Allodynia as a complication of migraine: Background and management

Young, William B.

doi:10.1007/s11940-009-0001-0

Cited by 15 publications

(7 citation statements)

References 32 publications

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“…Numerous studies, using quantitative sensory testing (QST) and/or a questionnaire [see (1,2) for review], have now reported CA in episodic migraine patients, although with very different prevalence. Using a semistructured interview, CA was found in 50-75% of episodic migraine patients (3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

Are there differences between cephalic and extracephalic cutaneous allodynia in migraine patients?

et al. 2009

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Cutaneous allodynia (CA), pain in response to innocuous cutaneous stimuli, is recognized as a sign of central sensitization during migraine episodes. It is either restricted within the pain area on the ipsilateral head, or extends within and outside the head. Moreover, CA can be elicited in response to thermal (heat or cold) and/or mechanical stimuli. This raises the question as to whether cephalic and extracephalic CAs share the same properties. We assessed cephalic and extracephalic CAs in migraine episodic patients using a questionnaire completed at home during migraine attacks. A total of 67 episodic migraine patients (58 women, nine men; 4013 years old) addressed all questions in the questionnaire. Forty-nine patients (73%) cited one or more allodynic symptoms during or immediately after the migraine attack. Almost all 49 patients reported cephalic CA, whereas 24 (49%) also reported extracephalic CA. Occurrence and extension of CA correlated (P = 0.005) with headache intensity. Modalities of cephalic and extracephalic CA were different (chi2 = 12.03; P = 0.002), extracephalic CA being mostly thermal (75%) whereas cephalic CA was mostly mechanical (92%). This suggests that cephalic and extracephalic CAs involve different mechanisms.

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Section: Introductionmentioning

confidence: 99%

Are there differences between cephalic and extracephalic cutaneous allodynia in migraine patients?

et al. 2009

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“…1). The significant presence of cephalic, cervical, and remote sensory hyperalgesia in patients with CWAH mirrors the presentation of primary headache 15,[17][18][19][20][21][22][83][84][85][86][87]94 and is considered a clinical manifestation of central sensitization. 19,95,96 Given this centrally-sensitized environment, the augmentation of light-induced pain in our CWAH group is not surprising.…”

Section: Discussionmentioning

confidence: 97%

“…). The significant presence of cephalic, cervical, and remote sensory hyperalgesia in patients with CWAH mirrors the presentation of primary headache and is considered a clinical manifestation of central sensitization …”

Section: Discussionmentioning

confidence: 99%

The Role of the Trigemino Cervical Complex in Chronic Whiplash Associated Headache: A Cross Sectional Study

Watson

Drummond

2016

Headache

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Objective To investigate signs of central sensitization in a cohort of patients with chronic whiplash associated headache (CWAH). Background Central sensitization is one of the mechanisms leading to chronicity of primary headache, and thus might contribute to CWAH. However, the pathophysiological mechanism of CWAH is poorly understood and whether it is simply an expression of the primary headache or has a distinct pathogenesis remains unclear. Thus, the factors involved in the genesis of CWAH require further investigation. Methods Twenty‐two patients with CWAH (20 females, 2 males; age 25–50 years, mean age 36.3 years) and 25 asymptomatic participants (13 females, 12 males; age 18–50 years, mean age 35.6 years) rated glare and light‐induced discomfort in response to light from an ophthalmoscope. Hyperalgesia evoked by a pressure algometer was assessed bilaterally on the forehead, temples, occipital base, and the middle phalanx of the third finger. The number, latency, area under the curve, and recovery cycle of nociceptive blink reflexes elicited by a supraorbital electrical stimulus were also recorded. Results Eight and 6 CWAH patients had migrainous and tension‐type headache (TTH) profiles, respectively; the remainder had features attributable to both migraine and TTH. Patients in the whiplash group reported significantly greater light‐induced pain than controls (8.48 ± .35 vs 6.66 ± .43 on a 0–10 scale; P = .001). The CWAH patients reported significantly lower pressure pain thresholds at all sites. For stimuli delivered at 20 second intervals, whiplash patients were more responsive than controls (4.8 ± .6 blinks vs 3.0 ± .6 blinks in a block of 10 stimuli; P = .036). While R2 latencies and the area under the curve for the 20 second interval trials were comparable in both groups, there was a significant reduction of the area under the curve from the first to the second of the 2‐second interval trials only in controls (99 ± 8% of baseline in whiplash patients vs 68 ± 7% in controls; P = .009). The recovery cycle was comparable for both groups. Conclusions Our results corroborate previous findings of mechanical hypersensitivity and photophobia in CWAH patients. The neurophysiological data provide further evidence for hyperexcitability in central nociceptive pathways, and endorse the hypothesis that CWAH may be driven by central sensitization.

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“…Many methods, including clinical questionnaires, are available to assess the pain morbidity caused by allodynia, but we still lack an objective framework with which to quantify the pain invoked by the allodynia. The contribution of allodynia to the pain morbidity and disability resulting from migraine attacks is still unclear (Young, ). More studies are needed to investigate the exact mechanisms that lead to the extracephalic (body pain) symptoms during migraine attacks.…”

Section: Introductionmentioning

confidence: 99%

Recent progress in migraine pathophysiology: role of cortical spreading depression and magnetic resonance imaging

Bhaskar

Saeidi

Borhani

et al. 2013

Eur J of Neuroscience

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Migraine is characterised by debilitating pain, which affects the quality of life in affected patients in both the western and the eastern worlds. The purpose of this article is to give a detailed outline of the pathophysiology of migraine pain, which is one of the most confounding pathologies among pain disorders in clinical conditions. We critically evaluate the scientific basis of various theories concerning migraine pathophysiology, and draw insights from brain imaging approaches that have unraveled the prevalence of cortical spreading depression (CSD) in migraine. The findings supporting the role of CSD as a physiological substrate in clinical pain are discussed. We also give an exhaustive overview of brain imaging approaches that have been employed to solve the genesis of migraine pain, and its possible links to the brainstem, the neocortex, genetic endophenotypes, and pathogenetic factors (such as dopaminergic hypersensitivity). Furthermore, a roadmap is proposed to provide a better understanding of pain pathophysiology in migraine, to enable the development of strategies using leads from brain imaging studies for the identification of early biomarkers, efficient prognosis, and treatment planning, which eventually may help in alleviating some of the devastating impact of pain morbidity in patients afflicted with migraine.

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Allodynia as a complication of migraine: Background and management

Cited by 15 publications

References 32 publications

Are there differences between cephalic and extracephalic cutaneous allodynia in migraine patients?

Are there differences between cephalic and extracephalic cutaneous allodynia in migraine patients?

The Role of the Trigemino Cervical Complex in Chronic Whiplash Associated Headache: A Cross Sectional Study

Recent progress in migraine pathophysiology: role of cortical spreading depression and magnetic resonance imaging

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