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Headache


Cambia® (Diclofenac Potassium for Oral Solution) in the Management of Acute Migraine


Kevin Kahn, MD Director, Clinical Care Center, Carolina Headache Institute


Abstract


Migraine is a prevalent and disabling disorder involving central and peripheral neurologic processes that generate inflammatory mediated pain. Cambia® (diclofenac potassium for oral solution), a novel patented form of the anti-inflammatory medication diclofenac potassium, has been approved by the US Food and Drug Administration for the acute treatment of migraine. Clinical trial data have demonstrated that this formulation offers a four-fold decrease in time of onset of relief compared with conventional diclofenac, which has comparable efficacy to triptan medication. It has also proven effective in a real-world setting. Over the past few years, it has been established that migraine treatment that is administered early may prevent central sensitization and improve treatment outcomes. Given the importance of early intervention in migraine treatment, this medication offers rapid, convenient, and effective relief with a favorable side-effect profile. This review describes migraine pathophysiology, treatment rationale, clinical trial results, and real-world experience with the use of this new medication.


Keywords


Diclofenac, Cambia, migraine, headache, pathophysiology, anti-inflammatory, non-steroidal anti-inflammatory drug, treatment, early intervention, central sensitization, Diener, Lipton


Disclosure: Kevin Kahn, MD, is a consultant for Zogenix and Allergan, and is on the speakers bureau for Allergan, Endo, Nautilus, and Pfizer. Received: October 5, 2011 Accepted: December 2, 2011 Citation: US Neurology, 2011;7(2):139–43 Correspondence: Kevin Kahn, MD, Clinical Care Center, Carolina Headache Institute, 103 Market Street, Chapel Hill, NC 27516. E: kahnk@carolinaheadacheinstitute.com


Support: The publication of this article was funded by Nautilus Neurosciences, Inc. The views and opinions expressed are those of the author and not necessarily those of Nautilus Neurosciences, Inc.


Migraine is one of the most prevalent neurological illnesses occurring in approximately 10 % of the US population, with a total prevalence of up to 29.6 % if probable migraine is also considered.1,2


With nearly one in four households affected by migraine,2 the


The disorder


manifests as episodic pain that is disabling in 50–75 % of patients with migraine.2


disease results in direct and indirect costs of about $23 billion per year.3,4 Despite the disabling nature of migraine, 50 % of patients with migraine go undiagnosed.5


The diagnosis of migraine is made almost exclusively by history. Secondary headaches must be excluded when the neurologic exam is abnormal or headache is of new onset or has atypical features.


The American Migraine Prevalence and Prevention study reported that acute migraine-specific treatment was only used by 19 % of patients with migraine. The lack of effective treatment and the limited uptake means there is a significant clinical unmet need for treatment and patient education.6


Migraine Diagnosis


The typical features and criteria of migraine (see Table 1) have been established by the International Headache Society (IHS) and are the basis for the study and diagnosis of migraine.7


A self-administered © TOUCH BRIEFINGS 2011


migraine screener, ID Migraine, has been validated for use in the primary care setting, and has reported sensitivity of 81 %, specificity of 75 %, and positive predictive value of 93 %.8


If a patient expresses at


least two of the following three features the likelihood of migraine is high: disability, nausea, and sensitivity to light.


When migraine attacks are inadequately treated, it is common for headaches to increase in frequency leading to a process of ‘chronification’.9 This process occurs in approximately 3% of patients with episodic migraine each year.10


Migraine Pathophysiology


The progression from episodic migraine to chronic migraine has been explained through a combination of experimental paradigms based on the current understanding of migraine pathophysiology. Although the pain from migraine is caused by inflammation of meningeal vessels and pericranial structures, the event originates from an electrical instability within cortical and subcortical neurons. The cortical event leads to the symptoms of migraine aura which manifests in 15–20 % of patients with migraine and the subcortical event leads to activation within


139


When headaches occur more than 15 days per month for more than three months these patients are classified as having chronic migraine.7


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