The Clinical Global Impression (CGI) scale is brief, comprehensive, Youth with panic attacks (which often do not meet diagnostic criteria open-label study, neuro psycho physical optimization-radio electric may be useful for some patients with refractory illness . ;– fm meet the world beat Photo taken in Suita-shi by たっち. concluded that, to meet the many demands of performing their functions . we live in a world where good management requires good leaders Admired Firms for , , mephistolessiveur.info Applied Psychology, 82, – Kinicki, A. J., McKee-Ryan, F. M., Schriesheim, C. A., & Carson, K. P. ( ).
Metabolic disturbances generally appear to be higher with olanzapine, intermediate with risperidone and quetiapine, and lower with aripiprazole, asenapine, lurasidone, and ziprasidone [ - ]. Atypical antipsychotics have varying sedative effects, with quetiapine, clozapine, asenapine, and olanzapine generally causing more sedation than ziprasidone, risperidone, lurasidone, or aripiprazole . Data on cognitive effects are conflicting, with some studies suggesting improvements [ ], while other data suggest greater cognitive dysfunction in patients using, versus those not using, antipsychotics [ ].
Because of the risks of diabetes and weight gain, and the fact that there is limited RCT evidence of the efficacy of these agents in anxiety and related disorders, atypical antipsychotics are generally recommended as second-line, third-line, or adjunctive therapies see Sections 3—9 for evidence and references.
Anticonvulsants are associated with gastrointestinal side effects, somnolence, weight gain, tremor, as well as dermatologic and hematologic side effects . In addition, several anticonvulsants have a potential risk of serious rash, erythema multiforme, Stevens-Johnson syndrome, or toxic epidermal necrolysis [ ]. Regular monitoring of serum medication levels and liver function is required for patients on divalproex [ 84].
Follow-up Anxiety and related disorders are often chronic and a systematic approach to treatment should include patient education, assessment of comorbidities, and evidence-based pharmacological and psychological interventions with adequate monitoring and duration.
Pharmacological treatment is often associated with a delay of about two to eight weeks in onset of symptom relief, with full response taking up to 12 weeks or more. Longer-term therapy has been associated with continued symptomatic improvement and the prevention of relapse, and therapy should be continued for at least months for most patients [ 32 ].
Medication should be initiated at low doses and titrated to the recommended dosage range at one- to two-week intervals over four to six weeks. Once the therapeutic range has been achieved, improvement is usually seen over the next four to eight weeks. Follow-up should occur at two-week intervals for the first six weeks and monthly thereafter [ 32 ].
For a patient undergoing psychotherapy, the treatment schedule is structured around weekly contact with a therapist for about weeks, although shorter protocols and minimal intervention programs have also proven effective see Sections 3—9 for evidence and references. A follow-up appointment four weeks later and then every two to three months is usually sufficient [ 32 ]. Assessing response to treatment Therapy should seek to improve symptoms and distress.
The optimal goal is full remission of symptoms and return to a premorbid level of functioning [ 3285 ].
However, goals may need to be individualized for some patients with disorders that have been present since childhood as they may never have had adequate premorbid functioning.
Remission is often defined as loss of diagnostic status, a pre-specified low score on an appropriate disorder-specific scale, and no functional impairment in fully recovered patients as measured by a scale such as the Sheehan Disability Scale or SF [ 32, ]. The Clinical Global Impression CGI scale is brief, comprehensive, and can easily be used at each appointment to assess improvement.
The clinician-rated Hamilton Anxiety Rating Scale HARS can assess anxiety symptoms in general and is often used in clinical trials but is less practical in clinical practice. A variety of self-report and clinician-rated scales are available to assess the specific anxiety or related disorder.
Panic disorder and agoraphobia Epidemiology The lifetime and month prevalence of panic disorder have been estimated at 4. The estimated prevalence of panic attacks is considerably greater at The precise pathophysiological steps from transient vascular changes to systemic hypertension are far from clear but may involve oxidative stress, upregulation of vasoactive substances Caples et al.
During even the lowest phase, blood pressure during REM was higher than in the awake state. Most case-control studies detecting a relationship with myocardial infarction found adjusted odds ratios of around 4 Young et al. The adjusted OR for stroke was 1.
A higher probability of stroke associated with OSA is also supported by other studies Bassetti and Aldrich, ; Parra et al. In the Sleep Heart Health Study, apnea-hypopnea index was deter mined by polysomnography, and adjustments were made for a variety of confounding factors, including hypertension.
That the hypertension adjustment did not eliminate the effect suggests that hypertension is not the exclusive means by which OSA may lead to cardiovascular disease. A limitation of cross-sectional and case-control analyses is that cause and effect cannot be determined: However, an observational cohort study of 1, individuals, where 68 percent of individuals had OSA apnea-hypopnea index of 5 or highershowed that OSA syndrome significantly increased the risk of stroke or death from any cause, and the increase is independent of other risk factors, including hypertension Yaggi et al.
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Other studies have confirmed the risk of OSA syndrome with stroke or death from any cause Ayas et al. Furthermore, other large prospective studies also have shown an association between snoring—a marker for OSA—and incidence of cardiovascular diseases Jennum et al. As will be discussed in the next section, OSA is associated with glucose intolerance and diabetes, both of which are independent risk factors for cardiovascular disease.
The events included myocardial infarction, stroke, and coronary artery bypass surgery. The untreated patients had refused CPAP but were followed regularly. A second study found an increased mortality rate from cardiovascular disease in individuals who did not maintain CPAP treatment over a 5-year follow-up period Doherty et al.
However, the number of new cases of cardiovascular disease was independent of CPAP treatment compliance. Although observational evidence of this type is not conclusive proof, because it may be subject to confounding by indication and other biases, it still lends weight to the strength of the association.
Most studies finding elevated cardiovascular disease risk have been conducted in adults. Whether or not children with sleep-disordered breathing are at risk for cardiovascular effects is not known. Children with OSAas noted previously, do experience changes in blood pressure profiles, heart rate variability, and ventricular wall changes as measured by echocardiography Marcus et al. The paucity of longitudinal data on OSA in children, in whom levels of OSA may vary during growth and development and in whom responses to therapies such as tonsillectomy may be variable Morton et al.
Nonetheless, evidence that as many as 20 to 25 percent of children may have persistent OSA even after tonsillectomy underscores the potential importance of OSA as an early childhood risk factor for later cardiovascular diseases Amin et al. Those outcomes were more prevalent in those with the highest apnea-hypopnea index.
The study also found a relationship between sleep-related hypoxemia and glucose intolerance, which has implications for understanding mechanisms behind the OSA-glucose intolerance link see below. The Sleep Heart Health Study, as noted earlier, was a large, cross-sectional, community-based study that used polysomnography to identify OSA. The analyses adjusted for obesity BMI and waist circumferenceself-reported sleep duration, and other confounding factors.
The findings suggest that OSA contributes to the onset of diabetes through the development of glucose intolerance and insulin resistance, which are established pathophysiological processes in diabetes Martin et al. The study found that, after 10 years of follow-up, occasional snoring versus nonsnoring was associated with an elevated risk of new onset diabetes in women, and the risk was even greater for regular snoring Al-Delaimy et al. Regular or habitual snoring is an indicator of OSA.
CPAP alleviates glucose intolerance in the short term and long term Brooks et al.
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The mechanisms by which OSA disrupts glucose metabolism are not established. Drawing on human studies and animal models, the biochemical cascade begins with intermittent hypoxia and recurrent sleep arousals sleep fragmentation. These events stimulate the sympathetic nervous system, hypothalamic-pituitary-adrenal axis, and adipocytes Punjabi and Beamer, Their activation, in turn, leads to release of catecholamines, cortisol, and inflammatory cytokines and other vasoactive intermediates, which may mediate the development of glucose intolerance, insulin resistance, and, ultimately, type 2 diabetes.
Because diabetes is also a risk factor for cardiovascular disease, the interrelationships may partly explain why OSA predisposes to cardiovascular disease Punjabi and Beamer, This finding may reflect the role of obesity as a well-established risk factor for the development of OSA.
It may also reflect obesity as a consequence of OSA, although the evidence is not yet conclusive Grunstein, b. Patients with newly diagnosed OSA, compared with controls matched for BMI and percent body fat, show recent weight gain Phillips et al. Data from the Wisconsin Sleep Cohort also show that individuals with OSA have reduced levels of physical activity; OSA-related sleepiness may contribute to changes in activity and energy expenditure, and thus contribute to weight gain.
OSA-related hormonal changes may also contribute to obesity. In general, patients with OSA have higher levels of leptin, the appetite-suppressing hormone Phillips et al. However, their morning levels are relatively lower than evening levels Patel et al. Furthermore, obesity also affects the severity of OSA. Significant weight loss in adolescents who underwent gastric bypass surgery mean, 58 kg was associated with a dramatic reduction of OSA severity Kalra et al.
Etiology and Risk Factors In simplest terms, OSA is caused by narrowing or collapse of the airway as a result of anatomical and physiological abnormalities in pharyngeal structures. Apnea episodes cause hypoxemia insufficient oxygen in the blood and hypercapnia high concentration of blood carbon dioxide.
The episodes also increase the output of the sympathetic nervous system Narkiewicz and Somers,the effect of which is to restore pharyngeal muscle tone and reopen the airway. Although increased sympathetic activity is beneficial for restoring normal breathing and oxygen intake over the short term, it has long-term deleterious effects on vascular tone and blood pressure, among other effects Caples et al.
These early events—which are mediated by a variety of chemoreceptors in the carotid body and brainstem—trigger pathophysiological changes that occur not only during the obstructive apneas, but also extend into wakeful states during the day. For example, during daytime wakefulness, people with OSA have higher sympathetic activity Somers, et al. The full pathophysiology of OSA remains somewhat elusive, although research is piecing together the relationships between OSA and a range of the previously described long-term health effects.
The etiology of central sleep apnea, although also not well understood, is hypothesized to result from instability of respiratory control centers White, There are a number of risk factors for OSAincluding: Obesity, male gender, and increasing age Table Young et al.
It is unclear how incidence changes with older age; some data suggest that snoring and OSA may decline after age 65 years Young et al. The pathophysiological roles of these risk factors are not well understood, although evidence suggests that fat deposition in the upper airways, which is more likely in males, contributes to the physical narrow ing that causes OSA Robinson et al.
Menopause also increases the risk of OSA Bixler et al. However, recent studies suggest that there may be a referral bias that results in a lower apparent rate of sleep apnea in females than in males Kapsimalis and Kryger, ; Shepertycky et al. Epidemiological evidence suggests that hormone replacement therapy lessens the risk of OSA Shahar et al.
In children, the main risk factor for OSA is tonsillar hypertrophy, although OSA may also occur in children with congenital and neuromuscular disorders and in children who were born prematurely Rosen et al. Asthma, a common childhood respiratory illness, is also associated with OSA in children Sulit et al.
In adolescents, risk factors may be more similar to those seen in adults and include obesity Redline et al. Being a minority is a risk factor for both increased prevalence and severity of sleep-disordered breathing in both children and adults Rosen et al. The prevalence of sleep-disordered breathing in the United States is approximately three times higher in middle-aged members of minority groups compared to non-Hispanic whites Kripke et al.
African American children are at increased risk, even after adjusting for obesity or respiratory problems Redline et al. Familial and probably genetic factors strongly contribute to OSA Buxbaum et al. Patients with cardiovascular disease and diabetes are also at higher risk for developing both OSA and central sleep apnea Sin et al. Patients with impaired baroreflexes e. In these patient groups, bradyarrhythmias, hypoxia, hypoperfusion, and sympathetic activation during apnea may predispose to sudden death Somers et al.
Risk Factors for Obstructive Sleep Apnea. Studies of patients at sleep clinics tend to show an association between sleep apnea and mortality He et al. The subgroup experienced twice the risk of mortality Lindberg et al. Other options, although less effective, include a variety of dental appliances Ferguson and Lowe, or surgery e. In children, the first-line treatment for most cases of OSA is adenotonsillectomy, according to clinical practice guidelines developed by the American Academy of Pediatrics Marcus et al.
Children who are not good candidates for this procedure can benefit from CPAP. Central apnea treatment is tailored to the cause of the ventilatory instability. Commonly used treatments include oxygen, CPAP, and acetazolamide, a drug that acts as a respiratory stimulant White, It is a highly prevalent disorder that often goes unrecognized and untreated despite its adverse impact on health and quality of life Benca, a see also Chapter 4.
The diagnostic criteria for primary insomnia include: Difficulty initiating or maintaining sleep or nonrestorative sleep. Causing clinically significant distress or impairment in social, occupational, or other important areas of functioning. Not occurring exclusively during the course of another sleep disorder. Not due to the direct physiological effects of a substance or a medical condition APA, Insomnia symptoms are remarkably common, affecting at least 10 percent of adults in the United States Ford and Kamerow, ; Ohayon et al.
Prevalence is higher among women and older individuals Mellinger et al. Severe insomnia tends to be chronic, with about 85 percent of patients continuing to report the same symptoms and impairment months or years after diagnosis Hohagen et al. The comorbidity of sleep disorders with psychiatric disorders is covered later in this chapter.
Etiology and Risk Factors The precise causes of insomnia are poorly understood but, in general terms, involve a combination of biological, psychological, and social factors. Insomnia is conceptualized as a state of hyperarousal Perlis et al.
Stress is thought to play a leading role in activating the hypothalamic-pituitary axis and setting the stage for chronic insomnia.
A key study showed that adults with insomnia, compared with normal sleepers, have higher levels, over a hr period, of cortisol and adrenocorticotropic hormone ACTHwhich are hormones released by the hypothalamic-pituitary-adrenal axis after stress exposure Vgontzas et al. The hour pattern of cortisol and ACTH secretion is different, however, from that in individuals who are chronically stressed. Cognitive factors, such as worry, rumination, and fear of sleeplessness, perpetuate the problem through behavioral conditioning.FM802 MEET THE WORLD BEAT 2018
Other perpetuating factors include light exposure and unstable sleep schedules Partinen and Hublin, Insomnia patients often attribute their difficulty sleeping to an overactive brain.
Several lines of evidence, from preclinical to sleep neuroimaging studies in insomnia patients, suggest that there are multiple neural systems arranged hierarchically in the central nervous system that contribute to arousal as well as insomnia complaints. Disturbances in these systems may differ according to the nature of insomnia. Structures that regulate sleep and wakefulness, for example the brainstem, hypothalamus and basal forebrain, are abnormally overactive during sleep in primary insomnia patients Nofzinger et al.
In addition, limbic and paralimbic structures that regulate basic emotions and instinctual behaviors such as the amygdala, hippocampus, ventromedial prefrontal cortex and anterior cingulate cortex have been shown to be abnormally active during sleep in individuals with primary insomnia and secondary insomnias related to depression Nofzinger et al.
Abnormal activity in neocortical structures that control executive function and are responsible for modulating behavior related to basic arousal and emotions has been observed in individuals with insomnias associated with depression Nofzinger et al. The two main risk factors of insomnia are older age and female gender Edinger and Means, One large, population-based study found that insomnia was nearly twice as common in women than men, although reporting bias cannot be ruled out as a contributing factor Ford and Kamerow, The reason behind the apparent higher prevalence in women is not understood.
Other risk factors for insomnia include family history of insomnia Dauvilliers et al. Although adolescent age is not viewed a risk factor, insomnia has rarely been studied in this age group. Treatment Insomnia is treatable with a variety of behavioral and pharmacological therapies, which may be used alone or in combination. While the therapies currently available to treat insomnia may provide benefit, the NIH State of the Science Conference on the Manifestations and Management of Chronic Insomnia concluded that more research and randomized clinical trials are needed to further verify their efficacy, particularly for long-term illness management and prevention of complications like depression NIH, Behavioral therapies appear as effective as pharmacological therapies Smith et al.
Behavioral therapies, according to a task force review of 48 clinical trials, benefit about 70 to 80 percent of patients for at least 6 months after completion of treatment Morin et al. The therapies are of several main types Table The major problem with current behavioral therapies is not their efficacy; rather it is lack of clinician awareness of their efficacy and lack of providers sufficiently trained and skilled in their use.
Other problems are their cost and patient adherence Benca, a. The most efficacious pharmacological therapies for insomnia are hypnotic agents of two general types, benzodiazepine or nonbenzodiazepine hypnotics Nowell et al. Nonbenzodiazepine hypnotics are advantageous because they generally have shorter half-lives, thus producing fewer impairments the next day, but the trade-off is that they may not be as effective at maintaining sleep throughout the night Morin, ; Benca, a.
It is still unclear whether hypnotics lead to dependence. It is suggested that they should not be taken for more than 10 days in a row; however, recent studies suggest that hypnotics do not always lead to dependence Hajak et al. There have been no large-scale trials examining the safety and efficacy of hypnotics in children and adolescents. Other pharmacological classes used for insomnia include sedating antidepressants, antihistamines, and antipsychotics, but their efficacy and safety for treating insomnia have not been thoroughly studied Walsh et al.
The most frequent types of sleep disturbances are insomnia, excessive daytime sleepiness hypersomniaand parasomnia. Sleep disturbances are so commonly seen as symptoms of certain psychiatric disorders that they are listed as diagnostic criteria under DSM-IV APA, For example, insomnia is a symptom used with others to diagnose major depression. The comorbidity, or coexistence, of a full-blown sleep disorder particularly insomnia and hypersomnia with a psychiatric disorder is also common.
Forty percent of those diagnosed with insomnia, in a population-based study, also have a psychiatric disorder Ford and Kamerow, Among those diagnosed with hypersomnia, the prevalence of a psychiatric disorder is somewhat higher— The reasons behind the comorbidity of sleep and psychiatric disorders are not well understood.
Comorbidity might be due to one disorder being a risk factor or cause of the other; they might both be manifestations of the same or overlapping physiological disturbance; one might be a consequence of the other. In some cases, the sleep disturbance can be both cause and consequence.
In generalized anxiety disorder, for example, the symptoms of fatigue and irritability used to diagnose it are often the result of a sleep disturbance, which itself is also a diagnostic symptom. Adolescents with major depressive disorders report higher rates of sleep problems and, conversely, those with sleep difficulties report increased negative mood or mood regulation Ryan et al. In addition, sleep-onset abnormalities during adolescence have been associated with an increased risk of depression in later life Rao et al.
The best studied and most prevalent comorbidity is insomnia with major depression. Insomnia as a symptom of depression is highly common. On the basis of longitudinal studies, insomnia is now established as a risk factor for major depression. Not all people with insomnia have a depression diagnosis; however, studies have found that 15 to 20 percent of people diagnosed with insomnia have major depression Ford and Kamerow, ; Breslau et al. Depressed individuals have certain abnormalities detected by polysomnography.
One is shorter rapid eye movement REM latency a shorter period of time elapsing from onset of sleep to onset of REM sleepan effect that persists even after treatment for depression.
Shorter REM latency and slow-wave sleep SWS deficits tend to run in families; these abnormalities are also found in first-degree relatives of people with major depression, but who are unaffected by depression Giles et al.
A variety of polysomnographic abnormalities have been found with other psychiatric disorders Benca, a. Etiology and Risk Factors The etiological basis for the comorbidity of sleep disorders and psychiatric disorders is not well understood.
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Most potential mechanisms for sleep changes in psychiatric disorders deal specifically with insomnia and depression. Possible mechanisms include neurotransmitter imbalance cholinergic-aminergic imbalancecircadian phase advance, and hypothalamic-pituitary-adrenal axis dysregulation Benca, a. Recent evidence implicating regions of the frontal lobe has emerged from imaging studies using positron emission tomography.
As they progress from waking to non- REM NREM sleep, depressed subjects have smaller decreases in relative metabolism in regions of the frontal, parietal, and temporal cortex when compared to individuals who are healthy Nofzinger et al. Normally, the transition from waking to NREM sleep is associated with decreases in these frontal lobe regions.
What appears to occur with depression is that the decrease is less pronounced. Because the amygdala also plays a role in sleep regulation Jones,this finding suggests that sleep and mood disorders may be manifestations of dysregulation in overlapping neurocircuits.
The authors hypothesize that increased metabolism in emotional pathways with depression may increase emotional arousal and thereby adversely affect sleep Nofzinger et al.
A major problem is underdiagnosis and undertreatment of one or both of the comorbid disorders. One of the disorders may be missed or may be mistakenly dismissed as a condition that will recede once the other is treated. In the case of depression, for example, sleep abnormalities may continue once the depression episode has remitted Fava, If untreated, residual insomnia is a risk factor for depression recurrence Reynolds et al.
Further, because sleep and psychiatric disorders, by themselves, are disabling, the treatment of the comorbidity may reduce needless disability. Insomniafor example, worsens outcomes in depression, schizophrenia, and alcohol dependence. Another concern is that medication for one disorder might exacerbate the other e.
The choice of medica tion for psychiatric disorder or vice versa should be influenced by the nature of the sleep complaint e. Insomnia and Psychiatric Disorders As mentioned above insomnia is associated with depression, acting as both a risk factor and a manifestation Ford and Kamerow, ; Livingston et al. Several studies done were longitudinal in design, including one that tracked more than 1, male physicians for 40 years Chang et al. Another study, which followed 1, young adults at a health maintenance organization for 3.
This figure is based on 16 percent of the sample who developed depression with a history of insomnia at baseline, as compared with 4.
Insomnia is also a predictor of acute suicide among patients with mood disorders Fawcett et al. The striking association between insomnia and depression in so many studies suggests that insomnia is also an early marker for the onset of depression, and the two may be linked by a common pathophysiology.