Depression clinical

The molten carbonate fuel ceU uses eutectic blends of Hthium and potassium carbonates as the electrolyte. A special grade of Hthium carbonate is used in treatment of affective mental (mood) disorders, including clinical depression and bipolar disorders. Lithium has also been evaluated in treatment of schizophrenia, schizoaffective disorders, alcoholism, and periodic aggressive behavior (56). 

Treatment goals for patients with psoriasis are to minimize signs such as plaques and scales, alleviate symptoms such as pruritus, reduce the frequency of flare-ups, and ensure appropriate treatment of associated conditions such as psoriatic arthritis or clinical depression, and minimize treatment-related morbidity. 

Psoriasis is a common inflammatory skin disorder which is estimated to affect 1.5% to 3% of the Caucasian population.1,2 It may present at any age.3,4 Ethnic factors influence disease prevalence. In the United States, prevalence among blacks (0.45% to 0.7%) is lower than in the remainder of the United States population (1.4% to 4.6%).1 Between 10% and 30% of patients with psoriasis will also have psoriatic arthritis.5 In 10% to 15% of psoriatic patients with arthritis, joint symptoms actually appear prior to skin involvement.3 Clinical depression is another frequent comorbid illness in these patients. A recent United States survey showed that 8% to 10% of psoriatic patients aged 18 to 54 years old actively contemplated suicide because of their psoriasis.6... 

One thing to learn from these data is that doing nothing is not the best way to respond to depression. People should not just wait to recover spontaneously from clinical depression, nor should they be expected just to snap out of it. There may be some improvement that is associated with the simple passage of time, but compared to doing nothing at all, treatment - even if it is just placebo treatment - provides substantial benefit. 

There is only one group of research subjects in whom rapid depletion of serotonin sometimes produces clinical depression. These are depressed patients in remission who are currently taking SSRIs. About half of these patients relapse when serotonin is depleted. Note that this only happens if they are still taking antidepressant medication. If they have stopped medication, depleting... 

How can this be How is it possible that a dummy pill with no active ingredients can produce substantial improvement in a condition as serious as clinical depression As it turns out, placebos can be surprisingly effective, not only in the treatment of depression, but also for various other conditions. As we shall see in this chapter, placebos can reverse the effects of powerful medications. They can affect the body as well as the mind. They produce side effects as well as beneficial effects. They can make people feel sick, and they can make them feel better. Placebo effects are part of a broader phenomenon - the power of suggestion to change how people feel, how they behave, and even their physiology. If placebos can produce such powerful effects, it is important to understand them. Only by unlocking the secrets of the placebo effect can we hope to harness its power so that it can be used in clinical practice. In this chapter we look at the power of the placebo its ability to produce therapeutic change and to cause harm. 

The evidence I have reviewed in this chapter indicates that placebos work for a wide variety of conditions. They can produce both positive and negative effects. They affect the body as well as the mind. They can be as strong as potent medications, and their effects can be lasting. We have also seen that placebos can produce negative effects. Furthermore, the nocebo effect maybe an important factor in clinical depression - at least for some depressed people. For this reason, understanding the placebo effect is essential to understanding how to treat depression effectively. How do inert substances produce both therapeutic and detrimental effects Chapter 6 provides an answer to this question. 

Physical exercise as a treatment for clinical depression has not been studied as extensively as dmgs or psychotherapy, but there are a number of clinical trials evaluating its effectiveness.41 In some of these studies, exercise was compared to no treatment at all. In others, it was compared to psychotherapy, medication or attention-control procedures intended to control for the nonspecific placebo aspects of the exercise programme. Some of the trials also looked at the combination of physical exercise with... 

Craft, Lynette L. and M. Daniel Landers, The Effects of Exercise on Clinical Depression and Depression Resulting from Mental Illness A Metaregression Analysis , Journal of Sport and Exercise Psychology 20 (1998) 339-57... 

Pinquart, M., P. M. Duberstein and J. M. Lyness, Effects of Psychotherapy and Other Behavioral Interventions on Clinically Depressed Older Adults A Meta-Analysis , Aging Mental Health 11, no. 6 (2007) 645-57... 

Vredenburg, K., Flett, G. L., Krames, L. (1993). Analogue versus clinical depression A critical appraisal. Psychological Bulletin, 113, 327-344-... 

Pharmacogenomics may be beneficial to people of color because of their high rates of morbidity and mortality from certain cancers, hypertension, cardiovascular disease, asthma, HIV /AIDS, Alzheimer disease, clinical depression, and other diseases. Thus more effective therapies help those individuals most in need of treatment. 

Anorexia nervosa sufferers can exhibit sudden angry outbursts or become socially withdrawn. One in ten cases of anorexia nervosa leads to death from starvation, cardiac arrest, other medical complications, or suicide. Clinical depression and anxiety place many individuals with eating disorders at risk for suicidal behavior. 

Nebes, R.D., Vora, I.J., Meltzer, C.C., et al. (2001) Relationship of deep white matter hyperintensities and apolipoprotein E genotype to depressive symptoms in older adults without clinical depression. Am. J. Psychiatry, 158, 878-884. 

It is also important to know about comorbid psychiatric disorders. If these are overlooked, treating the substance use disorder becomes significantly more difficult. Recognizing this, most treatment centers have developed dual diagnosis programs to treat those patients who have another major psychiatric illness in addition to a substance use disorder. It may be virtually impossible to discern at first, but the other psychiatric illnesses might either contribute to or be a result of substance use. The social toll of alcoholism alone can trigger a severe clinical depression. However,... 

Once chronic insomnia has developed, it hardly ever spontaneously resolves without treatment or intervention. The toll of chronic insomnia can be very high and the frustration it produces may precipitate a clinical depression or an anxiety disorder. Insomnia is also associated with decreased productivity in the workplace and more frequent use of medical services. Einally, substance abuse problems may result from the inappropriate use of alcohol or sedatives to induce sleep or caffeine and other stimulants to maintain alertness during the day. 

An unexpected discovery also arose during the therapeutic use of reserpine in the treatment of hypotension when it was found that approximately 15% of patients became clinically depressed. As it has been shown that reserpine depletes both the central and peripheral nervous system of noradrenaline, it was postulated that depression would be a consequence of the defective synthesis of noradrenaline and possibly serotonin. This helped to form the basis of the amine therapy of depression. 

Headache, chills, dry mouth, GI distress, worsening depression in patients who are clinically depressed, tachycardia, palpitations, chest pain... 

Loss of scalp hair, clinical depression Serious Reactions... 

Knox, M., King, C., Hanna, G.L., Logan, D., and Ghaziuddin, N. (2000) Aggressive behavior in clinically depressed adolescents./ Am Acad Child Adolesc Psychiatry 39 611-617. 

Advances in this area have perhaps been the most profound over the past 5 to 10 years, occurring as a result of imaging studies followed by focused postmortem studies of the brains of patients with both bipolar and unipolar depression. Neuroimaging studies of patients with familial pure major depression have identified neurophysiological abnormalities in multiple areas of the orbital and medial prefrontal cortex (PFC), the amygdala, and related parts of the striatum and thalamus. Some of these abnormalities appear to be state dependent (i.e., present only when the patient is clinically depressed), whereas other abnormalities appear to be trait dependent (i.e., present whether the patient is depressed or not) ( 27). 

Nevertheless, receptor studies in these areas are consistent with a role for biogenic amine function in the pathophysiology of major depression. Two of the most replicated findings are increased 5-FIT 2a receptor binding in the PFC and reduced 5-FIT receptor number and function in the brains of depressed suicide victims. These findings have led to positron emission tomography studies to quantitate the number of 5-FIT 2 and 5-FIT a receptors in the brain of patients with clinical depression (31, 32). This work has documented a 42% and a 27% reduction in 5-FIT a receptors in the raphe and mesiotemporal cortex, respectively, in unmedicated patients with primary, recurrent, familial major depression. 

Severe depression is another term that is frequently seen in the literature discussing clinical depression and antidepressant trials. There is no uniform definition of this term. One or more of the following criteria may be used to differentiate patients with nonsevere versus severe depression ... 

There is considerable debate as to how effective SSRIs are in patients with more severe clinical depression, particularly those who have been hospitalized. Part of this debate may be because the vast majority of studies done with SSRIs involved outpatients. As mentioned earlier, hospitalization is not simply determined by severity of an episode but may be driven by other variables such as concomitant substance abuse or a medical illness. 

The use of herbs has also been fueled by the increased awareness of clinical depression and its treatment as a result of the marketing efforts of major pharmaceutical companies. That effort has transformed prescription antidepressants into one of the largest dollar sales category in pharmaceuticals such that the sales for a block buster antidepressant can be more than 2 billion dollars per year. Not surprisingly, then, herbal remedies or phytomedicine has also become a multibillion dollar industry in the United States with an estimated one in ten Americans having used herbal agents within the past year, with or without their physician s knowledge. 

A number of studies have been performed on the efficacy of St. John s Wort as an antidepressant. Several meta-analyses of these studies have also been published. The first such metaanalysis involved 23 randomized trials (15 placebo-controlled and eight active-controlled) involving 1,757 outpatients. It concluded that there was preliminary evidence supporting hypericum extracts as being superior to placebo in patients with mild to moderate clinical depression ( 233). Two more recent reviews of subsequent, placebo-controlled studies also concluded that hypericum is more effective than placebo but possibly less effective than TCAs ( 234, 235). At least two large-scale, multicenter, double-blind, placebo- and active-controlled studies are ongoing in the United States, testing the efficacy of hypericum versus an SSRI in patients with major depression. The results of these studies should further clarify the role of hypericum in the treatment of depressive disorders. 

These older antidepressants have a therapeutic range that is bound on the lower end by lack of efficacy and on the upper end by risk of serious toxicity. These drugs also have substantial interindividual variability in drug metabolism so that ineffective concentrations can develop in some patients on the usual dose and toxic concentrations can develop in others. For that reason, TDM is a standard of care issue when using TCAs to treat clinical depression ( 325). 

Thus, the upper limit to the therapeutic range is a function of toxicity rather than reduced efficacy in contrast to the other TCAs. Perry et al. ( 326) proposed a minimal threshold for this tertiary amine TCA of 265 ng/mL (imipramine plus desimipramine) with a remission rate of 42% above this threshold versus 15% below it. Of note, this threshold for optimal antidepressant response is closer to the threshold for CNS and cardiac toxicity than for any other TCA. Preskorn and colleagues ( 327) found a lower optimal threshold for imipramine plus desimipramine (125 ng/mL) when it was used to treat clinical depression in children and adolescents than when used in adults. 

Aprison MH, Takahashi R, Tachiki K. Hypersensitive serotonergic receptors involved in clinical depression a theory. In Halver B, Aprison MH, eds. Neuropharmacology and behavior. New York Plenum, 1978 23-48. 

First-line therapy of CAD depends on modification of risk factors such as smoking, hypertension (see Chapter 11), hyperlipidemia (see Chapter 35), obesity, and clinical depression. In addition, antiplatelet drugs (see Chapter 34) are very important. 

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