Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AFFECT”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources
PubMed2004

Do the siblings of schizophrenia patients demonstrate affect perception deficits?

Affect perception deficits have been extensively documented in schizophrenia and are associated with the social dysfunction that is characteristic of this disorder. The two previous studies examined facial affect perception in genetically at-risk samples and yielded mixed results. The current study was designed to provide a rigorous test of affect perception abilities among schizophrenia patients (n=58), their biological siblings without psychosis (n=51), and nonpsychiatric controls (n=49). Participants completed three measures of affect perception, including facial, vocal, and combined modality. Schizophrenia patients performed significantly worse than controls on two of the three affect perception tests as well as a composite index based on all three tests. The performance of the sibling group fell between the patient and control groups on each of the affect perception tests. However, group differences achieved statistical significance only for the composite index with the siblings performing significantly worse than controls and significantly better than the schizophrenia group. These findings demonstrate that subtle deficits in affect perception are detectable in the unaffected siblings of schizophrenia patients when multiple measures of different types of affect perception abilities are used in combination.

Adult↗
PubMed2001

Gender ratio differences between Parkinson's disease patients and their affected relatives.

Mitochondrial dysfunction in Parkinson's disease (PD) is suspected to arise from either acquired or inherited mutation of mitochondrial DNA (mtDNA). If inherited, epidemiologic analysis may reveal maternal transmission. We looked for maternal inheritance bias in our PD clinical database. About 13% of 600 PD probands reported an affected parent. Although 60% of the PD probands were male, only 42% of the affected parents were. The gender ratios for the proband and affected parent generations were dissimilar (p<0.005), indicating an underrepresentation of affected fathers or an overrepresentation of affected mothers. To address these possibilities we analyzed a non-PD control cohort. Four percent of the controls had a PD affected parent, and 75% of these affected parents were male. Apparent maternal inheritance bias in our PD cohort is therefore more likely due to overrepresentation of affected mothers, and is consistent with mitochondrial inheritance in some of our ascertained cases.

Journal Article↗
PubMed2001

Body image, strategies to change muscles and weight, and puberty: do they impact on positive and negative affect among adolescent boys and girls?

The purpose of this study was to examine the impact of strategies to both decrease weight and increase muscle tone on negative (depression, anxiety) and positive affect among adolescent males and females. The respondents were 1185 adolescents (587 males, 598 females) who were enrolled in grades 7 and 9 (mean age for males=13.22 years; mean age for females=13.21 years). Respondents completed the Body Image and Body Change Inventory that assessed body image satisfaction, body image importance, body change strategies to decrease weight, body change strategies to increase muscle tone, and food supplements. Respondents also completed the Pubertal Development Scale, the depression and anxiety scales of the Depression Anxiety and Stress Scale, and the positive affect items from the Positive and Negative Affect Scale. Structural equation modelling was used to determine how body satisfaction and importance, body change strategies, and puberty impacted on depression, anxiety, and positive affect. The results demonstrated that for both boys and girls, there was a strong association between body change strategies and negative affect. For boys, body dissatisfaction did not predict negative affect, although this was a strong predictor for girls. Body change strategies did not strongly predict positive affect for either boys or girls, although body image satisfaction was a strong predictor for both genders. The implications of these findings for obtaining a better understanding of the role of pubertal development, body image, and body change strategies in predicting positive and negative affect among adolescent males and females are discussed.

Journal Article↗
PubMed2000

Effects of age at onset on the power of the affected sib pair and transmission/disequilibrium tests.

Information on the age of a patient at disease onset, an important feature of complex diseases, is often collected in studies designed to map the disease genes. Penetrance-model-free methods, requiring no specification of penetrance functions, have been used extensively for detecting linkage and association between marker and disease loci. In this paper, we conduct an analytical study to examine the effects of incorporation of age at onset information on the power of two commonly used penetrance-model-free methods, the affected sib-pair (ASP) and transmission/disequilibrium tests (TDT). Assuming a Cox model with a major gene effect for the age at onset, we quantify analytically how age at onset affects the identity by descent (IBD) probabilities, the mean IBD values, and the expected numbers of alleles transmitted from heterozygous parents to affected children under various genetic models. We show that the power of the mean IBD test and the TDT can be greatly affected by the ages at onset of affected siblings or children used in the study. Generally, the most powerful test for ASPs is that based on affected sib pairs both having early disease onset and for TDT analyses is that based on trios with early-onset children. Naively combining affected sib pairs with different ages at onset or parent-children trios with different ages at onset of affected children can result in reduced power for detecting linkage or association. These results may be used to guide collection and analysis of sib pairs or families for diseases with variable age at onset.

Adult↗
PubMed1992

Clients/patients with a principal diagnosis of affective disorder served in the inpatient, outpatient, and partial care programs of specialty mental health organizations, United States, 1986.

Of the 1.7 million persons under care on April 1, 1986 in the psychiatric inpatient, outpatient, and partial care programs of specialty mental health organizations nationwide, approximately 365,500 persons, or 22 percent, had a principal diagnosis of affective disorder. The vast majority of these persons, 84 percent, were under care in outpatient programs; 10 percent, in inpatient programs; and 6 percent, in partial care programs. Approximately 833,000, or 21 percent, of the 3.9 million persons admitted during 1986 to these same psychiatric programs had a diagnosis of affective disorder. Fifty-nine percent of persons with affective disorders were admitted to inpatient programs; 37 percent, to outpatient programs; and 4 percent, to partial care programs. Overall, most persons with affective disorders admitted to and under care in each of the three program types were female, white, and between the ages of 25 and 64. Most persons admitted to and under care in inpatient and partial care programs had a history of prior inpatient mental health care, while most persons in outpatient programs had never been treated in an inpatient psychiatric care setting. The principal source of payment used by persons with affective disorders varied by type of program setting. Blue Cross or other commercial insurance was the most common source of payment used by persons within inpatient programs, personal resources were used most often by persons under care in outpatient programs, and some type of public funds was used most often within partial care programs. Most persons with affective disorders were referred to inpatient and outpatient programs by family or friends, or were self-referrals. Most persons in partial care programs with affective disorders were referred to the program by an inpatient, outpatient, or another partial care mental health service. Services received by persons with affective disorders also varied by program setting. In general, drug and individual therapy were the leading types of treatment provided in inpatient programs. Individual therapy was the leading type of treatment provided, followed by drug therapy, in outpatient programs. Within partial care programs, no single type of treatment predominated.

Adult↗
PubMed1998

Two commonly expanded CAG/CTG repeat loci: involvement in affective disorders?

An association between bipolar affective disorder and CAG/CTG trinucleotide repeat expansions (TRE) has previously been detected using the repeat expansion detection (RED) method. Here we report that 89% of RED products (CAG/CTG repeats) > 120 nt (n = 202) detected in affective disorder patients as well as unaffected family members and controls correlate with expansions at two repeat loci, ERDA1 on chromosome 17q21.3 and CTG18.1 on 18q21.1. In a set of patients and controls in which we had previously found a significant difference in RED size distribution, the frequency of expansions at the CTG18.1 locus was 13% in bipolar patients (n = 60) and 5% in controls (n = 114) (P < 0.07) with a significantly different size distribution (P < 0.03). A second set of patients were ascertained from 14 affective disorder families showing anticipation. Twelve of the families had members with RED products > 120 nt. The RED product distribution was significantly different (P < 0.0007) between affected (n = 53) and unaffected (n = 123) offspring. Using PCR, a higher frequency (P < 0.04) of CTG18.1 expansions as well as a different (P < 0.02) repeat size distribution was seen between affected and unaffected offspring. In addition, a negative correlation between RED product size and the age-of-onset could be seen in affected offspring (rs = -0.3, P = 0.05, n = 43). This effect was due to an earlier onset in individuals with long CTG18.1 expansions. No difference in ERDA1 expansion frequency was seen either between bipolar patients (35%, n = 60) and matched controls (29%, n = 114), or between affected and unaffected offspring in the families. We conclude that expanded alleles at the CTG18.1 locus confers an odds ratio of 2.6-2.8 and may thus act as a vulnerability factor for affective disorder, while the ERDA1 locus seems unrelated to disease.

Bipolar Disorder↗
PubMed2001

Novel animal models of affective disorders.

Is there an appropriate animal model for human affective disorders? The traditional difficulties in accepting animal models for psychopathology stem from the argument that there is no evidence for concluding that what occurs in the brain of the animal is equivalent to what occurs in the brain of a human. However, if one models any or some core aspects of affective disorder, this model can become an invaluable tool in the analysis of the multitude of causes, genetic, environmental, or pharmacological, that can bring about symptoms homologous to those of patients with affective disorders. Animal models can also allow the study of the mechanisms of specific behaviors, their pathophysiology, and can aid in developing and predicting therapeutic responses to pharmacologic agents. Although animals exhibit complex and varied social and emotional behaviors for which well-validated and standardized measures exist, an understanding that a precise replica of human affective disorders cannot be expected in a single animal model is crucial. Instead, a good animal model of a human disorder should fulfill as many of the four main criteria as possible: (1) strong behavioral similarities, (2) common cause, (3) similar pathophysiology, and (4) common treatment. An animal model fulfilling any or most of these criteria can be used to elucidate the mechanisms of the specific aspect of the model that is homologous to the human disorder. A wide range of animal models of affective disorders, primarily depression, has been developed to date. They include models in which "depressive behavior" is the result of genetic selection or manipulation, environmental stressors during development or in adulthood, or pharmacologic treatments. The assessment of these animal models is based either on behavioral tests measuring traits that are homologous to symptoms of the human disorder they model, or behavioral tests responsive to appropriate pharmacologic treatments. The goal of this review is to focus on relatively recent developments of selected models, to aid in understanding their strengths and weaknesses, and to help those choosing the difficult task of developing novel animal models of affective disorders. The ideal animal model of affective disorders of the future would be an endogenous, genetic model that reiterates the essential, core aspects of the human disease and responds to the standard regimens of therapy. Because complex diseases have been approached from the genetic startpoint by using rodent models, a genetic model of affective disorder would open up possibilities for genetic analysis of polygenic traits that seem to underlie these disorders.

Animals↗
PubMed1981

Depressive disorders and HLA: a gene on chromosome 6 that can affect behavior.

To determine whether HLA-linked genes on chromosome 6 influence susceptibility to depressive disorders, we tested hypotheses concerning the distribution of HLA haplotypes among specific constellations of affected and unaffected family members. HLA haplotype identity among pairs of affected siblings in families with two affected siblings and among pairs of older unaffected siblings in families with one or two affected siblings was increased over random expectation (P less than 0.005). There was no increase in HLA haplotype identity among affected siblings in sibships with more than two affected members. When parents had a relative difference in estimated load of genes for susceptibility, HLA haplotypes were randomly transmitted to unaffected or affected children from the affected, "high-load" parent, but not from the unaffected, "low-load" parent (P less than 0.001). These results locate a gene contributing to susceptibility to depressive illness on chromosome 6 and provide a second example of the value of the hypotheses in defining the genetic bases of nonmendelian, familial diseases.

Adolescent↗
PubMed1999

A Colombian family with X-linked juvenile retinoschisis with three affected females finding of a frameshift mutation.

X-linked retinoschisis (XLRS) is a vitreoretinal disease responsible for most cases of juvenile macular degeneration in males. Retinoschisis carrier females generally manifest no pathological symptoms. However, a large affected family from Colombia presented three affected females with typical RS phenotype similar to their 27 affected male relatives. Fundus examination as well as electroretinograms (ERG) indicate that the disease in these three affected females is as severe as in their affected male counterparts. DNA sequence analysis of the XLRS1 gene in the affected members of this family indicates a single base (G) deletion at the 639 base position (639delG). This deletion causes a frameshift during translation and results in a larger (235 amino acids) than normal peptide (224 amino acids) with grossly altered discoidin domain, which is considered critical for the cellular function of the protein. The co-segregation of this gene mutation with the RS phenotype and the RS carrier status as well as its complete absence in normal controls indicates that this genetic change is responsible for the RS pathology in this family. This (639delG) is a novel RS mutation and reported here for the first time. Furthermore, the analysis of the three affected females indicates that the RS pathology in affected females (a very rare occurrence) is due to XLRS1 mutations carried on both of their X chromosomes.

Adolescent↗
PubMed1993

Genetic studies of affective disorders: should we be starting with childhood onset probands?

OBJECTIVE: The objective of this study is to test whether the presence of childhood onset affective disorder identifies families with increased incidence and severity of affective disorders. METHOD: Family history information was collected on the first and second degree relatives and first cousins age > or = 15 years of 22 children with bipolar affective disorder, 54 children with major depressive disorder, and 31 psychiatrically normal children. RESULTS: Compared with the relatives of normal children, relatives identified through children with bipolar affective disorder or major depressive disorder had elevated rates of affective disorders and increased severity of affective disorders as judged by earlier age of onset and increased suicide attempts. Segregation analyses could reject purely environmental transmission of illness. CONCLUSION: Ascertaining families through childhood onset affective disorder probands identifies extended pedigrees with high incidence and severity of affective disorders. These families may be more appropriate for genetic analyses than are families of adult probands.

Adolescent↗
PubMed1994

Prevalence of affective disorder in the child and adolescent offspring of a single kindred: a pilot study.

OBJECTIVE: The study determined the prevalence of psychiatric disorders among the child and adolescent offspring of an extended family identified through a proband with bipolar affective disorder. METHODS: All of the not mentally retarded offspring (ages 6 to 17 years) of a single extended bipolar affective disorder pedigree were studied. Data regarding psychiatric diagnoses, intelligence, school achievement, temperament, and family functioning were collected using structured and standardized instruments. RESULTS: When the child and adolescent offspring were stratified by degree of genetic relationship to an adult with an affective disorder, there were no differences in demographic variables, IQ, school achievement, or most temperamental and family characteristics. In contrast, there were increases in the rates of affective disorders and disruptive behavior disorders in the offspring that correlated with the degree of genetic relationship to an affected adult. CONCLUSIONS: The risk of developing an early onset affective disorder is correlated with the degree of genetic relatedness to affected adults in this single, extended family. This pilot study demonstrates that the inclusion of extended relatives in high-risk studies can enhance the discrimination of genetic and environmental contributions to the development of affective disorders.

Adolescent↗
PubMed1996

Origins of comorbidity between conduct and affective disorders.

OBJECTIVE: This analysis used methods of structural equation modeling to assess the extent to which comorbidity between conduct and affective disorders could be explained by (1) common or correlated causal factors that influenced both outcomes or (2) reciprocal causation between these conditions. METHOD: Data were obtained during the course of a 16-year longitudinal study of a birth cohort of New Zealand children. The data analyzed comprised measures of conduct and affective disorders at ages 15 and 16 years and data on a series of antecedent childhood factors. RESULTS: Structural equation modeling suggested that a substantial component of the comorbidity between conduct and affective disorders arose because the risk factors associated with the development of conduct disorders in teenagers overlapped and were correlated with the risk factors for adolescent affective disorders; of the shared variance between conduct disorder and affective disorders, more than two thirds was explained by common risk factors. These conclusions were replicated using diagnostically scored measures and methods of categorical data analysis. Model extensions suggested an absence of direct causal pathways between conduct and affective disorders. CONCLUSIONS: A substantial amount of the correlation and comorbidity between conduct and affective disorders arises because the risk factors and life pathways that predispose adolescents to one outcome are also associated with the risk factors and life pathways that predispose adolescents to the other outcome. Nonetheless, even after control for common causal factors, there was evidence of some unexplained comorbidity between conduct and affective disorders.

Adolescent↗
PubMed2006

'Bow and lean test' to determine the affected ear of horizontal canal benign paroxysmal positional vertigo.

OBJECTIVE: One of the problems in the management of horizontal semicircular canal benign paroxysmal positional vertigo (HSC-BPPV) is the difficulty in determining the affected ear using Ewald's second law. The purpose of this study is to develop the new "bow and lean test (BLT)" to easily determine the affected ear of HSC-BPPV and evaluate its efficiency. METHODS: We compared the efficiency between the classic method and BLT in 26 patients with HSC-BPPV. The classic method is based on Ewald's second law comparing the intensity of nystagmus or symptoms in the head roll test. BLT is based on the direction of both "bowing nystagmus" and "leaning nystagmus" at the head's bowing and leaning state in a sitting position. The affected ear is the same direction of bowing nystagmus in canalolithiasis and the same direction of leaning nystagmus in cupulolithiasis. RESULTS: In 26 patents (15 canalolithiasis, 11 cupulolithiasis), 3 (11.5%) patients did not show a prominent affected ear in the classic method, and 7 (26.9%) patients showed the different affected ear between the two methods. All 10 patients were successfully treated with just one trial of barbecue rotation based on the affected ear in BLT. Three patients did not show any bowing or leaning nystagmus. The side with canal paresis in all four patients, who showed significant canal paresis in bithermal caloric tests, was equal to the affected ear based on BLT. CONCLUSIONS: The "bow and lean test" (also called "Choung's test") is a new method that can easily determine the affected ear of HC-BPPV.

Adolescent↗
PubMed1983

Mutations that affect neural cell lineages and cell fates during the development of the nematode Caenorhabditis elegans.

We have described 19 genes that affect neural cell lineages and cell fates during the development of C. elegans. These genes differ markedly in the nature, breadth, and specificity of their effects. Their only obvious common characteristic is that they all lack specificity for the nervous system, affecting both neural and nonneural development. For some of these genes (lin-5, lin-6, unc-59, unc-85), this nonspecificity probably reflects a general utilization of their products in cellular replication. In contrast, most of these genes appear to be highly specific in their effects, but their specificity is not on the basis of cell type but rather on the basis of some particular aspect of development. Specifically, unc-83 and unc-84 mutations affect certain precursor cells that generate both neural and nonneural descendants; lin-22 and lin-26 mutants lead to the generation of supernumerary neural cells with a concomitant loss of nonneural cells; lin-4, lin-14, lin-28, and lin-29 mutants perturb global aspects of developmental timing, altering the time of appearance (or preventing the appearance) of both neural and nonneural cells; lin-1, lin-8, lin-9, and lin-15 mutations affect the cell lineages of certain nonneuron -producing ectoblasts in hermaphrodites and of homologous neuron-producing ectoblasts in males; lin-12 mutations affect many sets of nonidentical homologs (cells of similar lineage history that express different fates), only some of which are neural; ced-3 mutations prevent all programmed cell deaths, again only some of which are neural. Of these 19 genes, only unc-86 is specific for neural as opposed to nonneural cell lineages. However, some unc-86 mutants are abnormal in chromosome segregation at meiosis, indicating that this gene also may affect nonneural aspects of development. One implication of these observations is that genes (and molecules) involved in neural development are likely to function in nonneural development as well. The genes lin-22, lin-12, unc-86, and ced-3 may play decision-making roles during C. elegans neurogenesis, as mutations in each of these genes cause specific transformations in the fates of particular cells. These genes and others like them may act within a hierarchy to effect decisions at different levels within cell lineages. For example, lin-22 animals display transformations affecting entire postembryonic cell lineages, unc-86 animals are altered at an intermediate level of certain cell lineages, and ced-3 animals are affected only in the ultimate fates of cells produced by terminal cell divisions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2004

Psychosocial variables in children and teens of extended families identified through bipolar affective disorder probands.

OBJECTIVES: This multi-site study investigated the frequency of risk-related variables for developing an affective disorder using a within-pedigree control group. We wished to determine the effect of life events, social relationships, self-perceived competence, and aspects of home environment for youngsters from extended families with loading for bipolar disorder. Using a within-family contrast group, we address the following two issues: (1) Do offspring or their parents from families who do and do not have an affected parent report differences (i) in home environment? (ii) in frequency and type of offspring life events? and (iii) in social relations and self-perception? and (2) Do children or their parents who do or do not have an affective disorder report differently on these areas? METHODS: Juvenile offspring (n = 50) and their parents from 14 bipolar pedigrees were assessed. Structured interviews and self- or parent-reported instruments were used to compare offspring with an affected first-degree relative to those without and to compare offspring with or without an affective disorder. RESULTS: Only one significant psychosocial difference was found between offspring with or without a parent with an affective disorder but several were found between offspring who themselves did or did not have an affective disorder. These differences are in the areas of the need for discipline, social support, and dependent negative life events. CONCLUSIONS: The findings identify potential early psychosocial markers for affective disorder in high risk offspring.

Adolescent↗
PubMed2006

Relationship between depressive affect and malnutrition-inflammation complex syndrome in haemodialysis patients.

BACKGROUND: Depression is associated with high mortality in haemodialysis (HD) patients, and can be associated with the poor oral intake that contributes to malnutrition. Malnutrition-inflammation complex syndrome (MICS) causes increased morbidity and mortality in HD patients. We investigated relationships between depressive affect, social support and various components of MICS in HD patients. METHODS: The subjects were 110 patients (65 men and 45 women, mean age 45.39 +/- 14.73 years) on maintenance HD. The Beck Depression Inventory (BDI), Cognitive Depression Index (CDI), and the Multidimensional Scale of Perceived Social Support (MSPSS) were used to assess aspects of depressive affect in each subject. RESULTS: The mean dialysis duration was 53.04 +/- 38.15 months. The mean BDI and CDI scores were 12.10 +/- 7.43 and 8.40 +/- 5.72, respectively. Patients were divided into two subgroups according to CDI score (depressive affect >10 (n = 71) and non-depressive affect <or=10 (n = 39)). CDI score was correlated with malnutrition-inflammation score (MIS) (r = 0.24; P < 0.05), haemoglobin level (r = -0.23; P < 0.05) and MSPSS score (r = -0.28; P < 0.01). The subgroup with depressive affect had higher MIS (P < 0.01) and lower social support (P = 0.001) than the non-depressive affect group. Logistic regression analysis identified high MIS and low MSPSS score as independent risk factor for depression. CONCLUSIONS: The results suggest that MIS and MSPSS are the strongest predictors of depressive affect in HD patients. Further research is needed to understand the causal relationship between depressive affect and MICS in HD patients.

Adult↗
PubMed1996

Patterns of diagnoses, comorbidities, and treatment in late-middle-aged and older affective disorder patients: comparison of mental health and medical sectors.

OBJECTIVE: To compare the diagnoses, psychiatric and medical comorbidities, and prior and current treatment received by late-middle-aged and older affective disorder patients in mental health and medical service settings and to identify predictors of these patients' length of inpatient care. DESIGN: Department of Veterans Affairs (VA) nationwide databases are used to examine the prevalence, diagnoses, and inpatient and outpatient treatment received by affective disorder patients in mental health and medical units in Fiscal Year 1990. RESULTS: Compared with late-middle-aged and older index medical patients (n = 11,701), index mental health patients (n = 9039) were more likely to have affective psychoses and major depressive disorder and less likely to have depressive disorder NOS. Almost 60% of affective disorder patients in mental health settings had comorbid psychiatric diagnoses; this was true of 30% of patients in medical settings. Moreover, more than 80% of affective disorder patients in mental health settings had concomitant medical disorders. Affective disorder patients also had very high rates of prior mental health and medical care. Patients who had more severe affective disorders and comorbid psychiatric and medical diagnoses had longer episodes of inpatient care; in contrast, more intensive prior medical and mental health outpatient care was associated with shorter episodes of inpatient care. CONCLUSIONS: The findings highlight affective disorder patients' high rates of comorbidity and intensive use of health care resources, emphasize the value of outpatient care in reducing the amount of subsequent inpatient care, and underscore the need for closer integration of mental health and medical care.

Age Distribution↗
PubMed2001

Affective-prosodic deficits in schizophrenia: comparison to patients with brain damage and relation to schizophrenic symptoms [corrected].

OBJECTIVE: Although affective prosody seems to be a dominant and lateralised communication function of the right hemisphere, focal lesions of either hemisphere may cause problems with its modulation. When impairment occurs after brain damage, the profiles of affective-prosodic disturbances differ depending on the hemisphere injured. Patients with left brain damage (LBD) improve their performance whereas patients with right brain damage (RBD) do not when the verbal-articulatory demands of the test stimuli are reduced systematically. One of the major arguments for a right hemispheric contribution to schizophrenia has been the documentation of affective prosodic deficits under the assumption that these abnormalities reflect right hemispheric dysfunction. Thus, an essential question to resolve is whether the profile of affective prosodic disturbances in schizophrenia is similar to LBD or RBD, or represents a unique variation. METHODS: Data were collected from four subject groups: 45 chronic, medication-stabilised, schizophrenic patients, 10 patients with focal LBD, nine patients with focal RBD, and 19 controls. All groups were tested on the aprosodia battery, which uses stimuli having incrementally reduced verbal-articulatory demands. Schizophrenic and aphasic symptoms were evaluated using standard assessment tools. RESULTS: For patients with impaired performance on the aprosodia battery, schizophrenic patients were statistically identical to patients with RBD and robustly different from those with LBD. Thirty eight schizophrenic patients (84.4%) were found to have some type of affective prosodic deficit with the predominant pattern indicating, at minimum, right posterior sylvian dysfunction (57.8%). When schizophrenic symptoms and aprosodic deficits were examined using a principal component analysis, affective comprehension and repetition loaded uniquely as separate factors. CONCLUSIONS: The profile of affective-prosodic deficits found in impaired schizophrenic patients is characteristic of RBD, supporting the concept that schizophrenia is a bihemispheric disease process. These deficits may also represent cardinal symptoms of schizophrenia as they are highly prevalent and, except for spontaneous affective prosody, are not associated statistically with traditional clusters of schizophrenic symptoms.

Adult↗