(taken from the application): The well-established comorbidity of fibromyalgia (FMS) and major depression (MDD) has motivated speculations about the direction of the relationship. Three principal hypotheses to be tested here are: (l)that FMS is a variant of depression; (2) that MDD in FMS sufferers is a reaction to FMS; and (3) that high rates of MDD in FMS patients are an artifact of studying treatment-seekers. The proposed study's first aim is to support one and refute other hypotheses, by conducting a family study. Community women meeting criteria for FMS (n= 120) will be stratified so that half (n=60) have a lifetime history of MDD. Demographically-matched non-FMS controls (n= 120) from the same sampling frame will also be stratified on MDD status. Direct psychiatric interviews and physical examinations will be conducted with probands and all their available adult first degree relatives. To support the first hypothesis, familial MDD rates should be elevated in FMS probands, even among probands with no personal depression histories; to support the second, probands with FMS and MDD should have low familial depression rates, as their depression should be more likely reactive to FMS; to support the last, familial MDD should be elevated in probands with MDD histories themselves, regardless of FMS status.
A second aim, prompted by the comorbidity of FMS and myofascial temporomandibular disorder (M/TMD), is test (1) whether M/TMD is a regional manifestation of FMS or (2) whether M/TMD comorbid with FMS is different from M/TMD expressed as a regional disorder. To accomplish this aim, we will first reconfirm that FMS is familial, utilizing data gathered to satisfy the first aim. Second, we will reconstitute the groups from Aim 1, according to both FMS and M/TMD status. Rates of familial M/TMD in FMS and control probands, broken down by proband M/TMD status, will be examined. If M/TMD is found in the family of FMS probands, regardless of proband M/TMD status, this will support the first hypothesis. If only FMS probands have familial M/TMD but M/TMD probands do not, this will support the 2nd hypothesis and indicate that the two disorders are provoked through different pathogenic processes.
