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Biol Psychiatry 1998;44: correlates of treatment response in first-episode schizophrenia discount top avana 80 mg amex. Neuropsychology Chapter 56: Therapeutics of Schizophrenia 799 of first-episode schizophrenia: initial characterization and clini- ization during maintenance treatment of schizophrenia order top avana 80mg fast delivery. Study of Recent Onset Psychosis: one-year follow-up of first- 125 generic top avana 80mg overnight delivery. Arch Gen Psychia- fectiveness for patients in state hospitals: results from a random- try 1991;48:739–745. A study of the pharmaco- clinical symptoms in first-episode schizophrenia: response to logic treatment of medication-compliant schizophrenics who low-dose risperidone. Olanzapine versus of patients recently discharged on a regimen of risperidone or haloperidol treatment in first-episode psychosis. Psychosocial treatments in results of a 52 week randomized double blind trial. Multiple-family groups haloperidol in the treatment of first-episode psychosis. Research update on the psychosocial chosis and outcome in first-episode schizophrenia. Is there an association Conceptual model, treatment program, and clinical evaluation. Compliance with medication regi- schizoaffective disorder. Medication compliance and substance Schizophr Bull 1996;22:305–326. Why do schizophrenic patients refuse to take Bull 1996;22:283–303. A self-report scale predictive tive-behavioural interventions in early psychosis. Br JPsychiatry of drug compliance in schizophrenics: reliability and discrimina- (Suppl) 1998;172:101–106. Predicting medication compliance in a expressed emotion and relapse in recent onset schizophrenic psychotic population. Depot neuroleptics: the relevance of psychosocial 143. Subjective utility ratings factors—a United States perspective. JClin Psychiatry 1984;45: of neuroleptics in treating schizophrenia. Subjective experience of treatment, side- netics of long-acting injectable neuroleptic drugs: clinical impli- effects, mental state and quality of life in chronic schizophrenic cations. Compliance therapy: an inter- lized treatment option. Clozapine: pattern of efficacy in treatment-resis- outpatients. Addition of lithium to haloperidol in non-affec- drugs. Patient re- blind, placebo controlled, parallel design clinical trial. Psycho- sponse and resource management: another view of clozapine pharmacology 1993;111:359–366. Am JPsychiatry choosing among alternative somatic treatments for schizophre- 1995;152:821–825. Carbamazepine in violent non-epileptic schizo- 1374–1379. Carbamazepine as adjunctive treatment in nonepi- parative study of risperidone and conventional neuroleptics for leptic chronic inpatients with EEG temporal lobe abnormalities. The Quebec Schizophrenia JClin Psychiatry 1983;44:326–331. Treatment-resistant study of adjunctive carbamazepine versus placebo on excited schizophrenic patients respond to clozapine after olanzapine states of schizophrenic and schizoaffective disorders. Drug interactions in psychiatry, first pine therapy in chronic schizophrenics. Effects of switching induced reduction of plasma haloperidol levels worsen psychotic inpatients with treatment-resistant schizophrenia from cloza- symptoms? Randomized, double- controlled pilot study of divalproex sodium in the treatment of blind, controlled trial of risperidone versus clozapine in patients acute exacerbations of chronic schizophrenia. The clinical use of clozapine plasma concentrations on behavior and plasma amino acid concentrations in chronic in the management of treatment-refractory schizophrenia. Risperidone versus olanza- ergic drugs in the treatment of schizophrenia. JClin Psychophar- pine in patients with schizophrenia or schizoaffective disorder. Recent patterns and azepines for psychotic disorders: a literature review and prelimi- predictors of antipsychotic medication regimens used to treat nary clinical findings. Risperidone and clozapine combina- phrenic patients. Arch Gen Psychiatry 1988; tion for the treatment of refractory schizophrenia. Pimozide augmentation for Schizophr Bull 1996;22:27–39. Electrical convulsion therapy in 500 se- tation in people with schizophrenia partially responsive to clo- lected psychotics. Results obtained from the administration of 12,000 213. Negative symptoms: a path analytic doses of Metrazol to mental patients. Psychiat Quart 1941;15: approach to a double-blind, placebo- and haloperidol-con- 772–778. Lancet 1980; robiological models and treatment response. Thymosthenic agents, a novel approach in the response to electroconvulsive therapy in patients with schizo- treatment of schizophrenia. J of atypical neuroleptics in relation to the phencyclidine model of Gen Psychol 1954;50:79–86. Outcome in dementia praecox rat A10 dopamine neurons in vivo. Acta Physiol Scand 1989; under electro-shock therapy as related to mode of onset and to 136:497–498. Combined use of clozapine and electroconvulsive tients.
Quality improvement through clinical communities: eight lessons for practice buy 80 mg top avana amex. Reengineering Health Care: The Complexities of Organizational Transformation order 80mg top avana with mastercard. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed buy discount top avana 80 mg on-line, the full report) may be included in professional journals 101 provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising. Applications for commercial reproduction should be addressed to: NIHR Journals Library, National Institute for Health Research, Evaluation, Trials and Studies Coordinating Centre, Alpha House, University of Southampton Science Park, Southampton SO16 7NS, UK. Delivering Healthcare Through Managed Clinical Networks (MCNs): Lessons From the North. Southampton: National Institute for Health Research Service Delivery and Organisation; 2010. Process Improvement and Lean Thinking: Using Knowledge and Information to Improve Performance. Connecting Knowledge and Performance in Public Services. Dent M, Bourgeault IV, Denis JL, Kuhlman E, editors. The Routledge Companion to Professions and Professionalism. The Routledge Companion to Professions and Professionalism. The System of Professions: An Essay on the Division of Expert Labour. The enabling role of social position in diverging from the institutional status quo: evidence from the UK NHS. Agency at the managerial interface: public sector reform as institutional work. Understanding radical organisational change: bringing together the old and new institutionalism. Imison C, Curry N, Holder H, Castle-Clarke S, Nimmons D, Appleby J. Greenhalgh T, Humphrey C, Hughes J, Macfarlane F, Butler C, Pawson R. A realist evaluation of whole-scale transformation in London. Fitzgerald L, Ferlie E, Addicott R, Baeza J, Buchanan D, Gerry M. Service improvement in healthcare: understanding change capacity and change context. Theory building from cases: opportunities and challenges. Institutional work: refocusing institutional studies of organizations. Institutional Work: Actors and Agency in Institutional Studies of Organizations. Managing the rivalry of competing institutional logics. The Institutional Logics Perspective: A New Approach to Culture, Structure and Process. A tale of three discourses: the dominant, the strategic and the marginalized. Challenging Operations: Medical Reform and Resistance in Surgery. In Bryman A, Collinson D, Jackson B, Grint K, Uhl-Bien M, editors. National Improvement and Leadership Development Board. Developing People – Improving Care: A National Framework for Action on Improvement and Leadership Development in NHS-Funded Services. London: National Improvement and Leadership Development Board; 2016. Leadership and strategic change under conditions of ambiguity. The Iron Cage Revisited: Institutional Isomorphism and Collective Rationality in Organizational Fields. The New Institutionalism in Organisational Analysis. Institutional entrepreneurship by elite firms in mature fields: the big five accounting firms. Institutional contradictions, praxis, and institutional change: a dialectical perspective. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed, the full report) may be included in professional journals 103 provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising. Applications for commercial reproduction should be addressed to: NIHR Journals Library, National Institute for Health Research, Evaluation, Trials and Studies Coordinating Centre, Alpha House, University of Southampton Science Park, Southampton SO16 7NS, UK. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed, the full report) may be included in professional journals 105 provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising. Applications for commercial reproduction should be addressed to: NIHR Journals Library, National Institute for Health Research, Evaluation, Trials and Studies Coordinating Centre, Alpha House, University of Southampton Science Park, Southampton SO16 7NS, UK. Training and development Respondents were presented with a scale from minimal to major training and development provision. Only 8% of respondents reported that there had been major initiatives to provide training and development (Figure 27). Figure 28 suggests, however, that there has been a decline in GP engagement with leadership in and around CCGs. Figure 20) have shown reason for an optimistic picture of clinical leadership in and around CCGs, Figure 28 shows a degree of pessimism. There was an overall view that GPs are now less engaged in leadership than they were previously. There was broad agreement that, increasingly, service redesign is being tackled above the CCG level and that co-ordinated commissioning across multiple CCGs was increasingly common. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed, the full report) may be included in professional journals 107 provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising. Applications for commercial reproduction should be addressed to: NIHR Journals Library, National Institute for Health Research, Evaluation, Trials and Studies Coordinating Centre, Alpha House, University of Southampton Science Park, Southampton SO16 7NS, UK. APPENDIX 2 35 30 25 Year 20 2014 2016 15 10 5 0 Minimal training An uneven Moderate Significant Major initiatives and development pattern of amounts for training and have taken place training and most development to provide the development development needed FIGURE 27 How much training and development have clinical leaders received?
This study suggests that less than optimal perinatal circumstances impact on the individual top avana 80mg without a prescription, perhaps through personality development top avana 80 mg with mastercard, limiting coping skills in later life top avana 80 mg generic. Sociological factors have a profound effect on the rate of suicide. Thus, suicide is not simply a matter for mental health services. In 1970, Stengel identified the important risk factors as being male, older, widowed, single or divorced, childless, high density population, residence in big towns, a high standard of living, economic crisis, alcohol consumption, broken home in childhood, mental disorder, and physical illness. While many of these hold today, residence in the country has replaced “residence in big towns” and low socioeconomic status has replaced “a high standard of living”. Lists of risk factors have been gathered for decades, but, they have high sensitivity and low specificity, while suicide has a low base rate - leading to unmanageably large numbers of both false positives and false negatives. A Sydney based group has extremely robustly stated that risk categorization (using risk factors) plays little or no role in the prevention of suicide (Large and Ryan, 2014 a&b; Large et al, 2011 a&b). These authors recommend that patients with mental disorder and other suffering individuals should be closely examined and all possible treatment/assistance should be provided – it is the treatment/management of issues rather than the classification of risk which is helpful. Some recent studies reported certain factors playing a stronger role than mental disorder. Almeida et al (2012) examined the suicidal thoughts of older people, found social disconnectedness and stress accounted for a larger proportion of cases than the mood disorders. Park et al (2013) have emphasized the importance of strained family relationships and a tolerant attitude to suicide. Schneider et al (2013) have emphasized the importance of obesity, smoking and living alone and conclude, “Suicide prevention measures should not only subjects with mental disorders but also address other adverse conditions”. Some medically orientated groups make observations which encourage the belief that mental health professionals can prevent suicide. For example, a recent study (Beautrais, 2004) of people who had made a suicide attempt found that after 5 years, 6. The paper concludes, “These findings imply the need for enhanced follow-up, treatment, and surveillance of all patients making serious suicide attempts”. This argument is logical, but impractical; most services are already doing their best and there is little evidence that any form of therapy is effective and maintaining intensive follow-up for 5 years would be impossible (from many points of view). In another example (Burgess et al, 2000), “Data on patient and treatment characteristics were examined by three experienced clinicians” and they found that “20% of the suicides were considered preventable. An exemplary admission procedure does not stop the patient out on leave getting drunk or being rejected by a lover; it does not strengthen the last straw for that individual. Beck et al (1999) studied outpatients at high risk of suicide, people 100 times more likely to suicide than members of the general population. They found the suicide rate among this high risk population was only 0. Thus, to save one life, even in this high risk group, it would be necessary to provide infallible care, 24 hours per day to 500 people for one year. Also, the support offered would need to be in a form acceptable to each individual. Powell et al (2000) studied psychiatric inpatient suicide. They compared those who had suicided as inpatients with a control group and identified risk factors. However, they concluded, “Although several factors were identified that were strongly associated with suicide, their clinical utility is limited by sensitivity and specificity, combined with the rarity of suicide, even in this high-risk group”. Appleby et al (1999) conducted comprehensive analysis of 10 040 suicides. They found, “Most… (of the deceased)… were thought to have been at no or low immediate risk at the final contact”. Fahy et al (2004) asked 7 experienced mental health professionals to read the notes of 78 psychiatric patients, and attempt to predict which 39 had suicided. The readers considered all known suicide risk factors. The result was that these skilled clinicians did no better than chance. The authors state, “…these disappointing findings call into question the clinical utility of risk factor findings to date”. There have been a number of well resourced small studies, in which high risk groups have been given sustained attention with special counseling and additional support. In none of these was there a significant difference in outcome when the experimental was compared to a control group. Reviewing these studies, Gunnell and Frankel (1994) found, “No single intervention has been shown in a well conducted randomized controlled trial to reduce suicide”. Similar conclusions have recently been made with respect of suicide among young people (Robinson et al, 2010). To date, 5 men have completed suicide at Guantanamo prison camp. Even with the reputation of the most powerful nation in the world in the balance, in the most secure environment on the planet, and with all possible resources, suicide could not be indefinitely prevented. Hospital admission Not infrequently, following a suicide, there is criticism of mental health professionals and systems for failing to admit people to hospital or, having admitted them, failing to provide some particular service/supervision. Most psychiatrists, however, have known closely supervised patients who have suicided. Powell et al (2000) described their experience, “…two inpatients were under continuous observation. One of these two jumped through a window and deliberately cut his neck with the broken glass, the other ran to a railway line and was hit by a train. In response to budgetary constraints, admissions to psychiatric hospital in Fulton County Georgia, USA, had to be reduced. Over the same time period, the suicide rate of the county did not increase, but fell, from 12 to 10/100 000 (not statistically significant). Thus, ready admission to hospital does not improve the suicide rate of a general population. Another group admitted to hospital for their own safety are people with an episode of a disorder like major depressive disorder, who appear to be in some danger of suicide. The idea here is that hospital is a safe place where the mental disorder can be most efficiently treated. The Sydney based researchers mentioned above have put forward a revolutionary idea, “Nosocomial Suicide” - that psychiatric admission may increase the risk of suicide (Large et al, 2014). For some individuals, adverse aspects of psychiatric ward admission may include stigmatization, a sense of abandonment and heightened vulnerability. This idea needs close examination and may change psychiatric practice. The impact of suicide on others Impact on relatives and friends. There is surprisingly little standardized data on the effect of relatives and friends of those who suicide.
In contrast purchase top avana 80mg with mastercard, receptors order top avana 80 mg mastercard, which are en- changes in levels may be secondary to such features as activ- tirely postsynaptic buy top avana 80 mg mastercard, stimulate adenylate cyclase and cAMP ity or agitation. Urinary MHPG levels have been explored as possible 2 Receptor numbers and activity have been reported in tests for predicting antidepressant response. The earliest multiple studies to be increased in the platelets of depressed studies (14,15) pointed to low MHPG levels predicting pos- patients (22,23), although there is also at least one negative itive responses to imipramine but not amitriptyline. These ing cAMP responses to challenges with agonists. Mooney findings led Maas (14) to hypothesize that there were two and associates (25) reported that epinephrine suppression forms of depression—one a low MHPG state reflected a of prostaglandin-E induced cAMP formation is decreased norepinephrine depression; another characterized by high in the platelets of depressed patients. Siever and colleagues MHPG levels signified a serotonin depression. This hypoth- (26) reported norepinephrine stimulation results in blunted esis, although heuristic, has not been borne out. Subsequent adenylate cyclase responses in an E1– 2 prostaglandin cou- studies failed: (a) to demonstrate that high MHPG levels pled model. Platelet aggregation that results from 2 stimu- predicted amitriptyline response (16); and (b) in the light of lation has also been reported to be altered in depressed pa- the development of selective serotonin reuptake inhibitors tients (27). Mooney and colleagues (25) using stimulation (SSRIs) the serotonergic potency of amitriptyline was also of 2 receptors with a variety of agents, including NaF, thrown into question. In contrast, several studies have re- which directly affects G1 coupled proteins have hypothe- ported that low urinary MHPG levels do indeed predict sized that this down-regulation is not agonist specific and response to noradrenergic agents—nortriptyline, desipra- have argued that a fundamental uncoupling of the recep- mine, and maprotiline (17,18). Application of urinary tor–G-protein–AC complex occurs in some depressed pa- MHPG levels has been limited in part because of: difficulty tients. Chapter 72: Molecular and Cellular Mechanisms in Depression 1041 Growth hormone (GH) responses to challenge with form 5-HT. The principal metabolite of 5-HT is 5-hydrox- clonidine, an 2 agonist, has also been employed as a func- yindole acetic acid (5-HIAA), which is easily measurable in tional test of 1 activity. Consistent blunting of GH re- cerebrospinal fluid (CSF) and urine. MAO mediates part sponses in depressed patients has been reported (28,29). Blunted GH response appears to be a trait marker; it is found in remitted patients (30). The significance of blunted Metabolite Studies GH responses to clonidine is not entirely clear, however. Clonidine could be affecting presynaptic or postsynaptic Much of the early interest in serotonin was generated by receptors (31). Also, somatostatin, an inhibitor of GH re- observations that low CSF 5-HIAA levels in hospitalized lease, may play a role in the GH response to clonidine chal- depressives were associated with an increased risk for suicide lenge. Further studies revealed a relationship, particularly 2 Receptors have also been explored in postmortem with violent methods of suicide (e. Increased binding sites have been subsequently with difficulties with impulse control in sub- reported in several studies (32–34), although findings re- jects with antisocial personality (45). Current theories em- garding the specific isoform and location of the increased phasize a more general relationship between low serotonin binding sites have not been consistent. Results have been less consistent than depressed (46). Decreased binding in leukocytes of depressives has been reported inconsistently (35,36). Simi- Transporter larly, in postmortem brain tissue, increased -adrenergic receptor density has been reported by Mann and colleagues The serotonin transporter (SERT), a 12-transmembrane (37); however, decreased max was reported by Crow and molecule, actively pumps 5HT into the presynaptic neuron. Effects Originally, the transporter was studied in platelets using of previous medication may enter into these discrepant find- tritiated (3H) imipramine and more recently with the higher ings, as could biological heterogeneity of catecholamine se- affinity (3H)-paroxetine. Numerous studies have reported cretion in depressed patients. A metaanalysis by Ellis and Salmond (47) of 70 studies demonstrated an over- Depletion Strategies all significant difference between patients and controls, al- -Methylparatyrosine (AMPT) inhibits TH and ultimately though not all studies concur. Medication did not appear synthesis of norepinephrine. When given to healthy controls to account for these differences. Although mean values ap- or depressives it does little to lower mood (39,40); however, pear to differ between patients and controls, there is consid- remitted depressed patients on noradrenergic antidepres- erable overlap in values among patients and controls such sants show a worsening of symptoms when challenged with that there are numbers of patients who do not appear to AMPT, suggesting that norepinephrine availability or tone have decreased binding; this overlap limits the use of the is needed for maintaining response to NE agents (41). AMPT in previously depressed pa- be a trait marker, that is, did not normalize with treatment. Taken together, these imipramine binding does normalize with treatment but one data suggest the test could be a possible trait marker for must wait for sufficient periods to allow for protein regener- depressive vulnerability and that maintaining NE tone is ation. The transporter has also been the subject of examination in postmortem brain tissue. Early studies in this area pointed to decreased binding in suicide brains (48); however, more SEROTONIN recent studies have failed to confirm these findings (49). These data raise questions regarding the significance of ab- Serotonin (5-HT) is a monoamine neurotransmitter in- normalities in the activity SERT in the pathophysiology of volved in mood and appetite regulation. In brain, it is syn- depression and the relationship of peripheral and central thesized within the raphe from l-tryptophan. There are a number of methodo- self does not cross the blood–brain barrier. Synthesis logic problems inherent in postmortem tissue that may ac- includes an initial conversion to 5-hydroxytryptophan (5 count for differences among studies, including accuracy of HTP) via the enzyme, tryptophan hydroxylase. This system has been 123I- -CIT), that bind selectively to the transporter has al- studied in the brains of suicide victims. In one study, a significant ates reported [3H] phorbol dibutyrate binding to protein difference in binding using SPECT was observed between kinase C in prefrontal cortex was lower in teenage suicide depressed patients and controls (50). More recently they observed that both phos- cant differences were not observed in platelet binding to pholipase C activity and the 1 isozyme protein level were 3H-paroxetine, raising questions regarding whether the decreased of teenage suicide victims (63). Depression per transporter is regulated differently in the two tissues. In contrast Hrdina and associates (64) reported unaltered protein kinase C activity in antidepres- Receptors sant free depressives who suicided, and Coull and colleagues Presynaptic and postsynaptic 5HT receptors have also been (65) reported that phorbol dibutyrate binding sites were studied in depressed patients. Over a dozen serotonin recep- increased in the prefrontal cortex of adults with similar his- tors have been identified, although the possible roles for tories. Age, diagnosis of depression, antidepressant use, and many have not. Two that have attracted most study for the time to collection of brain may play a role in these disparate longest periods are the 5HT1A and 5HT2a types. As with the transporter, multiple studies have ple groups have explored the potential use of pindolol, a investigated 5HT2a binding sites in the platelets of depressed 5HT1a antagonist, to hasten response to antidepressants or patients. An increase in binding sites (B-max) has been re- bring out responses in refractory patients. These studies ported in depressed and suicidal patients with some sugges- have yielded mixed results suggesting that pindolol may tion that increased binding in suicidal patients may be inde- hasten response to antidepressants in milder or first-episode pendent of a diagnosis of major depression (51–53).
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