Association of pain catastrophizing with labor pain and analgesia consumption in obstetrical patients.

INTRODUCTION: Pain catastrophizing is an exaggerated negative orientation to painful stimuli which in obstetric patients is associated with fear of overwhelming labor pain and negative pain-related outcomes. This study aimed to quantitatively examine the association of pain catastrophizing with maternal labor pain outcomes. METHODS: We conducted a prospective observational study of women admitted for a vaginal trial of labor. Subjects completed the 13-item Pain Catastrophizing scale (PCS) questionnaire (scored 0 to 52, higher scores representing greater catastrophizing). Pain was assessed at baseline and at request for neuraxial labor analgesia. Labor and postpartum pain intensity was assessed as the average area under the pain intensity by time curve. Pain at request for analgesia, labor pain, postpartum pain, analgesic consumption, and quality of recovery was compared between high (PCS ≥ 17) and low catastrophizing groups. RESULTS: Data from 138/157 (88%) subjects were included in the analysis. Median (IQR) pain scores at request for analgesia were 9 (8,10) and 8 (6,9), a difference of 1 (95% CI 0 to 2.5, P = 0.008) in high-catastrophizing and in low-catastrophizing groups, respectively. Adjusted pain during labor, postpartum pain and opioid analgesic use were not significantly different. High-catastrophizers reported less comfort, ability to mobilize and less control during hospitalization. Post-discharge there were no differences in pain or analgesic use. CONCLUSION: We did not observe greater labor or post-delivery pain or increased analgesic use in high-catastrophizing parturients. High catastrophizers reported greater pain when requesting analgesia, which is consistent with the role of catastrophizing in intensifying the experience of pain.

Novel trabecular meshwork inducible glucocorticoid response mutation in an eight-generation juvenile-onset primary open-angle glaucoma pedigree.

OBJECTIVE: This study aimed to update a large kindred with juvenile-onset primary open-angle glaucoma (POAG) first described in 1940 and to identify the underlying genetic cause of the disease. DESIGN: Molecular genetic study of a single kindred, including clinical examination, retrospective review of clinical and family history records, linkage analysis, and mutation screening. PARTICIPANTS: The retrospective review included 957 members of a single large family. The linkage study included 40 members of 1 branch of the family in which juvenile-onset POAG is segregating in an autosomal-dominant pattern. Mutation screening included 15 at-risk family members with juvenile-onset POAG, probands of 40 families with adult-onset POAG, probands of 11 additional unrelated juvenile-onset POAG families, and 43 unrelated normal control subjects. INTERVENTION: Clinical and family history records were obtained, ophthalmologic examinations were performed, and blood samples were drawn for use in genotyping. MAIN OUTCOME MEASURES: Allele sizes of microsatellite repeat genetic markers from the vicinity of the GLC1A glaucoma gene on chromosome 1q were assigned based on size fractionation of DNA fragments generated by polymerase chain reaction (PCR). Linkage was established by the method of lod scores. Mutations were identified by determination of the DNA sequence of PCR products amplified from the trabecular meshwork inducible glucocorticoid response (TIGR) gene. Glaucoma status for purposes of linkage and mutation analysis was based on a combination of ophthalmologic examination, clinical records, family history, and previously published information. For some individuals reported in the pedigree, but not included in the genotyping studies, less information was available as presented in the text and tables. RESULTS: Autosomal-dominant POAG was confirmed or reported for 78 members of an 8-generation family. Linkage analysis showed significant evidence for linkage of juvenile-onset POAG in one branch of the family to D1S452 (maximum lod score of 6.42 at a recombination fraction of 0.00) and other markers in the vicinity of the GLC1A gene on chromosome 1q. Screening of the TIGR gene identified a mutation that results in substitution of asparagine for isoleucine at codon 477 near the carboxyterminal end of the protein. CONCLUSIONS: The authors' findings strongly suggest that the juvenile-onset POAG locus in this family is the GLC1A locus and that the underlying cause of the disease is the IIe477Asn TIGR mutation that cosegregates with juvenile-onset POAG in one branch of this large family. Lack of samples from deceased individuals prevented the authors from determining whether reported adult-onset cases in this family could also be attributed to the IIe477Asn TIGR mutation. Absence of the IIe477Asn TIGR mutation from other juvenile- and adult-onset POAG families implies that this TIGR mutation is not a common cause of glaucoma.

The impact of a decade of policy on home health care utilization.

The Medicare home health care eligibility changes, which occurred during the 1980s, were designed to make home health care more accessible to older adults. Ideally, by the 1990s, older adults in need of home health care services should no longer have encountered barriers to accessing this benefit. Therefore, an individual's need for home health care services should have been the primary determinant of service utilization. This paper examined whether need was predictive of home health care use. Client-level data on the case mix of home health care agencies in San Francisco and Philadelphia, as well as agency administrator interview data, were analyzed to determine which characteristics were the best predictors of home health care use. The regression analyses results revealed that, although client characteristics were important predictors of the amount and type of home health care services received during an episode of care, client characteristics alone did not adequately predict the amount and type of home health care services received by older adults.

Mapping of a gene for autosomal dominant juvenile-onset open-angle glaucoma to chromosome Iq.

A large Caucasian family is presented, in which a juvenile-onset form of open-angle glaucoma is transmitted in an autosomal dominant fashion. Sixteen affected family members were identified from 31 at-risk individuals descended from the affected founder. Affected patients developed high intraocular pressures (sometimes > 40 mm Hg) within the first 2 decades of life. Linkage analysis between the disease phenotype and 12 microsatellite repeat markers located on chromosome 1q gave a maximum lod score of 8.38 at a recombination fraction of zero for marker D1S210. Analysis of recombinant haplotypes suggests a total inclusion region of about 14 cM between markers D1S194 and D1S218 at 1q21-q31. This represents the second juvenile-glaucoma family, in which the disease has been mapped to the long arm of chromosome 1.