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MRI white matter Arch Gen Psychiatry 1998;55:145–152 500mg naproxen visa arthritis in feet remedies. Compromised white Chapter 55: Structural MRI Studies in Schizophrenia 771 matter tract integrity in schizophrenia inferred from diffusion thalamus in never-medicated patients with schizophrenia purchase naproxen 250 mg online arthritis treatment mexico. Image processing for Buchsbaum MS purchase 500 mg naproxen with amex arthritis in neck spinal cord, Yang S, Hazlett E, et al. Ventricular volume and diffusion tensor magnetic resonance imaging. In: Proceedings of asymmetry in schizotypal personality disorder and schizophrenia Second International Conference on Medical Image Computing and assessed with magnetic resonance imaging. Schizophr Res 1997; Computer-Assisted Interventions, Cambridge, UK: 1999:441–452. Uncinate fasciculus Casanova MF, Zito M, Goldberg T, et al. Shape distortion of the in schizophrenia: a diffusion tensor study. American Psychiatric corpus callosum of monozygotic twins discordant for schizophre- Association New Research Abstracts, 2000. Increase in caudate nuclei volumes of first-episode schizophrenic patients taking anti- Table 55. Caudate nuclei volumes Andreasen NC, Ehrhardt JC, Swayze II VW, et al. Magnetic reso- in schizophrenic patients treated with typical antipsychotics or nance imaging of the brain in schizophrenia: the pathophysiologic clozapine. Arch Gen Psychiatry 1990; Colombo C, Abbruzzese M, Livian S, et al. Psychiatry Res Neu- Andreasen NC, Arndt S, Swayze II VW, et al. Regional brain abnor- Psychiatry Clin Neurosci 1994;243:244–248. Reduction in temporal lobe J Psychiatry 1990;147:1457–1462. Volumes of ventricular system pared to normal controls. MRI findings in the medial episode schizophrenic patients. Arch Gen Psychiatry 1992a;49: temporal lobe structures in schizophrenia. Increased prevalence of the Becker T, Elmer K, Schneider F, et al. Confirmation of reduced cavum septum pellucidum in magnetic resonance scans and post- temporal limbic structure volume on magnetic resonance imaging mortem brains of schizophrenic patients. Psychiatry Res: Neuroim- in male patients with schizophrenia. Abnormalities of the septum Bilder RM, Wu H, Bogerts B, et al. Absence of regional hemispheric pellucidum on MR scans in first-episode schizophrenic patients. Am J Psychiatry Am J Neuroradiology 1992c;13:835–840. Magnetic reso- DeLisi LE, Hoff AL, Schwartz JE, et al. Brain morphology in first- nance imaging in schizophrenia: Altered brain morphology associ- episode schizophrenic-like psychotic patients: a quantitative mag- ated with P300 abnormalities and eye tracking dysfunction. The timing of brain morpho- Bogerts B, Ashtari M, Degreef G, et al. Reduced temporal limbic logical changes in schizophrenia and their relationship to clinical structure volumes on magnetic resonance images in first episode outcome. Increased prevalence of cavum Bogerts B, Lieberman JA, Ashtari M, et al. Psychiatry Res: Neuroimag volumes and psychopathology in chronic schizophrenia. Asymmetries in the superior Bornstein RA, Schwarzkopf SB, Olson SC, et al. Third-ventricle en- temporal lobe in male and female first-episode schizophrenic pa- largement and neuropsychological deficit in schizophrenia. Biol tients: measures of the planum temporale and superior temporal Psychiatry 1992;31:954–961.

Analysis of responses by 150 Estimates of the incidence of treatment resistance have var- schizophrenia patients to a 'Drug Attitude Inventory' re- ied with changes in the diagnostic classification of schizo- vealed that discount naproxen 250mg online arthritis what is it, based on responses to 10 items cheap naproxen 500mg mastercard arthritis meaning, 89% of patients phrenia and definitions of treatment response (149) cheap naproxen 500 mg visa arthritis medication nsaid, which could be correctly assigned to compliant versus non- have tended to obscure potential improvements in outcome compliant categories as determined by clinician assessment associated with advances in pharmacologic and psychosocial of compliance (140). For example, Hegarty and colleagues (150) re- was a positive experience with medication—this factor ac- viewed results of 320 clinical trials and found that, since the counted for 60% of the total variance, whereas the factor introduction of modern antipsychotics in the mid-twentieth representing a negative subjective experience accounted for century, about 50% of patients were improved at follow- 12%. Factors representing attitudes and beliefs about medi- up, whereas the rate of improvement dropped to 35% in cation had minimal predictive power. Rates of response have tended to be higher in first- Whereas many clinicians expect atypical agents to achieve episode psychosis, although dropout rates have been high higher levels of compliance by virtue of reduced or absent in this population, particularly with conventional agents EPS, this view may seriously underestimate the impact of (102,107). Persistence of psychotic symptoms is more com- other side effects. Two studies have found that clinicians mon in drug trials involving chronic patients, presumably tend to misjudge the relative distress produced by different reflecting progression of the illness as well as a possible selec- medication side effects (142,143). Side effects associated tion bias favoring participation by more refractory patients. The advan- or failure to achieve premorbid levels of functioning, treat- tage of atypical agents in terms of compliance may stem ment resistance can be considered the rule rather than the less from their reduced EPS and more from their improved exception. Whether targeting cognitive deficits and impairment in in- Psychotic Symptoms sight will improve compliance remains to be seen. Antipsychotic Monotherapy Response of psychotic symptoms to conventional antipsy- Psychosocial Interventions chotics, risperidone, and olanzapine has been associated Most approaches to noncompliance involve psychoeduca- with D2 receptor occupancy in excess of 65% (18,57), al- tion, supervision, and supportive therapy in which the bene- though persistence of psychotic symptoms has been shown fits of treatment are emphasized, whereas barriers to adher- to occur despite adequate D2 blockade in a subgroup of ence and medication side effects are minimized (145). As noted, only clozapine has con- Family therapy and social skills training may also exert a sistently demonstrated efficacy for psychotic symptoms in positive impact on compliance. Cognitive behavioral ap- treatment of refractory patients; the mechanism responsible proaches have recently been applied to noncompliance by for this therapeutic advantage remains uncertain. In a sam- Kemp and colleagues (146,147), who developed 'compli- ple of 268 patients prospectively established to be neurolep- ance therapy,' a four- to six-session intervention based on tic resistant, 30% in the clozapine group met criteria for motivational interviewing techniques that targets attitudes response at 6 weeks compared to 7% treated with chlorpro- towards medication and discharge planning during acute mazine (11). Response rates as high as 60% have been re- Chapter 56: Therapeutics of Schizophrenia 785 ported after 6 months in open trials with clozapine in pa- therapy as an intervention for neuroleptic-resistant patients; tients less rigorously defined as treatment refractory (152). Given the risk mine efficacy of clozapine and other atypical agents is the of agranulocytosis, the burden of side effects, and the re- subject of debate (153,154). Marder and colleagues (155) found that priate first choice among these agents is unclear; two con- schizophrenia patients presumed to be treatment-resistant trolled studies that compared olanzapine and risperidone on the basis of having been hospitalized for 6 months or have produced divergent results, probably reflecting differ- longer at the time of study entry did not respond to haloper- ences in dosing of the two agents and the use of intent-to- idol 20 mg per day but significantly improved with risperi- treat versus completer analyses (63,163). The focus of this done 6 mg per day or 16 mg per day compared to placebo. Many clinicians response of psychotic symptoms to olanzapine (mean dose express the impression that certain patients do respond pref- 11 mg per day) than haloperidol (mean dose 10 mg per erentially to a single agent of this class. Sequential controlled day); this difference was significant in the intent-to-treat trials of the newer agents in treatment-resistant patients will analysis but not in a comparison of completers (76). In 67 schizophrenia patients with his- The practice of combination therapy is gaining widespread tories of neuroleptic resistance, risperidone 6 mg per day popularity in the absence of controlled data in its support significantly improved total BPRS scores compared to halo- (164). In part based on empirical experience and the dem- peridol 15 mg per day at 4 weeks, but response did not differ onstration that clozapine at optimal doses achieves relatively between groups at 8 weeks (156). In contrast, risperidone low degrees of D2 occupancy, European clinicians com- produced significantly higher response rates than haloperi- monly add low-doses of neuroleptics to clozapine in par- dol in a large, randomized open trial involving 184 schizo- tially responsive patients (165). Uncontrolled trials and case phrenia patients with a history of poor response (157). Rela- reports have described benefits associated with the addition tive response of psychotic symptoms to risperidone of risperidone (4 mg per day) (159,166) and pimozide (167) increased over time and reached a maximum improvement to clozapine in partially responsive patients. In a small, pla- compared to haloperidol at the final 12-month assessment. The same group cians perceive improved response during the cross-tapering reported that 41% of 44 patients identified as unresponsive phase of switching from one to the other. A theoretical to olanzapine in the preceding study or in an open trial rationale for this combination is less apparent, given that subsequently exhibited a response to clozapine (158). In each agent produces maximal D2 and 5-HT2 occupancy addition, open trials in which patients have been switched when appropriately dosed (57). If combined treatment with from clozapine to olanzapine or risperidone have reported olanzapine and risperidone is found in suitably controlled a high incidence of clinical deterioration, casting doubt on study designs to offer advantages over optimal monotherapy claims for therapeutic equivalence between clozapine and with either agent, such a finding would argue in favor of the second-generation agents, at least at the doses tested the existence of additional contributory receptor actions (159,160). Of interest, two controlled trials have found unique to each drug. How- ever, in one 4-week trial, the 59 participants were not Adjunctive Treatments screened for treatment resistance at baseline and, despite A diverse range of adjunctive treatments has been proposed equivalence in outcomes between groups using an LOCF for antipsychotic-resistant schizophrenia, although thera- analysis, 25% of the risperidone group dropped out owing peutic effects generally have been small or inconsistent in to lack of efficacy compared to only 5% in the clozapine controlled trials. Very little data are available from con- group (161). Lithium augmentation frequently has been cited as 786 Neuropsychopharmacology: The Fifth Generation of Progress the best-established intervention based on positive results unresponsive to ECT and a diagnosis of schizoaffective dis- from three small studies (170–172); however, two recent order did not predict a favorable response (192–195). Cases placebo-controlled studies found no benefit when well-char- describing the successful combination of ECT with cloza- acterized neuroleptic-resistant patients were treated with pine in refractory patients have also been reported, suggest- lithium (approximately 1. Recently, interest has fo- lithium may enhance response of some patients, particularly cused on the potential use of transcranial magnetic stimula- in the presence of affective symptoms or excitement (175, tion (TMS) as an alternative to ECT in schizophrenia.

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Interestingly buy 250 mg naproxen amex treating arthritis in dogs with aspirin, growth factors that facilitate branch- branching tubulogenesis cheap 250mg naproxen with mastercard arthritis in feet diagnosis. A large variety of growth factors have ing tubulogenesis in vitro also enhance the recovery of injured been tested for their ability either to m ediate ureteric branching renal tubules generic naproxen 250 mg with visa arthritis in back of hand. Nigam SK, Denisenko N, Rodriguez-Boulan E, Citi S: The role of phos- kidney to ischem ia: Assessm ent of adenine nucleotide and catabolite phorylation in development of tight junctions in cultured renal epithelial profiles. N igam SK, Rodriguez-Boulan E, Silver RB: Changes in intracellular 304:93–108. Toback FG: Regeneration after acute tubular necrosis. Kidney Int Proc N atl Acad Sci USA 1992, 89:6162–6166. Liu S, Humes HD: Cellular and molecular aspects of renal repair in calcium in tight junction biogenesis. Doctor RB, Bennett V, M andel LJ: Degradation of spectrin and ankyrin 16. Stuart RO , N igam SK: Regulated assem bly of tight junctions by pro- in the ischemic rat kidney. Doctor RB, Bacallao R, M andel LJ: M ethod for recovering ATP con- 17. Stuart RO , Sun A, Bush KT, N igam SK: Dependence of epithelial tent and m itochondrial function after chem ical anoxia in renal cell intercellular junction biogenesis on thapsigargin-sensitive intracellular cultures. Edelstein CL, Ling H , Schrier RW : The nature of renal cell injury. Denker BM , Saha C, Khawaja S, N igam SK: Involvem ent of a het- Kidney Int 1997, 51:1341–1351. Fish EM , M olitoris BA: Alterations in epithelial polarity and the Chem 1996, 271:25750–25753. Denker BM , N igam SK: M olecular structure and assem bly of the tight 9. M andel LJ, Bacallao R, Zam pighi G: Uncoupling of the m olecular junction. Gething M -J, Sam brook J: Protein folding in the cell. Goligorsky M S, Lieberthal W , Racusen L, Sim on EE: Integrin recep- tors in renal tubular epithelium : N ew insights into pathophysiology of 21. Kuznetsov G, Bush KT, Zhang PL, N igam SK: Perturbations in m atu- Invest 1989, 84:1757–1761. Tsukam oto T, N igam SK: Tight junction proteins becom e insoluble, factors on renal proximal tubule cells. M iller SB, M artin DR, Kissane J, H am m erm an M R: Insulin-like m odel for reversible junction disassem bly. J Biol Chem 1997, growth factor I accelerates recovery from ischem ic acute tubular 272:16133–16139. Border W , N oble N : Transform ing growth factor beta in tissue fibro- 47. Kawaida K, M atsum oto K, Shim azu H , N akam ura T: H epatocyte where the level of tyrosine phosphorylation is elevated. J Cell Biol growth factor prevents acute renal failure and accelerates renal regen- 1991, 113:867–879. Citi S: Protein kinase inhibitors prevent junction dissociation induced 26. M iller S, M artin D, Kissane J, H am m erm an M : H epatocyte growth by low extracellular calcium in M DCK epithelial cells. J Cell Biol factor accelerates recovery from acute ischem ic renal injury in rats. M iller S, M artin D, Kissane J, H am m erm an M : Rat m odels for clini- catenin: The tyrosine kinase substrate pl20cas associates with E-cad- cal use of insulin-like growth factor I in acute renal failure. J Cell Biol 1994, lar obstruction: Therapeutic role of synthetic RGD peptides in acute 125:583–594. Franklin S, M oulton M , H am m erm an M R, M iller SB: Sustained 52. Citi S, Denisenko N : Phosphorylation of the tight junction protein im provem ent of renal function and am elioration of sym ptom s in cingulin and the effects of protein kinase inhibitors and activators in patients with chronic renal failure (CRF) treated with insulin-like M DCK epithelial cells. N ilsson M , Fagm an H , Ericson LE: Ca2+-dependent and Ca2+-inde- 31. Farquhar M , Palade GE: Junctional com plexes in various epithelia. J pendent regulation of the thyroid epithelial junction com plex by pro- Cell Biol 1963, 17:375–412. Anderson JM , Itallie CM V: Tight junctions and the m olecular basis 54.

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This increase in coupling persisted for at least 28 days following amphetamine withdrawal buy discount naproxen 500 mg on-line arthritis in lower back how to treat, but was not present if the rats were tested during the treatment phase 500 mg naproxen for sale does arthritis in dogs come on suddenly. These data suggested that dopamine depresses excitation (89) buy cheap naproxen 500mg working with arthritis in back. Specifically, D1-receptor stimulation en- the excitatory postsynaptic conductance (EPSC) by causing hances NMDA-mediated currents (90), which may occur an NMDA receptor-dependent increase in extracellular via a combination of two effects: (a) a facilitation of L-type adenosine, which acts presynaptically to depress glutamate calcium conductances on dendrites (90), and (b) activation release (104). The D1–NMDA-R interaction appears to be of cAMP-PKA cascade (91). A similar D1-mediated cascade postsynaptic and acts via PKC activation (105). It is of also attenuates responses to GABA in the striatum (92,93). Thus, a recent study by ate non–NMDA-mediated responses (89). There is also evi- Gines and colleagues (106) have shown that D1 and adeno-´ dence that the activation of DA neuron firing by stimulation sine A1 receptors have the capacity to form heteromeric of DA axons (70,94) occurs via a D1-mediated facilitation complexes, which appear to play a role in receptor desensiti- of glutamate transmission (94). This suggests that, within the striatal complex, with glutamate contributing to under physiologic conditions, D1-induced facilitation of DA release and DA causing a two-pronged inhibition of glutamate transmission in the striatum is mediated by burst- glutamate release, both directly via D2 presynaptic receptors firing–dependent phasic DA release (44). Finally, In addition to its ability to modulate neurotransmitter glutamate-released NO also appears to play a significant actions on postsynaptic neurons in the striatum, DA also role in modulating DA systems and striatal neuron respon- plays a significant modulatory role in the presynaptic regula- sivity. The tight interdependence and coregulation between tion of neurotransmitter release. D2 stimulation is reported DA and glutamate suggest that the system is designed to to presynaptically decrease GABA release from intrinsic maintain stable levels of transmission to the striatal neurons neurons (95) and glutamate release from corticostriatal ter- over the long term, whereas short-term changes in activity minals. Several studies report that D2 agonists cause a in either system in response to a signal are amplified by down-regulation of glutamate-mediated EPSPs on neurons their coordinated effects on each of these interdependent in the nucleus accumbens (96–99). Specifically, DA was presumed to be the glutamatergic corticostriatal afferents. In cases in which striatal excitatory acute depletion of endogenous DA, all corticoaccumbens amino acid afferents arising from the cortex are stimulated EPSPs are sensitive to DA (99). This suggests that under with high frequencies in the absence of magnesium (to en- normal circumstances, the presynaptic DA receptors may hance NMDA conductances), a long-term facilitation in already be saturated with DA, as suggested by the observa- synaptic transmission is induced, known as long-term po- tion that sulpiride increase EPSP amplitude in a majority tentiation. In contrast, if the stimulation is carried out at a of cases when administered alone (99). This unusual phar- low frequency, the opposite type of plasticity is induced; macology may reflect a contribution of presynaptic D4 re- that is, long-term depression (LTD) (107). These forms of ceptors on the corticoaccumbens terminals to this response synaptic plasticity have been proposed to play a major role (102). Although another group has reported a D1-mediated in learning and memory formation in other structures, such presynaptic action EPSPs evoked by intrastriatal stimulation as the hippocampus. Such plasticity within the striatum in slices, which was interpreted as a presynaptic effect on may be involved in such phenomena as the acquisition of corticostriatal terminals (103), this study employed exceed- complex motor skills. Repetitive stimulation of corticostria- ingly high doses of the D1 agonist to achieve these effects tal fibers to release glutamate is required for the induction (i. Moreover, anatomic studies have shown that D1 im- pretreatment prevents the induction of LTD (107), suggest- munoreactive axons are exceedingly rare in the striatum ing that a synergistic interaction between these receptor sub- (77). In contrast, recent studies suggest that DA acting on types is required for this process to occur. In contrast, corti- postsynaptic D1 receptors may actually cause a transsynap- cal stimulation-induced LTP is blocked selectively by D1 tic feed-forward inhibition of glutamate release. Both antagonists, but is actually enhanced by D2 antagonists or NMDA antagonists and adenosine antagonists can block in D2 receptor knockout mice (109). Thus, although studies done in vivo have consistently shown that direct DA application inhibits PFC neuron fir- ing, studies using in vitro slice preparations have found a DA-mediated increase (110,111) and a decrease (112,113) in neuronal excitability in this region. D1 stimulation has been shown to affect sodium conductances by increasing the sodium plateau potential and shifting the activation of sodium currents to more negative potentials (114). This increase in excitability was augmented by a D1-induced decrease in slow potassium conductances (110). D1 stimula- tion may also activate L-type calcium conductances located in proximal dendrites of pyramidal neurons to further in- crease excitability in these neurons (66). Such an interaction has been postulated to differentially modulate afferent input to these neurons (Fig. Indeed, the highly organized DAergic input onto virtually every dendrite of PFC pyrami- dal neurons in the primate provides a means for this neuro- transmitter to regulate nearly the entire complement of glu- tamatergic afferents to this cell type (115). In contrast, at least part of the inhibitory action of DA on PFC pyramidal neurons may occur by DA-induced excitation of GABAer- FIGURE 9. A simplified diagram illustrating the basic process- ing units within the prefrontal cortex.