The dentist's role in diagnosis and therapy. Sleep disordered breathing.
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Although technologic advances and insights into the mechanisms of cancer and cancer treatments have resulted in hope of increased survival and even cure in many cancer populations, parallel efforts to promote quality of life through a commitment to rehabilitation and aggressive palliation have lagged. Recent studies have demonstrated fatigue to be the most distressing phenomenon experienced by cancer patients. This article examines fatigue from a rehabilitation perspective. Application of innovations in therapeutic exercise training, diet therapy, sleep therapy, cognitive therapy, and pharmacologic therapy and their attendant rationales are discussed. From clinical as well as research perspectives of palliation and rehabilitation, the manifestations of fatigue are better appreciated if fatigue is conceptualized as a syndrome, namely, cancer-related fatigue syndrome (CRFS). Experience of CRFS by cancer patients, regardless of their diagnosis, stage of disease, treatment regimen, or age, influences all aspects of quality of life and aggravates the experience of other distressing symptoms such as pain, nausea, and dyspnea. Understanding the underlying mechanisms for energy loss and gain, as well as the relationship between the right amount and type of activity and sleep, can lead toward more effective and innovative rehabilitation programs. Development of research based clinical interventions in these areas holds promise for significant improvement in functioning and quality of life for cancer survivors and may constitute valuable rehabilitative techniques that can be adjunctive to standard therapies.
Sleep apnea has been increasingly recognized for its prevalence and its impact on cardiovascular health. The disorder has considerable impact on cardiovascular disease states, particularly congestive heart failure. Implantable cardiac pacing devices may have a role in both the diagnosis and therapy of sleep apnea, which may be of particular importance given the seemingly wide coprevalence of cardiac disorders and sleep apnea.
BACKGROUND AND PURPOSE: Earlier studies have shown an association between mood disorders and sleep regulation. Total or partial sleep deprivation was demonstrated to have rapid antidepressive effects in depression. Depressive symptoms recur after one night of recovery sleep, but relapse is less when patients are receiving medication. In this study, we examined the subjective sleep quality changes with the antidepressive therapy using partial sleep deprivation plus sertraline and sertraline monotherapy in patients with major depressive disorder. PATIENTS AND METHODS: Thirteen patients received six partial sleep deprivation therapies in addition to sertraline; the sleep schedule on deprivation nights started at 11:00 p.m. and ended at 3:00 a.m. Eleven patients were treated with sertraline monotherapy as a control group. Six nights of partial sleep deprivation were completed in the first two weeks. Subjective sleep quality was evaluated with the Pittsburgh Sleep Quality Index (PSQI); depression and the accompanying anxiety were also assessed at baseline and at the end of the fourth week. RESULTS: The late partial sleep deprivation (LPSD) group showed less increase in estimated sleep duration and less significant improvement in subjective sleep quality than the control group. Although decreased sleep latency and increased sleep efficiency are associated with the sleep deprivation, contrary results were found in our study. CONCLUSIONS: In conclusion, changes in subjective sleep quality could occur relative to the combined partial sleep deprivation therapy and to pharmacotherapy and must be differentiated from the rapid effects of sleep deprivation therapy and objective polysomnographic measures.
A study of sleep deprivation therapy was made in 62 females and 15 males, aged 20-72, with monopolar (60 patients) and bipolar (17 patients) types of manic-depressive psychosis. Of these patients, 30 had suffered only the current depression, 29 a maximum of five depressions, and 18 more than five depressions before the sleep deprivation therapy. Twenty-five patients had been treated with antidepressant drugs for less than 10 days, 12 patients for 10-24 days, and 36 patients for more than 24 days. Twenty-four patients were treated with one sleep deprivation, 29 patients with one sleep deprivations per week (average 1.59), and 24 patients with two sleep deprivations per week (average 2.5). The effect of the sleep deprivation therapy was evaluated clinically and by means of Cronholm-Ottosson's rating scale. The effect was found good and lasting in 29%, good but temporary in 38%, and poor in 32% of the cases. The best results were achieved with twice-weekly treatments, the poorest results with once-weekly treatment. The results were equal in monopolar and bipolar cases and were independent of the number of previous depressions as well as antidepressant drug treatment. No side effects have been observed, in particular no conversion to mania. The results of the present investigation indicate that depression and sleep disturbances are symptoms produced by a common factor which, however, it as yet unknown. Sleep deprivation therapy is seen to have at least some effect on all cases of endogenous depression. Sleep deprivation therapy has no side effects and is more quick-acting than any other treatment procedure hitherto known. It should therefore be considered the first treatment offer to all endogenously depressed patients in whom immediate ECT is not necessitated.
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Sleep apnea is associated with many adverse cardiovascular sequelae, including hypertension, nocturnal angina, decreased cardiac output, and bradyarrhythmias. The purpose of this study was to determine if patients referred for pacemaker therapy with asymptomatic bradyarrhythmias have underlying sleep apnea as the etiology of their bradyarrhythmias. This study included eight patients (7 males, 1 female) referred to a cardiac electrophysiology practice for pacemaker therapy. Patients included had asymptomatic bradyarrhythmias that consisted of severe sinus bradycardia, second-degree atrioventricular block, and complete heart block. In 7 of 8 patients, the bradyarrhythmias occurred at night or during the day while asleep. No patients were conditioned athletes. Symptoms often associated with bradyarrhythmias, such as lightheadedness and syncope, were not present. However, seven patients had at least one symptom suggestive of sleep apnea, such as excessive daytime fatigue, snoring, cessation of breathing during sleep (apnea), or frequent night-time awakenings. Overnight polysomnography studies were obtained on patients who had one or more symptoms suggestive of sleep apnea. In this study 7 of 8 patients (88%) referred for pacemaker therapy with asymptomatic bradyarrhythmias were documented by polysomnography to have sleep apnea. When treated with either sleep position modification, nasal continuous positive airway pressure (nasal CPAP), or tracheostomy, all seven patients had improvement in sleep apnea symptoms and remained asymptomatic from their bradyarrhythmias without pacemaker therapy over an average follow-up period of 22 months. One patient without symptoms suggestive of sleep apnea declined pacemaker therapy and remained asymptomatic. From these results, we concluded that asymptomatic transient bradyarrhythmias may suggest a diagnosis of sleep apnea. The evaluation of a patient referred for pacemaker therapy with asymptomatic bradyarrhythmias should include questions related to sleep apnea symptoms. Establishing the diagnosis of sleep apnea may reduce the need for pacemaker therapy and permit appropriate treatment of the underlying cause of these bradyarrhythmias.
STUDY OBJECTIVE: This study evaluated the effect of sleep posture on oral appliance therapy to elucidate the interindividual difference of response to the device. DESIGN: Seventy-two unselected patients with sleep apnea syndrome were studied polysomnographically before and after insertion of the individually fabricated and adjusted device. Sleep positions were measured using a body position sensor. The patients were classified into three groups; supine, lateral and prone groups, according to the position in which apneas were most frequently observed. SETTING: N/A. PATIENTS OR PARTICIPANTS: N/A. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: The mean apnea-hypopnea index (AHI) of all patients before treatment [43.0+/-25.6 (SD)] was significantly (p<0.0001) decreased after insertion of the appliance (21.6+/-18.3). The device decreased the mean AHI significantly from 29.8 to 11.3 in the supine position and 5.5 to 1.6 in the prone position, and increased, but not significantly, from 7.7 to 8.7 in the lateral posture. The supine (n=44) and prone (n=13) groups showed significant reduction of AHI with the oral appliance, while the lateral group (n=15) revealed only a slight decrease, although not significantly. Responders defined by AHI<10 accounted for 61.4% in the supine group, 0% in the lateral group and 84.6% in the prone group. Responders defined by a 50% drop in AHI accounted for 84.1%, 6.7%, and 46.7%, respectively. CONCLUSIONS: The effectiveness of oral appliance therapy is greatly influenced by sleep posture. Sleep posture recorded by polysomnography may be useful to predict the future success or failure of the device.
Therapies for obstructive sleep apnea other than positive airway pressure, oral appliances, and surgical modifications of the upper airway are reviewed in this practice parameter. Several of these therapies such as weight loss and positional therapy hold some promise. Others, such as serotonergic agents, may gain credibility in the future but lack well-designed clinical trials. No practice parameters could be developed for a number of possible therapeutic modalities that had little or no evidence-based data on which to form a conclusion. The role of an organized, targeted weight-loss program either as a single therapy or as a supplement to PAP needs to be clarified. Although bariatric surgery is increasingly performed for refractory medically complicated obesity, its long-term effectiveness in treatment of obstructive sleep apnea in morbidly obese patients is not yet demonstrated. Positional therapy, or methods for preventing sleep in the supine position, has probably been underutilized due to lack of easily measured predictive factors and randomized controlled trials.
Insomnia is a common complaint with potentially significant medical and psychologic complications. In some cases insomnia presents as a symptom of another underlying medical, psychiatric or environmental condition. In these cases, management of insomnia depends on accurate diagnosis and successful treatment of the underlying condition. In other cases, insomnia is a primary disorder requiring direct treatment. Pharmacologic treatments include nonprescription medications, sedating tricyclic antidepressants, benzodiazepines and related drugs. Behavior management methods that may be administered in the office setting include stimulus control therapy, sleep restriction therapy and sleep hygiene education. Although prescription medications and behavior therapy have similar short-term efficacy, behavior interventions are recommended as the first line of treatment for primary insomnia because of their greater safety and long-term efficacy.
Sleep disorders are very common in depression. They have been quantitatively and qualitatively described by polysomnographical recordings. It is of interest to know how treatments act on polysomnographical data. In this article, we propose to evaluate five treatment approaches proposed for depressive illness. Pharmacological treatment induces marked changes in sleep continuity, sleep architecture and REM sleep. However, no specific sleep profiles emerge neither for each treatment class nor for molecules within the same pharmacological class. But actually, sleep data cannot be viewed as markers of treatment response. Psychotherapeutic interventions have only few effects on sleep of depressed patients. Treatment efficiency does not seem to be correlated to abnormal sleep parameters. Sleep deprivation induces marked changes in nearly all sleep parameters and in temporal distribution of sleep stages during the night. Actually, the efficiency of sleep deprivation cannot longer be explained by suppression of REM sleep. Sleep deprivation has only a transient effect and treatment indications are therefore secondary. Sleep parameters do not distinguish responders from non-responders. Sleep deprivation shows that there is a depressogenic effect of sleep in the end of the night. Bright light therapy shows marked changes in sleep continuity parameters. Among all studies that examine the impact of treatment on sleep EEG, ECT has received little attention. The few studies available are either case studies or with poor effectifes++. For this reason and because of methodological bias, results are heterogeneous and no definite conclusions can be drawn. But all of them agree that ECT modifies sleep EEG. So, changes in polysomnographical data cannot predict response to any treatment. Prospective sleep studies are difficult to realise on a great number of patients explaining absence of treatment predictors.
OBJECTIVE: Our purpose was to evaluate the effect of estrogen replacement therapy on sleep complaints by postmenopausal women and to assess the predictive factors involved. STUDY DESIGN: Sixty-three postmenopausal women entered a 7-month prospective, randomized, double-blind, crossover study consisting of two 3-month treatments with estrogen and placebo with a 1-month washout period between. Eight Visual Analogic Scale statements about different sleep complaints, the Basic Nordic Sleep Questionnaire, scoring of climacteric symptoms, The Beck Depression Inventory, and serum estradiol and follicle-stimulating hormone level controls were the main outcome measures. RESULTS: Estrogen replacement therapy improved sleep quality, facilitated falling asleep, and decreased nocturnal restlessness and awakenings (p < 0.001). The subjects were less tired in the mornings and in the daytime (p < 0.001) when taking estrogen replacement therapy. Estrogen-induced sleep improvement was associated with alleviation of vasomotor symptoms (r range 0.27 to 0.55), alleviation of somatic symptoms (palpitations and muscular pain, r range 0.26 to 0.36), and alleviation of mood symptoms (r range 0.28 to 0.37) on estrogen replacement therapy. The severity of initial insomnia predicted only one estrogen-induced sleep improvement effect: the more the subjects experienced insomnia, the better the estrogen replacement therapy facilitated falling asleep (r = 0.26, p = 0.040). Estrogen-induced sleep improvement was also reported by the 15 climacterically asymptomatic subjects. In these subjects initial insomnia scores strongly predicted estrogen-induced sleep improvement (r range 0.50 to 0.75). CONCLUSIONS: Estrogen replacement therapy significantly diminished sleep complaints among postmenopausal women. Alleviation of climacteric symptoms was the most important predictive factor for the beneficial effect of estrogen replacement therapy on sleep complaints. The use of estrogen replacement therapy in women without self-reported climacteric symptoms could also be considered because women do not always recognize their climacteric symptoms or they ignore them.
BACKGROUND: Total or partial sleep deprivation was showed to have rapid antidepressive effects in depression. Sleep deprivation therapy in major depression constitutes insufficient antidepressive treatment response and depressive symptoms reoccur after one night of recovery. Combination of antidepressant medication with sleep deprivation therapy is generally indicated. These combination therapies were found more favorable overall therapeutic effect than antidepressive monotherapy. METHODS: In this study, we examined the Quality of Life changes with the antidepressive therapy using partial sleep deprivation plus sertraline and sertraline monotherapy in patients with major depressive disorder. Thirteen patients received six partial sleep deprivation therapies in addition to sertraline, that sleep schedule in deprivation nights started at 11:00-12:00 p.m. to 03:00 a.m. and 11 patients treated with sertraline monotherapy as a control group. Quality of Life was evaluated with the WHOQOL-100, depression and the accompanying anxiety were also assessed at baseline and at the end of the 4th week. RESULTS: Patients treated with combination therapy improved significantly and more rapidly. Rapid improvement in quality of life in major depressive disorder was showed in patients treated with combination of late partial sleep deprivation and sertraline. LIMITATIONS: Small sample size, the lack of placebo group and short duration of the study are the main limitations. CONCLUSIONS: In clinical practice, QOL improvement can be accelerated using combination of partial sleep deprivation with the sertraline therapy.
A sleep deprivation/chlorimipramine therapy was compared to chlorimipramine therapy in endogenous depression. In the sleep deprivation/chlorimipramine group a quick and long-lasting remission of depressive symptoms could be demonstrated. In the chlorimipramine group a marked prolonged onset of action was seen.
BACKGROUND: Sleep disturbance is common among disaster survivors with posttraumatic stress symptoms but is rarely addressed as a primary therapeutic target. Sleep Dynamic Therapy (SDT), an integrated program of primarily evidence-based, nonpharmacologic sleep medicine therapies coupled with standard clinical sleep medicine instructions, was administered to a large group of fire evacuees to treat posttraumatic insomnia and nightmares and determine effects on posttraumatic stress severity. METHOD: The trial was an uncontrolled, prospective pilot study of SDT for 66 adult men and women, 10 months after exposure to the Cerro Grande Fire. SDT was provided to the entire group in 6, weekly, 2-hour sessions. Primary and secondary outcomes included validated scales for insomnia, nightmares, posttraumatic stress, anxiety, and depression, assessed at 2 pretreatment baselines on average 8 weeks apart, weekly during treatment, posttreatment, and 12-week follow-up. RESULTS: Sixty-nine participants completed both pretreatment assessment, demonstrating small improvement in symptoms prior to starting SDT. Treatment and posttreatment assessments were completed by 66 participants, and 12-week follow-up was completed by 59 participants. From immediate pretreatment (second baseline) to posttreatment, all primary and secondary scales decreased significantly (all p values < .0001) with consistent medium-sized effects (Cohen's d = 0.29 to 1.09), and improvements were maintained at follow-up. Posttraumatic stress disorder subscales demonstrated similar changes: intrusion (d = 0.56), avoidance (d = 0.45), and arousal (d = 0.69). Fifty-three patients improved, 10 worsened, and 3 reported no change in posttraumatic stress. CONCLUSION: In an uncontrolled pilot study, chronic sleep symptoms in fire disaster evacuees were treated with SDT, which was associated with substantive and stable improvements in sleep disturbance, posttraumatic stress, anxiety, and depression 12 weeks after initiating treatment.
Manifestations of sleep disturbances can potentially serve as external criteria for the diagnosis of specific subtypes of major depressive disorder (MDD). Depressed patients generally experience disturbances of sleep continuity and rapid eye movement (REM) sleep. Disturbances in nonrapid eye movement (NREM) sleep (stages III and IV) also occur. Characteristic of primary sleep disturbance in many depressed patients are shortened REM latency periods and instabilities in NREM sleep identified by increases in the number of stage shifts, decreases in the duration of stage III and IV sleep, and a shift towards lighter sleep stages (sleep efficiency disturbances). Treatment modalities for these sleep disturbances include sleep deprivation therapy and antidepressant therapy. Sleep deprivation alone has been only moderately successful, while antidepressant therapy usually results in symptomatic improvement. To restore normative sleep, REM sleep periods and stage III and IV sleep must be returned to normal. Trazodone therapy has been shown to reduce the frequency of arousals, the severity of drowsiness, and the duration of REM sleep, and increase restorative slow wave sleep and stage III and IV NREM sleep.
The influence of hormone therapy on sleep states, pulse, respiration and seizure activities of infantile spasms was examined by means of overnight sleep polygraphy. Also the correlation between the changes of these parameters and the prognosis was investigated. The results were as follows: 1) In all cases, the awake time of TIB during hormone therapy was longer than before hormone therapy. The reduction of REM sleep time of SPT and lowering of REM density were remarkable during hormone therapy in cases with delayed psychomotor development as compared with cases with a considerable degree of psychomotor development. During hormone therapy, the NREM sleep time of SPT was shortened in cases with ACTH therapy, and prolonged in case with hydrocortisone therapy. 2) During hormone therapy, the pulse rate increased significantly in cases with a considerable degree of psychomotor development, but decreased significantly in cases with delayed psychomotor development. The change of respiratory rate by hormone therapy was not remarkable in all cases. 3) In cases with hypsarhythmic EEG records, the number of spikes decreased drastically by hormone therapy. In the case with EEG record of focal spikes, the number of spikes increased by hormone therapy. From the results mentioned above, the mechanism for effectiveness of hormone therapy and correlation between the administration of hormone therapy and prognosis was discussed.