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PubMed1992

Are personality assessments valid in acute major depression?

A number of recent studies indicate that identification of Axis II comorbidity in depressed patients may influence both the initial treatment plan and subsequent prognosis. Nevertheless, the validity of personality disorder diagnoses may be compromised by the effects of the patients' depression on historical recall, which distort presentation of their premorbid strengths and liabilities. These problems are illustrated in this study of 53 acutely depressed unipolar outpatients, with (N = 14) or without (N = 39) personality disorder diagnoses as defined by the Personality Disorder Examination (PDE). We found that: 1) pretreatment PDE diagnoses had no significant associations with any measure of demography, symptomatic status, illness course, or treatment response; and 2) pretreatment PDE diagnoses typically were not confirmed when patients were reassessed following effective treatment with cognitive behavior therapy. These findings provide strong empirical support for the wisdom of deferring definitive assessment of Axis II until an acute depressive disorder has been optimally treated.

Acute Disease↗
PubMed1995

Paroxysmal microarousals in amygdala-kindled kittens: could they be subclinical seizures?

Amygdala-kindled kittens exhibit frequent epileptiform EEG transients, often in conjunction with phasic arousal events of sleep [k-complexes, pontogeniculo-occipital (PGO) waves, and/or sleep spindles]. In this study, paroxysmal microarousals occurred throughout the sleep-wake cycle after kindling, but were most frequent during seizure-prone states of slow-wave sleep (SWS) and the transition into rapid-eye-movement sleep (REM). Their incidence correlated with interictal sleep fragmentation as well as onset of spontaneous convulsions. Results could reflect transsynaptic kindling effects on brainstem and forebrain arousal mechanisms with which amygdala is reciprocally connected. Increased discharge rates of neural generators for normal EEG and behavioral arousal could disrupt sleep at some times and recruit epileptic neurons in the kindled focus to precipitate seizures at others. Alternatively, epileptiform EEG paroxysms were accompanied by subtle behavioral stereotypes (a head nod, limb elevation, eye twitch, lip smack, or a combination of these). Behavioral correlates were elements of partial kindled seizures, suggesting that paroxysmal microarousals may be subclinical seizures. Whether or not the microarousals are true seizures, our findings may link ictal onset and interictal sleep disorders to a subclinical paroxysmal arousal disorder and suggest a common epileptic mechanism.

Amygdala↗
PubMed2003

Pharmacotherapy of dementia with Lewy bodies.

The syndrome of dementia with Lewy bodies (DLB) is characterised by the clinical triad of fluctuating cognitive impairment, recurrent visual hallucinations and spontaneous motor features of Parkinsonism. In an attempt to define DLB as a distinct clinical syndrome separate from Alzheimer's disease (AD) and Parkinson's disease (PD) with dementia, a consensus workshop in 1995 established a new set of diagnostic criteria. Dementia that precedes or accompanies the onset of spontaneous (i.e., not neuroleptic-induced) Parkinsonism is termed DLB. In addition, fluctuations in alertness, cognition and function and visual hallucinations are emphasised and included as core features of DLB. The degree to which an individual patient exhibits cognitive impairment, behavioural problems and Parkinsonian features is variable. Therefore, treatment must be individualised. Although there are no officially approved drugs for DLB, limited experience from clinical trials, as well as past experience with the treatment of AD and PD patients, provide some basis for making drug choices. The cholinergic deficit seen in DLB makes cholinesterase inhibitor drugs the mainstay of treatment for cognitive impairment. This class of drugs has also shown therapeutic benefit in reducing hallucinations and other neuropsychiatric symptoms of the disease. Because of their relatively greater therapeutic window, cholinesterase inhibitors are also used as first-line therapy for the treatment of psychosis in DLB. Patients with DLB are extremely sensitive to the extrapyramidal side effects of neuroleptic medications. Thus, only atypical antipsychotic agents such as quetiapine, should be considered as alternative treatment for psychosis. Anxiety and depression are best treated with selective serotonin re-uptake inhibitors, whereas REM sleep behaviour disorder may be treated with low dose clonazepam. Parkinsonism responds to dopaminergic agents; however, precipitation or aggravation of hallucinosis may occur. Levodopa is preferred over dopamine agonists due to its lower propensity to cause hallucinations and somnolence. As the diagnostic criteria for DLB become more refined and validated by postmortem studies, it is hoped that rigorous, well-designed trials will be performed, aimed at alleviating the primary target symptoms of dementia, psychosis and Parkinsonism.

Antipsychotic Agents↗
PubMed2005

Delta and spindle components in the integrated EEG during nocturnal sleep for infants with developmental disabilities.

The delta and spindle components in the integrated EEG for 121 infants with developmental disabilities (from 4 mo. to 6 yr. of age: M=1.79, SD=0.14; 57 girls and 64 boys) were studied throughout nocturnal sleep. In 80 (66.1%, Group A) of 121 subjects, periodic changes of delta and spindle rhythm powers were noted in measurements of EEG made during sleep. In 28 (23.1%, Group B), delta but not spindle rhythm powers were found, and in the remaining 13 subjects (10.7%, Group C) neither delta nor spindle rhythm powers were found throughout measurements of EEG made during sleep. The Tsumori-Inage Questionnaire for Infants was administered to the parents to estimate subjects' behavioral developmental level as Developmental Quotients. Significantly lower mean Developmental Quotients were found for Groups B and C than Group A. These findings suggested that the presence or absence of delta and spindle rhythm powers in EEG measurements made during nocturnal sleep could be taken as an index of the severity of developmental disorders in infants with developmental disabilities.

Child↗
PubMed1986

The role of the central monoaminergic system and rapid eye movement sleep in development.

Transmission of information in the brain is of a chemical nature. Neurotransmitters are present at very early stages of brain development, having trophic effects on maturation of target neurons as well as mediating the behavioral repertoire of the immature brain. Many centrally acting psychoactive drugs which are commonly used (also during pregnancy) for treatment of depression, asthma, hypertension, epilepsy, parkinsonism, hyperkinetism and other neurological and psychiatric disorders act directly on brain neurotransmitters (in particular monoamines) and behavioral states. Disturbances observed later in life in animals and man, as a result of early interference with brain neurotransmitters, using these drugs, are not gross physical malformations but are in fact subtle behavioral and neurological symptoms such as hyperactivity, emotional lability, attentional distractability and sleep disturbances, similar to symptoms observed in the minimal brain dysfunction syndrome.

Animals↗
PubMed1991

Neurobiological evidence for epilepsy-induced interictal disturbances.

It is not in the best interest of persons with epilepsy to deny the possibility that seizures could cause enduring behavioral disturbances. Rather, it is essential to pursue clinical and animal investigations in order to identify any such changes that might occur and to elucidate their mechanisms. Many testable hypotheses can be developed from existing evidence. Antiepileptic medication may produce interictal behavioral disturbances in patients with epilepsy by indirect mechanisms. Some aberrant behaviors could be due to medication-induced systemic disorders, neuroendocrine dysfunction, or REM deficit, whereas depression following successful treatment with drugs, as well as with surgery, may be related more specifically to cessation of seizures. The underlying neuropathological process also induces neurological and mental deficits, but it is not always possible to differentiate those behavioral disturbances due to destructive effects of the lesion from those due to recurrent epileptic seizures. Behavioral disturbances are associated more frequently with epileptogenic lesions in limbic structures than with those elsewhere in the brain, but a relationship between hemispheric lateralization of the epileptogenic lesion and specific interictal behavioral symptoms remains controversial. When considering the effects of seizures per se on interictal behavior, it is important to realize that some "interictal" behavioral disturbances may actually be ictal events. Prolonged affective, autonomic, and psychic disturbances can occur in clear consciousness with unilateral limbic seizures that are not associated with scalp EEG changes. When epilepsy is acquired as a result of cerebral damage, the epileptogenic process takes time to develop before spontaneous seizures appear. It is more reasonable to assume that this progressive process continues than to postulate that it stops completely at the time the first seizure occurs. Epilepsy-induced protective homeostatic mechanisms that act to terminate ictal events, prevent ictal spread, and maintain the interictal state may also disrupt interictal function. Furthermore, seizures could indirectly influence interictal behavior as a result of their effects on neuroendocrine function and sleep. Because of confounding biological factors, it is difficult to document the association of any epilepsy disorder, by itself, with progressive behavioral disturbances in humans. Secondary epileptogenesis, protective homeostatic mechanisms, and epilepsy-induced disturbances in development can be readily demonstrated, however, in experimental animal models. In experimental animals, endogenous opoids are released during seizures and mediate some postictal behaviors. A physiological dependency on high levels of endogenous opioids released during seizures could produce depression as a withdrawal symptom interictally or when seizures no longer occur as a result of successful therapy. Experimental animal models of depression exist to test hypotheses concerning pro- and antidepressant effects of epileptogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

A polysomnographically documented case of adult somnambulism with long-distance automobile driving and frequent nocturnal violence: parasomnia with continuing danger as a noninsane automatism?

A case of childhood-onset somnambulism is reported in which a 43-year-old man presented with repeated sleep-related injuries incurred during violent nocturnal activity, which included frenzied running, throwing punches and wielding knives. He had also driven an automobile a long distance during a presumed somnambulistic state. His wife had been repeatedly injured, and she felt that her life was threatened by his nocturnal violence 2-3 times yearly. Polysomnography (PSG) documented multiple episodes of complex and violent behaviors arising exclusively from stage 3/4 sleep, thus confirming the diagnosis of somnambulism. Other causes of sleep-related violence were excluded. The patient responded promptly to treatment with bedtime clonazepam, and benefit was maintained at 5-year follow-up. Although this strictly clinical case did not have any legal repercussions, it does carry forensic implications, particularly when placed in the context of the published medical literature on PSG-documented parasomnias (somnambulism, rapid eye movement sleep behavior disorder) containing explicit examples of recurrent violence, at times life-threatening, directed toward the bed partner and others. Thus, a new medical-legal concept is proposed, consisting of "parasomnia with continuing danger" as a noninsane automatism. Treatment guidelines, within the context of forensic medicine, are presented.

Adult↗
PubMed1997

Sleep-onset rapid eye movement periods in neuropsychiatric disorders: implications for the pathophysiology of psychosis.

This paper reviews the literature describing the occurrence of sleep-onset rapid eye movement periods in narcolepsy, schizophrenia, psychotic depression, and delirium tremens; the association of narcolepsy with psychotic disorders; the neuropathology of the brainstem in narcolepsy and schizophrenia; and other behavioral disorders resulting from probable brainstem pathology. These findings suggest that some forms of psychosis are a manifestation of pathophysiological changes in the brainstem. Some implications of this hypothesis for the treatment of psychoses are discussed. Future research should investigate psychoses and the psychobiological correlates of such biological markers as sleep-onset rapid eye movement periods across diagnostic categories.

Alcohol Withdrawal Delirium↗
PubMed2003

The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation.

OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h (s.e. 0.73 h). CONCLUSIONS: Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults. Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits, which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign. Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses, but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions. This suggests that sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.

Adult↗
PubMed1987

Increased adult behavioral 'despair' in rats neonatally exposed to desipramine or zimeldine: an animal model of depression?

Occurrence of depressive behavior at mature age was studied in rats exposed neonatally to antidepressant drugs. Early antidepressant treatments have been shown to increase voluntary alcohol consumption and the percentage of rapid-eye-movement (REM) sleep relative to total sleep time in adult rats as well as to cause long-lasting reduction in the concentrations of monoamines in the forebrain. In the present study rats were daily given either 5 mg/kg desipramine or 25 mg/kg zimeldine from the 7th to the 18th postnatal days. When they were 2 months and 5 months of age behavioral 'despair' was studied by using a modified version of Porsolt's swim-test. At both ages the desipramine-treated and zimeldine-treated rats expressed lengthened immobility times in the water pail. The findings indicate that neonatal exposure of rats to desipramine or zimeldine induces behavioral 'despair' at mature age. Thus, early exposure of rats to antidepressants causes long-lasting behavioral disorders, and, moreover, may be used to devise an animal model of subsequent depression.

Animals↗
PubMed2002

Heterogeneity in EEG sleep findings in adolescent depression: unipolar versus bipolar clinical course.

BACKGROUND: EEG sleep measures in child and adolescent subjects with depression have shown considerable variability regarding group differences between depressed and control subjects. This investigation was designed to assess whether some of the observed variability is related to undifferentiated unipolar and bipolar disorders in a sample that was reported previously. METHODS: Twenty-eight adolescents who met criteria for unipolar major depression and 35 controls with no lifetime psychiatric disorder participated in a cross-sectional sleep polysomnography study. Approximately 7 years later, follow-up clinical evaluations were conducted in 94% of the original cohort. Clinical course during the interval period was assessed without knowledge of subjects' initial diagnostic and psychobiological status. Re-analysis of the original sleep data were performed with the added information of longitudinal clinical course. RESULTS: Depressed subjects who had a unipolar course showed reduced REM latency, higher REM density, and more REM sleep (specifically in the early part of the night) compared with depressed adolescents who converted to bipolar disorder and controls who remained free from psychopathology at follow-up. In contrast to the unipolar group, depressed subjects who would later switch to bipolar disorder had demonstrated more stage 1 sleep and diminished stage 4 sleep. CONCLUSIONS: These preliminary results indicate that some of the observed variability in EEG sleep measures in adolescent depression appear to be confounded by latent bipolar illness. The findings also suggest that sleep regulatory changes associated with unipolar versus bipolar mood disorders may be different.

Adolescent↗
PubMed2002

Mesolimbic dopaminergic system is involved in diurnal blood pressure regulation.

Parkinson's disease (PD) patients with autonomic failure show no nocturnal decrease in blood pressure (BP). At present, it is not clear if this symptom is attributable to the disturbance of the dopaminergic (DA) system that is responsible for PD. In the present study, we determined that the mesolimbic DA system is involved in diurnal profiles of the mean BP (MBP) by destroying the A10 DA system in rats with 6-hydroxydopamine. In control rats, a clear dip in the MBP and heart rate (HR) occurs during the light, that is, resting period, analogous to the nocturnal dip in normal humans. This normal daytime decrease in MBP and HR was disturbed by inducing a lesion of the ventral tegmental area (VTA) DA neurons, although the rhythms of wake-sleep duration and behavioral activity remained relatively intact. On the basis of this evidence, the absence of a nocturnal dip in BP in PD patients is attributed to impairment of the mesolimbic DA system.

Animals↗
PubMed1995

REM sleep without atonia at early stage of sporadic olivopontocerebellar atrophy.

In order to investigate whether REM sleep without atonia (RWA) is detected even at early stage of sporadic olivopontocerebellar atrophy (OPCA), all-night polysomnography with video monitoring was performed on 5 patients presenting with no nocturnal behavioral complaints. RWA associated with sleep talk and/or minor movements in the head, neck, face and extremities was documented in all cases. Preserved proper NREM/REM cycle and relatively normal sleep architecture suggest the abnormality is confined to REM sleep. Dysfunction of the mechanisms underlying muscle atonia in REM sleep, especially functional or anatomical interruption of ponto-medullary pathways mediating REM sleep atonia, seems to cause RWA in these patients. RWA may be a clinically important finding as a sign of brainstem dysfunction at early stage of neurodegenerative diseases.

Aged↗
PubMed1991

Sleep-related eating disorders: polysomnographic correlates of a heterogeneous syndrome distinct from daytime eating disorders.

Over a 5-yr period, 19 adults presented to our sleep disorders center with histories of involuntary, nocturnal, sleep-related eating that usually occurred with other problematic nocturnal behaviors. Mean age (+/- SD) at presentation was 37.4 (+/- 9.1) yr (range 18-54); 73.7% of the patients (n = 14) were female. Mean age of sleep-related eating onset was 24.7 (+/- 12.9) yr (range 5-44). Eating occurred from sleep nightly in 57.9% (n = 11) of patients. Chief complaints included excessive weight gain, concerns about choking while eating or about starting fires from cooking and sleep disruption. Extensive polysomnographic studies, clinical evaluations and treatment outcome data identified three etiologic categories for the sleep-related eating: (a) sleepwalking (SW), 84.2% (n = 16); (b) periodic movements of sleep (PMS), 10.5% (n = 2) and (c) triazolam abuse (0.75 mg hs), 5.3% (n = 1). DSM-III Axis 1 psychiatric disorders (affective, anxiety) were present in 47.4% (n = 9) of the patients, and only two patients had a daytime eating disorder (anorexia nervosa), each in remission for 3-7 yr. Nearly half of all patients fulfilled established criteria for being overweight, based on the body mass index. Onset of sleep-related eating was linked directly to the onset of SW, PMS, triazolam abuse, nicotine abstinence, chronic autoimmune hepatitis, narcolepsy, encephalitis or acute stress. In the SW group, 72.7% (8/11) of patients had nocturnal eating and other SW behavior suppressed by clonazepam (n = 7) and/or bromocriptine (n = 2) treatment. Both patients with PMS likewise responded to treatment with combinations of carbidopa/L-dopa, codeine and clonazepam. Thus, sleep-related eating disorders can generally be controlled with treatment of the underlying sleep disorder.

Adolescent↗
PubMed2005

Diagnosis and assessment of sleep and circadian rhythm disorders.

Sleep and wakefulness are fundamental behavioral and neurobiological states that characterize all higher animals, including human beings. This article presents an overview of the current state of our knowledge concerning the function of sleep and sleep-wake rhythms, the neurobiology of circadian rhythms, how wakefulness and sleep are studied, and the clinical assessment and diagnosis of sleep and circadian rhythm disorders. Major theories of the function of sleep and sleep-wake rhythms are reviewed, including ecological or environmental advantage, physical restoration, optimizing waking function, learning and integration of experience, and survival. The author then reviews what is known about the neurobiology of endogenous circadian rhythms and how they are affected by environmental time cues. How sleep is studied using polysomnography (PSG) is explained, and the PSG characteristics of the three major neurobehavioral states, wakefulness, rapid eye movement (REM) sleep, and non-rapid eye movement (NREM) sleep, are described. Systems of classifying sleep disorders are reviewed, including those of the DSM-IV-TR, the International Classification of Sleep Disorders, and the ICD-10. Methods of assessing sleep complaints are then described, including taking an accurate history from the patient and bed partner, use of sleep history questionnaires and sleep-wake diaries, use of actigraphy, and use of PSG.

Adult↗
PubMed2004

Sleep in children with attention deficit/hyperactivity disorder.

Attention-deficit hyperactivity disorder (ADHD) is one of the most common psychological disorders in children. Sleep disturbances are also very prevalent among the pediatric age range and can lead to substantial behavioral and cognitive consequences that may mimic ADHD. Conversely, children with ADHD may suffer from significant sleep disturbances that may originate in the biochemical disturbances that underlie their deficits in executive function and attention. This review addresses both these issues and provides a concise yet timely assessment of the potential links between sleep disorders and ADHD.

Age Factors↗
PubMed1980

Sleep and sleepiness in children and adolescents.

We have attempted to review the current "state of the art" regarding the ontogenetic course of sleep-wake state organization and possible disruptions in this course from infancy through adolescence. It is becoming increasingly important for clinicians to learn about physiologic functioning during sleep. Much more research is required, directed at the relationship between waking behaviors and sleeping behaviors. Investigations of daytime sleepiness in adolescence, of the relationship of hyperactivity to excessive sleepiness, of the relationship between disorders such as depression and anorexia nervosa with disturbed sleep state organization, and of primary sleep disorders such as narcolepsy and the sleep apnea syndrome only scratch the surface in terms of the future work that needs to be done.

Adolescent↗
PubMed1982

Phencyclidine produces aggressive behavior in rapid eye movement sleep-deprived rats.

This study examined effects of acute doses of phencyclidine (PCP; 0.025, 0.05, 0.10, and 0.20 mg/kg intraperitoneally) on intra-specific aggressive behavior and muricide in normal rats and rats deprived of rapid eye movement (REM) sleep. Dose-related changes in intra-specific aggression and muricide occurred in REM sleep-deprived rats only. Dose-response curves are inverted-U shaped with the .05 mg/kg dose producing increases in aggression. Intra-specific aggression and muricide may serve as models of PCP-induced aggression in humans.

Aggression↗