A Comparison of Migraine Patients With and Without Allodynic Symptoms

Kalita, Jayantee; Yadav, Rama Kant; Misra, Usha Kant

doi:10.1097/ajp.0b013e3181b12dd3

Cited by 27 publications

(23 citation statements)

References 8 publications

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“…The relevance of our finding is not contradicting the notion that headache is the principal trigeminal pain in migraine. Nonetheless, an extensive clinical study carried out on 1,413 patients has indicated that, during an attack of migraine, the majority of them suffer from allodynia affecting the entire trigeminal territory [63], a finding confirmed to be independent from the presence of aura [64].…”

Section: Discussionmentioning

confidence: 99%

TNFα Levels and Macrophages Expression Reflect an Inflammatory Potential of Trigeminal Ganglia in a Mouse Model of Familial Hemiplegic Migraine

et al. 2013

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Latent changes in trigeminal ganglion structure and function resembling inflammatory conditions may predispose to acute attacks of migraine pain. Here, we investigated whether, in trigeminal sensory ganglia, cytokines such as TNFα might contribute to a local inflammatory phenotype of a transgenic knock-in (KI) mouse model of familial hemiplegic migraine type-1 (FHM-1). To this end, macrophage occurrence and cytokine expression in trigeminal ganglia were compared between wild type (WT) and R192Q mutant CaV2.1 Ca2+ channel (R192Q KI) mice, a genetic model of FHM-1. Cellular and molecular characterization was performed using a combination of confocal immunohistochemistry and cytokine assays. With respect to WT, R192Q KI trigeminal ganglia were enriched in activated macrophages as suggested by their morphology and immunoreactivity to the markers Iba1, CD11b, and ED1. R192Q KI trigeminal ganglia constitutively expressed higher mRNA levels of IL1β, IL6, IL10 and TNFα cytokines and the MCP-1 chemokine. Consistent with the report that TNFα is a major factor to sensitize trigeminal ganglia, we observed that, following an inflammatory reaction evoked by LPS injection, TNFα expression and macrophage occurrence were significantly higher in R192Q KI ganglia with respect to WT ganglia. Our data suggest that, in KI trigeminal ganglia, the complex cellular and molecular environment could support a new tissue phenotype compatible with a neuroinflammatory profile. We propose that, in FHM patients, this condition might contribute to trigeminal pain pathophysiology through release of soluble mediators, including TNFα, that may modulate the crosstalk between sensory neurons and resident glia, underlying the process of neuronal sensitisation.

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Section: Discussionmentioning

confidence: 99%

TNFα Levels and Macrophages Expression Reflect an Inflammatory Potential of Trigeminal Ganglia in a Mouse Model of Familial Hemiplegic Migraine

et al. 2013

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“…The abnormalities in the brainstem aminergic pathway are well documented in migraine and these influence the neuronal excitability of the cortical neurons. 4,24 This may indirectly suggest that the anti-inflammatory drugs may be capable of reducing sensitization of the cortical neurons. 23 Nonsteroidal anti-inflammatory drugs are effective in both allodynic and nonallodynic migraineurs, 4 whereas triptans are more effective in nonallodynic patients.…”

Section: Discussionmentioning

confidence: 99%

“…4,5 The checklist of allodynia triggers was administered in which combing, fan air, shower, shaving, laying head on pillow, wearing necklace, necktie, ornaments, scarf, and veil were enquired. The duration of migraine, distribution and frequency of headache, migraine triggers, and family history of headache were noted.…”

Section: Methodsmentioning

confidence: 99%

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Is Lack of Habituation of Evoked Potential a Biological Marker of Migraine?

Kalita¹,

Bhoi²,

Misra³

2014

The Clinical Journal of Pain

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“…On at least eight days, the headache features should be of a migraine headache and the pain possibly relieved by a triptan or ergot derivative 3 . Cutaneous allodynia, a risk factor for chronic migraine 4 , increases the discomfort and disability of patients with acute migraine attacks 5 and is recognized as a clinical manifestation of central sensitization in migraine patients 6 . Cutaneous allodynia is defined as the perception of pain or discomfort in response to innocuous thermal (heat or cold) and/or mechanical (static or dynamic) stimuli applied to normal skin 6 .…”

mentioning

confidence: 99%

Cutaneous allodynia is more frequent in chronic migraine, and its presence and severity seems to be more associated with the duration of the disease

Benatto

Carvalho

Dach

et al. 2017

Arq. Neuro-Psiquiatr.

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Objective To evaluate cutaneous allodynia among patients with chronic and episodic migraine in a tertiary headache clinic. Methods 80 subjects with episodic migraine and 80 with chronic migraine were assessed in a tertiary hospital. The 12-item Allodynia Symptom Checklist/Brazil questionnaire was applied to classify subjects according to the presence and severity of cutaneous allodynia. Results Cutaneous allodynia was identified in 81.3% of the episodic migraine group and 92.5% of the chronic migraine group (p = 0.03). No increased association could be attributed to chronic migraine when adjusted by years with disease (PR = 1.12; 95%CI = 0.99 to 1.27; p = 0.06). The groups also did not differ in the severity of allodynia, and severe presentation was the most frequent. Discussion Both groups seemed to be similarly affected in the cephalic and extracephalic regions, with the same severity. Conclusion Cutaneous allodynia is more frequent in chronic migraine, and its presence and severity seems to be more associated with the duration of the disease.

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A Comparison of Migraine Patients With and Without Allodynic Symptoms

Abstract: Allodynic symptoms occurred in 57.1% patients with migraine. In allodynic patients with moderate-to-severe headache, rizatriptan resulted in greater pain relief compared with ibuprofen. These results need further confirmation in larger study.

Cited by 27 publications

References 8 publications

TNFα Levels and Macrophages Expression Reflect an Inflammatory Potential of Trigeminal Ganglia in a Mouse Model of Familial Hemiplegic Migraine

TNFα Levels and Macrophages Expression Reflect an Inflammatory Potential of Trigeminal Ganglia in a Mouse Model of Familial Hemiplegic Migraine

Is Lack of Habituation of Evoked Potential a Biological Marker of Migraine?

Cutaneous allodynia is more frequent in chronic migraine, and its presence and severity seems to be more associated with the duration of the disease

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