Biomedical subjects

H P Landolt

Publications and source records attributed to H P Landolt.

At least 19 recordsLinked to original sources

PubMed2005

Exposure to pulse-modulated radio frequency electromagnetic fields affects regional cerebral blood flow.

We investigated the effects of radio frequency electromagnetic fields (RF EMF) similar to those emitted by mobile phones on waking regional cerebral blood flow (rCBF) in 12 healthy young men. Two types of RF EMF exposure were applied: a 'base-station-like' and a 'handset-like' signal. Positron emission tomography scans were taken after 30 min unilateral head exposure to pulse-modulated 900 MHz RF EMF (10 g tissue-averaged spatial peak-specific absorption rate of 1 W/kg for both conditions) and sham control. We observed an increase in relative rCBF in the dorsolateral prefrontal cortex on the side of exposure. The effect depended on the spectral power in the amplitude modulation of the RF carrier such that only 'handset-like' RF EMF exposure with its stronger low-frequency components but not the 'base-station-like' RF EMF exposure affected rCBF. This finding supports our previous observation that pulse modulation of RF EMF is necessary to induce changes in the waking and sleep EEG, and substantiates the notion that pulse modulation is crucial for RF EMF-induced alterations in brain physiology.

Adult↗

PubMed2001

Sleep and sleep electroencephalogram in depressed patients treated with phenelzine.

BACKGROUND: The beneficial effect of antidepressant interventions has been proposed to depend on suppression of rapid eye movement (REM) sleep or inhibition of electroencephalographic (EEG) slow-wave activity (SWA) in non-REM sleep. Use of the monoamine oxidase inhibitor phenelzine sulfate can eliminate REM sleep. We studied the relation between REM sleep suppression and antidepressant response and the effect of phenelzine therapy on sleep EEG power spectra. METHODS: Open-labeled prescriptions of 30 to 90 mg of phenelzine were given to 11 patients with major depressive disorder (6 men and 5 women; mean age, 41.4 years); all were physically healthy. Mood, dream recall, sleep, sleep EEG, and ocular and muscular activity during sleep were studied before treatment and during the third and fifth weeks of pharmacotherapy. RESULTS: Six patients remitted from depression, 2 responded partially, and 3 showed no antidepressant response. Independent from clinical response, REM sleep was dramatically suppressed. On average, only 4.9 minutes of REM sleep was observed in treatment week 5, and it was completely absent in 6 patients. This effect was compensated for by increased stage 2 sleep. In non-REM sleep, EEG power was higher than at baseline between 16.25 and 25 Hz. Slow-wave activity (power within 0.75-4.5 Hz) and the exponential decline of SWA during sleep were not affected. CONCLUSIONS: Antidepressant response to phenelzine treatment does not depend on elimination of REM sleep or inhibition of SWA in non-REM sleep. In depressed patients, REM sleep is regulated independently from non-REM sleep and can be manipulated without altering the dynamics of SWA.

Adult↗

PubMed2001

Effect of chronic phenelzine treatment on REM sleep: report of three patients.

Antidepressants belonging to the class of monoamine oxidase inhibitors (MAOI) such as phenelzine have long been known to drastically suppress REM sleep. Sleep and the electroencephalogram (EEG) in sleep and waking were studied in three depressed patients at regular time intervals before, during and after 6 to 18 months of phenelzine treatment. While REM sleep was initially eliminated in all patients, short REM sleep episodes reappeared after three to six months of medication. Total sleep time and EEG slow-wave activity (SWA, spectral power within 0.75-4.5 Hz) in nonREM sleep (stages 1-4) were not changed. In contrast, EEG theta frequency activity (TFA, power within 4.75-8.0 Hz) during a 5-min wake interval recorded prior to the sleep episodes was initially enhanced, and tended to correlate negatively with the percentage of REM sleep (p =.06). This observation indicates that compensatory REM sleep mechanisms may occur in wakefulness during chronic MAOI treatment.

Adult↗

PubMed2001

Age-dependent changes in sleep EEG topography.

OBJECTIVE: To assess age-related topographic changes in the sleep electroencephalogram (EEG). METHODS: The sleep EEG records of young (mean age, 22.3 years) and middle-aged (mean age, 62.0 years) healthy men were compared. The EEG was obtained from 3 bipolar derivations (frontal-central (FC), central-parietal (CP), and parietal-occipital (PO)) along the antero-posterior axis. RESULTS: The total sleep time, sleep efficiency, stage 2 and slow wave sleep (SWS) were lower in the middle-aged group, while sleep latency, stage 1 and wakefulness after sleep onset were higher. Spectral analysis documented the age-related reduction of EEG power in non-REM sleep (0.25-14 Hz), and REM sleep (0.75-10 Hz). However, the reduction was not uniform over the 3 derivations, but was most pronounced in the anterior derivation (FC) in the theta (both sleep states) and high-alpha/low-sigma bands (non-REM sleep). CONCLUSIONS: These changes can be interpreted as age-related shifts of power from the anterior (FC) towards the middle derivation (CP). Aging not only reduces power in the sleep EEG, but causes frequency-specific changes in the brain topography. The results are consistent with the notion of sleep as a local process.

Adult↗

PubMed2001

Sleep abnormalities during abstinence in alcohol-dependent patients. Aetiology and management.

Virtually every type of sleep problem occurs in alcohol-dependent patients. Typically, these individuals take a longer time to fall asleep and show decreased sleep efficiency, shorter sleep duration and reduced amounts of slow wave sleep when compared with healthy controls. Their sleep patterns are fragmented, and the typical time course of electroencephalogram (EEG) delta wave activity is severely disrupted. The amount of rapid eye movement (REM) sleep may be reduced or increased. Sleep changes can persist during months or years of abstinence, and recent studies indicate that certain alterations in sleep architecture, as well as subjective sleep complaints, predict relapse to alcoholism. The mechanisms of action of short and long term alcohol administration on sleep are incompletely understood. They may arise from an interaction with gamma-aminobutyric acid (GABA), serotonin (5-hydroxytryptamine; 5-HT), adenosine or other neurotransmitter systems. While only a few pharmacological and nonpharmacological strategies to improve or normalise disturbed sleep in individuals who have recovered from alcoholism have been studied, the use of benzodiazepines, other hypnosedatives or selective serotonin reuptake inhibitors is not recommended. Therapies include sleep hygiene, bright light therapy, meditation, relaxation methods, and other nonpharmacological approaches. Further studies are needed to clarify the relationship between sleep, sleep abnormalities and alcoholism, and to establish new approaches to improve sleep in alcohol-dependent patients and to prevent withdrawal reactions that affect sleep during abstinence.

Alcoholism↗

PubMed2000

Clinical and physiological consequences of rapid tryptophan depletion.

We review here the rapid tryptophan depletion (RTD) methodology and its controversial association with depressive relapse. RTD has been used over the past decade to deplete serotonin (5-hydroxy-tryptamine, or 5-HT) in humans and to probe the role of the central serotonin system in a variety of psychiatric conditions. Its current popularity was stimulated by reports that RTD reversed the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs) in remitted patients with a history of depression but not in patients treated with antidepressants which promote catecholaminergic rather than serotonergic neurotransmission (such as tricyclic antidepressants or buproprion). However, RTD has inconsistent effects in terms of full clinical relapse in depressed patients. Pooling the data from all published reports, patients who are either unmedicated and/or fully remitted are much less likely to experience relapse (7 of 61, or approximately 9%) than patients who are recently medicated and partially remitted (63 of 133, or approximately 47%; although, the numbers here may reflect patient overlap between reports). Recently remitted patients who have been treated with non-pharmacological therapies such as total sleep deprivation, electroconvulsive therapy, or bright light therapy also do not commonly show full clinical relapse with RTD. We briefly review RTD effects in other psychiatric disorders, many of which are treated with SSRIs. There is accumulating evidence to suggest that RTD affects central serotonergic neurotransmission. Nevertheless, many questions remain about the ability of RTD to reverse the beneficial effects of SSRIs or MAOIs, or to induce symptoms in unmedicated symptomatic or asymptomatic patients.

Antidepressive Agents↗

PubMed2000

[Alcohol and sleep disorders].

Despite an initial sedative effect, alcohol disrupts sleep persistently and should not be used as a sleeping aid. Nocturnal withdrawal symptoms may lead to an increased duration of wakefulness, and to tachycardia and sweating in the second half of the night. It is not known by which mechanism alcohol affects sleep; however, effects do not appear to depend on the stimulation of benzodiazepine receptors or the antagonism at adenosine receptors. Alcohol can exacerbate primary sleep disturbances such as sleep apnea and nocturnal myoclonus, and thereby contribute to excessive daytime sleepiness. The sleep of alcoholic patients is characterized by increased sleep latency, and reduced sleep efficiency, total sleep time, slow wave sleep and non-REM sleep. Even during abstinence, the changes in sleep architecture can persist for months or years, and might contribute to a relapse into alcoholism. The use of benzodiazepines or other hypnotics to treat alcohol-related sleep disturbances is not recommended.

Alcohol Drinking↗

PubMed2000

Functional neuroanatomy of human sleep states after zolpidem and placebo: a H215O-PET study.

Changes in the functional organization of the brain during the course of sleep and waking are reflected by different patterns of regional cerebral blood flow (rCBF). To investigate the effect of the hypnotic zolpidem, a benzodiazepine receptor agonist, drug or placebo were administered to eight young, healthy men prior to bedtime. The subjects were sleep-deprived to promote sleep during the 4-h recording period in the positron emission tomography scanner. Intravenous injections of labelled water were administered during pre-drug wakefulness, and during Stage 2, Stage 4 and rapid eye movement (REM) sleep, each injection being followed by an emission scan. Statistical parametric mapping was used to investigate the effects of treatment and sleep states. During sleep (combined Stages 2 and 4, and REM sleep) relative rCBF was lower after zolpidem than after placebo in the basal ganglia and insula, and higher in the parietal cortex. A 'multiple study' analysis of REM sleep revealed that rCBF in the anterior cingulum was lower after zolpidem than after placebo, whereas rCBF in the occipital and parietal cortex, parahippocampal gyrus and cerebellum was higher. When the pooled data (drug and placebo) of Stages 2 and 4 were compared with wakefulness, rCBF was lower in prefrontal cortex and insula, and higher in the occipital and parietal cortex. The results indicate that some differences in rCBF from wakefulness to non-REM sleep are further augmented by zolpidem.

Adult↗

PubMed2000

Zolpidem and sleep deprivation: different effect on EEG power spectra.

To study the role of GABA-ergic mechanisms in sleep regulation, the combined action of 40 h sleep deprivation and either 20 mg zolpidem or placebo on the sleep electroencephalogram (EEG) were investigated by quantitative EEG analysis in eight young men who participated in a positron emission tomography study. Compared with baseline, sleep deprivation increased low-frequency (1.25-7.0 Hz) EEG power in non-rapid eye movement (NREM) sleep in the placebo night. After administration of zolpidem, power in the 3.75-10.0 Hz range and 14. 25-16.0 Hz band was reduced. The largest decrease was observed in the theta band. Comparison with placebo revealed that zolpidem attenuated power in the entire 1.75-11.0 Hz range. The plasma concentration of zolpidem at 4.5 h after intake showed a positive correlation with the drug-induced difference in power from placebo in the 14.25-16.0 Hz band. Regional EEG analysis based on bipolar derivations along the antero-posterior axis disclosed, for NREM sleep, a drug-induced posterior shift of power in the frequency range of 7.75-9.75 Hz. Zolpidem did not affect rapid eye movemnt sleep spectra. We conclude that sleep deprivation and agonistic modulation of GABAA receptors have separate and additive effects on power spectra and that their effects are mediated by different neurophysiological mechanisms.

Adult↗

PubMed1999

Serotonin-2 receptors and human sleep: effect of a selective antagonist on EEG power spectra.

To investigate the effect on the sleep EEG, a 1-mg oral dose of SR 46349B, a novel 5-HT2 antagonist, was administered three hours before bedtime. The drug enhanced slow wave sleep (SWS) and reduced stage 2 without affecting subjective sleep quality. In nonREM sleep (NREMS) EEG slow-wave activity (SWA; power within 0.75-4.5 Hz) was increased and spindle frequency activity (SFA; power within 12.25-15 Hz) was decreased. The relative NREMS power spectrum showed a bimodal pattern with the main peak at 1.5 Hz and a secondary peak at 6 Hz. A regional analysis based on bipolar derivations along the antero-posterior axis revealed significant 'treatment' x 'derivation' interactions within the 9-16 Hz range. In enhancing SWA and attenuating SFA, the 5-HT2 receptor antagonist mimicked the effect of sleep deprivation, whereas the pattern of the NREMS spectrum differed.

Adult↗

PubMed1998

Human versus porcine insulin in patients with insulin-dependent diabetes mellitus: differences in sleep and the sleep EEG during near-normoglycemia.

To investigate whether porcine insulin (PI) and human insulin (HI) have different effects on brain functions outside of hypoglycemia, sleep and the sleep EEG were recorded in eight insulin-dependent diabetes mellitus (IDDM) patients in three separate sessions of 2 consecutive nights. Near-normoglycemia was confirmed by measurements of capillary blood glucose before and after sleep and at 0145 hours. The treatment effect (PI compared to HI) consisted of a change in the NREM sleep EEG in the spindle frequency range. Spectral power density in the 14-Hz bin was reduced upon transfer from PI (session 1) to HI (session 2) in all subjects, and increased upon reversal to PI (session 3) in all but one subject. There were no significant treatment effects on any other sleep EEG variable or on sleep stages. The subjects rated their sleep as more sound and their state in the morning as more relaxed during PI treatment. They were, however, not blinded to the type of insulin they were using. Porcine insulin and human insulin may exert differential effects on spindle-generating mechanisms in the thalamocortical system. The results indicate that human insulin may affect brain functions differently compared to animal insulin under near-normoglycemic conditions.

Adult↗

PubMed1998

Effect of frequent brief awakenings from nonREM sleep on the nonREM-REM sleep cycle.

In the framework of a selective sleep deprivation study, eight young men were repeatedly awakened during 3 nights from nonREM sleep (nonREMS). The mean number of awakenings per night was 27.4, 29.5 and 32.8. In order to avoid excessive suppression of slow wave sleep, no awakening occurred in the first nonREMS episode. Compared to baseline, cycle 2 was significantly prolonged in all 3 nights, and cycle 3 in night 3 only. However, after subtracting the waking intervals, the differences from baseline was eliminated. The results show that the mechanisms underlying sleep cycle control keep track of sleep time and disregard epochs of waking.

Adult↗

PubMed1998

Selective REM sleep deprivation in humans: effects on sleep and sleep EEG.

To investigate rapid eye movement (REM) sleep regulation, eight healthy young men were deprived of REM sleep for three consecutive nights. In a three-night control sleep deprivation (CD) session 2 wk later, the subjects were repeatedly awakened from non-REM sleep in an attempt to match the awakenings during the REM sleep deprivation (RD) nights. During the RD nights the number of sleep interruptions required to prevent REM sleep increased within and across consecutive nights. REM sleep was reduced to 9.2% of baseline (CD nights: 80.7%) and rose to 140.1% in the first recovery night. RD gave rise to changes in the EEG power spectra of REM sleep. Power in the 8.25- to 11-Hz range was reduced in the first recovery night, an effect that gradually subsided but was still present in the third recovery night. The rising REM sleep propensity, as reflected by the increase of interventions within and across RD nights, and the moderate REM sleep rebound during recovery can be accounted for by a compensatory response that serves REM sleep homeostasis. The changes in the electroencephalogram power spectra, which were observed during enhanced REM sleep propensity, may be a sign of an altered quality of REM sleep.

Adult↗

PubMed1996

Effect of age on the sleep EEG: slow-wave activity and spindle frequency activity in young and middle-aged men.

The effect of age on sleep and the sleep EEG was investigated in middle-aged men (mean age: 62.0 years) and in young men (mean age: 22.4 years). Even though the older men reported a higher number of nocturnal awakenings, subjective sleep quality did not differ. Total sleep time, sleep efficiency, and slow wave sleep were lower in the middle-aged, while stage 1 and wakefulness after sleep onset were higher. The differences in wakefulness within nonREM-REM sleep cycles was most pronounced in the third and fourth cycle. In the older men, EEG power density in nonREM sleep was reduced in frequencies below 14.0 Hz, whereas in REM sleep age-related reductions were limited to he delta-theta (0.25-7.0 Hz) and low alpha (8.25-10.0 Hz) band. Slow-wave activity (SWA, power density in the 0.75-4.5 Hz range) decreased in the course of sleep in both age groups. The between-group difference in SWA diminished in the course of sleep, whereas the difference in activity in the frequency range of sleep spindles (12.25-14.0 Hz) increased. It is concluded that frequency and state specific changes occur as a function of age, and that sleep dependent decline in SWA and increase in sleep spindle activity are attenuated with age.

Adult↗

PubMed1996

Late-afternoon ethanol intake affects nocturnal sleep and the sleep EEG in middle-aged men.

The effect of a moderate dose of ethanol (0.55 g/kg of body weight), administered 6 hours before scheduled bedtime, on performance, nocturnal sleep, and the sleep electroencephalogram (EEG) was investigated in 10 healthy, middle-aged men (mean age: 61.6 +/- 0.9 years). By the beginning of the sleep episode, breath-ethanol concentrations had declined to zero in all subjects. Compared with the control condition (mineral water), sleep was perceived as more superficial. Sleep efficiency, total sleep time, stage 1, and rapid eye movement (REM) sleep were reduced. In the second half of the sleep episode, wakefulness exhibited a twofold increase. EEG power density in low delta frequencies was enhanced in non-REM sleep (1.25-2.5 Hz) and REM sleep (1.25-1.5 Hz). In slow wave sleep (i.e., stages 3 + 4), power density was increased not only in the low-frequency range (1.25-1.5, 2.25-4.0, 4.75-5.0 Hz) but also within the alpha (8.25-9.0 Hz) and sigma (12.25-13.0 Hz) band. The data demonstrate that late-afternoon ethanol intake in middle-aged men disrupts sleep consolidation, affects the sleep stage distribution, and alters the sleep EEG.

Caffeine↗

PubMed1995

Melatonin effect on daytime sleep in men: suppression of EEG low frequency activity and enhancement of spindle frequency activity.

The effect of melatonin (5 mg, p.o.) on electroencephalographic (EEG) activity during sleep was investigated in eight men in a placebo-controlled cross-over design. Melatonin was administered immediately prior to a 4-h daytime sleep episode (13-17 h) after a partial sleep deprivation. The non-REM sleep stages and REM sleep duration were not significantly affected. Melatonin enhanced EEG power density in non-REM sleep in the 13.75-14.0 Hz bin (i.e., within the frequency range of sleep spindles), and reduced activity in the 15.25-16.5 Hz band. In the first 2 h spectral values within the 2.25-5.0 Hz range were reduced. These changes in the EEG are to some extent similar to those induced by benzodiazepine hypnotics and to the contribution of the endogenous circadian pacemaker to the spectral composition of the sleep EEG when sleep occurs at night.

Adult↗

PubMed1995

Intracranial temperature across 24-hour sleep-wake cycles in humans.

The 24 h time course of intracranial temperature, recorded subdurally at the parahippocampal gyrus in six patients (19 24 h periods), exhibited a prominent 24 h rhythm with its crest located at 20-21 h. The declining trend of intracranial temperature between lights off and sleep onset persisted in the first nonREM sleep episode (studied in two patients, seven sleep episodes). The correlation between EEG slow-wave activity (SWA) in nonREM sleep and the change in temperature explained < 25% of the variance. Although the change in temperature tended to be more positive in REM sleep episodes than in nonREM sleep episodes, no significant increase was observed in REM sleep. The data indicate that intracranial temperature exhibits a marked 24 h rhythm, the time course of which is only slightly affected by nonREM/REM sleep and EEG synchronization.

Adult↗

PubMed1995

Caffeine intake (200 mg) in the morning affects human sleep and EEG power spectra at night.

Adenosine has been implicated in the physiological regulation of sleep propensity. The adenosine-receptor-antagonist, caffeine (100 mg), administered immediately prior to a nocturnal sleep episode, has previously been shown to lower sleep propensity as indexed by a reduced sleep efficiency, a reduced EEG power density in low delta frequencies and enhanced power density in the frequency range of sleep spindles. To further investigate the role of adenosine in sleep regulation we administered 200 mg of caffeine at 07.10 h and analyzed the sleep stages and EEG power spectra during the subsequent night in nine healthy men. Caffeine levels in saliva decreased from a maximum of 17 mumol/l one hour after intake, to 3 mumol/l immediately prior to the sleep episode starting at 23.00 h. Compared to placebo, sleep efficiency and total sleep time were significantly reduced. EEG power density in nonREM sleep was suppressed in the 0.25-0.5 Hz band and enhanced in the frequency range of sleep spindles (11.25-12.0 Hz and 13.25-14.0 Hz). In REM sleep EEG power density was suppressed in the frequency range of 0.75-4.5 and 5.25-6.0 Hz. The data indicate that a saliva level of caffeine as low as 3 mumol/l directly affects sleep propensity or, alternatively, that the presence of caffeine in the central nervous system during the waking episode reduces the progressive increase of sleep propensity associated with wakefulness.

Adult↗