Biomedical subjects
Publications and source records attributed to P Cosyns.
This paper reports on the development of a videotape "Depression ... the answers" for use in cognitive behavioral therapy with depressed inpatients. 17 patients evaluated the videotape. The described psychoeducational video program was constructed as an introduction for, an opening to, and as a facilitation and clarification of the psychotherapeutic and pharmacological treatments.
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Recently, some authors have reported defective neutrophil phagocytosis during depression. The present study investigated neutrophil function in 19 healthy controls and in 41 depressed inpatients categorized according to DSM-III into minor, simple major, and melancholic depression. We determined neutrophil function by means of phagocytosis, chemotaxis, and superoxide release. The results show no significant differences in neutrophil function among any of the subtypes of depression and normal volunteers. This suggests that overall neutrophil function is normal during depression. Thus, neutrophils are unlikely to be involved in the increased susceptibility to physical illness of patients with depression.
Recently, true seasonal variation with significant periodicities (circannual, semiannual, circatrimensual, circabimensual) and a significant meteotropism have been observed in a number of self-rated characteristics of normal man (arousal, mood, physiology and social behaviour). In order to replicate these findings, two normal controls (a married couple) were asked daily to complete a self-rating scale concerned with the characteristics mentioned above during one calendar year. By means of time series analysis, significant rhythmicities with recurrent cycles in the autorhythmometric data of all of the above characteristics were found. An important part of the variance in these characteristics was found, using multiple regression, to be related to various weather variables, such as mean atmospheric pressure, temperature, relative humidity, wind speed, minutes of sunlight/day and precipitation/day. These results support the hypothesis that temporal variations in human psychological and physiological characteristics may be dictated by the composite effects of past and present atmospheric activity.
To date, there has been a small number of reports that severe depression is accompanied by disturbances in total white blood cell (i.e. leukocytosis) and leukocyte subset (i.e. neutrophilia, monocytosis, lymphopenia) counts. These results, however, have not yet been validated in a large-scale, well-controlled study. To this end, we have counted the number of leukocytes, monocytes, lymphocytes and granulocytes (neutrophils, eosinophils, basophils) in 22 healthy controls and in 109 depressed inpatients. We noted leukocytosis in major depressed patients compared with normal subjects, whilst minor depressives manifested intermediate findings. Leukocytosis was significantly more pronounced in major depressed males compared with major depressed females. Major depression related leukocytosis appears to be characterized by neutrophilia and monocytosis. There was a significant positive relationship between the overall severity of illness on one hand, and the degrees of leukocytosis, neutrophilia and monocytosis on the other. The total number of both phagocytic cell populations (i.e. monocytes and neutrophils) was significantly and positively related. Our results might point to the existence of an inflammatory process in major depressed subjects, particularly in males.
Pattern recognition methods were carried out on a sample of 80 depressed men, assessed by means of 14 items relevant to depressive symptomatology of the Structured Clinical Interview for DSM-III-R. 1985 edition (SCID). A cluster analysis generated two classes, which were described as a vital (n = 35) and a nonvital cluster (n = 45). Vital depressives were characterized by psychomotor disorders, loss of energy, cognitive disturbances, a distinct quality of mood, early morning awakening and nonreactivity (the "vital" symptoms). Our findings support the descriptive validity of the DSM-III melancholia diagnostic category, although the DSM-III criteria are too conservative and include nonrelevant symptoms (e.g., diurnal variation, anorexia-weight loss) whilst excluding some important items (e.g., loss of energy, cognitive disorders). Vital depressed men were significantly older, more severely depressed and they exhibited biological disturbances (abnormal dexamethasone suppression test, lower basal thyroid secreting hormone) as opposed to nonvital depressives. There are several arguments to support the possibility that both clusters constitute relevant stages in the overall severity of illness continuum, whilst showing qualitative differences with regard to the vital symptoms. In other words, both clusters are continuous categories within the overall severity of illness continuum and form discrete categories with regard to the vital symptoms. By merging the dimensional and categorical hypotheses, we were able to construct a new integrated threshold model: unipolar depression in men is probably a homogeneous disease with reference to overall severity of illness, but--as severity increases--vital symptoms emerge, grouping together into a distinct profile, i.e., vital depression.
Recently, some investigators have established a blunted natural killer cell activity (NKCA) in severely depressed patients. In order to replicate these findings NKC cytotoxicity assays--on fresh cell suspensions in human plasma and fetal calf serum--were performed in healthy controls and depressed inpatients. Instead of the commonly used 51Cr-release assay we have used a fluorescent NKC cytotoxicity assay, which allows a greater sensitivity. We observed a significantly blunted NKCA in melancholic patients as compared with healthy controls and minor depressives, whilst simple major depressives exhibited an intermediate position. NKC cytotoxicity assays in fetal calf serum were significantly and negatively correlated with the severity of illness. We were unable to establish any relationship between NKCA and measures of hypothalamic-pituitary-adrenal-axis function, such as baseline, postdexamethasone plasma cortisol and 24 hr urinary cortisol secretion. In addition, we did not find any effects of dexamethasone administration (1 mg orally) on NKCA.
Recently, there have been some reports that depression may be accompanied by indices of polyclonal B cell proliferation. In order to examine whether depression is characterized by an altered B cell subset profile we determined the number and percentage of the following B cells: HLADR+, CD19+, CD20+, and CD21+. We found a significantly increased number of HLADR+ and CD19+ B cells in depressed subjects compared with normal controls. Depressed patients exhibited a significantly higher percentage of HLADR+ and CD21+ B cells than normal controls. The number of CD21+ cells and the percentage of CD19+ cells were higher in melancholics than in normal controls. The increase in the number of the various B cells was highly sensitive (63%) and specific (94%) for melancholia. Our results may indicate B cell proliferation in depression, and particularly in melancholia.
Recently, a few reports have shown that severe depression may be associated with higher levels of positive acute phase proteins (APPs), such as haptoglobin (Hp), alpha 1-acid glycoprotein (alpha 1S) and lower levels of negative APPs (visceral proteins), such as albumin (Alb) and transferrin (Tf). In order to reassess whether depression is related to alterations in the expression of plasma APP concentrations, we measured in 84 normal controls and depressed inpatients positive APPs such as Hp, alpha 1-antitrypsin (alpha 1AT), hemopexin (Hpx), ceruloplasmin (Cp), complement component C3C and one visceral protein, i.e., retinol binding protein (RBP). We found increased plasma concentrations of Hp, alpha 1AT, and Cp in major depressed subjects as compared with healthy controls, with minor depressives exhibiting an intermediate position. RBP was significantly lower in minor and major depressives than in normal controls. The disorders in these proteins were rather sensitive (62%) for major depression, with a specificity equalling 96%. Our findings are compatible with the hypothesis that major depression may be accompanied by inflammatory changes with higher levels of positive APPs (i.e., alpha 1AT, Hp, Cp, alpha 1S) and lower levels of visceral proteins (i.e., RBP, Tf, Alb).
Several authors have reported attenuated adrenocorticotropin hormone (ACTH) responses to corticotropin releasing factor (CRF) administration in melancholic patients as compared with healthy controls. In order to explore the integrity of the hypothalamic-pituitary-adrenal (HPA)-axis in melancholics, we examined the following parameters in 98 subjects: the ACTH; beta-endorphin; and cortisol responses to ovine CRF (oCRF) (100 micrograms/i.v.); and the postdexamethasone cortisol values. We found significant lower CRF-induced ACTH responses in melancholic patients as opposed to healthy controls and minor depressives, while major depressives occupied an intermediate position. The psychopathological correlates of the blunted CRF-induced ACTH responses were feelings of worthlessness, self-reproach, or excessive guilt. The CRF-stimulated beta-endorphin and cortisol response did not differ between the study samples. Higher baseline plasma cortisol was associated with attenuated CRF-induced ACTH responses, but these effects were not pertinent to melancholia. There were no relationships between the disordered oCRF test results, and postdexamethasone cortisol values, age, body size, sex and severity of illness. The diagnostic power of the oCRF and the dexamethasone suppression test for melancholia is enhanced when both test results are combined.
This study investigated the leukocyte T helper and T suppressor-cytotoxic cell (sub)set profile of minor, simple major and melancholic depressives versus normal controls. Using both monoclonal antibody staining and flow cytometry, we determined the absolute numbers and percentages of the following T cell immune subsets: T helper (CD4+), T virgin (CD4+CD45+), T memory (CD4+CD45-), T suppressor/cytotoxic (CD8+), CD8+ T suppressor (CD8+CD57-) and CD8+ T cytotoxic (CD8+CD57+) cells. After computing the CD4+/CD8+ ratio, we detected a significantly increased ratio in depressed patients as compared with healthy controls. Depression per se is characterized by a higher percentage of CD4+ and a lower percentage of CD8+CD57- cells. Melancholic depressed subjects exhibit a significantly increased number of CD4+ and CD4+CD45- cells. The combined use of various percentages of CD4+ and CD8+ (sub)sets yields a high degree of marker positivity for melancholia: through cumulative evaluation of those percentages, the marker positivity increases to 68% (sensitivity) and the specificity is 95%. These results together with our previous reports may refer to a depression-related state of T cell activation.
In this study, we have measured the following biological variables in 78 depressed inpatients: adrenocorticotrophic hormone (ACTH) responses to corticotropin releasing factor (CRH: 100 micrograms intravenously), postdexamethasone cortisol and ACTH values, and circulating concentrations of L-tryptophan (L-TRP). Patients were categorized according to the DMS-III as (1) minor depression, (2) simple major depression, and (3) major depression with melancholia/psychotic features. By means of various pattern recognition methods, we determined whether these diagnostic groups constitute discrete biological classes or form relevant stages (i.e., continuous categories) in a continuum of progressing biological dysfunction. We established that unipolar depression constitutes one biological continuum characterized by a progression of lower CRH-induced ACTH responses, lower L-TRP levels, and higher postdexamethasone cortisol and ACTH values along the diagnostic spectrum. However, the biological differences in these markers between melancholia and minor depression are quantitatively prominent to the extent that they become qualitative. These findings support the biological heterogeneity hypothesis of melancholia. Simple major depression is a heterogeneous class with regard to the biological markers employed.
Recently, some researchers noted significant positive relationships between postdexamethasone serum cortisol and prolactin levels, whilst endogenous depressives exhibited a significantly lower suppression of prolactin by dexamethasone than non-endogenous patients or normal controls. To ascertain the extent of prolactin responses to dexamethasone in severely depressed patients, we measured 8 a.m. pre- and postdexamethasone prolactin levels in 104 depressed and 42 normal subjects. Serum cortisol levels were also determined in depressed patients before and after dexamethasone administration. We found a significant suppressive effect of dexamethasone on prolactin levels. There were no significant differences either in pre- or postdexamethasone prolactin, or in actual dexamethasone-induced decrements in prolactin between normal controls, melancholics, simple major or minor depressed subjects. We have not found any significant relationships between cortisol and prolactin, either under baseline or postdexamethasone conditions.
Several authors have reported enlarged lateral brain ventricles in major depressive patients as compared to healthy controls. Also, the enlargement of brain lateral ventricles has been related to delusions, psychomotor retardation and some biochemical data such as cortisol secretion and L-tryptophan serum levels. The present study was undertaken to investigate if melancholic depressives are characterised by a higher degree of brain atrophy than normal controls and minor depressives, the origin of any brain atrophy, and whether measures of brain atrophy are related to cortisol secretion and L-tryptophan serum levels. We investigated 10 healthy controls and 35 depressive patients categorised according to DSM-III. In contrast to previous studies, we determined a combination of indices which makes it possible to differentiate between central and cortical diffuse atrophy. We found no evidence for the existence of abnormal atrophy of the brain in melancholics; nor did we find any correlation between CT scan measurements and cortisol or tryptophan.
In order to investigate pituitary alpha-melanocyte-stimulating hormone (alpha-MSH), intact (1-39 structure) adrenocorticotropic hormone (ACTH), and adrenal cortisol secretion, we measured 8 a.m. plasma levels of those hormones before and after administration of 1 mg dexamethasone in 39 depressed inpatients and 10 healthy controls. We found a significantly lower baseline alpha-MSH secretion in melancholic patients as opposed to healthy controls. There were no significant relations between alpha-MSH secretion on the one hand and ACTH or cortisol secretion on the other. Dexamethasone did not affect the 8 a.m. alpha-MSH circulating levels. The post-dexamethasone intact ACTH and cortisol values were significantly higher in melancholics as compared with healthy, minor and simple major depressed subjects. ACTH non-suppression was defined as post-dexamethasone intact ACTH greater than or equal to 12 pg/ml. ACTH non-suppression was found to be more sensitive (70%) and specific (100%) for melancholia than cortisol non-suppression. By means of pathway analysis we have established that cortisol non-suppression during a severe depression is completely determined by an augmented ACTH escape from suppression by dexamethasone. It is concluded that the assay of post-dexamethasone intact ACTH could, in the future, replace post-dexamethasone cortisol determination.
The clinical description provided by the MMPI Scale 0 (Social Introversion, Si) reflects an apparent and striking affinity with the DSM-III--R concept of the avoidant personality disorder which was here investigated by comparing the MMPI variables of 22 avoidant with 60 other, nonavoidant personality disordered inpatients. Both of the groups were diagnosed by use of a semistructured interview (SCID-II). The avoidant group obtained for mean MMPI profile a 2-6-7 (D-Pa-Pt) code. Significant differences were found between groups on MMPI Scales 2 (D), 7 (Pt), 9 (Ma), and 0 (Si). ROC analysis of the diagnostic performance showed the importance and utility of the evaluation of Scale 0 (Si) in the psychodiagnostic assessment of the avoidant personality disorder.
This study investigated the diagnostic performance of the MMPI validity and clinical scales, and especially of Scale 7 (Pt), for the DSM-IIII--R obsessive-compulsive personality disorder by comparing the MMPI variables for 24 obsessive-compulsive with those for 58 nonobsessive-compulsive inpatients. Both groups were diagnosed by semistructured interview (SCID-II). The obsessive-compulsive group obtained for the mean MMPI profile a 2-(6-1) (D-Pa-Hs) code, with a tendency for a lowered Scale 4 (Pd) score, compared to the nonobsessive-compulsive group. Neither the ROC analysis of the individual MMPI scales, including Scale 7 (Pt), nor the analyses of frequency of two-point codes and elevated (T greater than 69) scales showed any clear indications of good diagnostic performance for the DSM-III--R obsessive-compulsive personality disorder.
Cluster analyses were carried out on a sample of 100 depressed females. The study was based on the 14 items relevant to depressive phenomenology of the Structured Clinical Interview for DSM-III-R (SCID). Our findings support the existence of two classes, i.e., a vital (melancholic) vs. a nonvital cluster. The vital cluster is characterized by the following symptoms: a distinct quality of depressed mood, nonreactivity, early morning awakening, anorexia-weight loss, and cognitive and psychomotor disturbances. Patients belonging to the vital cluster exhibit disorders in the hypothalamic-pituitary-adrenal and thyroid axes and a markedly decreased availability of L-tryptophan to the brain. The vital depressives score significantly higher on the Hamilton Rating Scale for Depression as compared to those suffering from nonvital depression. The cluster-analytically derived class of vital depression and the DSM-III subtype of melancholia tend to be quite similar. Our findings support the isolation and the descriptive validity of a vital (melancholic) depressive syndrome.