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PubMed1987

Differential time course of antidepressant effects after sleep deprivation, ECT, and carbamazepine: clinical and theoretical implications.

The pattern and time course of antidepressant response to different treatment modalities provide important clinical information and hints about underlying neurobiological mechanisms. Depressed patients who responded to 1 night's sleep deprivation (11 of 33 patients) showed maximal improvement on day 1 and deterioration in mood thereafter. In contrast, slower onset and more sustained effects were observed following carbamazepine (12 of 37) or electroconvulsive therapy (ECT) (8 of 8). Nearly maximal improvement required about 2 weeks for ECT and 3 weeks for carbamazepine. Possible differential or common biological mechanisms with differential times of action are implied by these data, which are of importance to the neuroscientist attempting to uncover neural substrates of antidepressant response and the clinician attempting to find rapid onset, yet sustained antidepressant treatments.

Carbamazepine↗
PubMed1999

Accelerating antidepressant response in geriatric depression: a post hoc comparison of combined sleep deprivation and paroxetine versus monotherapy with paroxetine, nortriptyline, or placebo.

Speed of response is an important clinical issue in the treatment of depressed elderly patients. Our objective was to compare rapid response rates in a study combining therapeutic sleep deprivation (TSD) with paroxetine with two earlier randomized, double-blind studies in late-life depression, one of paroxetine versus nortriptyline and another of nortriptyline versus placebo. We measured depressive symptoms with the 17-item Hamilton Rating Scale of Depression (HRSD), defining rapid response as an HRSD < or = 10 by 2 weeks. With combination therapy (TSD + paroxetine), 9 of 13 patients (69%) experienced a rapid response. In the nortriptyline versus paroxetine study, nortriptyline brought about rapid response in 12 of 37 (32%) and paroxetine in 11 of 43 patients (26%). In the third study, rapid response to nortriptyline occurred in 10 of 41 patients (24%) and to placebo in 6 of 39 patients (15%). The overall chi square, including the rate of rapid response to placebo, was 14.87 (P = .005). The chi square on the four active treatment groups, excluding placebo, was 10.28 (P = .016). This preliminary observation suggests that combined therapy with TSD plus paroxetine may be twice as successful at achieving rapid response in elderly depressed patients than conventional monotherapy with medication or placebo. A prospective, placebo-controlled evaluation of this dual therapy is warranted.

Aged↗
PubMed2006

Nocturnal ghrelin, ACTH, GH and cortisol secretion after sleep deprivation in humans.

Ghrelin is an endogenous ligand of the growth hormone (GH) secretagogue (GHS) receptor. It is hypothesised to play a key role in energy balance stimulating food intake and body weight. Besides GH-releasing hormone (GHRH) and somatostatin, it is thought to be a regulating factor of GH release. Ghrelin also appears to be involved in sleep regulation. We showed recently that ghrelin promotes slow-wave sleep and the nocturnal release of GH, cortisol and prolactin in humans. Similarly, promotion of non-rapid-eye-movement (NREM) sleep was reported in mice after systemic ghrelin. If ghrelin is a factor that induces and/or maintains sleep, it should be enhanced after a period of sleep deprivation (SD). To clarify this issue, nocturnal ghrelin, GH, ACTH and cortisol plasma concentrations were determined and simultaneously sleep electroencephalogram (EEG) was recorded (2300-0700 h) during sleep before and after 1 night of total SD in 8 healthy subjects. Compared to baseline, ghrelin levels increased earlier by a non-significant trend, already before the beginning of recovery sleep. Further a non-significant trend occurred, suggesting higher ghrelin secretion in the first half of the night. The ghrelin maximum was found significantly earlier after SD than at baseline. GH secretion during the first half of the night and total night after SD were elevated. ACTH and cortisol were also elevated, which was most pronounced during the second half of the night. No effects of SD on the time of the maximum were found for GH, ACTH and cortisol. The increase in ACTH after SD is a novel finding. Whereas the effects of SD on ghrelin levels were relatively weak, our findings are in line with the hypothesis that ghrelin is a sleep-promoting factor in humans. Ghrelin may be involved in sleep promotion after SD.

Adrenocorticotropic Hormone↗
PubMed2003

Antidepressant effects of light therapy combined with sleep deprivation are influenced by a functional polymorphism within the promoter of the serotonin transporter gene.

BACKGROUND: A functional polymorphism within the promoter of the serotonin transporter has been shown to influence the antidepressant response to serotonergic drug treatments and to total sleep deprivation (TSD). The short-term relapse that follows acute response to TSD has been successfully prevented by combining TSD with light therapy. The mechanism of action of this combined treatment is unknown. METHODS: We tested the hypothesis that allelic variation of the serotonin transporter (5-HTT) linked polymorphic region (5-HTTLPR) could influence the response to the combination of light therapy and TSD. Twenty-two bipolar depressed inpatients were administered a night of TSD combined with 30 min light therapy given during the TSD night and in the morning after recovery sleep. 5-HTTLPR was genotyped using polymerase chain reaction techniques. Changes in perceived mood were rated on a visual analog scale. RESULTS: Light therapy sustained the effect of TSD. The effect was more marked in homozygotes for the long variant of 5-HTTLPR than in heterozygotes and homozygotes for the short variant. CONCLUSIONS: The influence of 5-HTTLPR on response to the combination of TSD and light therapy is similar to that observed on response to TSD and serotonergic drug treatments.

Adult↗
PubMed1980

Reversal of paradoxical sleep deprivation by amygdaloid stimulation during learning.

Rats were subjected to a partial, selective paradoxical sleep (PS) deprivation. Two groups were trained in a shuttle avoidance task, one receiving posttraining amygdaloid stimulations (AS). A third group received AS, but was not trained. Levels of PS in the AS trained group were higher than in the AS non-trained controls, while the reverse was true for the slow wave sleep (SWS) measure. Both AS groups had levels of PS and SWS superior to the non-AS trained rats. In a second experiment, a group of normally rested AS animals was trained in the same task with a non-AS control group. These groups did not differ in terms of learning performance. Results were believed to support the hypothesis of a close relationship between sleep and learning.

Amygdala↗
PubMed2005

Rapid eye movement sleep deprivation in post-critical period, adolescent rats alters the balance between inhibitory and excitatory mechanisms in visual cortex.

Suppression of rapid eye movement sleep (REMS) in developing animals has both anatomical and physiological consequences. We have recently shown that initiating REMS deprivation (REMSD) prior to the end of the critical period in young rats delays termination of the critical period (CP) in visual cortex, and, consequently, the synaptic plasticity mechanisms that support a developmentally regulated form of long-term potentiation (LTP) are maintained in an immature state [J.P. Shaffery, C.M. Sinton, G. Bisset, H.P. Roffwarg, G.A. Marks, Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats, Neuroscience, 110 (2002) 431-443]. In CP animals, high-frequency, theta burst stimulation (TBS) directed at the white matter (WM) below visual cortex produces LTP in the post-synaptic cells in layer II/III (LTPWM-III). However, LTPWM-III can be induced in cortical tissue taken from REMS-deprived animals for up to a week beyond the usual end of the CP [J.P. Shaffery, C.M. Sinton, G. Bisset, H.P. Roffwarg, G.A. Marks, Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats, Neuroscience, 110 (2002) 431-443]. Further, in post-CP, adolescent animals (as late as postnatal day 60), REMSD appears to unmask synaptic plasticity mechanisms that allow for production of developmentally regulated LTPWM-III [J.P. Shaffery, J. Lopez, G. Bissette, H.P. Roffwarg, Rapid eye movement sleep deprivation revives a form of developmentally regulated synaptic plasticity in the visual cortex of post-critical period rats, Neurosci Lett., (2005), in press]. It has been proposed that REMSD's effects on production of LTPWM-III result from a reduction in efficiency of the inhibitory mechanisms thought to precipitate termination of the CP of brain development [J.P. Shaffery, J. Lopez, G. Bissette, H.P. Roffwarg, Rapid eye movement sleep deprivation revives a form of developmentally regulated synaptic plasticity in the visual cortex of post-critical period rats, Neurosci Lett., (2005), in press]. In this study we tested the hypothesis that low-frequency stimulation (LFS) of the fibers of the WM, which usually produces the related form of synaptic plasticity, long-term depression (LTD), will also reflect the reduction in inhibitory tone. We report here that LFS protocols, which in normally sleeping, adolescent rats usually produce either LTD or no change in response magnitude, in REMS-deprived, adolescent rats are more likely to produce LTP.

Age Factors↗
PubMed2000

Sleep and sleep deprivation as EEG activating methods.

OBJECTIVES: We examined retrospectively 19 patients with a history of clinical seizures, but normal activity or unclear epileptiform abnormalities in wake EEG recordings and obtained preliminary data for a controlled cohort study to evaluate the effects of sleep deprivation (SD) on interictal epileptic activity. METHODS: Nineteen patients referred to our EEG department for diagnostic or follow-up purposes were divided in two groups on the basis of the different EEG protocols applied. The first group (n=5) underwent two laboratory polysomnographies during afternoon naps, after SD, but the patients failed to fall asleep in one of the two occasions. The second group (n=14) was submitted to two polysomnographies, the first without SD and the second after SD. RESULTS: The first group of patients demonstrated focal epileptic discharges in 4 patients in which wake after SD appeared to be less activated that sleep after SD. In the second group the results obtained from the waking part of the recordings suggest a lack of activating effect due to SD. CONCLUSIONS: SD does not seem to offer greater activation than sleep alone. However, a mild SD may be a convenient activating method for inducing sleep and drowsiness without using any drug.

Brain↗
PubMed1983

Response to dexamethasone suppression and total night sleep deprivation in an affectively disordered Klinefelter patient.

A 50-year-old Klinefelter patient acutely developed a psychotic depression which rapidly responded to treatment with amitriptyline. This patient exhibited an early escape from dexamethasone suppression and became hypomanic the morning after total night sleep deprivation. The findings suggest that the use of biological tests to study affective syndromes occurring in Klinefelter patients might yield clues regarding the existence of pathophysiological common denominators of primary and Klinefelter-associated affective disorders.

Affective Disorders, Psychotic↗
PubMed2002

Plasma catecholamines and selective slow wave sleep deprivation.

The present study evaluated the effect of slow wave sleep (SWS) deprivation on plasma levels of catecholamines in healthy male volunteers. Eleven volunteers spent 4 nights in the sleep laboratory (2 nights of habituation and 2 further nights); during the latter, 1 night served as control, and in the other, SWS deprivation was performed. Blood was drawn at 30-min intervals. SWS was reduced by 86%; no sleep stage 4 was observed during the SWS-deprived nights. SWS reduction was found not to correlate with catecholamine levels. However, epinephrine levels were found to be sensitive to sleep fragmentation. The time interval between arousals in the SWS-deprived night as well as the difference in sleep efficiency were related to increases in epinephrine levels (p < 0.01 and p < 0.025, respectively). These results support the view that continuity rather than the duration of SWS is important for the recuperative value of sleep.

Adult↗
PubMed1997

Repeated REM sleep deprivation after chronic haloperidol administration in the rat.

Repeated haloperidol administration produces up-regulation of dopamine (DA) receptors. REM sleep deprivation (REMSD) does also, but in addition, has been shown to produce REM sleep rebound. Should DA receptor up-regulation play a role in REM sleep rebound, haloperidol could conceivably have effects similar to those observed following REMSD. This is the central question investigated in this study. Male Wistar rats were prepared for sleep recordings. They were randomly assigned to the following groups: group 1, REMSD by small platforms (40 h REMSD + 8 h recording); group 2, was the large platform control group (40 h in large platforms + 8 h of recording); group 3, received 2-week daily administration of haloperidol (3 mg/kg, i.p.) plus REMSD (40 h REMSD + 8 h of recording); group 4, 2-week administration of haloperidol (3 mg/kg) without sleep manipulation and at the end 40 h were allowed to elapse, following which 8 h of sleep recordings was carried out. In each group the sleep manipulation and/or sleep recordings were repeated five consecutive times. Repeated REMSD produced increases of REM sleep time after each recovery in group 1. Large platforms did not produce increases of REM sleep during the recovery trials. The 2-week administration of haloperidol plus REMSD prevented REM sleep rebound (group 3). The 2-week administration of haloperidol without sleep manipulation (group 4) produced a REM sleep reduction. Dopamine modulation seems not to be important for REM sleep rebound. Hypersensitivity of DA receptors developed after REMSD may be an epiphenomenon associated with this sleep manipulation, but seems not to participate in REM sleep enhancement after REMSD.

Animals↗
PubMed1992

Evaluation of the effects of total sleep deprivation on cerebral blood flow using single photon emission computerized tomography.

HMPAO-single photon emission computerized tomography (SPECT) is a useful technique in studying cerebral blood flow (CBF). This method is suitable to evaluate the differences of CBF with reference to total sleep deprivation (TSD) within 24 h because of the short half-life of the radiopharmaceutical compound. In the present study, CBF before and after TSD was analysed in patients suffering from major depression. The morning before and after TSD, Tc-HMPAO-SPECT was performed in 20 patients. Hamilton Rating Scale for Depression scores and subjective ratings were obtained daily. Eleven patients responded to TSD; 9 were nonresponders. The main finding was a significant left temporal and mainly right parietal increase of CBF, which was observed in the responders only. CBF values and the severity of depression correlated inversely.

Adult↗
PubMed1995

Sleep deprivation differentially alters the mRNA and protein levels of neurogranin in rat brain.

The mRNA level of the 17-kDa protein neurogranin (NG), a postsynaptic substrate of the protein kinase C, has previously been found to be decreased in rat forebrain after 24-h sleep deprivation (SD). To investigate the functional significance of this finding in various forebrain regions, the effect of 24-h SD on the mRNA level and the protein level of NG was determined in the cerebral cortex, hippocampus, and the total of the remaining subcortical forebrain plus midbrain areas (SFMA) of rats. In these areas, high levels of both NG mRNA and NG protein were detected by in situ hybridization and immunohistochemistry, respectively. NG protein was recognized in brain tissue by newly developed polyclonal antibodies. As determined by RNase protection assays, the level of NG mRNA was decreased in SFMA by 34 +/- 7% (P < 0.05) after 24-h SD, and was not significantly affected in the cerebral cortex and hippocampus. In contrast, on Western blots, the protein concentration of NG was reduced in the cerebral cortex by 37 +/- 7% (P < 0.05) whereas no significant changes were present in other brain areas tested. The results indicate that the mRNA and protein levels of NG are differentially modulated in rat brain by the prolongation of the waking period.

Animals↗
PubMed1990

Neuroendocrinological investigations during sleep deprivation in depression. I. Early morning levels of thyrotropin, TH, cortisol, prolactin, LH, FSH, estradiol, and testosterone.

Measurements of 12 hormones were conducted in patients with major depressive disorder at 8 AM on the morning before and at 8 AM on the morning after total sleep deprivation (SD). Thyrotropin (TSH), thyroxine (T4), triiodothyronine (T3), and free T3 (fT3) were measured in 50 patients, free T4 in 39 patients, reverse T3, cortisol, prolactin, luteinizing hormone, and follicle-stimulating hormone in 21, estradiol in 20 (women), and testosterone in 14 (men). After SD, there was a significant rise in TSH, T4, T3, and fT3 concentrations and a significant fall in testosterone levels. The increases in TSH levels were significantly correlated to clinical response. Responders to SD had higher T4, fT4, rT3, and testosterone concentrations before SD. Neither age, gender, polarity, nor antidepressant medication had a clearly significant effect on the response to SD.

Adult↗
PubMed1996

Rapid eye movement sleep deprivation in kittens amplifies LGN cell-size disparity induced by monocular deprivation.

The abundance of rapid eye movement (REM) sleep in the neonatal mammal and its subsequent decline in the course of development, as well as the dramatic and widespread enhancement of CNS activity during REM sleep, led us to propose that this state plays a functional role in the normative physiological and structural maturation of the brain [54]. When, after 1 week of monocular deprivation (MD), a second week of MD was coupled with behavioral deprivation of REM sleep, the structural alteration in the visual system provoked by MD alone (interlaminar relay cell-size disparity in the lateral geniculate nucleus (LGN) was amplified. With the addition of REM deprivation during MD, the LGN cells connected to the surgically patched eye, which are smaller than normal after MD, became even smaller, whereas the LGN cells receiving input from the seeing eye, which display compensatory hypertrophy after MD, grew even larger. We believe that the interlaminar disparity effect widened because during REM deprivation, the already vision-compromised LGN cells associated with the patched eye also lose the ascending brainstem activation reaching them during the REM state. Loss of the two main sources of 'afference' by these LGN cells permits their seeing-eye LGN counterparts to gain even greater advantage in the competition for synaptic connections in cortex, which is reflected in the relative soma sizes of the LGN relay cells. It is likely that the relatively abundant REM state in early maturation provides symmetric stimulation to all LGN relay cells, irrespective of eye of innervation. The symmetric activation propagated from brainstem to LGN acts to 'buffer' abnormal, asymmetric visual input and, thereby diminishes the extreme, asymmetric structural alteration that results from MD in the absence of REM sleep. We conclude that REM sleep-generated CNS discharge in development has the effect of 'protecting' the CNS against excessive plasticity changes. This is consistent with the possibility that REM sleep plays a role in the genetically programmed processes that direct normative brain development.

Animals↗
PubMed2005

Caffeine maintains vigilance and marksmanship in simulated urban operations with sleep deprivation.

PURPOSE: The purpose of this study was to examine the effects of caffeine (CAF) on physical, vigilance, and marksmanship tasks in soldiers during a sustained 55-h field exercise. METHODS: There were 30 soldiers (23.6 +/- 4.5 yr, 81.8 +/- 10.3 kg) who were divided into a placebo (PLAC) and a CAF group. After a period of restricted sleep of 3 h during the first night, a period of sustained wakefulness began that ended at 11:00 of the third day. PLAC or CAF doses of 100 mg, 200 mg, 100 mg, and 200 mg were administered at 21:45, 23:45, 01:45, and 03:45, respectively. At 22:00 of day 2, subjects began two cycles of marksmanship, urban operations vigilance, and psychomotor vigilance (PVT) testing which ended at 06:00 of day 3. RESULTS: CAF maintained marksmanship vigilance at 85% throughout the second night as compared with PLAC, who significantly declined to 61.4 +/- 28.2% overnight. Marksmanship accuracy also decreased significantly in PLAC from 95.1 +/- 8.3% to 83.3 +/- 19.2%, but no change was observed in CAF. Urban operations vigilance decreased for both groups over the night, but the decrease was less for CAF (81.2 +/- 14.4% to 63.4 +/- 24.1%) compared with PLAC (77.6 +/- 19.2% to 44.0 +/- 30.2%). Reaction time and the number of major and minor lapses with the PVT significantly increased in PLAC but were unaffected in CAF. CONCLUSIONS: It was concluded that CAF was an effective strategy to sustain vigilance and psychomotor performance during military operations involving sleep deprivation.

Adult↗
PubMed1994

Sleep deprivation as a diagnostic instrument.

A 59-year-old man with chronic treatment-resistant depression developed severe cognitive impairment. The severity of depression and the mode of presentation led to difficulty in diagnosis between a dementing disorder and a depressive illness. The diagnostic conundrum was resolved by the use of sleep deprivation (SD), which demonstrated clear subjective and objective improvements in his condition. These changes were quantified by a range of psychometric tests, which showed that initial deficits in cognitive performance improved temporarily after SD, and these improvements were maintained after effective treatment of the depression with electroconvulsive therapy.

Cognition Disorders↗