Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the FDA recommends imipramine hydrochloride (IMI) only for temporary relief of symptoms of enuresis nocturna (EN), the drug has been applied to a number of other pediatric situations, including the Hyperkinetic Syndrome (HS), childhood depression, somnambulism and pavor nocturnus, school phobia, petit mal epilepsy, allergies, autism, encorpresis and head-banging. We have reviewed the literature, with particular attention to the pharmacokinetics of IMI in children, and its putative mechanisms of action. The drug probably works through a number of different actions, and the futher delineation of these will be of considerable heuristic value. We review the toxic effects of IMI treatment and IMI poisoning in children, and the pediatric literature concerning other antidepressant drugs and lithium carbonate (Li).
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PMID:Imipramine and children: a review and some speculations about the mechanism of drug action. 40 23

The development and clinical course of night terrors and the personality patterns of patients with this disorder were evaluated in 40 adults who had a current complaint of night terrors. Compared with a group of adult sleepwalkers, the patients with night terrors had a later age of onset for their disorder, a higher frequency of events, and an earlier time of night for the occurrence of episodes. Both groups had high levels of psychopathology, with higher values for the night terror group. This sleepwalkers showed active, outwardly directed behavioral patterns, whereas the night terror patients showed an inhibition of outward expressions of aggression and a predominance of anxiety, depression, tendencies obsessive-compulsive/, and phobicness. Although night terrors and sleepwalking in childhood seem to be related primarily to genetic and developmental factors, their persistence and especially their onset in adulthood are found to be related more to psychological factors.
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PMID:Night terrors. Clinical characteristics and personality patterns. 744 22

Aging is a physiological process that shares many behavioral, biochemical and neuroendocrine phenomena with the pathophysiological situation of unresolved stress, as well as with a pharmacologically induced syndrome resulting from chronic benzodiazepine (BZ) consumption. Behavioral findings include symptoms such as drowsiness, ataxia, fatigue, confusion, weakness, dizziness, vertigo, syncope, reversible dementia, depression, impairment of intellectual, psychomotor and sexual function, agitation, auditory and visual hallucinations, paranoid ideation, panic, delirium, depersonalization, sleepwalking, aggressivity, orthostatic hypotension, and insomnia. Neuroendocrine findings include: central depletion of noradrenaline (NA), dopamine, adrenaline (AD), and serotonin (5-HT); reduction in the ratio of circulating NA/AD as well as platelet 5-HT and increase of AD, plasma free 5-HT and cortisol. These disturbances together with the increased platelet aggregability observed in the three groups are typical of unresolved-stress situations. Immunological findings include significant reduction of peripheral T lymphocytes (CD3, CD4, CD8) and the CD4/CD8 ratio, CD16 and gamma-delta cells. On the other hand, the three groups (elderly subjects, subjects faced with unresolved stress, and BZ consumers) show increase of the CD57 lymphocyte subset as well as natural killer cytotoxicity. Alterations of several biological markers have also been found, specifically in the oral glucose tolerance test, the intramuscular clonidine test, and the supine/orthostasis/exercise test. From a clinical point of view, the three groups appear to be more susceptible to the appearance and progression of many acute and chronic diseases (infectious and malignant diseases). As a result, chronic consumption of BZs should be avoided in both the elderly and subjects in unresolved-stress situations.
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PMID:Benzodiazepines: tolerability in elderly patients. 884 97

There is a general tendency to restrict the notion of sleep disorders to insomnia and consequently to limit treatment to the prescription of hypnotics. However, it is very often of benefit to prescribe psychotropic agents, in particular antidepressants, not only in insomnia but also in certain cases of hypersomnia, parasomnia and dysomnia associated with organic diseases. In some conditions, however, antidepressants may either induce or aggravate sleep disorders. This is the case with a number of psychostimulants that occasionally induce insomnia. It is also true of the tricyclic antidepressants, which may worsen or even induce a restlessleg syndrome that is often associated with periodic movement syndrome. On the other hand, the antidepressants may play a therapeutic role in certain sleep disorders : - depression-related insomnia is of course the << primary >> indication for antidepressants. Furthermore, certain antidepressants exhibit a sedative action resulting in a hypnogenic-type effect which appears well before the antidepressant effect; - the other types of insomnia may also often be treated with antidepressants : not acute reactional insomnia, against which hypnotics are remarkably effective, but chronic insomnia. In addition, all antidepressants may eventually correct depressive hypersomnia, but in these cases, it is evidently preferable to prescribe non-sedative drugs. Although some tricyclic antidepressants have been proposed for use in hypersomnia due to sleep apnea, their therapeutic interest is minor compared with mechanical and surgical treatment. In contrast, antidepressants play an important role in the treatment of narcolepsy, particularly for the correction of attacks of cataplexy. Antidepressants have also been used for some time in the treatment of parasomnia related to slow deep sleep (night terrors and sleepwalking), but the antidepressants may also be used in enuresis and in parasomnia related to REM sleep : nightmares, sleep paralysis, behavioral problems associated with REM sleep. Antidepressant (mainly serotoninergic drugs) are often used in the treatment of fibrolitis syndrome. Finally, antidepressants (particularly the serotoninergic antidepressants) play an important role in the drug treatment of fibromyalgia.
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PMID:[Use of antidepressants in sleep disorders: practical considerations]. 892 78

Nocturnal eating disorder (NED) is a rare syndrome that includes disorders of both eating and sleeping. It is characterized by awakening in the middle of the night, getting out of bed, and consuming large quantities of food quickly and uncontrollably, then returning to sleep. This may occur several times during the night. Some patients are fully conscious during their nocturnal eating, while some indicate total amnesia. The etiology of NED is still unclear, as research findings are contradictory. Those suffering from NED exhibit various levels of anxiety and depression, and many lead stressful life-styles. Familial conflict, loneliness and personal crises are commonly found. Recently, a connection has been discovered between NED and unclear self-definition, faulty interpersonal communication, and low frustration threshold. Several authors link it to sleepwalking, leg movements during sleep, and sleep apnea. Treatment is still unclear and there have been trials of pharmacotherapy, psychotherapy, or a combination of both. However, pharmacological treatment has generally been found to be the most effective, although each case must be considered individually. In 1998, 7 women referred to our Eating Disorders Clinic, 5% of all referrals, were subsequently diagnosed as suffering from NED. Of these, 3 suffered from concurrent binge-eating disorder and 4 also from bulimia nervosa. 2 case studies representative of NED are presented.
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PMID:[Nocturnal eating disorder--sleep or eating disorder?]. 1088 92

The enduring and contentious hypothesis that sleepwalking and night terrors are symptomatic of a protective dissociative mechanism is examined. This is mobilised when intolerable impulses, feelings and memories escape, within sleep, the diminished control of mental defence mechanisms. They then erupt but in a limited motoric or affective form with restricted awareness and subsequent amnesia for the event. It has also been suggested that such processes are more likely when the patient has a history of major psychological trauma. In a group of 22 adult patients, referred to a tertiary sleep disorders service with possible sleepwalking/night terrors, diagnosis was confirmed both clinically and polysomnographically, and only six patients had a history of such trauma. More commonly these described sleepwalking/night terrors are associated with vivid dream-like experiences or behaviour related to flight from attack. Two such cases, suggestive of a dissociative process, are described in more detail. The results of this study are presented largely on account of the negative findings. Scores on the dissociation questionnaire (DIS-Q) were normal, although generally higher in the small "trauma" subgroup. These were similar to scores characterising individuals with post-traumatic stress disorder. This "trauma" group also scored particularly highly on the anxiety, phobic, and depression scales of the Crown-Crisp experiential index. In contrast the "no trauma" group scored more specifically highly on the anxiety scale, along with major trends to high depression and hysteria scale scores. Two cases are presented which illustrate exceptional occurrence of later onset of sleepwalking/night terrors with accompanying post-traumatic symptoms during wakefulness. It is concluded that a history of major psychological trauma exists in only a minority of adult patients presenting with sleepwalking/night terror syndrome. In this subgroup trauma appears to dictate the subsequent content of the attacks. However, the symptoms express themselves within the form of the sleepwalking/night terror syndrome rather than as rapid eye movement sleep related nightmares. The main group of subjects with the syndrome and with no history of major psychological trauma show no clinical or DIS-Q evidence of dissociation during wakefulness. The proposition that, within the character structure of this group, the mechanism still operates but exclusively within sleep remains a possibility.
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PMID:Is there a dissociative process in sleepwalking and night terrors? 1126 87

Anorectics and bulimics often complain sleep onset insomnia and disrupted sleep. During awakenings bulimics can have binges. Conversely, eating disorders can be a clinical expression of a concomitantly occurring sleep disorder. Two clinical entities have been recently described: the Night Eating Syndrome (NES) and the Sleep Related Eating Disorders. The main goal of this literature review was to better characterize the relationships between eating disorders and sleep disturbances. No specific EEG sleep pattern emerges in anorectic and bulimic patients. However, all studies include several methodological limitations: a few number of patients, heterogeneous patient groups, various diagnostic criteria. The results of studies evaluating the impact of depression on sleep EEG in eating disorder patients are also subject to controversy. The only study examining the relationship between sleep EEG and morphological alterations in anorectics and normal weight bulimics shows that patients with enlarged cerebrospinal fluid spaces spent more time in slow wave sleep and that the duration of rapid eye movement (REM) sleep was reduced. The ventricular brain ratio was negatively correlated with REM sleep. The Night Eating Syndrome consists in insomnia, binge eating and morning anorexia. Other criteria are proposed to characterize the NES: more than 50% of the daily energy intake is consumed after the last evening meal, awakenings at least once a night, repetition of the provisional criteria for more than 3 months, subjects do not meet criteria for bulimia nervosa or binge eating disorder. Patients have no amnesia nor alteration of alertness, and no other sleep disorder. There is no modification of sleep EEG except sleep maintenance. The prevalence of the NES is 1.5% in the general population. Some neuroendocrine disturbances have been found in the NES. The delimitation with eating disorders is not yet clearly established. If it shares the compulsive features with eating disorders, particularly the "Binge Eating Disorder", and occurs during full awakenings, the night eating syndrome may be recognized as a specific eating disorder. The sleep related eating syndrome is also characterized by compulsive binge eating during awakenings. But in this case, night eating is linked with a reduced consciousness and sleep disorders, mainly somnambulism. Patients never experience hunger, abdominal pain, nausea or hypoglycemia. Night-eating takes place invariant across weekdays, weekend and vacations. Patients consumed high caloric foods and fluids but never alcohol and purging does not occur. Diurnal bulimia is frequently associated with the sleep-related eating disorder. In conclusion, the sleep related eating disorder seems rather be a clinical subtype of sleep disorders whereas the NES could be considered as an eating disorder.
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PMID:[Correlation between eating disorders and sleep disturbances]. 1176 Jun 92

Although sleep-related problems are a frequent finding in patients with Parkinson's disease (PD), the aetiology is still unknown. We examined the associations between disease severity, sleep-related problems and social status in 116 PD patients participating in the FAQT Study, a prospective, German cohort study evaluating determinants of quality of life in PD patients. 47.4% of the patients reported sleep onset difficulties, 26.7% sleep interruptions, 14.7% had five or more sleep-related events during the night and 71.6% showed symptoms of increased daytime somnolence. The disease severity was significantly associated with sleep-related events (p = 0.01), the depression score with sleep onset difficulties (p = 0.04), sleep interruptions (p = 0.01) and the levodopa dose (p < 0.01). We conclude that depressive symptoms and increasing levodopa doses in PD patients mainly cause sleep onset difficulties and sleep interruptions, while the severity of motor symptoms contributes to sleep-related events like sleep walking, heavy sweating and nightmares.
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PMID:The association between disease severity and sleep-related problems in patients with Parkinson's disease. 1237 26

Depression, dementia, and physiologic changes contribute to the high prevalence of sleep disturbances in patients with Parkinson's disease (PD). Antiparkinsonian drugs also play a role in insomnia by increasing daytime sleepiness and affecting motor symptoms and depression. Common types of sleep disturbances in PD patients include nocturnal sleep disruption and excessive daytime sleepiness, restless legs syndrome, rapid eye movement sleep behavior disorder, sleep apnea, sleep walking and sleep talking, nightmares, sleep terrors, and panic attacks. A thorough assessment should include complete medical and psychiatric histories, sleep history, and a 1- to 2-week sleep diary or Epworth Sleepiness Scale evaluation. Polysomnography or actigraphy may also be indicated. Treatment should address underlying factors such as depression or anxiety. Hypnotic therapy for sleep disturbances in PD patients should be approached with care because of the risks of falling, agitation, drowsiness, and hypotension. Behavioral interventions may also be useful.
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PMID:Sleep disorders in Parkinson's disease. 1525 35

Adult sleepwalking affects 2.5% of the general population and may lead to serious injuries. Fifty young adults with chronic sleepwalking were studied prospectively. Clinical evaluation, questionnaires from patients and bed partners, and polysomnography were obtained on all subjects in comparison with 50 age-matched controls. Subjects were examined for the presence of psychiatric anxiety, depression and any other associated sleep disorder. Isolated sleepwalking or sleepwalking with psychiatric disorders was treated with medication. All other patients with other sleep disorders were treated only for their associated problem. Prospective follow-up lasted 12 months after establishment of the most appropriate treatment. Patients with only sleepwalking, treated with benzodiazepines, dropped out of follow-up testing and reported persistence of sleepwalking, as did patients with psychiatric-related treatment. Chronic sleepwalkers frequently presented with sleep-disordered breathing (SDB). All these patients were treated only for their SDB, using nasal continuous positive airway pressure (CPAP). All nasal CPAP-compliant patients had control of sleepwalking at all stages of follow-up. Non-compliant nasal CPAP patients had persistence of sleepwalking. They were offered surgical treatment for SDB. Those successfully treated with surgery also had complete resolution of sleepwalking. Successful treatment of SDB, which is frequently associated with chronic sleepwalking, controlled the syndrome in young adults.
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PMID:Adult chronic sleepwalking and its treatment based on polysomnography. 1581 20


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