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Biomedical subjects

E Seifritz

Publications and source records attributed to E Seifritz.

At least 37 records · Page 2Linked to original sources
PubMed2000

Inhibition of phenprocoumon anticoagulation by carbamazepine.

Carbamazepine inhibits warfarin and dicoumarol anticoagulation through induction of cytochrome P450-enzymes. Inhibition of phenprocoumon anticoagulation by carbamazepine has been supposed in some reviews, however, without hard empirical evidence. We report a patient who was anticoagulated with phenprocoumon in whom carbamazepine produced a dramatic increase in prothrombin time ratio (Quick). After discontinuation of carbamazepine, Quick-values returned to therapeutic levels. Valproate did not affect phenprocoumol's anticoagulant properties. The potentially hazardous carbamazepine-phenprocoumon interaction should be emphasized in reference drug manuals.

Anticoagulants↗
PubMed2000

Sleep in depression and sleep deprivation: a brief conceptual review.

Risk factors for somnipathies are psychological stress or psychiatric illness. More severe sleep difficulties have been found to be clearly related to psychiatric illness such as depression and phobias, as well as to addiction. Somnipathies can objectively be identified by means of polygraphy. Overall, polysomnographic measures in patients with affective disorders differ most frequently and significantly from those in normal control subjects. Persistent sleep disturbances are associated with significant risk of both relapse and recurrence in mood disorders and an increased risk of suicide. In addition to changes in sleep architecture, patients with major depression show profoundly altered patterns of nocturnal hormone secretion, possibly through mechanisms that link regulation of sleep with neuroendocrine activity. Basic and clinical approaches of sleep research established neurobiological models into the underlying pathophysiology associated with psychiatric disorders.

Major Depressive Disorder↗
PubMed1999

Rapid cortical hemoglobin deoxygenation after heroin and methadone injection in humans: a preliminary report.

The short-term effects of intravenous opioids (heroin 20-300 mg, methadone 30-180 mg) on cortical hemoglobin oxygenation were examined by near infrared spectroscopy in ten opioid-dependent subjects and were compared with the effects of saline in ten age-matched normal controls. Heroin and methadone produced a rapid and dramatic decrease in cortical hemoglobin oxygenation. Saline had no effects. Opioid-induced acute deoxygenation of cortical hemoglobin is most likely associated with respiratory depression. Thorough medical monitoring is strongly recommended in intravenous opioid maintenance treatments.

Adult↗
PubMed1999

Titration of the BOLD effect: separation and quantitation of blood volume and oxygenation changes in the human cerebral cortex during neuronal activation and ferumoxide infusion.

Most functional magnetic resonance imaging (fMRI) techniques are sensitive to susceptibility variations and rely on the change in blood oxygenation level in response to neuronal activation (BOLD). The BOLD effect is accompanied by a change in cerebral blood flow (rCBF) and cerebral blood volume (rCBV). Intravascular contrast agents, such as magnetite nanoparticles, can be used to measure changes in rCBV. A new measuring protocol has been developed that enables the separate quantification of changes in blood volume and oxygenation levels. A combination of alternating acoustic stimulation blocks and infusion of a superparamagnetic contrast agent offers the possibility to disentangle the competing influences of oxygenation and blood volume changes. Serial blood sampling during infusion was used to assess the actual contrast agent concentration during infusion in order to calculate absolute blood volume changes during neuronal resting and activation states. Magn Reson Med 42:829-836, 1999.

Acoustic Stimulation↗
PubMed1998

Sleep electroencephalographic response to muscarinic and serotonin1A receptor probes in patients with major depression and in normal controls.

BACKGROUND: To test the hypothesis that depression is associated with an increased ratio of cholinergic to serotonergic neurotransmission, we compared the effects of pilocarpine, a muscarinic agonist, and ipsapirone, a serotonin (5-HT)1A agonist, on electroencephalographic (EEG) sleep in depressed and healthy subjects. We hypothesized, adopting the reciprocal interaction model, that the effects on REM sleep of these probes within the same individuals are negatively correlated and unmask neurobiological changes in depression. METHODS: Polysomnographic recordings were obtained in 12 unmedicated patients with a current major depression and 12 normal controls. They received placebo, pilocarpine 25 mg, or ipsapirone 10 mg (orally, 15 min before bedtime, after premedication with the peripheral anticholinergic probanthine 30 mg, double blind, counterbalanced) on three occasions. RESULTS: Pilocarpine shortened and ipsapirone prolonged REM latency equally in both groups. These effects were not correlated. Pilocarpine decreased slow-wave sleep and EEG delta power during the first nonREM episode more in controls than in patients, and enhanced EEG sigma power equally in both groups. Ipsapirone had no significant effects on EEG power. CONCLUSION: These data do not support the postulate of muscarinic receptor up-regulation and 5-HT1A receptor down-regulation in depression. The significance of blunted delta power suppression in patients following pilocarpine warrants further investigations.

Adult↗
PubMed1998

Microsleep during partial sleep deprivation in depression.

BACKGROUND: Sleep deprivation (SD) exerts a beneficial effect on mood and sleep in about 60% of depressed patients usually followed by a relapse into depression after the recovery night. Short phases of sleepiness, especially naps in the early morning, may be responsible for this phenomenon. METHODS: To evaluate the effect of short, even ultrashort phases of sleep-microsleep (MS) during partial sleep deprivation (PSD) on mood, cognitive psychomotor performance (CPP), and sleep, an electroencephalograph (EEG) was continuously recorded over 60 hours in 12 patients with major depression. Subjective mood was assessed by a visual analogue scale and CPP by a letter cancellation test. RESULTS: The results illustrate that in depressed patients during PSD the amount of MS is increased, predominantly in the early morning, which was subjectively unrecognized and not observed by nursing staff. Patients with a low cumulative amount of MS during PSD improved significantly in mood, CPP, and sleep pattern compared to the patients with a high amount of MS who showed only slight changes. CONCLUSION: Therefore, accumulated MS may influence the SD-induced positive effects in depressed patients.

Adult↗
PubMed1998

Effects of a tryptophan-free amino acid drink challenge on normal human sleep electroencephalogram and mood.

BACKGROUND: Serotonin has been implicated in the regulation of sleep and mood. In animals a tryptophan-free amino acid drink (TFD) challenge has been found to reduce brain serotonin. We hypothesized this TFD would produce alterations in electroencephalographic (EEG) sleep commonly associated with depression, i.e. an enhancement of rapid eye movement (REM) sleep, and adversely affect mood ratings in humans. METHODS: We investigated the effects of a TFD challenge in 11 healthy male subjects on EEG sleep and mood (assessed by Profile of Mood States). All subjects received on separate occasions an experimental drink containing approximately 100 g of an amino acid mixture (100% TFD) and a control drink containing one fourth strength (25% TFD) of the experimental drink 5 hours prior to sleep (6:00 PM). RESULTS: Both drinks significantly decreased plasma tryptophan levels 5 hours postchallenge (11:00 PM). Both drinks significantly decreased REM latency, and the 25% TFD also increased REM time and REM% compared to baseline. No significant changes were found in subjective ratings of depression; however, subjects reported confusion and tension and a decrease in elation, vigor, and friendliness compared with baseline. CONCLUSIONS: These TFD findings further support the involvement of serotonin deficiency in EEG sleep findings commonly seen in depression.

Adult↗
PubMed1998

Rapid tryptophan depletion, sleep electroencephalogram, and mood in men with remitted depression on serotonin reuptake inhibitors.

BACKGROUND: In previous studies, depletion of brain serotonin by administration of a tryptophan-free amino acid drink (TFD) (1) temporarily reversed the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) in euthymic patients who had a history of major depression, and (2) enhanced rapid eye movement (REM) sleep in normal volunteers. In this study, we hypothesized that the TFD would not only increase depressive symptoms but also the propensity for REM sleep in euthymic patients treated with SSRIs. METHODS: Ten fully remitted, medicated male patients who had a history of major depressive episode ingested a 100-g TFD (the experimental dose) or a 25-g TFD (designed to be the control drink) in double-blind, random order on separate days. The effects were assessed with mood ratings, plasma tryptophan concentrations, and an all-night sleep electroencephalogram. RESULTS: The TFDs produced a dose-dependent reduction in plasma tryptophan concentrations, sleep latency, and REM latency, as well as increased REM percentage, REM minutes, REM density, and total sleep time. Neither strength of TFD altered mood to a clinically significant degree. CONCLUSIONS: Although the TFD affected plasma tryptophan concentrations and various sleep measures, our study did not confirm previous reports that TFD temporarily reversed the antidepressant effects of SSRIs in euthymic patients. Our patients, however, had been treated for a longer period with SSRIs and were more fully remitted at the time of the study. Our results suggest that TFD-induced relapse in SSRI-treated patients in remission decreases as a function of treatment duration, degree of remission, or both.

Amino Acids↗
PubMed1998

Effects of corticotropin-releasing factor on circadian locomotor rhythm in the golden hamster.

Stress produces a reduction in the amplitude of some circadian rhythms. The neurochemical mechanisms underlying stress-induced changes in circadian rhythms are not known. To investigate a possible role of corticotropin-releasing factor (CRF) in this phenomenon, three related experiments were carried out: activity rhythms of male golden hamsters (10/14 hours light/dark entrained, lights on at 0800 h) were measured 1) following the intracerebroventricular administration of CRF (0.5, 1.0, 2.0, or 4.0 microg) at two different times of day, 2) following social stress (30-min resident-intruder confrontation), 3) and following the administration of the CRF-antagonist alpha-helical CRF9-41 (2.0 microg) prior to a 15-min resident-intruder confrontation. CRF produced a significant, dose-related decrease in circadian rhythm amplitude following administration in the morning hours, but not in the afternoon. CRF also induced transient increases in activity post injection concomitant with an activation of the hypothalamic-pituitary-adrenocortical (HPA) system. Stress similarly reduced the amplitude of activity patterns and stimulated the HPA system. The stress-induced depression of circadian rhythm amplitude was significantly attenuated following alpha-helical CRF9-41. These data suggest a role for CRF in the stress-related modulation of circadian locomotor rhythm amplitude.

Aggression↗
PubMed1997

Human sleep EEG following the 5-HT1A antagonist pindolol: possible disinhibition of raphe neuron activity.

The sleep electroencephalogram (EEG) was used to assay central effects of pindolol (10 and 30 mg p.o.), a mixed beta(1/2)-adrenoceptor/5-hydroxytryptamine (5-HT)(1A/1B) receptor blocker, in humans. Compared to placebo, pindolol produced a dose-related suppression of rapid-eye-movement (REM) sleep, including a prolongation of REM latency, and a decrease of REM time and REM density. At the higher dose, it also reduced EEG spectral power during non-REM sleep in portions of the delta, theta, and alpha frequencies (1.125-5.125 Hz, 7.125-9.625 Hz). By contrast, betaxolol (20 mg p.o.), a selective beta1-antagonist devoid of serotonergic affinity, affected neither REM sleep nor EEG power. REM sleep is, in part, under the inhibitory control of serotonergic neurons projecting from the dorsal raphe nucleus to pontine cholinergic/cholinoceptive cells. The EEG power spectrum induced by pindolol tended to be opposite to what has previously been reported for ipsapirone, a 5-HT1A agonist. Therefore, the present data, tentatively, are consistent with the contention that pindolol inhibits, possibly selectively, somatodendritic 5-HT1A autoreceptors in humans and may antagonize self-inhibition of midbrain raphe nuclei 5-HT neurons.

Adrenergic beta-Antagonists↗
PubMed1997

Side effects of adjunct light therapy in patients with major depression.

Adjunct bright-light therapy has been suggested to augment antidepressant drug treatment in patients with non-seasonal major depression. Side effects of the combined therapy have not been investigated thus far. Therefore, somatic complaints and side effects of combined therapy were evaluated in 28 patients with major depression (DSM-III-R) randomly assigned to either trimipramine or trimipramine and serially applied adjunct bright-light therapy. Response rates were comparable in both treatment groups and rates of newly emergent side effects during treatment were generally low. The most prominent unfavourable side effects of adjunct bright-light therapy as compared with trimipramine monotherapy were aggravated sedation, persisting restlessness, emerging sleep disturbance and decreased appetite as well as the worsening of vertigo. Discriminant analysis revealed that the combination of trimipramine with bright light results in a different side effect profile compared with drug monotherapy.

Antidepressive Agents, Tricyclic↗
PubMed1997

Category fluency is also predominantly affected in Swiss Alzheimer's disease patients.

OBJECTIVES: To establish the comparative efficacy to differentiate between Swiss patients with dementia of the Alzheimer type (DAT) and elderly normal control subjects (NC) on two different verbal fluency tasks: category fluency and letter fluency. MATERIAL AND METHODS: Fifty Swiss German DAT patients in the early stages of the disease and 50 matched normal control subjects were compared on letter and category fluency tasks. RESULTS: DAT patients exhibited an overproportional impairment on category fluency as compared with letter fluency. Receiver operating characteristic curves (ROC) showed that category fluency correctly classified a significantly higher number of DAT patients and NC subjects (84%) than letter fluency (70%). CONCLUSION: As similar findings have been described for English-speaking DAT patients, we conclude that deficiencies in category fluency are a general phenomenon, reflecting impaired structures of semantic knowledge occurring early in the course of Alzheimer's disease.

Aged↗
PubMed1997

CRF/NPY interactions: a potential role in sleep dysregulation in depression and anxiety.

Neuropeptide Y (NPY) has neuromodulatory actions on multiple brain functions including endocrine, behavioral, and circadian processes and has been implicated in the pathophysiology of both anxiety and depression. Behavioral studies suggest that NPY is a potent anxiolytic, whereas CRF is anxiogenic, thus it seems that a balance of these two peptides may exert important influences on behavioral state regulation. However, little is known about how the NPY/CRF balance affects general arousal, attention, and/or sleep states. The present study evaluated the effects of CRF alone, and co-administered with NPY, on spontaneous brain activity as well as on auditory processing using electrophysiological measures. Electroencephalographic (EEG) and event-related potentials (ERPs) were obtained in rats following intracerebroventricular administration of CRF (0.5 microgram) and CRF (0.5 microgram)/NPY (5.0 or 15 micrograms). Auditory processing, as assessed by ERPs, was affected most significantly in the frontal cortex where CRF produced increases in the N1 and P3 components of the ERP, and NPY/CRF co-administration produced significant decreases. These data are consistent with a role for CRF in hyperarousal, and further suggest that NPY may be capable of reversing such states. Administration of CRF also produced a significant increase in the time to sleep onset and a decrease in the amount of time spent in non-rapid eye movement (NREM) sleep as quantified by scoring the EEG paper records. Co-administration of NPY with CRF reversed the effects of CRF on sleep duration and sleep onset in a dose-dependent fashion. Spectral analysis revealed that CRF produced quantitative changes in the EEG that were similar to what has previously been reported. CRF-induced increases in fast frequency activity were found to be reversed by co-administration of NPY. Taken together these data suggest that "dysregulation" of sleep and arousal states in depression and anxiety may be consistent with an upset of the balance between hypothalamic neuropeptide systems.

Animals↗
PubMed1996

The 5-HT1A agonist ipsapirone enhances EEG slow wave activity in human sleep and produces a power spectrum similar to 5-HT2 blockade.

The REM sleep-suppressing effect of postsynaptic 5-HT1A stimulation has been well established. Here we investigate the effects of the 5-HT1A agonist ipsapirone (10 and 20 mg) on sleep EEG power spectra during non-REM sleep in nine healthy humans. At the lower dose, slow wave activity (SWA; EEG power in the delta (1-4.5 Hz) range) was significantly enhanced. At the higher dose, where side-effects occurred, the enhancement in SWA was not significant. The spectral profile was characterized by a bimodal increase of power in the lower delta and in the theta (5-8 Hz) frequencies, and by troughs at 4 Hz and at 11 Hz, a pattern compellingly similar to that reported for a 5-HT2 antagonist (seganserin). We propose that the spectral data following the lower ipsapirone dose reflect a net decrease of neuronal activity at 5-HT2 receptors, mediated through stimulation of somatodendritic autoreceptors in the raphe nuclei (presynaptic) and/or through stimulation of postsynaptic 5-HT1A receptors colocalized with 5-HT2 receptors. The spectral non-REM sleep EEG profile might be used to investigate central 5-HT function in humans.

Adult↗