"Pet things" and "penny drops"-Factors influencing clinicians' teaching of pelvic anatomy.

Pelvic anatomy is considered challenging to teach and learn, partly because its complexity can make it difficult to conceptualize. Educational researchers recognize the value of a spiraling curriculum to develop clinically orientated anatomy knowledge for health professionals, but most studies have focused on the preclinical years. It is unclear how the complexities of pelvic anatomy are taught in the clinical setting by clinician educators. Understanding pelvic anatomy teaching from the perspectives of clinician educators is important because of their critical role in supporting medical students to become knowledgeable, safe practitioners. This study sought to examine factors that influence clinician educators' teaching of pelvic anatomy to medical students during clinical placement. Using established qualitative research methods, this exploratory study used semi-structured interviews with 10 participants from obstetrics/gynecology (n = 4) and urology (n = 6) in Australia. Interviews were transcribed, and data were analyzed using a reflexive thematic analysis framework. Two overarching factors were identified as influencing clinician educators' teaching: (1) how they defined the scope of knowledge, and (2) pedagogical understanding. Scope of knowledge was underpinned by patient safety considerations and guided by past experience and student aspirations. Pedagogical understanding also relied on experience and encompassed multiple teaching strategies, including approaches informed by sensitivities surrounding pelvic anatomy. Multiple factors influence how clinician educators define the scope of pelvic anatomy knowledge required of medical students. Clinician educators' awareness of syllabus and teaching approaches can enable them to support students to attain threshold concepts such as three-dimensional spatial relationships and sociocultural sensitivities associated with pelvic anatomy.

Ultrastructure of dorsal root ganglia.

Dorsal root ganglia (DRG) contains thousands of sensory neurons that transmit information about our external and internal environment to the central nervous system. This includes signals related to proprioception, temperature, and nociception. Our understanding of DRG has increased tremendously over the last 50 years and has established the DRG as an active participant in peripheral processes. This includes interactions between neurons and non-neuronal cells such as satellite glia cells and macrophages that contribute to an increasingly complex cellular environment that modulates neuronal function. Early ultrastructural investigations of the DRG have described subtypes of sensory neurons based on differences in the arrangement of organelles such as the Golgi apparatus and the endoplasmic reticulum. The neuron-satellite cell complex and the composition of the axon hillock in DRG have also been investigated, but, apart from basic descriptions of Schwann cells, ultrastructural investigations of other cell types in DRG are limited. Furthermore, detailed descriptions of key components of DRG, such as blood vessels and the capsule that sits at the intersection of the meninges and the connective tissue covering the peripheral nervous system, are lacking to date. With rising interest in DRG as potential therapeutic targets for aberrant signalling associated with chronic pain conditions, gaining further insights into DRG ultrastructure will be fundamental to understanding cell-cell interactions that modulate DRG function. In this review, we aim to provide a synopsis of the current state of knowledge on the ultrastructure of the DRG and its components, as well as to identify areas of interest for future studies.

A Single Session of a Digital Health Tool-Delivered Exercise Intervention May Provide Immediate Relief from Pelvic Pain in Women with Endometriosis: A Pilot Randomized Controlled Study.

BACKGROUND: Endometriosis is a debilitating chronic condition that is commonly associated with chronic pelvic pain, affecting approximately 10% of women of reproductive age worldwide. The general principle of pain management in this population involves both pharmacological and surgical interventions. There is also increasing interest in the use of exercise as an alternative non-pharmacological analgesic, but adherence and accessibility to face-to-face exercise-delivery modalities are poor. This study aims to determine the immediate impact of a single session of 'supervised' telehealth-delivered exercise compared to 'self-managed' virtual reality (VR)-delivered exercise on pelvic pain associated with endometriosis. METHODS: Twenty-two women experiencing pelvic pain due to endometriosis were included and randomized into three groups: (i) VR-delivered exercise group (n = 8); (ii) telehealth-delivered exercise group (n = 8); and (iii) control group (n = 6). The visual analogue scale (VAS) was used to assess the severity of pelvic pain. RESULTS: There was no statistically significant between-group difference (p = 0.45) in the participants' pain score following a single session of the study interventions (VR or telehealth) or the control. However, a 'medium-to-large' group x time interaction effect (η2 = 0.10) was detected, indicating a more favorable pain score change following a single session of telehealth- (pre-post ∆: +10 ± 12 mm) and VR-delivered exercise (pre-post ∆: +9 ± 24 mm) compared to the control group (pre-post ∆: +16 ± 12 mm). CONCLUSIONS: Our study suggests that a single bout of a 'self-managed' VR-delivered exercise may be as efficacious as a single session of 'supervised' telehealth-delivered exercise in providing immediate relief from pelvic pain associated with endometriosis.

Clodronate Treatment Prevents Vaginal Hypersensitivity in a Mouse Model of Vestibulodynia.

INTRODUCTION: Improved understanding of vestibulodynia pathophysiology is required to develop appropriately targeted treatments. Established features include vulvovaginal hyperinnervation, increased nociceptive signalling and hypersensitivity. Emerging evidence indicates macrophage-neuron signalling contributes to chronic pain pathophysiology. Macrophages are broadly classified as M1 or M2, demonstrating pro-nociceptive or anti-nociceptive effects respectively. This study investigates the impact of clodronate liposomes, a macrophage depleting agent, on nociceptive signalling in a mouse model of vestibulodynia. METHODS: Microinjection of complete Freund's adjuvant (CFA) at the vaginal introitus induced mild chronic inflammation in C57Bl/6J mice. A subgroup was treated with the macrophage depleting agent clodronate. Control mice received saline. After 7 days, immunolabelling for PGP9.5, F4/80+CD11c+ and F4/80+CD206+ was used to compare innervation density and presence of M1 and M2 macrophages respectively in experimental groups. Nociceptive signalling evoked by vaginal distension was assessed using immunolabelling for phosphorylated MAP extracellular signal-related kinase (pERK) in spinal cord sections. Hyperalgesia was assessed by visceromotor response to graded vaginal distension. RESULTS: CFA led to increased vaginal innervation (p < 0.05), increased pERK-immunoreactive spinal cord dorsal horn neurons evoked by vaginal-distension (p < 0.01) and enhanced visceromotor responses compared control mice (p < 0.01). Clodronate did not reduce vaginal hyperinnervation but significantly reduced the abundance of M1 and M2 vaginal macrophages and restored vaginal nociceptive signalling and vaginal sensitivity to that of healthy control animals. CONCLUSIONS: We have developed a robust mouse model of vestibulodynia that demonstrates vaginal hyperinnervation, enhanced nociceptive signalling, hyperalgesia and allodynia. Macrophages contribute to hypersensitivity in this model. Macrophage-sensory neuron signalling pathways may present useful pathophysiological targets.

Effects of Lactate on One Class of Group III (CT3) Muscle Afferents.

A class of Group III muscle afferent neurons has branching sensory terminals in the connective tissue between layers of mouse abdominal muscles ("CT3 muscle afferents"). These sensory endings are both mechanosensitive and metabosensitive. In the present study, responses of CT3 afferents to lactate ions and changes in temperature were recorded. Raising muscle temperature from 32.7°C to 37°C had no consistent effects on CT3 afferent basal firing rate or responses to either von Frey hair stimulation or to an applied load. Superfusion with lactate ions (15 mM, pH 7.4) was associated with an increase in firing from 6 ± 0.7 Hz to 11.7 ± 6.7 Hz (14 units, n = 13, P < 0.05, P = 0.0484) but with considerable variability in the nature and latency of response. Reducing the concentration of extracellular divalent cations, which mimicked the chelating effects of lactate, did not increase firing. Raised concentrations of divalent cations (to compensate for chelation) did not block excitatory effects of lactate on CT3 afferents, suggesting that effects via ASIC3 were not involved. Messenger RNA for the G-protein coupled receptor, hydroxyl carboxylic acid receptor 1 (HCAR1) was detected in dorsal root ganglia and HCAR1-like immunoreactivity was present in spinal afferent nerve cell bodies retrogradely labeled from mouse abdominal muscles. HCAR1-like immunoreactivity was also present in axons in mouse abdominal muscles. This raises the possibility that some effects of lactate on group III muscle afferents may be mediated by HCAR1.

Immortalized Dorsal Root Ganglion Neuron Cell Lines.

Pain is one of the most significant causes of suffering and disability world-wide, and arguably the most burdensome global health challenge. The growing number of patients suffering from chronic pain conditions such as fibromyalgia, complex regional pain syndrome, migraine and irritable bowel syndrome, not only reflect the complexity and heterogeneity of pain types, but also our lack of understanding of the underlying mechanisms. Sensory neurons within the dorsal root ganglia (DRG) have emerged as viable targets for effective chronic pain therapy. However, DRG's contain different classes of primary sensory neurons including pain-associated nociceptive neurons, non-nociceptive temperature sensing, mechanosensory and chemoreceptive neurons, as well as multiple types of immune and endothelial cells. This cell-population heterogeneity makes investigations of individual subgroups of DRG neurons, such as nociceptors, difficult. In attempts to overcome some of these difficulties, a limited number of immortalized DRG-derived cell lines have been generated over the past few decades. In vitro experiments using DRG-derived cell lines have been useful in understanding sensory neuron function. In addition to retaining phenotypic similarities to primary cultured DRG neurons, these cells offer greater suitability for high throughput assays due to ease of culture, maintenance, growth efficiency and cost-effectiveness. For accurate interpretation and translation of results it is critical, however, that phenotypic similarities and differences of DRG-derived cells lines are methodically compared to native neurons. Published reports to date show notable variability in how these DRG-derived cells are maintained and differentiated. Understanding the cellular and molecular differences stemming from different culture methods, is essential to validate past and future experiments, and enable these cells to be used to their full potential. This review describes currently available DRG-derived cell lines, their known sensory and nociceptor specific molecular profiles, and summarize their morphological features related to differentiation and neurite outgrowth.

Emerging Evidence of Macrophage Contribution to Hyperinnervation and Nociceptor Sensitization in Vulvodynia.

Vulvodynia is an idiopathic chronic pain disorder and a leading cause of dyspareunia, or pain associated with sexual intercourse, for women. The key pathophysiological features of vulvodynia are vaginal hyperinnervation and nociceptor sensitization. These features have been described consistently by research groups over the past 30 years, but currently there is no first-line recommended treatment that targets this pathophysiology. Instead, psychological interventions, pelvic floor physiotherapy and surgery to remove painful tissue are recommended, as these are the few interventions that have shown some benefit in clinical trials. Recurrence of vulvodynia is frequent, even after vestibulectomy and questions regarding etiology remain. Vestibular biopsies from women with vulvodynia contain increased abundance of immune cells including macrophages as well as increased numbers of nerve fibers. Macrophages have multiple roles in the induction and resolution of inflammation and their function can be broadly described as pro-inflammatory or anti-inflammatory depending on their polarization state. This state is not fixed and can alter rapidly in response to the microenvironment. Essentially, M1, or classically activated macrophages, produce pro-inflammatory cytokines and promote nociceptor sensitization and mechanical allodynia, whereas M2, or alternatively activated macrophages produce anti-inflammatory cytokines and promote functions such as wound healing. Signaling between macrophages and neurons has been shown to promote axonal sprouting and nociceptor sensitization. This mini review considers emerging evidence that macrophages may play a role in nociceptor sensitization and hyperinnervation relevant to vulvodynia and considers the implications for development of new therapeutic strategies.

Human Dorsal Root Ganglia.

Sensory neurons with cell bodies situated in dorsal root ganglia convey information from external or internal sites of the body such as actual or potential harm, temperature or muscle length to the central nervous system. In recent years, large investigative efforts have worked toward an understanding of different types of DRG neurons at transcriptional, translational, and functional levels. These studies most commonly rely on data obtained from laboratory animals. Human DRG, however, have received far less investigative focus over the last 30 years. Nevertheless, knowledge about human sensory neurons is critical for a translational research approach and future therapeutic development. This review aims to summarize both historical and emerging information about the size and location of human DRG, and highlight advances in the understanding of the neurochemical characteristics of human DRG neurons, in particular nociceptive neurons.

Innervation Changes Induced by Inflammation in the Murine Vagina.

Vulvodynia is a prevalent chronic pain disorder associated with high medical costs and often ineffective treatments. The major pathological feature is proliferation of vaginal nerve fibers. This study aimed to develop a highly reproducible animal model to study neuroproliferation in the vagina and aid the identification of appropriately targeted treatments for conditions such as vulvodynia. Mild chronic inflammation was induced using microinjection of complete Freund's adjuvant in the distal vagina of C57Bl/6 mice. Control mice received saline. Inflammation and innervation density were assessed at 7 and 28 days after a single administration or 14 days following repeated administration of complete Freund's adjuvant or saline. Histochemistry and blinded-analysis of images were used to assess vaginal morphology (H & E) and abundance of macrophages (CD68-labeling), mast cells (toluidine blue staining, mast cell tryptase-immunoreactivity), blood vessels (αSMA-immunoreactivity) and nerve fibers immunoreactive for the pan-neuronal marker PGP9.5. Subpopulations of nerve fibers were identified using immunoreactivity for calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY). Single administration of complete Freund's adjuvant resulted in vaginal swelling, macrophage infiltration, vascular proliferation and increased abundance of nerve fibers immunoreactive for CGRP, SP, VIP and/or PGP9.5 but not NPY, evident at seven days. Inflammation further increased following repeated administration of complete Freund's adjuvant but nerve fiber proliferation did not. Nerve fiber proliferation continued to be evident at 28 days. The inter-individual differences within each treatment group were small, indicating that this model may be useful to study mechanisms underlying vaginal nerve fiber proliferation associated with inflammation.

Peptidergic nerve fibers in the urethra: Morphological and neurochemical characteristics in female mice of reproductive age.

BACKGROUND: Peptidergic nerve fibers provide important contributions to urethral function. Urethral innervation of female mice is not well documented. AIMS: To determine the distribution and projection sites of nerve fibers immunoreactive for vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP), substance P (SP), and neuropeptide Y (NPY) in the urethra of wild-type control mice and compare innervation characteristics between the proximal and distal urethra of young nullipara and older multipara mice. Furthermore, to identify the location and neurochemical coding of the spinal afferent nerve endings in the urethra, whose sensory neurons reside in lumbosacral dorsal root ganglia (DRG). METHODS: Multiple labeling immunohistochemistry of urethral sections of nulliparous (6-8 weeks old), and multiparous (9-12 months old) mice, and anterograde axonal tracing from L5-S2 (DRG) in vivo. RESULTS: Abundant VIP-, CGRP-, SP-, and NPY-immunoreactive nerve fibers were identified in the adventitia, muscularis, and lamina propria of proximal and distal segments of the urethra. A proportion of fibers were closely associated with blood vessels, glands, and cells immunoreactive for PGP9.5. The epithelium contained abundant nerve fibers immunoreactive for CGRP and/or SP. Epithelial innervation was increased in the distal urethra of multipara mice. Abundant fibers were traced from L5-S2 DRG to all urethral regions. CONCLUSIONS: We present the first identification of spinal afferent endings in the urethra. Peptidergic nerve fibers, including multiple populations of spinal afferents, provide rich innervation of the female mouse urethra. The morphology of fibers in the epithelium and other regions suggests multiple nerve-cell interactions impacting on urethral function.

Morphological and neurochemical differences in peptidergic nerve fibers of the mouse vagina.

The vagina is innervated by a complex arrangement of sensory, sympathetic, and parasympathetic nerve fibers that contain classical transmitters plus an array of neuropeptides and enzymes known to regulate diverse processes including blood flow and nociception. The neurochemical characteristics and distributions of peptide-containing nerves in the mouse vagina are unknown. This study used multiple labeling immunohistochemistry, confocal maging and analysis to investigate the presence and colocalization of the peptides vasoactive intestinal polypeptide (VIP), calcitonin-gene related peptide (CGRP), substance P (SP), neuropeptide tyrosine (NPY), and the nitric oxide synthesizing enzyme neuronal nitric oxide synthase (nNOS) in nerve fibers of the murine vaginal wall. We compared cervical and vulvar areas of the vagina in young nullipara and older multipara C57Bl/6 mice, and identified differences including that small ganglia were restricted to cervical segments, epithelial fibers were mainly present in vulvar segments and most nerve fibers were found in the lamina propria of the cervical region of the vagina, where a higher number of fibers containing immunoreactivity for VIP, CGRP, SP, or nNOS were found. Two populations of VIP-containing fibers were identified: fibers containing CGRP and fibers containing VIP but not CGRP. Differences between young and older mice were present in multiple layers of the vaginal wall, with older mice showing overall loss of innervation of epithelium of the proximal vagina and reduced proportions of VIP, CGRP, and SP containing nerve fibers in the distal epithelium. The distal vagina also showed increased vascularization and perivascular fibers containing NPY. Immunolabeling of ganglia associated with the vagina indicated the likely origin of some peptidergic fibers. Our results reveal regional differences and age- or parity-related changes in innervation of the mouse vagina, effecting the distribution of neuropeptides with diverse roles in function of the female genital tract.

The role of the trigeminal sensory nuclear complex in the pathophysiology of craniocervical dystonia.

Isolated focal dystonia is a neurological disorder that manifests as repetitive involuntary spasms and/or aberrant postures of the affected body part. Craniocervical dystonia involves muscles of the eye, jaw, larynx, or neck. The pathophysiology is unclear, and effective therapies are limited. One mechanism for increased muscle activity in craniocervical dystonia is loss of inhibition involving the trigeminal sensory nuclear complex (TSNC). The TSNC is tightly integrated into functionally connected regions subserving sensorimotor control of the neck and face. It mediates both excitatory and inhibitory reflexes of the jaw, face, and neck. These reflexes are often aberrant in craniocervical dystonia, leading to our hypothesis that the TSNC may play a central role in these particular focal dystonias. In this review, we present a hypothetical extended brain network model that includes the TSNC in describing the pathophysiology of craniocervical dystonia. Our model suggests the TSNC may become hyperexcitable due to loss of tonic inhibition by functionally connected motor nuclei such as the motor cortex, basal ganglia, and cerebellum. Disordered sensory input from trigeminal nerve afferents, such as aberrant feedback from dystonic muscles, may continue to potentiate brainstem circuits subserving craniocervical muscle control. We suggest that potentiation of the TSNC may also contribute to disordered sensorimotor control of face and neck muscles via ascending and cortical descending projections. Better understanding of the role of the TSNC within the extended neural network contributing to the pathophysiology of craniocervical dystonia may facilitate the development of new therapies such as noninvasive brain stimulation.

Cushing's mechanism maintains cerebral perfusion pressure in experimental subarachnoid haemorrhage.

Mortality following subarachnoid haemorrhage (SAH) is high, especially within the first 48 h. Poor outcome is predicted by high intracranial pressure which causes diminished cerebral perfusion pressure unless a compensatory increase in mean arterial blood pressure occurs. Therefore blood pressure elevation can be protective following subarachnoid haemorrhage despite the potential for rebleeding. This study investigated blood pressure responses to SAH and the impact on cerebral perfusion pressure and outcome, as demonstrated by two experimental models. Various blood pressure responses were demonstrated, both at the ictus and within the following 5h. Elevated MABP at the ictus and at 2h following experimental SAH was associated with maintenance of CPP in the presence of raised ICP. Poor outcome (arrest of the cerebral circulation) was predicted by failure of MABP to increase significantly above sham levels within 2h of SAH. Rat SAH provides relatively inexpensive models to investigate physiological mechanisms that maintain cerebral perfusion in the presence of intracranial hypertension.

New therapeutic approaches to subarachnoid hemorrhage.

INTRODUCTION: Subarachnoid hemorrhage (SAH) is associated with significant morbidity and mortality, even for patients who receive early neurointerventionist management. AREAS COVERED: Early mechanisms of secondary brain injury precede the delayed vasospasm phase and contribute to the poor outcome. These mechanisms and their intervention are discussed, including high intracranial pressure (ICP), low cerebral perfusion pressure (CPP), acute vasospasm, disturbed cerebral autoregulation, cerebral edema, oxidative stress, seizures, microvascular damage and hyperglycemia. Erythropoietin, statins and magnesium have been particularly promising in experimental studies. EXPERT OPINION: Multiple mechanisms, including delayed vasospasm, may contribute to cerebral ischemia and poor outcome following SAH. Treatments that simultaneously target multiple secondary injury pathways show significant potential as therapeutic agents, particularly those that attenuate vasospasm in addition to having other neuroprotective properties.

Implementing 'translational' biomedical research: convergence and divergence among clinical and basic scientists.

Universities are increasingly regarded as key actors in the new 'knowledge economy', with requirements to produce market-oriented knowledge and engage in commercialization. This is of particular significance in the biomedical field, reflecting the perceived gap between success in terms of scientific discoveries and its transformation into products. The dominant discourse attributes this situation to 'blocks' in the translational pathway from 'bench to bedside', leading to policies to 'reengineer' the research enterprise. This study examines a pilot initiative established by the UK's Medical Research Council (MRC). This involved employing a change agent (Research Translator) supported by a small amount of translational funding to promote the culture and practice of translational research at a university/hospital site in England. An ethnographically informed case study involving semi-structured and open exploratory interviews, observation and document review, was conducted in 2008. Analysis and interpretation were informed by Bourdieu's logic of practice applied to science. The requirements of translational research promoted by the Research Translator and its sources of capital (authority, prestige etc) were largely congruent with the 'field' of clinical science. In contrast, translational research diverged from perceptions of 'legitimate' science and requirements for capital accumulation held by the majority of basic scientists who often described this research as 'high risk' and were resistant to the Research Translator's advice. However some differences in motivations and practices were identified within groups of scientists associated with career stage, work environment and specialty. We argue that there are convergent and divergent forces that influence scientists' readiness to adopt a market-oriented translational research model and in turn facilitate or constrain the effectiveness of a knowledge broker. We also identify ways in which current structures and policies continue to promote a continuum of forms of knowledge production, thus challenging notions of a linear shift.

Characterizing the role of the neuropeptide substance P in experimental subarachnoid hemorrhage.

BACKGROUND: Raised intracranial pressure (ICP) following SAH predicts poor outcome and is due to hemorrhage volume and possibly, brain edema, hydrocephalus and increased volume of circulating intracranial blood. Interventions that reduce edema may therefore reduce ICP and improve outcome. The neuropeptide substance P (SP) mediates vasogenic edema formation in animal models of ischemic stroke, intracerebral hemorrhage and brain trauma, and may contribute to development of increased ICP. SP (NK1 tachykinin receptor) blockade using n-acetyl-l-tryptophan (NAT) reduces edema and improves outcome in these models. This study therefore assessed whether SP mediates edema formation in experimental SAH. METHODS: SAH was induced in rats by either injection of autologous blood into the prechiasmatic cistern (injection SAH) or by arterial puncture of the Circle of Willis (filament SAH). NAT was injected (i.v.) 30min after SAH induction. Subgroups were assessed for brain water content, SP and albumin immunoreactivity, and functional outcome at 5, 24 and 48h or ICP over 5h. RESULTS: A secondary ICP increase occurred within 2h of SAH. Brain edema followed filament SAH (p<0.001) and correlated with functional deficits (r=0.8, p<0.01). Increased albumin immunoreactivity (p<0.001) indicated vasogenic edema. However, NAT treatment did not improve ICP, edema or outcome. CONCLUSIONS: Experimental SAH produced secondary ICP elevation, vasogenic brain edema and functional deficits, although it is unclear if edema contributed to ICP. Blockade of SP did not improve any outcome parameters, suggesting that neurogenic inflammation may be less critical than other factors in these models.

The role of evidence in alternative medicine: contrasting biomedical and anthropological approaches.

The growth of alternative medicine and its insurgence into the realms of the biomedical system raises a number of questions about the nature of evidence. Calls for 'gold standard' randomised controlled trial evidence, by both biomedical and political establishments, to legitimise the integration of alternative medicine into healthcare systems, can be interpreted as deeply political. In this paper, the supposed objectivity of scientific, biomedical forms of evidence is questioned through an illumination of the multiple rhetorics embedded in the evidence-based medicine phenomenon, both within biomedicine itself and in calls for its use to evaluate alternative therapeutic systems. Anthropological notions of evidence are constructed very differently from those of biomedical science, and offer a closer resonance with the philosophy of alternative medicine. Examples are given of the kinds of evidence produced by anthropologists researching alternative medicine. Ethnographic evidence of 'what works' in alternative medicine includes concepts such as transcendent, transformational experiences; changing lived-body experience; and the gaining of meaning. It is proposed that the promotion of differently constructed modes of evidence can be used to legitimise alternative medicine by widening the definition of what works in therapy, and offering a critique of what people feel is lacking from much of orthodox medical care.

The expression of aversion to medicines in general practice consultations.

Although the relevance of patients' views about medicines for their medicine taking behaviour is now well established, little is known about the ways in which these views are discussed in primary care consultations. In particular, many studies have demonstrated patients' aversion to medicines. This paper examines the form that aversion talk takes in the consultation and how doctors respond to patients' expression of aversion to medicines. It is based on a dataset of 35 case studies of general practice consultations in England. In interviews with researchers, aversion to medicines was expressed in 34 of the 35 cases. In consultations with doctors, aversion was expressed in 10 cases. The interactional dimension of aversion talk in consultations was analysed using Conversation Analysis, and two general patterns were identified. Aversion could be used as an interactional resource, or it could be a topic in its own right. If used as an interactional resource, no real discussion of patients' views of medicines took place. When aversion was a conversational topic in its own right, two situations were observed. Firstly, the doctor elicited patients' views directly. Secondly, patients initiated aversive talk using a range of indirect strategies to do so. Even when patients managed to express their aversion to medicines, doctors did not engage them in any real discussion of their views. A scheme of interpretation is suggested to explain these findings. In this scheme patients perceive medicines to be an extension of the doctor and to be beneficial. In this view it is right for doctors to prescribe medicines and for patients to take medicines. The results of this paper suggest that using aversion as an interactional resource might be the only safe way for patients to express their aversion without seeming to breach the social contract.

Self-treatment and its discussion in medical consultations: how is medical pluralism managed in practice?

Recent policy changes in the UK such as deregulation of prescribed medicines and the introduction of telephone helpline services are intended to promote self-treatment. Drawing on interviews with, and consultations between, 35 patients and 20 general practitioners, we use Kleinman's (Patients and Healers in the context of culture: an exploration of the Borderland between Anthropology, Medicine and Psychiatry, University of California Press Ltd., London) model of the three sectors of health care in order to examine the range of self-treatments people use and the discussion of these treatments in medical consultations. We argue that despite the availability of a range of treatment options and policy changes advocating greater use of self-treatment, patients are inhibited from disclosing prior self-treatment, and disclosure is affected by patients' perceptions of the legitimacy of self-treatment. The findings are in keeping with Cant and Sharma's (A New Medical Pluralism, Alternative Medicines, Doctors, Patients and the State, UCL Press, London) contention that although there has been a pluralisation of "legitimate" providers of health care and a restructuring of expertise, biomedicine itself remains dominant.