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Intrathecal injection

Vincristine -vinca alkaloid inhibits tubulin polymerization G2 phase specific -neurotoxicity—peripheral neuropathy -vesicant if extravasated -nausea and vomiting -bone marrow suppression—mild -transient transaminase elevation -constipation (often secondary to neuropathy induced ileus) —intrathecal injection is ALWAYS FATAL... [Pg.180]

Suh HW, Song DK, Lee KJ, Choi SR, Kim YH. (1996). Intrathecally injected nicotine enhances the antinociception induced by morphine but not beta-endorphin, D-Pen2,5-enkephalin and U50,488H administered intrathecally in the mouse. Neuropeptides. 30(4) 373-78. [Pg.532]

Intrathecal Administer undiluted solution by various intrathecal routes (20 mg/dose) as an adjunct to IV treatment in fungal meningitis. Succeeding intrathecal injections may be alternated between lumbar, cervical, and cisternal punctures every 3 to 7 days. [Pg.1659]

Mitoxantrone must not be given by intrathecal injection. Neuropathy and neurotoxicity have been reported. These reports have included seizures leading to coma and severe neurologic sequelae, and paralysis with bowel and bladder dysfunction. [Pg.2024]

On intrathecal injection, it acts on substantia gelatinosa of dorsal horn of spinal cord and inhibit the release of excitatory transmitters. At supraspinal sites, it acts on medulla, mid brain, limbic and cortical areas. [Pg.76]

Lepore, A.C., Bakshi, A., Swanger, S.A., Rao, M.S., Fischer, I. (2005). Neural precursor cells can be delivered into the injured cervical spinal cord by intrathecal injection at the lumbar cord. Brain Res, 1045, 206-16. [Pg.31]

Kristensen, J. D., Karsten, R., Gordh, T., Berge, O.-G. The NMDA antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) has antinociceptive effect after intrathecal injection in the rat, Pain 1994, 56, 59-67. [Pg.420]

Studies to elucidate the functional role of NO have used inhibitors of NO synthase such as L-NAME and L-NMMA (see below). Systemic and intrathecal injections of NO synthase inhibitors have been shown to reduce noxious responses to formalin and carrageenan-induced hyperalgesia (Sakurada et al., 2001). Furthermore, NO-induced mechanical hyperalgesia has been reported to be mediated by supraspinal centers and does not occur in in vitro preparations of the spinal cord. [Pg.560]

The effects of intrathecal administration, both wanted and unwanted, are still much debated (448). The question as to whether oral glucocorticoid therapy should be preferred to intrathecal injections is raised by the harmful effects that have sometimes occurred after the latter, although some of these may have been caused by irritative substances in the injection fluid (SEDA-6, 331). The same local glucocorticoid concentrations can probably be attained with fewer problems with oral administration. Epidural injection of glucocorticoids seems to be safer than intrathecal injection, but injection of high doses can cause the same systemic adverse effects as seen with oral treatment. Facial flushing and erythema after lumbar... [Pg.50]

Glucocorticoids given intrathecally can cause a rise in cerebrospinal fluid protein and carry the risk of arachnoiditis (SED-8, 820). Chemical meningitis has been reported after two intrathecal injections of methylpredni-solone acetate (450) and after lumbar facet joint block (SEDA-17, 450). Intraspinal injections of hydrocortisone for multiple sclerosis apparently led in one case to a cauda equina syndrome, with subsequent ulceromutilating acro-pathy (SEDA-17, 450). Intra-discal injections of triamcinolone acetonide in a number of French cases led to disk or epidural calcification, sometimes symptomless (SEDA-17, 450). [Pg.50]

Methotrexate acts by inhibition of dihydrofolate reductase, the enzyme requisite for the reduction of dihydrofolic acid (3) to 5,6,7,8-tetrahydrofolic acid (4). In turn, (4) is a precursor to a series of enzyme cofactors (5-7) essential for the transfer of one carbon unit necessary for the biosynthesis of purines and pyrimidines and hence, ultimately, DNA. As an inhibitor of dihydrofolate reductase, methotrexate kills cells during the S phase of the cell cycle, when the cells are in the log phase of growth. Unfortunately, this cytotoxicity is non-selective, and rapidly proliferating normal cells, e.g., gastrointestinal epithelium cells and bone marrow, are dramatically affected as well. In addition, recent use of high dose methotrexate therapy with leucovorin rescue has led to additional clinical problems arising from a dose-related nephrotoxic metabolite, 7-hydroxy methotrexate (8). Finally, the very polar nature of methotrexate renders it virtually impenetrable to the blood-brain barrier, which can necessitate direct intrathecal injection in order to achieve therapeutic doses for the treatment of CNS tumours. [Pg.87]

D-Ala-deltorphin-II induces 6-opiate receptor mediated analgesia in frogs [55] and also in the invertebrate land snail (Cepaea nemoralis) [56]. When administered by intrathecal injection in rats, D-Ala-deltorphin-II produces a dose-related inhibition of the tail-flick response (threshold 0.6 nmol/rat). Its inhibitory effect lasts 10 60 min, depending on the dose, and is naltrindole reversible [57]. Wang et al. [25] demonstrated that D-Ala-deltorphin-II inhibited A6 and C fiber evoked responses from nociceptive neurons in the superficial and deeper dorsal horn of the rat medulla. [Pg.181]

After intrathecal injection, delta opioid agonists slow transit in the small intestine [116,117] and inhibit diarrhea [114,118]. Based on these studies, it appears that delta opioid receptors in the spinal cord, unlike those in the... [Pg.440]

As indicated in Table 2.1, drugs may be injected into veins, muscles, subcutaneous tissue, arteries, or into the subarachnoid space of the spinal canal (intrathecal). For obvious reasons, intraarterial and intrathecal injections are reserved for specialized drug administration requirements, such as regional perfusion of a tumor with a toxic drug or induction of spinal anesthesia, respectively. Therefore, the more routine injection routes are intravenous (IV), intramuscular (IM), and subcutaneous (SC). Because these three modalities involve skin puncture, they carry the risks of infection, pain, and local irritation. [Pg.31]

Cheng J-K, Lin C-S, Chen C-C et al. (2007) Effects of intrathecal injection of T-type calcium channel blockers in the rat formalin test. Behav Pharmacol 18 1-8... [Pg.50]

Adverse effects Nausea, vomiting, diarrhea, and severe myelo-suppression (primarily granulocytopenia) are the major toxicities. Hepatic dysfunction is also occasionally encountered. At high doses or intrathecal injection, ara-C may cause seizures or altered mental states. [Pg.395]


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See also in sourсe #XX -- [ Pg.16 ]

See also in sourсe #XX -- [ Pg.296 , Pg.297 ]




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Intrathecal

Irritancy after Intrathecal (Spinal) Injection

Irritancy after intrathecal injection

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