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

One hundred and nine out of one hundred and twenty-two cases of endogenous depression were followed-up after their index diagnosis 3-13 years earlier. No recurrence occurred in 28 cases. Forty-two cases turned out to be bipolar and 21 remained unipolar. Manic episodes outnumbered the depressive ones. The change of polarity from depression to mania occurred within three years after the initial depression, though in others the shift occurred between three years and twelve years. The number of episodes of depression before the onset of mania varied from 1 to 3. While the onset of depression before the age of 40 years predisposed to recurrences, there was risk of chronicity in those patients who developed the illness after 40.
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PMID:The course and outcome in depressive illness. A follow-up study of 122 cases in Madurai, India. 85 14

To evaluate the possible abnormality in MAO activity in affective disorders, blood platelet samples were obtained from 80 patients with mania and depression. Blood-platelet MAO activity was measured by a newly developed assay procedures using serotonin as substrate. MAO activities in 121 normal adult subjects were in a range of 2.49-12.05 nM/mg protein/hour, with the mean values of 4.91 +/- 1.72 (+/-S.D.) for men and 6.88 +/- 1.99 for women. (p less than 0.001) MAO activities in the manic and depressed patients were in a range of 0.65-13.40 nM/mg protein/hour, and both manic and depressed patients showed the mean value very familiar to that in the normal subjects. Bipolar depressed patients did not exhibited lower MAO activity in the blood platelets than other clinical subtypes of depressive illness, including unipolar, involutional, neurotic and chronic characterological, and first-episode depression. No significant differences were established between these five subcategories of depression, while significant higher values were evident in female than male patients (p less than 0.001). No correlation was found between the MAO activity and serotonin levels in the blood platelets either in the normal subjects or in the depressed patients.
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PMID:Monoamine oxidase activity in blood platelets from manic and depressed patients. 86 45

The efficacy of ECT in the treatment of depression is well recognized. In mania its efficacy is less well acknowledged. This report compares ECT, chlorpromazine, and no active treatment in mania. Twenty-eight control patients diagnosed as manic were selected from consecutive admissions to the University of Iowa Psychiatric Hospital in the period 1935-1941 when there was no active treatment given. Twenty-eight patients treated with ECT were selected from the period 1945-1949, and 28 chlorpromazine-treated patients were selected from the period 1958-1964. Symptoms sufficient to fulfill a research diagnosis of mania had to be documented in the record for all patients. Results compare symptomatology, duration of hospital admission, discharge condition, discharge category, social recovery, and follow-up. Both ECT and chlorpromazine were superior to no active treatment for outcome measures considered. Ten chlorpromazine-treated patients did not respond satisfactorily to the chlorpromazine treatment but recovered with ECT treatment.
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PMID:ECT versus chlorpromazine in mania. 87 95

The authors present detailed clinical and follow-up data on 12 patients with agitated psychotic depressions who developed serious hypomanic or manic episodes. In six patients, each type of affective episode seemed to merge into the others, while in the other patients there was always a clear temporal distinction between each type of episode. The authors suggest that the older ages of their patients may have contributed to the syndrome. They also offer several possible theoretical explanations: the patients 1) had mixed affective states and were trapped in the "switch" state from depression to mania, 2) inherited both unipolar and bipolar diseases, 3) represent a subgroup of bipolar patients, and 4) were schizoaffective.
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PMID:Agitated psychotic depression associated with severe hypomanic episodes: a rare syndrome. 93 66

Three different syndromes produced by congeners of morphine have been identified in the nondependent chronic spinal dog. These syndromes have been attributed to interaction of agonists with three distinguishable receptors (mu, kappa and sigma). Morphine is the prototype agonist for the mu receptor, ketocyclazocine for the kappa receptor and SKF-10,047 for the sigma receptor. The morphine syndrome (mu) in the dog is characterized by miosis, bradycardia, hypothermia, a general depression of the nociceptive responses and indifference to environmental stimuli. Ketocyclazocine (kappa) constricts pupils, depresses the flexor reflex and produces sedation but does not markedly alter pulse rate or the skin twitch reflex. SKF-10,047 (sigma), in contrast to morphine and ketocyclazocine, causes mydriasis, tachypnea, tachycardia and mania. The effects of these three drugs can be antagonized by the pure antagonist naltrexone, indicating that they are agonists. Further, chronic administration of morphine, ketocyclazocine and SKF-10,047 induces tolerance to their agonistic effects. Morphine suppresses abstinence in morphine-dependent dogs while ketocyclazocine does not. Ketocyclazocine at best precipitated only a liminal abstinence syndrome in the morphine-dependent dog, indicating that it had little affinity for the morphine receptor. Ketocyclazocine thus appears to be a selective agonist at the kappa receptor. Further, it has been shown that buprenorphine is a partial agonist of the mu type which both suppressed and precipitated abstinence in the morphine-dependent dog while morphine and propoxyphene are stronger agonists. Apomorphine and SKF-10,047 produce similar pharmacologic effects suggesting that sigma activity may involve a dopaminergic mechanism.
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PMID:The effects of morphine- and nalorphine- like drugs in the nondependent and morphine-dependent chronic spinal dog. 94 47

A study of sleep deprivation therapy was made in 62 females and 15 males, aged 20-72, with monopolar (60 patients) and bipolar (17 patients) types of manic-depressive psychosis. Of these patients, 30 had suffered only the current depression, 29 a maximum of five depressions, and 18 more than five depressions before the sleep deprivation therapy. Twenty-five patients had been treated with antidepressant drugs for less than 10 days, 12 patients for 10-24 days, and 36 patients for more than 24 days. Twenty-four patients were treated with one sleep deprivation, 29 patients with one sleep deprivations per week (average 1.59), and 24 patients with two sleep deprivations per week (average 2.5). The effect of the sleep deprivation therapy was evaluated clinically and by means of Cronholm-Ottosson's rating scale. The effect was found good and lasting in 29%, good but temporary in 38%, and poor in 32% of the cases. The best results were achieved with twice-weekly treatments, the poorest results with once-weekly treatment. The results were equal in monopolar and bipolar cases and were independent of the number of previous depressions as well as antidepressant drug treatment. No side effects have been observed, in particular no conversion to mania. The results of the present investigation indicate that depression and sleep disturbances are symptoms produced by a common factor which, however, it as yet unknown. Sleep deprivation therapy is seen to have at least some effect on all cases of endogenous depression. Sleep deprivation therapy has no side effects and is more quick-acting than any other treatment procedure hitherto known. It should therefore be considered the first treatment offer to all endogenously depressed patients in whom immediate ECT is not necessitated.
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PMID:Sleep deprivation therapy in depression. 97 Jan 95

Eighty-five cases of atypical schizophrenia were compared with 200 of schizophrenia, 100 of bipolar (mania), and 225 of unipolar (depression) affective disorder. Comparisons were made on the basis of sex, age at admission, precipitating factors, outcome, and a family history of schizophrenia or of affective disorder. The atypical schizophrenia differed remarkably from the schizophrenia and most closely resembled the bipolar affective disorder when allowance was made for a younger age at onset and a higher frequency of precipitants. An analysis of symptoms verified the predominance of schizophrenic features in the atypical schizophrenia, but also showed a high percentage (80%) of patients who had one or more manic symptoms at index admission. It is concluded that great care should be taken in diagnosing schizophrenia in a patient who also has manic symptoms.
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PMID:A study of "atypical schizophrenia". Comparison with schizophrenia and affective disorder by sex, age of admission, precipitant, outcome, and family history. 97 Oct 26

By treating rats with lithium chloride or cocaine hydrochloride, or lithium chloride followed by cocaine hydrochloride, we have shown the antagonistic effects of these drugs on two mechanisms that may be involved in regulating serotonin 5-HT) synthesis in the striate cortex. Lithium chloride (5 to 10 meq/kg/day) stimulates the relative velocity of the active uptake of labelled tryptophan and proportionally enhances the conversion of labelled tryptophan to 5-HT in synaptosomally enriched preparations. With continued administration of lithium chloride, the activity of tryptophan hydroxylase from the median raphe and subsequently in lysed synaptosomal preparations from striate cortex is reduced; the substrate uptake remains enhanced, but the conversion of substrate to transmitter returns to control levels. In contrast, an injection of cocaine hydrochloride inhibits the high affinity uptake of tryptophan, reducing the conversion of the amino acid to 5-HT and resulting in an increase in the biosynthetic enzyme activity. However, administration of cocaine hydrochter three daily lithium chloride injections (10 meq/kg) results in no apparent effects on substrate uptake, conversion, or enzyme activity. We theorize that the effect of lithium was to push two regulatory parameters (the uptake of substrate and the enzyme activity) to their respective functional upper and lower limits, leaving the serotonergic neurons "buffered" against the "usual" effects of the stimulant drug, and offer this neurobiological model for consideration in relation to the clinical effects of lithium in the prophylaxis of both mania and depression in some patients.
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PMID:A neurobiological model for the symmetrical prophylactic action of lithium in bipolar affective disorder. 98 97

The Chair of the University Nervenklinik in Homburg/Saar was held by Klaus Conrad from 1949-58 and by H.-H. Meyer, a former pupil and colleague of Kurt Schneider, from 1962-72. As the catchment area and admission policy of the clinic remained substantially unchanged throughout, comparison of the relative proportions of all admissions allocated to different diagnostic categories in 1949-58 and 1962-72 can be used to elucidate the similarities and differences between Conrad's and Schneider's diagnostic criteria. The results of this comparison indicate that Schneider's concept of schizophrenia was broader than Conrad's, and his concept of manic-depressive depression more restricted. More detailed comparisons are complicated by differences in nomenclature and in the varieties of functional mental illness recognized in the two periods. However, it seems that Conrad's concept of mania was wider only when the atypical schizophrenia-like psychoses diagnosed during the Conrad era were added to the Conrad-oriented cases of mania; when this was not done, the Schneiderian concept of mania was broader.
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PMID:Schneider-oriented versus Conrad-oriented psychiatric diagnosis in the same German clinic. 99 Jun 59

Blood platelet serotonin levels were measured in unmedicated 12 manic and 74 depressive patients with 118 normal control subjects employed. Blood platelets were separated by multiple centrifugation in the medium of Na2-EDTA solution, and the loss of serotonin during collecting procedures was about 11%. The mean value of blood platelet serotonin levels in depressed patients was 594 +/- 288 ng/mg platelet protein (+/- S.D.), which was significantly lower than that for normal controls, 780 +/- 253 ng/mg protein (p less than 0.001). Age does not account for the reduction of serotonin levels both in depressed and in normal population. Unipolar and involutional depressed patients exhibited to have the most pronounced reduced levels of serotonin of various subtypes of depression, while bipolar depressed patients, neurotic and chronic characterological depressed patients as well as patients with first-episode depression had the values which were comparable with those in normal controls. Manic patients did not show enhancement but did reduction of serotonin levels, the mean being 580 +/- 152 ng/mg protein, which made a contrast with their clinical manifestations of exhilaration and hyperactivity. Changes in blood platelet serotonin levels were determined before, during and after administration of L-5-HTP with a maintenance dose of 300 mg daily in nine depressed patients. Serotonin levels in all subjects were lifted to normal levels during the L-5-HTP treatment, while clinical symptoms were not improved with the treatment. Reduction of blood platelet serotonin levels in depressed patients may be due to their psychobiological distinction, which involves abnormal biogenic amine metabolism in the brain.
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PMID:Reduction of blood platelet serotonin levels in manic and depressed patients. 102 43


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