Relevant bibliographies by topics / Intrathecal injection

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Academic literature on the topic 'Intrathecal injection'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 June 2025

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Journal articles on the topic "Intrathecal injection"

1

Kim, Yeo Ok, Ji A. Song, Woong Mo Kim, and Myung Ha Yoon. "Antiallodynic Effect of Intrathecal Korean Red Ginseng in Cisplatin-Induced Neuropathic Pain Rats." Pharmacology 105, no. 3-4 (2019): 173–80. http://dx.doi.org/10.1159/000503259.

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Background: Chemotherapy-induced neuropathic pain (CINP) is a serious side effect of chemotherapy. Korean Red Ginseng (KRG) is a popular herbal medicine in Asian countries. We examined the therapeutic potential of intrathecally administered KRG for CINP and clarified the mechanisms of action with regard to 5-hydroxytryptamine (5-HT)7 receptor at the spinal level. Methods: CINP was evoked by intraperitoneal injection of cisplatin in male Sprague-Dawley rats. After examining the effects of intrathecally administered KRG on CINP, 5-HT receptor antagonist (dihydroergocristine [DHE]) was pretreated to determine the involvement of 5-HT receptor. In addition, intrathecal 5-HT7 receptor antagonist (SB269970) was administered to define the role of 5-HT7 receptor on the effect of KRG. 5-HT7 receptor mRNA expression levels and 5-HT concentrations were examined in the spinal cord. Results: Intrathecally administered KRG produced a limited, but a dose-dependent, antiallodynic effect. Intrathecally administered DHE antagonized the antiallodynia caused by KRG. Furthermore, intrathecal SB269970 also reversed the effect of KRG. No changes in 5-HT7 receptor mRNA expression were seen in the dorsal horn of the spinal cord after cisplatin injection. After injecting cisplatin, 5-HT levels were decreased in the spinal cord, whereas those of 5-HT were increased by intrathecal KRG. Conclusions: Intrathecally administered KRG decreased CINP. In addition, spinal 5-HT7 receptors contributed to the antiallodynic effect of KRG.
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Jhamandas, K., M. Sutak, and S. Lemaire. "Comparative spinal analgesic action of dynorphin1-8, dynorphin1-13, and a kappa-receptor agonist U50,488." Canadian Journal of Physiology and Pharmacology 64, no. 3 (1986): 263–68. http://dx.doi.org/10.1139/y86-042.

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The effect of intrathecal injections of dynorphin1-8 (DYN1-8), dynorphin1-13 (DYN1-13), and a putative kappa agonist, U50,488 was tested in the rat tail-flick test. DYN1-8 and DYN1-13 (5, 10, 20 μg) produced a dose-related biphasic antinociceptive response consisting of an initial and a delayed response. Injection of U50,488 (20, 40 60 μg) produced a monophasic response. The antinociceptive effect of DYN1-8 (5, 10, 20 μg) and DYN1-3 (20 μg), but not U50,488 (20 μg), was present 24 h postintrathecal injection. Pretreatment with systemic naloxone (2 mg/kg s.c.) attenuated the delayed response, but not the initial response induced by DYN1-8 and DYN1-13. The initial response was attenuated by pretreatment with intrathecal naloxone at a dose of 0.5 and 2.0 μg. The antinociceptive effect of U50,488 (20,60 μg) was not affected by pretreatment with 2.0 μg intrathecal naloxone, but was significantly reduced by 4 μg of the antagonist. Both DYN1-8 and DYN1-13 (5 μg) augmented the antinociceptive effect of intrathecally administered morphine (5, 10 μg). Intrathecal injection of DYN1-8 (5, 10, 20 μg), DYN1-13 (5 μg), and morphine (10 μg) reduced the spontaneous output of urine measured at 2 and 24 h postintrathecal injection. A similar injection of U50,488 (20 μg) had no significant action on the urinary output. The results show that long and short dynorphin fragments have a comparable activity and the spinal antinociceptive actions of dynorphin are sensitive to low doses of intrathecal naloxone. The activity profile of spinally administered dynorphins differs from that of the kappa agonist U50,488.
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Li, Gehui, Hao Wang, Xiaofei Qi, Xiaolei Huang, and Yuantao Li. "Intrathecal dexmedetomidine improves epidural labor analgesia effects: a randomized controlled trial." Journal of International Medical Research 49, no. 4 (2021): 030006052199953. http://dx.doi.org/10.1177/0300060521999534.

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Objective α2‑agonists and opioids have been used as intrathecal adjuvants to local anesthetics for several years, but the effect of intrathecal dexmedetomidine (Dex) or sufentanil combined with epidural ropivacaine in labor analgesia is not fully understood. Methods A total of 108 parturient women receiving combined spinal-epidural labor analgesia were randomly divided into three groups. Group C received l mL saline (0.9%) intrathecally, Group D received 5 µg Dex intrathecally, and Group S received 5 µg sufentanil intrathecally. All parturient women then received 0.1% epidural ropivacaine and 0.2 µg/mL sufentanil for patient-controlled epidural analgesia with standard settings. The visual analog scale score, onset time, duration of intrathecal injection, local anesthetic requirements, and side effects were recorded. Results The labor analgesia effects in Groups D and S were better than those in Group C. Groups D and S displayed significantly shorter onset times, longer durations of intrathecal injection, and reduced local anesthetic requirements compared with Group C. The incidence of shivering and pruritus in Group D was lower than that in Group S. Conclusion Intrathecal administration of 5 µg Dex could improve epidural labor analgesia effects. This randomized controlled clinical trial was registered with the Chinese Clinical Registry Center (ChiCTR-1800014943, http://www.chictr.org.cn/ ).
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Pan, Hui-Lin, Shao-Rui Chen, and James C. Eisenach. "Role of Spinal NO in Antiallodynic Effect of Intrathecal Clonidine in Neuropathic Rats." Anesthesiology 89, no. 6 (1998): 1518–23. http://dx.doi.org/10.1097/00000542-199812000-00031.

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Background The role of spinal nitric oxide (NO) in neuropathic pain remains uncertain. Although intrathecal clonidine causes NO release in the spinal cord, the functional role of spinal NO in clonidine-produced analgesia has not been examined. The objectives of this study were to assess the role of spinal NO in maintenance of allodynia and to determine the role of spinal NO in the antiallodynic effect of intrathecal clonidine. Methods Allodynia was produced in rats by tight ligation of the left L5-L6 spinal nerves. Intrathecal catheters were inserted with tips in the lumbar intrathecal space. Mechanical allodynia was determined by application of von Frey filaments to the left hindpaw. In the first series of experiments, allodynia was assessed before and after intrathecal injection of saline, L-arginine, an NO donor (SNAP), two NO synthase inhibitors (TRIM and NMMA), or an NO scavenger (PTIO). In the second series of experiments, 20 microg of clonidine was injected intrathecally 15 min after intrathecal injection of saline, TRIM, NMMA, or PTIO. Results Allodynia was not affected significantly by intrathecal injection of L-arginine, SNAP, TRIM, NMMA, or PTIO. The antiallodynic effect produced by intrathecal injection of clonidine was attenuated significantly by pretreatment with TRIM, NMMA, or PTIO. Conclusions These results demonstrate that spinal NO neither contributes significantly to maintenance of allodynia nor produces detectable antiallodynic effect in this neuropathic pain model. Furthermore, this study provides functional evidence that spinal NO plays an important role in the antiallodynic effect of intrathecal clonidine in neuropathic pain.
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Ouyang, Handong, Peizong Wang, Wan Huang, Qiang Li, Bilin Nie, and Weian Zeng. "Spinal Antinociceptive Action of Amiloride and Its Interaction with Tizanidine in the Rat Formalin Test." Pain Research and Management 20, no. 6 (2015): 321–26. http://dx.doi.org/10.1155/2015/902914.

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BACKGROUND: Amiloride has been reported to produce a wide variety of actions, thereby affecting several ionic channels and a multitude of receptors and enzymes. Intrathecal α2-adrenergic receptor agonists produce pronounced analgesia, and amiloride modulates α2-adrenergic receptor agonist binding and function, acting via the allosteric site on the α2A-adrenergic receptor.OBJECTIVES: To investigate the antinociceptive interaction of intrathecal amiloride and the α2-adrenoceptor agonist tizanidine using a rat formalin test.METHODS: Sprague-Dawley rats were chronically implanted with lumbar intrathecal catheters and were tested for paw flinching using formalin injection. Biphasic painful behaviour was recorded. Amiloride, tizanidine or an amiloride-tizanidine mixture was administered 10 min before formalin injection. To characterize any interactions, isobolographic analysis was performed. The effects of a pretreatment using intrathecally administered yohimbine was also tested.RESULTS: Intrathecally administered amiloride (12.5 μg to 100 μg) and tizanidine (0.5 μg to 5 μg), given separately, produced a significant dose-related suppression of the biphasic responses in the formalin test. Isobolographic analysis revealed that the combination of intrathecal amiloride and tizanidine synergistically reduced phase I and II activities. Intrathecally administered yohimbine antagonized or attenuated the antinociceptive effect of amiloride, tizanidine and the amiloride-tizanidine mixture. Intrathecally administered amiloride synergistically interacts with tizanidine to reduce the nociceptive response in the formalin test, most likely by activating α2-adrenoceptors in the spinal cord.CONCLUSIONS: Although intrathecal tizanidine produced pronounced analgesia, antinociceptive doses of intrathecal tizanidine also produced several side effects, including bradycardia and sedation. Amiloride produced antinociceptive action against the thermal nociceptive test without side effects in rats.
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Pan, Hui-Lin, Shao-Rui Chen, and James C. Eisenach. "Intrathecal Clonidine Alleviates Allodynia in Neuropathic Rats." Anesthesiology 90, no. 2 (1999): 509–14. http://dx.doi.org/10.1097/00000542-199902000-00027.

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Background Intrathecally administered clonidine increases release of spinal acetylcholine, which may be related to its analgesic action in neuropathic pain. The current study determined the role of spinal muscarinic and nicotinic receptors in the antiallodynic effect of intrathecally administered clonidine in spinal nerve-ligated rats. Methods Allodynia was produced in rats by ligation of the left L5-L6 spinal nerves. Mechanical allodynia was determined by application of von Frey filaments to the left hindpaw. The effect of intrathecal injection of saline, two muscarinic receptor antagonists (atropine and scopolamine), and two nicotinic receptor antagonists (mecamylamine and hexamethonium) on the antiallodynic action produced by intrathecal administration of 20 microg clonidine was assessed in six groups of animals. Each group consisted of six to eight rats. Results Intrathecal injection of saline or muscarinic or nicotinic receptor antagonists did not alter the withdrawal thresholds. The antiallodynic effect produced by intrathecally administered clonidine was attenuated in a dose-dependent manner by intrathecal treatment with muscarinic and nicotinic antagonists. Although nicotinic receptor antagonists only partially attenuated the effect of clonidine, blockade of spinal muscarinic receptors almost abolished the antiallodynic effect of clonidine. Conclusions These results demonstrate that the analgesic effect of intrathecally administered clonidine on neuropathic pain is mediated by spinal muscarinic and nicotinic receptors. Therefore, this study provides functional evidence that spinally released acetylcholine plays a role in the antiallodynic effect of intrathecally administered clonidine in neuropathic pain.
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Guo, Tian-Zhi, Jian-Yu Jiang, Ann E. Buttermann, and Mervyn Maze. "Dexmedetomidine Injection into the Locus Ceruleus Produces Antinociception." Anesthesiology 84, no. 4 (1996): 873–81. http://dx.doi.org/10.1097/00000542-199604000-00015.

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Background Alpha(2)-Adrenergic agonists such as clonidine and dexmedetomidine are known to produce sedation and analgesia in humans. The sedative effect of these agents is thought to occur through supraspinal pathways, involving the locus ceruleus (LC) and its projections in rats. While the antinociceptive response to alpha(2) agonists, given intrathecally, is mediated predominantly in the spinal cord, other sites of action have not been systematically studied. The authors examined whether alpha(2)-adrenergic receptors in the LC mediate an antinociceptive effect. Methods For administration of different drugs into the LC, guide cannulas were placed with their tips in the LC in male Sprague-Dawley rats. Dexmedetomidine (3.5 micrograms/0.2 microliter) was microinjected into the LC through the cannula, or given systemically by intraperitoneal injecton (50 micrograms/kg). The antinociceptive effect of dexmedetomidine was measured using the tail-flick latency response. To determine the sites through which dexmedetomidine injection into the LC produces antinociception, the authors examined whether this response could be perturbed by the specific alpha(2)-adrenergic antagonists atipamezole and L659,066 and pertussis toxin administered either into the LC or intrathecally before injection of dexmedetomidine systemically or directly into the LC. To eliminate the possibility that drug administered in one site (LC or intrathecal) could reach the other site, the dispositional characteristics of radiolabeled dexmedetomidine (LC) or atipamezole (intrathecal) were studied. Results Dexmedetomidine placed into the LC produces a dose-dependent increase in the tail-flick latency. This antinociceptive effect was blocked by pertussis toxin and by the alpha(2) antagonists atipamezole and L659,066 placed in the LC. Intrathecal administration of atipamezole and pertussis toxin also blocked the antinociceptive effect of dexmedetomidine placed in the LC. (3)H-dexmedetomidine introduced into the LC did not reach the spinal cord in pharmacologically active concentrations; also, intrathecally administered (3)H-atipamezole did not reach the LC in appreciable amounts. The systemic administration of dexmedetomidine produced an increase in tail-flick latency, and this effect was attenuated by the injection of atipamezole and L659,066 into the LC. Conclusions Part of the mechanism by which dexmedetomidine produces an antinociceptive effect is by an action directly on the LC, demonstrated by these studies in which antinociception produced by injection of this drug into the LC can be blocked by specific alpha(2) antagonists injected into the LC. Furthermore, the action of dexmedetomidine in the LC in turn may result in an increase in activation of alpha(2) adrenoceptors in the spinal cord, because the antinociceptive effect of LC dexmedetomidine injection also can be blocked by intrathecal injection of antipamezole and pertussis toxin.
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Gordin, Vitaly. "Gadolinium Encephalopathy After Intrathecal Gadolinium Injection." Pain Physician 5;13, no. 5;9 (2010): E321—E326. http://dx.doi.org/10.36076/ppj.2010/13/e321.

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Background: Gadolinium-induced encephalopathy is a well documented complication due to the inadvertent entrance of a high dose of gadolinium into the intrathecal compartment. In lab animals, injecting gadolinium into the intrathecal compartment resulted in neurotoxicity and seizures. It is also well recognized that the presence of autologous blood in the intrathecal compartment can cause a broad range of neurological changes that can include seizures and mental status changes. At the time of writing this report, there were no references in the literature of simultaneous injection of gadolinium and blood into the subarachnoid space. Case: We present a case of a patient who received a high dose of gadolinium in the epidural space for needle placement confirmation during a fluoroscopically-guided epidural steroid injection for the treatment of lumbar radiculopathy. The injection was complicated by a wet tap necessitating an epidural blood patch for post-dural puncture headache. Shortly after the injection of the autologous blood, the patient developed grand-mal seizures and mental status changes requiring endotracheal intubation and admission to an intensive care unit. We describe the clinical course and management, as well as brain MRI findings and cerebrospinal fluid (CSF) changes. The patient made a complete recovery and was discharged. Conclusion: This case reinforces the need for using a low dose of gadolinium for the confirmation of needle placement in the epidural space, especially in procedures that carry the risk of inadvertent intrathecal injection. We attribute these findings to inadvertent simultaneous intrathecal injection of high dose gadolinium and autologous blood. A literature review of the cases of gadolinium-induced encephalopathy is provided followed by discussion. Key words: Postdural puncture headache, epidural blood patch, intrathecal gadolinium, seizures, mental status changes, encephalopathy
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Zada, Gabriel, and Thomas C. Chen. "A Novel Method for Administering Intrathecal Chemotherapy in Patients With Leptomeningeal Metastases and Shunted Hydrocephalus: Case Report." Operative Neurosurgery 67, no. 3 (2010): ons. http://dx.doi.org/10.1227/01.neu.0000383138.78632.ba.

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Abstract BACKGROUND AND IMPORTANCE: Leptomeningeal metastatic disease occurs in a minority of patients with systemic neoplastic disease. Before the initiation of intrathecal chemotherapy, hydrocephalus must be addressed with a cerebrospinal fluid (CSF)-diverting shunt. CSF diversion can theoretically prematurely divert chemotherapeutic drugs that are administered intrathecally, thereby potentially reducing the efficacy of such treatments. CLINICAL PRESENTATION: We report on a patient with leptomeningeal disease and hydrocephalus secondary to metastatic bladder carcinoma requiring insertion of a programmable ventriculoperitoneal shunt and intrathecal chemotherapy. A novel method was utilized to administer intrathecal chemotherapy, in which the valve pressure setting was transiently increased during a 4-hour treatment session for intrathecal chemotherapy. No clinical complications occurred. Nuclear imaging was obtained sequentially after the injection of indium tracer into the ventricular system with the programmable valve at its baseline setting as well as at a maximal pressure setting. In the maximal valve setting condition, reduced outflow of nuclear tracer was observed at 1.5 and 4 h after injection, and normalized by 24 hours after injection. CONCLUSION: Programmable shunt valves can be utilized in a safe, controlled fashion to treat hydrocephalus associated with leptomeningeal disease, as well as regulate the outflow of CSF and minimize diversion of intrathecal chemotherapeutic agents.
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Lonjaret, L., T. Geeraerts, J.-F. Albucher, et al. "Early Encephalic Toxicity after Inadvertent Intrathecal Injection of Low Osmolar Contrast Medium." Neuroradiology Journal 25, no. 2 (2012): 222–24. http://dx.doi.org/10.1177/197140091202500212.

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Only nonionic contrast media are allowed for intrathecal use because of their lower neurotoxicity. In case of inadvertent intrathecal administration of an ionic contrast medium, the typical following syndrome is called ascending tonic clonic seizure syndrome. We describe the case of a 61-year-old woman with low back pain who underwent myelography. Ioxaglate, a water-soluble ionic low osmolar contrast medium was accidentally injected intrathecally. She first presented encephalic signs of neurotoxicity, followed by opisthotonic spasms and respiratory distress. In our case, ioxaglate is a low osmolar agent, leading to early encephalic toxicity (preceding medullary signs), because of its cephalic migration. The patient was successfully treated by sedation, anticonvulsant therapy and fluid hydration. Intrathecal administration of an ionic contrast medium is clearly contraindicated. In case of inadvertent injection of a low osmolar product, encephalic signs are seen first.
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Dissertations / Theses on the topic "Intrathecal injection"

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DUALE, CHRISTIAN JEAN. "Effets analgesiques du midazolam intrathecal : etude experimentale chez le rat." Clermont-Ferrand 1, 1991. http://www.theses.fr/1991CLF13829.

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Machino, Masaaki, Yasutsugu Yukawa, Tetsuro Hida, et al. "A Prospective Randomized Study for Postoperative Pain Relief of Lower Extremity Fractures: Efficacy of Intrathecal Morphine Administration." Nagoya University School of Medicine, 2010. http://hdl.handle.net/2237/14176.

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Moroto, Denise. "A dexametasona administrada pela via subaracnoidea é toxica à medula espinal e meninges de coelhos?" Universidade Estadual Paulista (UNESP), 2018. http://hdl.handle.net/11449/153620.

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Submitted by DENISE MOROTO (de_moroto@hotmail.com) on 2018-04-18T15:30:46Z No. of bitstreams: 1 Tesev6.pdf: 9989693 bytes, checksum: b1f5424e844b4857860140c0b71b3cca (MD5)<br>Rejected by Luciana Pizzani null (luciana@btu.unesp.br), reason: Solicitamos que realize uma nova submissão seguindo as orientações abaixo: Necessário fazer as seguintes correções no arquivo submetido: problema 1: o arquivo submetido não contém capa padrão, item obrigatório de acordo com as normas do seu programa. Assim que tiver efetuado as correções submeta o arquivo em PDF novamente. Agradecemos a compreensão. on 2018-04-19T13:02:09Z (GMT)<br>Submitted by DENISE MOROTO (de_moroto@hotmail.com) on 2018-04-19T14:03:21Z No. of bitstreams: 1 Tesev7.pdf: 10060555 bytes, checksum: bf4975d0b77a02d79ca9201cb11a74b8 (MD5)<br>Approved for entry into archive by Luciana Pizzani null (luciana@btu.unesp.br) on 2018-04-19T14:53:49Z (GMT) No. of bitstreams: 1 moroto_d_dr_bot.pdf: 10060555 bytes, checksum: bf4975d0b77a02d79ca9201cb11a74b8 (MD5)<br>Made available in DSpace on 2018-04-19T14:53:49Z (GMT). No. of bitstreams: 1 moroto_d_dr_bot.pdf: 10060555 bytes, checksum: bf4975d0b77a02d79ca9201cb11a74b8 (MD5) Previous issue date: 2018-02-21<br>Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)<br>Introdução: Dor perioperatória desencadeia resposta neuroendócrina ao estresse, responsável por efeitos adversos em vários órgãos e sistemas. Estratégias foram desenvolvidas para controle da dor e dessa resposta ao trauma, como a injeção de dexametasona, glicocorticoide de alta potência, no espaço peridural e subaracnoideo. Embora a injeção de corticosteroides no neuroeixo seja realizada com aparentes benefícios em seres humanos no contexto da dor aguda e crônica, a eficácia e segurança desse procedimento continuam discutíveis e alvo de controvérsia na literatura. O objetivo deste estudo foi avaliar os efeitos histológicos que a dexametasona administrada no espaço subaracnoideo determina sobre o tecido nervoso da medula espinal e das meninges dos coelhos. Método: Após aprovação pela Comissão de Ética no Uso de Animais, 28 coelhos adultos jovens foram randomizados em dois grupos (G) experimentais com 14 animais cada: G1 recebeu solução salina a 0,9% pela via subaracnoidea e G2, dexametasona na dose de 0,37 mg.kg-1. Os animais foram mantidos em cativeiro por 21 dias, durante os quais se avaliou motricidade e sensibilidade dolorosa. Depois desse período, sob anestesia venosa, foram submetidos a sacrifício para retirada da porção lombar e sacral da medula espinal e das meninges para avaliação histológica pelo método de Hematoxilina-eosina (HE) e de marcação imuno-histoquímica para Proteína Glial Fibrilar Ácida (GFAP). Resultados: Todos os animais permaneceram sem alterações clínicas durante o período de cativeiro. Nenhum animal do G1 apresentou alterações histológicas à microscopia óptica. No G2, 13 animais exibiram infiltrado inflamatório linfoplasmocitário perivascular nos vasos das meninges, com ou sem acometimento também das meninges e do parênquima nervoso. Os animais do G2 também tiveram percentual de células marcadas pelo GFAP inferior aos do G1 (p<0,05). Conclusão: Neste modelo experimental em coelhos, a solução de dexametasona determinou alterações histológicas no tecido nervoso da medula espinal e, principalmente, nas meninges.<br>Background: Perioperative pain triggers neuroendocrine response to stress, responsible for adverse effects on various organs and systems. Strategies were developed to control pain and this response to trauma, such as the injection of dexamethasone, a high-potency glucocorticoid, into the epidural and subarachnoid space. Although corticosteroid spinal injection is performed with apparent benefits in humans in the context of acute and chronic pain, the efficacy and safety of this procedure remain controversial in the literature. The objective of this study was to evaluate the histological effects that dexamethasone administered into the subarachnoid space determines on the nervous tissue of the spinal cord and the meninges of rabbits. Methods: After approval by the animal research ethics committee, 28 young adult rabbits were randomized in two experimental groups (G) with 14 animals each: G1 received 0.9% saline solution into the intrathecal space and G2 received 0.37mg.kg-1 of dexamethasone by the same route. The animals were clinically evaluated for 21 days. After this period of observation, sacrifice was performed under intravenous anesthesia and then the lumbar and sacral portion of their spinal cords were removed for histological examination by Hematoxylin-eosin (HE) and Glial Fibrillary Acidic protein (GFAP) immunohistochemical staining. Results: All animals remained without clinical changes during the period of captivity. No histological changes were observed in G1 animals. In G2, 13 animals exhibited perivascular lymphoplasmocytic inflammatory infiltrate in the meninges vessels, with or without involvement of the meninges and the nervous parenchyma. G2 animals also showed lower percentage of GFAP stained cells than rabbits of G1 (p<0.05). Conclusion: In this experimental model, the dexamethasone solution determined histological changes in the nervous tissue of the spinal cord and, especially, the meninges of rabbits.<br>FAPESP: 2014/23740-2
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Ratzlaff, Viviane. "Padronização e validação de um novo modelo de febre induzida pela injeção intratecal de prostaglandina e2 em ratos jovens." Universidade Federal de Santa Maria, 2006. http://repositorio.ufsm.br/handle/1/11148.

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The fever response, besides being part of host defense response to infection or inflammation, is associated with discomfort and anxiety and may constitute a risk for febrile seizures in children. Therefore, antipyretic therapy is routinely prescribed for febrile patients. The animal models of fever using the systemic injection of lipopolysaccharide (LPS) and Baker yeast, described in the literature, are suitable for screening of novel antipyretics, but they do not provide information regarding the mechanism of action of these compounds. Therefore, the present study aimed to describe and validate a model of fever induction by prostaglandin (PG) E2, the final mediator of febrile response in the central nervous system, in young male Wistar rats (25-30 days of age). In this protocol, PGE2 was injected intrathecally without implantation of cannula. Rectal temperature (TR) was recorded every thirty minutes for three hours after PGE2 injection (08:00 11:00 h). The intrathecal (i.t.) injection of PGE2 10 ηg in 100 μL/animal induced fever in the animals, which was prevented by administration of EP1 and EP3 receptors antagonists, but did not by antagonist of EP4 receptor. In addition, the classic antipyretics dipyrone and acetaminophen, at doses that had no effect per se on TR of animals, did not revert the fever induced by i.t. injection of PGE2. This model seems suitable to investigate whether the action of antipyretics occurs upstream or downstream the prostaglandin coupling in EP receptors. In addition, this protocol is advantageous from the technical, ethical and economical point of view compared to others PGE2-induced fever protocols described in the literature, because trepanation for cannula implantation is not required, reducing the inflammatory response, animals suffering and experimental costs.<br>A febre, apesar de fazer parte da resposta de defesa do hospedeiro à infecção ou inflamação, está associada com desconforto e ansiedade, além de representar um risco iminente de convulsões febris em crianças. Por isso, terapia antipirética é rotineiramente prescrita a pacientes febris. Os modelos animais de febre empregando a injeção sistêmica de lipopolissacarídeo (LPS) e fermento de padeiro, descritos na literatura, são úteis para a triagem de novos antipiréticos, mas não fornecem informações a respeito do mecanismo de ação desses compostos. Diante disso, o presente estudo objetivou padronizar e validar um modelo de indução de febre por prostaglandina (PG) E2, o mediador final da resposta febril no sistema nervoso central, em ratos machos jovens da raça Wistar (25-30 dias). Neste protocolo, a PGE2 foi injetada pela via intratecal (i.t.), não necessitando a implantação de cânula. A temperatura retal (TR) foi registrada a cada trinta minutos durante três horas após a injeção da PGE2 (08:00-11:00 h). A injeção i.t. de PGE2 10 ηg em 100 μL/animal induziu febre nos animais, a qual foi prevenida pela administração de antagonistas dos receptores EP1 e EP3, mas não por antagonista do receptor EP4. Além disso, os antipiréticos clássicos dipirona e paracetamol, em doses que não tiveram efeito per se na TR dos animais, não reverteram a febre induzida por PGE2 i.t. Este modelo parece útil para investigar se a ação dos antipiréticos ocorre antes ou depois da ligação da PGE2 em seus receptores EP. Além disso, este protocolo é vantajoso do ponto de vista técnico, ético e econômico em relação aos outros protocolos de indução de febre por PGE2 descritos na literatura, porque a trepanação para implantação de cânula não é necessária, reduzindo a resposta inflamatória, o sofrimento dos animais e os custos experimentais.
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Rane, Lindgren Kerstin. "Intrathecal adenosine for treatment of acute pain : safety assessments and evaluation in experimental, surgical and labour pain /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-750-9.

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Maher, Sue Ellen. "A study of the antinociceptive and toxicological effects of intrathecal dexmedetomidine and methoxamine in the rat." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0003/MQ34204.pdf.

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Charpentier, Éric. "Acropathie ulcero-mutilante par arachnoidite de la queue de cheval apres injections intrathecales d'hydrocortisone : a propos d'une observation." Nancy 1, 1991. http://www.theses.fr/1991NAN11105.

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Lionnet, Ludivine. "Administration d'Eugénol intrathécal pour le traitement de la douleur neuropathique." Thèse, 2009. http://hdl.handle.net/1866/3724.

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Le projet porte sur l’étude de l’effet de l’eugénol, composant principal du clou de girofle, sur la douleur neuropathique. L’objectif principal du projet était de déterminer la contribution du système nerveux central dans l’effet analgésique de l’eugénol. Lors d’une étude préliminaire, la pénétrabilité de l’eugénol a été évaluée dans le système nerveux central du rat. Des échantillons de sang, de cerveau et de moelle épinière ont été prélevés et les concentrations d’eugénol dans ces différents tissus ont été analysées à l’aide d’un spectromètre de masse. Les résultats ont montré que l’eugénol pénètre bien le système nerveux central avec une distribution plus importante dans la moelle épinière. Après l’induction de la douleur neuropathique à des rats Sprague-Dawley par le modèle de ligatures du nerf sciatique, des injections intrathécales d’eugénol furent réalisées afin d’évaluer l’effet central de l’eugénol. La plus forte dose d’eugénol a atténué l’allodynie secondaire après 15min, 2h et 4h et a aussi amélioré l’hyperalgésie thermique après 2h et 4h. Ces résultats confirment l’hypothèse que l’eugénol atténue les deux aspects de la douleur neuropathique que sont l’allodynie et l’hyperalgésie. Les injections au niveau lombaire permettent de penser que l’eugénol, un agoniste/antagoniste des récepteurs vanilloïdes pourrait diminuer la douleur neuropathique en agissant notamment au niveau des récepteurs vanilloïdes situés dans la corne dorsale de la moelle épinière.<br>The project is based on the study of the effects of eugenol, the main component of clove oil, on neuropathic pain. The main objective was to determine the central effect of eugenol. In a preliminary study we evaluated the penetrability of eugenol in the central nervous system of rats. Blood, brain and spinal cord samples were collected and concentrations were determined by mass spectrometry. Brain-toplasma and spinal cord-to-plasma ratios suggest that eugenol penetrates the central nervous system of rats relatively well, with a preferential distribution in the spinal cord. Following the induction of neuropathic pain in male Sprague-Dawley rats using the sciatic nerve ligation model, intrathecal injections of eugenol were done to evaluate the central effect of eugenol. Treatment with the high dose of eugenol significantly decreased secondary mechanical allodynia measured by the Von Frey test after 15min, 2h and 4h and improved thermal hyperalgesia measured by the Hargreaves device after 2h and 4h. Results support the hypothesis that eugenol may alleviate neuropathic pain, both allodynia and hyperalgesia. Eugenol, a vanilloid agonist/antagonist may therefore reduce neuropathic pain by acting on vanilloid receptors at the level of the dorsal horn of the spinal cord.
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Books on the topic "Intrathecal injection"

1

Gianino, Janet M. Intrathecal drug therapy for spasticity and pain: Practical patient management. Springer, 1996.

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McClenahan, Maureen F., and William Beckman. Pain Management Techniques. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190217518.003.0011.

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This chapter provides a broad review of various interventional pain management procedures with a focus on indications, anatomy, and complications. Specific techniques reviewed include transforaminal epidural steroid injection, lumbar sympathetic block, stellate ganglion block, cervical and lumbar radiofrequency ablation, gasserian ganglion block, sacroiliac joint injection, celiac plexus block, lateral femoral cutaneous nerve block, ilioinguinal block, lumbar medial branch block, obturator nerve block, ankle block, occipital nerve block, superior hypogastric plexus block, spinal cord stimulation, and intrathecal drug delivery systems. The chapter reviews contrast agents, neurolytic agents, botulinum toxin use, corticosteroids, and ziconotide pharmacology and side effects in addition to diagnosis and management of local anesthetic toxicity syndrome. It also discusses indications for neurosurgical techniques including dorsal root entry zone lesioning. In addition, information on radiation safety and the use of anticoagulants with neuraxial blocks is covered.
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Paech, Michael J., and Patchareya Nivatpumin. Postdural puncture headache. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0027.

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Postdural puncture headache (PDPH) may follow either deliberate or unintentional (accidental) penetration of the interdigitating meninges, the dura and arachnoid mater. It is one of the most common and clinically important complications of regional anaesthesia and analgesia in the obstetric population. The headache develops as a consequence of cerebrospinal fluid loss, low intracranial pressure and cerebrovascular changes in the upright position and can prove debilitating. The diagnosis is clinical, making thorough assessment and regular review all the more important, to revise treatment plans, exclude rare serious pathology such as subdural haematoma, and avoid misdiagnosis. This chapter reviews the pathophysiology, incidence, risk factors (needle, technical and patient related), features, natural history, diagnosis, and management of PDPH. High level evidence supports prevention by using small gauge, non-cutting spinal needles, but other preventative strategies against either unintentional dural puncture or PDPH are poorly supported. The absent or poor efficacy of measures such as bed rest, hydration, cerebral vasoconstrictor therapy, epidural or intrathecal saline injection, intrathecal catheter placement or prophylactic epidural blood patch, is noted. Validation of better evidence supporting epidural morphine or intravenous cosyntropin is required. Symptomatic treatment of PDPH is also unreliable. Very limited evidence that requires substantiation supports a modest benefit from caffeine, gabapentinoids or intravenous hydrocortisone. The intervention of epidural blood patch is highly likely to relieve post-spinal PDPH, but only completely resolves epidural needle-induced PDPH in 30–50% of cases. Much detail about EBP remains undetermined, but delayed intervention and injection of approximately 20 mL of autologous blood appear appropriate.
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(Preface), R. D. Penn, ed. Intrathecal Drug Therapy for Spasticity and Pain: Practical Patient Management. Springer, 1995.

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Andrew, Koman L., Smith Beth Paterson, and Kolaski Kat, eds. Management of spasticity in cerebral palsy: The role of intrathecal baclofen. Data Trace Pub., Co., 2005.

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Koman, L. Andrew. Management of Spasticity in Cerebral Palsy: The Role of Intrathecal Baclofen. Data Trace Pub. Co., 2005.

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Book chapters on the topic "Intrathecal injection"

1

Herndon, Robert M. "The Medical Uses of Injection into the Cerebrospinal Fluid Space (Intrathecal and Intraventricular Injection)." In The Cerebrospinal Fluid. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1591-9_5.

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Peterson, Cristina D., Alexander G. J. Skorput, Kelley F. Kitto, George L. Wilcox, Lucy Vulchanova, and Carolyn A. Fairbanks. "AAV-Mediated Gene Delivery to the Spinal Cord by Intrathecal Injection." In Methods in Molecular Biology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9139-6_11.

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Kemshead, J. T., K. I. Hopkins, and C. L. Chandler. "Treatment of Diffuse Leptomeningeal Malignancy by Intrathecal Injection of 131I Radioimmunoconjugates." In Systemic Radiotherapy with Monoclonal Antibodies. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79952-5_10.

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Schwarz, M., T. Klockgether, L. Turski, and K. H. Sontag. "Intrathecal Injection of Antispastic Drugs in Rats: Muscle Relaxant Action of Midazolam, Baclofen, 2-Aminophosphonoheptanoic Acid (AP7) and Tizanidine." In Local-spinal Therapy of Spasticity. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-72954-6_6.

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Petitjean, P., P. Mouchet, G. Pellissier, M. Manier, C. Feuerstein, and P. Demenge. "Cardio-vascular Effects of Intrathecal Thoracic Injections of Apomorphine." In Dopaminergic Systems and their Regulation. Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-07431-0_80.

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"Intrathecal Injection." In Encyclopedia of Pain. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_201081.

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"Intrathecal Administration of Local Anesthetics and Glucocorticoids." In Spinal Injection Techniques, edited by Theodoros Theodoridis and Juergen Kraemer. Georg Thieme Verlag, 2009. http://dx.doi.org/10.1055/b-0034-66346.

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McCutchen, Thomas, and J. C. Gerancher. "Epidural Anesthesia: Unintended Intrathecal Injection." In Complications in Anesthesia. Elsevier, 2007. http://dx.doi.org/10.1016/b978-1-4160-2215-2.50064-8.

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"Medical procedure for intrathecal baclofen trial injection." In Spasticity Management. CRC Press, 2006. http://dx.doi.org/10.3109/9780203090541-18.

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Lazar, Alina. "Spinal Anesthesia." In Pediatric Anesthesia Procedures, edited by Anna Clebone and Barbara K. Burian. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190685188.003.0010.

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Spinal anesthesia is the injection of local anesthetics and additives into the subarachnoid space, providing analgesia by creating a sensory block and providing suitable surgical conditions by creating a motor block. In the pediatric population, spinal “intrathecal” anesthesia can be used as an alternative to general anesthesia for lower extremity and abdominal surgery in high-risk patients (e.g., premature or former premature infants, teenagers with malignant hyperthermia susceptibility or chronic respiratory disease). Preservative-free morphine injected into the intrathecal space can also be used for postoperative pain control, for example, after scoliosis repair.
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Conference papers on the topic "Intrathecal injection"

1

Sutherland, Emily, Jonathan Baird-Gunning, Laura Rudaks, Natalie Palavra, Michal Lubomski, and Martin Krause. "075 Gadolinium encephalopathy presenting as status epilepticus following intrathecal injection." In ANZAN Annual Scientific Meeting 2021 Abstracts. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/bmjno-2021-anzan.75.

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Liu, James, Phabinly Gabriel, Gurkirat Kohli, and Jean Eloy. "Direct Orbital Injection of Intrathecal Fluorescein to Identify Orbital Defect Causing Postoperative Pneumocephalus." In 29th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679653.

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Lueshen, Eric, Indu Venugopal, and Andreas Linninger. "Intrathecal Magnetic Drug Targeting: A New Approach to Treating Diseases of the Central Nervous System." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93117.

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Intrathecal (IT) drug delivery is a standard technique which involves direct injection of drugs into the cerebrospinal fluid (CSF)-filled space within the spinal canal to treat many diseases of the central nervous system. Currently, in order to reach the therapeutic drug concentration at certain locations within the spinal canal, high drug doses are used. With no method to deliver the large drug doses locally, current IT drug delivery treatments are hindered with wide drug distributions throughout the central nervous system (CNS) which cause harmful side effects. In order to overcome the current limitations of IT drug delivery, we have developed the novel method of intrathecal magnetic drug targeting (IT-MDT). Gold-coated magnetite nanoparticles are infused into a physiologically and anatomically relevant in vitro human spine model and then targeted to a specific site using external magnetic fields, resulting in a substantial increase in therapeutic nanoparticle localization at the site of interest. Experiments aiming to determine the effect of key parameters such as magnet strength, duration of magnetic field exposure, location of magnetic field, and ferrous implants on the collection efficiency of our superparamagnetic nanoparticles in the targeting region were performed. Our experiments indicate that intrathecal magnetic drug targeting and implant-assisted IT-MDT are promising techniques for concentrating and localizing drug-functionalized nanoparticles at required target sites within the spinal canal for potential treatment of diseases affecting the central nervous system.
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Shokuhfar, T., P. Nazari, S. Ansari, et al. "P-018 Transforaminal intrathecal access for injection of nusinersen in children with spinal muscular atrophy." In SNIS 15TH ANNUAL MEETING, July 23–26, 2018, Hilton San Francisco Union Square San Francisco, CA. BMJ Publishing Group Ltd., 2018. http://dx.doi.org/10.1136/neurintsurg-2018-snis.54.

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Matchynski, James, Rayyan Manwar, Karl Kratkiewicz, et al. "Photoacoustic imaging of fear conditioning neuronal ensembles using a Fos-Lacz gene reporter system in the rat brain in vivo after intrathecal X-gal injection." In Neural Imaging and Sensing 2021, edited by Qingming Luo, Jun Ding, and Ling Fu. SPIE, 2021. http://dx.doi.org/10.1117/12.2579526.

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Gutierrez, Maya, Emmanuelle Mouret Fourme, Emilie Le Rhun, et al. "Abstract P5-19-17: Final results of the phase I "HIT" study: A multicenter phase I-II study evaluating trastuzumab administered by intrathecal injection for leptomeningeal meningitis of HER2+ metastatic breast cancer (MBC)." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p5-19-17.

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Reports on the topic "Intrathecal injection"

1

Koiro, Brenda J. The Effect of the Time of Injection of Intrathecal Analgesia on the Length of Early and Advanced Labor. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ad1012145.

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