The Experts below are selected from a list of 12 Experts worldwide ranked by ideXlab platform
Kim J Burchiel - One of the best experts on this subject based on the ideXlab platform.
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inflammatory mass lesions associated with intrathecal Drug infusion catheters report and observations on 41 patients
Neurosurgery, 2001Co-Authors: Robert J Coffey, Kim J BurchielAbstract:OBJECTIVE: Several reports have described inflammatory mass lesions at the tip of Intraspinal Drug Administration catheters. We evaluated the number of patients reported with this condition and whether data support hypotheses that have been put forth regarding the cause of these lesions. METHODS: Information that was reported in the medical literature, and by Medtronic, Inc., to the United States Food and Drug Administration as of November 30, 2000, was reviewed. RESULTS: Forty-one cases were identified, including 16 from the literature and 25 that were not published previously in the literature. Because of voluntary reporting and other methodological limitations, the actual number of cases must be higher than reported. All of the patients had chronic pain. The mean duration of therapy was 24.5 months. Most masses were located in the thoracic region. Intrathecal Drugs included morphine or hydromorphone, either alone or mixed with other Drugs, in 39 of 41 cases. No masses were reported in patients who received baclofen as the only intrathecal medication. Thirty patients underwent surgery to relieve spinal cord or cauda equina compression. Eleven patients were nonambulatory at last follow-up, and one died of a pulmonary embolus. Surgical specimens revealed noninfectious chronic inflammation, granuloma formation, and fibrosis or necrosis. DISCUSSION: The most plausible hypothesis with regard to the cause of intrathecal catheter tip mass lesions implicates the Administration of relatively high-concentration or high-dose opiate Drugs or the use of Drugs and admixtures that are not labeled for intrathecal use. CONCLUSION: Patients who require high-dose Intraspinal opioid therapy and those who receive Drugs or admixtures that are not approved for intrathecal use should be monitored closely for signs of an extra-axial mass or catheter malfunction. Prompt diagnosis and treatment may preserve neurological function.
Robert J Coffey - One of the best experts on this subject based on the ideXlab platform.
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inflammatory mass lesions associated with intrathecal Drug infusion catheters report and observations on 41 patients
Neurosurgery, 2001Co-Authors: Robert J Coffey, Kim J BurchielAbstract:OBJECTIVE: Several reports have described inflammatory mass lesions at the tip of Intraspinal Drug Administration catheters. We evaluated the number of patients reported with this condition and whether data support hypotheses that have been put forth regarding the cause of these lesions. METHODS: Information that was reported in the medical literature, and by Medtronic, Inc., to the United States Food and Drug Administration as of November 30, 2000, was reviewed. RESULTS: Forty-one cases were identified, including 16 from the literature and 25 that were not published previously in the literature. Because of voluntary reporting and other methodological limitations, the actual number of cases must be higher than reported. All of the patients had chronic pain. The mean duration of therapy was 24.5 months. Most masses were located in the thoracic region. Intrathecal Drugs included morphine or hydromorphone, either alone or mixed with other Drugs, in 39 of 41 cases. No masses were reported in patients who received baclofen as the only intrathecal medication. Thirty patients underwent surgery to relieve spinal cord or cauda equina compression. Eleven patients were nonambulatory at last follow-up, and one died of a pulmonary embolus. Surgical specimens revealed noninfectious chronic inflammation, granuloma formation, and fibrosis or necrosis. DISCUSSION: The most plausible hypothesis with regard to the cause of intrathecal catheter tip mass lesions implicates the Administration of relatively high-concentration or high-dose opiate Drugs or the use of Drugs and admixtures that are not labeled for intrathecal use. CONCLUSION: Patients who require high-dose Intraspinal opioid therapy and those who receive Drugs or admixtures that are not approved for intrathecal use should be monitored closely for signs of an extra-axial mass or catheter malfunction. Prompt diagnosis and treatment may preserve neurological function.
A. Urban Höglund - One of the best experts on this subject based on the ideXlab platform.
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Spinal cholinergic involvement after treatment with aspirin and paracetamol in rats.
Neuroscience letters, 2004Co-Authors: Klas S P Abelson, Mahinda Kommalage, A. Urban HöglundAbstract:Aspirin and paracetamol have been shown to suppress non-inflammatory pain conditions like thermal, visceral and mechanical pain in mice and rats. The non-inflammatory antinociception appears to be mediated by central receptor mechanisms, such as the cholinergic system. In this study, we tested the hypothesis that the non-inflammatory antinociception of aspirin and paracetamol could be mediated by an increase of Intraspinal acetylcholine release. Microdialysis probes were placed Intraspinally in anesthetized rats for acetylcholine sampling. Subcutaneously administered aspirin 100 and 300 mg/kg increased, while paracetamol 300 mg/kg decreased Intraspinal acetylcholine release. Intraspinal Drug Administration did not affect acetylcholine release. Our results suggest that an increased Intraspinal acetylcholine release could be involved in part of the non-inflammatory pain suppression by aspirin, but not by paracetamol.
Klas S P Abelson - One of the best experts on this subject based on the ideXlab platform.
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Spinal cholinergic involvement after treatment with aspirin and paracetamol in rats.
Neuroscience letters, 2004Co-Authors: Klas S P Abelson, Mahinda Kommalage, A. Urban HöglundAbstract:Aspirin and paracetamol have been shown to suppress non-inflammatory pain conditions like thermal, visceral and mechanical pain in mice and rats. The non-inflammatory antinociception appears to be mediated by central receptor mechanisms, such as the cholinergic system. In this study, we tested the hypothesis that the non-inflammatory antinociception of aspirin and paracetamol could be mediated by an increase of Intraspinal acetylcholine release. Microdialysis probes were placed Intraspinally in anesthetized rats for acetylcholine sampling. Subcutaneously administered aspirin 100 and 300 mg/kg increased, while paracetamol 300 mg/kg decreased Intraspinal acetylcholine release. Intraspinal Drug Administration did not affect acetylcholine release. Our results suggest that an increased Intraspinal acetylcholine release could be involved in part of the non-inflammatory pain suppression by aspirin, but not by paracetamol.
Ryan W. Bavis - One of the best experts on this subject based on the ideXlab platform.
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Serotonin-dependent respiratory plasticity
Respiratory Research, 2001Co-Authors: Gordon S. Mitchell, Tracy L. Baker, David D. Fuller, Ryan W. BavisAbstract:Serotonin initiates neuroplasticity in a number of invertebrate and vertebrate experimental models. The first report of serotonin-dependent plasticity in respiratory motor control was a long-lasting facilitation of phrenic activity following episodic stimulation of chemoafferent neurons [1], a phenomenon now known as long-term facilitation (LTF). Recent progress has contributed considerably towards an understanding of the mechanisms and manifestations of this potentially important model of respiratory plasticity. In this presentation, recent progress in understanding the mechanism of LTF will be reviewed. In all studies, we exposed awake or anesthetized Sprague Dawley rats to episodic hypoxia as an experimental model of LTF. Both awake and anesthetized rats express LTF following episodic hypoxia. Intermittent, but not continuous hypoxia elicits LTF, indicating remarkable pattern sensitivity in its underlying mechanism. Both episodic chemoafferent activation by stimulation of the carotid sinus nerve and episodic hypoxia in carotid denervated rats elicit LTF, suggesting that at least two discrete mechanisms contribute to LTF in anesthetized rats. Hypoxia-induced LTF requires serotonin receptor activation during, but not following episodic hypoxia, indicating that serotonin is necessary to initiate but not maintain LTF. Phrenic LTF following episodic hypoxia is blocked by intrathecal Administration of a serotonin receptor antagonist (methysergide) or protein synthesis inhibitors (cyclohexamide, emetine) to the cervical spinal cord. On the other hand, Intraspinal Drug Administration had no effect on hypoglossal LTF. Thus, the relevant serotonin receptors in phrenic LTF are within the spinal cord, suggesting a location within the respiratory motor nucleus itself. These observations form the basis of our working hypothesis that LTF is initiated by episodic activation of 5-HT2 receptors on respiratory motoneurons, thereby initiating a cell-signaling cascade leading to new protein synthesis. Although the specific protein(s) necessary for LTF is (are) unknown, we recently found that episodic hypoxia and LTF are associated with elevations in ventral spinal concentrations of brain derived neurotrophic factor (BDNF). The elevation in BDNF following episodic hypoxia is blocked by local application of methysergide, suggesting that it may be a causal agent in LTF. Although the physiological (or pathophysiological) role of LTF is uncertain, it may reflect a general mechanism whereby intermittent activation of raphe serotonergic neurons elicits plasticity in respiratory motoneurons. Thus, the same fundamental mechanism may be operational in a number of physiological (eg. altitude or repetitive exercise) or pathophysiological (eg. lung disease or neural injury) states.