Antidepressants mood stabilizers

Management of Agitation and Psychosis. Like antidepressants, mood stabilizers do not work immediately. It often takes a week or longer for a mood stabilizer to reach a therapeutic level and exert its beneficial treatment effects. Meanwhile, one may have a labile, impulsive, and agitated patient on one s hands. Clearly, rapidly acting tranquilizing medications are needed at this juncture to calm an agitated patient. 

Nefazodone, sertraline, mirtazapine, tricyclic antidepressants Mood stabilizers... 

Psychotropic effect is the main effect, with the desired action Psvchopharmaceuticals Antipsychotics Antidepressants Mood stabilizers Anxiolytics, hypnotics Psychostimulants Nootropics, antidementia drugs Social drugs , drugs Alcohol Nicotine Cocaine, heroin, etc. 

The following sections of this chapter concentrate on psychopharmaceuticals in the sense of Table 1.1, Le. antipsychotics. antidepressants, mood stabilizers, anxiolytics and psychostimulants attention also will be paid to hypnotics and antidementia drugs. 

Problems of optimal dosage and duration of drug treatment for mental disorders have also been addressed in numerous controlled studies and are presented separately below for antipsychotics, antidepressants, mood stabilizers, anxiolytics and psychostimulants. This division again makes sense because the disorders treated and the therapeutic approaches used differ in significant aspects and the empirical studies carried out in the individual indications show major qualitative and quantitative differences. 

Electroconvulsive therapy has been used as antidepressive, mood-stabilizing and antipsychotic treatments (Eitan and Lerer 2006 Shapira et al., 1991). It is reported that electroconvulsive shocks (ECS), an animal model for the ECT, affect the NE system. Thus, both acute and chronic ECS increase cortical and hippocampal NE release. Chronic ECS also desensitize a2-adrenergic autoreceptors in the PFC (Thomas et al., 1992). Paradoxically, electrophysiological studies report that chronic ECS suppress the firing activity of NE neurons in the ECS (Grant and Weiss 2001). Based on the evidences of ECS-induced increase in brain NE levels, it can be concluded that the benefitial effect of the ECT is mediated, at least in part, via NE system. 

For each of these three symptom clusters, there is a specific algorithm of treatment, sequencing various antidepressants, mood stabilizers, and antipsychotics in varying orders of preference, doses, and combinations of use. 

UGTs are responsible for the metabolism of many anxiolytics, antidepressants, mood stabilizers and antipsychotics. Inhibition of the metabolism of carbamazepine by valproic acid in part results from an effect on UGTs. Amitriptyline and clomipramine decrease the metabolism of morphine by affecting UGTs. 

There is ample evidence from preclinical and clinical research that the glutamatergic system is involved in the pathophysiology of mood disorders and that many of the somatic treatments used in the treatment of mood disorders, including current conventional antidepressants, mood stabilizers, atypical antipsychotic drugs, and electroconvulsive therapy, have direct and indirect inhibitory effects on the glutamatergic system.The monoamine-based therapies (i.e. the currently available antidepressants) ultimately inhibit the N-methyl-D-aspartate (NMDA) receptor for glutamate (although it is not classically conceived as their main therapeutic action). 

Maes M, Goossens F, Scharpe S, Calabrese J, Desnyder R, Meltzer HY (1995) Alterations in plasma prolyl endopeptidase activity in depression, mania, and schizophrenia effects of antidepressants, mood stabilizers, and antipsychotic drags. Psychiatry Res... 

Lara DR, Bisol LW, Munari LR. Antidepressant, mood stabilizing and procognitive effects of very low dose sublingual ketamine in refractory unipolar and bipolar depression. Int J Neuropsychopharmacol/Off Sci J CoU Int Neuropsychopharmacol 2013 16 2111-7. 

There is, however, a unique risk in the bipolar form that antidepressant treatment may trigger a switch into mania. This may occur either as the natural outcome of recovery from depression or as a pharmacological effect of the drug. Particular antidepressants (the selective serotonin reuptake inhibitors) seem less liable to induce the switch into mania than other antidepressants or electroconvulsive therapy. Treatment for mania consists initially of antipsychotic medication, for instance the widely used haloperidol, often combined with other less specific sedative medication such as the benzodiazepines (lorazepam intramuscularly or diazepam orally). The manic state will usually begin to subside within hours and this improvement develops further over the next 2 weeks. If the patient remains disturbed with manic symptoms, additional treatment with a mood stabilizer may help. 

The primary treatment for depressive episodes in bipolar disorder is mood-stabilizing agents, often combined with antidepressant drugs. 

Optimize the dose of mood stabilizing medication(s) before adding on lithium, lamotrigine, or antidepressant (e.g., bupropion or an SSRI) if psychotic features are present, add on an antipsychotic ECT used for severe or treatment-resistant depressive episodes or for psychosis or catatonia... 

Guidelines agree that when antidepressants must be used, they should be combined with a mood-stabilizing drug to reduce the risk of mood switch to hypomania or mania.17,41 The question of which antidepressant drugs are less likely to cause a mood switch is not resolved. Anecdotal reports suggested bupropion may be less likely to cause this effect, but systematic reviews have not supported this conclusion. Prevailing evidence recommends that tricyclic antidepressants be avoided.41,43... 

Duration of antidepressant therapy is also an unsettled question. It may be possible in some patients to prevent depressive relapse with a mood-stabilizing drug without maintenance antidepressant therapy following acute treatment with an antidepressant. If so, the risk of a mood switch with continued antidepressant therapy would be reduced. 

Prescribing of psychotropic drugs, such as antipsychotics, antidepressants, anxiolytics and mood stabilizers, is common in psychiatric inpatients for acute and maintenance treatment of psychiatric illness. 

Chen G, H.K., Bebchuk JM et al. Regulation of signal transduction pathways and gene expression by mood stabilizers and antidepressants. Psychosomat Med 1999 61 599-617. 

Lamotrigine is effective for the maintenance treatment of bipolar I disorder in adults. It has both antidepressant and mood-stabilizing effects, and it may have augmenting properties when combined with lithium or valproate. It has low rates of switching patients to mania. Although it is less effective for acute mania compared to lithium and valproate, it may be beneficial for the maintenance therapy of treatment-resistant bipolar I and II disorders, rapidcycling, and mixed states. It is often used for bipolar II patients. 

TDM has improved the performance of anticancer, antidementia, antidepressant, antiepileptic, anticonvulsant, antifungal, antimicrobial, antipsychotic, antiretroviral, anxiolytic, hypnotic, cardiac, addiction treatment, immunosuppressant, and mood stabilizer drags for more than 30 years.2-9 Many analytical procedures evolved as analytical techniques and instrumentation have advanced. This chapter briefly reviews the different types of analytical methods the applications of high-throughput techniques in TDM are discussed in detail. 

One popular miscouception is that modem autidepressauts also induce euphoria. This is not true. Autidepressauts do not lift the mood of nondepressed individuals. Antidepressants simply relieve depression and hopefully return a person to a normal euthymic mood. The lone exception is the bipolar patient who may have a manic episode triggered by taking an antidepressant without a mood stabilizer. Because antidepressants do not produce pleasurable euphoric feelings in nondepressed people, they are not addictive. 

The distinction between major depression and bipolar depression is an important one. Treating a depressed bipolar patient with antidepressant monotherapy (i.e., withont a concomitant mood stabilizer) can propel such a patient into a manic or hypomanic episode. Although it may not be prudent to initiate a mood stabilizer when the evidence for bipolar illness is equivocal, the clinician should be particularly vigilant for the emergence of manic or hypomanic symptoms when starting antidepressant treatment for the first time in a depressed patient. 

In contrast to MDD, the bipolar disorders consist of episodes of depression and episodes of hypomania or mania. This poses a problem for treating the depressed phase of this illness, becanse, as noted earlier, antidepressants can trigger hypomania, mania, or mixed dysphoric mania and can increase the freqnency of manic episodes. Therefore, the hallmark of treating BPAD is the nse of mood stabilizers, with and withont snpplemental antidepressant therapy. Please refer to Table 3.16 for a comparison of the traditional mood stabilizers. 

If we dehne a mood stabilizer as a medication that is both an effective anti-manic and antidepressant, then lithium arguably remains to this day the prototypical mood stabilizer. Lithium not only reduces the symptoms of acute BPAD, it also prevents the recurrence of additional mood episodes. Despite the fact that lithium has revolutionized the treatment of BPAD and remains nearly 50 years after its introduction as the single best treatment for many patients with BPAD, there is still no consensus as to how it works. Lithium exerts effects on several neurotransmitter systems (e.g., serotonin, dopamine, norepinephrine, acetylcholine), on second messenger systems inside the nerve cell, and on nerve cell gene expression. Yet, precisely how these varied effects produce lithium s therapeutic benefit remains unclear. 

Lithium remains the treatment of choice for bipolar patients who experience classic euphoric episodes of mania. Current evidence suggests that those with mixed episodes or rapid cycling episodes respond preferably to anticonvulsants or atypical antipsychotic drugs. In addition to its use as a mood stabilizer, lithium is effective in converting unipolar antidepressant nonresponders to responders. Finally, lithium may also be an effective treatment for patients with clnster headaches. 

It appears that SSRls and bnpropion are less likely than TCAs to indnce mania. Venlafaxine, perhaps becanse of its dnal effects on serotonin and norepinephrine like the TCAs, also appears to increase the likelihood of switching into mania. Rarely, if ever, shonld an antidepressant be nsed in bipolar patients withont concomitant treatment with a mood stabilizer. 

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