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Bipolar disorder response

The total costs are likely to reflect the efficacy of treatment. In one industry-sponsored study (Keck et al, 1996b) treatment with lithium or valproate was compared in relation to classical, mixed and rapid-cycling disorder. Treatment with lithium was associated with lower costs than treatment with valproate for classical bipolar disorder, but treatment with valproate was associated with lower costs than treatment with lithium for mixed and rapid-cycling disorders. This is in keeping with the evidence that valproate is more effective than lithium for certain patients with rapid-cycling disorder and probably also for certain patients with mixed affective states. However, these associations are a guide to predicting response to treatment but are not very specific. [Pg.75]

Based on all information presented, create a care plan for this patient s bipolar disorder. Your plan should include (1) a statement of the drug-related needs and/or problems, (2) the goals of therapy, (3) a patient-specific therapeutic plan, and (4) a plan for follow-up to assess therapeutic response and adverse effects. [Pg.590]

Educate the patient on the nature of bipolar disorder and its treatment, what to expect with regard to response and side effects, and stress the need for adherence to treatment, even when feeling well. [Pg.603]

Turecki, G., Grof, R, Grof, E. etal. (2001). Mapping susceptibility genes for bipolar disorder a pharmacogenetic approach based on excellent response to lithium. Mol. Psychiatry, 6, 570-8. [Pg.85]

These data show that for three psychotic disorders (schizophrenia, bipolar disorder and unipolar depression) the genetic contribution is over 50% but for reactive depression (in response to a traumatic life event ) and tuberculosis, an infectious disease caused by a species of Mycobacterium, environmental factors account for over 90% of the variance. [Pg.159]

Mood stabilisers are used to regulate the cyclical change in mood characteristic of bipolar disorder, since they can attenuate both manic and depressive phases. Their main use is as a prophylactic for manic depression and unipolar mania. However, they can also be administered concomitantly with antidepressants for refractory (non-responsive) unipolar depression. [Pg.182]

The positive symptoms are the most responsive to antipsychotic medications, such as chlorpromazine or halo-peridol. Initially, these drugs were thought to be specific for schizophrenia. However, psychosis is not unique to schizophrenia, and frequently occurs in bipolar disorder and in severe major depressive disorder in which paranoid delusions and auditory hallucinations are not uncommon (see Ch. 55). Furthermore, in spite of early hopes based on the efficacy of antipsychotic drugs in treating the positive symptoms, few patients are restored to their previous level of function with the typical antipsychotic medications [2]. [Pg.876]

Bipolar disorder patients have shown abnormalities of the hypothalamic-pituitary-thyroid axis, demonstrated by an exaggerated TSH response to TRH and elevated basal... [Pg.893]

Thus, it is possible that recurrent mood disorders, as in the case of bipolar disorder, may lower the threshold for cell death and/or atrophy in response to a variety of other physiological (e.g. normal aging) and pathological (e.g. ischemic) events, and thereby contribute to a variety of deleterious health-related effects. [Pg.895]

To date, there have only been a limited number of studies directly examining PKC in bipolar disorders [77], Although undoubtedly an oversimplification, particulate (membrane) PKC is sometimes viewed as the more active form of PKC, and thus an examination of the subcellular partitioning of this enzyme can be used as an index of the degree of activation. Friedman etal. [78] investigated PKC activity and PKC translocation in response to serotonin in platelets obtained from bipolar-disorder patients before and during lithium treatment. They reported that the ratios of platelet-membrane-bound to cytosolic PKC activities were elevated in the manic patients. In addition, serotonin-elicited platelet PKC translocation was found to be enhanced in those patients. With respect to brain tissue, Wang and Friedman [74] measured PKC isozyme levels, activity and translocation in postmortem brain tissue from patients with bipolar disorder, and reported increased PKC activity and translocation in the brains of bipolar patients compared with controls, effects which were accompanied by elevated levels of selected PKC isozymes in cortices of bipolar disorder patients. [Pg.897]

The term "bipolar disorder" originally referred to manic-depressive illnesses characterized by both manic and depressive episodes. In recent years, the concept of bipolar disorder has been broadened to include subtypes with similar clinical courses, phenomenology, family histories and treatment responses. These subtypes are thought to form a continuum of disorders that, while differing in severity, are related. Readers are referred to the Diagnostic and Statisticial Manual of Mental Disorders of the American Psychiatric Association (DSM-IV) for details of this classification. [Pg.193]

Bipolar disorder The initial dosage is 200 mg twice daily. Adjust in 200 mg daily increments to achieve optimal clinical response. Doses greater than 1,600 mg/day have not been studied. [Pg.1247]

The most common mood disorders are major depression (unipolar depression) and manic-depressive illness (bipolar disorder). Major depression is a common disorder that continues to result in considerable morbidity and mortality despite major advances in treatment. Approximately 1 in 10 Americans will be depressed during their lifetime. Of the 40,000 suicides occurring in the United States each year, 70% can be accounted for by depression. Antidepressants are now the mainstay of treatment for this potentially lethal disorder, with patients showing some response to treatment 65 to 80% of the time. [Pg.385]

Sovner, R. (1991) Divalproex-responsive rapid cycling bipolar disorder in a patient with Down s syndrome implications for the Down s syndrome-mania hypothesis. J Ment Defic Res 35 171-173. [Pg.327]

Duffy, A., Alda, M., Kutcher, S., Fusee, C., and Grof, P. (1998) Psychiatric symptoms and syndromes among adolescent children of parents with lithium-responsive or lithium-nonresponsive bipolar disorder. Am Psychiatry 155 431 33. [Pg.495]

The treatment of the major depressive disorders such as unipolar and bipolar depressions was initially considered to be uniform, ffowever, with psychopharmacological advances, it has been demonstrated that the patients with bipolar depression may be partially responsive, at least prophylactically responsive, to lithium therapy, whereas the patients with unipolar depression are not as responsive (Abou-Saleh 1992). In addition, the treatment of depression may contribute through serendipity to the confirmation of a subgroup of patients with a bipolar disorder referred to as bipolar II. These patients, following treatment with antidepressants, will switch over to a hypomanic or fully manic phase resulting from pharmacological mechanisms. Thus, another subgroup of the bipolar disorder may be identified in the future. [Pg.42]

Carbamazepine produces complex effects in a variety of neurotransmitters, receptors, and second messenger and neuropeptide systems (Post et al. 1992, 1994a). Determining which of these effects is most closely associated with its psychotropic properties in bipolar disorder and which of these or other effects may be responsible for the augmentation response in combination therapy with dihydropyridine L-type CCBs remains to be further evaluated. However, discussion of two possibilities might be beneficial. One possibility, of course, is that actions of carbamazepine unrelated to calcium dynamics account for its augmenting effects with nimodipine. The plethora of these other... [Pg.103]

Considerable effort over the years has been expended to identify specific neurotransmitter systems that might mediate the therapeutic action of lithium in the treatment of patients with bipolar disorder. As we critically review the evidence from these studies, it will be evident that lithium can affect a variety of neurotransmitter systems, but these effects may be secondary to more fundamental modulation of signal transduction responsible for regulating the balance of signaling in critical regions of the brain. [Pg.114]


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See also in sourсe #XX -- [ Pg.143 ]




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