Letter: Sickling pain and season.

Amjad, Halima; Bannerman, R M; Judisch, Janifer M.

doi:10.1136/bmj.2.5909.54

Cited by 35 publications

(22 citation statements)

References 6 publications

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“…Previous studies have both hypothesized and investigated a correlation between meteorological or seasonal factors and frequencies of VOC (9,25,26). The results of these studies were, however, inconclusive.…”

Section: Discussionmentioning

confidence: 90%

“…The results of these studies were, however, inconclusive. Pain due to VOC in 78 patients of all ages was related to seasonal changes in Buffalo, NY, with a tendency for more episodes of pain to be associated with lower temperature and higher humidity (25). Hospital admission rates for severe painful crises were also associated with low temperature in Jamaica, but occurrence of painful crises peaked in both winter and summer in Kuwait (26,27).…”

Section: Discussionmentioning

confidence: 97%

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Pediatric Vasoocclusive Crisis and Weather Conditions

Rogovik

Persaud

Friedman

et al. 2011

The Journal of Emergency Medicine

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 97%

Pediatric Vasoocclusive Crisis and Weather Conditions

Rogovik

Persaud

Friedman

et al. 2011

The Journal of Emergency Medicine

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“…Genetic as well as environmental factors contribute to the frequency and severity of acute pain produced by VOC [24]. As for environmental factors, a number of studies found an association between cold temperatures and painful episodes [1,20,40]. Moreover, skin cooling due to wind was also associated with acute painful episodes [35], underscoring the exquisite sensitivity of VOC crises to cold.…”

Section: Discussionmentioning

confidence: 99%

Sensitization of nociceptive spinal neurons contributes to pain in a transgenic model of sickle cell disease

Cataldo

Rajput

Gupta

et al. 2015

Pain

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Chronic pain is a major characteristic feature of sickle cell disease (SCD). The refractory nature of pain and the development of chronic pain syndromes in many patients with SCD suggest that central neural mechanisms contribute to pain in this disease. We used HbSS-BERK sickle mice, which show chronic features of pain similar to those observed in SCD, and determined whether sensitization of nociceptive neurons in the spinal cord contributes to pain and hyperalgesia in SCD. Electrophysiological recordings of action potential activity were obtained from single, identified dorsal horn neurons of the spinal cord in anesthetized mice. Compared to control HbAA-BERK mice, nociceptive dorsal horn neurons in sickle mice exhibited enhanced excitability as evidenced by enlarged receptive fields, increased rate of spontaneous activity, lower mechanical thresholds, enhanced responses to mechanical stimuli, and prolonged after-discharges following mechanical stimulation. These changes were accompanied by increased phosphorylation of mitogen activated protein kinases (MAPKs) in the spinal cord that are known to contribute to neuronal hyperexcitability, including c-Jun N-terminal kinase (JNK), p44/p42 extracellular signaling-regulated kinase (ERK), and p38. These findings demonstrate that central sensitization contributes to pain in SCD.

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“…Environmental factors are likely to explain much of this variability, but have not been studied in depth, at least in part because of the logistical difficulties in conducting these studies. For example, the importance of climatic factors as precipitants of acute pain has been recognized for many years, particularly an increased frequency of pain in cold and rainy seasons, 14,15 although this is not a consistent finding. 16,17 Other potentially relevant environmental factors include air quality, housing, socio-economic status, physical activities and infections.…”

Section: Introductionmentioning

confidence: 99%