Communication skills in psychiatry residents-- how do they handle patient concerns? An application of sequence analysis to interviews with simulated patients

BACKGROUND: The main focus of the training of psychiatrists is on diagnosis and treatment based on the traditional doctor-centered approach to the psychiatric interview. Less attention is given to the correct handling of patients' emotional concerns, which is crucial for the patient-physician relationship, but also for improving diagnostic and treatment decisions. The aim of this study is to assess psychiatrists' responses to patients' concerns and worries. METHOD: 118 consultations, conducted by 10 residents in psychiatry with 20 simulated patients, have been coded using the Verona Psychiatric Interview Classification System. Lag1 sequential analysis and a multinomial logit regression analysis were performed to investigate the relationship between patients' expressions of concern and psychiatrists' subsequent interventions in terms of patient-centered skills. RESULTS: Compared to doctor-centered interventions, all patients' expressions of concern increased the probability of passive listening (odds ratios between 2.4 and 4.2). They also increased the occurrence of emotion focusing interventions (odds ratios between 3.3 and 1.7), which however remained rare (4% of residents' total responses). A small although significant increase in the likelihood of active listening expressions was observed as a response to two types of patient expressions of concern: statements of feelings (odds ratio 1.4) and expression of opinions regarding problematic psychosocial issues (odds ratio of 1.7). CONCLUSIONS: Young psychiatrists are good passive listeners but need to improve active listening skills which, together with emotion focusing skills, should be a major learning target in psychiatry. These patient-centered interviewing skills should integrate those traditionally used for attributing ICD-10 and/or DSM-IV categories.     

Recurrence patterns and surveillance for patients with early stage endometrial cancer

Introduction

To evaluate the recurrence patterns and the clinical and economic role of surveillance with vaginal cytology in women with low risk endometrial cancer.

Methods

Patients undergoing primary surgery with final pathology consistent with a grade 1 endometrial cancer confined to the endometrium (FIGO 1988 stage IA) between 9/1997–12/2007 were retrospectively identified. Follow-up data for at least 2 years was also collected, including diagnosis of a recurrence, symptomatology at that time, and method of detection. Costs for vaginal cytology were estimated using Medicare charge-to-cost ratios adjusted to 2010 costs.

Results

One hundred fifty-four patients met study inclusion criteria. The mean age was 54.4 years and the mean follow-up was 46.9 months. Four recurrences were detected, occurring 16–73 months after the initial diagnosis. During a scheduled visit, one patient was found to have an asymptomatic vaginal cuff recurrence, detected on physical examination. The remaining three cases were diagnosed at an unscheduled visit after the presence of symptoms (vaginal bleeding, abdominal pain, shortness of breath) prompted further evaluation. In all, cytology detected no cases of recurrence and the estimated cost associated with cytology alone for all patients over the study time frame was approximately $7,760 per year.

Conclusions

Patients with grade 1 endometrial cancer confined to the endometrium have a low risk of recurrence (2.6%) and were detected on clinical findings alone. Emphasis should be placed on counseling patients on symptoms of recurrence and performing a thorough physical examination. The elimination of vaginal cytology for this select group of patients may be appropriate and result in a significant reduction in health care costs.     

T cells generated in the absence of a thoracic thymus fail to establish homeostasis

Cervical thymus mimics the thoracic thymus in supporting T‐cell development and exists in a subset of mice and humans. Importantly, it remains unknown whether the cervical thymus can generate T cells that are self‐tolerant in the complete absence of signals from the thoracic thymus. Using a fetal liver reconstitution model in thoracic thymectomized RAG^?/? mice, we found that T cells could be generated without contribution from the thoracic thymus. However, these mice had decreased T cells, increased proportions of effector memory T cells and Treg phenotype cells, increased serum IgG1/2b, and increased frequency of T cells expressing IFN‐γ, IL‐17 or IL‐10. Half of the mice that received a thoracic thymectomy and fetal liver cells, unlike sham surgery controls, developed substantial morbidity with age. Disease was associated with lymphopenia‐driven activation rather than inherent defects in the cervical thymus, as both thoracic and cervical thymocytes could generate disease in lymphopenic recipients. Administration of the homeostatic cytokine IL‐7 caused a rapid, transient increase in T‐cell numbers and reduced the time to disease onset. Together the data suggests that the cervical thymus can function in the complete absence of the thoracic thymus; however, the T cells generated do not establish homeostasis.     

Type I interferons have opposing effects during the emergence and recovery phases of colitis

The contribution of the innate immune system to inflammatory bowel disease (IBD) is under intensive investigation. Research in animal models has demonstrated that type I interferons (IFN‐Is) protect from IBD. In contrast, studies of patients with IBD have produced conflicting results concerning the therapeutic potential of IFN‐Is. Here, we present data suggesting that IFN‐Is play dual roles as regulators of intestinal inflammation in dextran sodium sulfate (DSS)‐treated C57BL/6 mice. Though IFN‐Is reduced acute intestinal damage and the abundance of colitis‐associated intestinal bacteria caused by treatment with a high dose of DSS, they also inhibited the resolution of inflammation after DSS treatment. IFN‐Is played an anti‐inflammatory role by suppressing the release of IL‐1β from the colon MHC class II⁺ cells. Consistently, IL‐1 receptor blockade reduced the severity of inflammation in IFN‐I receptor‐deficient mice and myeloid cell‐restricted ablation of the IFN‐I receptor was detrimental. The proinflammatory role of IFN‐Is during recovery from DSS treatment was caused by IFN‐I‐dependent cell apoptosis as well as an increase in chemokine production and infiltrating inflammatory monocytes and neutrophils. Thus, IFN‐Is play opposing roles in specific phases of intestinal injury and inflammation, which may be important for guiding treatment strategies in patients.     

Rare copy number variation in cerebral palsy

Recent studies have established the role of rare copy number variants (CNVs) in several neurological disorders but the contribution of rare CNVs to cerebral palsy (CP) is not known. Fifty Caucasian families having children with CP were studied using two microarray designs. Potentially pathogenic, rare (<1% population frequency) CNVs were identified, and their frequency determined, by comparing the CNVs found in cases with 8329 adult controls with no known neurological disorders. Ten of the 50 cases (20%) had rare CNVs of potential relevance to CP; there were a total of 14 CNVs, which were observed in <0.1% (<8/8329) of the control population. Eight inherited from an unaffected mother: a 751-kb deletion including FSCB, a 1.5-Mb duplication of 7q21.13, a 534-kb duplication of 15q11.2, a 446-kb duplication including CTNND2, a 219-kb duplication including MCPH1, a 169-kb duplication of 22q13.33, a 64-kb duplication of MC2R, and a 135-bp exonic deletion of SLC06A1. Three inherited from an unaffected father: a 386-kb deletion of 12p12.2-p12.1, a 234-kb duplication of 10q26.13, and a 4-kb exonic deletion of COPS3. The inheritance was unknown for three CNVs: a 157-bp exonic deletion of ACOX1, a 693-kb duplication of 17q25.3, and a 265-kb duplication of DAAM1. This is the first systematic study of CNVs in CP, and although it did not identify de novo mutations, has shown inherited, rare CNVs involving potentially pathogenic genes and pathways requiring further investigation.     

Menopausal hormone therapy in Germany: Results of three national surveys from 1997 to 2003

Objective

To determine regional variations in the prevalence and applied therapy regimes of current menopausal hormone therapy (HT) in Germany.

Methods

Three population-based surveys, analysing data of 45–74 years old women, were compared: The Study of Health in Pomerania (SHIP; 1123 participants; northeast Germany, October 1997–May 2001), Cooperative Health Research in the Augsburg Region Survey 2000 (KORA; 1253 participants; south Germany, October 1999–April 2001) and Heinz Nixdorf Recall Study (HNR; 2257 participants; west Germany, December 2000–August 2003). A standardized interview technique provided data on current medication.

Results

The age-standardized prevalence of HT was 17.0% (95% confidence interval (CI): 14.9–19.1) in SHIP, 25.9% (95% CI: 23.6–28.3) in KORA and 24.7% (95% CI: 22.9–26.4) in HNR. Mean average time of intake of HT was 5.1 (SHIP), 7.5 (KORA) and 10.1 years (HNR). The use of estrogen plus progestogen combinations was equally common in all three surveys with proportions of about 15%, the use of unopposed estrogen in KORA and HNR was twice as high as in SHIP. In all three surveys oral estradiol was taken most often. Transdermal estradiol was preferred by KORA women whereas conjugated estrogens were taken most frequently by HNR women.

Conclusions

Compared to northeast Germany HT was more often applied in the south and west of Germany. HT as long-term therapy was more common in West than in East Germany. In each study region there was a specific pattern of used HT components.     

Long-term neurological outcome of term-born children treated with two or more anti-epileptic drugs during the neonatal period

Background

Neonatal seizures may persist despite treatment with multiple anti-epileptic drugs (AEDs).

Objective

To determine in term-born infants with seizures that required two or more AEDs, whether treatment efficacy and/or the underlying disorder were related to neurological outcome.

Design/methods

We included 82 children (born 1998-2006) treated for neonatal seizures. We recorded mortality, aetiology of seizures, the number of AEDs required, achievement of seizure control, and amplitude-integrated-EEG (aEEG) background patterns. Follow-up consisted of an age-adequate neurological examination. Surviving children were classified as normal, having mild neurological abnormalities, or cerebral palsy (CP).

Results

Forty-seven infants (57%) had status epilepticus. The number of AEDs was not related to neurological outcome. Treatment with three or four AEDs as opposed to two showed a trend towards an increased risk of a poor outcome, i.e., death or CP, odds ratio (OR) 2.74; 95% confidence interval (CI) 0.98-7.69; P = .055. Failure to achieve seizure control increased the risk of poor outcome, OR 6.77; 95%-CI 1.42-32.82, P = .016. Persistently severely abnormal aEEG background patterns also increased this risk, OR 3.19; 95%-CI 1.90-5.36; P < .001. In a multivariate model including abnormal aEEG background patterns, failure to achieve seizure control nearly reached significance towards an increased risk of poor outcome, OR 5.72, 95%-CI 0.99-32.97, P = .051. We found no association between seizure aetiology and outcome.

Conclusions

In term-born infants with seizures that required two or more AEDs outcome was poorer if seizure control failed. The number of AEDs required to reach seizure control and seizure aetiology had limited prognostic value.     

A comprehensive survey for polymorphisms in the bovine IFN-gamma gene reveals a highly polymorphic intronic DNA sequence allowing improved genotyping of Bovinae.

This study aimed to identify interferon-gamma (IFN-gamma) gene variants in cattle for diagnostic purposes. Therefore, the entire bovine IFN-gamma gene (BoIFNG) and 2605 bp of its promoter DNA were sequenced. The BoIFNG DNA sequence conforms to the published part of Bo-IFN-gamma cDNA. Primer extension experiments show the presence of a 5' extension of exon 1 by 42 nucleotides (nt). One SINE element (Bov-A2) is located in the 5'-region, and two SINE elements (Bov-tA, Bov-B) are contained in the 3'-region of BoIFNG. The variants were detected by comparative sequence analysis of PCR amplicons from different bovine species. Four polymorphic mononucleotide repeats are situated in the promoter and in intron 1. Four distinct series of single nucleotide polymorphisms (SNP) were found in functionally important regions of BoIFNG. The region between the two intron 1 microsatellites contains the highest density of SNPs in Bos taurus breeds. One G-T transversion in the coding region of exon 1 causes a Gly(14) to Val(14) exchange in the BoIFNG signal peptide of different bovine species. A G-A transition in exon 2 encodes a Ser(19) to Asn(19) change in the mature protein of the Tibetan yak. Genotyping of randomly sampled Holstein Friesian cows at selected SNPs and of both intron 1 microsatellites revealed two dominant BoIFNG microhaplotypes. The detected SNPs improve the recently reported genotyping system of cattle.     

Clinical and molecular basis of classical lissencephaly: Mutations in the LIS1 gene (PAFAH1B1)

Classical lissencephaly (LIS) and subcortical band heterotopia (SBH) are related cortical malformations secondary to abnormal migration of neurons during early brain development. Approximately 60% of patients with classical LIS, and one patient with atypical SBH have been found to have deletions or mutations of the LIS1 gene, located on 17p13.3. This gene encodes the LIS1 or PAFAH1B1 protein with a coiled‐coil domain at the N‐terminus and seven WD40 repeats at the C‐terminus. It is highly conserved between species and has been shown to interact with multiple proteins involved with cytoskeletal dynamics, playing a role in both cellular division and motility, as well as the regulation of brain levels of platelet activating factor. Here we report 65 large deletions of the LIS1 gene detected by FISH and 41 intragenic mutations, including four not previously reported, the majority of which have been found as a consequence of the investigation of 220 children with LIS or SBH by our group. All intragenic mutations are de novo, and there have been no familial recurrences. Eight‐eight percent (36/41) of the mutations result in a truncated or internally deleted protein—with missense mutations found in only 12% (5/41) thus far. Mutations occurred throughout the gene except for exon 7, with clustering of three of the five missense mutations in exon 6. Only five intragenic mutations were recurrent. In general, the most severe LIS phenotype was seen in patients with large deletions of 17p13.3, with milder phenotypes seen with intragenic mutations. Of these, the mildest phenotypes were seen in patients with missense mutations. Hum Mutat 19:4–15, 2002. © 2001 Wiley‐Liss, Inc.