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J C Gillin

Publications and source records attributed to J C Gillin.

At least 37 records · Page 2Linked to original sources
PubMed1999

Sleep deprivation-induced reduction in cortical functional response to serial subtraction.

Thirteen normal volunteers were studied with fMRI during arithmetic performance after a normal night of sleep and following sleep deprivation (SD). Aims included determining whether the prefrontal cortex (PFC) and the parietal lobe arithmetic areas are vulnerable to the effects of SD. After a normal night of sleep, activation localized to the bilateral PFC, parietal lobes and premotor areas. Following SD, activity in these regions decreased markedly, especially in the PFC. Performance also dropped. Data from the serial subtraction task are consistent with Horne's PFC vulnerability hypothesis but, based on this and other studies, we suggest the localized, functional effects of SD in the brain may vary, in part, with the specific cognitive task.

Adult↗
PubMed1999

Sleep EEG studies during early and late partial sleep deprivation in premenstrual dysphoric disorder and normal control subjects.

In this study of 23 patients with premenstrual dysphoric disorder (PMDD) and 18 normal comparison (NC) subjects, we examined sleep EEG measures during baseline midfollicular (MF) and late luteal (LL) menstrual cycle phases and after early sleep deprivation (ESD), in which subjects slept from 03.00 to 07.00 h, and late sleep deprivation (LSD), in which subjects slept from 21.00 to 01.00 h. Each sleep deprivation night was followed by a night of recovery sleep (ESD-R, LSD-R) (sleep 22.30-06.30 h) and was administered in the late luteal phase of separate menstrual cycles. During baseline studies, sleep EEG measures differed significantly by menstrual cycle phase, but not group. Both PMDD and NC groups showed longer REM latencies and less REM sleep (minutes and percent) during the luteal compared with the follicular menstrual cycle phase. PMDD subjects, however, did not show sleep architecture changes similar to those of patients with major depressive disorders. Sleep quality was better during recovery nights of sleep in PMDD compared with NC subjects. REM sleep measures changed in association with clinical improvement in responders to sleep deprivation. Both early and late sleep deprivation may help to correct underlying circadian rhythm disturbances during sleep in PMDD, although differential sleep changes during ESD vs. LSD did not correlate with clinical response. Further sleep studies addressing additional circadian variables may serve to elucidate mechanisms mediating the therapeutic effects of sleep deprivation in PMDD.

Affect↗
PubMed1999

Prediction of antidepressant effects of sleep deprivation by metabolic rates in the ventral anterior cingulate and medial prefrontal cortex.

OBJECTIVE: Sleep deprivation has been shown to have an antidepressant benefit in a subgroup of depressed patients. Functional imaging studies by the authors and others have suggested that patients with elevated metabolic rates in the anterior cingulate gyrus at baseline are more likely to respond to either sleep deprivation or antidepressant medications than patients with normal metabolic rates. The authors extend their earlier work in a larger group of patients and explore additional brain areas with statistical probability mapping. METHOD: Thirty-six patients with unipolar depression and 26 normal volunteers were studied with positron emission tomography before and after sleep deprivation. Response to sleep deprivation was defined as a 40% or larger decrease in total scores on the Hamilton Depression Rating Scale. RESULTS: One-third of the depressed patients had a significant response to sleep deprivation. Responders had higher relative metabolic rates in the medial prefrontal cortex, ventral anterior cingulate, and posterior subcallosal gyrus at baseline than depressed patients who did not respond to sleep deprivation and normal volunteers. Lower Hamilton depression scores correlated significantly with lower metabolic rates in the left medial prefrontal cortex. After sleep deprivation, significant decreases in metabolic rates occurred in the medial prefrontal cortex and frontal pole in the patients who responded positively to sleep deprivation. CONCLUSIONS: High pretreatment metabolic rates and decreases in metabolic rates after treatment in the medial prefrontal cortex may characterize a subgroup of depressed patients who improve following sleep deprivation and, perhaps, other antidepressant treatments.

Adolescent↗
PubMed1999

Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications.

The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.

Adult↗
PubMed1998

Is there a relationship between delta sleep at night and afternoon cerebral blood flow, assessed by HMPAO-SPECT in depressed patients and normal control subjects? Preliminary data.

We wished to explore the relationships between waking HMPAO uptake and visually scored polysomnography. We hypothesized that HMPAO activity would correlate positively with slow wave sleep measures the same night. Eight unmedicated unipolar patients with current DSM-IV major depression (17-item Hamilton Depression Rating Scale score 21.5+/-2.9) and seven control subjects received polysomnography on 2 consecutive nights. On the afternoon following the adaptation night, subjects received cerebral SPECT, with 15 mCi Tc-99m-HMPAO injected while subjects performed the Continuous Performance Task. Patients and control subjects did not significantly differ on demographic, polysomnographic, and SPECT variables. Slow wave sleep measures correlated positively (Spearman's) with global and regional tracer activity for depressed (n = 8), control (n = 7) and combined groups (n = 15); in other words, the greater the global or regional afternoon HMPAO uptake, the greater the slow wave sleep measures were the same night. In addition, the greater the waking afternoon global or regional HMPAO activity, the faster subjects fell asleep and the less Stage 2% they had. In patients, global and regional HMPAO activity correlated positively with REM density. Positive correlations between waking tracer activity and subsequent slow wave measures are consistent with previous hypotheses linking slow wave sleep with brain energy conservation and restoration. Further study is needed to determine whether these functional relationships differ in depression.

Adult↗
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

Comparative effects of nefazodone and fluoxetine on sleep in outpatients with major depressive disorder.

BACKGROUND: Sleep disturbances are common in major depressive disorder. In previous open-label trials, nefazodone improved sleep continuity and increased rapid eye movement (REM) sleep, while not affecting stage 3/4 sleep or REM latency: in contrast, fluoxetine suppressed REM sleep. This study compared the objective and subjective effects of nefazodone and fluoxetine on sleep. METHODS: This paper reports combined results of three identical, multisite, randomized, double-blind, 8-week, acute-phase trials comparing nefazodone (n = 64) with fluoxetine (n = 61) in outpatients with nonpsychotic major depressive disorder and insomnia. Sleep electroencephalographic (EEG) recordings were gathered at baseline and weeks 2, 4, and 8. Clinical ratings were obtained at weeks 1-4, 6, and 8. RESULTS: Nefazodone and fluoxetine were equally effective in reducing depressive symptoms; however, nefazodone differentially and progressively increased (while fluoxetine reduced) sleep efficiency and reduced (while fluoxetine increased) the number of awakenings in a linear fashion over the 8-week trial. Fluoxetine, but not nefazodone, prolonged REM latency and suppressed REM sleep. Nefazodone significantly increased total REM sleep time. Clinical evaluations of sleep quality were significantly improved with nefazodone compared with fluoxetine. CONCLUSIONS: Nefazodone and fluoxetine were equally effective antidepressants. Nefazodone was associated with normal objective, and clinician- and patient-rated assessments of sleep when compared with fluoxetine. These differential sleep EEG effects are consistent with the notion that nefazodone and fluoxetine may have somewhat different modes and spectra of action.

Adult↗
PubMed1998

Increased REM sleep density at admission predicts relapse by three months in primary alcoholics with a lifetime diagnosis of secondary depression.

BACKGROUND: Having previously reported that 3-month relapse was associated with increased admission REM pressure in nondepressed primary alcoholics, we hypothesized that baseline polysomnography would predict outcome in primary alcoholics with a lifetime diagnosis of secondary depression. METHODS: Twenty-one primary alcoholics with secondary depression received polysomnography and the Hamilton Depression Rating Scale during the first and fourth weeks of a 1-month inpatient alcohol treatment program. Exclusion criteria included serious illness, current major alcohol withdrawal symptoms, other Axis I diagnoses, sleep apnea, nocturnal myoclonus, and psychoactive substances within 14 days of polysomnography. Relapse was defined as drinking any alcohol between hospital discharge and 3-month follow-up. RESULTS: Relapsers' total sleep time was reduced, and REM density (reflecting REM sleep ocular activity) was increased significantly throughout admission compared with abstainers. Sleep continuity and Hamilton scores improved by discharge in sober and relapsing alcoholics. Factors derived from admission REM latency, REM percent, and REM density predicted sobriety vs. relapse within 3 months after hospital discharge in 76% of patients. Admission REM density was greater, and total sleep time was less in relapsers than in patients sober at 3 months. CONCLUSIONS: Results suggest that increased REM density and decreased total sleep time at about 2-4 weeks of abstinence predict relapse by 3 months in depressed alcoholics.

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

Neonatal scopolamine or antidepressant treatment: effect on development of hamster circadian rhythms.

Chronic treatment of young rodents with drugs altering monoamine metabolism has been reported to produce lasting effects on behavior that resemble human affective disorders. To test the generality of this finding, scopolamine, imipramine, or clomipramine was injected daily between the ages of 8 and 21 days in golden hamsters. Wheel-running rhythms were monitored continuously from the age of 4 to 20 weeks of age to test the hypothesis that neonatal treatments would lower the amplitude of biological activity rhythms in adults. Of these three neonatal treatments only scopolamine altered running rhythms, significantly increasing the amplitude of running rhythms in adult hamsters under both entrained and free-running conditions. Hamsters treated neonatally with scopolamine were also more sensitive to the hypothermic effects of the muscarinic agonist, oxotremorine, as adults. These data indicate that neonatal exposure to cholinergic receptor blockade may produce long-lasting changes in biological rhythm characteristics related to upregulation of muscarinic receptors.

Aging↗
PubMed1998

A comparison of descriptive characteristics of male outpatients and inpatients with affective disorders.

Recent studies of patients with affective disorders have found that there are biological differences between inpatients and outpatients. Concerned by these findings, we compared individuals admitted to our inpatient and outpatient affective disorders clinical research center who met criteria for major depression. We hypothesized that inpatients would be more severely ill, more suicidal, more functionally impaired, and have more co-morbid disorders and higher ratings of depression and mood state dysfunction. The demographic profiles, lifetime co-morbid Axis I diagnoses, consumption histories, symptom profiles, global assessment of functioning, and severity of current stressors (Axis IV) were compared and contrasted for the two groups. Inpatients had more severe current psychosocial stressors, lower current levels of functioning, increased lifetime co-morbid Axis I diagnoses, and increased rates of psychiatric hospitalizations, however, they did not have higher depression symptom ratings. In conclusion, inpatients and outpatients differed significantly in the severity of their stressors, coping abilities and history of previous hospitalizations, but not in most demographic variables or their current symptoms of depression.

Adaptation, Psychological↗
PubMed1998

Are sleep disturbances risk factors for anxiety, depressive and addictive disorders?

This paper reviews recent literature which suggests that sleep disturbance in members of the general population, whether or not they have ever had a formal psychiatric disorder, is a risk factor for the onset of a formal psychiatric diagnosis at a later time. Based upon the current literature, the strongest link is between subjective insomnia, lasting at least 2 weeks, and the later onset of depression. Less well-established data suggest that lifetime reports of at least 2 weeks of insomnia, hypersomnia, or both hypersomnia and insomnia, are risk factors for the later development of depression, anxiety disorders or substance abuse. More tentatively, preliminary data suggest that increasing subjective sleep disturbance may signal a relapse in remitted depressed patients. Sleep disturbances are common manifestations of major depressive and anxiety disorders. Therefore, sleep complaints may be among the most robust prodromal symptoms reflecting partial depressive or anxiety disorders, which eventually declare themselves as full-blown clinical episodes.

Anxiety Disorders↗
PubMed1998

The sleep of abstinent pure primary alcoholic patients: natural course and relationship to relapse.

Sleep in male pure primary alcoholic inpatients was examined at a mean of 16 days (n = 29), 19 weeks (n = 29), 14 months (n = 9), and 27 months (n = 4) of abstinence. Results were as follows: (1) the sleep of abstinent alcoholic patients is short, fragmented, and shallow early in abstinence; (2) a patient's sleep improves slowly over at least the first year of abstinence; however, (3) some facets of a patient's sleep remain abnormal even after 27 months of abstinence; (4) insomnia and sleep fragmentation after approximately 5 months of abstinence may be related to relapse by 14 months. The mechanism underlying the relationship between sleep and withdrawal in alcoholic patients is not well understood, and the issue of treating sleep problems as an adjunct to prevention of relapse warrants further investigation.

Adult↗
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

Cigarette smoking predicts development of depressive symptoms among U.S. adolescents.

To examine whether adolescent cigarette smoking predicts the development of depressive symptoms, we used a longitudinal follow-up survey of 6,863 adolescents ages 12 to 18 in the U.S. who did not report notable depressive symptoms at baseline. This study used a self-report measure of six depressive symptoms experienced within the past twelve months at follow-up as the outcome of interest. Results indicated that 11.5% developed notable depressive symptoms at follow-up. There were marked gender differences with 15.3% of girls developing notable depressive symptoms compared to 8.1% of boys. Gender differences in depressive symptoms were consistent across all age groups and were apparent by the age of twelve. For both genders, smoking status was the most significant predictor of developing notable depressive symptoms. Several other risk factors including involvement in organized athletics, availability of social support, and personality characteristics were also found to be associated with development of depressive symptoms. Adolescent cigarette smoking may have marked health consequences in terms of depressive symptoms. The reduction of cigarette smoking among adolescents should be a focus of depression prevention interventions. In addition, the development of gender-specific components of prevention interventions may be warranted.

Adolescent↗
PubMed1997

Subthreshold depressions: clinical and polysomnographic validation of dysthymic, residual and masked forms.

We summarize clinical and polysomnographic findings in support of the existence of a broad and prevalent spectrum of less than syndromal or subthreshold depressive conditions that constitute subeffective disorders. Many of these conditions were previously subsumed under such rubrics as 'neurotic,' 'characterological,' and 'existential' depressions. Prospective follow-up studies of neurotic depressions (defined by a predominance of the psychological features of, in most instances, less than syndromal depression) have demonstrated their transformation into moderate to melancholic or psychotic depressive, and even bipolar, disorders. Many characterological depressives (outpatients with early insidious onset and fluctuating chronicity of subthreshold manifestations falling short of full syndromal depression), were shown to have shortened REM latency, increased REM%, redistribution of REM to the first part of the night, classic diurnality, high rates of family history for mood disorders, positive response to antidepressants and sleep deprivation, and prospective follow-up course leading to major affective episodes. Shortened REM latency and related sleep neurophysiological disturbances have also been reported to characterize so-called 'borderline' personality disorder even when examined in the absence of concomitant major depression. Finally, among primary care referrals to a sleep disorders center, short REM latency was found in a large number of patients without subjective mood change but with somatic manifestations of depression (meeting Probable Feighner Depression and/or lesser subacute manifestations). Rather than being incidental, the REM disturbances in the foregoing studies appear consistently on consecutive nights of polysomnography in the subthreshold affective group; this was not the case for patients with non-affective personality and anxiety disorders. The findings overall tend to support a common neurophysiological substrate for subthreshold and melancholic depressions and, interpreted in the context of clinical observations, family history and follow-up course, uphold the validity of dysthymic, intermittent and subsyndromal depressions.

Bipolar Disorder↗