Relevant bibliographies by topics / Opioid agonist-induced seizures

Academic literature on the topic 'Opioid agonist-induced seizures'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Opioid agonist-induced seizures"

1

Socała, Katarzyna, Urszula Doboszewska, and Piotr Wlaź. "Salvinorin A Does Not Affect Seizure Threshold in Mice." Molecules 25, no. 5 (March 7, 2020): 1204. http://dx.doi.org/10.3390/molecules25051204.

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The κ-opioid receptor has recently gained attention as a new molecular target in the treatment of many psychiatric and neurological disorders including epilepsy. Salvinorin A is a potent plant-derived hallucinogen that acts as a highly selective κ-opioid receptor agonist. It has unique structure and pharmacological properties, but its influence on seizure susceptibility has not been studied so far. Therefore, the aim of the present study was to investigate the effect of salvinorin A on seizure thresholds in three acute seizure tests in mice. We also examined its effect on muscular strength and motor coordination. The obtained results showed that salvinorin A (0.1–10 mg/kg, i.p.) did not significantly affect the thresholds for the first myoclonic twitch, generalized clonic seizure, or forelimb tonus in the intravenous pentylenetetrazole seizure threshold test in mice. Likewise, it failed to affect the thresholds for tonic hindlimb extension and psychomotor seizures in the maximal electroshock- and 6 Hz-induced seizure threshold tests, respectively. Moreover, no changes in motor coordination (assessed in the chimney test) or muscular strength (assessed in the grip-strength test) were observed. This is a preliminary report only, and further studies are warranted to better characterize the effects of salvinorin A on seizure and epilepsy.
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2

Mohammadpour, Abbas, Mahmood Ashkezari, Behrokh Farahmand, and Mohammad Shokrzadeh. "Demographic Characteristics and Functional Performance of the Kidneys and Hearts of Patients with Acute Tramadol Toxicity." Drug Research 69, no. 04 (July 11, 2018): 207–10. http://dx.doi.org/10.1055/a-0646-3918.

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Abstract Background Tramadol overdose is disproportionately more common in Iran, and in recent years, it has become one of the most common causes of poisoning admissions to emergency departments in this country. Tramadol is a synthetic analogue of codeine and a weak opioid receptor (μ) agonist that can cause seizures even in commonly used doses. Aims This study aimed to examine the relationship between seizure and plasma tramadol concentration in patients with tramadol poisoning who referred to one of the hospitals in Ghaemshahr, Iran. Study Design This research is an analytical cross-sectional study. Methods A total of 121 tramadol users (non-seizure group=61 and seizure group=60) were admitted to hospital. Demographic characteristics and clinical findings were collected by a questionnaire. Plasma was harvested after separation from blood cells and quantified using the HPLC method. Biochemical parameters, including urea, creatinine, troponin I, and creatine phosphokinase (CPK–MB) were determined by spectrophotometry. This study was a single blind design study. Results The mean age of participants was 25 years. Ninety-five participants were classified as smokers. The mean serum concentrations of tramadol in subjects with seizures and those without seizures were 491.90 μg/ml and 374.42 μg/ml (p=0.211), respectively. Average concentrations of biochemical parameters in the seizure group were 53.33 (9.38) µg/ml urea, 1.71 (0.29) µg/ml Cr, 6.53 (2.89) µg/ml TPI, and 58.23 (22.20) µg/ml CPK- MB. Average concentrations of biochemical parameters were significantly higher in the seizure group than in the non-seizure group (p<0.001). Conclusion Tramadol-induced seizures were not found to be related to age, gender, or dosage. This complication can lead to cardiac and renal complications in individuals on tramadol experiencing seizures. This result indicates that stricter restrictions should be imposed on the distribution and administration of the drug tramadol.
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3

Bausch, Suzanne B., Joshua P. Garland, and Jaclyn Yamada. "The delta opioid receptor agonist, SNC80, has complex, dose-dependent effects on pilocarpine-induced seizures in Sprague–Dawley rats." Brain Research 1045, no. 1-2 (May 2005): 38–44. http://dx.doi.org/10.1016/j.brainres.2005.03.008.

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4

Lee, P. H. K., and J. S. Hong. "Ventral hippocampal dentate granule cell lesions enhance motor seizures but reduce wet dog shakes induced by mu opioid receptor agonist." Neuroscience 35, no. 1 (January 1990): 71–77. http://dx.doi.org/10.1016/0306-4522(90)90121-j.

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5

Mukau, Leslie, Kadia Wormley, Christian Tomaszewski, Bushra Ahmad, Rais Vohra, and Andrew Herring. "Buprenorphine for High-dose Tramadol Dependence: A Case Report of Successful Outpatient Treatment." Clinical Practice and Cases in Emergency Medicine 6, no. 1 (January 28, 2022): 83–86. http://dx.doi.org/10.5811/cpcem.2021.12.54602.

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Introduction: During the coronavirus disease 2019 pandemic caused by the severe acute respiratory syndrome coronavirus 2, deaths from opiate drug overdoses reached their highest recorded annual levels in 2020. Medication-assisted treatment for opiate use disorder has demonstrated efficacy in reducing opiate overdoses and all-cause mortality and improving multiple other patient-centered outcomes. Treatment of tramadol dependence in particular poses unique challenges due to its combined action as opioid agonist and serotonin-norepinephrine reuptake inhibitor. Tramadol puts patients with dependence at risk for atypical withdrawal syndromes when attempting to reduce use. Little evidence is available to guide treatment of tramadol dependence. Case Report: We present a case of high-dose tramadol addiction that began with misuse of medically prescribed tramadol for treatment of musculoskeletal back pain. The patient’s use reached oral consumption of 5000-6000 milligrams of illicit tramadol daily. She complained of common complications of tramadol use disorder including memory impairment, excessive sedation, and tramadol-induced seizures. The patient was referred to the emergency department in a withdrawal crisis seeking treatment where she was successfully managed with buprenorphine and phenobarbital and then linked to ongoing outpatient treatment. Conclusion: Our report adds to the limited guidance currently available on the acute management of tramadol withdrawal and treatment of tramadol use disorder. Our case suggests the initiation of high-dose buprenorphine may be an effective and feasible option for emergency clinicians.
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6

Blaine, Arryn T., Yiming Miao, Jinling Yuan, Sophia Palant, Rebecca J. Liu, Zhong-Yin Zhang, and Richard M. van Rijn. "Exploration of beta-arrestin isoform signaling pathways in delta opioid receptor agonist-induced convulsions." Frontiers in Pharmacology 13 (August 11, 2022). http://dx.doi.org/10.3389/fphar.2022.914651.

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The δ-opioid receptor (δOR) has been considered as a therapeutic target in multiple neurological and neuropsychiatric disorders particularly as δOR agonists are deemed safer alternatives relative to the more abuse-liable µ-opioid receptor drugs. Clinical development of δOR agonists, however, has been challenging in part due to the seizure-inducing effects of certain δOR agonists. Especially agonists that resemble the δOR-selective agonist SNC80 have well-established convulsive activity. Close inspection suggests that many of those seizurogenic δOR agonists efficaciously recruit β-arrestin, yet surprisingly, SNC80 displays enhanced seizure activity in β-arrestin 1 knockout mice. This finding led us to hypothesize that perhaps β-arrestin 1 is protective against, whereas β-arrestin 2 is detrimental for δOR-agonist-induced seizures. To investigate our hypothesis, we characterized three different δOR agonists (SNC80, ADL5859, ARM390) in cellular assays and in vivo in wild-type and β-arrestin 1 and β-arrestin 2 knockout mice for seizure activity. We also investigated downstream kinases associated with β-arrestin-dependent signal transduction. We discovered that δOR agonist-induced seizure activity strongly and positively correlates with β-arrestin 2 efficacy for the agonist, but that indirect inhibition of ERK activation using the MEK inhibitor SL327 did not inhibit seizure potency and duration. Inhibition of the PI3K/AKT/mTOR signaling with honokiol but not PQR530, attenuated SNC80 seizure duration in β-arrestin 1 knockout, but honokiol did not reduce SNC80-induced seizures in wild-type mice. Ultimately, our results indicate that β-arrestin 2 is correlated with δOR agonist-induced seizure intensity, but that global β-arrestin 1 knockout mice are a poor model system to investigate their mechanism of action.
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7

Blaine, Arryn, Sophia Palant, Jinling Yuan, and Richard Rijn. "Role of β‐arrestin Isoforms in Delta Opioid Receptor Agonist‐Induced Seizures." FASEB Journal 35, S1 (May 2021). http://dx.doi.org/10.1096/fasebj.2021.35.s1.02144.

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8

Dasgupta, Himadri Sekhar, Debashis Priyadarshan Sahoo, Bhupen Barman, and Dhriti Brahma. "Low-Dose Tramadol-Induced Seizure: A Case Report." Journal of Pharmacology and Pharmacotherapeutics, July 11, 2022, 0976500X2211074. http://dx.doi.org/10.1177/0976500x221107494.

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Tramadol is a weak mu (µ) opioid receptor agonist that acts by inhibiting serotonin and norepinephrine uptake. Tramadol undergoes extensive hepatic metabolism by a number of pathways, including CYP2D6 and CYP3A4, and by conjugation with subsequent renal excretion. The maximum recommended dose is 400 mg/day. One of the most important adverse effects of tramadol is a seizure, which usually occurs at high doses and is often generalized tonic–clonic type and self-limiting. Here, we present a case of a patient with inflammatory low backache who developed seizures while on low-dose oral tramadol. After 1 h of taking the first tablet of tramadol, he developed morbilliform rashes all over the body. One day later, he developed generalized tonic–clonic seizures followed by a loss of consciousness for 5 min. The patient was admitted to the hospital and managed conservatively with injection lorazepam and tramadol was stopped. In general, if applied in overdose, tramadol can only incite seizures in patients already suffering from some sort of disorder related to seizures or if it is administered along with antidepressants, alcohol, etc. But here, only with the use of 37.5 mg oral application, the incidence of seizure happened.
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