Carbamazepine potentiates morphine analgesia on postoperative pain in morphine-dependent rats

Naseri, Kobra; Sabetkasaei, Masoumeh; Zanjani, Taraneh Moini; Saghaei, Elham

doi:10.1016/j.ejphar.2011.10.026

Cited by 13 publications

(4 citation statements)

References 26 publications

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“…Bilateral activation of the descending diffuse noxious inhibitory controls (DNIC) with release of endorphins, due to the repetition of painful paroxysms of TN [24] could explain this finding, but this seems unlikely since during pain threshold determination no neuralgic pain putatively activating the inhibitory control has been triggered. A second possibility would be the antinociceptive effect of CBZ, which has been described in rats [25,26] and TN patients after noxious laser stimulation [23]. …”

Section: Discussionmentioning

confidence: 99%

Cuneus and fusiform cortices thickness is reduced in trigeminal neuralgia

et al. 2014

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BackgroundChronic pain disorders are presumed to induce changes in brain grey and white matters. Few studies have focused CNS alterations in trigeminal neuralgia (TN).MethodsThe aim of this study was to explore changes in white matter microstructure in TN subjects using diffusion tensor images (DTI) with tract-based spatial statistics (TBSS); and cortical thickness changes with surface based morphometry. Twenty-four patients with classical TN (37-67 y-o) and 24 healthy controls, matched for age and sex, were included in the study.ResultsComparing patients with controls, no diffusivity abnormalities of brain white matter were detected. However, a significant reduction in cortical thickness was observed at the left cuneus and left fusiform cortex in the patients group. The thickness of the fusiform cortex correlated negatively with the carbamazepine dose (p = 0.023).ConclusionsSince the cuneus and the fusiform gyrus have been related to the multisensory integration area and cognitive processing, as well as the retrieval of shock perception conveyed by Aδ fibers, our results support the role of these areas in TN pathogenesis. Whether such changes occurs as an epiphenomenon secondary to daily stimulation or represent a structural predisposition to TN in the light of peripheral vascular compression is a matter of future studies.

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Section: Discussionmentioning

confidence: 99%

Cuneus and fusiform cortices thickness is reduced in trigeminal neuralgia

et al. 2014

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“…The interaction of these drugs has not been previously examined, and synergy was demonstrated peripherally and orally via isobolographic analysis. Carbamazepine has been tested in analgesic combinations with paracetamol [Tomić et al, 2010], oxycodone [Siniscalchi et al, 2011], morphine [Naseri et al, 2012] and pregabalin [Hahm et al, 2012] while topimarate has been tested in combination with tramadol [Codd et al, 2008] and gabapentin [Paudel et al, 2011] in several experimental pain models. Gabapentin has also been co-administered with morphine [Shimoyama et al, 1997], ibuprofen [Yoon and Yaksh, 1999], naproxen [Hurley et al, 2002], amitriptyline [Heughan and Sawynok, 2002], tramadol [Granados-Soto and Arguelles, 2005] and metamizol [Ortega-Varela et al, 2007], yielding synergistic effects in inflammatory pain models.…”

Section: Antinociceptive Effect Of the Diacerhein-antiepileptic Drugsmentioning

confidence: 99%

Combination of Diacerhein and Antiepileptic Drugs After Local Peripheral, and Oral Administration in the Rat Formalin Test

Zúñiga-Romero

Ponce-Chávez

Gauthereau-Torres

et al. 2014

Drug Development Research

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Preclinical Research The present study was designed to evaluate the possible antinociceptive interaction between diacerhein and some antiepileptic drugs (carbamazepine, topiramate and gabapentin) on formalin-induced nociception. Diacerhein, each of the antiepileptics or a fixed dose-ratio combination of these drugs was assessed after local peripheral and oral administration in rats. lsobolographic analyses were used to define the interaction between drugs. Diacerhein, antiepileptic drugs (carbamazepine, topiramate and gabapentin) or their combinations yielded a dose-dependent antinociceptive effect when administered by both routes. Theoretical ED30 values for the combination estimated from the isobolograms were obtained as follows: diacerhein-carbamazepine (85.99 ± 7.07 μg/paw; 56.53 ± 4.56 mg/kg po), diacerhein-topiramate (197.97 ± 22.90 μg/paw; 13.06 ± 2.44 mg/kg po) and diacerhein-gabapentin (96.87 ± 17.73 μg/paw; 17.90 ± 4.70 mg/kg p.o.) for the local peripheral and oral administration routes, respectively. These values were significantly higher than the experimentally obtained ED30 values: diacerhein-carbamazepine (49.33 ± 3.37 μg/paw; 35.49 ± 7.91 mg/kg po), diacerhein-topiramate (133.00 ± 39.10 μg/paw; 8.87 ± 1.46 mg/kg po) and diacerhein-gabapentin (70.98 ± 14.73 μg/paw; 10.95 ± 3.23 mg/kg po). The combinations produced their antinociceptive effects without motor impairment in the rotarod test indicating synergistic interactions with a good side effect profile.

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“…Experts analyzing the available literature emphasize that in real-world clinical practice, anticonvulsants acting on Nav are often combined with opioids to manage trigeminal neuralgia [ 92 ], despite limited clinical evidence. Experiments in animal pain models have demonstrated that Nav blockers such as carbamazepine potentiate the morphine analgesia of postoperative pain in morphine-dependent rats [ 93 ] and in model of neuropathic pain [ 94 ]; that intrathecally co-administered lamotrigine attenuates antinociceptive tolerance to morphine in rats [ 95 ]; and that topiramate and lamotrigine synergistically interact with tramadol in a nociceptive pain model [ 96 ]. The potential molecular mechanisms by which anticonvulsants enhance opioid-induced analgesia may involve the blockade of overexpressed and overactive Nav1.7 in injured neurons [ 97 ] and Nav 1.6 in microglia [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Phenytoin Decreases Pain-like Behaviors and Improves Opioid Analgesia in a Rat Model of Neuropathic Pain

et al. 2023

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Neuropathic pain remains a clinical challenge due to its complex and not yet fully understood pathomechanism, which result in limited analgesic effectiveness of the management offered, particularly for patients with acute, refractory neuropathic pain states. In addition to the introduction of several modern therapeutic approaches, such as neuromodulation or novel anti-neuropathic drugs, significant efforts have been made in the repurposing of well-known substances such as phenytoin. Although its main mechanism of action occurs at sodium channels in excitable and non-excitable cells and is well documented, how the drug affects the disturbed neuropathic interactions at the spinal cord level and how it influences morphine-induced analgesia have not been clarified, both being crucial from a clinical perspective. We demonstrated that single and repeated systemic administrations of phenytoin decreased tactile and thermal hypersensitivity in an animal model of neuropathic pain. Importantly, we observed an increase in the antinociceptive effect on thermal stimuli with repeated administrations of phenytoin. This is the first study to report that phenytoin improves morphine-induced antinociceptive effects and influences microglia/macrophage activity at the spinal cord and dorsal root ganglion levels in a neuropathic pain model. Our findings support the hypothesis that phenytoin may represent an effective strategy for neuropathic pain management in clinical practice, particularly when combination with opioids is needed.

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Carbamazepine potentiates morphine analgesia on postoperative pain in morphine-dependent rats

Cited by 13 publications

References 26 publications

Cuneus and fusiform cortices thickness is reduced in trigeminal neuralgia

Cuneus and fusiform cortices thickness is reduced in trigeminal neuralgia

Combination of Diacerhein and Antiepileptic Drugs After Local Peripheral, and Oral Administration in the Rat Formalin Test

Phenytoin Decreases Pain-like Behaviors and Improves Opioid Analgesia in a Rat Model of Neuropathic Pain

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