Developmental prosopagnosia (DP) is a condition associated with severe difficulties recognising familiar faces, which occurs in individuals with normal intelligence, typical low-level vision, and in the absence of manifest brain injuries. The neuro-cognitive origins of DP are still debated. Cognitive accounts have attributed face recognition deficits to reduced holistic processing of faces (i.e., whereby individual features of faces are integrated into a unified perceptual whole), and mnemonic difficulties, whereby prosopagnosics may be able to form accurate percepts, but are unable to maintain those percepts over time. At the neurological level, differences have been reported in the structural and functional connectivity of occipito-temporal regions which include face selective areas. Chapter 2 of this thesis investigated facial emotion recognition in DP and revealed widespread difficulties recognising facial emotion in individuals with apperceptive profiles of DP (i.e., DPs exhibiting difficulties forming view-invariant structural descriptions of faces at early stages of encoding). Chapter 3 explored body recognition in DP and found evidence of impaired body and object recognition in DP individuals. Moreover, the lack of relationship between observers' object and body recognition performances suggested that body and object recognition impairments in DP may co-occur independently. Chapter 4 investigated the susceptibility to the composite face illusion in two independent samples of individuals with DP and failed to show evidence of diminished composite face effects in both samples. Finally, Chapter 5 considered the contribution of perceptual encoding and short term face memory in DP using a delayed match-to-sample task and found that recognition impairments in prosopagnosics were insensitive to changes in retention interval and viewing angle, supporting an apperceptive characterisation of DP. The implications of these findings for the characterisation of DP and for understanding its underlying cognitive mechanisms, are discussed in Chapter 6.

Recognition memory is one of the most basic types of memory. One type of recognition memory is visual familiarity, which is the sense that a visual stimulus has been encountered before. This type of memory is affected in different mental illnesses, like schizophrenia and autism. The perirhinal cortex, which is a part of the medial temporal lobe has long been believed to be crucial for recognition. This work had 2 main lines of research. The first part, described in chapters Chapter 3 and Chapter 4 , set out to investigate whether activity at either the population level or at the single-unit level in the mouse perirhinal cortex was correlated with visual familiarity. In these chapters, the recordings were made also in the visual cortex and the hippocampus to put the perirhinal response in the context of the activity both upstream and downstream from it, respectively. Visual stimuli evoked responses in the perirhinal cortex, no familiarity-related modulation could be detected at both levels of analysis. That was true even when the visual cortex demonstrated familiarity-related differences in response. The second part of the work, described in chapters Chapter 5 and Chapter 6 examined the mice with haplo-insufficiency of the CYFIP1 gene as a possible new model for mental illness. First, the animal’s validity as a model of mentalillness was tested using auditory-evoked potential, one of the most ubiquitous phenomena that appears with mental illness in people and animal models. Then, recognition memory and the neuronal activity in the perirhinal and the visual cortex was tested, to see if they demonstrate other symptoms relating to schizophrenia. In the second line of work, the CYFIP1 mice demonstrated an auditory-evoked potential profile more like that observed in fragile-X syndrome, rather than schizophrenia and did not present any changes in both recognition memory or the electrical activity in the visual and the perirhinal cortex. This work showed that the perirhinal cortex does not show any familiarity-related activity unlike the current assumption in the literature. It also showed that the CYFIP1 mice might be a possible model for autism and Fragile-X syndrome.

No description available.

The mammalian hippocampus is vitally involved in the formation of both episodic memory and semantic memory, and in learning and recognition. These functions are actively involved during spatial navigation through an environment. The rodent hippocampus in particular has been greatly studied, providing a wealth of experimental data; however collation of this data into universally accepted theories of hippocampal function is far from complete. The present study concentrates on events occurring in the rodent hippocampus during such navigation. There is particular emphasis on the hippocampal theta rhythm which is manifested during navigation; on the existence and characteristics of place fields and associated place cells; and on the phenomenon of phase precession. The study has been limited to the CA1 region. Testable assertions are made about these phenomena. These assertions have been incorporated into models which are described in the later chapters of the thesis. The model has been further extended to demonstrate features of serotonergic activity in the CA1 region.

Scottish people have a reputation for being high consumers of alcohol. Certainly this is the case today and was also the case throughout the nineteenth century - the most obvious comparison to be made, a comparison often made both then and now, is with supposedly more moderate English drinking habits. Less well known is the reversal of this perspective during the inter-war years (1918–1939), when Scotland was held in many quarters to be more sober than England. This turnaround was brought about by changes in popular culture alongside specific alcohol control legislation that had a greater impact in Scotland. This thesis is not an exploration per se of why alcohol consumption rose in nineteenth-century Scotland, fell in the first half of the twentieth century and rose again to damaging levels at the end of the twentieth century. This high level of consumption persists in 2017 and the Scottish government is still acting to reduce alcohol-related harm by a variety of measures. Rather this thesis seeks to explore the response of the Scottish medical profession to the changing conditions in relation to alcohol over a seventy-year period from 1855 to 1925. (Chapter 3 and Chapter 4 set the scene). The starting point of 1855 for the period examined in this thesis is taken from the 1855–57 Inquiry by the Scottish Lunacy Commission, which led to the Lunacy Act (Scotland) of 1857. This report demonstrates that Scottish psychiatry was already having to deal with the mental consequences of alcohol and describes oinomania, an early term for alcohol dependence. The report introduces the idea that alcohol can itself cause insanity – an estimated 20% or more of the cases in asylums were caused by intemperance around that time and this figure was deemed to rise as the century wore on. This seems like a curious and excessive causal attribution from today’s perspective. In this thesis I trace how the idea of a persistent form of alcoholic insanity evolved in the Scottish context (Chapters 4 and 6), and I outline changing terminology and ideas around the mental consequences of alcohol (Chapters 5, 6, 7 and 8). These ideas were expounded by physicians and alienists/psychiatrists in the public arena of parliamentary inquiries in the second half of the nineteenth century (Chapter 4) as well as in the specialised literature of the time (Chapters 5, 6, 7 and 8), including the medical reports within the Annual Reports of asylums. Original to this thesis in relation to primary sources is an in-depth analysis of the alcohol cases received by the Delirium Ward at the Royal Infirmary of Edinburgh between 1856 and 1867, in the May to July period of each of these years (Chapter 5). These 178 recorded cases (57% of all admissions with threatening or actual delirium) illustrate that alcohol problems in the form of incipient or established delirium tremens were a common reason for admission to hospital at this early date and that such cases were of particular interest to physicians. It is striking that beyond the acute episode of what was erroneously thought to be an intoxication-induced illness there is no apparent attempt to help the person with their underlying intemperance (Chapter 5). The idea that later emerged of an underlying condition of inebriety, differentiated from insanity, was to have practical consequences in that it led to the setting up and running of Inebriate Reformatories in Scotland, as elsewhere in the British Isles, in the first quarter of the twentieth century (Chapters 7 and 8). I trace this story in detail through to the closure of the Inebriate Reformatories in 1925,whilst examining this in a Scottish context. Other scholars have looked at the era of the Inebriate Reformatories in Scotland from the perspectives of sociology, of history and of feminist theory. I review the previous literature in Chapter 2, and provide a historiography spanning the last hundred years. I also bring a fresh medical perspective to the topic in Chapter 7, which uses records not available to some of the previous scholars, and produce a very detailed analysis of the female cases sent to the Glasgow Reformatory (Girgenti House). This is presented in Chapter 8. The time period cut-off of 1925 for the end of the thesis is made for pragmatic reasons, as the trends in the conception of alcoholism and alcohol use disorders, and in treatment provision, since 1925 would merit separate full consideration. I do, however, sketch out these trends for this later period in a Postscript (Chapter 9) in order to give a context for drawing out some historic lessons from 1855–1925 in my Conclusion and Discussion (Chapter 10) about the “alcohol question” in the Scotland of today. The period I cover therefore includes an historic high in alcohol consumption in the late nineteenth century and an historic low in the 1920s. I aim to show how practice and theory interconnected during these years in the work of medical men such as Thomas Laycock, David Yellowlees, Sir Thomas Clouston, William Tennent Gairdner, James Craufurd Dunlop, John Cunningham and Sir David Henderson. I also describe some of the connections between these key medical figures within the Scottish system in Chapter 4. The post-1920 period also illustrates a sea change from a time where psychiatrists were arguing for the separation of the “inebriate” from the “lunatic” in terms of service provision to one where the “alcoholic” is seen as deserving of new forms of psychiatric help. This shift in practice, around the end of the period of my study, is seen in the context of a changing emphasis from a more biological view of the problem to a more psychodynamic, or dynamic, view as seen in the work of Henderson and others. The fact that this shift in theory and practice coincides with a decline in the alcohol problem is discussed in the light of Skog’s idea that our concerns around alcohol vary in relation to where we are in relation to “waves of consumption” (Chapter 10). My overall aim in this thesis, then, is to set out how from 1855 to 1925 medicine in Scotland responded to the idea that habituated use of alcohol might represent a disease in its own right. The idea of such a “disease of the will” remains both legally and philosophically controversial to this day. This is perhaps why our diagnostic systems continue to change in this area without final resolution. An associated aim of the thesis is to look at three aspects of the “drinking disease”, in Scotland, namely delirium tremens, alcoholic insanity and inebriety, where practice can be examined from case records and related to theory as represented in a range of publications. I also prove, and highlight the fact, that institutionalised medicine cannot escape engagement with the problem of alcohol. From the beginning, Scottish doctors in both infirmaries and asylums were presented with the consequences of heavy drinking in a sizeable proportion of patients. As with recent epidemiological analyses, alcohol consumption levels in the general population during the nineteenth and early twentieth century are shown to correlate highly with the incidence and prevalence of such disease consequences from the Scottish national and local statistics available. Then, as now, doctors were inevitably drawn into the issue of how best to respond to the underlying habit of drinking both at an individual and societal level. I draw lessons from my study of the past for our continuing struggle in this regard.

Parkinson's disease (PD) is misdiagnosed throughout its disease course for conditions such as essential tremor, drug-induced parkinsonism, vascular pseudo-parkinsonism, Alzheimer's disease and other degenerative parkinsonian diseases. This thesis aims to verify the accuracy of dopaminergic imaging in early and uncertain parkinsonian/tremor disorders through 3 studies. The first is a prospective United Kingdom multicentre assessment of [1231] FP-CIT SPECT use in 190 patients in pre-defined diagnostic categories and with particular focus on clinical features to assess the influence of imaging in routine practice. The second is a 2 year follow-up study of 150 consecutive patients with normal SPECT, with specific attention to clinical progression and antiparkinson medication use, and includes focus on a subgroup who fulfilled PD criteria where successful antiparkinson medication withdrawal was achieved. The third is a multicentre prospective European study of the accuracy of [1231] FP-CIT SPECT in 99 patients that included serial clinical and imaging assessments. Notably, when initial diagnosis/scan mismatch cases occurred, and with awareness of the scan result, the clinician invariably changed the diagnosis in line with the scan result which confirms the considerable influence of imaging on the practising clinician. Parkinson's disease is clinically overdiagnosed early in its disease course, whereas imaging is more specific, in the vast majority of cases with normal dopaminergic imaging, there was no evidence of clinical or imaging progression which would be in keeping with degenerative parkinsonism.

There is a wide variation in the phenotypic expression, progression rates, therapy response and complications in Parkinson’s disease (PD). The primary research objective in this thesis was to analyse the variation in the 4 domains of phenotypic expression i.e. motor, non-motor, cognitive, and quality of life in a subset of early onset Parkinson’s disease (EOPD) patients from the PRoBaND study, in the United Kingdom. The secondary objective was to explore the factors responsible for this variation or heterogeneity in the clinical characteristics. Linking genotypes with phenotypes, besides evaluating environmental risk factors and iatrogenic influences, represents one mechanism of understanding this variation in the phenotypic expression of PD. We found subtle but significant variation across all domains of symptoms examined in this thesis by classifying patients into groups according to motor subtype, gender, age at diagnosis and heritability of the parkinsonian trait, despite statistically insignificant differences in risk factors such as head trauma, exposure to pesticides (including herbicides, insecticides, fungicides and fumigants), heavy metals, caffeine and a past history of oophorectomy (in females) with the exception of smoking (p=0.046) and exposure to solvents, which were more common in males compared to females (p<0.001). There were differences in the prevalence of motor symptoms such as balance problems being more prevalent in the postural instability gait difficulty (PIGD) subtype compared to the tremor dominant PD (TDPD) and ‘Mixed’ motor subtypes both subjectively (p<0.001) and objectively (p<0.001). Other axial problems such as speech difficulties and freezing were also more prevalent in those with the PIGD phenotype compared to the other motor subtypes both subjectively (p=0.004, p<0.001) and objectively (p=0.002, p<0.001). There was also variation in the prevalence of motor complications such as dyskinesia (p<0.001) and dystonia (p=0.020), being more prevalent in the PIGD subtype compared to other motor subtypes. 8 The prevalence of certain non-motor symptoms such as pain (p=0.022) and features of gastrointestinal dysfunction e.g. prandial bloating (p=0.024) and constipation (p=0.022) were more commonly reported by females compared to males. There were also differences in the prevalence of cognitive impairment (p=0.049) and neurobehavioural characteristics such as anxiety (p=0.002) and depression (p=0.006), after the diagnosis of PD, being more prevalent in PIGD compared to other motor subtypes. Finally, these differences contributed to the variation in the independence of activities of daily living scores which were lower in those with the PIGD phenotype compared to other motor subtypes (p<0.001). There were some differences in exposure to environmental risk factors for PD but not sufficient to explain all the variation. Iatrogenic influences from drugs contributed in part to the phenotypic variation. 10% of the cases in the EOPD cohort tested positive for mutations in one of three genes screened i.e. LRRK2, GBA and Parkin; their DNA remains banked and there is scope to test these cases for mutations in other genes, relevant to PD, in the future. There were too small numbers of cases in each subgroup to draw definite conclusions about the exact influence of genes on the overall phenotypic variation but differences between Parkin mutation carriers and gene test negative ‘controls’ such as early age of onset and long disease duration were obvious. PRoBaND is linked to other similar research studies in the UK, with the stated aim of sharing datasets, in the hope that larger numbers of patients and their DNA samples will increase the power, in statistical terms, to test hypotheses about the role of genetic markers in influencing the course and expression of symptoms. Our current understanding of PD as a complex trait suggests both genetic and environmental influences (including iatrogenic factors if patients are treated) play a role in the phenotypic expression of this condition. A lot more remains to be explored to improve our understanding of the finer details and molecular mechanisms underlying the variation in this disease.

The spinal cord dorsal horn is involved in the processing and transmission of sensory information to the brain. There are several distinct populations of dorsal horn projection cells that constitute the major output of the spinal cord. These cells are mostly found in lamina I and are scattered throughout the deep dorsal horn. There is a population of large lamina III projection cells that expresses the neurokinin 1 receptor (NK1r), which is the main target for substance P released by nociceptive primary afferents. These cells are densely innervated by peptidergic nociceptive afferents and more sparsely by low-threshold myelinated afferents. In addition, they also receive selective innervation from neuropeptide Y-containing inhibitory interneurons. However, not much is known about their input from glutamatergic spinal neurons. It has already been reported that the great majority of large lamina III NK1r expressing cells project to caudal ventrolateral medulla (CVLM) therefore in this study these cells were easily identified without retrograde tracer injection. Preliminary observations showed that these cells received contacts from preprodynorphin (PPD)-containing excitatory axons. The first part of the study tested the hypothesis that lamina III projection cells are selectively targeted by PPD-containing excitatory spinal neurons. Spinal cord sections from lumbar segments of the rat underwent immunocytochemical processing including combined confocal and electron microscopy to look for the presence of synapses at the sites of contact. The results showed that lamina III NK1r cells received numerous contacts from non-primary boutons that expressed vesicular glutamate transporter 2 (VGLUT2), and formed asymmetrical synapses on their dendrites and cell bodies. These synapses were significantly smaller than those formed by peptidergic afferents but provided a substantial proportion of the glutamatergic input to lamina III NK1r projection cells. Furthermore, it was observed that PPD was found to be present in ~58% of the VGLUT2 boutons that contacted these cells while a considerably smaller proportion of (5-7%) VGLUT2 boutons in laminae I-IV expressed PPD. These results indicate a highly selective targeting of the lamina III projection neurons by glutamatergic neurons that express PPD. Fine myelinated (Aδ) nociceptors are responsible for the perception of fast, well-localised pain. Very little is known about their postsynaptic targets in the spinal cord, and therefore about their roles in the neuronal circuits that process nociceptive information. In the second part of the study, Fluorogold injections were made into the lateral parabrachial region (LPb) of the rat brain on one side and cholera toxin B subunit (CTb) was injected into the sciatic nerve on the contralateral side to assess whether Aδ nociceptors provide input to lamina I projection cells. The vast majority of lamina I projection neurons belong to the spinoparabrachial tract, and these can be divided into two major groups: those that express NK1r, and those that do not. The results suggested that CTb labelled a distinct set of Aδ nociceptors, most of which lack neuropeptides. CTb-labelled Aδ afferents formed contacts on 43% of the spinoparabrachial lamina I neurons that lacked the NK1r, but on a significantly smaller proportion (26%) of NK1r projection cells. Combined confocal and electron microscopy established that the contacts were associated with synapses. Furthermore, the contact density of CTb labelled boutons was considerably higher on the NK1r- cells than on those with the NK1r. These results provide further evidence that primary afferents input to projection cells is organized in a specialized way and that both NK1r+ and NK1r- lamina I projection neurons are directly innervated by Aδ nociceptors, thus may have an important role in the perception of fast pain. Lamina I of the rat spinal cord dorsal horn contains a population of large spinoparabrachial projection neurons (giant cells) that receive numerous synapses from both excitatory (VGLUT2) and inhibitory (VGAT) interneurons. The giant cells are selectively innervated by GABAergic axons that express neuronal-nitric oxide synthase (nNOS) and are thought to originate from local inhibitory interneurons. In the rat, the nNOS inhibitory cells belong to a distinct functional population that differs from other inhibitory interneurons in terms of somatostatin receptor (sst2A) expression and also in responsiveness to painful stimuli. There is a population of inhibitory interneurons that express green fluorescent protein (GFP) in lamina II of mice in which GFP is under control of the prion promoter (PrP) and the great majority of these cells also express nNOS. In this part of the study, the inhibitory synaptic input from nNOS-containing GFP boutons to giant lamina I cells was investigated. The great majority of lamina I projection neurons express NK1 receptor; therefore, the possibility that lamina I NK1r-expressing projection neurons received innervation from GFP+/nNOS+ axons was also tested. Since retrograde tracing technique was not used in this part of the study, lamina I projection cells were identified based on the observations made in the previous studies in the rat. Lamina I giant cells were recognized with antibodies against glycine receptor associated protein gephyrin as well as VGLUT2 and VGAT boutons, all of which provide dense innervation to these cells while only those lamina I NK1cells were included in the sample that were large and strongly immunoreactive for NK1r. The results indicated that although GFP axons accounted for only 7-9% of the GABAergic boutons in superficial dorsal horn, they provided over 70% of the inhibitory synapses on most of the giant cells in the PrP-GFP mouse and the great majority of these boutons also contained nNOS. Moreover, a subset of large lamina I NK1r-expressing cells (18/60) received a substantial inhibitory input (> 30%) from GFP+ boutons while the majority of these neurons showed sparse (< 15%) synaptic input. Recently, it has been reported that loss of some inhibitory interneurons in mice lacking the transcription factor Bhlhb5 results in exaggerated itch, and the cells that are lost include many of those that would normally express nNOS. Therefore, in the final set of experiments was designed to test whether there is a reduction in the inhibitory synaptic input to the giant cells in Bhlhb5-/- mouse. Spinal cord sections from Bhlhb5-/- mice and the wild type littermates were processed and analysed to determine any difference in the inhibitory nNOS input to lamina I giant cells belonging to either group. The giant cells from the knockout mice showed a substantial reduction (~80%) in their inhibitory nNOS input; with a moderate reduction in their overall GABAergic input (~35%). There was a considerable increase in nNOS-/VGAT+ boutons in the Bhlhb5-/- mouse (18 ± 4.6 and 37.7 ± 8.2/100 µm of the dendrite in WT and KO, respectively), suggesting some compensation from other nNOS-negative inhibitory interneurons. These results suggest that the loss of nNOS-containing inhibitory synaptic input to lamina I projection cells may contribute to the abnormal scratching behaviour seen in the Bhlhb5-/- mouse. This raises the possibility that the giant cells and a subset of large lamina I NK1r-expressing cells are involved in perception of itch.

Parkinson’s disease (PD) is commonly treated with L-DOPA. Long-term treatment is associated with the development of motor side effects such as L-DOPA induced dyskinesia (LID), and pathological changes in the striatal circuitry. However, while this circuitry is implicated in both motor and non-motor behaviour, little is known about the effects of long-term L-DOPA treatment on non-motor function. This thesis used a rat model of PD and LID to test the hypothesis that long-term L-DOPA treatment also affects non-motor behaviour. Pharmacological studies typically utilise albino rats, while pigmented rats are preferred for operant studies. To guide later methodological decisions, Experiment 1 compared pigmented Listed Hooded and albino Sprague Dawley rats’ motor, dyskinetic, or operant response to L-DOPA. As there were no gross strain differences, and Lister Hooded rats are preferred in operant studies, they were used in later experiments measuring both LID and operant behaviour. Experiment 2 aimed to identify appropriate lesion screening tests. Success of unilateral 6-OHDA lesions is commonly measured using amphetamine-induced rotations. However, amphetamine interferes with goal-directed behaviour. The ability of amphetamine-induced rotations and four non-pharmacological motor tests to accurately identify lesion rats was therefore compared. The non-pharmacological spontaneous rotations and cylinder tests were identified as robust screening tests and used in later experiments. L-DOPA competes with dietary amino acids for transport across the blood-brain barrier, and chronic L-DOPA treatment sensitises dopamine receptors. It was therefore hypothesised that food restriction and chronic L-DOPA would both decrease the L-DOPA dose required to alleviate motor symptoms in the rat 6-OHDA model. Chapter 4 describes two dose response curves testing the effect of food restriction and chronic L-DOPA on the motor response to acute L-DOPA in rats with intra-striatal or MFB lesions. Chronic L-DOPA increased the motor response to acute L-DOPA in the MFB, but not intra-striatal, lesion model. Conversely, food restriction increased the motor response to acute L-DOPA in the intra-striatal, but not MFB, lesion model. Chapter 5 used microdialysis to test the hypothesis that the increased motor response following food restriction was caused by an increased influx of L-DOPA to the striatum. The data did not support the hypothesis but suggested that food restriction affects baseline neurotransmitter levels in the 6-OHDA lesion rat. Chapter 6 tested the hypothesis that LID onset, by disrupting cortico-striatal synaptic plasticity which is implicated in motor skill learning, impairs acquisition of novel motor skills by measuring rats’ performance on the staircase task. While an initial experiment suggested that chronic LID onset impaired lesion rats’ acquisition of the task, the phenomenon could not be replicated. Chapters 7 and 8 further explored the effect of chronic L-DOPA on non-motor function using a lateralized choice reaction time task reliant on the striatal system. Chronic L-DOPA exacerbated a lesion induced accuracy deficit that has been hypothesised to reflect extinction. This deficit was linked to LID onset, rather than L-DOPA exposure per se. The data therefore expand on current knowledge by suggesting that the effects of chronic L-DOPA extends beyond inducing motor side effects to also affect non-motor function.

interventions are recommended for people with bipolar disorder to enable them to effectively self-manage their health, prevent relapse and improve their long-term outcomes. Psychoeducation comprises expert information (on topics such as monitoring mood, lifestyle and medication) and is commonly presented by health care professionals in structured individual or group face-to-face sessions. This thesis reviewed the evidence from randomised controlled trials and qualitative studies that psychoeducational approaches in different formats may or may not be beneficial for patients with bipolar disorder, and consequently found the evidence base to be sparse, particularly with regard to the benefits and drawbacks of different formats of delivery. This thesis explores the feasibility, acceptability and impact of a group-based psychoeducation programme for people with bipolar disorder in Wales (Bipolar Education Programme – Cymru) and a novel internet-based psychoeducation programme (Beating Bipolar) for participants of a randomised controlled trial. Adopting a pragmatic approach, and using both qualitative and quantitative research methods in a predominantly qualitative study, I explored and compared both interventions from the perspectives of patients and facilitators, using qualitative interviews, data from the Beating Bipolar online discussion forum and quantitative outcome data from questionnaires. Findings principally describe the facilitators and barriers to delivery in different formats, what participants liked and disliked about the programmes, the potential impact of the programmes and recommendations for future use, and identify the potential therapeutic mechanisms of psychoeducation. Receiving social support from the groups and enhanced knowledge and understanding of bipolar disorder from the educational content and shared experiences were found to improve many participants’ self-reported confidence in their ability to manage their bipolar disorder, and many made beneficial changes to their lifestyles, coping strategies and their attitudes towards medication and bipolar disorder in general as a result. Future research should focus on widening access to both interventions.