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Attentional deficits in cerebral blood flow evidence generic prinivil 5 mg without prescription. Arch Gen Psychiatry 1986;43: patients with schizophrenia and in their non-psychotic first- 114–124 generic prinivil 5mg overnight delivery. Schizotypy and function of dorsolateral prefrontal cortex in schizophrenia purchase 2.5mg prinivil with visa. A new cohort and evidence for a monoaminergic mechanism. Attentional func- Arch Gen Psychiatry 1988;45:609–615. Schizotypy in community sam- Further evidence for regional and behavioral specificity. Arch ples: the three-factor structure and correlation with sustained Gen Psychiatry 1988;45:616–622. Span of apprehension and frontal lobe functioning: evidence from neuropsychology, in schizophrenia. In: Steinhauer SR, Gruzelier JH, Zubin J, cognitive neuroscience, and psychophysiology. Neuropsychology, psychophysiology and information processing Cummings JL, eds. The human frontal lobes: functions and disor- (Handbook of schizophrenia, vol 5). Information schizophrenia: transient 'on line' storage versus executive func- tioning. Neuropsychological indica- trasting attentional profiles in schizophrenic and depressed pa- tors of the vulnerability to schizophrenia. Vulnerability to schiz- pathophysiology of schizophrenia. Span of apprehen- cessing abnormalities as neuropsychological vulnerability indi- sion performance, neuropsychological functioning, and indices cators for schizophrenia. Acta Psychiatr Scand Suppl 1994;384: of psychosis-proneness. Further evidence for a multidimensional person- 136. Glucose metabolic ality disposition to schizophrenia in terms of cognitive inhibi- correlates of continuous performance test performance in adults tion. Information processing dysfunction continuous performance test. Arch Gen Psychiatry 1977;34: in paranoid schizophrenia: a two factor deficit. Effect of antipsychotic medication on Chapter 51: Endophenotypes in the Genetics of Schizophrenia 715 speed of information processing in schizophrenic patients. Am visual channels in the visual backward masking deficits of schizo- J Psychiatry 1982;139:1127–1130. Am J Psychiatry 1985;142: Ment Dis 1966;143:80–91 170–174. Electroencephalogr Clin Neurophysiol performance in unaffected siblings of schizophrenic patients. Electroencephalogr Clin Neurophysiol 1970;29: dysfunction in schizophrenia: studies of visual backward mask- 429–440. Very short-term memory dys- Steinhauer S, Gruzelier JH, eds. Defective short time constant infor- ogy, and information processing (Handbook of schizophrenia, vol mation processing in schizophrenia. On peripheral and central processes in vision: infer- 182. Auditory ences from an information-processing analysis of masking with P300 abnormalities and left posterior superior temporal gyrus patterned stimuli. P300 in schizophrenia: suppression and information processing. Psychol Rev 1976,83: interactions between amplitudes and topography.

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Actors at the margins 10mg prinivil otc, for example purchase prinivil 10mg overnight delivery, who have less invested in the status quo cheap 2.5mg prinivil fast delivery, may be prompted to initiate such action. However, on the other hand, they are less likely to have the resources to make a major impact. Disruption may occur to the role divisions (jurisdictions) of organisations (e. In the NHS, actors/change agents are likely to be interfacing with, and having an impact on, both of these. Resistance to change may come from both of these interests. Evidence from our cases suggests that disruption and the imagining of new forms of service was additionally complicated by the fact that in the NHS it is far from a simple matter to map which actors are more embedded in the status quo and which have a greater stake in challenging it. National policies and strategies emanating from senior levels in NHSE profoundly challenge the status quo in terms of the boundaries between primary and acute care. At the same time, front-line clinicians in district general hospitals are often the most passionate advocates of shoring up the status quo in terms of what happens in the acute sector. So, new models of service delivery can come both from apparently entrenched senior actors (such as those instances in cases B, E and F where the top two or three provided the vision and the impetus) and from more marginal actors (as in cases C and D where enthusiastic GPs with no formal place in the CCG hierarchy used their local knowledge to drive a path for change). Neither one could be said to be inherently superior. The latter, ground-up approach, needed to win resources and support from above. Their position in the field means that they can deploy resources based on expertise and local knowledge and can, credibly, bid for contracts from commissioners of a kind which represent new modes of service provision. These new elements may include improved access, extended hours, multidisciplinary teams and an extended range of services in community settings. Our cases revealed instances where clinical leaders within CCGs (e. In these cases, leaders could deploy the allocated resources (managerial and financial) to deliver the plan. However, given the complexity of the NHS, matters were not always quite so simple. Our cases revealed numerous examples of leadership of service redesign where the challenges were more complicated. The CCG might itself support the status quo because unpicking the tangled web of payments, contracts and systems maintenance appeared too daunting and they saw themselves as having more pressing immediate priorities. Commissioning as a platform for clinical leadership The second question asked about the extent and nature of the scope for clinical leadership and engagement in service redesign that is possible and facilitated by commissioning bodies. This question places the focus on the enabling conditions. Nor did clinicians engage in any meaningful way with these bodies. Representatives from CCGs at HWBs tended to be accountable officers and/or chairpersons. Of more direct interest was the role of the CCGs themselves. The first of these was within the CCGs: how much influence were clinicians able to exercise? The second aspect was the power and influence of CCGs as institutions: what weight did they carry among the many other players in the landscape? There were a significant number of cases where managers acted as the most influential players. However, this was by no means a universal phenomenon. Our data point to cases where GPs exercised extensive influence over the strategic direction of the CCG as a whole and significant influence within specific service areas.

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Comparison and monoaminergic variables in schizophrenic patients treated of the effects of venlafaxine order prinivil 10 mg mastercard, desipramine cheap prinivil 10 mg with visa, and paroxetine on with sulpiride or chlorpromazine order prinivil 5 mg. Acta Psychiatr Scand Suppl noradrenaline- and methoxamine-evoked constriction of the 1984;311:49–74. Catecholamine metabolism: basic aspects and clinical quin and haloperidol on plasma homovanillic acid concentra- significance. Plasma catecholamine subtype 5-HT1D on basal and stimulated growth hormone se- metabolites in schizophrenics: evidence for the two-subtype cretion. Serotonin and the regulation of hypothalamic-pitui- 59. Long-term effects of neuroleptic drugs on the neu- tary-adrenal axis function. Serotonin receptor subtypes in depression: evidence chopharmacol 1998;18:305–310. Multiple fixed doses of 'Seroquel' col 1993;16:S6–S18. Neuroendocrine nia: a comparison with haloperidol and placebo: the Seroquel effects of buspirone: mediation by dopaminergic and serotoner- Trial 13 Study Group. A positron emission tomog- Buspirone: mechanisms and clinical aspects. San Diego: Academic raphy study of quetiapine in schizophrenia: a preliminary find- Press, 1991:177–192. Arch Gen Psychiatry 2000;57: sleep in humans: role of 5-HT2A and 5-HT2C receptors. Use of surrogate markers in clinical psychopharma- 82. Clinical perazine decreases slow-wave sleep in humans. Biol Psychiatry pharmacology in psychiatry: finding the right dose of psychotropic 1993;33:49–51. Serotonin1Areceptor activa- as tools for enhancing our understanding of 5-HT neurotrans- tion by flesinoxan in humans: body temperature and neuroen- mission. Neuroen- mine to plasma proteins and to brain tissue: relationship to CSF docrine responses to serotonergic agonists as indices of the func- tricyclic levels in man. Beta-adrenoceptor a preliminary comparative analysis of neuroendocrine endpoints blockers and the blood-brain barrier. Br J Clin Pharmacol 1981; versus other endpoint measures. The effects of intravenous binding and CSF concentrations of valproic acid in man follow- clomipramine on neurohormones in normal subjects. Effect of pindolol on the L-5-HTP- trations of the N-methyl-D-aspartate (NMDA) receptor antago- nist meantime in man. Effects of ritanserin on compared with regional cerebral blood flow measured by PET: the behavioural, neuroendocrine, and cardiovascular responses effects of linearization. J Cereb Blood FlowMetab 1988;8: to meta-chlorophenylpiperazine in healthy human subjects. The 5-HT3 antagonist BRL 46470 changes in regional brain glucose metabolism. Psychopharmacol does not attenuate m-chlorophenylpiperazine (mCPP)-induced Bull 1998;34:229–232. Effects of circuits during cue-elicited cocaine craving. Proc Natl Acad Sci the serotonin reuptake inhibitor fluvoxamine on yohimbine- USA 1996;93:12040–12045. Role of noradrenergic mechanisms in the etiology of 11–18. The current status of the dopamine hypothesis of the third generation of progress. The influence of receptor blockage of neuroleptic drugs in the living human psychotropic drugs and releasing hormones on anterior pituitary brain.

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Finally prinivil 2.5 mg low price, plate- function play a primary buy 5mg prinivil overnight delivery, etiologic role in the pathogenesis let 2-adrenoreceptor density (196) order prinivil 2.5mg on-line, platelet basal adeno- of anxiety disorders, or instead reflect secondary, compensa- sine, isoproterenol, forskolin-stimulated cyclic adenosine tory changes in response to disorders in other systems. Altered 2-adrenoreceptor sensi- subjective anxiety ratings increase in response to exposure tivity is evidenced by findings that administration of the to phobic stimuli (199). Subjects with social anxiety disor- 2-adrenoreceptor agonist, clonidine, results in greater hy- der show greater increases in plasma NE during orthostatic potension and larger reductions in plasma 3-methoxy-4- challenge than healthy subjects or those with PD (200). The hydroxyphenylethylene glycol (MHPG) in PD relative to growth hormone response to intravenous clonidine (a control subjects (178–181). In addition, administration of the -adrenoreceptor antagonist, yohimbine (which stimu- marker of central 2-adrenoreceptor function) is blunted 2 lates NE release by antagonizing presynaptic -adrenore- in social anxiety disorder (201), although the density of 2 ceptors) produces exaggerated anxiogenic and cardiovascu- lymphocyte -adrenoreceptors has not differed between so- lar responses and enhanced plasma MHPG and cortisol cial anxiety–disordered and control samples (202) (Table increases in PD relative to control subjects (133,172,173, 63. Finally, yohimbine administration resulted in Finally, Gerra et al. However, the Chapter 63: Neurobiological Basis of Anxiety Disorders 913 pretest baseline NE concentrations did not differ between Conversely, positive early-life experiences during critical the anxious and control subjects. For example, daily postnatal handling of Corticotropin-Releasing Hormone rat pups by human experimenters within the first few weeks of life has been shown to produce persistent (throughout Exposure to acute stress of various types results in release life) increases in the density of type II glucocorticoid recep- of CRH, ACTH, and cortisol. This increase was associated with enhanced feedback during acute stress can produce a transient elevation of the sensitivity to glucocorticoid exposure and reduced glucocor- plasma cortisol concentration and partial resistance to feed- ticoid-mediated hippocampal damage in later life (214, back inhibition of cortisol release that persists during and 215). These effects are hypothesized to comprise a type of shortly after the duration of the stressful stimulus. Taken ticoid receptors, because elevated glucocorticoid levels such together with the data reviewed in the preceding paragraph, as those elicited by acute stress decrease the number of hip- these data indicate that a high degree of plasticity exists in pocampal glucocorticoid receptors, with a resulting increase stress-responsive neural systems during the prenatal and in corticosterone secretion and feedback resistance (204). The During some types of chronic stress, adaptive changes feedback inhibition of CRH function by glucocorticoids (to in ACTH and corticosterone secretion occur such that the suppress HPA-axis activity) occurs at the level of the PVN plasma ACTH and corticosterone concentrations achieved of the hypothalamus, where systemically administered glu- are lower than those seen in response to acute stress (205). In contrast, other types of chronic stress are associated with cocorticoids reduce CRH expression, and the anterior pitui- enhanced corticosterone secretion in rats (206). Moreover, tary, where glucocorticoids decrease CRH receptor expres- Dallman and Jones showed that the experience of prior sion (217–220). The regulation of CRH receptor mRNA stress can result in augmented corticosterone responses to expression shows a regional specificity that becomes altered subsequent stress exposure (207). The factors that deter- when stress occurs concomitantly with elevated glucocorti- mine whether adaptation or sensitization of glucocorticoid coid concentrations. After both short-term and long-term activity occurs after chronic stress remain poorly under- corticosterone (CORT) administration, the CRH receptor stood. RNA expression decreases in the PVN and the anterior pi- Some stressors experienced within critical periods of neu- tuitary (219). However, after acute or repeated immobiliza- rodevelopment exert long-term effects on HPA-axis func- tion stress sufficient to produce a large increase in plasma tion. In rats exposed to either severe prenatal (in utero) stress CORT levels, the CRH mRNA expression decreases in the or early maternal deprivation stress (208,209), the plasma anterior pituitary, but increases in the PVN. In contrast, concentrations of corticosterone achieved in response to neither CORT administration nor restraint stress alters the subsequent stressors are increased, and this tendency to CRH receptor expression in the CE of the amygdala or the show exaggerated glucocorticoid responses to stress persists BNST. Furthermore, CRH secretion is not constrained by into adulthood. Early postnatal adverse experiences such as glucocorticoids in the CE or the lateral BNST, and CRH maternal separation are associated with long-lasting altera- mRNA expression increases in these areas during systemic tions in the basal concentrations of hypothalamic CRH CORT administration (217,218,220). It is thus conceivable mRNA, hippocampal glucocorticoid-receptor mRNA, me- that the positive feedback of glucocorticoids on extrahypo- dian eminence CRH, and in the magnitude of stress-in- thalamic CRH function in the amygdala or the BNST may duced CRH, corticosterone, and ACTH release (210–212). Adult monkeys who were raised in such involves functional differences between CRH-receptor a maternal environment are also hyperresponsive to yohim- subtypes. The CRH1 and CRH2 receptors appear to play bine and have elevated CRH concentrations and decreased reciprocal roles in mediating stress responsiveness and anxi- cortisol levels in the CSF, findings that parallel those in ety-like behaviors (221). Mice genetically deficient in humans with PTSD (213). CRH1-receptor expression exhibit diminished anxiety and 914 Neuropsychopharmacology: The Fifth Generation of Progress stress responses to threat or stress (222,223). In contrast, tion, cortisol suppression was found to be normal (234) or mice deficient in CRH2 receptors display heightened anxi- enhanced (228,235,236) in PTSD, with the latter result ety in response to stress (224,225).

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