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These inhibitory output nuclei Nonhuman Primate Models stimuli are discount 16mg betahistine, in turn cheap 16mg betahistine free shipping, regulated by two parallel but opposing pathways from the caudate and putamen purchase betahistine 16 mg fast delivery, one excitatory Antipsychotic treatment in the nonhuman primate has been and the other inhibitory purchase betahistine 16 mg with visa. The primary cortical signal to basal studied to define the mechanism of acute drug-induced par- ganglia is mediated by an excitatory glutamatergic pathway. It would be rational to suspect some role of these parallel Gunne et al. This idea correlated with the known clinical phar- The cause of TD in antipsychotic drug–treated patients macology of TD, namely, that GABA agonist treatment can is, by definition, long-term drug treatment. Thus, putative improve drug-induced dyskinesias (65). Chapter 126: Tardive Dyskinesia 1835 Rodent Models transmission in nonhuman primate basal ganglia directly affected the output nuclei, and from there, the thalamic and Results from many laboratories suggested that rats treated frontal regions associated with the segregated motor circuit. In comparison, the newer antipsychotics, often called vacuous chewing movements (13,16,18,23,27,30, including clozapine, olanzapine, sertindole, and low-dose 56,61). The phenomenology of CMs resembles TD, in that risperidone, failed to induce the rat 'syndrome' of CMs movements have a gradual onset (61), partial penetrance (21,39). Can these preparations contribute to knowledge (34), and a delayed offset, and they are sensitive to stress of TD pathophysiology? However, the movements in rats remain limited to mation to the mechanism of antipsychotic drug action? The Comparison of several different animal treatment groups pharmacology of CMs resembles that of TD: CMs are sup- has been useful in addressing these questions: (a) haloperi- pressed by antipsychotics, but not by anticholinergics (52); dol-treated rats, with versus without rat CMs and (b) halo- they are reduced by GABAmimetics (20), and they are at- peridol-treated rats versus newer antipsychotic drug–treated tenuated with benzodiazepines. Antipsychotic drugs block advance the onset and severity of the rat CMs (24). The the inhibitory D2 receptor and disinhibit the medium spiny similarities across phenomenology and pharmacology are neuronal projections to the GP. In these studies, striatal close enough between human TD and rat CMs for investi- disinhibition is reflected in the glutamic acid decarboxylase gators to pursue the biochemical basis of CMs as a clue to mRNA increases in GP, especially in the CM rats (Table pathophysiology in TD. At the same time, activity in the direct striatonigral the two are similar enough for the use of this model as a pathway appears also to be altered possibly by the haloperi- screen for new antipsychotic drugs to rule out TD potential. In the reported that although all traditional antipsychotics are as- SNR, a primary basal ganglia output nuclei in the rat, ab- sociated with CMs (70,71), clozapine is not (19,27). Subse- quently, the other 'new' antipsychotics have been tested and have generated results consistent with clinical data, demonstrating low TD potential for the second-generation antipsychotics (29,39). Neither olanzapine nor sertindole produce the CM syndrome at drug doses that produce human therapeutic plasma levels in the animals (21); risperi- done at low doses is not associated with CMs, whereas high doses produce haloperidol-like CMs (Gao, unpublished ob- servations). Data using quetiapine or ziprasidone in this animal model have not been reported. NEUROCHEMICAL CHANGES WITHIN THE BASAL GANGLIA THALAMOCORTICAL PATHWAYS IN A RODENT MODEL OF TARDIVE DYSKINESIA We designed and carried out a series of studies in a putative rodent model of TD based on the broadly accepted, func- FIGURE 126. Specific binding of 3H-spiperone to D2-familydo- tional architecture of the basal ganglia and thalamus already pamine receptors in the nucleus accumbens of control and chroni- described. These studies were based not only on the exis- callyhaloperidol-treated rats. D2 binding data were similar in the tence of these theoretic models, but also on early experimen- caudate and putamen. Significant dopamine-receptor up-regula- tal data in nonhuman primates with chronic antipsychotic tion was apparent in the haloperidol-treated rats with chewing movements (CMs) and in those without CMs; there was no appar- treatment implicating GABAergic transmission in TD (30, ent difference between CM and non-CM rats in the magnitude 31). The drug- and time-induced changes in GABAergic of increase. Haloperidol Haloperidol Olanzapine, Sertindole, + VCMs – VCMs no VCMs no VCMs Striatum ↑D2R, ↑GAD ↑D2R, ↑GAD S1 ↑D2 o ∆ D2R No ∆ GAD ↑GAD Globus pallidus ↓GAD, No ∆ GAD, No ∆ GAD No ∆ GAD, ↓GABAA o ∆ GABAA o ∆ GABAAR ↓GABAAR Substantia nigra ↑GABAAR Tr ↑GABAAR∆ Nl, GABAAR Nl, GABAAR1 pars reticulata ↓D1 o ∆ D1 o ∆ D1 o ∆ D1R MD thalamus ↑GABAA o ∆ GABAA o ∆ GABAA o ∆ GABAAR GABAAR/ No correlation No correlation No correlation VCM correlation Right thalamus ↑GAD mRNA ↑GAD mRNA ↑GAD mRNA ↑GAD mRNA arrow, significant change; D1R, D1 family dopamine receptor; D2R, D2 family dopamine receptor; GABAAR, GABAA receptor; GAD, glutamic acid decarboxylase mRNA; Tr, trend; VCMS, vacuous chewing movements. Here the CM rats show reduced efferent pathway to thalamus. A reduction in GABA-me- nigral D1-receptor numbers, whereas the non-CM treated diated transmission from SNR to the target nucleus in the rats show no change in D1-receptor density (Fig. In the haloperidol-treated animals, a significant eleva- treatment with the GABA agonist progabide (Fig. The reduction in D1-receptor CMs in the mediodorsal thalamus (Fig. This posi- number in SNR could be associated with an antipsychotic- tive correlation implicates a nigral D1 defect along with induced increase in the dendritic release of dopamine (Fig. The Hence, an increase in dopamine release within SNR could idea that a reduction in the activity of the basal ganglia mediate the release of GABA at striatonigral terminals and output nuclei disinhibits the thalamus and is associated with subsequently could inhibit activity in the GABA-mediated drug-induced rat hyperkinetic oral CMs is consistent with the already established functional models of these interac- tions (2). Two second-generation antipsychotics tested in the same animal chronic treatment paradigm differed from haloperi- dol in their actions. Both olanzapine and sertindole, each at two doses, were compared with haloperidol after 6 months of treatment (56). Neither olanzapine nor sertin- dole substantially up-regulated striatal D2 binding in the rat, even though we know from human studies that D2 blockade of some strength and duration occurs with each of these drugs (21). Because of the relatively high receptor affinities of these drugs at the D2 receptor, the data suggest that any regional reduction in blockade may occur only at some of the D2 receptors, and the resultant antidopami- nergic action is weaker or of a reduced duration than with haloperidol. Nonetheless, olanzapine shows mild, haloperi- dol-like actions in striatum, and sertindole shows mild, FIGURE126. Specific bindingof 3H-SCH23390to D1-familydo- pamine receptors in the substantia nigra pars reticulata (SNR). Still, in SNR, nei- binding was down-regulated bychronic haloperidol (HAL) treat- ther new compound is associated with D1-receptor down- ment onlyin the rats that displayed the vacuous chewing move- regulation or GABA up-regulation (Table 126. This reduction was blocked bythe GABA agonist progabide (P), as were the CMs themselves. Progabide alone had GABAA receptors altered in mediodorsal thalamus by either no effect on the D1 binding. It is possible Chapter 126: Tardive Dyskinesia 1837 FIGURE126. Hypotheticalmodelforthe mechanism of chronic haloperidol-induced chewing movements (CMs) in rat. The data collected can be parsimoniouslyexplained bypostulating an increase in dendritic do- pamine release associated with the devel- opment of dyskinetic movements in the CM rats. An increase in dopamine could stimu- late the release of GABA presynaptically from the striatonigral GABAergic neurons and therebyincreasethe overall GABAergic inhibition on the GABA-containing nigral efferent fibers, including those to the thal- amus. This alteration would serve to de- crease the level of GABAergic inhibition on critical nuclei of the thalamus. This inter- pretation of the data, even though parsi- monious, is speculative. It may be that the common seroto- nergic influence exerted within the basal ganglia nuclei by both these compounds spares SNR changes. WORKING HYPOTHESIS OF THE CM-TD MECHANISM The data summarized here are consistent with many reports in the literature and confirm the central role of the basal ganglia output nuclei and thalamus in mediating hyperki- netic movements in chronic antipsychotic-treated animals. It would be our current notion that traditional antipsychotic drugs alter the dynamic balance of neurotransmitter activity within the indirect and direct striatonigral pathway. This change, perhaps associated with sustained increase in nigral dendritic dopamine release, results in rodent hyperkinetic oral movements through the feedback of this information to motor regions of neocortex through thalamus. This anti- psychotic-induced alteration acutely would merely inhibit activity within the indirect pathway and would be associated with parkinsonism. As treatment progresses and CMs begin, the indirect pathway inhibition could be progressively coun- FIGURE 126. Correlation of GABAA receptor densitywith chewing movements (CMs) in mediodorsal thalamus in rats terbalanced by direct pathway overactivity in the vulnerable treated chronicallywith haloperidol. We postulate that the changes in SNR in D1- relation between these two factors suggests their relationship. These available cant thalamic nuclei, evidenced bythe up-regulation in GABAA- data so far derive from animal model studies and provide receptor densityassociated with the putativelyreduced GABAer- a putative framework for TD pathophysiology. However, no other thalamic nuclei show this type of correlation, even the ventral nuclei traditionally must proceed with the human illness itself, by testing these associated with motor control in thalamus. CNS plasticity in response to chronic dopamine-receptor Speculations would then center most strongly on the role blockade. The difference between those animals who are of the serotonin2A-receptor blockade in striatum to attenu- vulnerable to develop CMs and those who are not remains ate the tardive motor effects of the dopamine-receptor obscure, as is the vulnerability to TD with antipsychotic blockade.
Six-month stability of psychiatric diagnoses in first- schizophrenia: the Jerusalem Infant Development Study cheap 16 mg betahistine overnight delivery. Am J Psychiatry 1994;151: Neurobehavioral deficits at school age buy betahistine 16mg without prescription. DSM-III-R noses of affective disorders and schizophrenia in public hospi- schizotypal personality traits in offspring of schizophrenic disor- tals discount betahistine 16 mg online. The concept of target features in Res 1989;23:229–239 purchase 16 mg betahistine with visa. Mental Health Project: demographic, pre-morbid and clinical 41. Vazquez-Barquero JL, Cuesta Nunez MJ, Herrera CS, et al. Sociodemographic and clinical variables as predictors of the di- 19. The ABC Schizophrenia agnostic characteristics of first episodes of schizophrenia. 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Results from the Cam- New York, Oxford University Press, 1982. Putatively psy- and intellectual markers for schizophrenia in apparently healthy chosis-prone subjects 10 years later. Generalizability of first-episode studies in children who develop schizophrenia in adult life: evidence for schizophrenia. Magical ideation and sode schizophrenia: marker or determinant of course? Biol Psy- social anhedonia as predictors of psychosis proneness: a partial chiatry 1999;46:899–907. Prediction of adult-onset schizophrenia ing the boundaries and connections between vulnerability and from childhood home movies of the patients. Prediction of psy- Chapter 47: Schizophrenia: Course Over the Lifetime 653 chosis: a step towards indicated prevention of schizophrenia. Premorbid IQ in patients Risk Project: diagnostic specificity and the role of attention. Electrodermal activation in relatives of schizophrenic patients. 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Acta Psychiatr Scand zation, and acute initial development reduce duration of un- 1999;100:359–366. Practice parameters for the assessment Psychiatry 2000;41:184–190. Early intervention American Academy of Child and Adolescent Psychiatry. JAm for schizophrenic disorders: implementing optimal treatment AcadChildAdolesc Psychiatry 1997;36:177S–193S. First-onset schizo- Br J Psychiatry Suppl 1998;172:33–38. Schizophrenia: from prediction to prevention: a chal- onset, early manifestations and typology. Acta Psychiatr Scand lenge for the 21st century [Editorial]. Early intervention and prevention in schizo- dopamine dysfunction in schizophrenia. Biol Psychiatry 1999; phrenia: experiences from a study in Stavanger, Norway. From fighting to preventing disease: is such a tion, and schizotypal symptoms in nonpsychotic relatives of paradigm possible for schizophrenic disorders? Arch Gen Psychiatry 1997;54: Psychiatr 1998;66:366–377. 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Patients start to complain at serum calcium level of 13 mg/dl generic betahistine 16 mg with mastercard, when abnormal EEG changes start to appear generic 16 mg betahistine. Patients suffering from hyperparathyroidism may manifest seizures independent of serum calcium level due to elevated serum parathormone order betahistine 16mg. Management: Hypercalcemia is corrected by saline diuresis betahistine 16 mg overnight delivery, augmented with furosemide, followed by a choice of mithramycin steroids, phosphate or etidronate. Encephalopathy in Diabetic Patients Hypoglycemia: Clinically, patients who develop hypoglycemia are graded: – At 20 mg/dl, immediate loss of consciousness in adults and children, neonates resist hypoglycemia better, – At 45 mg/dl, confusion, irritability. Sometimes unexplained focal lesions appear with hypoglycemia. Nonketotic hyperosmolar hyperglycemia (NHH): Usually occurs in diabetic patients whose insulin production is adequate to inhibit lipolysis, but insufficient to prevent hyperglycemia, which result in a marked osmotic diuresis. In such situations, serum glucose may rise to 800-1200 mg/dl, and serum osmolarity may exceed 350 mOsm/L, which may invite development of brain edema. Management: Normal saline is infused slowly to correct hypotension and improve osmolality, in addition to insulin Medical Diseases and Metabolic Encephalopathies | 107 infusion at the rate of 10 IU/h, with regular checking of plasma glucose, since these patients are very sensitive to insulin. Glucose should be added to saline when plasma glucose is approximately 300 mg/dl (Quinn 2002). Diabetic ketoacidosis (DKA): About 80% of DKA patients have encephalopathy and 10% are comatose. Management: Like NHH, but with higher amounts of insulin. If there is evidence of brain edema mannitol is used. If there is evidence of electrolyte imbalance, mandate correction. The use of IV sodium bicarbonate to compensate for metabolic acidosis is debatable (Quinn 2002). Hypoxic Ischemic Encephalopathy (HIE) Following cardiac or respiratory arrest, CO poisoning or cyanide poisoning, one of four clinical syndromes might appear: – Global encephalopathy – Memory loss – Postanoxic Parkinsonism – Lance-Adams syndrome (intention myoclonus) Findings predicting good prognosis are preserved pupillary responses, preserved roving eye movement, decorticate posture or better at initial examination. We predict good prognosis when we find in clinical examination after 24 hours, motor withdrawal from noxious stimuli or improvement of 2 grades in eye movement. Also, finding motor withdrawal or better, and normal spontaneous eye movements at 72 hours examination, carries a good prognosis. Also, when a patient obeys commands at the 1-week examination. Management is by hyperventilation and osmotic diuresis, for cerebral edema. Seizure control is live saving and has an impact on prognosis, as patients suffering from GTCS have a better outcome than those who suffer from myoclonic seizures. It is caused by a number of processes, such as direct bacterial invasion, toxic effects of endotoxins, inflammatory mediators, impairment of microcirculation, and neuroendocrine changes. The exact cellular and molecular mechanisms remain an enigma. Several mediators of inflammation have been assigned a key role in etiogenesis of encephalopathy, including cytokines, chemokines and complement cascade. With the observations that brain dysfunction in such sepsis disorders can be alleviated by regulation of the cytokines and complements in various species of animals, optimism is building for a possible therapy of the sepsis-damaged brain (Jacob 2011). Early aggressive treatment with antibiotics is key, along with modulators of cytokines and complements and anti- inflammatory medicines (Jacob 2011). Drug-induced Encephalopathies Commonly implicated drugs in encephalopathy etiology include salicylates, tricyclic antidepressants, lithium, sedatives, neuroleptics, methyldopa, amantadine, acyclovir, digitalis, propranolol, hydantoins, etc (Jain 2001). Drug-induced delirium results from disruption of the normal integration of neurotransmitters, including dopamine, acetylcholine, glutamate, gamma-aminobutyric acid (GABA), and/or serotonin (Young 1998). References Adams HP, del Zoppo G, Alberts MJ, et al. Guidelines for the Early Management of Adults With Ischemic Stroke. Management of hypertension in acute critical ill patients. Deciding when hemodynamic monitoring is appropriate. Intracranial Pressure and Cerebral Blood Flow Monitoring. Cambridge Books Online, Cambridge University Press (Accessed June 24, 2011, at http://dx. An introduction to the concepts and classification of impairments, disabilities and handicaps. Baldwin K, Orr S, Briand M, Piazza C, Veydt A, McCoy S. Clinical examination in diagnosis and subclassification of stroke. Berg K, Maki B, Williams JI, Holliday P, Wood-Dauphinee S. Clinical and laboratory measures of postural balance in an elderly population. The Sickness Impact Profile: development and final revision of a health status measure. The American-European consensus conference on ARDS, definitions, mechanisms, relevant outcomes, and clinical trials co-ordination. Medications attenuate stress response in critical illness. Neurologic intensive care unit catastrophes: airway, breathing, and circulation. Current Treatment Options in Neurology 2000;2:499–506. Angiography in brain death neuroradiology 1974;7:25-8. Measurements of acute cerebral infarction: a clinical examination scale. Predicting death and readmission after intensive care discharge. Cecil S, Chen PM, Callaway SE, Rowland SM, Adler DE, Chen JW. Traumatic brain injury: advanced multimodal neuromonitoring from theory to clinical practice. Clark WC, Muhlbauer MS, Lowery R, Hartman M, Ray MW, Watridge CB. Complications of intracranial pressure monitoring in trauma patients. The Rivermead Mobility Index: a further development of the Rivermead Motor Assessment. Mobility after stroke: reliability of measures of impairment and disability. Assessing motor impairment after stroke: a pilot reliability study. Cote R, Hachinski VC, Shurvell BL, Norris JW, Wolfson C. The Canadian Neurological Scale: a preliminary study in acute stroke. Crutchfeld JS, Narayan RK, Robertson CS, Michael LH. Evaluation of a fiberoptic intracranial pressure monitor. Clinical assessment of rehabilitation potential of older patients: a pilot study. Significance of intracranial pressure waveform analysis after head injury. 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Particular service redesign initiative Key topics What was the perceived need for change or the problem to be fixed? Who identified this and how was it brought to institutional attention? How were proposals for redesign developed buy betahistine 16 mg with amex, by whom and what was the content of these proposals? What is the role in these proposals of ideas of integrated care or improving value? How far did/do the new service redesigns challenge existing models of clinical work or clinical organisations discount 16 mg betahistine overnight delivery, as opposed to enhance what is already there? Who was involved order betahistine 16 mg fast delivery, in which kinds of ways buy 16mg betahistine mastercard, in getting agreement and implementing change? 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 111 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 4 What various stances and positions did different actors or agencies adopt? Which kinds of leadership, demonstrated by whom, were involved in achieving progress? What has happened in terms of results achieved – service redesign implemented and/or health outcomes? What reflections or views do various parties have on success/compromise/what next? Overall, what was revealed about clinical leadership and engagement by the change attempt? What has been revealed about the possibilities for more far-reaching service redesigns, particularly those that embody ideas of value-based care? What do you see as the key service redesign initiatives that have taken place recently in your area? What has happened to date and who (clinical and non-clinical) has been involved? What kinds of measures of success are relevant to these initiatives and is there, at this point, evidence that the new or changed form of services provides better care? What has made success achieved to date possible and what issues or blocks to progress have had to be overcome? Who has provided what kinds of leadership to make these initiatives work? Who else might it be worth talking to in order to gain further perspectives on this? What issues from your perspective would it be useful to focus on and understand better? With respect to service change, how did this come to be a priority? Build detailed chronology – when did it start and what milestone? What obstacles were faced and how were/are these (being) overcome? What role did clinical leaders play in these service changes? What role was played by managers in the service changes? Charts were produced using Microsoft Excel® (2010; Microsoft Corporation, Redmond, WA, USA). For the Kruskal–Wallis test, a randomisation procedure was used to calculate p-values because of the preponderance of ties. The analysis of variance results were taken into account only when residual plots indicated that the analysis of variance model was adequate. Questions where the p-value for the association was < 0. However, because of the multiple testing of many specific questions, attention concentrated on associations with smaller p-values. Not all such associations were reported on in Chapter 3, with a subjective choice being made depending on the statistical strength of the association and on its salience in the context of the study. Statistical calculations were performed using the R statistical programming language (version 3. 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 113 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. Patient centred, patient focused Outcome focused Clarity and structure, practical patient focus Clear evidence-based thinking. Clear understanding of what is needed to maximise the potential for front-line staff to work effectively together in the interest of their patients They have an understanding of resources Clear insight into the operational implications of challenges to services and service redesign Rapid option appraisal Relationships and Strategic clinical leadership influence and followed by all clinicians and officers collaboration Experience and judgment Patient engagement and member engagement;. 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 115 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. Agenda driven by managers Over managers Over secondary care Tiers and tiers of bureaucracy NHSE! Consultants are much more used to this environment Management blocking clinical change become of worry of loss of trust income. The clinical leadership is often sessional – lack of continuality, e. 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 117 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 119 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. Prime contractor arrangement and outcome-based commissioning Table 12 shows a brief overview of the answers with percentages rounded to the nearest 5%. The answers to this question suggested some fundamental differences in the beliefs and perspectives held by those who hold positions on CCGs. As Table 12 shows, the majority leaned towards a view that commissioning through the use of contracts with clearer specification of outcomes was the surest way to proceed. 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 121 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 6 committed to the general principle and logic. A surprisingly high number of CCG board members (10%) admitted that they did not know what the terms meant. Another significant group (around 15%) comprised persons opposed to these contracting approaches in principle and/or viewed them as too complicated, impractical and overhyped. A significant number of these sceptics were more attracted to what they saw as emerging models such as MCPs and the STPs, which gave hints that they leaned more towards planning and collaboration rather than completion and contracts. Other responses were: I think this will take longer than 2–3 years to have an impact. It is difficult to get good reliable outcome measures in a number of areas. I think the major issue will be that acute providers will have a disproportionate influence, and too much effort will be spent on managing this. Prime contractor arrangements could be hugely important due to the risk around sustainability of individual providers and the blurring of responsibilities for sector based activity (i. They will only work, however, if there is a strong and sustainable provider in the economy who can lead on them.