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Delusional Disorder Delusional Disorder: Molecular Genetic Evidence for Dopamine Psychosis Kiyoshi Morimoto, M.D., Ph.D., Ryosuke Miyatake, M.D., Ph.D., Mitsuo Nakamura, M.D., Ph.D., Takemi Watanabe, M.D., Ph.D., Toru Hirao, M.D., Ph.D., and Hiroshi Suwaki, M.D., Ph.D. Since delusional disorder is characterized by mono- significantly higher in patients with persecution-type symptomatic paranoid symptoms, it can be a good clinical delusional disorder (21%), compared with schizophrenic model for investigating the dopaminergic mechanism patients (6%) or controls (6%). (4) Patients homozygous responsible for paranoid symptoms. We examined for the DRD3 gene Ser9Ser had higher pretreatment levels neuroleptic responses, plasma homovanillic acid (pHVA) of pHVA than those heterozygous for Ser9Gly. (v) A and genes of the dopamine receptor (DR) and its significant positive correlation was found between the synthesizing enzyme (tyrosine hydroxylase: TH) in patients polymorphic (TCAT)n repeat in the first intron of the TH with delusional disorder and compared them with those of gene and pretreatment levels of pHVA in delusional schizophrenic patients and healthy controls. Results: (1) A disorder. We suggest that delusional disorder, especially the relatively small dose of haloperidol was more effective for persecution-type, includes a “dopamine psychosis,” and delusional disorder than for schizophrenia. (2) The that polymorphism of the DRD2, DRD3 and/or TH gene is pretreatment level of pHVA was higher in patients with part of the genetic basis underlying the hyperdopaminergic persecution-type, but not in those with jealousy-type state that produces paranoid symptoms. Further studies on delusional disorder, compared with age- and sex-matched a large sample size are required. controls. This increased pHVA level was decreased eight [Neuropsychopharmacology 26:794–801, 2002] weeks after successful haloperidol treatment. (3) The © 2002 American College of Neuropsychopharmacology. genotype frequency of the DRD2 gene Ser311Cys was Published by Elsevier Science Inc. KEY WORDS: Delusional disorder; Dopamine psychosis; ology remain unclear. The long-standing “dopamine pHVA; Polymorphism; DRD2 Ser311Cys; DRD3 Ser9Gly; hypothesis” of schizophrenia (Carlsson 1988) is partly supported by the action of neuroleptics, which block Although the neurobiological mechanism underlying dopamine receptors (DRs) and improve paranoid symp- schizophrenia has been investigated extensively during toms, such as delusion and hallucination (Seeman et al. the past few decades, its biochemical and molecular eti- 1976). It has further been supported by indirect evi- dence that repeated administration of dopamine agonists (e.g. amphetamine and cocaine) results in the develop- From the Department of Neuropsychiatry, Faculty of Medicine, Kagawa Medical University, Kagawa, Japan. ment of paranoid symptoms in humans (Ellinwood 1976; Address correspondence to: Kiyoshi Morimoto, M.D., Ph.D., Sato et al. 1992) and abnormal behavior (“behavioral Department of Neuropsychiatry, Faculty of Medicine, Kagawa sensitization”) in animals (Kalivas 1993). In schizo- Medical University, 1750-1 Ikenobe, Miki-cho, Kita-gun, 761-0793 Japan, Tel: ϩ81-87-891-2167, fax: ϩ81-87-891-2168, E-mail: neuropsy phrenic patients, dopamine agonists aggravate para- @kms.ac.jp noid symptoms (Janowski and Davis 1976; Lieberman Received August 2, 2001; revised October 29, 2001; accepted et al. 1987); this may be the result of an aberrant in- November 2, 2001. Online publication: 11/28/01 at www.acnp.org/citations/ crease in dopamine release (Laruelle et al. 1996; Breier Npp 112801213. et al. 1997). However, many clinical studies on plasma NEUROPSYCHOPHARMACOLOGY 2002–VOL. 26, NO. 6 © 2002 American College of Neuropsychopharmacology Published by Elsevier Science Inc. 0893-133X/02/$–see front matter 655 Avenue of the Americas, New York, NY 10010 PII S0893-133X(01)00421-3 NEUROPSYCHOPHARMACOLOGY 2002–VOL. 26, NO. 6 Molecular Genetics of Delusional Disorder 795 and cerebral spinal fluid (CSF), DR imaging, and post- age (and age at onset) was 57.5 Ϯ 2.2 years (54.6 Ϯ 2.2 mortem brain or DR genes have failed to obtain direct years) and the male/female ratio was 1/10. Neuroleptic hyperdopaminergic evidence, or if such evidence has responses, including effective neuroleptic dose (halo- been obtained, the results have been contradictory (Davis peridol equivalent, mg/day), duration of admission, et al. 1991; Willner 1997; Laruelle 1998; Zakzanis et al. and outcome at discharge (complete/incomplete remis- 1998; Harrison 1999; Soares and Innis 1999; see also Dis- sion) were examined. To evaluate social function, the cussion). Global Assessment of Functioning (GAF; DSM-IV One of the most important reasons for these complex (American Psychiatric Association 1994)) score was used. results may be etiological heterogeneity of the disorder, In addition, we compared the neuroleptic responses of since there is a considerable variety of clinical features 15 patients with schizophrenia, who presented their of schizophrenia, including symptoms, neuroleptic re- first psychotic episode and were admitted during the sponse and long-term prognosis, between the patients. same period, with those of the patients with delusional To evaluate and categorize the heterogeneity clinically, disorder. The average of age (at onset) of these schizo- some biology-based classifications have been proposed, phrenic patients was 25.1 Ϯ 1.4 years (22.7 Ϯ 1.3 years), for example “type I and type II syndromes” (Crow the male/female ratio was 7/8, and the ICD-10 sub- 1980), “3 syndromes” (Liddle 1987), and “deficit and types included 6 paranoid, 6 undifferentiated, 2 hebe- non-deficit forms” (Carpenter et al. 1988). phrenic, and 1 catatonic type. Another methodology that may allow us to break through the heterogeneity and clarify the role of pHVA in Delusional Disorder dopamine systems in psychosis is to select a psychiatric disorder with only one target schizophrenic symptom. Subjects. To investigate brain dopamine function, While paranoid symptoms are commonly seen in vari- pHVA levels were measured in patients with delu- ous psychiatric disorders, as known “paranoid spec- sional disorder and compared with those of age- and trum” (Fujinawa 1981), delusional disorder, a psychosis sex-matched controls. Thirteen neuroleptic-naive pa- previously called “paraphrenia” (Kraepelin 1909; Roth tients with delusional disorder (age at onset was 48.4 1987), is characterized by mono-symptomatic paranoid years; male/female ratio was 4/9) were subjects in our symptoms without other schizophrenic symptoms. In the inpatient and outpatient clinics. The subtypes involved ICD-10 diagnostic criteria (WHO 1992), delusional dis- were: nine persecution-type and four jealousy-type. order is diagnosed when: (1) delusions constitute the Written informed consent to participate this study was only, or the most conspicuous, clinical characteristic; (2) obtained from all patients. Blood for pHVA was drawn it cannot be classified as organic, schizophrenic, or af- between 9:00 A.M. and 11:00 A.M. before starting neuro- fective disorder; and (3) affect, speech, and behavior are leptic treatment. The Brief Psychiatric Rating Scale normal. Thus, delusional disorder can be a good clinical (BPRS) was used to evaluate the level of delusional psy- model for investigating the molecular genetic mecha- chopathology in each patient. In addition to the pre- nisms for paranoid symptoms. treatment examination, in eight patients, pHVA and In the present study, we hypothesized that a hyper- BPRS scores were measured eight weeks after neuro- dopaminergic state in the brain is responsible for pro- leptic treatment with a small dose of haloperidol (aver- ducing paranoid symptoms. To test this hypothesis, we age 2.7 mg/day). compared neuroleptic responses between patients with delusional disorder and schizophrenia, measured plasma Measurement of pHVA. pHVA concentrations were levels of homovanillic acid (pHVA), a dopamine metabo- determined by high-performance liquid chromatogra- lite and clinical marker of dopamine metabolism, in pa- phy using electrochemical detection analysis (Chang et tients with delusional disorder before and after neuro- al. 1983). The interassay coefficients of variance were leptic treatment, and analyzed the polymorphism of DR 1.2 and 1.7% for concentrations of 20 and 100 pmol/ml, and its synthesizing enzyme gene. respectively. The DR and Tyrosine Hydroxylase Gene in Delusional Disorder METHODS Subjects. To investigate the possible genetic basis un- Neuroleptic Response of Delusional Disorder derlying the hyperfunction of dopamine systems in de- Subjects. Eleven patients with delusional disorder lusional disorder, we analyzed the polymorphism of classified according to ICD-10, who were admitted to genes for DRD2 and DRD3 and their synthesizing en- our psychiatric ward, were studied. All patients pre- zyme tyrosine hydroxylase (TH). Twenty-three patients sented the first delusional episode without previous with delusional disorder, 48 patients with schizophre- neuroleptic medication. The average (mean Ϯ S.E.M.) nia, and 48 normal controls were studied. Delusional 796 K. Morimoto et al. NEUROPSYCHOPHARMACOLOGY 2002–VOL. 26, NO. 6 patients included the subjects for our pHVA study. nia. A clear gender difference was also seen in delusional The age at onset was 52.3 years, male/female ratio was disorder (femaleϾmale). A relatively smaller dose of halo- 4/19, and the subtypes were 19 persecution-type and
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