Pathophysiology of Medication-overuse Headache: Implications from Animal Studies

Bongsebandhu-phubhakdi, Saknan; Srikiatkhachorn, Anan

doi:10.1007/s11916-011-0234-y

Cited by 27 publications

(33 citation statements)

References 27 publications

(23 reference statements)

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“…Alteration of cortical neuronal excitability, central sensitization involving the trigeminal nociceptive system, and changes in serotonergic and dopaminergic expression and pathways including the endocannabinoid system have been suggested to play a part in the pathophysiology of MOH 85,86,89–92…”

Section: Pathogenesismentioning

confidence: 99%

Medication-overuse headache: a review

Kristoffersen

Lundqvist²

2014

JPR

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Medication-overuse headache (MOH) is a worldwide health problem with a prevalence of 1%–2%. It is a severe form of headache where the patients often have a long history of headache and of unsuccessful treatments. MOH is characterized by chronic headache and overuse of different headache medications. Through the years, withdrawal of the overused medication has been recognized as the treatment of choice. However, currently, there is no clear consensus regarding the optimal strategy for management of MOH. Treatment approaches are based on expert opinion rather than scientific evidence. This review focuses on aspects of epidemiology, diagnosis, pathogenesis, prevention, and treatment of MOH. We suggest that information and education about the risk of MOH is important since the condition is preventable. Most patients experience reduction of headache days and intensity after successful treatment. The first step in the treatment of MOH should be carried out in primary care and focus primarily on withdrawal, leaving prophylactic medication to those who do not manage primary detoxification. For most patients, a general practitioner can perform the follow-up after detoxification. More complicated cases should be referred to neurologists and headache clinics. Patients suffering with MOH have much to gain by an earlier treatment-focused approach, since the condition is both preventable and treatable.

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Section: Pathogenesismentioning

confidence: 99%

Medication-overuse headache: a review

Kristoffersen

Lundqvist²

2014

JPR

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“…Peripheral and central sensitization can explain the progression from episodic to chronic headache pain. In fact, cutaneous allodynia, a frequent event that develops during migraine attacks, reflects the decrease in nociceptive threshold, which is the key feature of sensitization [22]. There are many experimental evidences supporting a negative impact of opioids in migraine pathophysiology and progression.…”

mentioning

confidence: 99%

Controversies in migraine treatment: opioids should be avoided

Casucci¹,

Cevoli

2013

Neurol Sci

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The use of opioids for migraine is still controversial. Evidence-based guidelines do not recommend opioids as first-line treatment of migraine attacks, while clinical and epidemiological surveys demonstrate that the use of opioids is associated with more severe headacherelated disability, symptomology and comorbidities, and greater health-care resource utilization. There are concerns that opioids may be misused or abused, leading to opioid abuse or dependence and migraineurs are particularly prone and at risk for the development of chronic daily headache from opioids overuse. Since clinical and preclinical studies evidence a pathophysiological role of opioids in migraine progression, opioids should be avoided in migraine patients.The role of opioids in clinical practice for migraine: the state-of-the-art Migraine is a common disabling neurologic disorder, characterized by recurrent headache attacks manifesting with unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity, and association with nausea and/or photophobia and phonophobia [1]. The goals of acute migraine treatments are to treat attacks rapidly and consistently without recurrence, restore the patient's ability to function, minimize the use of back-up and rescue medications, optimize self-care and reduce subsequent use of resources, be cost-effective for overall management, and have minimal or no adverse events [2]. Acute treatments used for migraine include nonspecific agents such as aspirin, acetaminophen, non-steroidal anti-inflammatory drugs (NSAIDs), opioids, and barbiturates among others, as well as migraine-specific medications, including ergot alkaloids and triptans [2]. International guidelines recommend triptans and NSAIDs as first-line treatment of migraine attacks [2][3][4]. Use of opioids for treatment of migraine is controversial. Despite evidence-based guidelines do not recommend opioids as first-line treatment of migraine attacks [2][3][4], and no randomized controlled trial has shown any significant effect of opioids on migraine attacks when pain-free was the primary end-point of the study [5], their use in clinical practice [6][7][8] and, even more, in emergency departments (EDs) is very large, especially in USA and Canada [9,10]. Moreover, among studies about the efficacy of opioids as rescue medication for acute migraine in EDs recently revised, only one evidenced a superiority of meperidina 75 mg i.m. versus ketorolac 30 mg i.m., three reported superiority of competitors and eight reported similar results for opioids versus competitors such as DHE, metoclopramide, chlorpromazine, droperidol, and ketorolac [5]. In any case, opioids did not adequately restore the patient's ability to function. The negative impact of opioids on migrainous population is reported in several clinical and epidemiological studies. In fact, opioids use for migraine resulted associated with more severe headache-related disability, symptomology, and comorbidities (primarily, psychiatric, and cardi...

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“…Although the exact mechanisms underlying MOH remain undefined, cortical hyperexcitability is a possible explanation [16,17]. In our previous experiments, rats receiving chronic paracetamol exhibited a higher number of CSD waves, while the AUC of the waveforms was not different [8].…”

Section: Discussionmentioning

confidence: 86%

“…Changes in algogenic protein expression in trigeminal ganglia and latent sensitization have been demonstrated in rats chronically exposed to triptans [22]. A derangement of the central serotonin-dependent endogenous pain control system induced by chronic medication has been proposed [16]. Observation of a decrease in serotonin in patients with MOH supports this hypothesis [23].…”

Section: Discussionmentioning

confidence: 92%

Original article. Potential risk of dihydroergotamine causing medicationoveruse headache: preclinical evidence

Vibulyaseck

Bongsebandhu-phubhakdi

Grand

et al. 2014

Asian Biomedicine

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Background: Overuse of abortive medication is a common factor contributing to an increase in headache frequency in patients with migraine. Whether or not chronic exposure to dihydroergotamine (DHE) can lead to this transformation remains uncertain. Objective: To determine the effect of acute and chronic DHE exposure on development of cortical spreading depression (CSD) and trigeminal nociception. Methods: The study comprised two experiments, namely acute and chronic exposure. In the acute experiment, a single dose of DHE (100 μg/kg) was given to male Wistar rats after successful induction of CSD. In the chronic experiment, DHE was given daily for the period of 0, 7, 14, and 28 days. CSD was induced 30 minutes after the final injection and the cortical field potential was recorded. Expression of c-Fos in caudal brainstem was used as an indicator of trigeminal nociception. Results: Acute exposure to DHE attenuated the expression of c-Fos in the caudal brainstem without change in CSD response. By contrast, chronic exposure (14 and 28 days) to DHE increased the area under the curve of CSD waveforms. In parallel with the change in the CSD, there was significant increase of c-Fos expression within 14 days exposure to DHE and the expression remained significantly elevated for up to the 28 days examined. Conclusion: Our study demonstrated that chronic DHE administration can increase cortical excitability and increase c-Fos expression in caudal brainstem. Our preclinical evidence suggests the possible adverse effect of chronic DHE use in causing chronification of headache.

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Pathophysiology of Medication-overuse Headache: Implications from Animal Studies

Cited by 27 publications

References 27 publications

Medication-overuse headache: a review

Medication-overuse headache: a review

Controversies in migraine treatment: opioids should be avoided

Original article. Potential risk of dihydroergotamine causing medicationoveruse headache: preclinical evidence

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