesics↗