Identifying Cutaneous Allodynia in Chronic Migraine Using a Practical Clinical Method

Abstract

Cutaneous allodynia is common in migraine. In the majority of previous studies on allodynia in migraine, only patients with episodic migraine (EM) were included. Little is known on patterns of allodynia in chronic migraine (CM). Since the presence of allodynia is associated with a poor response to triptans, a clinically practical method to test migraine patients for allodynia would be useful to the clinician. The aim of this study was to assess the prevalence of dynamic mechanical (brush) allodynia (BA) in CM, using a clinically practical method. Eighty-nine CM patients were prospectively recruited. Patients were given a structured questionnaire regarding demographic data and migraine characteristics. Allodynia was tested using a 10 x 10-cm gauze pad to brush various areas of the skin lightly. The prevalence of BA in the entire study population and in different patient subgroups was calculated. BA was present in 42.7% (38/89) of the patients. The presence of allodynia was unrelated to age, disease duration or to the occurrence of an acute headache exacerbation at the time of testing. Allodynia was positively associated with a history of migraine aura. BA was most common in the cephalic area, but was also seen in cervical dermatomes. BA is common in CM and, unlike in EM, is not significantly affected by the occurrence of an acute headache exacerbation. This suggests that central trigeminovascular neurons are chronically sensitized in patients experiencing migraine headache >15 days per month. The testing of BA in the clinical setting is possible using a simple and brief approach. It allows the clinician to determine whether the patient is sensitized, a diagnosis that affects treatment decisions.

The role of intracranial hypertension in the chronification of migraine

“…Wang et al [13] compared the clinical features of 25 patients with IIHWOP with those exhibiting chronic daily headache (CDH) but with normal CSF pressure, and no difference in headache profile was found. Besides clinical presentation, IIH and CM also share some relevant risk factors such as S24 Neurol Sci (2015) 36 (Suppl 1):S23-S28 female gender, obesity and sleep disturbances [44][45][46] and both show a higher prevalence of allodynic symptoms [47][48][49][50]. Topiramate, a drug with documented efficacy in CM [51,52] that shares with acetazolamide the inhibition of carbonic anhydrase isoenzyme [53], has been found as effective as acetazolamide in IIH treatment [54], suggesting that the topiramate efficacy in CM could be mediated, at least partially, by an acetazolamide-like CSF pressure lowering effect.…”

“…We speculate that the opposite increased pressures acting on both, the blood and the CSF side of the venous wall, might promote the activation of dural sinus trigeminovascular nociceptors, leading to central sensitization of pain pathways [37]. Allodynia, a clinical marker of central sensitization, usually develops in the course of primary headache attacks [61][62][63][64][65] but is bilaterally detected during the intercritical phase in over 70 % of chronic headache subjects [49]. Amongst migraine sufferers, allodynia has been associated with female sex, frequent headache, increased BMI and depression [66,67].…”

Sensitization, glutamate, and the link between migraine and fibromyalgia

“…In the latter, allodynia was correlated to the duration of illness as well as frequency of migraine attacks and was most common in the cephalic and cervical areas, but was also found in cervical dermatomes. Unlike in episodic migraine, it was not significantly affected by the occurrence of an acute headache exacerbation, suggesting that central trigeminovascular neurons are chronically sensitized in patients who experience migraine headache more than 15 days/month [37].…”

Allodynia in Cluster Headache

“…Over the past decade, there has been considerable interest in the pathophysiology of this phenomenon in headaches (particularly in migraine) and in its clinical implications [2,3,[5][6][7][8]. CA in migraine is currently thought to result from sensitization of pain-signaling neurons in the trigeminal nucleus caudalis (TNC) that receive input from both intracranial structures and skin [9].…”

“…CA in migraine is currently thought to result from sensitization of pain-signaling neurons in the trigeminal nucleus caudalis (TNC) that receive input from both intracranial structures and skin [9]. Both clinic-and population-based studies have shown that CA is common in migraine patients, with a prevalence of up to 80% in some studies [2,7,8]. A clinic-based study of patients with chronic migraine has shown that these patients exhibit CA not only during acute headaches, but also in between headache exacerbations [8].…”