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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Only recently has there been interest in the systematic study of insight in schizophrenia. The present investigation was designed to evaluate the specific relationship between psychopathological symptoms, neurocognitive deficits and awareness of illness in chronic schizophrenia. Fifty-eight outpatients with the DSM-III-R diagnosis of schizophrenia were rated on David's Schedule for Assessing Insight, the Positive and Negative Syndrome Scale (PANSS), the Calgary Depression Scale and the Wisconsin Card Sorting Test (WCST). Results indicate that there is a significant association among these variables and that approximately 44% of the variance in the dependent variable could be explained by this combination of independent variables. Notably, however, negative symptoms were only moderately inversely correlated with awareness of illness, and they were not associated with scores on the WCST. Moreover, neither negative symptoms nor per cent perseverative errors contributed significantly to the prediction of insight in schizophrenia. These findings argue against the notion that unawareness of illness is the product of neuropsychological dysfunction in the frontal lobes. Instead, the most significant associations and predictors of insight were related to the positive symptoms of schizophrenia.
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PMID:Insight, neurocognitive function and symptom clusters in chronic schizophrenia. 937 93

The statistical associations between stress and cardiovascular and other prevalent diseases have not been explained. Perceived stress, resulting in an uncontrollable defeat reaction, has been shown by James Henry (Henry 1993) to be followed by specific endocrine abnormalities, including sensitization of the hypothalamo-pituitary-adrenal (HPA) axis, and inhibited sex steroid and growth hormone secretions. With an elevated waist/hip circumference ratio (WHR)--a simple, surrogate, measurement of intraabdominal, visceral fat masses--combined with insulin resistance, similar endocrine perturbations are found. Based on considerable evidence, such endocrine abnormalities seem to be followed by accumulation of intraabdominal, visceral fat masses and insulin resistance, both powerful risk factors for cardiovascular disease, diabetes and stroke. A postulated chain of events is therefore that the endocrine perturbations are primary factors, followed by visceral fat accumulation, insulin resistance and other risk factors dependent on the hyperinsulinemia following insulin resistance. This highlights the importance of elucidating the cause(s) to the endocrine abnormalities. These are identical to those described by Henry (1993) to follow a stress reaction of a defeat type. Findings of several psychosocial and socio-economic handicaps might provide a basis for such a reaction, supported by experimental studies in primates. Furthermore, depression, anxiety, alcohol consumption and smoking, all known activators of the HPA axis, are also often found. The low sex steroid and growth hormone secretions might be secondary to the hypersensitive HPA-axis. They could also be caused by other factors, and are, each alone, capable of causing both visceral fat accumulation and insulin resistance. Visceral fat accumulation is only an indirect, surrogate measurement of the underlying endocrine abnormalities, but is useful for screening purposes on a population basis. Developments of novel techniques for sensitive, yet simple measurements of HPA axis activity under undisturbed conditions seem to allow a better definition of pathogenetic factors. Utilizing such methods, subgroups of the syndrome including visceral fat accumulation, insulin resistance and other associated risk factors (Metabolic Syndrome), are beginning to emerge. A more detailed information on noxious factors in society leading to a defeat reaction to perceived stress, endocrine abnormalities and the Metabolic Syndrome, with increased risk for prevalent disease may hopefully be developed by these new methods.
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PMID:Stress and cardiovascular disease. 940 28

Coined by Sifneos in 1972, alexithymia refers to a relative narrowing in emotional functioning, an inability to find appropriate words to describe their emotions, and a poverty of fantasy life. Although initially described in the context of psychosomatic illness, alexithymic characteristics may be observed in patients with a wide range of medical and psychiatric disorders: Parkinson disease, depression, anxiety, substance abuse and eating disorders. Flattening of affect and poverty of speech, major negative symptoms, referred to chronic schizophrenia: there is a lack of outward display of emotions. Accordingly, some disturbances of alexithymia's scores would be expected in schizophrenic patients. The aims of this study were: first to establish some correlations between alexithymia and some symptoms of schizophrenia, and second to estimate the intensity of alexithymia in negative versus positive and undifferentiated schizophrenic patients. Twenty-nine patients, meeting DSM III-R criteria for schizophrenia have been studied. All of them treated by neuroleptics, were in a stable clinical status for at least one month. The patients were assessed by one trained psychiatrist (IN) using six rating scales: Beth Israel Questionnaire (BIQ) for alexithymia, Positive and Negative Syndrome Scale (PANSS), Depressive Retardation Rating Scale (DRRS), Montgomery and Asberg Depression Rating Scale (MADRS), revised Physical Anhedonia Scale (PAS), and finally, Extrapyramidal Symptom Rating Scale (ESRS). In the total sample, the mean score of BIQ was 4.79 +/- 1.68 (mean +/- SD). Significant correlations were found between alexithymia and blunted affect (r = 0.376; p < 0.05), poverty of speech (r = 0.471; p < 0.01), anxiety (r = 0.370; p < 0.05), total score of DRRS (r = 0.370; p < 0.05), and motor subscore of DRRS (r = 0.429; p < 0.05). The patients with negative symptoms of schizophrenia had significantly higher total scores in alexithymia (p < 0.05), blunted affect (p < 0.0001), poverty of speech (p < 0.0001), anxiety (p < 0.05), total score of DRRS (p = 0.01) and his motor subscore (p < 0.0001) as compared to positive and undifferentiated subtypes. In our study, alexithymia seems to be correlated with negative and depressive symptoms in negative forms of schizophrenia, regardless of medication status.
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PMID:[Negative symptoms, depression, anxiety and alexithymia in DSM III-R schizophrenic patients]. 941 92

Coined by Sifneos in 1972, alexithymia refers to a relative narrowing in emotional functioning, an inability to find appropriate words to describe their emotions and, a poverty of fantasy life. Although initially described in the context of psychosomatic illness, alexithymic characteristics may be observed in patients with a wide range of medical and psychiatric disorders: Parkinson disease, depression, anxiety, substance abuse and eating disorders. Flattening of affect and poverty of speech, major negative symptoms, referred to chronic schizophrenia: there is a lack of outward display of emotion. Accordingly, some disturbances of alexithymia's scores would be expected in schizophrenic patients. The purpose of this study was to estimate and compare the prevalence of alexithymia in deficit and non-deficit schizophrenia. The term "deficit symptoms" may be used as Carpenter, to refer specifically to those negative symptoms that are not considered secondary. The influence of patients' symptoms has also been studied on alexithymia scores: negative and positive symptoms of schizophrenia, depression, anxiety, anhedonia and effects of neuroleptics. Twenty-five patients, meeting DSM III-R criteria for schizophrenia have been studied. All of them treated by neuroleptics, were in a stable clinical status for at least one month. The patients have been categorized into deficit (n = 12) and non-deficit (n = 13) subgroups by one trained psychiatrist (SD), using the Schedule for the Deficit Syndrome. The subjects have been assessed by the same rater (IN), blind to deficit status, using six rating scales: Beth Israel Questionnaire (BIQ) and Toronto Alexithymia Scale (TAS) for alexithymia, Positive and Negative Syndrome Scale (PANSS), Montgomery and Asberg Depression Rating Scale (MADRS), revised Physical Anhedonia Scale (PAS), and finally, Extrapyramidal Symptom Rating Scale (ESRS). Using TAS, alexithymic characteristics were more prevalent in the deficit subgroup as compared to non-deficit subgroup (83% versus 30.76%; p < 0.01). Significant correlations were observed in the non-deficit subgroup between: TAS and anxiety (r = 0.743; p < 0.01), TAS and depression (r = 0.568; p < 0.05), BIQ and blunted affect (r = 0.636; p < 0.02), BIQ and poverty of speech (r = 0.629; p < 0.02). These correlations were not significant in the deficit group of patients. Alexithymia in schizophrenic patients seems to be a trait characteristic in deficit patients, and a state related to many symptoms, such as flattening of affect, poverty of speech, depression and anxiety in nondeficit patients.
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PMID:[Alexithymia in negative symptom and non-negative symptom schizophrenia]. 945 28

The Calgary Depression Scale for Schizophrenia (CDSS) is a nine-item structured interview scale developed by Addington et al. to assess depression in schizophrenics. This paper describes the testing of the reliability and validity of the French version of the CDSS in a population of 70 schizophrenic patients. The validity of the CDSS as a measure of depression was confirmed; a single factor accounted for 41% of the variance of the nine items. The total score on the CDSS was strongly correlated with those on the Montgomery-Asberg Depression Rating Scale (MADRS), the Hamilton Depression Rating Scale (HDRS) and also the G6 item (depression) of the Positive and Negative Syndrome Scale (PANSS). The correlation with the Psychomotor Retardation Scale (ERD) total score was much less significant and was better with the 'subjective' subscore. The internal consistency was good, with a Cronbach's alpha of 0.79. A high level of inter-rater reliability was observed (weighted kappa values were >0.75 in all cases). The CDSS has a lower stability over time than other depression scales. It is a simple, quick and reliable scale for assessing depression in schizophrenic populations.
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PMID:Calgary Depression Scale for Schizophrenia: a study of the validity of a French-language version in a population of schizophrenic patients. 950 1

In a multicenter, double-blind, parallel group trial, the efficacy of risperidone (RIS) was compared with a combination of haloperidol and amitriptyline (HAL/AMI) over 6 weeks in patients with coexisting psychotic and depressive symptoms with either a schizoaffective disorder, depressive type, a major depression with psychotic features, or a nonresidual schizophrenia with major depressive symptoms according to DSM-III-R criteria. A total of 123 patients (62 RIS; 61 HAL/AMI) were included; the mean daily dosage at endpoint was 6.9 mg RIS versus 9 mg HAL combined with 180 mg AMI. Efficacy results for those 98 patients (47 RIS; 51 HAL/AMI) who completed at least 3 weeks of double-blind treatment revealed in both treatment groups large reductions in the Positive and Negative Syndrome Scale-derived Brief Psychiatric Rating Scale (RIS 37%; HAL/AMI 51%) and the Bech-Rafaelsen Melancholia Scale total scores (RIS 51%; HAL/AMI 70%). The reductions in the Brief Psychiatric Rating Scale and the Bech-Rafaelsen Melancholia Scale scores in the total group were significantly larger in the HAL/AMI group than in the RIS group (p < 0.01), mostly because of significant differences in the subgroup of patients suffering from depression with psychotic features, whereas treatment differences in the other diagnostic subgroups were not significant. The incidence of extrapyramidal side effects as assessed by the Extrapyramidal Symptom Rating Scale was slightly higher under RIS (37%) than under HAL/AMI (31%). Adverse events were reported by 66% of RIS and 75% of HAL/AMI patients. The results of this trial suggest that the therapeutic effect of HAL/AMI is superior to RIS in the total group of patients with combined psychotic and depressive symptoms. However, subgroup differences have to be considered.
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PMID:Risperidone versus haloperidol and amitriptyline in the treatment of patients with a combined psychotic and depressive syndrome. 955 96

In the present pilot study, our aim was to investigate whether associations could be demonstrated in psychiatric patients between the changes in plasma lipid and lipoprotein levels expected during treatment with psychoactive drugs and the changes in the patients' depressive and hostile behavior. One hundred and fourteen patients with various psychiatric disorders (depressive episode in bipolar affective disorder, depressive episode or recurrent depressive disorder, paranoid schizophrenia, and schizoaffective disorders) were included in the study. The following examinations were carried out in each patient on admission and at discharge: (1) the plasma lipid parameters total cholesterol (TC), low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), high-density lipoprotein (HDL), and triglycerides (TRI) were determined, and (2) the psychopathological features were recorded employing the AMDP system and the AMDP Syndrome Scales. Within the context of a naturalistic clinical setting with a choice of psychoactive drugs available, patients were subdivided at the end of treatment into eight treatment groups, as follows: group 1, treatment with butyrophenones; group 2, treatment with tricyclics; group 3, treatment with butyrophenones and tricyclics; group 4, treatment with butyrophenones, tricyclics and selective serotonin reuptake inhibitors; group 5, treatment with butyrophenones and lithium; group 6, treatment with tricyclics and lithium; group 7, treatment with butyrophenones, tricyclics and lithium; and group 8, treatment with butyrophenones, tricyclics, selective serotonin reuptake inhibitors and lithium. To compare the changes in the eight treatment groups, mixed general linear models including diagnosis, gender, age, body mass index changes, and baseline values were applied using proc GLM of SAS. Butyrophenones induce an increase in TC, LDL, and TC/TRI ratio, whereas tricyclics lead to an increase in TC, LDL, VLDL, and TRI. In combined medication of butyrophenones and tricyclics the effects of tricyclics predominate. Comedication of lithium inhibits the increase in TC and LDL induced by butyrophenones and/or tricyclics. Treatment groups with lipid changes of the same type (decrease, no change, or increase) were combined in "lipid change groups". Analyses of variance or covariance (with psychopathological admission value as covariate where there were significant differences in psychopathological admission mean values between the groups) of these lipid change groups with regard to the changes in the Depressive Syndrome Scale and the Hostility Syndrome Scale gave results which are interpreted as follows: an increase in TC or LDL inhibits the remission of hostility, whereas an increase in TRI with concomitant decrease in TC, or else a relatively greater increase in TRI than in TC promotes the remission of hostility. A decrease in TRI or VLDL promotes the remission of depression. Our data and findings published in the literature may suggest that systemic changes in plasma lipid parameters, at the cellular level, induce changes in the fluidity of brain cell membranes. We hypothesize that an increase in plasma TC or LDL and/or a decrease in plasma TRI or VLDL may induce a relative decrease in brain cell membrane fluidity with decreased presynaptic serotonin reuptake and increased postsynaptic serotonin function. This proposed increase in brain serotonin function would finally result in an anti-depressive, aggression-promoting effect. Conversely, a decrease in plasma TC or LDL and/or an increase in plasma TRI or VLDL may induce a relative increase in brain cell membrane fluidity with increased presynaptic serotonin reuptake and decreased postsynaptic serotonin function. This proposed decrease in brain serotonin function would result in an anti-aggressive, depression-promoting effect.
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PMID:Are psychoactive-drug-induced changes in plasma lipid and lipoprotein levels of significance for clinical remission in psychiatric disorders? 956 10

This paper uses monthly symptom data on 90 first-onset schizophrenics in Madras, India, to characterize, in a continuous manner, the course of remission and relapse. Remission from the first episode occurs in about 6 months and in about 3 months for later episodes. Syndromes from the Present State Exam, assessed at the first episode, predict differentially to early and later parts of the course. Hypomania and simple depression predict early remission from the first episode; flat affect and grandiose delusions predict longer episodes and shorter remissions later in the course.
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PMID:Remission and relapse in schizophrenia: the Madras Longitudinal Study. 965 20

Research pertaining to the occurrence of depression and/or depression symptomatology after a Mild Traumatic Brain Injury (MTBI) was reviewed. We found that methodological differences such as the criteria used to assess MTBI and depression, time that elapsed since brain injury, and control group variations confounded comparisons across studies. Nevertheless, the studies are consistent with at least a 35% prevalence of, and left frontal damage with depression after MTBI, an overlap of symptoms of depression and Postconcussion Syndrome (PCS), and indicate that depression can continue for many years following the injury. Our conclusion is that MTBI is the triggering event for a set of pathophysiological changes and a concomitant depressive episode in a vulnerable subset of the population. Due to a paucity of research, it cannot be definitively concluded that the underlying substrates of depression seen after MTBI and clinical depression are the same. Implications for future investigations are discussed.
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PMID:Depression after mild traumatic brain injury: a review of current research. 965 12

A metabolic dysfunction contributes to the poor performance and mortality associated with Poult Enteritis and Mortality Syndrome (PEMS). Within 2 d after contact-exposed poults were removed from the presence of PEMS-infected poults and returned to their respective treatment rooms to infect experimental poults, the experimental poults began to huddle together and show signs of the disease. When separated from the huddle, body temperatures of exposure poults were depressed significantly. Body temperatures decreased progressively through 8 d after exposure with a maximum depression of 2 C and returned to a normal level at 18 d after PEMS exposure. Similar decreasing patterns in serum glucose, inorganic phosphorus, triiodothyronine, and thyroxine were observed, with maximum decreases in these serum constituents being found between 8 and 13 d after PEMS exposure. There were significant correlations among decreasing body temperatures, decreasing serum constituents, and mortality in the PEMS-exposed poults. Daily mortality rates associated with PEMS began at 6 d and peaked at 9 d after PEMS exposure. Mortality rates decreased from 9 to 15 d after experimental PEMS exposure. Depressions in serum constituents, body temperature, and increased mortality rates did not coincide with decreased feed intake associated with PEMS. Therefore, it was concluded that the agent(s) causing PEMS may have a direct effect on energy metabolism in afflicted poults.
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PMID:Hypothermia, hypoglycemia, and hypothyrosis associated with poult enteritis and mortality syndrome. 970 73


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