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Biomedical subjects

P Linkowski

Publications and source records attributed to P Linkowski.

At least 73 records · Page 4Linked to original sources
PubMed1991

Quantitative analysis of the 24-hour blood pressure and heart rate patterns in young men.

To characterize the normal nycterohemeral blood pressure and heart rate profiles and to delineate the relative roles of sleep and circadian rhythmicity, we performed 24-hour ambulatory blood pressure monitoring with simultaneous polygraphic sleep recording in 31 healthy young men investigated in a standardized physical and social environment. Electroencephalographic sleep recordings were performed during 4 consecutive nights. Blood pressure and heart rate were measured every 10 minutes for 24 hours starting in the morning preceding the fourth night of recording. Sleep quality was not significantly altered by ambulatory blood pressure monitoring. A best-fit curve based on the periodogram method was used to quantify changes in blood pressure and heart rate over the 24-hour cycle. The typical blood pressure and heart rate patterns were bimodal with a morning acrophase (around 10:00 AM), a small afternoon nadir (around 3:00 PM), an evening acrophase (around 8:00 PM), and a profound nocturnal nadir (around 3:00 AM). The amplitude of the nycterohemeral variations was largest for heart rate, intermediate for diastolic blood pressure, and smallest for systolic blood pressure (respectively, 19.9%, 14.1%, and 10.9% of the 24-hour mean). Before awakening, a significant increase in blood pressure and heart rate was already present. Recumbency and sleep accounted for 65-75% of the nocturnal decline in blood pressure, but it explained only 50% of the nocturnal decline in heart rate. Thus, the combined effects of postural changes and the wake-sleep transition are the major factors responsible for the 24-hour rhythm in blood pressure. In contrast, the 24-hour rhythm of heart rate may reflect an endogenous circadian rhythm, amplified by the effect of sleep. We conclude that modulatory factors different from those controlling nycterohemeral changes in blood pressure influence the 24-hour variation in heart rate.

Adolescent↗
PubMed1990

Fluoxetine in major depression: efficacy, safety and effects on sleep polygraphic variables.

Fluoxetine (60 mg), a selective inhibitor of the reuptake of 5-HT, was compared in a double-blind trial to amitriptyline (150 mg) in a sample of 34 patients fitting the Research Diagnostic Criteria for a major depressive disorder. Patients were studied after a drug washout period of 10 days and an active treatment period of 42 days. Sleep polygraphic recordings were performed before and at the end of the study. As indicated by the significant decrease in the Hamilton Depression scale and the Montgomery Asberg Depression scale, fluoxetine showed similar antidepressant effects to amitriptyline with significantly fewer adverse effects. Fluoxetine and amitriptyline decreased the amount of REM sleep, a well known effect of classical antidepressants. Fluoxetine showed some specific effects on sleep continuity (potentially dose related) as indicated by the significant increase in the number of awakenings and in stage shifts, without interfering with the therapeutic response.

Adolescent↗
PubMed1989

Specific determination of plasma dexamethasone by HPLC and RIA--application to standard dexamethasone suppression test in psychiatric patients.

Three radioimmunoassays (RIA), with or without preparative HPLC, were applied to the monitoring of plasma dexamethasone (DXM) levels during standard dexamethasone suppression test (DST) in psychiatric patients. Due to the robotic ease of the fully automated HPLC process, precision of the chromatographic assay was equivalent to that of the direct assays, but prepurification improved both sensitivity and specificity. These improvements allowed the elucidation of the following features: (1) half (36) of the patients (68) displayed infranormal DXM levels (less than or equal to 0.40 ng/ml) whatever the cortisol response; (2) 22% (15) patients (68) with DXM levels in the low control range showed a strong inhibition of cortisol suppression. These observations raise some doubts on the validity of the DST test and introduce the following questions. (1) What is the dependence of cortisol suppression upon DXM absorption and catabolism? (2) Does plasma DXM measurement several hours after its physiological action still reflect its effect on the hypothalamo-hypophyseal axis? (3) What is the reliability of DXM direct assays when measuring low DXM levels in the presence of high cortisol?

Adult↗
PubMed1989

The 24-hour profile of plasma prolactin in men with major endogenous depressive illness.

Plasma prolactin (PRL) levels were measured at 15-minute intervals for 24 hours in 18 men suffering from major endogenous depressive illness and in 7 age-matched healthy men. Eleven of the 18 depressed patients were restudied during clinical remission following either electroconvulsive therapy or treatment with amitriptyline hydrochloride. During the acute phase of the illness, the unipolar depressed patients had fragmented patterns of PRL secretion with an early timing of the nocturnal secretory phase of PRL, which started, on the average, 2 hours earlier than in healthy subjects. Moreover, the amplitude of the circadian variation of PRL was reduced in these patients, with subnormal PRL levels occurring during the midsleep period. This latter abnormality was also observed in bipolar patients, who had otherwise normal PRL profiles. These lower midsleep PRL concentrations were associated with a significant increase in the amount of time spent awake during the same period. Antidepressant treatment did not consistently correct the abnormalities in the patterns of PRL release observed during the acute phase of the illness. These results indicate that early timing of nocturnal PRL secretion and damping of the nighttime PRL elevation may be found in men with endogenous depressive disorders. In contrast to disturbances of the corticotropic and somatotropic axes, these abnormalities of PRL secretion may still be present during clinical remission following antidepressant treatment.

Adult↗
PubMed1989

EEG sleep patterns in man: a twin study.

All-night EEG sleep recording was performed for 3 consecutive nights in 26 pairs of normal male twins (14 monozygotic and 12 dizygotic) in order to investigate genetic components of sleep. The analysis was based on average values of repeated sleep measures and controlled for the effect of cohabitation. Our results indicate that a significant proportion of variance in stages 2, 4 and delta sleep as well as in REM density is genetically determined in man. Genetic influences on stage 1 and REM are strongly confounded by a synchronizing effect of the cohabitational status.

Adolescent↗
PubMed1989

[Sleep apnea syndrome : multidisciplinary management. Apropos of a preliminary experience].

The authors describe a multidisciplinary approach for patients with sleep apnea syndrome. During the first year 40 patients with obstructive sleep apnea documented by polysomnographic recordings were managed. Therapy proposed to the patient included weight loss and abstention from sedatives at night as sole treatment (n = 12) or, more often, combined with nasal and/or throat surgery (n = 21) or nasal continuous positive airway pressure (NCPAP) during sleep (n = 7). NCPAP was by far the most effective in reversing apneas but in view of its cost for the patient and its constraining aspects was proposed solely to those patients with the most severe apnea syndromes.

Adult↗
PubMed1989

Effects of intravenous catheter on sleep in healthy men and in depressed patients.

The effects of intravenous catheter and nocturnal blood samplings at frequent intervals on sleep electroencephalogram (EEG) variables were investigated in 8 male healthy controls and 12 depressed patients, who were studied in the same experimental conditions. After one night of habituation, sleep was recorded during 4 consecutive nights in the sleep laboratory. A catheter was inserted around noon the day before the fourth night, and blood was sampled every 15 min for 25 h. The night-to-night comparison of sleep EEG variables did not show significant sleep continuity modifications in the control subjects, other than a weak trend toward an increase in nocturnal awakenings during the night with the catheter. A lengthening of sleep onset latency during the fourth night was found in the depressed patients. No significant changes were detected in percentage of rapid eye movement (REM) sleep in the two groups. However, a gradual increase in Stage 3 was observed across the 4 nights in the control subjects. These results indicate that intravenous blood sampling via a catheter can be performed without inducing significant disruption of sleep length and structure.

Adult↗
PubMed1988

[Neuroendocrine rhythms in uni- and bipolar depressions].

Eighteen patients with major depressive disorder of the endogenous subtype (8 unipolars and 10 bipolars) were submitted to blood sampling at 15 min interval for 24 h with polygraphic sleep recording during an acute episode of depression. Plasma growth hormone (GH), adrenocorticotrophin (ACTH) and cortisol were measured in each sample. The depressed patients hypersecreted GH during the daytime and had hypercortisolism which was evident throughout the 24 h span. The nadir of ACTH and cortisol rhythms was advanced by an average of 3 h as compared to the timing observed in normal subjects. These abnormalities were more pronounced and more consistent in patients with unipolar rather than bipolar depression. These results are consistent with the hypothesis that disorders of circadian time-keeping may characterize major endogenous depression.

Adrenal Cortex Hormones↗
PubMed1988

Multivariate study of sleep EEG in depression.

The effects of four subtypes of major depressive disorder on four sleep EEG variables obtained in 153 depressed inpatients were analyzed taking into account the effects of age, gender, DST response and severity of depression. We have found that age significantly affected slow wave sleep. Sleep efficiency and total sleep time were shown to vary with age and severity of depression. Such effects were not detected for REM latency which was influenced by the endogenous subtype and the gender. Our data indicate that in depressed patients sleep EEG measures are influenced by multiple factors.

Adult↗
PubMed1987

24-hour profiles of adrenocorticotropin, cortisol, and growth hormone in major depressive illness: effect of antidepressant treatment.

Plasma ACTH, cortisol, and GH concentrations were measured at 15-min intervals for 24 h in 11 men suffering from major depressive illness during an acute episode of depression and during clinical remission following antidepressant treatment with either electroconvulsive therapy or amitriptyline. Seven age-matched normal men also were studied. During the acute phase of the illness, the patients had abnormally short rapid eye movement sleep latencies, hypercortisolism, early timing of the nadirs of the ACTH-cortisol rhythms, and shorter nocturnal periods of quiescent cortisol secretion. GH was hypersecreted during wakefulness, and a major pulse occurred before, rather than after, sleep onset. After treatment, rapid eye movement sleep latencies were lengthened, and cortisol levels returned to normal due to a decrease in the magnitude of episodic pulses. Moreover, the timing of the circadian rhythms of ACTH and cortisol as well as the duration of the quiescent period of cortisol secretion were normalized. The amount of GH secreted during wakefulness decreased to normal values, with fewer significant GH pulses. The major elevation of GH secretion in the early part of the night occurred later than that during the depressive episode. These results demonstrate that a disorder of circadian rhythmicity characterizes acute episodes of major depressive illness and that this chronobiological abnormality as well as the hypersecretion of ACTH, cortisol, and GH are state rather than trait dependent.

Adrenocorticotropic Hormone↗
PubMed1986

Sleep during mania in manic-depressive males.

Sleep polygraphic recordings were performed in six unmedicated male manics, in age and sex matched unipolar and bipolar depressives and in normal controls. No difference was evidenced between manics, depressives and controls when percentages of sleep stages 1, 2, 3, 4 and REM were considered. Manics demonstrated poorer sleep efficiency, longer sleep onset latency and reduced sleep period time than normal controls but no more so than in our depressed patients. None of the classical sleep disturbances reported in depression (short REM latency, decreased delta sleep and increased REM density) were observed in mania suggesting that with the exception of sleep continuity disturbances, sleep in mania is comparable to sleep in normal subjects.

Adult↗
PubMed1985

Sleep EEG recordings in depressive disorders.

Sleep polygraphic recordings were performed during 3 consecutive nights in a sample of 43 affectively ill inpatients. The patients were classified as major (n = 36) or minor depressive disorder (n = 7), according to the Research Diagnostic Criteria. Among the 36 patients with a major depressive disorder, 14 were in remission at the time of the sleep investigation. A two-way analysis of variance was performed to assess night and diagnostic effect on sleep variables. Shortening of REM latency was observed in depressed patients with major depressive disorder when compared to major depressive disorder patients in remission. Depressed patients with major depressive disorder also showed higher REM activity and REM density values than patients with minor depressive disorder. According to the linear discriminant analysis, sleep variables were able to correctly classify 68% of the patients.

Adult↗
PubMed1985

Effects of ECT on sleep and CSF biogenic amines in affective illness.

The effects of electroconvulsive therapy (ECT) on sleep and cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid (5HIAA) and homovanillic acid (HVA) were studied in 11 male patients suffering from major depressive disorders severe enough to require ECT. Total sleep time and sleep efficiency index increased significantly after ECT, while the number of awakenings, the ratio wake/total sleep time, and the time of intermittent awake decreased, indicating that sleep continuity improved after treatment. Sleep architecture was also favorably influenced by ECT as shown by a significant increase in time of stage 2 and rapid eye movement (REM) sleep. REM latency and REM density also normalized after ECT. CSF 5HIAA increased significantly after ECT, but this was not the case for CSF HVA. These results demonstrate a positive effect of ECT on sleep EEG and CSF neurochemical markers for depressive illness.

Adult↗
PubMed1985

Suicidal behaviour in major depressive illness.

We investigated past suicidal behaviour and family history of suicide in 713 inpatients with major depressive illness. A familial history of suicide (mainly violent) significantly increased the frequency of violent suicidal behaviour in depressive women; bipolar patients being more affected than unipolars. In depressed men, the presence of suicidal behaviour was not significantly affected by polarity. The occurrence of familial suicide significantly increased the risk of violent suicidal behaviour in male depressed attempters. The present study indicates that a familial history of violent suicide is associated with the presence of violent suicidal behaviour in major depressive patients.

Adolescent↗
PubMed1985

Diurnal hypersecretion of growth hormone in depression.

A 24-h profile of plasma GH concentrations was obtained together with polygraphic recordings of sleep in 16 men suffering from a major depressive disorder (8 unipolar and 8 bipolar) and in 8 age- and sex-matched normal men. None of the patients had any physical illness. All were studied after a drug-free period of at least 15 days. Blood was sampled every 15 min. The amount of GH released in every significant secretory spike was estimated using a computer program. Both unipolar and bipolar depressed patients secreted more GH than normal men (mean +/- SD, 441 +/- 189 micrograms/24 h for unipolar depressed men; 357 +/- 143 micrograms/24 h for bipolar depressed men vs. 172 +/- 101 micrograms/24 h for normal men (P less than 0.01). This hypersecretion occurred during waking hours rather than during sleep. The increase in daytime GH release was more marked in unipolar depressed patients. During sleep, depressed patients and normal men secreted similar amounts of GH despite an overall reduction in slow wave stages in depressed patients. An early sleep GH increase was found in all but one of the normal men, but was absent in seven of the eight unipolar depressed patients, who had, instead, a presleep increase in between 2100-0000 h. No consistent disturbance of the temporal association between sleep onset and GH secretion was found in bipolar depressed patients.

Adult↗