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Suppes mania were randomized to olanzapine (n 15) or lithium and co-workers randomized 85 patients with DSM-IV crite- (n 15) for 4 weeks (7) 150 mg bupropion fast delivery depression symptoms for elderly. Olanzapine was administered as ria for schizoaffective or BD with treatment-refractory ill- a fixed dose of 10 mg per day and lithium at 400 mg BID ness to add-on clozapine or treatment as usual (94) cheap bupropion 150mg fast delivery depression johanniskraut test. Concomitant lorazepam 1 year, patients receiving clozapine displayed significant re- 4 to 12 mg per day was permitted throughout the 4-week ductions in measures of mania, psychosis, and global im- trial. There were no significant differences between the two provement compared with patients receiving treatment as treatment groups on any of the primary outcome mea- usual. In addition, total medication use decreased signifi- sures—the Mania Scale and BPRS total scores and the CGI cantly in the clozapine group. However, olanzapine-treated patients trial confirmed earlier reports suggesting that clozapine ex- displayed significantly greater improvement than lithium- erted long-term mood-stabilizing effects in patients with treated patients on the CGI severity scale at the end of 4 treatment-refractory BD (102). Olanzapine Maintenance Acute Mania There are no controlled trials of olanzapine in the mainte- nance treatment of BD published to date. In an open-label The efficacy of olanzapine in the treatment of acute bipolar 52-week extension trial following the initial placebo-con- mania has been established in three double-blind, controlled trolled acute mania study, none of the 98 patients who trials (7,98,99). In the first of two placebo-controlled stud- participated developed tardive dyskinesia during long-term ies, 139 inpatients with bipolar I disorder were randomized treatment (99). Olanzapine was begun at 10 mg per day and adjusted by 5-mg per day increments within a range of 5 Risperidone to 20 mg per day; the median modal dose was 15 mg per Acute Mania day. Concomitant lorazepam up to 4 mg per day was per- mitted for the first 7 days as needed for agitation; 2 mg per There are two double-blind randomized active comparator day was permitted for the subsequent 3days. The olanzap- studies of risperidone in the treatment of acute bipolar ine group displayed significant improvement on the YMRS, mania (84,86). In the first study, 45 inpatients were ran- CGI-BP severity of mania, and the PANSS total and posi- domized to risperidone 6 mg per day (n 15), haloperidol tive symptom scores compared with the placebo group. Patients receiving placebo exhibited significantly for up to 4 weeks (86). There were no significant differences greater improvement in YMRS total scores compared with among the three treatment groups in reductions on the patients receiving gabapentin. YMRS, BPRS, CGI, and GAF from baseline to endpoint In the second controlled trial, 28 patients with bipolar (LOCF). In the second trial, 158 inpatients receiving lith- I(n 13) or bipolar II (n 15) disorder received 6-week ium or VPA were randomized to adjunctive therapy with crossover trials of gabapentin, lamotrigine, or placebo (29) risperidone 1 to 6 mg per day (n 52), haloperidol (n The reduction in manic symptoms as measured by the CGI- 53), or placebo (n 51) for up to 3weeks (84). Patients BP was not significantly different among the three treat- receiving risperidone or haloperidol displayed significantly ments. However, manic symptoms were quite low at base- greater improvement at 1 week, 2 weeks, and at endpoint line, raising the possibility that meaningful differences (LOCF), but not at 3weeks of treatment on the YMRS among the three groups might not have been detected. There were no motrigine was also compared with lithium in a 4-week dou- significant differences between the risperidone and placebo ble-blind, randomized trial in 30 inpatients with bipolar I groups from baseline to endpoint in BPRS and HamD total disorder (39). There are no controlled trials of risperidone in the lamotrigine 25 mg per day for the first week, 50 mg per maintenance treatment of patients with BD. At the conclusion of the study, both agents produced significant reductions in mean Mania Rat- Ziprasidone ing Scale, BPRS, and CGI total scores from baseline to Acute Mania endpoint. There were no significant differences between the two treatment groups. The small sample size, low lithium Ziprasidone has been studied in placebo-controlled trials dose, use of as needed lorazepam throughout the trial, and in the treatment of acute mania in patients with BD and absence of a placebo control group limit the results of this schizoaffective disorder, bipolar type (42,47). In this study, bipolar I produced significant reductions on the Manic Rating Scale (n 130) and bipolar II (n 52) patients who were (MRS) total score (from the SADS-C) at day two and stabilized on initial open-label lamotrigine monotherapy throughout the remainder of the trial compared with pla- were randomized to lamotrigine or placebo in a 26-week cebo. Based on a 50% reduction in MRS total scores, prevention trial. There were no significant differences be- significantly more ziprasidone-treated patients responded tween the lamotrigine and placebo groups in time to drop (50%) compared with placebo-treated patients (36%). This out for any reason and time to need for additional medica- study confirmed the findings of an earlier study that found tion among bipolar I patients.

How- It was found generic bupropion 150mg on line mood disorder 6 game, using a double-blind crossover technique buy bupropion 150 mg with mastercard depression symptoms vertigo, that ever, reading speed and numbers of words written in a timed 608 Neuropsychopharmacology: The Fifth Generation of Progress period were significantly enhanced in subjects treated with analysis and increasing attentional resources among dyslexic piracetam as compared with placebo. Effective reading and children when the stimuli are recognized as having linguistic writing ability, taking both rate and accuracy into considera- significance (96). These effects were shown to be dose re- tion, were also significantly improved in the piracetam lated in a subsequent study (97). One negative study examined the interaction of pirace- Two hundred twenty-five dyslexic children between the tam and tutoring (98). Sixty children with dyslexia (41 boys, ages of 7 years 6 months and 12 years 11 months whose 19 girls; ages 9 to 13 years) were enrolled in a 10-week reading skills were significantly below their intellectual ca- summer tutoring program that emphasized word-building pacity were enrolled in a multicenter, 36-week, double- skills. They were randomly and blindly assigned to receive blind, placebo-controlled study. Piracetam-treated children either placebo or piracetam. The children were subtyped as showed significant improvements in reading ability (Gray 'dysphonetic' or 'phonetic' on the basis of scores from Oral Reading Test) and reading comprehension (Gilmore tests of phonologic sensitivity and phoneme-grapheme cor- Oral Reading Test). Treatment effects were evident after respondence skills. Of the 53 children who completed the 12 weeks and were sustained for the total period (36 weeks) program, 37 were classified as dysphonetic and 16 as pho- (94). The phonetic group improved significantly more in The neurophysiologic mechanisms involved in the effects word-recognition ability than the dysphonetic group. Over- of piracetam were examined in studies using event-related all, the children taking medication did not improve more potentials. Eight- to 12-year-old dyslexic boys were ran- than the nonmedicated children in any aspect of reading. Chil- netic subgroup gained most in word recognition. Event-related potentials to letters and shapes, for active and SUMMARY AND CONCLUSIONS passive responses, were recorded at the vertex and left and right parietal areas of the scalp. Performance measures in- Significant difficulties continue to bedevil the definition of cluded letter and form hits, misses, commission errors, and LD, including problems surrounding various criteria such reaction times. Piracetam increased the amplitude of a late as an IQ/learning discrepancy or low absolute achievement positive component (believed to correspond to P300) at the level. Approaches that define the disorder by resistance to vertex for letter hits. Piracetam also increased the latency high-quality instruction may be the most valid for purposes of this component in both hemispheres, but only for active of identifying persons with LDs in genetic, neuroimaging, responses (letter hits) in the left hemisphere and passive and pharmacologic studies. The high degree of comorbidity responses (correct rejections and misses) in the right hemi- with many psychiatric disorders raises further issues for sphere. Reaction time to letter hits was significantly corre- studies requiring a homogeneous symptom pattern, and it lated with the latency of the P300 component, a finding seems likely that further advances will require replacing suggesting that letters created increased effort or attentional broad clinical patterns with more specific processing deficits demand on the subjects compared with forms. Despite these limitations, event-related potential component (P225) also showed in- existing research is encouraging regarding the possibility of creased amplitude to piracetam in both hemispheres, and precise genetic and neuroanatomic localization of LDs, par- effects were limited to form hits. Again, however, subtyping issues at the possibly to reflect slow negative potentials arising from stim- phenotypic level require elucidation before further progress ulus anticipation in the CNV-like paradigm. Evidence generally supports the finding that psy- In a subsequent study, 29 dyslexic children (aged 7 to chostimulants (e. Event-related potentials were obtained at the mance but less impact on long-term academic gains. Work end of treatment from a vigilance paradigm that required with nootropic drugs shows intriguing effects on verbal a response to letter or form matches. The drug group learning, single-word reading, and left-hemisphere process- showed a significant advantage in letter hits compared with ing of alphabetic stimuli. Good controlled trials indicate placebo and a reduced variance in reaction time. The drug that piracetam may be a safe and effective enhancer of read- increased the amplitude of three factors from a principal ing in school-aged children, with gains double the rate ex- components analysis of event-related potentials and was in- pected in seriously impaired readers. LD remains a large terpreted as increasing a processing negativity when stimuli public health problem, is significantly undertreated, has were letters. Piracetam was interpreted as enhancing feature devastating lifetime outcomes, and therefore merits greater Chapter 44: Learning Disorders 609 research efforts to understand its neurobiology and treat- 20. Learning disabilities: implications for psychiatric treatment, vol 19.

N eum ann H PH generic bupropion 150 mg without a prescription mood disorder ottawa, Zbar B: Renal cysts purchase 150 mg bupropion amex depression symptoms young adults, renal cancer and von H ippel- 19. Schievink W I, Torres VE, W iebers DO, Huston J III: Intracranial arterial Lindau disease. Schievink W I, H uston J III, Torres VA, M arsh W R: Intracranial cysts in autosom al dom inant polycystic kidney disease. Gagnadoux M F, Broyer M : Polycystic kidney disease in children. Edited by Davison AM , Cam eron JS, Grünfeld JP, et al. Gabow PA: Autosom al dom inant polycystic kidney disease— m ore 1998:2385–2393. Schievink W I, Torres VE: Spinal m eningeal diverticula in autosom al som al recessive polycystic kidney disease (ARPKD) to chrom osom e dom inant polycystic kidney disease. J Am Soc N ephrol 1997, nile nephronophthisis (recessive m edullary cystic kidney disease) m aps 8:373A. Adv N ephrol 1997, SH 3 dom ain protein is m utated in nephronophthisis type 1. O xford: O xford University Press; the 2q13 region are a m ajor cause of juvenile nephronophthisis. Pirson Y, Chauveau D: Intracranial aneurysm s in autosom al dom inant 44. Edited by I: An unusual cause of hereditary cystic kidney disease. O xford:O xford University Press; Transplant 1997, 12:1247–1250. Feather SA, W inyard PJD, Dodd S, W oolf AS: O ral-facial-digital syn- 28. Pirson Y, Christophe JL, Goffin E: O utcom e of renal replacem ent therapy in autosom al dom inant polycystic kidney diseases. Scheinman variety of m etabolic conditions produce disease of the renal interstitium and tubular epithelium. In m any cases, disease Areflects the unique functional features of the nephron, in which the ionic com position, pH , and concentration of both the tubular and interstitial fluid range widely beyond the narrow con- fines seen in other tissues. Recent genetic discoveries have offered new insights into the m olecular basis of som e of these conditions, and have raised new questions. This chapter discusses nephrocalcinosis, the relatively nonspecific result of a variety of hypercalcem ic and hypercalciuric states, as well as the renal consequences of hyperox- aluria, hypokalem ia, and hyperuricem ia. In the parathyroid gland the calcium-sensing recep- tor allows the cell to sense extracellular levels of calcium and transduce that signal to regu- late parathyroid hormone production and release. In the nephron, expression of the calcium receptor can be detected on the api- cal surface of cells of the papillary collecting Hypercalcemia duct, where calcium inhibits antidiuretic inhibits reabsorption hormone action. Thus, hypercalcemia impairs of NaCl, Ca, and M g urinary concentration and leads to isotonic polyuria. The most intense expression of the calcium receptor is in the thick ascending limb of the loop of Henle, particularly the cortical portion, where the calcium receptor protein is located on the basolateral side of the cells; this explains the known effects of hypercalcemia in inhibiting reabsorption of calcium, magnesium, and sodium chloride in the thick ascending limb. In addition, Hypercalcemia inhibits hypercalcemia causes hypercalciuria through reabsorption an increased filtered calcium load and of water suppression of parathyroid hormone release with a consequent reduction in calcium reabsorption. Ca— calcium; M g— magne- sium; NaCl— sodium chloride. FIGURE 11-2 RENAL EFFECTS OF CALCIUM H ypercalcem ia leads to renal vasoconstriction and a reduction in the glom erular filtration rate. H owever, no expression of the calci- um -sensing receptor has been reported so far in renal vascular or Hypercalcemia glom erular tissue. Calcium receptor expression is present in the Collecting duct proxim al convoluted tubule, on the basolateral side of cells of the distal convoluted tubule, and on the basolateral side of m acula Resistance to vasopressin, leading to isotonic polyuria densa cells. Functional correlates of calcium receptor expression Thick ascending limb of the loop of Henle at these sites are not yet clear. Impaired sodium chloride reabsorption, leading to modest salt wasting H ypercalciuria leads to m icroscopic hem aturia and, in fact, is Inhibition of calcium transport, leading to hypercalciuria the m ost com m on cause of m icroscopic hem aturia in children.

It may be speculated that such of antidepressant-induced receptor activation (which may phosphorylation causes cytoskeletal changes that result in a occur quickly); rather bupropion 150mg without prescription anxiety young children, it results when such receptor activa- modification of neurotransmission and antidepressant- tion alters signaling pathways to cause more slowly develop- induced changes in gene expression (see below) 150mg bupropion overnight delivery anxiety 7 months pregnant, as PKA ing changes in gene expression. Two major areas have been translocation to the nucleus is microtubule-dependent studied. One deals with effects of antidepressants on second (290). Antidepressant-induced activation of PKA is interest- messenger-regulated protein kinases in brain. The other ing in light of findings of decreased PKA activity in cultured deals with changes in activities of protein kinases that result fibroblasts of melancholic patients with major depression in changes in gene expression and perhaps even neurogene- (291), perhaps a consequence of reduced binding of cAMP sis. Given the estab- lished facilitative function of CaMKII on neurotransmitter Protein Kinases release (293), the effect of long-term antidepressant treat- Phosphorylation of proteins may well be the primary regula- ment on CMKII, with increased phosphorylation of sub- tory mechanism for intracellular events. Such phosphoryla- strates such as synapsin 1 and synaptotagmin, may underlie Chapter 79: Mechanism of Action of Antidepressants and Mood Stabilizers 1155 the facilitation of monoamine transmitter release produced increase in BDNF can oppose and perhaps overcome the by these drugs. Indeed, long-term anti- depressant treatment has been shown recently to increase neurogenesis of dentate gyrus granule cells (312). Gene Expression/Neuroplasticity Although the precise mechanism is not understood, long- term but not acute treatment with antidepressants has ef- CONCLUSION fects on the expression of specific genes that may be a conse- quence of the activation of protein kinases, particularly Our understanding of the mechanism of action of drugs PKA. It is known, for example, that PKA can phosphorylate that treat mood disorders such as depression and manic- the transcription factor CREB. CREB binds to specific pro- depressive illness derives for the most part from their inter- moter sites (cAMP response elements) to produce changes action with known signaling systems within the brain. It is in the expression of specific genes, such as those for brain- evident that intracellular effects initiated by antidepressant derived neurotrophic factor (BDNF) and its receptor, trkB. Al- of antidepressants increases the mRNA for CREB in addi- though much more research is needed to test this hypothesis tion to CREB protein in brain (294; see 221,295). More and establish whether and how such long-term changes are recently, it was shown that such treatments increase CREB of physiologic significance, current evidence suggests that expression and CREB phosphorylation, indicative of func- such changes in brain may be quite important for the now tional activation of CREB (296). Furthermore, long-term well-established prophylactic effects of mood stabilizers and antidepressant treatment increases BDNF and trkB expres- antidepressants in the treatment of recurrent mood disor- sion in hippocampus (294,297). Finally, exogenous BDNF has that use gene expression arrays, we have the opportunity been shown to have antidepressant-like activity in behav- to examine multiple targets in the brain, both known and ioral tests sensitive to antidepressant treatment (301). Within this chapter, Such results are viewed as evidence that long-term antide- we have tried to identify the most promising of the candi- pressant treatment causes sustained activation of the cAMP date targets of mood stabilizers and antidepressants. The noradren- ever, research to determine which current and future targets ergic and serotoninergic receptors producing increases in constitute a profile that is most relevant to the therapeutic cAMP are -adrenoceptors and 5-HT4, 5-HT6, and 5-HT7 action of these agents will continue to be hampered by a receptors. If such intracellular effects are responsible for clin- lackof animal models for these complex behavioral disor- ical improvement, then these receptors may be the impor- ders that have strong construct and predictive validity. The hypothesis which new mood stabilizers can be discovered has proved is fundamentally different from earlier views of antidepres- more challenging. We suggest that the creation of models sant action, in which depression was a problem of synaptic with both construct and predictive validity to permit the transmission and drugs acted within the synapse to improve discovery of novel targets directly related to therapeutic effi- behavior directly (301,302). The new view is more morpho- cacy will be significantly enhanced by the identification of logic in nature. It posits that depression may be caused by susceptibility and protective genes for these illnesses. It is well established that such atrophy occurs (303,304). Further, more recent REFERENCES data indicate a decrease in hippocampal volume in some 1. In: Nemeroff CB, Schatzberg depressive patients (305–307), although this need not indi- AF, eds. American Psychiatric Association textbook of psychophar- cate a loss of neurons. However, postmortem studies have macology, second ed. Washington DC: American Psychiatric revealed a loss of glia and neurons in the cortex of depressed Association, 1998:303–349. New York: the differentiation and growth of neurons in the developing McGraw-Hill, 1996:461–486.