Prednisolone reduces nitric oxide‐induced migraine

Tfelt‐Hansen, Peer; Daugaard, D.; Lassen, LH; Iversen, Helle K.; Olesen, Jes

doi:10.1111/j.1468-1331.2009.02654.x

Cited by 27 publications

(19 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This is supported by observations that NTG was able to increase the expression of nuclear factor κB in the trigeminocervical complex of rats (13, 24), which is a key player in the inflammation process controlled by cytokines. In human studies, Tfelt-Hansen and his group demonstrated that infusion of NTG can trigger inflammatory response by inducing inflammatory mediators, which response was inhibited by the anti-inflammatory drug, prednisolone (25). …”

Section: Discussionmentioning

confidence: 99%

The Effect of Systemic Nitroglycerin Administration on the Kynurenine Pathway in the Rat

et al. 2017

View full text Add to dashboard Cite

The primary headache disorders include migraine, which is one of the most frequent neurological disorders, which influences more than 14% of the whole population. Despite the research efforts, its exact pathomechanism is not fully revealed, but evidence points to the role of glutamate and its receptors. Kynurenic acid is an endogenous glutamate receptor antagonist produced by the kynurenine pathway (KP). Tryptophan 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO) convert l-tryptophan to N-formyl-l-kynurenine, to be further transformed to l-kynurenine. Kynurenine aminotransferase-II (KAT-II), l-kynurenine hydrolase (KYNU), and l-kynurenine 3-monooxygenase (KMO) are key enzymes in the later steps of the KP. Nitroglycerin (NTG) administration serves as both human and animal model of migraine, causing the activation and sensitization in the trigeminal system. A previous study demonstrated a reduction of KAT-II expression following NTG administration in animals. The goal of current tests was to identify the potential modulatory effect of NTG on other metabolizing enzymes of the KP in the caudal trigeminal nucleus (TNC) of rats. Four hours following the intraperitoneal injection of NTG (10 mg/kg), the rats were perfused transcardially and the TNC was extracted for Western blotting. Western blot studies revealed that the expression of TDO2, IDO1, KYNU, and KMO decreased in the TNC. The results demonstrated that NTG is able to downregulate the KP, with a potential influence on the glutamatergic system as well, contributing to the development of trigeminal activation and sensitization in animals.

show abstract

Section: Discussionmentioning

confidence: 99%

The Effect of Systemic Nitroglycerin Administration on the Kynurenine Pathway in the Rat

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Thus, NO has also been implicated in the mechanisms of other primary headaches. In addition, GTN‐induced attacks have been demonstrated to respond to typical acute headache treatments 158‐160 …”

Section: Nitric Oxide and Headachementioning

confidence: 99%

“…After taking a taste of the substance, he developed a severe headache 154 . Over a century passed before GTN was evaluated formally in the study of headache pathophysiology, and recognized to participate in the delayed headache and migrainous features associated with NO 159 . In recent decades, the GTN model has become valued for its importance and potential in elucidating migraine mechanisms and seeking new treatments.…”

Section: Nitric Oxide and Headachementioning

confidence: 99%

Chemical Mediators of Migraine: Preclinical and Clinical Observations

2011

View full text Add to dashboard Cite

Migraine is a neurovascular disorder, and although the pathophysiology of migraine has not been fully delineated, much has been learned in the past 50 years. This knowledge has been accompanied by significant advancements in the way migraine is viewed as a disease process and in the development therapeutic options. In this review, we will focus on 4 mediators (nitric oxide, histamine, serotonin, and calcitonin gene-related peptide) which have significantly advanced our understanding of migraine as a disease entity. For each mediator we begin by reviewing the preclinical data linking it to migraine pathophysiology, first focusing on the vascular mechanisms, then the neuronal mechanisms. The preclinical data are then followed by a review of the clinical data which support each mediator’s role in migraine and highlights the pharmacological agents which target these mediators for migraine therapy.

show abstract

“…It is conceivable that glucocorticoids might modulate this neuroimmune interaction. Therefore, antiinflammatory and immunosuppressive effects of corticosteroids are indicated to improve pain by inhibiting the production of inflammatory mediators, reducing prostaglandin synthesis, and suppressing ectopic neural discharges from the injured or inflamed fibers [15-17]. …”

Section: Discussionmentioning

confidence: 99%

Effects of a Short Course of Oral Prednisolone in Patients with Bladder Pain Syndrome with Fluctuating, Worsening Pain despite Low-Dose Triple Therapy

Jeong

2012

Int Neurourol J

View full text Add to dashboard Cite

PurposeTriple therapy with gabapentin, amitriptyline, and nonsteroidal antiinflammatory drugs is efficacious for chronic bladder pain syndrome/interstitial cystitis (BPS/IC). However, transient, fluctuating, worsening pain or flare-up symptoms may develop during treatment for a variety of reasons. Here, we assessed the validity of our observational experience regarding a short course of oral prednisolone therapy, which might be of value in the management of flare-up symptoms of BPS/IC.MethodsBetween May 2007 and May 2012, 7 women (mean age, 61.5 years; range, 44.8 to 75.4 years) with BPS/IC presenting with transient, fluctuating, worsening pain as a flare-up symptom despite low-dose triple therapy received a 1- to 3-month course of oral prednisolone 10 mg. The outcome measures used were the IC symptom scale (ICSS, O'Leary-Sant Interstitial Cystitis Symptom Index) and a visual analogue scale (VAS), which were completed at baseline and after treatment.ResultsThere were statistically significant differences in the ICSS and VAS score before and after prednisolone treatment (P<0.05 by Wilcoxon singed-rank test). The pretreatment IC symptom index (ICSI), IC problem index (ICPI), and VAS score were 16.7± 2.2, 13.7±2.3, and 8.3±1.5 (mean±standard deviation [SD]), and the posttreatment scores were 4.9±2.3, 4.3±1.1, and 2.5±0.9 (mean±SD), respectively. The ICSI, ICPI, and VAS scores were improved after prednisolone treatment by 70.7%, 68.6%, and 69.9%, respectively. Low-dose triple therapy with prednisolone caused no significant adverse effects.ConclusionsIn patients with BPS/IC who show transient, fluctuating, worsening pain as flare-up symptoms despite undergoing low-dose triple therapy, a short course of oral prednisolone therapy was sufficiently effective. However, large-scale studies should be performed to verify our findings.

show abstract

Prednisolone reduces nitric oxide‐induced migraine

Cited by 27 publications

References 27 publications

The Effect of Systemic Nitroglycerin Administration on the Kynurenine Pathway in the Rat

The Effect of Systemic Nitroglycerin Administration on the Kynurenine Pathway in the Rat

Chemical Mediators of Migraine: Preclinical and Clinical Observations

Effects of a Short Course of Oral Prednisolone in Patients with Bladder Pain Syndrome with Fluctuating, Worsening Pain despite Low-Dose Triple Therapy

Contact Info

Product

Resources

About