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Paranoid schizophrenia was studied in 365 patients who constitute a nonrepresentative sample group inhabiting three urban districts. The population under study included groups with juvenile (31 patients), middle-aged (266) and late (68) onsets of the disease. Clinical variants of the disease were established with respect to its phenomenology and the course of delirium syndromes.
Paranoid schizophrenics, non-paranoid schizophrenics and normals were assessed on tasks designed to demonstrate their tendency to perceive illusory correlations. It was hypothesized that paranoids would show stronger illusory correlations than normals due to the predominance of their schemata when processing information, and that non-paranoids would show weaker correlations than normals because of their impaired ability to establish conceptual categories. Results were broadly consistent with predictions.
The history of nosologic approaches to paranoid schizophrenia and the other paranoid psychoses is traced from the time of Kraepelin. Kraepelin, emphasizing the course of illness, proposed a narrow definition for paranoid dementia praecox (paranoid schizophrenia). He created the entity of paraphrenia for cases with symptoms similar to those in paranoid dementia praecox but without a deteriorating course. Bleuler, emphasizing underlying psychological mechanisms, broadened the concept of paranoid schizophrenia to include nearly all delusional functional psychotic states. After Bleuler, the controversy continued as to whether the paranoid psychoses belonged within or separate from the schizophrenic disorders. Emerging from these historical controversies, current nosologic approaches to paranoid schizophrenia and paranoid psychosis differ substantially. Approaches to paranoid schizophrenia range from broad global criteria, which include patients with thought disorder and affective deterioration (e.g., ICD-9), to narrow criteria such as those proposed by Tsuang and Winokur (1974), which specifically exclude such patients. While some criteria for paranoid psychosis exclude patients with hallucinations or other than persecutory or jealous delusions (e.g., DSM-III), other criteria include such patients.
Genetic and biochemical findings in paranoid schizophrenia and other paranoid psychoses are reviewed. Although the data suggesting a lower genetic loading for schizophrenia in paranoid versus nonparanoid schizophrenia are unclear, paranoid schizophrenia does, to a limited extent, breed true within families. Monozygotic twins concordant for schizophrenia tend to be either both paranoid or both nonparanoid schizophrenics. In all studies, the risk for schizophrenia in the relatives of patients with paranoid psychosis is close to that found in the normal population. Genetic studies provide no evidence for a link between affective illness and either paranoid schizophrenia or paranoid psychosis. Although reports of low platelet monoamine oxidase activity in paranoid schizophrenia have not been confirmed, recent results suggest that brain norepinephrine levels may be higher in paranoid than in nonparanoid schizophrenics. Genetic and biochemical findings suggest some differences between paranoid and nonparanoid schizophrenia, but definitive clarification of the relationship between these two syndromes must await future research. From a genetic perspective, paranoid psychosis appears to bear little relationship to schizophrenia.
BACKGROUND: Paranoid schizophrenia is considered to be a rare condition in adolescence. Since this is contrary to the authors' clinical experience, they hypothesized that a controlled study would show that a significant number of adolescents would be diagnosed with paranoid schizophrenia and that scores from the childhood version of the Schedule for Affective Disorders and Schizophrenia (K-SADS) would differentiate between the paranoid schizophrenic adolescents and adolescents with other types of schizophrenia or with affective disorder. METHOD: The authors conducted a prospective study of 120 adolescents admitted consecutively to an adolescent psychiatric inpatient department. Patients were diagnosed on the basis of DSM-III after an 8-week period during which they were evaluated with a structured psychiatric history and psychiatric examination, the K-SADS, repeated nonstructured interviews, and extensive ward observations. RESULTS: Thirty-eight percent of the schizophrenic adolescents and 14% of the total hospitalized population met the DSM-III criteria for paranoid schizophrenia. The symptom profile of the paranoid schizophrenic adolescents clearly distinguished them from adolescents with other psychiatric disorders. CONCLUSIONS: Given the incidence of paranoid schizophrenia in an adolescent population, adolescent psychiatrists are likely to encounter this disorder. DSM-III-R should be used in future studies to further clarify the issue of the prevalence of paranoid schizophrenia in adolescents.
Based on test comparisons involving psychotic depressives and chronic paranoid schizophrenics, Carter (J. Nerv. Ment. Dis. 174: 336-341, 1986) inferred that cognitive disorder may reflect a general psychosis factor rather than a differential diagnostic marker. Review of the design and analysis raises methodological and conceptual issues that obviate such interpretation. Problems include absence of control for IQ and chronicity of illness, sample bias incurred by selectively matching groups for education, use of parametric statistics on ordinal data, measures that do not differentially assess cognitive deficit, plausible alternative explanations for nonsignificant outcome, and inadequate data base for generalizing about larger diagnostic groups or psychosis itself. Significant differences found by Carter and others suggest, instead, some fundamental distinctions in the nature if not extent of cognitive disorder in these two groups. It was proposed that a general psychosis factor may be a pervasive interfering variable that obscures diagnostic differences in cognition and thus needs to be rooted out by proper statistical or research design.
To explore whether or not patients with schizophrenia display a more profound impairment of negative emotion processing, we assessed the implicit evaluation of positive and negative emotional stimuli. Twenty patients with schizophrenia (9 paranoid, 11 non-paranoid) and 22 normal controls were instructed to classify emotional pictures according to the intrinsic valence if the pictures were black and white. If the stimuli were color-filtered, participants were instructed to press the positive/negative response key according to the extrinsic valence (assigned valence of color). The error rates of the color-filtered stimuli were used as dependent measures. Normal controls made more errors on trials of the positive pictures when the correct response was the negative response key than when the correct response was the positive response key. The reverse was true on trials of the negative pictures. Patients with schizophrenia, especially paranoid schizophrenia, committed more errors in trials of the positive pictures when the correct response key was the negative response key. However, the reverse was not true on trials of the negative pictures. These findings suggest that patients with paranoid schizophrenia might suffer from an impaired ability to evaluate negative emotions and have a loosening of association within their negative emotional networks.
Epidemiological data available on paranoid schizophrenia are noteworthy for their paucity and poor quality. Although it is commonly said that the paranoid subtype is less common in developing countries, published studies are contradictory. It has also been said that paranoid schizophrenia occurs more frequently among educated persons, but the evidence is not conclusive. Two Scandinavian studies suggest that the paranoid subtype increased in frequency during this century. Assertions that some cultures produce large numbers of paranoid persons are of great interest since schizophrenic symptomatology is partly dependent on culture. The most famous such culture, the Dobuans, are found to be a product of ethnographic bias and probably do not exist as described. This leaves the question of cultural influence on paranoid schizophrenia wide open. Two studies on the seasonality of paranoid schizophrenic births found that their birth pattern does not differ from the seasonal pattern previously established for schizophrenic births as a whole. It is concluded that the epidemiology of paranoid schizophrenia is an area of potentially fruitful inquiry and one that is mostly terra incognita.
The incidence of paranoid schizophrenia (the number of new cases per year) was examined in a population. The figure was found to be 0.17 per 10,000 of the population, being greatly dependent on the age and sex structure of the population examined. The method of the examination is presented in detail. It is shown, in particular, that the results are considerably influenced by the disease duration in the patients. With a short duration of the disease the results appear to be greatly underestimated because of the difficulties in making the correct diagnosis in many cases. The exact number of such cases can be determined by using the law of statistical distribution of the duration of the paranoid schizophrenia stages.
To investigate the nature of emotional experience in schizophrenia, we examined emotional responses to affective stimuli. Twenty-one outpatients with schizophrenia (9 paranoid, 12 nonparanoid) and 20 normal controls rated the arousal and valence that they experienced from the presentation of 60 pictures. Schizophrenia patients displayed less emotional responsivity to the positive stimuli and they displayed diverse responsivity to the negative stimuli, which depended upon arousal level. Further analysis, using schizophrenia subtype, indicated that nonparanoid patients reported increased negative responsivity and decreased positive responsivity, regardless of arousal level. However, paranoid schizophrenia patients showed enhanced self-reported experiences of emotion to the low arousing stimuli and diminished responsivity to the high arousing stimuli. This pattern was robust to the negative stimuli. These findings suggest that paranoid schizophrenia patients might suffer from aberrantly flattened responses to negative emotional stimuli, and that this may account for paranoid tendency and secondary social isolation in paranoid schizophrenia.
The pharmacological treatment for paranoid schizophrenia is based on antipsychotic drugs. Their actions is only suspensive but not curative. In 1980 Crow proposed a division of schizophrenia in two major syndromes, type 1 being characterized by prominent positive symptoms. Andreasen in 1982 suggested similar criteria for positive subtype. Many others have described schizophrenia subtypes over the years. The paranoid schizophrenia criteria are very close to Crow's type 1 criteria. Since chlorpromazine was synthetized in France in 1952, the French speaking psychiatrists have classified neuroleptics according to their therapeutic efficacy and their side effects. So Deniker and Ginestet categorized neuroleptics on the basis of their behavioural efficacy and distinguished sedative neuroleptics from anti-delusional neuroleptics and anti-autistic neuroleptics. French psychiatrists consider that there are qualitative differences between various neuroleptics. In USA, equivalent doses are established with chlorpromazine for many neuroleptic drugs, but equivalency doses are considered as crude at best by some, such as J.M. Kane. The typical neuroleptic treatment is reviewed: target symptoms, choice of drug, dosage, route of administration, combined medications, predictive clinical and biological parameters of response, duration of treatment. Failure to response to neuroleptic treatment is not uncommon. Some strategies are detailed for the treatment-resistant patients. Combination of neuroleptics like haloperidol + thioproperazine or haloperidol + trifluoperazine may be useful.(ABSTRACT TRUNCATED AT 250 WORDS)
Two patients with paranoid schizophrenia had delusions involving the internet. Additionally, one of them experienced computer databases as being distributed to other people in a phenomenologically similar way to that encountered in thought broadcasting. The presented cases illustrate the historical association of the contents of delusions in schizophrenia.
BACKGROUND: Early differentiation of the nervous system and adult CNS neuroplasticity is modulated by PAX-6. We have shown previously that a highly polymorphic, functional AC/AG repeat in the 5' regulatory region of the gene showed significantly increased promoter activity, if containing > or = 29 repeats, and that the heterozygous genotype (< or = 28/> or = 29) revealed increased mRNA PAX-6 levels in human brain tissue compared to the homozygous short variant. METHODS: In a case-control study of 655 unrelated individuals, allele frequencies and genotype distributions of the functional PAX-6 promoter polymorphism were investigated comprising patients with DSM-IV schizophrenia, patients with affective disorders, and population controls. RESULTS: No allelic or genotypic association of the PAX-6 promoter polymorphism to affective disorder or to schizophrenia as one disease entity was observed. After subtyping schizophrenia into paranoid and nonparanoid forms, potential evidence was found for a genotypic association of the high-activity variant with the paranoid subtype of schizophrenia (p = .02). The estimated odds ratio was 1.7 (95% CI .98 to 2.95) for those heterozygous and 1.4 (95% CI .82 to 2.42) for those heterozygous or homozygous for the high-activity variant compared to the homozygous low-activity variant. CONCLUSIONS: Our finding indicates that early developmental genes may be involved in the etiopathogenesis of schizophrenia subtypes via variable transcriptional regulation in the developing and adult human brain.
OBJECTIVES: It was hypothesized that people with paranoid schizophrenia would differ from depressed and normal participants in their interpretation of complex communications in which the affect conveyed verbally was either congruent or incongruent with the affect conveyed non-verbally. DESIGN: A 3 (group) x 3 (positive, negative, neutral facial expression) x 3 (positive, negative, neutral verbal content) experimental design was used. There were eight participants per group, and the paranoid and depressed groups comprised inpatients in an acute psychiatric facility for either their first or second psychiatric episode. METHODS: Participants, tested individually, were asked to interpret the affect conveyed by the various communications presented. RESULTS: All participants interpreted most of the communications in a similar way. Paranoid schizophrenia patients, however, differed in their interpretation of communications in which negative feelings were expressed verbally. In contrast to both the normal and depressed groups, the paranoid schizophrenia group interpreted these communications as virtually devoid of any affect whatsoever. CONCLUSIONS: Paranoid schizophrenia patients show an information-processing bias in response to communications involving both congruent and incongruent negative verbal content. It is not obvious why the bias observed would be specific to negative verbal messages and not extend to negative non-verbal messages. Replication and further study are required.
OBJECTIVES: Genetic associations between delusional disorder and paranoid schizophrenia are not well understood, although involvement of biological factors has been suspected. We investigated the incidence of human leukocyte antigen (HLA) class I alleles in patients with delusional disorder and paranoid schizophrenia, first, to explore a possible immunogenetic etiology of these paranoid disorders and, second, to determine whether they share similar etiologic mechanisms. METHOD: We employed a nested case-control study design. Psychiatric reference data were available for 38,500 patients attending a hospital-based psychiatric outpatient department between 1998 and 2005. We enrolled 100 patients with delusional disorder and 50 patients with paranoid schizophrenia as the subject cases, using DSM-IV criteria. We considered equivalent numbers of healthy volunteers matched for age and ethnic background as control subjects. All subjects came from an India-born Bengali population. We applied the polymerase chain reaction-based molecular typing method to all patients and healthy subjects. RESULTS: The HLA-A*03 gene is significantly associated with delusional disorder as well as with paranoid schizophrenia. This HLA gene alone or in linkage disequilibrium with other HLA genes or other closely linked non-HLA genes may influence susceptibility to delusional disorder and paranoid schizophrenia. CONCLUSIONS: The study reveals important associations between HLA genes and paranoid disorders. Delusional disorder and paranoid schizophrenia may share similar etiologic mechanisms. This preliminary observation may help our understanding of the genetic basis of these paranoid disorders.
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The objective of the present study was to investigate the relationship between schizophrenia subtype and morphological characteristics of trees drawn in the Baum test. Subjects comprised the following three groups: 20 patients diagnosed with paranoid schizophrenia according to International Classification of Diseases (10th revision; ICD-10) criteria; 26 patients with non-paranoid schizophrenia according to ICD-10 criteria; and 53 healthy individuals. Differences in psychiatric symptoms as assessed using the Brief Psychiatric Rating Scale (BPRS) score were compared between patients with paranoid and non-paranoid schizophrenia. In addition, differences in two morphological characteristics of trees, namely trunk-to-crown ratio and trunk end opening, were compared between the three groups. No differences in psychiatric symptoms were identified between patients with paranoid and non-paranoid schizophrenia. Conversely, mean +/- SD trunk-to-crown ratio was 13.1 +/- 8.0 for patients with non-paranoid schizophrenia, 8.8 +/- 4.6 for patients with paranoid schizophrenia, and 5.4 +/- 3.4 for healthy individuals. Significant differences were identified between all three groups. Furthermore, mean trunk end opening was 0.80 +/- 0.7 for patients with paranoid schizophrenia, 0.38 +/- 0.6 for patients with non-paranoid schizophrenia, and 0.06 +/- 0.3 for healthy individuals. Again, significant differences were apparent between all three groups. These findings suggest that morphological differences in trees drawn in the Baum test can be observed between the two schizophrenia subtypes in terms of not only psychopathological interpretation, but also gestalt formation, as assessed on the basis of trees with collapsed gestalt or with some degree of gestalt. This suggests the possibility of multiple disorders at a physiological level. The present study confirmed that the Baum test can quantitatively assess facets of schizophrenia that existing scales such as BPRS are unable to analyze, and is useful for investigating brain function in patients with schizophrenia.
Most paranoid patients have traditionally been diagnosed as schizophrenic, although considerable evidence points to the dissimilarities between paranoid and nonparanoid schizophrenic patients and to commonalities between paranoid and affective disorder groups. Based on a review of research, it is suggested that paranoid schizophrenia, at least in some of its varieties, may more fruitfully be conceptualized as a phenotypic expression of an underlying depressive mode than as a schizophrenic form. This formulation is presented within the framework of a broad examination of diagnostic issues.