Bladder function during lumbar myelography. An experimental investigation in cats.
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Anesthesia, Spinal↗
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Results for “Injections, Spinal”
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Patient-controlled spinal analgesia for postoperative pain control.
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Aged↗
Intrathecal meperidine and shivering in obstetric anesthesia.
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Adult↗
Continuous Intrathecal Infusion of Nivolumab in Advanced Melanoma With Concomitant Leptomeningeal Disease: Efficacy, Safety, and Pharmacokinetics.
BACKGROUND AND OBJECTIVES: Prognosis of melanoma with leptomeningeal disease (LMD) is poor (median overall survival of 5.1 months). Intrathecal (IT) nivolumab appears safe, although its efficacy remains uncertain. We investigated the feasibility, safety, and efficacy of continuous IT nivolumab. METHODS: This was a retrospective analysis of 11 melanoma patients with progressive LMD (MelBase; NCT02828202) treated as part of the patients' care with continuous IT nivolumab administered through spinal (n = 10) or ventricular catheter (n = 1). RESULTS: Patients (5 women, median age 52) with Eastern Cooperative Oncology Group ≤1 (except for 1) and stable extracranial disease (except for 4) were treated over a median duration of 1.5 months and followed for 2.5 months. Seven presented symptomatic LMD. Primary tumors were mostly cutaneous (n = 8) and BRAF-mutated (n = 10). All patients had progressed on systemic immunotherapy; 7 had received brain radiotherapy (whole brain radiotherapy [n = 3]; stereotactic radiosurgery [n = 4]). Concomitant therapies included corticosteroids >10 mg (n = 5), intravenous nivolumab (first 3 months of IT therapy, n = 1), and targeted therapies (n = 7). The median overall survival was 2.5 months, with 3 patients surviving for more than a year. Reversible treatment-related adverse events occurred in 5 patients: meningoencephalitis (grade 3, n = 1), intracranial hemorrhage (grade 1, n = 1), intracranial hypotension (grade 2, n = 2; grade 1, n = 1). Baseline levels of nivolumab in the cerebrospinal fluid (CSF) were <2 µg/mL, even among patients with plasma detection. CSF concentrations of nivolumab at steady state varied from 36 to 97 µg/mL, with clearances of 4.3-15.7 mL/h. Next-generation sequencing identified CSF genomic profiles correlating with clinical progression in 4 patients. CONCLUSION: These findings warrant further trials on IT nivolumab.
Humans↗
[Intrathecal 2% tetracaine causes mild histological lesions in the spinal cord without detectable sensory deficits on paw stimulation test in rats].
The purpose of this study is to determine if intrathecal 2% tetracaine (TC) causes histological changes by its neurotoxicity, and to examine the relationship between the lesions and neurological functions. Twenty-two rats received either 2% TC or 0% TC dissolved in 10% glucose, via an intrathecal catheter terminated at T 13 level. Neurological deficits were evaluated by rat's behavior and paw stimulation test (UCSF). Five days after drug administration, the L 1 spinal cord with the anterior and posterior roots and cauda equina were excised for light and electron microscopy. Four rats out of 8 in 2% TC group showed mild pathological changes induced by neurotoxicity mainly in the posterior roots and slightly in the posterior column. However, there were no significant differences in sensory and behavioral function between the rats who had received 2% TC with lesion and the others with no lesion. As many rootlets enter one segment of the spinal cord, mild and restricted lesions may be difficult to detect by sensory tests. These findings may explain the fact that the patients with transient neurologic symptoms (TNS) are normal by neurological tests.
Anesthesia, Spinal↗
Somatostatin causes vasoconstriction, reduces blood flow and increases vascular permeability in the rat central nervous system.
Using radiolabeled microspheres, spinal cord blood flow was measured after spinal subarachnoid injections of 3.1- to 12.5-nmol doses of somatostatin through either indwelling i.t. catheters or acutely inserted intervertebral needles. With either injection technique, somatostatin caused significant dose-dependent reductions in thoracic and lumbosacral blood flow that could be partially blocked by a 5-min preinjection of the somatostatin receptor antagonist cyclo[7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)], which has previously been shown to block the hindlimb flaccidity produced by these doses of somatostatin in conscious rats. The duration of these blood flow changes were appreciably less in the rats injected through indwelling i.t. catheters. Somatostatin-induced reductions in spinal cord perfusion were accompanied by transient pressor responses, reduced cardiac output, 3-fold increases in spinal cord cerebrospinal fluid lactic acid concentrations and breakdown of the blood-spinal cord barrier, as reflected by significantly increased extravasation of [125I]bovine serum albumin. By 24 hr postinjection, a 12.5-nmol dose of somatostatin caused appreciable spinal cord cellular injury, as evidenced by significant elevations in cerebrospinal fluid concentrations of lactate dehydrogenase. After topical application to exposed pial vessels of the parietal cortex, comparable doses of somatostatin caused immediate intense dose-related arteriolar vasospasm and subsequent extravasation of the visible macromolecular tracer Evans blue dye. We conclude that somatostatin has significant vasoconstrictory effects on the blood vessels of the brain and spinal cord of the rat that must be recognized and appreciated when studying its neuropharmacological actions in vivo.
Animals↗
[Intrathecal meperidine on the effects of anesthesia and postoperative pain relief].
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Adult↗
[Drainage of the extradural space through the sacral canal].
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Anesthesia, Spinal↗
Subarachnoid bupivacaine increases human cerebrospinal fluid concentration of serotonin.
BACKGROUND AND OBJECTIVES: Serotonin (5-hydroxytryptamine [5-HT]) has antinociceptive properties at the spinal level. Activation of descending serotonergic neurons or topically applied 5-HT at the spinal cord inhibits rostral spread of sensory information. Epidural anesthesia has been shown to increase 5-HT in plasma, and local anesthetics may interfere with 5-HT reuptake and metabolism. For these reasons, the action of subarachnoid local anesthetics on cerebrospinal fluid (CSF) 5-HT concentrations has been studied. METHODS: Six volunteers received lumbar spinal anesthesia with 0.5% bupivacaine through subarachnoid catheters, and CSF and plasma 5-HT concentrations were determined radioenzymatically before and after anesthesia. RESULTS: Plasma 5-HT was unchanged, but CSF 5-HT increased by 300% after bupivacaine administration (P < .02). CONCLUSION: Subarachnoid bupivacaine increases local 5-HT concentration. This may have implications for nociceptive gating as well as for local vasoregulation.
Adult↗
Spinal morphine in remote practice.
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Analgesia, Obstetrical↗
Kainic acid injection in NTS evokes hypertension and c-fos expression in spinal cord.
Kainic acid injected into rat nucleus tractus solitarius (NTS) caused a slowly developing hypertension, with a 2-fold increase in Fos-immunoreactive (Fos-IR) nuclei in the area of the presympathetic bulbospinal neurons in the rostral ventrolateral medulla (RVLM) and a widespread activation of sympathetic preganglionic neurons (SPN) in the spinal cord, particularly in the mid to lower thoracic cord. The highest segmental concentration of Fos-IR SPN was in T8, with Fos-IR nuclei increased 12-fold compared with the vehicle injected group. More than 60% of retrogradely labelled sympathoadrenal neurons in T8 were Fos-IR after kainic acid injection, consistent with the 60-fold increases in plasma adrenaline levels observed in these rats.
Animals↗
Spinal anaesthesia: effect of the site of injection on the spread of analgesia.
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Anesthesia, Spinal↗
Studies of activated microglia and macrophages in lumbosacral spinal cord following an intraperitoneal injection of 6-aminonicotinamide into adult rats.
The anterior horns of the lumbosacral segment of the spinal cord in rats showed an extensive lesion following an intraperitoneal administration of 6-amino-nicotinamide (6-AN). Neuronal chromatolysis was observed in some of the large efferent neurons 1-7 days after the injection of 6-AN. The capability in their uptake of fluorogold and its retrograde transport was comparable to those in the normal rats. Small neurons presumably internuncial cells underwent degeneration. 8 weeks after 6-AN injection, all the surviving neurons appeared normal. 1 day after 6-AN injection microglial cells appeared activated as evidenced by the hypertrophy and expansion of their processes. A large number of macrophages were observed in the lesioned site 7 days after the administration of 6-AN. The activated microglia and macrophages showed intense immunoreactivity with the monoclonal antibody OX-42. The immunoreactivity declined with time so that by 4 weeks after the injection of 6-AN very weak immunoreactivity was seen on some very branched cells. A similar pattern of immunoreactivity was observed with the monoclonal antibodies OX-18 and OX-6. It was concluded from this study that neuronal chromatolysis and neuronal degeneration induced the expression of CR3 receptors (marked by OX-42) and MHC encoded antigens (marked by OX-18 and OX-6) in activated microglia and macrophages. With time the immunoreactivity decreased so that by 4 weeks after the administration of 6-AN only faint immunoreactivity was observed on some branched cells.(ABSTRACT TRUNCATED AT 250 WORDS)
6-Aminonicotinamide↗
Intramedullary injection of contrast into the cervical spinal cord during cervical myelography: a case report.
STUDY DESIGN: A case of iatrogenic intramedullary contrast injection during a C1-C2 cervical myelography is reported. OBJECTIVE: To investigate the occurrence of iatrogenic intramedullary contrast injection during a current C1-C2 cervical myelography. SUMMARY OF BACKGROUND DATA: Intramedullary injection of contrast is a rare but serious complication of C1-C2 cervical myelography that has not been reported since the widespread use of magnetic resonance imaging and the NASCIS III study protocol. METHODS: A 39-year-old woman received an iatrogenic intramedullary contrast injection during a C1-C2 cervical myelography. RESULTS: During the procedure the patient reported right-side face, neck, and arm pain and parethesias. After the procedure, right arm weakness and diffuse hyperreflexia developed. Postmyelography imaging demonstrated intramedullary contrast and cord swelling. High-dose methylprednisolone was administered intravenously and the patient's symptoms improved. The literature and management of this rare complication are reviewed. CONCLUSIONS: Intramedullary cord injection is a rare complication of cervical myelography. The mechanism of spinal cord injury appears to involve a combination of physical compression from the injected liquid and neurotoxicity of the contrast material. Iohexol rather than metrizamide should be used when C1-C2 myelography is indicated in patients who are unable to undergo magnetic resonance imaging, or those whose pathology is inadequately demonstrated magnetic resonance imaging alone. In the event of contrast injection into the spinal cord, administration of high-dose methylprednisolone is recommended.
Adult↗
c-Fos expression in the myenteric plexus, spinal cord and brainstem following injection of formalin in the rat colonic wall.
Fos expression induced by injection of dilute formalin (50 microl, 5% in physiological saline) into the colonic wall was examined in the myenteric plexus, lumbosacral spinal cord and brainstem of the rat. The aims of this study were (i) to determine whether neurons in these regions express Fos in response to the injection of formalin into the colon and (ii) to examine whether administration of an alpha 2 adrenoceptor agonist modulates Fos expression. Tissues were removed 2 h after the injection of saline or formalin. Saline injected in the colon induced Fos in enteric glia in the myenteric plexus. The number of Fos immunoreactive nuclei significantly increased in both myenteric neurons and enteric glia after the injection of formalin. Similarly, Fos immunoreactive neuronal nuclei were significantly increased in the spinal cord, area postrema and nucleus of the solitary tract after the injection of formalin. Pretreatment of rats with the alpha 2 adrenoceptor agonist xylazine (2, 4 and 8 mg/kg) 15 min before the injection of formalin, dose-dependently reduced the number of Fos immunoreactive neuronal and glial nuclei in the myenteric plexus, and neuronal nuclei in the spinal cord and brainstem. Simultaneous administration of xylazine (8 mg/kg) and the alpha 2 adrenoceptor antagonist yohimbine (1 mg/kg) reversed the effects of xylazine in the spinal cord and brainstem, but not in the myenteric plexus. These data show that injection of formalin in the colonic wall results in Fos expression in myenteric neurons and enteric glia, and neurons in the spinal cord and brainstem. This may be due to the direct chemical stimulation of the innervation of the colon and/or the subsequent acute colitis. The observed neuronal Fos expression can be modulated by an alpha 2 adrenoceptor agonist through noradrenergic pathways and/or reduction of the excitability of the enteric neural circuitry.
Adrenergic alpha-Agonists↗
c-Fos expression in the myenteric plexus, spinal cord and brainstem following injection of formalin in the rat colonic wall.
Fos expression induced by injection of dilute formalin (50 microl, 5% in physiological saline) into the colonic wall was examined in the myenteric plexus, lumbosacral spinal cord and brainstem of the rat. The aims of this study were (i) to determine whether neurons in these regions express Fos in response to the injection of formalin into the colon and (ii) to examine whether administration of an alpha 2 adrenoceptor agonist modulates Fos expression. Tissues were removed 2 h after the injection of saline or formalin. Saline injected in the colon induced Fos in enteric glia in the myenteric plexus. The number of Fos immunoreactive nuclei significantly increased in both myenteric neurons and enteric glia after the injection of formalin. Similarly, Fos immunoreactive neuronal nuclei were significantly increased in the spinal cord, area postrema and nucleus of the solitary tract after the injection of formalin. Pretreatment of rats with the alpha 2 adrenoceptor agonist xylazine (2, 4 and 8 mg/kg) 15 min before the injection of formalin, dose-dependently reduced the number of Fos immunoreactive neuronal and glial nuclei in the myenteric plexus, and neuronal nuclei in the spinal cord and brainstem. Simultaneous administration of xylazine (8 mg/kg) and the alpha 2 adrenoceptor antagonist yohimbine (1 mg/kg) reversed the effects of xylazine in the spinal cord and brainstem, but not in the myenteric plexus. These data show that injection of formalin in the colonic wall results in Fos expression in myenteric neurons and enteric glia, and neurons in the spinal cord and brainstem. This may be due to the direct chemical stimulation of the innervation of the colon and/or the subsequent acute colitis. The observed neuronal Fos expression can be modulated by an alpha 2 adrenoceptor agonist through noradrenergic pathways and/or reduction of the excitability of the enteric neural circuitry.
Journal Article↗
Sustained microglial immunoreactivity in the caudal spinal trigeminal nucleus after formalin injection.
Recent studies indicate that glia may be involved in altered nociceptive processing after a peripheral inflammatory lesion produced by injection of inflammatory reagents such as formalin and zymosan. Most of these studies, however, confined their observations to a period shortly after the injections. This study investigated the immunohistochemical responses of microglia in the caudal part of the spinal trigeminal nucleus for up to 60 days after subcutaneous injection of formalin into the lateral faces of Wistar rats. The results showed obvious up-regulation of microglial markers such as OX-18, OX-42 and OX-6 up to 21 days after formalin injection. These were somewhat reduced at 30 days after injection. Electron microscope investigation revealed no evidence of significant phagocytosis of degenerative neuronal elements by microglia in the nucleus at the time--that is, 7 days after formalin injection, when microglial activation was at its peak. Significantly, however, the period of microglial activation corresponded closely to that showing enhanced nociceptive behavior after perioral formalin injection (Cadet et al., 1995). This study indicates a microglial role in the genesis of enhanced nociceptive behavior.
Animals↗
[The effect of epidural saline injection on analgesic level during combined spinal and epidural anesthesia].
The purpose of this study is to clarify the volume effect of epidural saline injection 20 min after spinal anesthesia. Thirty patients undergoing combined spinal and epidural anesthesia for orthopedic surgery were randomly divided into two groups: a control group (n = 15) and a saline group (n = 15). In the control group, 2% lidocaine 3 ml with 0.4% tetracaine was injected into the subarachnoid space from L 4-5 interspace using Durasafe (Becton Dickinson, USA) and saline was not injected into the epidural space. In the saline group, saline 10 ml was injected through an epidural catheter 20 min after spinal anesthesia. The levels of analgesia 20 min after spinal anesthesia were not significantly different between the groups. However, the levels of analgesia 3, 5, 10, 40 and 100 min after epidural saline injection in the saline group were significantly higher than those in the control group (P < 0.05). The highest analgesic level was obtained 10 min after epidural saline injection and reached to T 4.3 +/- 1.1. In conclusion, epidural saline injection increases the analgesic level 20 min after spinal anesthesia because of the volume effect.
Adjuvants, Anesthesia↗