Pain
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Multicenter Study
The migraine eye: distinct rod-driven retinal pathways' response to dim light challenges the visual cortex hyperexcitability theory.
Migraine-type photophobia, most commonly described as exacerbation of headache by light, affects nearly 90% of the patients. It is the most bothersome symptom accompanying an attack. Using subjective psychophysical assessments, we showed that migraine patients are more sensitive to all colors of light during ictal than during interictal phase and that control subjects do not experience pain when exposed to different colors of light. ⋯ Unexpectedly, it was the amplitude of the retinal rod-driven b wave, which was consistently larger (by 14%-19% in the light-adapted and 18%-34% in the dark-adapted flash ERG) in the migraineurs than in the controls, rather than the retinal cone-driven a wave or the visual-evoked potentials that differs most strikingly between the 2 groups. Mechanistically, these findings suggest that the inherent hypersensitivity to light among migraine patients may originate in the retinal rods rather than retinal cones or the visual cortex. Clinically, the findings may explain why migraineurs complain that the light is too bright even when it is dim to the extent that nonmigraineurs feel as if they are in a cave.
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Multicenter Study
CACNG2 polymorphisms associate with chronic pain following mastectomy.
Chronic postmastectomy pain (PMP) imposes a major burden on the quality of life of the ever-increasing number of long-term survivors of breast cancer. An earlier report by Nissenbaum et al. claimed that particular polymorphisms in the gene CACNG2 are associated with the risk of developing chronic PMP after breast surgery (Nissenbaum J, Devor M, Seltzer Z, Gebauer M, Michaelis M, Tal M, Dorfman R, Abitbul-Yarkoni M, Lu Y, Elahipanah T, delCanho S, Minert A, Fried K, Persson AK, Shpigler H, Shabo E, Yakir B, Pisante A, Darvasi A. Susceptibility to chronic pain following nerve injury is genetically affected by CACNG2. ⋯ We found that the biomarker is selective because it did not predict pain after laparoscopic hernia repair and was not associated with pain sensitivity to experimentally applied noxious thermal stimuli. We conclude that the A-C-C haplotype at the 3 single-nucleotide polymorphisms (rs4820242, rs2284015, and rs2284017) in the CACNG2 gene is associated with increased risk of developing PMP. This information may advance current knowledge on pathophysiology of PMP and serve as a step forward in the prediction of clinical outcomes and personalized pain management.
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Multicenter Study
Obesity increases the risk of chronic pain development following motor vehicle collision.
Obesity has been found to increase the risk of musculoskeletal pain (MSP) in other settings, but to our knowledge, the influence of increased body mass index on pain outcomes after common trauma exposures such as motor vehicle collision (MVC) has not been assessed. In addition, obesity results in biomechanical changes, as well as physiologic changes including reduced hypothalamic pituitary adrenal axis negative feedback inhibition, but mechanisms by which obesity may result in worse post-traumatic outcomes remain poorly understood. ⋯ After adjusting for an array of sociodemographic factors, obesity (particularly morbid obesity) was an independent risk factor for worse MSP after MVC (eg, RR 1.41 [95% CI 1.11, 1.80] for moderate or severe MSP 6 months after MVC among morbidly obese vs normal weight MVC survivors). Interestingly, substantial effect modification was observed between obesity risk and a genetic variant known to reduce hypothalamic pituitary adrenal axis negative feedback inhibition (FKBP5 rs9380526). (eg, 41% vs 16% increased risk of moderate or severe MSP at 6 months among obese individuals with and without the risk allele.) Further studies are needed to elucidate mechanisms underlying chronic pain development in obese trauma survivors and to develop interventions that will reduce chronic pain severity among this common, at-risk group.