Search

Background\ud Psychological therapy assessments are a key point at which a person is accepted into a service or referred on. There is evidence of service users experiencing harm, dropping out of services and potentially experiencing poor outcomes because of inadequate assessment practices. Approaches to assessment tend to be developed by individual services, with a lack of research identifying what makes a good assessment.\ud \ud Methods\ud This survivor-led study, based in England, aimed to generate guidelines for conducting trauma-informed psychological therapy assessments. The study was guided by a Service User Advisory Group and a Clinician Advisory Group. The study was conducted in three key stages: (i) identifying, modelling and drafting guideline content (ii) modified Delphi study and (iii) guideline finalization. Stage 1 was informed by literature reviews, qualitative research, data workshops with Advisory Groups and an expert consultation. Fifty-nine people with relevant experiences then participated in a single-stage modified Delphi (Stage 2). The guidelines were finalized through an analysis of Delphi open comments and a final expert consultation (Stage 3).\ud \ud Results\ud The guidelines evolved through each stage of the process, and all items were deemed important by >90% of Delphi participants. The final trauma-informed guidelines contain eight principles, including ‘focus on relationships’, ‘from systems to people’ and ‘healing environments’.\ud \ud Conclusions\ud Experiential knowledge was key in generating the guidelines and conceptualizing content, with a consequent focus on areas, such as recognizing power differentials, understanding oppression as trauma and the relational aspects of assessments. Future research should focus on guideline implementation and investigate whether this impacts service user dropout, engagement with therapy, and outcomes.\ud \ud Patient or Public Contribution\ud This study is an example of survivor research, with several authors, including the study lead, identifying as survivors. We consider the ways in which our identities as survivor researchers impacted the study findings.

Hyponatremia is a known but underrecognized presentation of sellar lesions. Herein, we present a series of patients who presented with single or multiple episodes of hyponatremia.Over 5 years, patients undergoing endonasal surgery for a de novo sellar mass with hyponatremia as an initial presentation were included. Pathology, sodium levels, pituitary hormonal status, and treatment course were documented.Of 282 patients, 16 (5.7%) (9 males, 7 females, age 32 to 84 years) presented with severe hyponatremia, with a mean serum sodium level of 115 ± 6 mmol/L (range, 101 to 125 mmol/L), and 3 patients had 2 or more episodes. Severe hyponatremia was a presenting sign in 0, 4.1, 14.3, and 37.5% of patients with craniopharyngiomas (n = 10), pituitary adenomas (n = 243), Rathke's cleft cysts (RCCs) (n = 21), and sellar arachnoid cysts (n = 8), respectively (P.01). Half of the patients presenting with hyponatremia, including 6 of 10 patients with adenomas and 2 of 3 patients with RCCs, had pituitary apoplexy or cyst rupture. All patients had anterior pituitary gland dysfunction, including 81% with hypoadrenalism and 69% with hypothyroidism. Following surgery, hormonal status was unchanged or improved in 15 patients (median follow-up, 14 months). No patient had tumor/cyst recurrence or recurrent hyponatremia.Severe hyponatremia was a presenting sign in 5.7% of patients with sellar pathology, most frequently in patients with arachnoid cysts, RCCs, and pituitary apoplexy. Patients with new-onset severe hyponatremia and no obvious pharmacologic or systemic cause should undergo pituitary hormonal evaluation and brain imaging. Surgical resection and correction of hormonal deficiencies are associated with resolution of recurrent hyponatremic episodes.

The chromosome 1q23.3 region, which includes the RGS4 gene has been implicated in genetic susceptibility to schizophrenia by two linkage studies with lod scores of 6.35 and 3.20 and with positive lod between 2.00 and 3.00 scores in several other studies. Reduced post mortem RGS4 gene expression in the brain of schizophrenics was reported as well as positive allelic association between markers at the RGS4 gene locus and schizophrenia. We have attempted to replicate the finding of allelic association with schizophrenia in a UK based sample of 450 subjects with schizophrenia and 450 supernormal controls. We genotyped the same SNP marker alleles investigated in the earlier studies and also a di-nucleotide (GT)(14) repeat microsatellite marker, which was 7 kb distal to RGS4. In the new UK sample there was no evidence for allelic or haplotypic association between RGS4 markers and schizophrenia. This might reflect genetic heterogeneity between the population samples, genotyping or other methodological problems. The finding weakens the evidence that mutations or variation in the RGS4 gene have an effect on schizophrenia susceptibility. (c) 2006 Wiley-Liss, Inc.

Chromosome 5q33 is a region that has previously shown good evidence of linkage to schizophrenia, with four LOD scores >3.00 in independent linkage studies. We studied 450 unrelated white English, Irish, Welsh, and Scottish research subjects with schizophrenia and 450 ancestrally matched supernormal controls. Four adjacent markers at the 5' end of the Epsin 4 gene showed significant evidence of linkage disequilibrium with schizophrenia. These included two microsatellite markers, D5S1403 (P = .01) and AAAT11 (P = .009), and two single-nucleotide-polymorphism markers within the Epsin 4 gene, rs10046055 (P = .007) and rs254664 (P = .01). A series of different two- and three-marker haplotypes were also significantly associated with schizophrenia, as confirmed with a permutation test (HapA, P = .004; HapB, P = .0005; HapC, P = .007; and HapD, P = .01). The Epsin 4 gene encodes the clathrin-associated protein enthoprotin, which has a role in transport and stability of neurotransmitter vesicles at the synapses and within neurons. A genetically determined abnormality in the structure, function, or expression of enthoprotin is likely to be responsible for genetic susceptibility to a subtype of schizophrenia on chromosome 5q33.3.

Background Linkage studies have confirmed that chromosome 1q23.3 is a susceptibility locus for schizophrenia. It was then claimed that markers at the carboxyl-terminal PDZ ligand of neuronal nitric oxide synthase (CAPON) gene showed allelic association with schizophrenia in Canadian families. A second Chinese study found a base pair polymorphism at the CAPON gene also associated with schizophrenia. Methods We attempted replication using eight markers from the Canadian study in a UK based sample of 450 cases and 450 supernormal controls. Results We found no evidence for allelic or haplotypic association with schizophrenia for any of the markers found to be associated in the Canadian sample. Conclusions The negative results might reflect genetic heterogeneity between the Canadian, Chinese and UK samples or be due to methodological problems. The present finding weakens the evidence that mutations or variation in the CAPON gene are causing genetic susceptibility to schizophrenia in European populations.