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The occurrence of schizophrenia as a worsening of schizoid traits previously present has been a topic of interest for some time.1–4 However, it is generally the case that information on a day-to-day basis about the premorbid personalities of psychotic patients when they come into care is fragmented and limited. In this article, I describe my own experience of schizoidism, into which I had insight, before I became psychotic. I also give some comments on how this worsened into psychosis.

Background: No prior study of morbid risk in relatives of schizophrenia probands has, to our knowledge, focused solely on those with a recent onset of illness. Given that studies starting with chronic schizophrenia probands may exclude some individuals who have a more benign illness course, the examination of morbid risks among first-degree relatives of recent-onset schizophrenia patients is of substantial interest.

In the "Special Report on Schizophrenia" published in the Schizophrenia Bulletin in 1987, the genetic basis of schizophrenia was reviewed. Here, we provide our perspective on the current status of this area of investigation, focusing largely but not exclusively on recent findings. Methodologically rigorous family studies have now clearly shown that schizophrenia substantially aggregates in families. Familial factors that predispose to schizophrenia also increase the risk for certain schizophrenia-related personality disorders and probably for some forms of non-schizophrenic nonaffective psychosis. Results from one new twin study and updates from two ongoing adoption studies continue to support the hypothesis that genetic factors play a major role in the etiology of schizophrenia. Little is known about how genetic liability to schizophrenia is transmitted, although statistical models suggest that transmission is probably not due solely to a single major gene. Schizophrenia is clearly a complex disorder in that gene carriers need not manifest the illness (incomplete penetrance), affected individuals need not have the gene (environmental forms of phenocopies), diagnostic uncertainties cannot be avoided, and different families may carry different susceptibility genes (genetic heterogeneity). Therefore, segregation or linkage analyses are far more difficult to perform with schizophrenia than with Mendelian genetic disorders. Given this complexity, it is not too surprising that no replicated positive evidence for linkage to schizophrenia has been reported to date. However, just as linkage analysis of schizophrenia should not be excessively embraced as the only form of viable genetic research in schizophrenia, it also shouldn't be prematurely spurned. If one or several genes of major effect exist for schizophrenia, large samples using new statistical and laboratory methodologies have a good chance of detecting them. The authors thus recommend a balanced research approach to the genetics of schizophrenia that includes traditional methods of family, twin, and adoption studies as well as a major effort in large-sample linkage studies.

In the New York High-Risk Project (NYHRP) we followed subjects at risk for schizophrenic or affective disorders and low-risk controls from childhood to adulthood, with the goal of identifying early predictors of later schizophrenia-related psychopathology. In this article, we focus on two potential predictors: the Physical Anhedonia Scale administered in adolescence and the Attention Deviance Index obtained in childhood. Subjects of this report are 161 members of the NYHRP's first sample (sample A), who had scores on both attention and anhedonia and had followup clinical assessments in adulthood. We used a path analysis model and several separate regression analyses to examine the relationships of the parent diagnostic groups, attentional dysfunction, and anhedonia to each other and to each of three psychopathological outcomes: schizophrenia and schizophreniarelated psychoses, major affective disorder, and social isolation in nonpsychotic subjects. Subject groups did not differ in anhedonia scores but did differ in childhood attentional dysfunction, psychosis, and social isolation, all of which are more common in subjects at risk for schizophrenia. In these subjects at risk for schizophrenia, but not in the other two groups of subjects, childhood attentional dysfunction is related to anhedonia, social isolation, and possibly nonparanoid psychosis. Anhedonia is associated with social isolation and with psychosis in females. Several other gender effects are also noted. Anhedonia, an inability to experience pleasure in activities that normally produce it, has been proposed as an important negative symptom of schizophrenia . In their classic descriptions of schizophrenic patients, both Kraepelin (1919/1971) and Bleuler (1919/ 1950) referred to anhedonic symptoms as one aspect of their patients' emotional impairment. Rado (1956) and Meehl (1962) not only regarded anhedonia as a key clinical feature, but also believed it was a fundamental aspect of a hereditary predisposition to schizophrenia. A large body of data (Edell and

Background: Insight in psychosis and schizophrenia is considered a complex biopsychosocial phenomenon. Premorbid personality is regarded by some authors as part of the substrate to many psychiatric phenomena, but it is not clear if this applies to insight. Aim: To examine longitudinal relationships between personality traits and insight dimensions in first-episode psychosis. Methods: One hundred consecutive antipsychotic-naive first-episode nonaffective psychotic patients admitted to hospital were included in the study. Eighty-one patients completed at 1 month a premorbid personality evaluation, plus baseline, and 6-month insight assessments. We used the Assessment and Documentation of Psychopathology inventory for assessing insight dimensions (not feeling ill, lack of insight, and refusal of treatment) and the Personality Assessment Schedule for ascertaining 5 dimensions of premorbid personality (schizoid, passive-dependent, anancastic, sociopathic, and schizotypy). Results: At baseline, personality dimensions did not show any association with insight dimensions, with the exception of schizotypy traits. At 6 months, schizoid and sociopathic personality showed a significant association with not feeling ill (r = .30, P ≤ .007; r = .27, P = .01) and lack of insight (r = .36, P = .001; r = .41, P < .001), respectively. When we calculated insight change, schizoid and sociopathic personality had moderate correlation with the lack of insight dimension (r = −.34, P = .002; r = .38, P < .001, respectively). After applying partial correlations for potential confounders and Bonferroni correction, the associations remained significant. Moreover, using a regression model, sociopathic and schizoid personality significantly predicted lack of insight at 6 months and change from baseline to the 6 months assessment. Conclusions: Sociopathic and schizoid personality dimensions were not only significantly associated with lack of insight at 6 months but also predicted change on lack of insight over 6 months. Therefore, exploring premorbid personality traits at the beginning of a psychotic episode may be helpful in identifying patients at high risk for lack of insight during the initial course of the illness.

This study aimed to assess the boundaries of the schizophrenia spectrum and whether inclusion of such phenotypes increases power for linkage analysis of schizophrenia. Participants were 234 first degree relatives (FDRs) of 94 schizophrenia probands in Northern Taiwan who completed a direct interview using the Diagnostic Interview for Genetic Studies (DIGS). Based on best estimate diagnosis, the morbidity risk in the relatives for schizophrenia was 2.5 percent (Weinberg's shorter method) or 3.9 percent (Kaplan-Meier estimate). Depending on the stringency of diagnosis, lifetime prevalence was 2.6 percent to 4.7 percent for schizotypal personality disorder, 3.4 percent to 8.6 percent for paranoid personality disorder, and 1.3 percent to 3.4 percent for schizoid personality disorder. These figures are significantly higher than the corresponding figures in the general population. However, none of the recurrence risk ratio for any spectrum that included both schizophrenia and a personality disorder (3.0 to 5.9) was greater than that of schizophrenia alone (9.3 to 14.4). Thus, including schizophrenia-related personality disorders in the spectrum did not increase power for linkage analysis of schizophrenia.

In light of current linkage studies in schizophrenia, research on the "schizophrenia spectrum" deserves increased attention for an exact determination of the affected phenotype: Those disorders that have a much higher prevalence among biological relatives of schizophrenia patients are supposed to share common etiological factors with "core" schizophrenia. However, there is controversy over which of the DSM-III-R personality disorders should be included in the spectrum. In a controlled family study of inpatients with a DSM-III-R diagnosis of schizophrenia (n = 101), schizophreniform and schizoaffective disorders (n = 69), and unipolar major depression (n = 160), familial rates of personality disorders were assessed through personal interviews and compared with prevalence rates in 109 control families from the community. As predicted, schizotypal personality disorder occurred more frequently in the nonpsychotic relatives of schizophrenia probands (2.1%) than in the families of unscreened controls (0.3%). Paranoid personality disorder was more frequent in relatives of probands with unipolar depression (2.9%) than in relatives of schizophrenia patients (1.7%), and controls revealed the lowest rate (0.9%). Schizoid personality disorder, however, was extremely rare in all sample groups (between 0.3% and 0.7%), providing no sufficient statistical power for detection of group differences. Further analysis of the DSM-III-R criterion symptoms of schizotypal personality disorder demonstrated that items describing "negative" symptomatology are the main source of familial aggregation, but "psychotic-like" personality features are also contributing factors.

We compared 20 patients with late-onset schizophrenia, 7 with delusional disorder with hallucinations (paraphrenia), and 13 with delusional disorder without hallucinations (late-onset paranoia). We found that these three categories could be distinguished from each other on some clinical parameters. Late-onset schizophrenia was characterized by bizarre delusions; auditory hallucinations; to a lesser degree, first-rank and negative symptoms; and premorbid personality of the paranoid or schizoid type. Paraphrenia was associated with predominantly nonbizarre delusions, auditory hallucinations, earlier onset of symptoms, and paranoid or schizoid personality. Paranoia (late-onset) was characterized by late onset of symptoms, nonbizarre delusions, relatively intact premorbid personality, and an underlying physical stratum.

A retrospective study of 61 acute schizophrenic patients examined whether any demographic, clinical, and outcome characteristics distinguished patients who improved with placebo or low dosages of antipsychotics (PLD patients) from patients who required high conventional dosages of antipsychotics (HCD patients). Patients in the PLD group (n = 30) and HCD group (n = 31) were similar in overall level of psychopathology at admission. Prominent excitement and certain somatic and auditory hallucinations were significantly more frequent in the HCD patients. PLD patients were more likely to be female, were hospitalized more rapidly after the onset of psychosis, and were more often first admissions. Although paranoid symptoms and premorbid schizoid personality did not differentiate the two groups, nonschizoid patients who were nonparanoid tended to be in the PLD group while nonschizoid patients who were paranoid tended to be in the HCD group. PLD patients were less psychotic at discharge, remained out of the hospital for longer periods, and had fewer rehospitalizations. These results confirm other reports of better outcome for patients successfully treated without medication. PLD patients were also functioning better as family members 1 year after discharge. Further research is indicated to improve the prediction of which acute psychotic patients will respond without medication or to low dose neuroleptic treatment and to determine if these predictions are generalizable to other treatment settings.

Everything we now are-including our anatomy, functioning, and emotional life—arises from past forms, functions, and feelings and, as such, is shaped at least as much by the distant past as by the near past and the present. It is therefore difficult to understand why psychiatry has paid so little attention to evolutionary processes; but perhaps, this neglect can be traced to the fact that man has so long considered himself to be unique that the comparatively recent idea of his unity with and descent from the rest of the animal world has taken something over 100 years since Darwin's time to percolate into the general consciousness. The variability in phenotype afforded by genetic inheritance provides each generation of a species with a sufficient range of individuals that some, proving more adaptive to the contemporary environment than others, prosper and over time come to suffuse and dominate the gene pool of their population. Thus the appearance of a variation that proves valuable for survival in even a single creature in a population will be found at a geometrically progressive rate in succeeding generations until a large proportion if not all members of the breeding group manifest it. The earlier form or function, however, is not entirely eliminated. It is retained recessively in the genetic potential of the group and occasionally emerges. It remains available, so to speak, should circumstances favor it once again. The form and function of any creature at any given point in time, therefore, is in effect a selection made by environmental pressures out of a repertoire of forms and functions genetically available to it. Hindsight, viewing the sequence of actual realizations, generates a notion of purpose or direction.

Studies of adopted individuals and their biological and adoptive families offer a means of disentangling the genetic and environmental contributions to a disorder such as schizophrenia and permit an examination of the effects of one type of influence while the other is randomized or controlled. Using this strategy in a series of studies, we have obtained results pertinent to genetic and family-interaction theories of etiology subject in a considerably lesser degree to the confounding of these influences that have flawed previous studies in both fields. There is every reason that these studies should be presented and criticized in an issue of the Schizophrenia Bulletin devoted to genetics, just as another strategy—high risk studies—was previously examined. The masterful review by Garmezy (Garmezy with Streitman 1974 and Garmezy 1974) on individuals at high risk for schizophrenia, published in the Schizophrenia Bulletin, presented the hypotheses, research design, results obtained, and conclusions permissible in that area, as reported by the various investigators. The reader could readily judge the pertinence and validity of the reviewer's critique. In contrast, the reviews of the adoption studies to be found in the critical essays by Gottesman and Shields (1976) and by Lidz (1976) suffer from a selective and incomplete presentation of the data obtained in the studies under examination, the omission of important conclusions, and the paraphrasing