Osteoarthritis (OA), depression and anxiety are common problems in primary care. OA coexisting with depressive and/or anxiety symptoms has detrimental consequences to the individual. To inform recognition and management of these important problems in primary care a better understanding of their coexistence is needed. A systematic review with meta-analysis was undertaken to determine the prevalence of depression and anxiety in adults with OA/joint pain in the community. Elevated anxiety symptoms were more common (45%) than depression symptoms (24%) in persons with OA joint pain. Sources of between study variance include methods of ascertainment and geographical location. A review of measurement properties of several recommended patient-reported depression and anxiety measures found evidence to support properties in some populations, but some critical properties warrant investigation in adults with OA in the community. A secondary data analysis was conducted for older consecutive primary care patients with musculoskeletal pain recruited to a cohort (n=443) of the PROGnostic Research study. Latent Class Growth Analyses identified clusters of individuals who exhibited different trajectories of anxiety and depression symptoms over a 12-month period: three anxiety and two depression symptom trajectories. In total, 56% and 63% of participants experienced persistent anxiety and depression symptoms respectively for at least 12 months. Pain characteristics and coping strategies were the most prominent risk factors for persistent anxiety and depression symptoms. With the aim of identifying individuals with sub- threshold persistent anxiety and depression symptoms, characteristics predisposing to symptoms persistence may be considered. A medical records review found that only half of all older musculoskeletal patients with persistent anxiety and depression symptoms have their mental health problems detected by their GP. Frequent consulters and those with more severe anxiety were more likely to be detected. This reinforces the need to recognise and manage OA coexisting with depression and/or anxiety by patients and health professionals alike.

The cerebellum receives information from the hindlimbs through several populations of spinocerebellar tract neurons. Although the role of these neurons has been established in electrophysiological experiments, the relative contribution of afferent fibres and central neurons to their input, their organization and mechanisms of control of transmission has only been estimated approximately so far. The present study aimed to investigate the input properties of four populations of spinocerebellar tract neurons: dorsal spinocerebellar tract neurons located in Clarke´s column (ccDSCT) and in the dorsal horn (dhDSCT) and ventral spinocerebellar tract (VSCT) neurons including spinal border (SB) neurons. There were three major aims: (1) to investigate the excitatory inputs to four types of spinocerebellar tract neurons in the cat and rat thoraco-lumbar spinal cord; (2) to analyze the inhibitory inputs to four types of spinocerebellar tract neurons in the cat and rat thoraco-lumbar spinal cord; (3) to determine the origin of excitatory and inhibitory inputs to four types of spinocerebellar tract neurons in the cat and rat thoraco-lumbar spinal cord. Two series of experiments were carried out. In the first series of experiments in cats, spinocerebellar tract neurons were identified electrophysiologically and labelled intracellularly with rhodamine-dextran and Neurobiotin. In the second series of experiments in rats, cells were labelled by retrograde transport of b-subunit of Cholera toxin (CTb) from the cerebellum. In addition, to address the third aim, reticulospinal (RetS) and corticospinal (CS) terminals were identified by anterograde transport of CTb from the caudal medulla and hindlimb sensory motor cortex respectively in rats along with labelling of spinocerebellar tract neurons by retrograde injection of Fluorogold in the cerebellum. Following this, immunohistochemistry was carried out. The first aim was achieved by utilizing the difference in the immunohistochemistry of glutamatergic terminals of peripheral afferents and of central neurons with vesicular glutamate transporters, VGLUT1 or VGLUT2, respectively. All SB neurons with dominating inhibitory input from the periphery possessed very few VGLUT1 contacts and remarkably higher numbers of VGLUT2 contacts. In VSCT neurons with excitatory primary afferent input, the number of VGLUT1 contacts was relatively high although VGLUT2 contacts likewise dominated. In contrast, DSCT neurons were associated with numerous VGLUT1 contacts; ccDSCT neurons with strong input from group I afferents had higher density of VGLUT1 contacts than dhDSCT neurons with major input from group II and cutaneous afferents. In order to fulfill the second aim, quantification of contacts formed by inhibitory axon terminals on spinocerebellar tract neurons along with excitatory terminals was carried out. Inhibitory axon terminals were characterised as either GABAergic, glycinergic or both GABAergic/glycinergic by using antibodies against vesicular GABA transporter (VGAT), glutamic acid decarboxylase (GAD) and gephyrin. Similarly, excitatory terminals were characterised by using combination of VGLUT1 and 2. The comparison revealed the presence of much higher proportions of inhibitory than excitatory contacts on SB neurons but similar proportions were found on VSCT, ccDSCT and dhDSCT neurons. In all types of cell, the majority of inhibitory terminals were glycinergic. The density of contacts was higher on somata and proximal in comparison with distal dendrites of SB and VSCT neurons but more evenly distributed in ccDSCT and dhDSCT neurons. To achieve the third aim, a series of immunohistochemical reactions was performed to characterize contacts that originate from proprioceptors, different types of interneurons and descending RetS and CS pathways. Among the four populations of spinocerebellar tract neurons, ccDSCT neurons had the highest proportion of contacts formed by VGLUT1 terminals double labeled with parvalbumin (PV) which indicated that majority of direct excitatory sensory inputs to ccDSCT neurons are derived from proprioceptors. A small proportion of excitatory and inhibitory contacts on these neurons originated from Calbindin/ Calretinin/ PV expressing neurons. Quantitative analysis revealed that SB and VSCT neurons have significantly higher numbers of appositions from VGLUT2 expressing RetS axon terminals than DSCT neurons. A small proportion of the RetS contacts on these neurons were VGAT positive. In contrast, DSCT neurons had higher numbers of appositions made by CS axon terminals in comparison to SB and VSCT neurons. The present findings provide a new basis for understanding the organization and functional connectivity of four populations of spinocerebellar tract neurons and strengthen previous indications of their functional differentiation. SB and VSCT neurons principally receive inputs from spinal and supraspinal neurons although direct input from primary afferents is also stronger in VSCT neurons. DSCT neurons have major direct input from primary afferents and also to some extent from the CS pathway but monosynaptic inputs from proprioceptors dominated in ccDSCT neurons and dhDSCT neurons have mixed proprioceptive and low threshold cutaneous afferent input.

In studies on the pathophysiology of the autoimmune neuropathy, Miller Fisher syndrome (MFS), monoclonal antibodies to the disialosyl epitopes on GQ1b, GT1a and GD3 gangliosides have been produced. Antibodies to these complex gangliosides are thought to be crucial in the pathogenesis of MFS. These antibodies have recently been shown to produce complement dependent, glial and/or neuronal injury at mouse neuromuscular junctions (NMJs). Three antibodies (EG1, LB1 and R24) were identified as producing selective terminal Schwann cell (TSC) injury whilst sparing neuronal membranes at NMJs in BALB/c and C57BL/6 mouse strains in a dose dependent manner. These changes occur in the absence of observable acute physiological or morphological changes to the nerve terminal, suggesting that TSC injury or loss has no major short-term influence on synapse function. Having compared the suitability of two common ex vivo muscle preparations for use in characterisation studies, TSC selective antibodies were compared, and EG1 was identified as most suitable for further investigations on the role of the TSC in mammalian NMJ function and as a possible disease target in MFS. The effect of this antibody when combined with normal human serum as a source of complement in ex vivo hemidiaphragm preparations was independent of complement regulators DAF1 and CD59a. Cell specific promoter sequences have been used to produce a mouse line that expresses green-fluorescent protein (GFP) in TSCs, and cyan-fluorescent protein (CFP) in axons (CK mouse). Live imaging techniques were used to study the acute and chronic effects of EG1 mAb mediated, complement dependent glial injury in this system. It is shown that TSC injury is characterised by loss of GFP staining, occurring within 20 minutes of complement exposure. Repopulation of the NMJs with GFP-positive cell bodies is first evident at day 2. The origin of these returning Schwann cells is discussed, and three possible sources are considered – the last myelinating Schwann cell, non-myelinating Schwann cells lying more proximally in the peripheral nervous system, and muscle stem cells. At day 7, the number of GFP-positive cell bodies seen at the NMJ is higher (7-12 per NMJ) than prior to antibody exposure (3-5 per NMJ). This process of enhanced repopulation is not dependent on an intact axon as it is retained following axotomy. At 3 months, minor remodelling of the NMJ is seen, and is more pronounced at one year. Repeat antibody exposure within 48 hours does not injure returning processes, or delay repopulation. Instead, extra-junctional TSC processes are formed, with associated axon sprouts in the absence of gross terminal axon injury. Anti-GQ1b containing serum from a MFS patient is shown to induce murine TSC death in a similar manner to murine monoclonal antibodies described previously. This suggests that TSCs are a potential new disease target in human disease if the ganglioside profile of mouse and human TSCs is equivalent. Ganglioside distribution and antibody binding are examined on a series of human muscles. These studies demonstrate for the first time that components of the human NMJ are potentially susceptible to anti-ganglioside antibody mediated injury, by virtue of their ganglioside profile. This study suggests that TSCs may be a previously unrecognised site of immune-mediated nerve injury. It also describes a new technique for observing chronic TSC injury and recovery in an in vivo mouse model system, which could be used for human disease modelling.

Many spinal cord injuries (SCI) are incomplete, variable numbers of spared fibres passing the lesion level and supporting some residual function below the injury. One approach to improving function following injury is to develop therapies that maximise the potential of these spared fibres. The aim of the work in this thesis was to investigate the spontaneous plasticity that occurs in spinal cord pathways following injury and then determine whether olfactory ensheathing cell (OEC) transplants or treatment with antibodies blocking the function of the myelin inhibitors Nogo and MAG could enhance this plasticity. An electrophysiological approach was used to investigate these questions in rats which were subjected to a lesion of the dorsal columns at the C4/5 segmental level. This lesion interrupts the main component of the corticospinal tract which descends in the ventromedial dorsal column and also interrupts the ascending collaterals of sensory fibres from forelimb nerves. In this study, changes in the function of both of these pathways were assessed by recording cord dorsum potentials (CDPs) after stimulation in the pyramids (corticospinal activation) or of the radial nerve (sensory fibre activation). To enable plasticity in the corticospinal system to be investigated a method was developed for maximally activating the corticospinal projection on one side of the pyramids, whilst avoiding activation of the opposite pyramid and structures surrounding the pyramids. It was found that this could be achieved by careful positioning of bipolar stimulating electrodes. Before investigating the effect of potential plasticity inducing agents, the degree to which plasticity occurs in the absence of treatments was first assessed in F344 rats. The function of corticospinal and sensory pathways was compared in normal animals, acutely lesioned animals, and at 1 week and 3 months after a dorsal column lesion. Corticospinally-evoked CDPs above the lesion were not altered following an acute lesion but were larger in 1 week and 3 month dorsal column lesioned animals than in normal animals. The increase in amplitude was similar in both lesioned animal groups. This suggests that plasticity occurs at the intact connections formed by corticospinal fibres axotomised more distally, that it occurs within a week of the lesion and persisits for at least 3 months. Corticospinally-evoked CDPs were almost abolished below an acute dorsal column lesion and remained of minimal amplitude 1 week after lesioning. However, there was some recovery of CDPs between 1 week and 3 months. This suggests plasticity either at the connections formed by spared fibres of the minor non-dorsal column components of the corticospinal tract or in propriospinal pathways originating above the lesion. This plasticity has a longer time-course than that at the connections of axotomised fibres above the lesion. Plasticity of the connections formed by larger diameter sensory fibres in the radial nerve was also seen below the level of the dorsal column lesion. This had a similar time course to the plasticity of corticospinal connections above the lesion CDPs being larger both 1 week and 3 months after injury compared to normal animals. A modest enhancement of transmission in both corticospinal and sensory systems therefore occurred following a dorsal column lesion. To investigate whether OEC transplants enhance plasticity after spinal cord injury, OECs were transplanted such that they became distributed within the spinal cord for several mm either above or below the lesion. Electrophysiological methods were then used, as above, to investigate whether transmission in the corticospinal and sensory fibre systems following a dorsal column lesion was improved in transplanted animals compared to 3 month survival animals. However, corticospinal actions rostral to the lesion were not enhanced by OEC transplants above the lesion and sensory transmission caudal to the lesion was not enhanced by cells below the lesion. OEC transplants are therefore unlikely to support recovery by promoting plasticity in the spinal cord after injury. To investigate whether antibodies designed to block the function of the myelin inhibitors Nogo and MAG would enhance plasticity following spinal cord injury, antibodies were delivered intrathecally via implanted osmotic minipumps over a period of six weeks following a dorsal column lesion. Vehicle treated and normal animals were investigated for comparison. Placement of the cannula and/or delivery of vehicle alone was found to have a detrimental effect on corticospinal actions above the lesion when compared to normal animals. Treatment with an anti-Nogo antibody (GSK577548) raised against a human Nogo-A fragment and targeting the amino-Nogo terminal was found to enhance transmission of corticospinal actions both above and below the dorsal column lesion. Corticospinal actions above the lesion were significantly greater than in the vehicle treated controls but did not exceed those in normal animals because of the detrimental effect of the intrathecal cannulae/vehicle treatment. Transmission at the terminals of sensory afferent fibres below the level of the lesion was also enhanced by anti-Nogo treatment. In this case the actions of sensory pathways were significantly greater than those in both vehicle treated and normal animals. The fact that enhanced transmission occurs on the ‘wrong side’ of the lesion to be explained by axonal regeneration and the sensory transmission is enhanced over normal, strongly suggests that anti-Nogo induces plasticity in spinal pathways. In contrast, treatment with the anti-MAG antibody (GSK249320A) had no effect on either corticospinal or sensory-evoked activity in the spinal cord above or below the lesion, CDPs evoked by these pathways being comparable to that in vehicle treated controls. Anti-MAG does not appear to induce plasticity but may have neuroprotective actions which cannot be adequately tested in this lesion model. The results show that both corticospinal and sensory fibre systems show modest spontaneous plasticity following a dorsal column lesion. Plasticity at the terminations of axotomised fibres occurs relatively rapidly (within one week) while plasticity in spared systems occurs more slowly. This spontaneous plasticity does not appear to be enhanced by transplants of OECs, so that improvements in spinal cord function previously demonstrated in transplanted animals are probably due to a neuroprotective mechanism. The results obtained using function blocking antibodies targeting myelin inhibitors suggest that anti-Nogo but not anti-MAG treatment may enhance plasticity in the spinal cord after injury. This observation adds to the accumulating evidence that interfering with Nogo-A signalling may be a useful approach for improving function after spinal cord injury.

Thesis Overview Psychogenic nonepileptic seizures (PNES) can be defined as paroxysmal events that resemble epileptic seizures, without being associated with either abnormal electrical activity of the brain or primary physiological disturbances otherwise. It is estimated that about 10% of new presentations seen in an epilepsy clinic, and up to 30% of patients with intractable epilepsy will eventually be diagnosed as having PNES (Benbadis & Hauser, 2000). Attributing a specific ‘cause’ to PNES is conceptually and clinically contentious but it seems reasonable to say that they represent a physical expression of psychological distress involving behaviour that the patient finds difficult or impossible to control or disavows as being intentional. Most patients with PNES are initially thought to have epilepsy and treated with antiepileptic drugs (AED), sometimes for many years. Up to 40% of patients are inappropriately maintained on AEDs after the diagnosis of PNES has been established. As such, rather than being intrinsic to the condition, the widely reported poor outcomes associated with PNES may be substantially confounded by continued inappropriate medical management and iatrogenic harm. Withdrawing or continuing antiepileptic medication in patients with PNES could have important physical and psychological consequences, which may affect the prognosis of the attack disorder. If this is the case, manipulating medication following the diagnosis of PNES may have a role in the management of this disorder. The work contained in this thesis aims to explore some aspects of the effects that continuing or withdrawing AED has on the course and outcome of PNES. Following an initial general overview on the subject of PNES (chapter 1), a systematic review of the literature is presented in chapter 2; the conclusion being a lack of good quality and reliable evidence for the effects of AED treatment in patients with PNES and a need for further original research in this area. The rationale and programme of research is presented in chapter 3 Chapter 4 presents the results of a large observational study to establish the feasibility and safety of supervised AED withdrawal in patients with an established diagnosis of PNES. Only 3 of the 78 patients included reported a new type of event requiring the reintroduction of AED, and no serious medical events were reported. The study therefore shows that, with appropriate diagnostic investigations and surveillance during follow-up, withdrawal of AED can be achieved safely in patients with PNES. A randomised controlled trial presented in chapter 5 aims to evaluate the potential therapeutic effect of AED withdrawal. Of the 25 subjects recruited, 14 were randomised to immediate withdrawal (IW) and 11 to delayed withdrawal (DW). Patients randomised to IW had a significant reduction in the use of emergency treatment for PNES, and a lower proportion was found to be using emergency services. The IW group also had a sustained reduction of attacks throughout the study and by 18 months post-diagnosis 50% were attack free as compared with 27% in the DW group. The results of this exploratory trial suggested a possible therapeutic effect of AED withdrawal, with a sustained reduction of attacks following the withdrawal of medication, coupled with a significant reduction in health care utilisation and no evidence of any deterioration. The last original paper presented in chapter 6 investigates the longer term psychosocial outcome of PNES with an observational study of the 25 patients included in the RCT. This study reports a significant improvement in some psychological measures; particularly in illness representations and mood, as well as for some measures of social adjustment. The evidence presented in these three studies (chapter 4, 5 and 6) suggests that a clear delivery of the diagnosis of PNES, followed by AED withdrawal, is safe and has possible beneficial effects on the clinical and psychosocial outcome of PNES. In particular medication withdrawal in and of itself appears to be a helpful concomitant in the successful removal of an inappropriate label of label of epilepsy, reduces the potential for iatrogenic harm, may help patients to shift towards a more psychologically-based explanation, and is associated with positive psychosocial outcomes. Finally, chapter 7 gives a summary of the main findings as well as discussing methodological limitations of the current research. The clinical implications of the evidence from this body of work are also discussed, as well as possible avenues for future research in the field.

No description available.

This thesis explores perspectives on living and working with dementia. Chapter one reviews the literature related to the experience of dementia and identity. Themes within theoretical and empirical papers are identified which contribute to an understanding of how the available information can be utilised to inform clinical work with people with dementia. It is argued that maintaining the integrity of a person with dementia's identity is possible and important for well-being, however, more research is needed to establish what 'identity work' should contain and when it should be delivered. Directions for future research are discussed. Assessment and diagnosis have been identified as being difficult aspects of work by clinicians in areas of healthcare, such as oncology, and as crucial to the experience of clients with memory problems. Despite this, and the importance of understanding the experience of staff members to support recruitment, retention and staff well-being, research exploring the experience of clinicians of assessing and diagnosing clients within dementia services is lacking. Chapter two therefore uses interpretative phenomenological analysis to examine the experience of staff members who perform this role. Themes are identified that highlight the complex nature of this role and the conflicting aspects of it. Participants appeared to be trying to meet conflicting needs within the context of a progressive illness and service restrictions, which influenced their perceived effectiveness and caused conflict and stress. Clinical and service implications are discussed and suggestions for future research made. Chapter three utilises the author's experience of completing the research presented in chapter two to reflect on tensions between the roles of researcher and clinician. How these roles can come into conflict with each other and the implications of this for the research process is explored.

This research study is concerned with the motivation of psychotherapists who choose to train in Psychosynthesis. Psychosynthesis sits within the transpersonal school of psychology and is less well known than the mainstream schools of Psychoanalytic, Behavioural and Humanistic psychology. There has been considerable research into the motivation of those who choose a career as a psychotherapist, in general, but none into why someone should be drawn to this Spiritual model. Life narrative interviews were conducted with twelve eminent Psychosynthesis psychotherapists. The interviews were recorded on audiotape and transcribed. The format was of a semistructured interview based on five key questions. At the end of each life narrative interview, the participant was asked to reconnect with the moment of choosing, to allow an image to come and then to draw. The drawings were then explored with the participants, who were invited to explain the meanings of the images and symbolism contained in them. Comparative thematic analysis was used to identify key and minor themes in the interview data. The symbolism and imagery in the drawings were considered in relation to transpersonal theory. The initial results suggested that those choosing to train as Psychosynthesis therapists shared, to a considerable extent, the 'dysfunctional' childhood backgrounds reported in earlier research as common among psychotherapists trained in a wider range of therapies. The earlier research had framed the choice to train as a psychotherapist as stemming from a 'negative' motivation. This is an interpretation from the perspective of 'depth' psychology. This research study suggests another possible motivation, from the perspective of 'height' psychology. 'Height' psychology suggests that human behaviour and human choices, can be motivated by 'higher' as well as 'lower' needs. The findings support the concept of 'dual motivation', a term which was used by one of the research participants, based on her observations of the many therapists she had trained in Psychosynthesis over a long period of time. This term captures the essence of the two dimensions of motivation. The anticipated strong interest in Spirituality was confirmed in the data results but the dimension of Mysticism, which had not been anticipated, emerged as a strong feature in three of the life histories. All twelve participants been drawn by the inclusive nature of the model, which they felt facilitated an unusual degree of freedom in therapeutic practice, without compromising the integrity of the model. The central Psychosynthesis techniques of visualisation, meditation, imagery and disidentification, emerged as strong factors in the choice because clear and effective results had been experienced in both personal work and work with clients. Two therapists identified the dual focus on Heart and Mind as attractive to them. In Psychosynthesis theory, Heart is more than emotions; it encompasses a dimension of the Will (Good Will or the Will to Good). Surprisingly, the marginality of the model was identified as a positive attraction by two of the therapists, as it echoed their own marginalised life positions, especially in childhood. Lastly, the experiential nature of Psychosynthesis therapy was valued as giving a creative and enlivening dimension to practice. The analysis of the drawings further confirmed the strong Spiritual orientation of the therapists. The symbolism in the drawings was overwhelmingly of a Spiritual nature with the dominant symbol of Light appearing in ten of the drawings. Other transpersonal symbols appearing included a path or journey, a chalice, the rose and new birth. The results suggest that Psychosynthesis offers a model of what it is to be a human being, which is validating and affirming at a personal level to those who are attracted to a transpersonal psychology. Furthermore, it offers experiential and creative techniques, which are experienced as powerful and successful ways to work therapeutically.

The Derby Functional Communication Scale (DFCS) was developed to assess functional communication in patients in hospital and rehabilitation settings. The validity of the DFCS and its sensitivity to low mood was also examined. In this study, correlation analysis was undertaken between DFCS and other existing measures of communication and mood. Assessments took place on local Stroke and Rehabilitation units. Sixteen hospital inpatients with acquired communication problems due to mixed aetiologies were assessed on the DFCS and other measures of communication and mood. Measures used included the DFCS, Frenchay Aphasia Screening Test (FAST), Edinburgh Functional Communication Profile (EFCP), Speech Questionnaire (SQ) and speech and language therapists (SaLT) ratings of global communication ability were used to assess communication. The Visual Analogue Mood Scales (VAMS) and the Stroke Aphasic Depression Questionnaire (SADQ) were administered as measures of low mood. The data indicated that DFCS scores were significantly related to other measures of communication (r = .75-.9, p<.01). Inter-rater reliability was generally good for the DFCS with the exception of the 'understanding' subscale, where a low correlation between staff and SaLT ratings was found. No significant (p>0.05) correlations between DFCS and measures of mood were found. In conclusion, the DFCS may be used for assessing observable communication skills in patients with acquired communication disorders. However, further validation and evaluation of the sensitivity to low mood is required.

Introduction The topic of study is concerned with the impact that working with sexual abuse survivor groups has on therapists. The existing literature primarily utilises quantitative methodologies and is, on the whole, concerned with the negative impact of trauma work. Previous studies have suggested that qualitative research exploring the experiences of therapists working in this field would provide a richer understanding of the potential impacts. The methodological limitations and shortcomings of the existing research base are addressed, specifically the lack of research on group therapists. Objectives This study aimed to provide a qualitative, phenomenological exploration of the impact that therapists state, working with sexual abuse survivor groups, has had on them. Design Interpretative Phenomenological Analysis (IPA) was used to conduct an in-depth study of a small sample of group therapists. Methods Multi-site ethics approval was gained to conduct the study within two local NHS trusts and an independent sector service. Therapists were selected using purposive sampling from these services. Semi-structured interviews were conducted with five therapists who ran groups for adult survivors of sexual abuse. Verbatim transcripts were analysed using IPA. Results Two concurrent theme groups were described. Themes concerned with the impact that the work has on the therapists, were discussed under the headings ‘Sense of Responsibility’, ‘Impact’, ‘Protecting and Maintaining Sense of Self’, ‘Contradictions in Narratives’ and ‘Evolving Impact’. Furthermore, findings related to the aspects of working within a group setting, were titled ‘Unique Aspects of the Group Setting’ and ‘Group Milieu’. Discussion Therapists did not ascribe to having ‘positive’ or ‘negative’ impacts, but seemed to simultaneously experience both, having created meaning for the impact of the work. Furthermore, in contradiction to previous literature, the therapists felt that working in a group setting had less potential to traumatise the facilitators. Implications for clinical practice and future research are discussed.