Antipsychotics SSRIs

Low doses of antipsychotics SSRI antidepressants Antidepressants Antidepressants... 

SGA second-generation antipsychotic SSRI selective serotonin reuptake inhibitor... 

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... 

Consider augmentation ) (non-SSRI antidepressant, lithium, thyroid homione, atypical antipsychotic)/ ... 

Infrequently, SSRIs produce dystonic reactions, which are intense mnscle spasms nsnally of the face and neck. They may cause akathisia, a restless inability to sit still. Dystonic reactions and akathisia are more commonly side effects of the dopamine-blocking antipsychotics. It is believed that SSRIs prodnce these effects because increasing 5HT activity tends to decrease dopamine. When these side effects occur, the SSRI should be switched to another antidepressant. 

Atypicai Antipsychotics. In the 1980s and early 1990s, the SSRIs began a revolution in the treatment of depression. Tried-and-true but side effect laden tricyclic antidepressants fell into disfavor as newer and safer medications became available. A similar revolution is taking place in the treatment of psychosis. A new generation of antipsychotics that have fewer of the more disturbing side effects and may well be more effective are now available. 

The key has been to avoid using treatments that worsen the disease. In this instance, this means avoiding anticholinergic (acetylcholine-blocking) medications that worsen dementia. As a result, when newer antidepressants such as the SSRIs became available, they quickly replaced the older tricyclic antidepressants because the latter are potent anticholinergics. For the same reason, the low potency anti-psychotics like chlorpromazine (Thorazine) were replaced by the higher potency antipsychotics like haloperidol (Flaldol) and more recently by the atypical antipsychotics. 

Among these choices, bnspirone is preferred if the patient is also experiencing anxiety. If the patient is depressed and agitated, a SSRI should be tried first. Second line choices inclnde carbamazepine (Tegretol) or one of the atypical antipsychot-ics—ziprasidone (Geodon), risperidone (Risperdal), olanzapine (Zyprexa), quetiap-ine (Seroquel), or aripiprazole (Abilify) can be tried. If psychotic symptoms are present, one of the atypical antipsychotics should be tried first. 

Chronic Agitation. For chronic agitation with physical aggression, sodium divalproex is the preferred treatment. If divalproex is ineffective, haloperidol or an atypical antipsychotic can be added or snbstituted. Other options include trazodone, carbamazepine, and SSRI antidepressants. 

Antidepressants. In our experience, clinicians who are trying to manage the behavior of impulsive or aggressive patients too often overlook antidepressants. Antidepressants are often just as effective as anticonvulsants, antipsychotics, or benzodiazepines, especially when managing mild-to-moderate behavioral disturbances. Furthermore, antidepressants are generally easier to use and easier to tolerate than these alternatives. Once again, the SSRIs are best studied and so represent the favored first-line treatment for managing mild-to-moderate behavioral lability... 

As anxiolytics, benzodiazepines have faster onset of effect than SSRIs or antipsychotics. Their use is best limited to short-term situations, although there are likely to be comparable risks of dependence in these populations from all major classes of drugs. 

Extrapyramidal side effects (EPS) associated with SSRI medications used as single agents were reported as early as 1979 (Meltzer et ah, 1979). Since then, several case reports have been published on use of fluoxetine (Elamilton and Opler, 1992), paroxetine (Nicholson, 1992), and sertraline (Opler 1994). The SSRI medications in combination with neuroleptics can cause severe EPS (Tate, 1989 Ketai, 1993) above and beyond what may be associated with increased levels of antipsychotic medications (Goff et ah, 1991), and are perhaps related to pharmacokinetic drug interactions. 

There are several antipsychotics that are substrates to CYP2D6 (von Bahr et ah, 1991 Jerling et ah, 1996 Ring et ah, 1996 (Fang and Gorrod, 1999 Flockhart and Oesterheld, 2000) (Table 26.3). Moreover, several antipsychotics may act as inhibitors of CYP2D6-mediated biotransformation. These include thioridazine, chlorpromazine, haloperidol, fluphenazine, and pimozide (Desta et ah, 1998 Shin et ah, 1999). Of particular salience is the fact that the serotonin selective reuptake inhibitors (SSRIs) fluoxetine and paroxetine are metabolized to a significant extent by this isoenzyme. 

PMD responds less well to a TCA alone than does NPMD. It is unknown, but unlikely, whether other antidepressants alone would fare any better. The combination of an antidepressant and an antipsychotic appears effective in most cases of PMD. Preliminary data suggest no differences in the combination of an SSRI and an antipsychotic versus a TCA and an antipsychotic. However, the vast majority of studies have employed TCA and antipsychotic combinations. 

Some patients will decline ECT, and the available data suggest that combination antidepressant/antipsychotic treatment or amoxapine may be equally effective. Given the preponderance of data supporting TCA/antipsychotic combinations in the treatment of PMD, it may be reasonable to consider TCA combinations before other antidepressant combinations. Currently, the literature shows debates as to whether the SSRIs are as efficacious as the... 

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