Change of Excitability in Brainstem and Cortical Visual Processing in Migraine Exhibiting Allodynia

Shibata, Koichi; Yamane, Kiyomi; Iwata, Makoto

doi:10.1111/j.1526-4610.2006.00612.x

Cited by 20 publications

(14 citation statements)

References 47 publications

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“…However, using these conditions, a low-contrast (29%) pattern also resulted in increased amplitude. Similar to previous results [60], hyperreactivity of the P pathway is not likely to result in migraine.…”

Section: Resultssupporting

confidence: 86%

Spatial frequency differentially affects habituation in migraineurs: a steady-state visual-evoked potential study

et al. 2011

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A lack of habituation in visual-evoked potentials (VEPs) is the main abnormality observed in migraineurs. However, no study of steady-state VEPs has yet evaluated pattern-reversal stimuli with respect to habituation behavior or spatial frequency. The aim of this study was to clarify habituation behavior in migraineurs between attacks and to establish characteristics of VEPs in these patients. Steady-state VEPs were sequentially recorded as checkerboard patterns in four consecutive blocks from 12 patients with migraine without aura (MO), 12 patients with migraine with aura (MA), and 12 healthy controls (HC) at four spatial frequencies of 0.5, 1.0, 2.0, and 4.0 cycles per degree (cpd) with a stimulus rate of 7.5 Hz (15 reversal/s). VEP amplitudes were consistently higher in migraineurs. However, habituation was not demonstrated in HCs, and migraineurs did not reveal a clear lack of habituation. MAs exhibited high-amplitude VEPs, depending on spatial frequency. In the MA patients, amplitude differences reached statistical significance at 2.0 cpd. The sequential amplitude changes at 0.5 cpd were significantly different in MAs compared with HCs. Migraine patients exhibited high-amplitude VEPs, which were dependent on spatial frequency, and may be related to altered excitability in pre-cortical and cortical visual processing.

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Section: Resultssupporting

confidence: 86%

Spatial frequency differentially affects habituation in migraineurs: a steady-state visual-evoked potential study

et al. 2011

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“…Shared genetic risk factors may similarly account for the association between comorbid disorders (14). Finally, independent genetic or environmental risk factors may produce a brain state that gives rise to both migraine and a comorbid conditions (36). …”

Section: Discussionmentioning

confidence: 99%

Migraine in women with chronic pelvic pain with and without endometriosis

Karp¹,

Sinaii²,

Nieman³

et al. 2011

Fertility and Sterility

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Objective To examine the prevalence of migraine in women with chronic pelvic pain with and without endometriosis. Design Prospective study of headache, pelvic pain, and quality of life before laparoscopic surgery for pelvic pain. Endometriosis was diagnosed pathologically. Headaches were classified as migraine or non-migraine using International Headache Society criteria. Setting Clinical research hospital. Patient(s) 108 women in a clinical trial for chronic pelvic pain (NCT00001848). Intervention(s) Laparoscopy to diagnose endometriosis, assessment by neurologist to assess headaches. Main Outcome Measure(s) Prevalence of migraine and other headaches in women with chronic pelvic pain with or without endometriosis. Headache frequency, severity and relationship to pelvic pain and endometriosis. Result(s) Lifetime prevalence of definite or possible migraine was 67% of women with chronic pelvic pain. An additional 8% met criteria for possible migraine. Migraine was no more likely in women with endometriosis than those without. Women with the most severe headaches had a lower quality of life compared with those with pelvic pain alone. Conclusion(s) Migraine headache is common in women with chronic pelvic pain, regardless of endometriosis, and contributes to disability in those with both conditions. The strong association suggests a common pathophysiology.

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“…This was then followed by the observation by Bernstein and colleagues that cutaneous allodynia developed in 79% of patients during migraine attacks in, and sometimes beyond the area of referred pain [36–37]. This finding has been repeated in several studies since then [161; 135; 207; 52]. While cephalic and extracephalic allodynia are well described, spontaneous body pain and allodynia has also been reported as preceding migraine attacks [56].…”

Section: To Which Clinical Syndromes Does Central Sensitization Contrmentioning

confidence: 98%

Central sensitization: Implications for the diagnosis and treatment of pain

Woolf¹

2011

Pain

3,548

2,733

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Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and postsurgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk both of developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.

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Change of Excitability in Brainstem and Cortical Visual Processing in Migraine Exhibiting Allodynia

Cited by 20 publications

References 47 publications

Spatial frequency differentially affects habituation in migraineurs: a steady-state visual-evoked potential study

Spatial frequency differentially affects habituation in migraineurs: a steady-state visual-evoked potential study

Migraine in women with chronic pelvic pain with and without endometriosis

Central sensitization: Implications for the diagnosis and treatment of pain

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