NOTES 3514 Kapur, S. and Seeman, P. “Does fast dissociation from the dopamine D 2 receptorexplain the action of atypical antipsychotics? A new hypothesis,” American Journal of<strong>Psychiatry</strong>, 158:360–9, 2001.5 Kinon, B.J. and Lieberman, J.A., “Mechanisms of action of atypical antipsychoticdrugs: A critical analysis,” Psychopharmacology, 124:2–34, 1996; Sartorius, “Theusefulness of the second-generation antipsychotic medications.”6 For reviews of research on the dopamine hypothesis of schizophrenia see Meltzer,H.Y. and Stahl, S.M., “The dopamine hypothesis of schizophrenia: A review,”<strong>Schizophrenia</strong> Bulletin, 2:19–76, 1976; Haracz, J.L., “The dopamine hypothesis: Anoverview of studies with schizophrenic patients,” <strong>Schizophrenia</strong> Bulletin, 8:438–69,1982; <strong>And</strong>reasen, N.C., Carson, R., Diksic, M. et al., “Workshop onschizophrenia, PET, and dopamine D 2 receptors in the human neostratum,”<strong>Schizophrenia</strong> Bulletin, 14:471–84, 1988; Kapur, S. and Remington, G., “DopamineD 2 receptors and their role in atypical antipsychotic action: Still necessary and mayeven be sufficient,” Biological <strong>Psychiatry</strong>, 50:873–83, 2001. For a discussion of thedopamine theory of schizophrenia and the novel antipsychotic medications seeKapur, S. and Seeman, P., “Does fast dissociation from the dopamine D 2 receptorexplain the action of atypical antipsychotics? A new hypothesis,” American Journal of<strong>Psychiatry</strong>, 158:360–9, 2001.7 Kapur, S., Zipursky, R., Jones, C. et al. “Relationship between dopamine D 2occupancy, clinical response, and side effects: A double-blind PET study of firstepisodeschizophrenia,” American Journal of <strong>Psychiatry</strong>, 157:514–20, 2000.8 Smythies, J.R. and Adey, W.T., The Neurological Foundation of <strong>Psychiatry</strong>, NewYork: Academic Press, 1966, pp. 150–7.9 Melamud, N., “Psychiatric disorder with intracranial disorders of the limbicsystem,” Archives of Neurology (Chicago), 17:113–24, 1967; Horowitz, M.J. andAdams, J.E., “Hallucinations on brain stimulation: Evidence for revision of thePenfield hypothesis,” in W.Keup (ed.), Origins and Mechanisms of Hallucinations, NewYork: Plenum Publishing, 1970, pp. 13–22; Torrey, E.F. and Peterson, M.R.,‘<strong>Schizophrenia</strong> and the limbic system,’ Lancet, 2:942–6, 1974.10 Abi-Dargham, A., Gil, R., Krystal, J. et al., “Increased striatal dopaminetransmission in schizophrenia: Confirmation in a second cohort,” American Journal of<strong>Psychiatry</strong>, 155:761–7, 1998; Kapur, S., “Psychosis as a state of aberrant salience: Aframework linking biology, phenomenology, and pharmacology in schizophrenia,”American Journal of <strong>Psychiatry</strong>, 160:13–23, 2003; Wong, D.F., Wagner, H.N., Tune,L.E. et al., “Positron emission tomography reveals elevated D 2 dopamine receptorsin drug-naïve schizophrenics,” Science, 234:1558–63, 1986; Farde, L., Wiesel, F.-A.,Stone-Enlander, S. et al., “D 2 dopamine receptors in neuroleptic-naïveschizophrenic patients: A positron emission tomography study with [ 11 C]raclopride,” Archives of General <strong>Psychiatry</strong>, 47:213–19, 1990.11 Kapur, “Does fast dissociation explain the action of atypical antipsychotics?;” Kapur,“Relationship between dopamine D 2 and side effects.”12 Judd, L.L., Goldstein, M.J., Rodnick, E.H. and Jackson, N.L.P., “Phenothiazineeffects in good premorbid schizophrenics divided into paranoid non-paranoidstatus,” Archives of General <strong>Psychiatry</strong>, 29:207–11, 1973.13 Rosen B., Engelhardt, D.M., Freedman, N et al., “The hospital proneness scale as apredictor of response to phenothiazine treatment. II: Delay of psychiatrichospitalization,” Journal of Nervous and Mental Disease, 152:405–11, 1971.
352 NOTES14 Bowers, M.B., “Central dopamine turnover in schizophrenic syndromes,” Archives ofGeneral <strong>Psychiatry</strong>, 31:50–4, 1974.15 Burt, D.R., Creese, I. and Snyder, S.H., “Antischizophrenic drugs: Chronictreatment elevates dopamine receptor binding in brain,” Science, 196:326–8, 1977;Muller, P. and Seeman, P., “Brain neurotransmitter receptors after long-termhaloperidol: Dopamine, acetylcholine, serotonin, -noradrenergic and naloxonereceptors,” Life Sciences, 21:1751–8, 1977; Abi-Dargham, “Increased striataldopamine transmission in schizophrenia;” Kapur, “Relationship between dopamineD 2 and side effects;” Kapur, “Does fast dissociation explain the action of atypicalantipsychotics?”16 Farde, “D 2 dopamine receptors in neuroleptic-naïve schizophrenic patients;” Kapur,“Dopamine D 2 receptors and their role in atypical antipsychotic action;” Kapur,“Relationship between dopamine D 2 and side effects.”17 Rosen, B., Engelhardt, D.M., Freedman, N. et al, “The hospitalization pronenessscale as a predictor of response to phenothiazine treatment. I: Prevention ofpsychiatric hospitalization,” Journal of Nervous and Mental Disease, 146:476–80, 1968.18 Rosen B., Engelhardt, D.M., Freedman, N. et al, “The hospital proneness scale as apredictor of response to phenothiazine treatment. II: Delay of psychiatrichospitalization,” Journal of Nervous and Mental Disease, 152:405–11, 1971.19 Goldstein, M.J., “Premorbid adjustment, paranoid status, and patterns of response tophenothiazine in acute schizophrenia,” <strong>Schizophrenia</strong> Bulletin, 3:24– 37,1970; Evans,J.R., Rodnick, E.H., Goldstein, M.J. and Judd, L.L., “Premorbid adjustment,phenothiazine treatment, and remission in acute schizophrenics,” Archives of General<strong>Psychiatry</strong>, 27:486–90, 1972.20 Judd, L.L., Goldstein, M.J., Rodnick, E.H. and Jackson, N.L.P., “Phenothiazineeffects in good premorbid schizophrenics divided into paranoid non-paranoidstatus,” Archives of General <strong>Psychiatry</strong>, 29:207–11, 1973.21 Goldstein, M.J., Rodnick, E.H., Evans, J.R. et al., “Drug and family therapy in theaftercare of acute schizophrenics,” Archives of General <strong>Psychiatry</strong>, 35:1169–77, 1978.22 Rappaport, M., Hopkins, H.K., Hall, K. et al. “Are there schizophrenics for whomdrugs may be unnecessary or contraindicated?’ International Pharmacopsychiatry, 13:100–11, 1978, p. 107.23 Carpenter, W.T., McGlashan, T.H. and Strauss, J.S., “The treatment of acuteschizophrenia without drugs: An investigation of some current assumptions,”American Journal of <strong>Psychiatry</strong>, 134:14–20, 1977, p. 19.24 Klein, D.G. and Rosen, B., “Premorbid asocial adjustment and response tophenothiazine treatment among schizophrenic inpatients,” Archives of General<strong>Psychiatry</strong>, 29:480–5, 1973.25 May, P.R.A., Tuma, A.H. and Dixon, W.J., “<strong>Schizophrenia</strong>—A follow-up study ofresults of treatment. I: Design and other problems,” Archives of General <strong>Psychiatry</strong>, 33:474–8, 1976; May, P.R.A., Tuma, A.H. and Dixon, W.J., “<strong>Schizophrenia</strong>: Afollow-up study of the results of five forms of treatment,” Archives of General<strong>Psychiatry</strong>, 38:776–84, 1981.26 Schooler, N.R., Goldberg, S.C., Boothe, H. and Cole, J.O., “One year afterdischarge: Community adjustment of schizophrenic patients,” American Journal of<strong>Psychiatry</strong>, 123:986–95, 1967.
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Recovery from SchizophreniaRecovery
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First edition published 1985by Rout
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ContentsAcknowledgments viIntroduct
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devotion to excellence in creating
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ixA NOTE ON THEORYThe materialist t
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Part IBackground
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Table 3.3 Recovery rates in the USA
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Part IIITreatment
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TREATMENT 247indicated, unemploymen
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