Female predominance in certain chronic pain syndromes begins to arise in adolescence, suggesting that age or puberty may be a marker for the emergence of gender differentiation in pain. Research shows estrogen affects pain sensitivity. However, studies have not always found higher pain responsivity in the luteal phase of menses (when estrogen levels are high) compared to the follicular phase (when estrogen is relatively low). This suggests that there are other factors which modulate the effects of estrogen on pain responses. Psychological vulnerability, as manifested in heightened physiological reactivity, sensitivity to somatic sensations, and a threat-oriented attentional focus, has been linked to increased pain responsivity. A composite of these psychological vulnerability factors may interact with estrogen levels (and thus puberty status) to produce enhanced pain responsivity in late puberty females. Experimental work to test this hypothesis is lacking; the developmental trajectory for the emergence of adult chronic pain has not been studied. A gender (male vs. female) by puberty status (early: Tanner Stages I-II vs. late: Tanner Stages III-V) by psychological vulnerability (low vs. high composite score) by task type (thermal, pressure and cold pressor pain) between-within factorial design will be used to examine the role of puberty in laboratory pain responsivity among 240 health children, ages 8-17 years.
The aims of the study are to: (1) examine among health children the effects of gender, puberty and psychological vulnerability on pain responsivity as measured by subjective, behavioral, autonomic, gonadal and pituitary-adrenal responses to three types of laboratory pain tasks; (2) examine interactions between gender, puberty, and psychological vulnerability in three types of pain responses (tolerance, intensity ratings and distress ratings); and (3) determine the effects of stage of menses (luteal vs. follicular) and dysmenorrhea on pain responsivity among post-menarchal females adolescents. Puberty status will be identified by self-rating pictorial questionnaires tied to Tanner staging and confirmed by hormone assays (FSH, E2, progesterone, testosterone and DHEA-S). Physiologic (ANS) behavioral (tolerance) and subjective measures (pain intensity and distress ratings) will be recorded in response to each pain task. Two finger pricks for spot blood analyses 20 minutes apart will test for stress reactivity in two systems (cortisol, prolactin). Potential psychosocial moderators of pain responsivity (e.g., concurrent negative life events, past experiences with pain, and adherence to traditional gender roles which emphasize passivity and helplessness among females) will also be assessed. This study is an initial step in understanding the role of puberty in the developmental trajectory of gender differences in pain responsivity from childhood to adulthood.
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