Gender Differences in Pain and Secondary Hyperalgesia After Heat/Capsaicin Sensitization in Healthy Volunteers

Jensen, Magnus Thorsten; Petersen, Karin L.

doi:10.1016/j.jpain.2005.10.013

Cited by 62 publications

(47 citation statements)

References 37 publications

(33 reference statements)

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“…5,51 Such a control could increase test-retest reliability. However, a recent study on experimental pain, 16 using the heat/capsaicin sensitization model, 39 found no sex differences in heat pain detection thresholds, total pain during capsaicin stimulation, or areas of secondary hyperalgesia to pin-prick stimulation, which were points of interest in our study.…”

Section: Neurogenic Flare Response and Neurosecretory Changescontrasting

confidence: 47%

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Psychophysics, Flare, and Neurosecretory Function in Human Pain Models: Capsaicin Versus Electrically Evoked Pain

Geber

Fondel

Krämer

et al. 2007

The Journal of Pain

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Section: Neurogenic Flare Response and Neurosecretory Changescontrasting

confidence: 47%

“…Sizes (cm 2 ; above) and intensities (perfusion units, PU; below) of the neurogenic flare response were measured at baseline, during (minutes 1,6,16,21,26,31), and after (minute 42) the stimulation period, using LDI. Test (CAP_1, ES_1) and retest (CAP_2, ES_2) are presented by dashed lines (each n ϭ 10).…”

mentioning

confidence: 99%

Psychophysics, Flare, and Neurosecretory Function in Human Pain Models: Capsaicin Versus Electrically Evoked Pain

Geber

Fondel

Krämer

et al. 2007

The Journal of Pain

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“…A greater degree of peripheral and central sensitization in females has been suggested in the literature. Human studies indicate that women have a greater pain response to intradermal capsaicin than men, indicating greater peripheral sensitization (Gazerani et al, 2005; Gazerani et al, 2007), and a larger area of secondary hyperalgesia, indicating central sensitization (Jensen and Petersen, 2006; Gazerani et al, 2007). Sex differences in nocifensive responses to intraplantar capsaicin have also been noted in rats (Lu et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Female sex and obesity increase photophobic behavior in mice

2016

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Migraine affects predominantly women. Furthermore, epidemiological studies suggest that obesity is a risk factor for migraine and this association is influenced by sex. However, the biological basis for this bias is unclear. To address this issue, we assessed light avoidant behavior, a surrogate of photophobia, in female C57BL/6J mice fed regular diet (RD) or high fat diet (HFD, 60% kcal from fat). We first assessed sex differences in basal photophobia in 20-25 week old mice and found that both obese and lean females spent significantly less time in light than their male counterparts. Next, we assessed photophobia evoked by trigeminal stimulation with intradermal capsaicin. Females at 20-25 weeks of age did not display capsaicin-evoked photophobic behavior unless they had diet-induced obesity. When we tested 8-11 week old females to determine if the diet alone could be responsible for this effect, we found that both HFD and RD 8-11 week old females exhibit capsaicin-evoked photophobic behavior. This is in contrast to what we have previously shown in males and indicates a sex difference in the photophobic behavior of mice. Comparison of 20-25 week old RD mice with 8-11 week old RD mice suggests that age or age-related weight gain may contribute to capsaicin-evoked photophobic behavior in males, but not in females. These findings suggest that obesity exacerbates photophobia in both sexes, but additional work is needed to understand the sex- and age-specific mechanisms that may contribute to photophobia and trigeminal pain.

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“…Interestingly, while gender has been described as important for differences in nociceptive pain sensitivity, a study on the secondary hyperalgesia induced by heat and capsaicin did not reveal a gender difference [119]. Nevertheless, recent data show that pain sensitivity including secondary hyperalgesia and brush evoked allodynia is heritable, with an estimated 50% genetic contribution to the pain variance [172].…”

Section: Central Sensitization In Human Volunteersmentioning

confidence: 99%

Central sensitization: Implications for the diagnosis and treatment of pain

Woolf¹

2011

Pain

3,497

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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Gender Differences in Pain and Secondary Hyperalgesia After Heat/Capsaicin Sensitization in Healthy Volunteers

Cited by 62 publications

References 37 publications

Psychophysics, Flare, and Neurosecretory Function in Human Pain Models: Capsaicin Versus Electrically Evoked Pain

Psychophysics, Flare, and Neurosecretory Function in Human Pain Models: Capsaicin Versus Electrically Evoked Pain

Female sex and obesity increase photophobic behavior in mice

Central sensitization: Implications for the diagnosis and treatment of pain

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