This study aimed to explore the terms used by old-age psychiatrists and psychologists to describe subjective and mild cognitive impairment and functional cognitive disorders (FCD) in clinical practice.

Participants were selected from across the United Kingdom based on their clinical involvement in the assessment of cognitive complaints. 9 old-age psychiatrists and 4 psychologists were interviewed about their use of terminology in clinical practice and their awareness and understanding of FCD terminology via semi-structured interview questions and case vignettes. Interviews were conducted between December 2020 and February 2021 using online platforms Zoom and Microsoft Teams. Participants were recruited by email and Twitter. All questions were asked verbally; however, the four case vignettes were displayed via screen-share. All discussions and answers were transcribed and transcripts were coded manually using the exploratory case study methodology in order to identify themes in participants’ responses.

This study has highlighted the variable use of terms used to describe and diagnose patients presenting with symptoms of cognitive disorders. The terms ‘mild cognitive impairment’, ‘subjective cognitive decline’ and ‘functional cognitive disorder’ were used most commonly amongst participants, though the terms ‘subjective cognitive impairment’ and ‘pseudodementia’ were also presented. This theme of language discontinuity is underscored by participants’ varying use of terminology when describing or presenting their diagnoses for the case vignettes. The data also reveals a sub-theme of variability in application of the term FCD. Whilst all participants gave similar definitions for this term, the application of FCD as a diagnosis in practice was inconsistent. Six participants described FCD as associated with or secondary to other functional or psychiatric conditions, four participants viewed FCD as an isolated diagnosis, and one participant considered FCD to be either part of another illness or a separate diagnosis. Two participants neither used nor recognised the term FCD.

It is evident that there is varied use of terms describing or diagnosing forms of cognitive symptoms. The findings of this study highlight the need for a clear, adoptable definition of FCD in practice as well as implementable management plans for FCD patients. This is critical in order to avoid misdiagnosis and mismanagement, which may have harmful effects on patients living with debilitating cognitive symptoms.

There is very little research into the challenges of training in intellectual disability psychiatry or into interventions which may address these challenges. Using focus groups, we explored the experiences of intellectual disability psychiatry trainees, and evaluated a leaderless trainee support group developed in Bristol.

Five distinct themes were identified via framework analysis: that trainees felt unprepared for the difference from previous posts; the need for support; the value of the group; that trainees were concerned about judgement in supervision; that the group structure was valued.

Our findings highlight the support needs specific to intellectual disability psychiatry trainees. Leaderless peer support groups may be a valued resource to address such issues, and may be a useful model to be considered by other training schemes.

The importance of the neurotransmitter serotonin (5-HT) in the pathophysiology of anxiety is well known. A key role for postsynaptic 5-HT1A receptors has recently been suggested in studies of genetic knockout mice.

To measure 5-HT1A receptor binding in patients with panic disorder in the untreated state and after recovery on treatment with selective serotonin reuptake inhibitors (SSRIs).

Nine symptomatic untreated patients with panic disorder, seven patients recovered on SSRI medication and nineteen healthy volunteers underwent a single positron emission tomography (PET) scan using the 5-HT1A tracer [11C]WAY-100635.

In comparison with controls, both presynaptic and postsynaptic 5-HT1A receptor binding was reduced in untreated patients, with the most significant reductions being in the raphe, orbitofrontal cortex, temporal cortex and amygdala. In recovered patients presynaptic binding was reduced, but there was no significant reduction in postsynaptic binding.

Panic disorder is associated with reduced 5-HT1A receptor availability, which is also known to have a key role in depression.

Sleep effects of antidepressants are important clinically and for elucidating mechanism of action: selective serotonin reuptake inhibitors disturb sleep and 5-HT2 receptor-blocking compounds may enhance sleep quality.

To compare the objective and subjective effects on sleep of paroxetine and nefazodone in patients with moderate to severe depression.

Forty patients with depression were randomised to take paroxetine 20-40 mg/day or nefazodone 400–600 mg/day for 8 weeks. Objective and subjective quality of sleep and depression measures were assessed throughout.

Nefazodone significantly increased objective sleep efficiency and total sleep time, and improved subjective sleep on days 3 and 10. Paroxetine decreased sleep efficiency early in treatment and some sleep disruption remained at week 8. Paroxetine but not nefazodone produced marked suppression of rapid eye movement (REM) sleep.

Nefazodone improves sleep in early treatment compared with paroxetine in patients with moderate to severe depression. These effects are seen within the first 2 weeks of treatment and diminish thereafter.