Academic literature on the topic 'Mood stabilizer drugs'

Phenytoin is a first-generation antiepileptic drug characterized by a good range of antiepileptic indications, with an acceptable interaction profile in polytherapy. The reasons for the decreased use of phenytoin in patients with epilepsy include its narrow therapeutic index and potential for long-term toxicity, as well as the development of other antiepileptic drugs throughout the second half of the twentieth century. Phenytoin has a good behavioural tolerability profile and a restricted range of psychiatric uses. Despite occasional reports of adverse behavioural effects (especially at higher

The past two decades have seen significant advances in the development of evidence-based treatments for pediatric bipolar disorder. Practice guidelines recommend pharmacotherapy with mood stabilizers or second-generation antipsychotics (SGAs) as the first-line treatment. Lithium, risperidone, aripiprazole, quetiapine, and olanzapine are approved by the U.S. Food & Drug Administration for treating bipolar disorder in children and adolescents. The pharmacological literature suggests that SGAs are faster and more effective than mood stabilizers in treating acute manic or mixed episodes, but t

Increased appetite and weight gain represent a significant problem related with particular antipsychotic drugs, antidepressants, mood stabilizers, and—to a lesser extent—anxiolytic drugs. Psychotropic drug-induced weight gain may contribute to obesity-related metabolic changes and pathological conditions such as dyslipidaemia, type-2-diabetes and hypertension—summarized as the metabolic syndrome—with an increased risk for cardiovascular morbidity and mortality. Interestingly, psychotropic drugs are also used for the treatment of diabetes-related complications. For example, antidepressants are

In this chapter, essential aspects of the treatment of psychiatric disorders are reviewed including pharmacokinetics, pharmacodynamics, drug interactions, psychogenomics and the use of antidepressants, mood stabilizers, antianxiety agents, antipsychotics, psychostimulants, hypnotics and sedatives, ECT and psychotherapy

Despite the lack of approval by the U.S. Food & Drug Administration, drugs are used widely to treat personality disorders, particularly borderline personality disorder, based on their effects known from clinical trials in other psychiatric disorders (off-label use). The role of medications in personality disorders is limited to moderate effects on some but not all of the symptom domains. There are no medications available that improve the global severity of any personality disorder as a whole. In borderline personality disorder, evidence is strongest for second-generation antipsychotics an

A “mood stabilizer” is a drug that prevents mania and depressive episodes in bipolar disorder. The four drugs that have reasonable evidence that they can do this are lithium, Depakote, carbamazepine, and Lamictal. Second generation antipsychotics are not mood stabilizers, despite the FDA maintenance indications that many have received, because of the invalidity of the enriched, randomized, discontinuation maintenance design. Thus, all patients with bipolar illness should receive one of those four mood stabilizers, and dopamine blockers should be used as adjuncts, but not by themselves. In this chapter, a summary is given of the major drug classes, and the agents within those classes. Specific dosing guidelines are provided for most agents. Main clinical side effects and drug interactions are reviewed.

‘Drugs and other physical treatments’ provides coverage of the current drug and physical treatments used in the management of general psychiatric disorders. Following a historical introduction and general principles governing drug use and prescription, agents are considered according to the major psychotropic classes, namely: anxiolytic and hypnotic, antipsychotic, antidepressant, mood stabilizer, and psychostimulant. Each class is described according to its pharmacology, followed by the indications, pharmacokinetics, adverse effects and clinical use of individual compounds. Subsequent sections describe the indications, practical management, and adverse effects of electroconvulsive therapy, as well as other treatments designed to influence brain activity directly. Included here are descriptions of neurosurgery and various neurostimulation techniques (deep brain stimulation, transcranial magnetic stimulation, transcranial direct current stimulation, and vagal nerve stimulation), together with the evidence for their effectiveness as well as their proposed indications and adverse effects.

Lithium is the paradigmatic mood stabilizer. It is effective in the acute and prophylactic treatment of both mania and, to a lesser magnitude, depression. These characteristics are generally paralleled by the widely accepted anticonvulsant mood stabilizers valproate, carbamazepine (Table 6.2.4.1), and potentially by the less well studied putative mood stabilizers oxcarbazepine, zonisamide, and the dihydropyridine L-type calcium channel blocker nimodipine. In contrast, lamotrigine has a profile of better antidepressant effects acutely and prophylactically than antimanic effects. Having grouped lithium, valproate, and carbamazepine together, it is important to note they have subtle differences in their therapeutic profiles and differential clinical predictors of response (Table 6.2.4.1). Response to one of these agents is not predictive of either a positive or negative response to the others. Thus, clinicians are left with only rough estimates and guesses about which drug may be preferentially effective in which patients. Only sequential clinical trials of agents either alone or in combination can verify responsivity in an individual patient. Individual response trumps FDA-approval. Given this clinical conundrum, it is advisable that patients, family members, clinicians, or others carefully rate patients on a longitudinal scale in order to most carefully assess responses and side effects. These are available from the Depression Bipolar Support Alliance (DBSA), the STEP-BD NIMH Network, or www.bipolarnetworknews.org and are highly recommended. The importance of careful longitudinal documentation of symptoms and side effects is highlighted by the increasing use of multiple drugs in combination. This is often required because patients may delay treatment-seeking until after many episodes, and very different patterns and frequencies of depressions, manias, mixed states, as well as multiple comorbidities may be present. Treating patients to the new accepted goal of remission of their mood and other anxillary symptoms usually requires use of several medications. If each component of the regimen is kept below an individual's side-effects threshold, judicious use of multiple agents can reduce rather than increase the overall side-effect burden. There is increasing evidence of reliable abnormalities of biochemistry, function, and anatomy in the brains of patients with bipolar disorder, and some of these are directly related to either duration of illness or number of episodes. Therefore, as treatment resistance to most therapeutic agents is related to number of prior episodes, and brain abnormalities may also increase as well, it behooves the patient to begin and sustain acute and long-term treatment as early as possible. Despite the above academic, personal, and public health recommendations, bipolar disorder often takes ten years or more to diagnose and, hence, treat properly. In fact, a younger age of onset is highly related to presence of a longer delay from illness onset to first treatment, and as well, to a poorer outcome assessed both retrospectively and prospectively. New data indicate that the brain growth factor BDNF (brain-derived neurotrophic factor) which is initially important to synaptogenesis and neural development, and later neuroplasticity and long-term memory in the adult is involved in all phases of bipolar disorder and its treatment. It appears to be: 1) both a genetic (the val-66-val allele of BDNF) and environmental (low BDNF from childhood adversity) risk factor; 2) episode-related (serum BDNF decreasing with each episode of depression or mania in proportion to symptom severity; 3) related to some substance abuse comorbidity (BDNF increases in the VTA with defeat stress and cocaine self-administration); and 4) related to treatment. Lithium, valproate, and carbamazepine increase BDNF and quetiapine and ziprasidone block the decreases in hippocampal BDNF that occur with stress (as do antidepressants). A greater number of prior episodes is related to increased likelihood of: 1) a rapid cycling course; 2) more severe depressive symptoms; 3) more disability; 4) more cognitive dysfunction; and 5) even the incidence of late life dementia. Taken together, the new data suggest a new view not only of bipolar disorder, but its treatment. Adequate effective treatment may not only (a) prevent affective episodes (with their accompanying risk of morbidity, dysfunction, and even death by suicide or the increased medical mortality associated with depression), but may also (b) reverse or prevent some of the biological abnormalities associated with the illness from progressing. Thus, patients should be given timely information pertinent to their stage of illness and recovery that emphasizes not only the risk of treatments, but also their potential, figuratively and literally, life-saving benefits. Long-term treatment and education and targeted psychotherapies are critical to a good outcome. We next highlight several attributes of each mood stabilizer, but recognize that the choice of each agent itself is based on inadequate information from the literature, and sequencing of treatments and their combinations is currently more an art than an evidence-based science. We look forward to these informational and clinical trial deficits being reduced in the near future and the development of single nucleotide polymorphism (SNP) and other neurobiological predictors of individual clinical response to individual drugs. In the meantime, patients and clinicians must struggle with treatment choice based on: 1) the most appropriate targetting of the predominant symptom picture with the most likely effective agent (Table 6.2.4.1 and 6.2.4.2) the best side-effects profile for that patient (Table 6.2.4.2 and 6.2.4.3) using combinations of drugs with different therapeutic targets and mechanisms of action (Table 6.2.4.3 and 6.2.4.4) careful consideration of potential advantageous pharmacodynamic interactions and disadvantageous pharmacokinetic drug-drug interactions that need to be avoided or anticipated.

This chapter on basic mechanisms of, and treatment targets for, bipolar disorder examines the cause and treatment of bipolar disorder from the perspective of intracellular signalling pathways implicated by the convergence of evidence from efficacious drugs, pathophysiology, and genetics and concludes that the unifying concept is calcium signalling. It discusses the pathways for cyclic adenosine monophosphate and inositol trisphosphate/calcium in the context of the action of drugs, with emphasis on lithium, the most effective true mood stabilizer. It proposes that the calcium signalling pathway and its components, such as channels, pumps, messengers, and enzymes, can explain both how dysfunction can affect neural activity and how this can be remedied by drugs. It argues for the central role of calcium, based on new evidence for the inositol depletion hypothesis and evidence of calcium dysregulation in peripheral and inducible pluripotent stem cells, as well as genome-wide association studies and drugs implicating a plasma membrane calcium channel.

The chapter on mood stabilizers discusses and reviews the use of available treatments for bipolar disorder, including lithium, selected anticonvulsants (such as valproate, carbamazepine, oxcarbazepine, and lamotrigine) and second-generation antipsychotics. It reviews each medication’s mechanism of action, clinical characteristics, potential medication interactions, and adverse effects. The chapter also reviews emerging pharmacotherapies such as the use of ketamine. It also briefly discusses complementary and alternative pharmacotherapies and the use of omega-3 fatty acids. The chapter includes an in-depth review of the clinical use of the previously listed medications for bipolar depression, mania, mixed episodes, and bipolar maintenance. It also reviews the risks of using antidepressants for bipolar depression. It also discusses the use of mood stabilizers in women of childbearing age, notably for pregnancy and breastfeeding considerations. Finally, the chapter includes a table of mood stabilizers that includes each medication’s generic and brand names, usual adult doses, pertinent clinical comments, black box warnings and Food and Drug Administration indications.

Background: Elderly patients with and without dementia are especially vulnerable to COVID-19 infection due to their disease status, age and comorbidities, needing to face measures of social restrictions. However, it is known that social isolation is a risk factor for decline of cognitive functions. Objectives: Gather information about consequences of isolation in elderly patients with and without dementia during the COVID-19 pandemic. Methods: Narrative literature review through active search for publications on the topic on the PubMed platform, resulting in 17 articles for evaluation. Results