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REFLECTION VERSUS REACTION Positioning one partner as listener as the other partner speaks highlights subtle differences that might become obscured in debate-style conversa- tions generic 120mg sildalis fast delivery. This structure also guards against one voice becoming too dominant in the session generic sildalis 120mg with mastercard. The following questions illustrate how the therapist invites reflection: "Has the pattern of Interruption helped or hindered your hopes of un- derstanding each other differently? By being mindful of the assumptions that underlie our work as narrative therapists discount sildalis 120mg without a prescription, we reinforce our clients’ 170 THEORETICAL PERSPECTIVES ON WORKING WITH COUPLES sense of choice generic sildalis 120mg free shipping, empowerment generic sildalis 120mg without a prescription, and personal agency. Since problems are viewed as external to couples, we look for nouns that name prob- lems, rather than adjectives that describe partners (as problematic). So, rather than viewing Marci and/or Max as "codependent," we’d be more inclined to see them "struggling with the effects of Codependency. Examples of social constructs and possibly problematic dis- courses are the following: Religion (I should not be gay), Media (I should have a partner), Patriarchy (I should have sex when my partner wants to). Couples are continually recruited into evaluating themselves against dominant norms. If they don’t conform to these norms, couples often experience themselves as failures. It is not uncommon for couples to speak of exceptions to their problems as small or in- significant: "It was just that one time," or "It only lasted about five seconds. Every unique exception is a piece of gold, waiting to be grown (from 1 time to 2, from 5 seconds to 10) into alternative stories. In the same way that we refrain from to- talizing descriptions of couples, we resist totalizing descriptions of what the couple defines as problematic. We turn a critical eye on ways in which the culture privileges certain belief systems over others, im- pacting couples and the ways in which they view their relationships. We view each couple as unique and in- dividual, and resist any ideas of holding them up to a normative stan- dard of what constitutes a healthy couple. Oftentimes, a couple’s resources have been obscured by the strength of the problem. It is our job as narrative Narrative Therapy with Couples: Promoting Liberation 171 therapists to reconnect the couple to the resources that support their preferred ways of relating in partnership. We seek to make visible the dynamics of power in partner relationships, addressing all of its sources. By naming taken-for-granted truths embedded in power rela- tions, we invite couples to research the effects of power imbalance on their relationship. We question the assumptions that partners carry about their relationship and each other. One per- son’s unexpressed ideas about being a man/partner/lover/parent/ provider are not necessarily the same as his or her partner’s. Can partners agree to disagree, or is there a polarized, debate-style manner of seeing dif- ferences, as in "either I win or you win"? We aim to create a space where couples feel they have the right to evaluate the usefulness of our questions: "Does one of these questions capture your attention? Assuming a genuinely cu- rious stance requires the therapist to ask questions from a place of not knowing, free of interpretations. We are less interested in how we make meaning of the couple’s experience, and more interested in how the couple makes meaning of their own experience. Therapists share their own beliefs, assumptions, and experi- ences related to the therapy conversation, so that couples can situate and judge the therapist’s biases in deciding what is useful for them. We are willing 172 THEORETICAL PERSPECTIVES ON WORKING WITH COUPLES to share the impact that therapeutic conversations have on our lives, ac- knowledging the recursive quality of dialogue. We consider our position of power and the weight given to our pro- fessional knowledge. Narrative therapists collaborate with couples around diagnosis and correspondence with others, keeping them in the position of co-authors of the stories that get circulated. In profes- sional, academic, and supervisory settings, narrative therapists aim to speak about couples as if they were present in the room. This adher- ence to respectful practice invites generative conversations and shapes the lens that others use in viewing couples. If you’re looking for Re- sourcefulness in couples, you’re more likely to find it. DISCOURSE AND DECONSTRUCTION Until lions have their own historians, tales of hunting will always glorify the hunter.

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A book more sympathetic to the possibilities of CAM therapies in MS cheap sildalis 120 mg visa, but which is still based on rigorous evaluations effective 120mg sildalis, has been written by A purchase 120 mg sildalis amex. Bowling (Alternative Medicine and Multiple Sclerosis) order sildalis 120 mg on line, and there is an associated website that may be helpful to people with MS (see Appendix 2) cheap sildalis 120 mg online. For another sympathetic view of the possible benefits of complementary medicine, you might try the Institute of Complementary Medicine (see Appendix 1), which adopts a very rigorous approach to the evaluation of such therapies, or the individual professional associations of the therapy concerned. This would also enable you to check the qualifications, experience and regulation of their members. Safety of complementary therapies Few complementary therapies have been fully scientifically evaluated, especially in relation to MS. Almost any therapy, scientifically evaluated or not, that has the power to produce very good and positive results, has the potential to do harm. Although complementary therapies are considered as ‘natural’ and, almost by association, to be intrinsically safe, this is not always the case. For example, some herbal medicines have to be very carefully targeted to symptoms and very sensitively administered, otherwise they may be harmful. Note that practitioners may expect initial ‘reactions’ or ‘aggravations’ or symptoms as part of the effective working of the therapy. A competent therapist should both warn you about these and what to do, if and when they occur. Finding a practitioner Finding a competent practitioner for a complementary therapy is not always easy. There is little statutory regulation for qualifications or practice for most of the therapies and therapists. However, the best ways of finding a practitioner are through: • an MS resource or therapy centre, where often other people with MS and staff in the centre will have experience of particular therapists; • a recommendation or referral from a neurologist, GP or other healthcare professional; • registers set up by the professional bodies of whichever therapy you are interested in; • referral for homeopathy to one of the NHS hospitals providing this service; • contacting the British Complementary Medicine Association, or the Institute of Complementary Medicine (see Appendix 1). Ask whether practitioners are trained and licensed; whether they are insured for malpractice, negligence or accident; and how complaints are handled. One of the key things is to try and ensure that whichever therapist you go to has a good understanding of MS. Costs involved Many complementary therapies (acupuncture and osteopathy to name only two) are increasingly recognized as having significant benefits and can, in certain circumstances and limited geographic areas, be made available through the NHS. The appropriate registration bodies can provide details of registered practitioners in your local area and provide guidance on how much you might expect to pay. You may find COMPLEMENTARY THERAPIES AND MS 35 the addresses of these registration bodies through the British Com- plementary Medicine Association or the Institute of Complementary Medicine (see Appendix 1). Some types of CAM therapy There are many, many types of CAM therapy that may be used by people with MS, most of which we cannot consider in detail here (see the book by Bowling for more detailed information on individual therapies in Appendix 2). Furthermore the popularity of such therapies in MS can change very rapidly, with new therapies or new variations of previously available therapies regularly appearing, and the use of others decreasing rapidly after only a brief high profile existence. Thus in this section we consider some of the key CAM therapies that appear to have gained longer term use, or appear to be on the verge of doing so. Cannabis There has been a great deal of discussion about the use of cannabis recently in relation to the symptoms of MS. Based originally on individual reports by people with MS that at least two of the more problematic symptoms of MS, tremor and spasticity, seemed to respond well to cannabis, there has been an increasing interest in its use by people with MS. However, at present, cannabis is illegal in Britain – some people with MS have already been prosecuted for possessing, growing or supplying it – and it cannot be prescribed for MS. Nonetheless the pressure from people with MS to research the effects of cannabis more formally has resulted in the setting up of major clinical trials, the most significant of which are funded by the Medical Research Council, although some are being undertaken by pharmaceutical companies. These trials are not using cannabis in its original form, but are using what are called cannabinoids (one or more of the very many active substances in cannabis). Thus if the trials are a success, it will not mean that cannabis itself will be made available to people with MS, but almost certainly will lead to the use of manufactured drugs that have some cannabinoids as constituents. The results of some of the key trials are now beginning to appear indicating that a statistically significant beneficial effect on such MS symptoms as spasticity (and particularly pain associated with such spasticity). In due course one or more products based on such cannabinoids will become available. However, it is important to note that becoming ‘available’ will almost certainly mean 36 MANAGING YOUR MULTIPLE SCLEROSIS only by prescription from a medical practitioner who is willing to offer such drugs. Furthermore, even then such drugs may not become available through the NHS for some time, and may only be available initially through private payment. Currently, there is evidence that an increasing number of people with MS are using cannabis on an occasional or sometimes regular basis; it has become a very difficult issue because, although they do feel that they gain from taking it, they are having to balance what they feel is a significant reduction in their symptoms against committing an illegal act. Using the drug in any form is illegal, including ‘inactivated’ tinctures with limited narcotic effects.

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Hiatt buy 120mg sildalis with amex, MD 120mg sildalis for sale, Novartis Professor of Cardiovascular Research generic sildalis 120mg fast delivery, Section of Vascular Medicine buy 120mg sildalis overnight delivery, Unversity of Colorado Health Sciences Center order 120 mg sildalis fast delivery, Denver, CO 80203, USA Patrick R. Hof, MD, Associate Regenstreif Professor of Neuroscience, Kastor Neuro- biology of Aging Laboratories, Mount Sinai School of Medicine, New York, NY 10029, USA Sharon K. Inouye, MD, MPH, Professor of Medicine, Department of Internal Medi- cine, Yale University School of Medicine, Yale-New Haven Hospital, New Haven, CT 06504, USA Angela Inzerillo, MD, Assistant Professor of Medicine and Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA Jameel Iqbal, BS, Research Associate, Mount Sinai School of Medicine, New York, NY 10029, USA Nancy S. Jecker, PhD, Professor, Department of Medical History and Ethics, Univer- sity of Washington School of Medicine, Seattle, WA 98195, USA Fran E. Kane, MD, Professor, Minnesota Chair in Long Term Care and Aging, Uni- versity of Minnesota School of Public Health, Minneapolis, MN 55455, USA Wishwa N. Kapoor, MD, MPH, Falk Professor of Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA Marshall B. Kapp, JD, MPH, Professor, Departments of Community Health and Psychiatry; Director of Geriatric Medicine and Gerontology, Wright State University School of Medicine, Dayton, OH 45435-0001, USA Jason H. Karlawish, MD, University of Pennsylvania, Institute on Aging, Philadel- phia, PA 19104, USA Gary J. Kennedy, MD, Professor of Psychiatry and Behavioral Science, Albert Einste- ing College of Medicine; Director, Division of Geriatric Psychiatry and Fellowship Training Program, Montefiore Medical Center, Bronx Psychiatric Center, Bronx, NY 10024-2490, USA Gerard J. Kerins, MD, FACP, Assistant Professor of Medicine, Division of Geriatrics, University of Connecticut Health Center, Farmington, CT 06030-3956, USA Harold G. Koenig, MD, MHSc, Associate Professor of Psychiatry and Medicine, Department of Psychiatry and Behavioral Science, Duke University Medical Center, Durham, NC 27710, USA Contributors xxi Brandon Koretz, MD, Assistant Clinical Professor of Medicine, Division of Geriatrics, UCLA School of Medicine, Los Angeles, CA 90024, USA Amy Krupnick Freeman, MD, Dermatology Resident, Department of Dermatology, Mount Sinai School of Medcine, New York, NY 10029, USA Eric B. Larson, MD, MPH, Director, Center for Health Studies, Group Health Coop- eratives; Professor of Medicine, University of Washington Medical Center, Seattle,WA 98195, USA Rosanne M. Leipzig, MD, PhD, Vice-Chair for Education, Gerald and May Ellen Ritter Professor of Geriatrics, Brookdale Department of Geriatrics and Adult Devel- opment, Mount Sinai School of Medicine, New York, NY 10029, USA Sharon A. Levine, MD, Associate Professor of Medicine, Director of Medical Educa- tion and the Geriatric Medicine, Dentistry, and Psychiatry Fellowship Program, Geriatrics Section, Boston University Medical Center, Boston, MA 02218, USA Edward M. Liebers, MD,Clinical Fellow,Department of Medicine,Section of Hematol- ogy and Oncology, Dartmouth Hitchcock Medical Center, Lebanon, NH 03756, USA David A. Marin, MD, Professor of Psychiatry, Vice Chair, Department of Psychia- try, Mount Sinai School of Medicine, New York, NY 10029, USA Robert E. Martell, MD, PhD, Assistant Professor of Medicine, Divisions of Geriatrics and Medical Oncology, Duke University Medical Center, Durham, NC 27710, USA José C. Masdeu, MD, PhD, Professor and Director of Neurology and the Neuroscience Center, Department of Neurology, University of Navarre Medical School, Pamplona, Spain Khalid Matin, MD, Fellow, Division of Hematology-Oncology, Department of Medi- cine, University of Pittsburgh, Pittsburgh, PA 15213, USA Robert J. Mayer, MD, Director, Center for Gastrointestinal Oncology; Professor of Medicine, Department of Adult Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA 02115-5013, USA Wayne C. McCormick, MD, MPH, Associate Professor, Department of Medicine, Divi- sion of Gerontology and Geriatric Medicine, University of Washington Medical Center; Program Director, Long Term Care Services, Harborview Medical Center, Seattle, WA 98104, USA Diane E. Meier, MD, Director, Hertzberg Palliative Care Institute; Catherine Gaisman Professor of Medical Ethics; Professor, Brookdale Department of Geriatrics and Adult Development, Mount Sinai School of Medicine, New York, NY 10029, USA Kenneth L. Minaker, MD, Associate Professor of Medicine, Harvard Medical School; Chief, Geriatric Medicine Unit, Massachusetts General Hospital, Boston, MA 02114, USA xxii Contributors Charles Mobbs, PhD, Associate Professor, Neurobiology of Aging Laboratories, Brookdale Department of Geriatrics and Adult Development, Mount Sinai School of Medicine, New York, NY 10029, USA Anna Monias, MD, Victory Springs, Inc. Morrison, PhD, Professor and Director, Kastor Neurobiology of Aging Lab- oratories, Mount Sinai School of Medicine, New York, NY 10029, USA R. Sean Morrison, MD, Associate Professor, Brookdale Department of Geriatrics, and Adult Development; Research Director, Hertzberg Palliative Care Institute, Mount Sinai School of Medicine, New York, NY 10029, USA Thomas Mulligan, MD, AGSF, Chair, Consortium on Successful Aging, McGuire VAMC, Virginia Commonwealth University, Richmond, VA 23249, USA Aman Nanda, MD, Assistant Professor of Medicine, Division of Geriatrics, Brown Medical School, Rhode Island Hospital, Providence, RI, 02903, USA Mark R. Nehler, MD, Assistant Professor of Surgery, Section of Vascular Surgery, Uni- versity of Colorado Health Sciences Center, Denver, CO 80203, USA Linda C. Niessen, DM, MPH, MPP, Vice President, Clinical Education, DENTSPLY International, York, PA 17405, USA Eugene Z. Oddone, MD, MHSc, Director, Center for Health Services Research in Primary Care,VA Medical Center; Chief, Divison of General Internal Medicine, Duke University Medical Center, Durham, NC 27710, USA S. Jay Olshansky, PhD, Associate Professor, Department of Medicine, Harris Graduate School of Public Policy Studies, University of Chicago, Chicago, IL 60089, USA Robert M. Palmer, MD, MPH, Department of General Internal Medicine, The Cleve- land Clinic Foundation, Cleveland, OH 44195, USA Cynthia X. Pan, MD, Assistant Professor and Director of Education, Palliative Care Program, Brookdale Department of Geriatrics and Adult Development, Mount Sinai School of Medicine, New York, NY 10029, USA Ann Partridge, MD, Breast Oncology Center, Dana Farber Cancer Institute, Brigham and Women’s Hospital, Boston, MA 02115, USA Robert H.

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AMPA (a) (b) Response Response Measure by: Measure by: –electrophysiology –electrophysiology –behaviour –behaviour NK-R Mg2 –humans –humans (b) removed (a) AMPA-R (a) AMPA-R Transmitter Transmitter Peptides release Glu release Glu Stimulus number Stimulus number (c) (d) Amplification of response Response Response (d) NMDA-R Measure by: Measure by: activation –electrophysiology –electrophysiology –behaviour NK-R Mg2 –behaviour NK-R Mg2 –humans (b) (c) removed –humans (b) (c) removed (a) AMPA-R (a) AMPA-R Transmitter Peptides Transmitter Peptides release Glu release Glu Stimulus number Stimulus number (e) Injury generic sildalis 120 mg with mastercard, continued (e) stimulation Spinal Response (d) hyperexcitability NMDA-R Measure by: activation –electrophysiology –behaviour NK-R Mg2 –humans (b) (c) removed (a) AMPA-R Transmitter Peptides release Glu Stimulus number Injury discount sildalis 120mg free shipping, continued (f) stimulation Spinal Response (d) hyperexcitability NMDA-R Measure by: activation –electrophysiology (f) –behaviour NK-R Mg2 –humans (c) removed (b) (a) AMPA-R Transmitter Peptides release Glu Stimulus number Figure 5 cheap 120mg sildalis with amex. Repeated stimulation (at sufficient intensity to activate C-fibres) leads to an elevated level of response that can be measured in electrophysiology and behavioural experiments in animals buy sildalis 120 mg visa, and psychophysical experiments in humans cheap 120 mg sildalis with visa. This phenomenon is referred to as wind-up, and illustrates the importance of NMDA receptor activation in starting the processes of central sensitization. The sequence of events during a train of stimuli is explained in these four figures. AMPA-R, AMPA receptor; Glu, glutamate; NK-R, neurokinin receptor; NMDA-R, NMDA receptor; Hist, histamine. In response Importantly, the membrane depolarizations caused by to a noxious stimulus glutamate is released, AMPA tachykinin receptor activation are slower to rise than receptors are activated and action potentials are gen- AMPA currents and are longer lasting (Figure 5. This potentials begin to summate and the membrane is is a fast and faithful transmission of the nociceptive 2 depolarized sufficiently to remove the Mg block information (Figure 5. The released glutamate can now activate the channel, allowing a The NMDA receptor differs from the AMPA recep- 2 2 large Ca influx (Figure 5. Consequences of unchecked ele- vated Ca2 could be severe, so the channel is tightly It is probably not an overstatement to say that the regulated. It is blocked by Mg2 ions at physiolog- mechanisms discussed below all depend absolutely on ical membrane potentials, the block only being NMDA receptor activation for their initiation and in released during sustained membrane depolarization. The key element is increased [Ca2 ] , which is i mate will still be binding to the NMDA receptor, the only generated in sufficient amounts from influx channel cannot open to pass Ca2 ions. In the presence of a more persistent noxious stimulus, Effects on the NMDA receptor peptides are released along with glutamate from afferent fibre terminals. This delay in peptide release Ca2 influx through NMDA receptors feeds back to occurs partly because peptides are located in termin- increase channel open probability. This is thought to als of high-threshold C-fibre afferents, but also be mediated through PKC phosphorylation of sites in because neuropeptide vesicles are stored at some dis- the C-terminus of the NMDA receptor NR1 subunit. However, PKC may The tachykinins and CGRP are the predominant exci- also mediate Ca2 -dependent inactivation of the tatory peptide transmitters in the DH. Tyrosine kinases also enhance tachykinin peptides – SP, neurokinin A (NKA) and NMDA receptor function, mediating the effects of neurokinin B (NKB) – which prefer the tachykinin several transmitters and maybe also PKC itself. It is certainly receptor have been studied in more detail than the an important molecule in inflammatory hyperalgesia, others. Most spinal cord neurones that respond to SP as a neuronal-specific modulatory subunit of PKA are in lamina I and express NK1 receptors. These (R1 ) is required for the development of inflam- SP-responsive neurones are not absolutely required for matory, but not neuropathic pain (Malmberg et al. It is an intriguing possibility that in differ- and manifestation of behavioural inflammatory hyper- ent injury states distinct subsets of afferent neurones algesia. Many behavioural and electrophysiological may drive the development of DH hyper-excitability pharmacological studies using NK1 receptor antago- by distinct intracellular pathways. However, despite this convincing Brain-derived neurotrophic factor (BDNF) can be pre-clinical evidence that SP and its receptors form an released from afferent neurones, and acts via its tyro- important part of the nociceptive pathway, NK1 recep- sine kinase B (TrkB) receptor to activate an Src kinase tor antagonists have been disappointing in human tri- that further enhances NMDA receptor function als for analgesia in a variety of clinical pain states. PERIPHERAL AND CENTRAL SENSITIZATION 35 N/P VDCC N/P VDCC (a) (b) Ca2 Ca2 SP SP Glu Glu BDNF BDNF NK1 TrkB NK1 TrkB Gq/11 Gs NMDA-R AMPA-R Gq/11 Gs NMDA-R AMPA-R KA-R PLC AC KA-R Na Na IP DAG cAMP 3 Src PKA PKCγ Ca2 2 Ca Post-synaptic neurone, projects to higher centres N/P VDCC (c) 2 Ca SP Glu NO BDNF PGE2 NK TrkB 1 NMDA-R AMPA-R Gq/11 Gs PLC AC KA-R Na IP DAG cAMP 3 Src Gs EP PKA PKA PKCγ cAMP AC 2 COX/LOX Ca PGE 2 Increased excitability NOS NO Figure 5. Receptor effects combine to depolarize the membrane, generate action potentials and activate the NMDA receptor (see Figure 5. N/P VDCC, N- and P-type voltage-dependent Ca2 channel; Src, pp60c-src, a well-characterized protein tyrosine kinase; COX/LOX, cyclooxygenase/lipoxygenase. Elevated [Ca ]i activates PLA2 and leads to formation • The resulting increased activity in nociceptors of COX and LOX products. Many noxious events and leads to increased afferent drive in the DH of the injury have been shown to generate PGE2, and applica- spinal cord. PKC and PKA) interact with release from the post-synaptic neurone signalling to enhance NMDA receptor function, with among changes back to the pre-synaptic terminal (Figure 5. Nitric oxide • These changes increase the excitability of the DH Nitric oxide synthase (NOS) is expressed by spinal neurone (spinal hyper-excitability), allowing: cord neurones and its activation is Ca2 dependent. NO activates guanylyl cyclase and gener- i In this way, weak peripheral inputs that impinge upon ates cGMP, but subsequent cellular mechanisms under- a hyper-excitable spinal cord can produce high levels lying its effects are not completely understood. Receptor pathways Further reading Tachykinins activate several intracellular pathways such as: Caterina, M. Impaired nociception and pain sensation in mice lacking • cAMP-mediated PKA activation. Vanilloid receptor 1 is essential for inflammatory thermal • Activation of NOS and NO release.

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