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

A study on 61 subjects who meet Spitzer's Research Diagnosis Criteria of schizophrenia and on 56 normal subjects has been conducted to explore anhedonia. Anhedonia was evaluated by two rating scales, the Physical Anhedonia Scale (PAS) and a sub-scale of physical pleasure (FCPCS-PP) extracted from the pleasure scale of Fawcett. The reliabilities of the scales were studied in the schizophrenic group by the Cronbach alpha and the Kuder Richardson (KR 20) coefficient and by the correlation between the two scales (concurrent validity). The Cronbach alpha was 0.77 for the FCPCS-PP and the KR 20 was 0.82 for the PAS. The correlation between the two scales was -0.37 (p < 0.01). The schizophrenics were significantly more anhedonic than normals with higher score on the PAS and with a lower score on the FCPCS-PP. Using the Beck Depression Inventory to rate depression in the schizophrenic group and to dichotomize these subjects into depressed schizophrenics and no depressed schizophrenics, we failed to find significantly differences concerning anhedonia scales between these two sub-groups of schizophrenics. There was no difference between in and outpatients concerning the anhedonia scales. Our results suggest that anhedonia would be a possible marker of schizophrenic disease. The distribution of the anhedonia scales in the schizophrenic group is normal or unimodal and it doesn't support the hypothesis of a qualitative sub-group of schizophrenics characterised by severe anhedonia.
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PMID:[Anhedonia in schizophrenia]. 867 70

Activation of the immune system produces psychological and physiological effects, which resemble the characteristics of depression. The present study was designed to investigate further, in rats, the similarity between the behavioral effects of immune activation and a model of depression in animals. Reduction in the preference for and consumption of saccharin solutions and suppression of sexual behavior were used as models of one essential feature of depression, the inability to experience pleasure (anhedonia). Other measures testing this model were the reduction in food consumption, body weight, locomotor activity, and social interaction. It was found that systemic injection of lipopolysaccharide (endotoxin), which is a potent activator of the immune system, significantly decreased saccharin preference in fluid-deprived rats. Lipopolysaccharide (LPS) also decreased free consumption of saccharin, but not water, in non-deprived rats. Several indices of male sexual behavior were significantly suppressed following LPS administration. Chronic, but not acute, treatment with the tricyclic antidepressant imipramine abolished the suppressive effect of LPS on saccharin preference. Moreover, chronic, but not acute, treatment with imipramine also reduced and facilitated the recovery from the suppressive effects of LPS on food consumption, body weight, social interaction and activity in the open-field test. The results suggest that activation of the immune system in rats produces anhedonia and other depressive-like symptoms, which can be attenuated or completely blocked by chronic treatment with an antidepressant drug.
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PMID:Endotoxin produces a depressive-like episode in rats. 868 Aug 60

The aim of the study was to precise the relationship between physical anhedonia and depression in healthy subjects. The construct validity of these two dimensions were determined using a principal components analysis. 224 normal subjects were recruited for the study. They filled out the abrigded version of the Beck Depression Inventory (BDI) and a physical pleasure scale (Fawcett Clark Pleasure Capacity Scale--FCPCS-PP). A principal components analyses following by a varimax rotation was done. The correlation matrix comprising items from both the BDI and the FCPCS-PP yielded a three-factor solution (two "pleasure" factors and one "depression factor") with no overlap of the significant factor loading for the items from each scale. The findings support the view that physical anhedonia is a construct that is distinct and separate from depression.
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PMID:[Physical anhedonia and depression: distinct concepts? Study of the construct validity of these dimensions in a group of 224 normal subjects]. 876 45

The tripartite model of depression and anxiety suggests that depression and anxiety have shared (generalized negative affect) and specific (anhedonia and physiological hyperarousal) components. In one of the 1st studies to examine the structure of mood-related symptoms in youngsters, this model was tested among 116 child and adolescent psychiatric inpatients, ages 8-16 (M = 12.46; SD = 2.33). Consistent with the tripartite model, a 3-factor (Depression, Anxiety, and Negative Affect) model represented the observed data well. Follow-up analyses suggested that a nonhierarchical arrangement of the 3 factors may be preferable to a hierarchical one.
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PMID:Tripartite structure of positive and negative affect, depression, and anxiety in child and adolescent psychiatric inpatients. 877 10

Clinical and preclinical studies provide convincing evidence for persistent neurological/psychiatric impairments and possible neuronal degeneration associated with chronic cocaine/stimulant abuse. These impairments include multifocal and global cerebral ischemia, cerebral hemorrhages, infarctions, optic neuropathy, cerebral atrophy, cognitive impairments, and mood and movement disorders. These findings may encourage the placement of stimulant addiction into the category of organic brain disorders. Functional and microanatomical anomalies in the frontal and temporal cortex as well as other brain regions may be responsible for certain aspects of phenomenology and neuropsychopathology that are characteristic of stimulant polydrug addictions. These may include broad spectrum of deficits in cognition, motivation, and insight; behavioral disinhibition; attention deficits; emotional instability; impulsiveness; aggressiveness; depression; anhedonia; and persistent movement disorders. Although it is still debated whether the hypofrontality and other brain anomalies observed in stimulant abusers are a consequence or an antecedent of drug abuse, this debate seems purely academic and irrelevant with respect to the importance of compensating for these deficits in the development of treatment strategies. The neuropsychiatric impairments accompanying stimulant abuse may contribute to the very high rate of relapse in addicts that can take place after long periods (years) of abstinence. It is possible that the neurological deficits present in stimulant addicts, whether they are primary or secondary to stimulant abuse, are responsible for perpetual drug abuse which may be a form of self-medication (Weiss et al. 1991, 1992). In this context, addiction to stimulants, once fully developed, may represent a true biological dependency on drugs that temporarily compensate for existing neurological deficits. The concept of self-medication by drug addicts is supported by major theories of biological psychiatry. While a majority of drug addicts are polydrug users, there seems to be a preference for a particular type of drug among different populations of addicts. Addicts who experience distress, anxious dysphoria, and turbulent anger prefer the calming actions of opiates, whereas addicts with preceding attention deficit disorder, depression, or bipolar disorder often prefer stimulants (Khantzian 1985). Figure 1 presents conceptual relationships between brain damage and cocaine/stimulant abuse. More clinical studies are needed to establish unequivocally the epidemiological relationships between preexisting neurological deficits-resulting either from genetic, developmental, traumatic, or neurotoxic factors- and vulnerability to drug addictions. Nonetheless, deducing from the results of preclinical studies, it is conceivable that individuals with neurological deficits associated with attention deficit disorder, developmental neuroanatomical abnormalities, lead poisoning, alcoholism, posttraumatic brain lesions, and PTSD may be more vulnerable to stimulant addiction. This notion has significant empirical support as preclinical studies have shown that animals with lesioned prefrontal cortex became supersensitive to cocaine (Schenk et al. 1991) and animals with lesions at the amygdala, VTA, or raphe nuclei manifest more rapid acquisition of amphetamine self-administration than control rats (Deminiere et al. 1989). The above arguments, postulating neuropathology as an intrinsic component of stimulant addiction, should be taken into consideration with the caveat that the clinical manifestations of the disease are heterogenous and addicts may express varying stages and degrees of the disease as determined by environmental and genetic factors. Therefore, it is likely that stimulant addicts who have less advanced neuropathology may recover spontaneously after detoxification with proper nutritional and psychotherapeutic support if they can sustain abstinence. (ABSTR
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PMID:Cocaine addiction as a neurological disorder: implications for treatment. 880 51

We conducted Goldberg's 30-item General Health Questionnaire (GHQ) on 1,216 Japanese general population aged 40-92. Among them, 9.8% of males and 13.7% of females scored over the cut-off point which is used to indicate minor psychiatric disorders. Factor analysis was carried out using the Likert method and eight factors labelled as follows were selected: depression, anxiety and tension, anergia, interpersonal dysfunction, difficulty in coping, insomnia, anhedonia and social avoidance. The mean value of the standardized scores for each age-sex group indicated that changes in sex-age social roles with age affect the mental health of the general population.
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PMID:The factor structure of the general health questionnaire (GHQ-30) in Japanese middle-aged and elderly residents. 881 50

Potential antidepressant properties of preferential 5HT2C receptor agonists were investigated in stress-induced anhedonia, a validated simulation of depression. This simulation evaluates the hedonic state of stressed rats by recording variations in self-stimulation threshold measured before, during, and after exposure to intermittent, unpredictable, mild stressors. This stress regimen gradually elevates self-stimulation threshold, suggesting the development of an anhedonic state. In stressed animals, chronic treatment with the preferential 5HT2C receptor agonists Ro 60-0175 and Ro 60-0332 (3 mg/kg i.p. b.i.d.) prevented the loss of sensitivity to reward. Similarly, when stressed anhedonic animals were curatively treated with Ro 60-0175 (3 mg/kg i.p. b.i.d.), the stress-induced anhedonia was gradually reversed. These results suggest a role for 5HT2C receptors in some aspects of depression, and potential antidepressant properties for selective 5HT2C receptor agonists. Such compounds may offer an innovative approach to the treatment of mood disorders.
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PMID:5HT2C receptor agonists exhibit antidepressant-like properties in the anhedonia model of depression in rats. 888 75

Ratings on a 10-item affect checklist yielding composite positive affect and negative affect scores were made daily for 30 days by older people in residential care: 19 were diagnosed as having major depression, 21 had minor depression, and 37 were without psychiatric diagnosis ("normal"). Mean levels of positive affect were highest in normal people and least in those with major depression; negative affect was lowest in normal ones and highest in those with a major depression. Variability was least among those with major depression in positive affect and among normal people in negative affect, while residents with minor depression showed some tendency, although inconsistent, toward greater day-to-day variability in positive affect. Patterns of invariance were such that those with major depression tended to be consistently lacking in positive affect but were variable in negative affect; normal people showed variability in positive affect but a relatively unvarying lack of negative affect. Clinical major depression was thus characterized less by "pervasive" depressive affect than by anhedonia.
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PMID:Affective states in normal and depressed older people. 893 18

The aim of the present study is to present a model of depressive vulnerability centered on anhedonia. After a review of the literature, we suggest a specific symptomatic profile associating anhedonia, introversion, low sensation-seeking, autonomy, dysfunctional attitudes, high displeasure capacity, obsessive-compulsive features, passitivity and pessimism. This symptomatic profile could constitute a mild chronic mood disorder which, following stress, might decompensate into unipolar endogenomorphic depression. Several methods of research are suggested to test the validity of our model.
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PMID:Vulnerability to depression: a model centered on anhedonia. 893 4

The present review was aimed at re-evaluating results obtained from animal models of depression based on experimental stressors in the light of the most recent data on the effects of stress on mesolimbic dopamine (DA) functioning. The data reviewed reveal that the effects of stressful experiences on behaviour and on mesoaccumbens DA functioning can be very different or even opposite depending on the behavioural controllability of the situation, the genetic background of the organism and its life history. Exposure to a single unavoidable/uncontrollable aversive experience leads to inhibition of DA release in the accumbens as well as to impaired responding to rewarding and aversive stimuli. Moreover, the data reviewed indicate a strong relationship between these neurochemical and behavioural effects and suggest that they could model stress-induced expression and exacerbation of some depressive symptoms such as anhedonia and feeling of helplessness caused by life events as well as syndromal depression provoked by traumatic experiences in humans. Repeated and chronic stressful experiences can reduce the ability of stressors to disrupt behaviour, induce behavioural sensitisation to psychostimulants and promote adaptive changes of mesolimbic DA functioning. Opposite neural and behavioural changes, however, can be promoted in specific environmental conditions (repeated variable stressful experiences) or in genetically predisposed individuals. Thus, depressive symptoms may not represent the necessary outcome of stress experiences but be promoted by specific environmental conditions and by a genetically determined susceptibility.
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PMID:Stress, depression and the mesolimbic dopamine system. 898 3


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