Subgroup Of Depressed Patients Research Articles

Relationship of depressive symptoms to edentulousness, dental health, and dental health behavior

We investigated the relationship of edentulousness, dental health, and dental health behavior to depressive symptoms in the 55-year-old population of Oulu (a medium-sized Finnish town), 780 of whom (78%) participated. The dental examination included an assessment of oral health status. Depressive symptoms were determined with the Zung Self-Rating Depression Scale (ZSDS). The participants were also asked about their dental health behavior, smoking habits, health, life satisfaction, and factors related to their work. Depressive symptoms were associated with edentulousness among non-smoker men. When further evaluated by logistic regression analysis, edentulousness was independently associated with depressive symptoms in this subpopulation (odds ratio = 6.4, confidence interval = 1.4–29.2) after adjusting for confounding factors. Depressive symptoms were not associated with dental caries, periodontal status, or number of teeth. The dentate women with high rates of depressive symptoms had a more negative attitude towards preserving their natural teeth, used sugary products more frequently, reported a longer time since their last dental visit, and tended to have a lower percentage of filled tooth surfaces than the non-depressed dentate women. The aspect of depression should be borne in mind by dentists when treating edentulous patients. On the other hand, certain subgroups of depressed patients might benefit from dental implant therapy. Thus, the importance of teamwork between clinicians, psychiatrists, and dentists is emphasized.

Melatonin in Psychiatric Disorders – Subtyping Affective Disorder

Altered diurnal secretory patterns, i.e. altered phase and/or amplitude of melatonin have been reported in sleep and affective disorders. The alteration may depend on environmental factors which in vulnerable individuals may cause sleep and/or affective disorders. Early stress in conjunction with development of resistance to corticotropin-releasing hormone may be linked to the low melatonin syndrome in subgroups of depressed patients. Also the seasonal variation in melatonin as well as serotonin may be linked to the seasonal pattern seen in subgroups of affective disorders. Melatonin may be used as a combined marker for proneness to develop affective disorders especially in latent carriers of bipolar disorders.

Antiglucocorticoid treatments in psychiatry.

A confluence of evidence indicates that alterations in hypothalamic-pituitary-adrenal regulation can have profound effects on the symptom picture of psychiatric illnesses and that therapeutic interventions directly targeted at corticosteroid metabolism may have clinical benefit. This paper reviews the varying lines of inference that support such a hypothesis and reviews work by our group and others utilizing the cortisol synthesis inhibitor, ketoconazole and, more recently, dehydroepiandrosterone (DHEA), as potential novel mood-altering agents. The data thus far suggest that antiglucocorticoid drug treatment may be useful in certain subgroups of depressed patients and may offer a theoretical rationale for alternative drug design.

Heterogeneity of information-processing alterations according to dimensions of depression: An event-related potentials study

To identify alterations in elementary cognitive operations according to dimensions of depression, two stages of information processing, namely the response choice and the motor preparation stages, were explored using an event-related potential paradigm in two subgroups of depressed patients (retarded and blunted affect versus anxious-agitated and impulsive) compared to controls. Two results are common to all depressed patients: a slow encoding of stimuli (P1 wave) and a prolonged processing of stimulus-response compatibility (after P3b). This is compensated by a global velocity increase in stimulus evaluation or decision making (P3b) in anxious-agitated patients or, on the contrary, cumulated with its velocity decrease in retarded-blunted-affect patients. Such results could provide an explanation for the massive retardation observed in blunted-affect patients, contrary to anxious-agitated patients, whose normal reaction times may come from a very high energetical involvement at the P3b level. Results as a whole suggest that impairments in blunted-affect patients concern effort mechanisms, whereas those in anxious-agitated patients concern perceptual processes.

Sleep benefit and sleep deprivation in subgroups of depressed patients with Parkinson's disease

Sleep benefit and sleep deprivation in subgroups of depressed patients with Parkinson's disease

Major depression in coronary artery disease patients with vs. without a prior history of depression.

Major depression (MD) is common in patients with coronary artery disease (CAD). Some of these patients have a history of prior depressive episodes, whereas others experience their first episode around the same time that their CAD is diagnosed. The purpose of this study was to determine whether there are systematic differences between these two subgroups of depressed patients. Of 39 patients with recently diagnosed CAD who met DSM-III-R criteria for MD, 17 (44%) had a prior history of MD. This subgroup had a higher proportion of females (p less than 0.003), more severe depression (p less than 0.004), were marginally younger (p = 0.08), and had slightly less severe CAD (p = 0.07) compared with those with no prior history of MD. These results support the hypothesis that there may be two distinctive subtypes of MD in patients with CAD. Additional studies are needed to determine whether these subgroups differ with respect to course, treatment, and relationship to the coronary artery disease.

Urinary Excretion of Catecholamines and Their Metabolites in Relation to Circulating Catecholamines

Some depressed patients have been shown to excrete abnormal amounts of catecholamines and their metabolites in urine. Some studies suggest that hypersecretion of epinephrine by the adrenals and of norepinephrine by the peripheral sympathetic system cause increased excretion of urinary catecholamines and their metabolites in a subgroup of patients. To evaluate the effect of increased catecholamine levels in the peripheral circulation on urinary catecholamine and metabolite levels, we infused healthy volunteers during 6 hours with epinephrine, norepinephrine, or placebo, respectively, in a three-period, double-blind, crossover design. The results indicate that (1) urinary epinephrine and norepinephrine levels were the most sensitive indicators of increased circulating epinephrine and norepinephrine levels, respectively; (2) changes in circulating epinephrine or norepinephrine levels were not readily reflected in changes in urinary vanillylmandelic acid or 3-methoxy-4-hydroxyphenylglycol levels; and (3) increased normetanephrine excretion was not only induced by infusion of norepinephrine but also by epinephrine. This last finding may be due to activation of the sympathetic nervous system by circulating epinephrine. These results may help to explain the mechanism of adrenal epinephrine and sympathetic nervous system norepinephrine hypersecretion observed in subgroups of depressed patients.

The safety of antidepressants.

It is no exaggeration to say that, in the 30 years since antidepressants were introduced, they have revolutionised the management of depression, thus fulfilling, at least for depressive illness, Paracelsus' prophetic wish. We now have a group of drugs which can induce remission in a disease which is disabling and not infrequently fatal. Despite intensive research, however, our understanding of the mechanism of action of these drugs is still largely hypothetical. Even our methods of evaluation are sufficient only to enable one to decide whether an antidepressant drug is effective or ineffective; there is no experimental method which can rank them in an overall order of potency, and perhaps this should not be the aim, since there must be subgroups of depressed patients who will respond differently to any one agent.

Effects of major depression on estimates of intelligence.

This study examined whether patients with major depressive disorder manifest deficits in intelligence during affective episodes and following clinical improvement. WAIS-R scores were contrasted in 100 patients in an episode of major depression with 50 normal controls, matched to the patient sample in terms of demographic variables and estimates of premorbid IQ. The groups were equivalent in verbal IQ, but, in line with previous studies, the depressed patients had a pronounced deficit in performance IQ. A patient subsample was administered the WAIS-R under unlimited time conditions to determine whether the time constraints of performance IQ subtests contributed to the magnitude of the verbal-performance IQ discrepancy. This discrepancy was only slightly reduced with untimed scoring. Subgroups of depressed patients were retested with the WAIS-R within one week (n = 26) or two months (n = 33) following treatment with electroconvulsive therapy. In both subsamples, IQ scores were improved at posttreatment testing relative to pretreatment, but with little change in the verbal-performance IQ discrepancy. These and related findings suggested that a performance IQ deficit is characteristic of depressed patients regardless of affective state.

Stimmungsverlauf über 6 Jahre bei einer Patientin mit saisonal abhängiger Depressionsform (SAD)

Since the first description of seasonal affective disorder (SAD), many international studies have confirmed the existence of this subgroup of depressive patients. Even though the diagnosis of SAD has been incorporated into the DSM-III-R classification system, many psychiatrists maintain a certain skepsis as to the existence of SAD as a separate sub-group of depression. The diagnostic issues are important because of the apparent specificity of treatment of SAD with bright light. Most diagnoses have relied on retrospective descriptions of the patients' depressive and healthy phases with respect to time of year. We present prospectively gathered weekly depression self-ratings in a SAD patient over a period of six years that may provide valid criteria for diagnostic purposes. This is a particularly exemplary case with implications for the relationship between light therapy and the course of depressive phases, the possible interaction of light treatment with lithium, the relationship between weight-changes and mood changes over the year and aspects of family loading of the illness.

Clonidine causes antidepressant-like effects in rats by activating α 2-adrenoceptors outside the locus coeruleus

Clonidine,0.05, 0.1 and 0.5 mg/kg administered i.p. as a three-injection course but not as single doses, significantly reduced the immobility of rats in the forced swimming test. Doses of 0.1 and 0.5, administered the same way, significantly reduced activity in an open field. The effect of 0.05 and 0.5 mg/kg clonidine on immobility was prevented by 1 mg/kg idazoxan, an α 2-adrenoceptor antagonists, but not by 3 mg/kg prazosin, which blocks α 2-adrenoceptors. An infusion of 6 μg/μl 6-hydroxydopamine in the locus coeruleus, which markedly depleted noradrenaline in terminal regions, did not modify the effect of 0.05 and 0.5 mg/kg clonidine on immobility. Chronic treatment with 5 mg/kg i.p. desipramine or 0.1 mg/kg i.p. clonidine, twice daily for 15 days, did not modify the effect of a three-injection course with 0.1 mg/kg clonidine. It is suggested that clonidine exerts antidepressants-like effects on rats in the forced swimming test by acting on central α 2-adrenoceptors outside the locus coerlus and presumably postsynaptically to noradrenalin-containing neurons. No tolerance or sensitization of the clonidine effect was found after chronic treatment with desipramine or clonidine. These findings are of significance for these effects of clonidine in subgroups of depressed patients.

Personality and family history of depression in patients with affective illness

The presence of a family history of depression may distinguish clinically important subgroups of depressed patients. Depressed patients with and without a family history of depression may differ on several clinical features. There are limited data, however, on potential differences in personality variables between patients with and without familial depression. We examined personality measures in 41 depressed subjects with and without a familial history of depression in both the depressed and remitted state. Patients with no family history of depression had significantly higher mean personality trait scores on the dependent and compulsive personality scales. The clinical and theoretical implications of these findings are discussed.

Efficacy of a reversible monoamine oxidase‐A inhibitor versus imipramine in subgroups of depressed patients

Two multicentre studies comparing moclobemide with imipramine under similar conditions in patients undergoing a major depressive episode (DSM-III) were combined in the present analysis. A total of 353 patients received moclobemide (300-600 mg/day) and 356 imipramine (100-200 mg/day). In each study, the antidepressant efficacy of the 2 drugs was comparable, and subgroup analysis showed that moclobemide and imipramine were equally effective in endogenous depression. The response rate did not appear to be influenced by sex, but patients older than 60 years tended to respond less well to both drugs than did those under 60. The conclusion from the 2 studies is that, contrary to what is frequently stated for monoamine oxidase inhibitors, moclobemide appears as effective as a tricyclic in treating endogenous depression.

Platelet serotonin-2 receptor binding sites in depression and suicide

In order to examine the role of serotonin-2 (5HT 2) receptors in depression and suicide, we determined 5HT 2 receptors using 125I-lysergic acid diethylamine (LSD) as the binding ligand in platelets obtained from 20 normal control and 23 drug-free depressed patients. Our results indicate significantly increased 125I-LSD binding sites (B max) in the platelets of depressed patients compared with normal control subjects. We also observed that a subgroup of depressed patients with a recent history of suicide attempts or suicidal ideation had significantly higher 5HT 2 binding sites as compared with nonsuicidal depressed patients and normal controls. There were no significant differences in the apparent dissociation constant (K d) values in the platelets of depressed patients compared with normal control subjects. To examine if the baseline 5HT 2 receptors are related to either the severity of illness or treatment response, we determined the relationships of the baseline B max and K d with baseline Hamilton Depression Rating Scale (HDRS) and Brief Psychiatric Rating Scale (BPRS) scores and change in scores after treatment. We found no significant correlation between baseline B max and K d with the baseline HDRS or BPRS scores or change in these scores after psychoactive drug treatment. These results thus indicate increased platelet 5HT 2 receptors in depression, but much more so in depressed patients with suicidal ideation or attempts.

3H-Imipramine Binding to Previously Frozen Platelet Membranes from Depressed Patients, Before and After Treatment

3H-imipramine binding in 39 drug-free patients with major depression and 44 healthy controls did not differ significantly between the two groups, in male or female subjects or in subgroups of depressed patients divided by endogenicity or dexamethasone suppression test result. 3H-imipramine binding in depressed patients drug-free for less than three weeks did not differ from those drug-free for longer intervals or from controls. A significant seasonal variation of 3H-imipramine Bmax was found, with lower values in summer and autumn. Treatment of depressed patients with imipramine or lofepramine for six weeks increased KD and Bmax. Methodological modification (in preparation and storage of platelets) does not explain the major differences in results between this study (using frozen platelets), a previous one (using freshly prepared platelets) and others in general, although it might contribute to the range of values reported.

Investigations with the Specific μ-Opiate Receptor Agonist Fentanyl in Depressive Patients: Growth Hormone, Prolactin, Cortisol, Noradrenaline and Euphoric Responses

15 depressive patients and 15 controls, 9 of them age- and sex-matched, were administered 0.2 mg/70 kg i.v. fentanyl, a specific and highly potent mu-opiate receptor agonist. Growth hormone response was significantly reduced in depressive patients in comparison to controls, whereas prolactin response did not significantly differ between the two groups. Cortisol plasma concentration increased in depressive patients and decreased in controls. The difference between the groups failed to reach statistical significance. Only in patients, but not in controls, fentanyl led to a significant increase in plasma noradrenaline. In contrast, a significant increase in the visual analogue scale for the evaluation of psychotropic drug effects was found only in controls after fentanyl administration. From these preliminary results in connection with other studies we conclude a possible involvement of a disturbed opioid system at least in a subgroup of depressive patients.

Major Depressive Disorder and Immunity

An association between depression and altered immunity has been suggested but has not been consistently demonstrated. We have studied 91 patients with unipolar major depressive disorder, and no mean differences were found between the patients and concurrently studied matched controls in mitogen-induced lymphocyte proliferation, lymphocyte subsets, and natural killer cell activity. There were, however, significant age-related differences between the depressed patients and controls in mitogen responses and in the number of T4 lymphocytes. In contrast to age-related increases in mitogen response and in T4 cells in controls, depressed patients did not show increased lymphocyte responses or numbers of T4 lymphocytes with advancing age. Severity of depression and hospitalization status were also associated with immune system changes. Altered immunity does not appear to be a specific biologic correlate of major depressive disorder but may occur in subgroups of depressed patients.

Norepinephrine and its metabolites in cerebrospinal fluid, plasma, and urine. Relationship to hypothalamic-pituitary-adrenal axis function in depression.

Among 140 depressed and control subjects, there were significant positive correlations between indexes of noradrenergic activity in cerebrospinal fluid (CSF), plasma, and urine. Among the depressed patients, CSF levels of the norepinephrine (NE) metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) and urinary outputs of NE and its metabolites normetanephrine, MHPG, and vanillylmandelic acid correlated significantly with plasma cortisol levels in relation to dexamethasone administration. Also, CSF levels of MHPG were significantly higher among patients who were cortisol nonsuppressors than among either patients who were cortisol suppressors or controls. Urinary outputs of NE and normetanephrine were significantly higher among patients who were cortisol nonsuppressors than among controls. Patients who were cortisol suppressors had indexes of NE metabolism similar to those of controls. These results in the depressed patients extend recent observations suggesting that dysregulation of the noradrenergic system and hypothalamic-pituitary-adrenal axis occur together in a subgroup of depressed patients.

Cerebrospinal Fluid and Urinary Biogenic Amines in Depressed Patients and Healthy Controls

The National Institute of Mental Health-Clinical Research Branch Collaborative Study investigated 132 drug-free, severely depressed patients and 80 healthy controls. Forty-five percent of the depressed patients excreted markedly elevated levels of urinary epinephrine (E) and metanephrine (MET), while only 5% of healthy controls did so. Using gaussian mixture distributions, we identified two subgroups of depressed patients: one excreting normal levels and the other excreting high levels of urinary E, MET, norepinephrine, and normetanephrine. Cerebrospinal fluid homovanillic acid levels were low in a subgroup of depressed patients. When analyzed by subgroup, the elevated E + MET group had markedly lower cerebrospinal fluid homovanillic acid levels than controls, whereas depressed patients with normal catecholamine levels did not. Since it has been postulated that there are two subgroups of depressed patients, those with low 3-methoxy-4-hydroxyphenylglycol (MHPG) levels and normal 5-hydroxyindoleacetic acid (5-HIAA) levels and those with normal MHPG levels and low 5-HIAA levels, several analyses were performed to see if such a group could be identified. Our analysis failed to find evidence of a subgroup of depressives with low MHPG and normal 5-HIAA levels or normal MHPG and low 5-HIAA levels.

Function of the adrenal cortex in patients with major depression

Failure to suppress cortisol secretion after administration of dexamethasone occurs in up to 50% of depressed patients. To test whether this hypothalamic-pituitary-adrenal (HPA) overactivity is associated with adrenocortical hyperresponsiveness, we performed dexamethasone suppression tests (DSTs) and adrenocorticotropic hormone (ACTH) stimulation tests in depressed subjects and subjects with other psychiatric disorders. Three groups were defined: depressed nonsuppressors, depressed suppressors, and other suppressors. While predexamethasone and postdexamethasone cortisol concentrations were greater in the depressed nonsuppressor group, ACTH concentrations did not differ among groups. After receiving α-ACTH[1–24](4.2μ/kg), depressed nonsuppressors had greater increases in stimulated cortisol secretion than the other groups. These results demonstrate that in a subgroup of depressed patients, HPA over-activity is associated with adrenocortical hyperresponsiveness.