Reciprocal links between anxiety sensitivity and obsessive-compulsive symptoms in youth: a longitudinal twin study.

BACKGROUND: Anxiety sensitivity, the tendency to fear the symptoms of anxiety, is a key risk factor for the development anxiety disorders. Although obsessive-compulsive disorder was previously classified as an anxiety disorder, the prospective relationship between anxiety sensitivity and obsessive-compulsive symptoms (OCS) has been largely overlooked. Furthermore, a lack of genetically informative studies means the aetiology of the link between anxiety sensitivity and OCS remains unclear. METHODS: Adolescent twins and siblings (N = 1,579) from the G1219 study completed self-report questionnaires two years apart assessing anxiety sensitivity, OCS, anxiety and depression. Linear regression models tested prospective associations between anxiety sensitivity and OCS, with and without adjustment for anxiety and depressive symptoms. A phenotypic cross-lagged model assessed bidirectional influences between anxiety sensitivity and OCS over time, and a genetic version of this model examined the aetiology of these associations. RESULTS: Anxiety sensitivity was prospectively associated with changes in OCS, even after controlling for comorbid anxiety and depressive symptoms. The longitudinal relationship between anxiety sensitivity and OCS was bidirectional, and these associations were predominantly accounted for by nonshared environmental influences. CONCLUSIONS: Our findings are consistent with the notion that anxiety sensitivity is a risk factor for OCS during adolescence, but also suggest that experiencing OCS confers risk for heightened anxiety sensitivity. The reciprocal links between OCS and anxiety sensitivity over time are likely to be largely mediated by nonshared environmental experiences, as opposed to common genes. Our findings raise the possibility that interventions aimed at ameliorating anxiety sensitivity could reduce risk for OCS, and vice versa.

The CODATwins Project: The Current Status and Recent Findings of COllaborative Project of Development of Anthropometrical Measures in Twins.

The COllaborative project of Development of Anthropometrical measures in Twins (CODATwins) project is a large international collaborative effort to analyze individual-level phenotype data from twins in multiple cohorts from different environments. The main objective is to study factors that modify genetic and environmental variation of height, body mass index (BMI, kg/m2) and size at birth, and additionally to address other research questions such as long-term consequences of birth size. The project started in 2013 and is open to all twin projects in the world having height and weight measures on twins with information on zygosity. Thus far, 54 twin projects from 24 countries have provided individual-level data. The CODATwins database includes 489,981 twin individuals (228,635 complete twin pairs). Since many twin cohorts have collected longitudinal data, there is a total of 1,049,785 height and weight observations. For many cohorts, we also have information on birth weight and length, own smoking behavior and own or parental education. We found that the heritability estimates of height and BMI systematically changed from infancy to old age. Remarkably, only minor differences in the heritability estimates were found across cultural-geographic regions, measurement time and birth cohort for height and BMI. In addition to genetic epidemiological studies, we looked at associations of height and BMI with education, birth weight and smoking status. Within-family analyses examined differences within same-sex and opposite-sex dizygotic twins in birth size and later development. The CODATwins project demonstrates the feasibility and value of international collaboration to address gene-by-exposure interactions that require large sample sizes and address the effects of different exposures across time, geographical regions and socioeconomic status.

A bad night's sleep on campus: an interview study of first-year university students with poor sleep quality.

BACKGROUND: Poor sleep quality is common in university students and increases the risk of mental illness and poor academic attainment. It is therefore critical to understand what may cause or aggravate poor sleep in students. First-year students living on campus are particularly worthy of attention due to their distinctive sleeping circumstances: they are adapting to a new lifestyle, sleep in close proximity to new peers, and experience environmental noise and academic stress. METHOD: Fifteen first-year undergraduates with poor sleep quality completed in-depth interviews in which they were asked about aspects of university life that might contribute to their poor sleep quality. RESULTS: Four main themes were constructed from the data using thematic analysis: the social context of noise problems; the lure of socializing with peers; the cost of having an unstructured academic lifestyle; and the wide-reaching impact of poor sleep quality on university life. Flatmates and friends were central to poor sleep quality on campus because they caused excessive noise and provided an easy opportunity to socialize late into the night. Academic factors, including students working late at night and spending all day in their bedrooms, were also key. CONCLUSION: Fundamental aspects of moving to university, including living with peers and adapting to a new academic schedule, may increase the risk of students' poor sleep quality. When designing interventions to minimize the risk of poor sleep quality in first-year students, unique aspects of the campus environment, including the close proximity to new peers, must be addressed.

Are punitive parenting and stressful life events environmental risk factors for obsessive-compulsive symptoms in youth? A longitudinal twin study.

BACKGROUND: Punitive parenting and stressful life events are associated with obsessive-compulsive symptoms (OCS). However, the lack of longitudinal, genetically-informative studies means it remains unclear whether these factors represent environmentally-mediated risks for the development of OCS. METHODS: Twins and siblings from the Genesis1219 study completed self-report questionnaires two years apart (Time 1: N = 2616, mean age = 15.0; Time 2: N = 1579, mean age = 17.0 years) assessing OCS, maternal and paternal punitive parenting, and dependent stressful life events. Multiple regression models tested cross-sectional and longitudinal associations between the putative environmental risk factors and obsessive-compulsive symptoms using: (a) individual scores; and (b) monozygotic twin difference scores. The aetiologies of significant phenotypic associations between putative risk factors and OCS were further examined using multivariate genetic models. RESULTS: At a phenotypic level, maternal and paternal punitive parenting and stressful life events were all associated with OCS both cross-sectionally and longitudinally. However, only stressful life events predicted the subsequent development of OCS, after controlling for earlier symptoms. Genetic models indicated that the association between life events and change in OCS symptoms was due to both genetic (48%) and environmental (52%) influences. Overall, life events associated with change in OCS accounted for 1.2% of variation in OCS at Time 2. CONCLUSIONS: Stressful life events, but not punitive parenting, predict OCS change during adolescence at a phenotypic level. This association exists above and beyond genetic confounding, consistent with the hypothesis that stressful life events play a causal role in the development of obsessive-compulsive symptoms.

Sleeping with one eye open: loneliness and sleep quality in young adults.

BACKGROUND: Feelings of loneliness are common among young adults, and are hypothesized to impair the quality of sleep. In the present study, we tested associations between loneliness and sleep quality in a nationally representative sample of young adults. Further, based on the hypothesis that sleep problems in lonely individuals are driven by increased vigilance for threat, we tested whether past exposure to violence exacerbated this association. METHOD: Data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2232 twins born in England and Wales in 1994 and 1995. We measured loneliness using items from the UCLA Loneliness Scale, and sleep quality using the Pittsburgh Sleep Quality Index. We controlled for covariates including social isolation, psychopathology, employment status and being a parent of an infant. We examined twin differences to control for unmeasured genetic and family environment factors. RESULTS: Feelings of loneliness were associated with worse overall sleep quality. Loneliness was associated specifically with subjective sleep quality and daytime dysfunction. These associations were robust to controls for covariates. Among monozygotic twins, within-twin pair differences in loneliness were significantly associated with within-pair differences in sleep quality, indicating an association independent of unmeasured familial influences. The association between loneliness and sleep quality was exacerbated among individuals exposed to violence victimization in adolescence or maltreatment in childhood. CONCLUSIONS: Loneliness is robustly associated with poorer sleep quality in young people, underscoring the importance of early interventions to mitigate the long-term outcomes of loneliness. Special care should be directed towards individuals who have experienced victimization.

A longitudinal twin and sibling study of the hopelessness theory of depression in adolescence and young adulthood.

BACKGROUND: Maladaptive cognitive biases such as negative attributional style and hopelessness have been implicated in the development and maintenance of depression. According to the hopelessness theory of depression, hopelessness mediates the association between attributional style and depression. The aetiological processes underpinning this influential theory remain unknown. The current study investigated genetic and environmental influences on hopelessness and its concurrent and longitudinal associations with attributional style and depression across adolescence and emerging adulthood. Furthermore, given high co-morbidity between depression and anxiety, the study investigated whether these maladaptive cognitions constitute transdiagnostic cognitive content common to both internalizing symptoms. METHOD: A total of 2619 twins/siblings reported attributional style (mean age 15 and 17 years), hopelessness (mean age 17 years), and depression and anxiety symptoms (mean age 17 and 20 years). RESULTS: Partial correlations revealed that attributional style and hopelessness were uniquely associated with depression but not anxiety symptoms. Hopelessness partially mediated the relationship between attributional style and depression. Hopelessness was moderately heritable (A = 0.37, 95% confidence interval 0.28-0.47), with remaining variance accounted for by non-shared environmental influences. Independent pathway models indicated that a set of common genetic influences largely accounted for the association between attributional style, hopelessness and depression symptoms, both concurrently and across development. CONCLUSIONS: The results provide novel evidence that associations between attributional style, hopelessness and depression symptoms are largely due to shared genetic liability, suggesting developmentally stable biological pathways underpinning the hopelessness theory of depression. Both attributional style and hopelessness constituted unique cognitive content in depression. The results inform molecular genetics research and cognitive treatment approaches.

The stability and change of etiological influences on depression, anxiety symptoms and their co-occurrence across adolescence and young adulthood.

BACKGROUND: Depression and anxiety persist within and across diagnostic boundaries. The manner in which common v. disorder-specific genetic and environmental influences operate across development to maintain internalizing disorders and their co-morbidity is unclear. This paper investigates the stability and change of etiological influences on depression, panic, generalized, separation and social anxiety symptoms, and their co-occurrence, across adolescence and young adulthood. METHOD: A total of 2619 twins/siblings prospectively reported symptoms of depression and anxiety at mean ages 15, 17 and 20 years. RESULTS: Each symptom scale showed a similar pattern of moderate continuity across development, largely underpinned by genetic stability. New genetic influences contributing to change in the developmental course of the symptoms emerged at each time point. All symptom scales correlated moderately with one another over time. Genetic influences, both stable and time-specific, overlapped considerably between the scales. Non-shared environmental influences were largely time- and symptom-specific, but some contributed moderately to the stability of depression and anxiety symptom scales. These stable, longitudinal environmental influences were highly correlated between the symptoms. CONCLUSIONS: The results highlight both stable and dynamic etiology of depression and anxiety symptom scales. They provide preliminary evidence that stable as well as newly emerging genes contribute to the co-morbidity between depression and anxiety across adolescence and young adulthood. Conversely, environmental influences are largely time-specific and contribute to change in symptoms over time. The results inform molecular genetics research and transdiagnostic treatment and prevention approaches.

The effect of medial temporal lobe epilepsy on visual memory encoding.

Effective visual memory encoding, a function important for everyday functioning, relies on episodic and semantic memory processes. In patients with medial temporal lobe epilepsy (MTLE), memory deficits are common as the structures typically involved in seizure generation are also involved in acquisition, maintenance, and retrieval of episodic memories. In this study, we used group independent component analysis (GICA) combined with Granger causality analysis to investigate the neuronal networks involved in visual memory encoding during a complex fMRI scene-encoding task in patients with left MTLE (LMTLE; N=28) and in patients with right MTLE (RMTLE; N=18). Additionally, we built models of memory encoding in LMTLE and RMTLE and compared them with a model of healthy memory encoding (Nenert et al., 2014). For those with LMTLE, we identified and retained for further analyses and model generation 7 ICA task-related components that were attributed to four different networks: the frontal and posterior components of the DMN, visual network, auditory-insular network, and an "other" network. For those with RMTLE, ICA produced 9 task-related components that were attributed to the somatosensory and cerebellar networks in addition to the same networks as in patients with LMTLE. Granger causality analysis revealed group differences in causality relations within the visual memory network and MTLE-related deviations from normal network function. Our results demonstrate differences in the networks for visual memory encoding between those with LMTLE and those with RMTLE. Consistent with previous studies, the organization of memory encoding is dependent on laterality of seizure focus and may be mediated by functional reorganization in chronic epilepsy. These differences may underlie the observed differences in memory abilities between patients with LMTLE and patients with RMTLE and highlight the modulating effects of epilepsy on the network for memory encoding.

Social jetlag, obesity and metabolic disorder: investigation in a cohort study.

BACKGROUND: Obesity is one of the leading causes of preventable death worldwide. Circadian rhythms are known to control both sleep timing and energy homeostasis, and disruptions in circadian rhythms have been linked with metabolic dysfunction and obesity-associated disease. In previous research, social jetlag, a measure of chronic circadian disruption caused by the discrepancy between our internal versus social clocks, was associated with elevated self-reported body mass index, possibly indicative of a more generalized association with obesity and metabolic dysfunction. METHODS: We studied participants from the population-representative Dunedin Longitudinal Study (N=1037) to determine whether social jetlag was associated with clinically assessed measurements of metabolic phenotypes and disease indicators for obesity-related disease, specifically, indicators of inflammation and diabetes. RESULTS: Our analysis was restricted to N=815 non-shift workers in our cohort. Among these participants, we found that social jetlag was associated with numerous clinically assessed measures of metabolic dysfunction and obesity. We distinguished between obese individuals who were metabolically healthy versus unhealthy, and found higher social jetlag levels in metabolically unhealthy obese individuals. Among metabolically unhealthy obese individuals, social jetlag was additionally associated with elevated glycated hemoglobin and an indicator of inflammation. CONCLUSIONS: The findings are consistent with the possibility that 'living against our internal clock' may contribute to metabolic dysfunction and its consequences. Further research aimed at understanding that the physiology and social features of social jetlag may inform obesity prevention and have ramifications for policies and practices that contribute to increased social jetlag, such as work schedules and daylight savings time.

Cognitive content specificity in anxiety and depressive disorder symptoms: a twin study of cross-sectional associations with anxiety sensitivity dimensions across development.

BACKGROUND: The classification of anxiety and depressive disorders has long been debated and has important clinical implications. The present study combined a genetically sensitive design and multiple time points to investigate cognitive content specificity in anxiety and depressive disorder symptoms across anxiety sensitivity dimensions, a cognitive distortion implicated in both disorders. METHOD: Phenotypic and genetic correlations between anxiety sensitivity dimensions, anxiety and depressive disorder symptoms were examined at five waves of data collection within childhood, adolescence and early adulthood in two representative twin studies (n pairs = 300 and 1372). RESULTS: The physical concerns dimension of anxiety sensitivity (fear of bodily symptoms) was significantly associated with anxiety but not depression at all waves. Genetic influences on physical concerns overlapped substantially more with anxiety than depression. Conversely, mental concerns (worry regarding cognitive control) were phenotypically more strongly associated with depression than anxiety. Social concerns (fear of publicly observable symptoms of anxiety) were associated with both anxiety and depression in adolescence. Genetic influences on mental and social concerns were shared to a similar extent with both anxiety and depression. CONCLUSIONS: Phenotypic patterns of cognitive specificity and broader genetic associations between anxiety sensitivity dimensions, anxiety and depressive disorder symptoms were similar at all waves. Both disorder-specific and shared cognitive concerns were identified, suggesting it is appropriate to classify anxiety and depression as distinct but related disorders and confirming the clinical perspective that cognitive therapy is most likely to benefit by targeting cognitive concerns relating specifically to the individual's presenting symptoms across development.

Aetiological overlap between obsessive-compulsive and depressive symptoms: a longitudinal twin study in adolescents and adults.

BACKGROUND: Depression is commonly co-morbid with obsessive-compulsive disorder (OCD). However, it is unknown whether depression is a functional consequence of OCD or whether these disorders share a common genetic aetiology. This longitudinal twin study compared these two hypotheses. METHOD: Data were drawn from a longitudinal sample of adolescent twins and siblings (n = 2651; Genesis 12-19 study) and from a cross-sectional sample of adult twins (n = 4920). The longitudinal phenotypic associations between OCD symptoms (OCS) and depressive symptoms were examined using a cross-lag model. Multivariate twin analyses were performed to explore the genetic and environmental contributions to the cross-sectional and longitudinal relationship between OCS and depressive symptoms. RESULTS: In the longitudinal phenotypic analyses, OCS at time 1 (wave 2 of the Genesis 12-19 study) predicted depressive symptoms at time 2 (wave 3 of the Genesis 12-19 study) to a similar extent to which depressive symptoms at time 1 predicted OCS at time 2. Cross-sectional twin analyses in both samples indicated that common genetic factors explained 52-65% of the phenotypic correlation between OCS and depressive symptoms. The proportion of the phenotypic correlation due to common non-shared environmental factors was considerably smaller (35%). In the adolescent sample, the longitudinal association between OCS at time 1 and subsequent depressive symptoms was accounted for by the genetic association between OCS and depressive symptoms at time 1. There was no significant environmental association between OCS and later depressive symptoms. CONCLUSIONS: The present findings show that OCS and depressive symptoms co-occur primarily due to shared genetic factors and suggest that genetic, rather than environmental, effects account for the longitudinal relationship between OCS and depressive symptoms.

Phenotypic and genetic structure of anxiety sensitivity in adolescence and early adulthood.

Anxiety sensitivity is a risk factor for emotional disorders. The structure of anxiety sensitivity was examined using phenotypic and genetic analyses. Self-reported anxiety sensitivity was measured at three time points from adolescence into young adulthood by 2651 individuals from the G1219 twin study. Confirmatory factor analyses revealed comparable statistical support for anxiety sensitivity models consisting of three or four dimensions across all time points. The three-factor model depicting Physical, Social and Mental anxiety-related concerns was favoured due to greater interpretability and parsimony. Multivariate quantitative genetic analyses supported a hierarchical structure with general genetic (.09-.61) and non-shared environmental (.39-.72) influences acting via a higher-order factor as well as dimension-specific genetic (.09-.21) and non-shared environmental (.23-.68) influences. The findings provide further evidence for a hierarchical structure underlying different dimensions of anxiety sensitivity.

Associations between diurnal preference, sleep quality and externalizing behaviours: a behavioural genetic analysis.

BACKGROUND: Certain aspects of sleep co-occur with externalizing behaviours in youth, yet little is known about these associations in adults. The present study: (1) examines the associations between diurnal preference (morningness versus eveningness), sleep quality and externalizing behaviours; (2) explores the extent to which genetic and environmental influences are shared between or are unique to these phenotypes; (3) examines the extent to which genetic and environmental influences account for these associations. method: Questionnaires assessing diurnal preference, sleep quality and externalizing behaviours were completed by 1556 young adult twins and siblings. RESULTS: A preference for eveningness and poor sleep quality were associated with greater externalizing symptoms [r=0.28 (95% CI 0.23-0.33) and 0.34 (95% CI 0.28-0.39), respectively]. A total of 18% of the genetic influences on externalizing behaviours were shared with diurnal preference and sleep quality and an additional 14% were shared with sleep quality alone. Non-shared environmental influences common to the phenotypes were small (2%). The association between diurnal preference and externalizing behaviours was mostly explained by genetic influences [additive genetic influence (A)=80% (95% CI 0.56-1.01)], as was the association between sleep quality and externalizing behaviours [A=81% (95% CI 0.62-0.99)]. Non-shared environmental (E) influences accounted for the remaining variance for both associations [E=20% (95% CI -0.01 to 0.44) and 19% (95% CI 0.01-0.38), respectively]. CONCLUSIONS: A preference for eveningness and poor sleep quality are moderately associated with externalizing behaviours in young adults. There is a moderate amount of shared genetic influences between the phenotypes and genetic influences account for a large proportion of the association between sleep and externalizing behaviours. Further research could focus on identifying specific genetic polymorphisms common to both sleep and externalizing behaviours.

The presence of a perseverative iterative style in poor vs. good sleepers.

Catastrophizing is present in worriers and poor sleepers. This study investigates whether poor sleepers possess a 'perseverative iterative style' which predisposes them to catastrophize any topic, regardless of content or affective valence, a style previously found to occur more commonly in worriers as compared to others. Poor (n=23) and good sleepers (n=37) were distinguished using the Pittsburgh Sleep Quality Index (PSQI), from a sample of adults in the general population. Participants were required to catastrophize 2 topics: worries about sleep, and a current personal worry; and to iterate the positive aspects of a hypothetical topic. Poor sleepers catastrophized/iterated more steps to a greater extent than good sleepers to these three interviews, (F(1, 58)=7.35, p<.05). However, after controlling for anxiety and worry, this effect was reduced to non-significance for the 'sleep' and 'worry' topics, suggesting that anxiety may mediate some of the association between catastrophizing and sleep. However there was still a tendency for poor sleepers to iterate more steps to the 'hypothetical' topic, after controlling for anxiety and worry, which also suggests that poor sleepers possess a cognitive style which may predispose them to continue iterating consecutive steps to open-ended tasks regardless of anxiety and worry. Future research should examine whether the presence of this cognitive style is significant in leading to or maintaining insomnia.

Genetic and phenotypic heterogeneity in pattern dystrophy.

BACKGROUND: The pattern dystrophies (PD) represent a clinically heterogeneous family of inherited macular diseases frequently caused by mutations in the peripherin/RDS gene. Most previous studies have detailed the clinical findings in single families, making it difficult to derive data from which progression and visual outcome can be generalised. METHODS: Families were ascertained and clinically evaluated including angiography and electrophysiology where appropriate. RESULTS: In each of the six families with autosomal dominant PD, a mutation in the peripherin/RDS gene was identified, including a novel Cys250Phe variant. These data suggest that the condition is characterised by the accumulation of yellow to grey subretinal flecks, followed by pigmentary change accompanied by patches of chorioretinal atrophy. Subsequently, 50% (16/32) of individuals with PD developed poor central vision because of chorioretinal geographic atrophy or subretinal neovascularisation. The risk of these complications appears to increase with age. CONCLUSION: PD should not necessarily be considered a benign condition. Instead, patients should be counselled that there is a significant chance of losing central vision in their later years. Some elderly patients with probands showing PD may be misdiagnosed with age related macular degeneration owing to the phenotypic similarities between these conditions in the advanced state.

Gene-environment interaction analysis of serotonin system markers with adolescent depression.

We report analyses from a study of gene-environment interaction in adolescent depression. The sample was selected from 1990 adolescents aged 10-20 years: those with depression symptoms in the top or bottom 15% were identified and divided into high or low environmental risk groups. DNA was obtained from 377 adolescents, representing the four quadrants of high or low depression and high or low environmental risk. Markers within, or close to, each of the serotonergic genes 5HTT, HTR2A, HTR2C, MAOA (monoamine oxidase type A) and tryptophan hydroxylase (TPH) were genotyped. Environmental risk group was a nonsignificant predictor and sex was a significant predictor of the depression group. HTR2A and TPH significantly predicted the depression group, independent of the effects of sex, environmental risk group and their interaction. In addition, there was a trend for an effect of 5HTTLPR, which was significant in female subjects. Furthermore, there was a significant genotype-environmental risk interaction for 5HTTLPR in female subjects only, with the effect being in the same direction as another recent study, reaffirming that an important source of genetic heterogeneity is exposure to environmental risk.

SF-36 general health status survey to determine patient satisfaction at short-term follow-up after total hip and knee arthroplasty.

The purpose of this study was to determine whether the SF-36 general health status survey was sensitive enough to document early improvements in patient health after total hip arthroplasty (THA) and total knee arthroplasty (TKA). Early follow-up data were collected an average of 3 months after surgery. Results were striking, showing statistically significant improvements in all pain and function subcategories of the SF-36 for both THA and TKA. Further, the survey instrument successfully differentiated the course of healing after THA and TKA; at this early follow-up period, the patients who had had THA expressed greater improvement in pain, function, and overall health than did patients who had had TKA. These data suggest that the SF-36 is a simple, easy-to-administer, and effective instrument for monitoring improvements in patient health after THA and TKA.

Integral porous femoral stem. 5-to 8-Year follow-up study.

The outcome of total hip arthroplasty without cement was prospectively followed in patients who received a titanium taper wedge femoral component with a circumferential titanium plasma spray coating on the proximal surface (Integral femoral stem, Biomet, Warsaw, IN). One hundred ninety femoral components were implanted in 179 patients. Nine patients (9 hips) died prior to their 5-year examination, leaving 170 patients available for follow-up evaluation. Thirty-one of the 170 patients (33 hips) were lost at an intermediate follow-up period of 5 years. (mean, 5.8 years, range; 5-8 years), giving a follow-up rate of 82% for patients and hips. The preoperative diagnoses included osteoarthritis (91 hips), avascular necrosis (38), post-traumatic arthritis (10), rheumatoid arthritis (4), congenital dislocation of the hip (3), and fractures (2). The 78 men and 61 women had a mean age of 55 years (range, 18-81 years) and a mean weight of 81 kg (range, 50-136 kg). Pre-operative Harris pain and function scores for the hip were 19.9 (range, 0-40) and 55.6 (range, 12-84), respectively. At the most recent follow-up visit, the mean pain score increased to 41.2 (range, 10-44) and the mean function score increased to 93.5 (range, 6-100). Thigh pain was present in 4% of the hips at the most recent follow-up visit. Radiographically, 99% of the femoral components demonstrated spot welds in the porous-coated zone. Two hips had demarcation of the femoral component in the porous-coated zone consistent with fibrous fixation. None of the femoral stems had been revised and there were no signs of aseptic loosening. Additionally, there were no cases of pain that could be directly attributed to the stem and there was no evidence of distal femoral osteolysis. It is concluded that the integral femoral stem provides excellent clinical and radiographic results at intermediate follow-up periods.

Collection of surgical specimens in total joint arthroplasty. Is routine pathology cost effective?

A retrospective review of 715 consecutive cases of total joint arthroplasty (283 hips, 432 knees), performed for a variety of indications during 1992 and 1993, was undertaken to assess the cost effectiveness of routine pathologic examination. The charts were reviewed for preoperative, operative, and pathologic diagnosis, and any discrepancies in diagnosis were noted. Particular attention was paid to pathologic findings suggestive of neoplasia or rheumatoid arthritis that were not noted in the preoperative or operative diagnoses. Six of the 715 cases fit into this category, but all failed to have any clinical significance. No alteration in patient care resulted from routine pathologic examination. This paper questions the necessity of routinely submitting pathologic specimens in uncomplicated total hip and knee arthroplasty.