Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three biological markers of affective disorders and response to desipramine were used to study the relationship of posttraumatic stress disorder (PTSD) to affective illness. Blunted TRH response and decreased REM latency in eight patients with PTSD occurred at frequencies similar to those that have been found in patients with major affective disorder. Pretreatment Hamilton Rating Scale for Depression and Beck Depression Inventory scale scores were elevated; scores after 4 weeks' treatment with desipramine revealed significant (p less than .05 and p less than .005, respectively) improvement. These findings support a link between PTSD and affective illness.
 ...
PMID:Biological markers of affective disorders and posttraumatic stress disorder: a pilot study with desipramine. 311 42

Among patients referred for areactive depression who were polygraphically recorded after at least 2 weeks without any pharmacological treatment, some were found to present qualitative sleep symptoms similar to those already described in clinically diagnosed parkinsonian patients. A therapeutic trail with a dopamine agonist (Piribedil) was followed, in all of these patients, by a dramatic and rapid improvement of mood. As compared to areactive depressive patients whose sleep recordings were free of these qualitative abnormalities, some quantitative sleep criteria, mainly related to REM sleep, permit to diagnose this group of dopamine dependent depression (DDD). These data, together with the beneficial effect of Piribedil, favor a role of DA in the genesis of this type of depression. Some clinical signs now appear as sufficient to diagnose these DDD. The interest of this study is that all the patients (now 48), among whom no clinical parkinsonian symptoms were found, diagnosed according to the reported polygraphic criteria were cured following this treatment.
 ...
PMID:[Polygraphic, clinical and therapeutic markers of dopamine-dependent depressions]. 311 2

A group of 27 patients with definite (n = 20) or probable (n = 7) RDC major depressive disorder underwent 2 sleep EEGs and 1 TRH test while in a drug-free depressive phase. A short mean REM latency (less than 60 min) identified 55.5% of major depressives while added use of blunted TSH responses (delta max. less than 5 microU/ml) increased that percentage by 11%. When patients were subdivided into RDC endogenous and nonendogenous, mean REM latency and global depression scores distinguished the 2 groups, while delta TSH did not. A short mean REM latency identified endogenous depression with 80% specificity and 76% sensitivity. The combination of REM latency and delta TSH reduced the specificity to 60%, and therefore cannot be recommended for differentiating endogenous from nonendogenous depression.
 ...
PMID:Biological heterogeneity of major depressive disorder: indications by sleep EEG and TRH stimulation test findings. 312 30

The effects of 400-600 mg trazodone on the sleep patterns of ten depressed in-patients treated for 5 weeks were studied during the initial (days 1-3) and terminal (days 26-28) treatment periods. The sleep parameters were compared to those obtained from three sleep recordings performed just prior to the initiation of the treatment and after 2 adaptation nights at the end of a 2-week drug-free period. At the same time, the clinical evolution of patients was evaluated weekly using MADRS and Hamilton-Anxiety scales for anxiety-depression symptomatology and Spiegel and Norris sleep scales. Weekly blood samples were collected to measure plasma levels of trazodone and, at the end of the study, the elimination half-life at steady state was calculated by repeated measurements of plasma levels. Clinical improvement, as assessed by a reduction of more than 60% in MADRS scale scores, was accompanied by evidence of the definitely beneficial effects of trazodone on the disturbed sleep of these depressed patients. From the beginning of treatment, there was a hypnotic-like effect (increase in total duration of sleep and stage II, decrease in sleep latency and intrasleep awakenings). In addition, records at the end of the study showed an increase in delta sleep and an increase in REM latency, an effect classically associated with an antidepressant action. These particularly valuable effects of trazodone on sleep would suggest that this drug should especially be given in cases of depression with major insomnia.
 ...
PMID:Effects of trazodone on the sleep of depressed subjects--a polygraphic study. 313 13

The state of knowledge in the area of suggested biological markers that may delineate subpopulations of patients with borderline personality disorders (BPD) is reviewed. There is widespread disagreement as to the specificity of these markers. The clinical implications of Axis I--Axis II, state vs. trait, acute vs. chronic, and definite vs. probable diagnoses, all seem to contribute to the confusion in this area. Some patients with BPD and with schizotypal personality disorders (SPD) share neuroendocrine abnormalities with affective disorders (AD) and schizophrenic (SCH) patients respectively. This interface and/or potential overlap between personality disorders (PD) and the major mental disorders is discussed with special reference to the DST, TRH/TSH test, and REM latency which have already been established as valuable biological markers for certain subtypes of depression. In contrast, biologic abnormalities observed in chronic schizophrenia are also present in some SPD patients. Current data are supportive of the hypothesis that some PD patients are independent whereas others are genetically related to the major mental disorders.
 ...
PMID:Biological markers in borderline personality disorders: an overview. 313 5

Ritanserin (1.0 and 2.5 mg/kg i.p.) was administered to rats before the start, of the light period, and sleep was recorded during the subsequent 12 h. The higher dose reduced sleep in the first 3 h. Both doses caused a more prolonged suppression of REM sleep. Spectral analysis of the EEG in non-REM sleep showed an increase of power density in the low frequency range (1.5-6 Hz) and a depression in the high frequency range (8-25 Hz). Since these changes differ from those previously observed after sleep deprivation, it is premature to conclude that the drug induces a physiological sleep intensification.
 ...
PMID:Effect of ritanserin on sleep stages and sleep EEG in the rat. 314 44

Patients who met provincial criteria for atypical depression were contrasted with a group of patients who met RDC criteria for endogenous depression and a group of normal controls on a standard series of sleep variables. Atypical depressives were differentiated from normal controls by a shortened REMP latency. They did not, however, appear to have the sleep continuity disturbance exhibited by endogenous depressives. This preliminary work suggests that atypical depressives may have a unique pattern of sleep variables consisting of REM abnormalities without continuity disturbance. If this pattern is observed in additional studies, it would add to the validity of considering atypical depression a subtype of unipolar depressive illness.
 ...
PMID:Sleep of atypical depressives. 315 12

The sleep patterns of nine male subjects were studied on four consecutive nights comprising two baseline nights, one night on which environmental temperature was elevated from 21 degrees C to 30 degrees C one hour after lights out, and a recovery night. There was a suppression of stage 4 sleep during the initial three hours of sleep on the hot night. A significant increase in stage 4 sleep with a decrease in stage 2 sleep occurred during the first three hours of the recovery sleep. There was a shortening in sleep onset latency and an increase in sleep efficiency on the recovery night. There were no changes in REM latency or REM sleep time. Rectal temperature rose after the increase in ambient temperature on the hot night. These results indicate that elevations in environmental temperature during sleep affect sleep patterns in a manner opposite to elevations of body temperature occurring prior to sleep onset. The curtailing of the usual circadian temperature drop during the first few hours of sleep reduces slow-wave sleep during this period. These findings have implications for those conditions with both altered sleep and altered temperature rhythms, for example, depression.
 ...
PMID:Circadian temperature rhythm blunting and sleep composition. 324 67

Clomipramine, administered to neonatal rats, has been reported to produce adult behavioral and REM sleep abnormalities. They include decreased sexual behavior, increased ambulation in the outer part of an open-field arena, increased REM sleep % of total sleep time, and in descriptive data, short REM latency, and increased REM phasic events. Since these abnormalities resemble some found in human endogenous depression, we have hypothesized that the adult rats represent an animal model of depression. Diminished aggressive behavior is a common characteristic of endogenous depression. This study tested the validity of the animal depression model by determining in rats the effect of neonatal clomipramine on adult shock-induced fighting. Experimental rats were treated neonatally with clomipramine and control rats were treated neonatally with saline. When they matured, compared with control rats, experimental rats had significantly fewer offensive fighting responses, and significantly more defensive fighting responses. The findings add some support to the validity of the animal depression model produced by neonatal clomipramine.
 ...
PMID:Animal depression model by neonatal clomipramine: reduction of shock induced aggression. 325 40

Future sleep research in affective illness will probably continue the current evolution beyond cross-sectional to longitudinal studies, and beyond a largely descriptive emphasis to the testing of specific hypotheses and predictions derived from models of the pathophysiology of depression. These models are and will be variously neurochemical, chronobiological, genetic, and developmental in nature. Adequate testing of these models and predictions from them will require the use of pharmacologic and naturalistic probes and the use of sophisticated CNS imaging techniques. These probes will help further characterize the physiology of depression under conditions of disequilibrium or perturbation, such as following sleep deprivation, REM deprivation, phase advancement of the major sleep period, or the administration of antidepressant drugs with specific monoaminergic activity. Concurrently, if one is to understand further whether the sleep abnormalities of depression are part of a larger circadian rhythm disturbance, investigations will necessarily include 24-h measures of sleep-wake activity, psychomotor activity, and probably core body temperature rhythm under constant routine conditions. A complementary point of view would suggest that more intensive investigative efforts be focused on the first 100 min of sleep at night, since it is the first NREM-REM cycle that seems to show the greatest and most specific deviation in depressed patients from normal controls. Efforts to characterize further this part of the 24-h cycle, with respect to age- and gender-related variance as well as responses to physiologic, hormonal, pharmacologic, and naturalistic probes, are strongly warranted.
 ...
PMID:Sleep research in affective illness: state of the art circa 1987. 330 74


<< Previous 1 2 3 4 5 6 7 8 9 10