Recovery From Schizophrenia: Psychiatry And Political Economy

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 ofPsychiatry, 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,”Schizophrenia Bulletin, 2:19–76, 1976; Haracz, J.L., “The dopamine hypothesis: Anoverview of studies with schizophrenic patients,” Schizophrenia Bulletin, 8:438–69,1982; Andreasen, N.C., Carson, R., Diksic, M. et al., “Workshop onschizophrenia, PET, and dopamine D 2 receptors in the human neostratum,”Schizophrenia 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 Psychiatry, 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 ofPsychiatry, 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 Psychiatry, 157:514–20, 2000.8 Smythies, J.R. and Adey, W.T., The Neurological Foundation of Psychiatry, 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.,‘Schizophrenia 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 ofPsychiatry, 155:761–7, 1998; Kapur, S., “Psychosis as a state of aberrant salience: Aframework linking biology, phenomenology, and pharmacology in schizophrenia,”American Journal of Psychiatry, 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 Psychiatry, 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 Psychiatry, 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.