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)

A case of classical Sturge-Weber syndrome associated with infantile spasms (female infant, aged 4 months) was presented. The association of both conditions would be very rare since no similar case was found among 214 cases of Sturge-Weber syndrome and 1,180 cases of infantile spasms gathered from the literature, except for one who was reported by Millichap et al. Evolutional changes of electroencephalographic findings were followed up for about 3 years on average in 5 personal cases of Sturge-Weber syndrome. Unilateral depression of electrical activity in the cerebral hemisphere ipsilateral to the facial nevi was the constant finding. Focal spike discharges were noticed only in the contralateral hemisphere in 3 cases, only in the ipsilateral in 1, and in the bilateral in 1.
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PMID:A study on Sturge-Weber syndrome. Report of a case associated with infantile spasms and electroencephalographic evolution in five cases. 47 91

Sleep and respiration data from two French medical high altitude expeditions (Annapurna 4,800 m and Mt Sajama 6,542 m) are presented. Difficulties in maintaining sleep and a SWS decrease were found with periodic breathing (PB) during both non-REM and REM sleep. Extent of PB varied considerably among subjects and was not correlated to the number of arousals but to the intercurrent wakefulness duration. There was a positive correlation between the time spent in PB and the individual hypoxic ventilatory drive. The relation between PB, nocturnal desaturation, and mountain sickness intensity are discussed. Acclimatization decreased the latency toward PB and improved sleep. Hypnotic benzodiazepine intake (loprazolam 1 mg) did not worsen either SWS depression or apneas and allowed normal sleep reappearance after acclimatization.
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PMID:Sleep apneas and high altitude newcomers. 148 84

During the clinical latency phase of human immunodeficiency virus (HIV) disease the central nervous system may be infected and begin to manifest subtle dysfunction. Our early investigations demonstrated persistent alterations in the sleep architecture of HIV-infected asymptomatic men. The major aims of this study were to delineate alterations of sleep architecture in asymptomatic HIV-infected men, to identify and describe sleep behavior complaints and to seek a correlation between objective sleep parameters and subjective complaints of sleep behavior. The study sample consisted of 24 men, 14 HIV-infected and 10 HIV-negative, age-matched controls. The protocol included a comprehensive history and physical, two polysomnograms, urine toxicity, detailed written sleep questionnaire, the Pittsburgh Sleep Quality Index, the Spielberger State-Trait Anxiety Test and the Beck Depression Inventory. Our results indicated that sleep architecture differed from controls in that wakefulness, slow-wave sleep [SWS-stage 3 and 4 nonrapid eye movement (NREM) sleep] and stage rapid eye movement (REM) sleep were more evenly dispersed throughout the night. In particular, SWS was prevalent during the second half of recorded sleep. The observed changes in the NREM/REM cycle could not be explained on the basis of underlying psychopathology. Just as the course of individuals with HIV infection varies, it is expected that sleep abnormalities will vary. Considering the known relationships between NREM stage 3 and 4 and immune system function, it is possible that the observed alterations in the NREM/REM cycle are related to coincident changes in immunologic function. Quantitative measures of NREM sleep, especially SWS and REM sleep, are perhaps of greater significance than relative measures of sleep stages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep disturbances in men with asymptomatic human immunodeficiency (HIV) infection. 157 89

In rats with the persistent alcohol motivation the electrophysiological sleep pattern was studied during ethanol intake, after 24 and 48 hours of alcohol withdrawal. It was established that during the voluntary ethanol intake rats may be divided into two groups: with comparative deficit (1st group) and comparative abundance (2nd group) of REM sleep. Alcohol withdrawal caused differential alterations of sleep-wakefulness cycle: in the 1st group of rats REM sleep was more suppressed while in the 2nd group--more increased in comparison to those during ethanol intake. In all animals the SWS depression, increase of awakenings, the aggravation of falling asleep and decrease of sleep depth were observed. DSIP (0.1 mg/kg, i.p. 1 hour before sleep recording) was found to regulate sleep disorders caused by ethanol withdrawal. It makes the neuropeptide possible to be recommended for ethanol withdrawal syndrome treatment in clinical practice.
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PMID:[Effects of delta sleep-inducing peptide on electrophysiological parameters of sleep during alcohol withdrawal in rats]. 226 15

Sleep in depression is characterized by an increase in the number and duration of awakenings, sleep instability, and SWS decrease. REM sleep occurs earlier. REMs density during the 1st REM period is higher than in normal controls matched in age. Accordingly, sleep in depression is similar to sleep in normal aging. Endogenous depression cannot be distinguished from other types of depression by means of polygraphic criteria. Sleep recordings at the beginning of tricyclic compound treatment could be predictive of clinical response to treatment. Sleep modifications induced by antidepressive drugs are reviewed. Sleep recordings enabled us to formulate several physiopathological hypotheses of depression mechanisms: cholinergic-aminergic hypothesis, phase advance, deficiency of process S. Other hypotheses are reviewed: flattening of a hypothetical circadian rhythm of arousal, depressogenic property of sleep in itself (or only of SWS) or timing delay for the start of sleep. A significant phase advance of biological rhythms (temperature, cortisol) is rarely found. A reduction in the amplitude of rhythms (temperature, TSH, melatonine) is more frequent.
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PMID:[Sleep and biological rhythms in depression. Changes caused by antidepressants]. 812 20

The amino acids L-glutamate and L-aspartate have been shown to be excitatory neurotransmitters in mammalian central nervous systems. Antagonists acting selectively at excitatory amino acid receptors have shown antiepileptic properties in several animal models. We report the results of the first therapeutic trial of the competitive NMDA antagonist, D-CPP-ene (SDZ EAA-494), in eight patients with intractable complex partial seizures. All patients withdrew prematurely because of side-effects, including poor concentration (8), sedation (7), ataxia (6), depression (3), dysarthria (2), amnesia (2) and unilateral choreo-athetosis in a patient with contralateral Sturge-Weber syndrome. Seizures were unchanged in four patients and worse in three. A further patient with apparent improvement in seizures in the first week developed complex partial status epilepticus on withdrawal of DCPP-ene. EEG on treatment (5) or in the immediate post-treatment period (2) showed slowing of background activity and, in five cases, an increase in epileptiform activity. Serum concentrations of DCPP-ene were found to be unpredictable and higher than expected from pharmacokinetic data on normal subjects. There was no clear relationship between serum concentrations and the severity of side-effects. Preliminary experience with DCPP-ene in patients with refractory partial seizures is not promising. Evaluation of related compounds is warranted.
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PMID:The excitatory amino acid antagonist D-CPP-ene (SDZ EAA-494) in patients with epilepsy. 826 15

The effect of repeated Na-penicillin (PCN) microinjections in the temporal lobe amygdala (AM) of free-moving cats was investigated in order to establish if kindling epileptogenesis is possible with this procedure. The cortical propagation of the PCN-induced post-discharge in AM and the sequence of behavioral changes induced by PCN were similar to those of AM electrical kindling. Nevertheless, the epileptogenic effect of PCN had a different evolution from that of electrical kindling, since some PCN habituation was observed after several doses. Repeated microinjections of PCN did not produce lasting alterations in sleep onset and organization. The only mild changes recorded in the 23 h following PCN microinjections were an increased latency of the first rapid eye movement (REM) sleep episode, a SWS II total time and percentage increase, and, with the highest PCN doses, a not very significant diminution of REM sleep total time. Another finding was the occurrence of REM sleep ponto-geniculo-occipital (PGO) waves, coinciding with a depression of the frequency and amplitude of interictal amygdaloid and cortical spikes. The results showed that a microinjection of PCN in the AM produced a reliable model of interictal spikes, paroxysms and generalized convulsive seizures. Nevertheless, long lasting kindling effect was not observed.
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PMID:Repeated penicillin-induced amygdala epileptic focus in freely moving cats. EEG, polysomnographic (23-h recording), and brain mapping study. 877 99

During the third quarter of her pregnancy, a young woman with Sturge-Weber angiomatosis had a severe right hemiplegia with hemianopia and aphasia, followed 48 hours later by focal seizures. Neuroimaging did not show any cerebral lesion but contrast magnetic resonance imaging revealed a left hemispheric pial angiomatosis. The patient recovered progressively from the third day after a ceasarean. The hemianopia disappeared within 15 days, the hemiplegia within one month and the aphasia greatly improved within 3 months. Ten weeks after the clinical onset, we performed a positron emission tomography study. A decrease from 15 to 40% of the cerebral radioactivity was observed after injection of water (H2(15)O) or fluorodesoxyglucose (18FDG) in the left temporooccipital area adjacent to the meningeal angiomatosis. A chronic and focal olighemia, already reported in Sturge-Weber angiomatosis, might participate in the occurrence of this cortical metabolic depression.
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PMID:[Sturge-Weber angiomatosis responsible for hemiplegia without cerebral infarction in term pregnancy]. 899 Nov 75

The neuropeptides growth hormone-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) play a key role in sleep endocrine regulation. After pulsatile application of GHRH during the first few hours of the night in young normal controls SWS and GH increase, whereas cortisol is blunted. CRH however prompts inverse effects. The balance between these peptides is changed in favour of CRH physiologically during the second time of the night, during the acute episode of depression (due to overactivity of GRH) and in the elderly (due to reduced activity of CHRH). These changes explain the aberrances of sleep endocrine activity in these states, as shallow sleep, low GH and enhanced cortisol.
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PMID:[The role of neuropeptides in normal and disordered sleep regulation]. 901 57

Utilizing polysomnography (PSG) and psychometry, objective and subjective sleep and awakening quality was investigated in 11 drug-free patients (five females, six males) aged 35-75 years (mean age 54.1 +/- 11.4) suffering from nonorganic insomnia (F 51.0) related to a depressive episode (F 32) or recurrent depressive disorder (F 33). as compared with 11 age- and sex-matched normal controls (five females, six males) aged 36-75 years (mean age 53.0 +/- 13.5). PSG demonstrated decreased sleep efficiency, total sleep time (TST), total sleep period (TSP) and sleep stage S2, as well as increased wakefulness during TSP, early morning awakening, sleep latency to S1, S2, S3 and sleep stage S1 in depressed patients. Subjective sleep quality and the total score of the Self-Assessment of Sleep and Awakening Quality Scale (SSA) were deteriorated as were morning and evening well being, drive, mood and fine motor activity right. Evening and morning blood pressure, the O2 desaturation index and periodic leg movement (PLM) index were increased. In a subsequent acute, placebo-controlled cross-over design study, the acute effects of 100 mg of trazodone, a serotonin reuptake inhibitor with a sedative action due to 5-HT2 and alpha1 receptor blockade, were investigated in the patients. As compared with placebo, trazodone induced an increase in sleep efficiency (primary target variable), TST, TSP and SWS (S3 + S4), as well as a decrease in wakefulness during the TSP, early morning awakening and S2. There was no change in rapid eye movement (REM) sleep with the exception of an increase in the REM duration in minutes. Trazodone also caused an improvement in subjective sleep quality, affectivity, numerical memory and somatic complaints. All respiratory variables remained within normal limits. Critical flicker frequency and moming diastolic blood pressure were decreased. The present study demonstrated that depression induced significant changes in objective and subjective sleep and awakening quality, which were counteracted by 100 mg of trazodone, thus suggesting a key-lock principle in the treatment of depression.
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PMID:Insomnia in depression: differences in objective and subjective sleep and awakening quality to normal controls and acute effects of trazodone. 1181 1


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