Mania drug-induced

The commonest diagnoses associated with sl36 are schizophrenia, mania, drug-induced psychosis and personality disorder (Borschmann et ai, 2010). 

Note. BP = bipolar disorder D/C = discontinue Dep = depression Li = lithium M = mania SA = schizoaffective RBD = recurrent brief depression UP = unipolar. Drug-induced hypomania. 

Antidepressants do not prevent relapses into mania and may even precipitate a manic phase. For these reasons, a mood stabilizer (with or without concomitant antidepressants) is the prophylaxis of choice for bipolar depressions. If there is a reasonable hint of bipolarity (e.g., a family history of bipolar illness, a prior hypomanic episode, or drug-induced hypomania), a mood stabilizer should be considered (see Chapter 10 for more detailed discussion). 

Because there are also some data that concurrent use of antidepressants can lead to rapid cycling in vulnerable patients, these agents may best be cautiously used on an as-needed basis or as adjuncts when there are early signs of breakthrough depressive, psychotic, or anxious symptoms. In particular, antidepressants do not prevent manic episodes, and may even precipitate them. The fact that many patients on antidepressants experience a manic phase, however, could be coincidental, rather than drug-induced. To definitively answer this question, we need to show that the number who switch to mania is higher on, as opposed to off, antidepressant therapy. Given these concerns, however, we advocate the initial use of a mood stabilizer alone to lessen the chance of a switch to mania in bipolar depressed patients. If this is insufficient, a mood stabilizer should be used concurrently with an antidepressant. 

Psychiatric uses of benzodiazepines other than treatment of anxiety states include the initial management of mania and the control of drug-induced hyperexcitability states (eg, phencyclidineintoxication). Sedative-hypnotics are also used occasionally as diagnostic aids in neurology and psychiatry. 

Those disorders that require the presence of psychosis (Table 10—1) as a defining feature of the diagnosis include schizophrenia, substance-induced (i.e., drug-induced) psychotic disorder, schizophreniform disorder, schizoaffective disorder, delusional disorder, brief psychotic disorder, shared psychotic disorder, and psychotic disorder due to a general medical condition. Disorders that may or may not have psychotic symptoms (Table 10—2) as an associated feature include mania and depression as well as several cognitive disorders such as Alzheimer s dementia. 

Euphoria is unusual in patients treated with the neuroleptics because of the suppressive effects on the central nervous system (see chapter 2). It is more common among patients treated with antidepressants, stimulants, and benzodiazepine tranquilizers, especially alprazolam. Drug-induced mania is an extreme of medication spellbinding. 

Activation should be at the top of the differential diagnosis list when a patient s condition deteriorates while taking antidepressants. If the physician misidentifies drug-induced activation as caused by the patient s original psychiatric disorder, the doctor is likely to continue, or even increase, the antidepressant dose, ultimately causing mania and psychosis. 

The initial euphoria associated with mild cases of drug-induced mania often offer relief and hope, however unrealistic, to the patients who experience it. If the euphoria does not progress to full-blown mania, it is likely to wear off, and then apathy becomes more dominant over time. This often leads patients to ask for one antidepressant after another in the hope of recapturing that brief high. ... 

I want to reemphasize that drug-induced disturbances in mood or in behavior should be viewed as genuine neurological disorders rather than as vague mental illnesses. The capacity of speculative biochemical imbalances or genetic factors to cause or contribute to mania or depression remains unproven. Nor do we know the specific biochemical or neurological mechanisms whereby psychoactive substances cause mental disturbances. But the capacity for psychoactive substances to disrupt brain function and hence mental function is beyond dispute. Furthermore, a great deal of empirical data confirm their capacity to cause disinhibition, mania, depression, and other mental phenomena associated with violence toward oneself and others, as well as other destructive behaviors. 

The most important finding of this review is that signs and symptoms of psychosis or mania, particularly hallucinations, can occur in some patients with no identifiable risk factors, at usual doses of any of the drugs currently used to treat ADHD. Current labeling for drug treatments of ADHD does not clearly address the risk of drug-induced signs or symptoms of psychosis or mania (such as hallucinations)... A substantial proportion of psychosis related cases were reported to occur in children age ten years or less, a population in which hallucinations are not common, (pp. 3—4)... 

Clonazepam is a benzodiazepine that is used predominantly in epilepsy, panic disorder, and mania, and also appears to be effective in relieving antipsychotic drug-induced akathisia (1). The use of clonazepam in psychiatric disorders is complicated by significant drowsiness in a majority of patients, and additional behavioral problems in children (SEDA-19, 34). 

To a lesser extent, antipsychotics also have been used in the treatment of mania, agitated depression, toxic (such as drug-induced) psychoses, emotionally unstable personalities, and psychoses associated with old age. Antipsychotic medications arc also known as neuroleptics or major tranquilizers (the latter term is used much less frequently now). The term neuroleptic is derived from the Greek word that means to clamp the neuron (Snyder 8c Largent, 1989). Antipsychotics the term more commonly used in the United States, with neuroleptics used more often in Europe. The terms are used interchangeably in this discussion. Representative antipsychotic medications are li.sted in Table 13.1. 

Schizophrenia involves the exhibiting of psychotic symptoms. For many social workers trying to help, these clients can be difflcult because the mental health conditions in this category usually include symptoms of delusions, hallucinations, uncooperativeness, and thought disorders (Kaplan Sadock, 1990). The specific conditions that are treated with antipsychotic medications usually include schizophrenia, delusional disorders, depressive psychoses, mania, and drug-induced psychoses (Kaplan Sadock, 1990). See Table 7.1 for a list and brief description of the schizophrenic or primary psychotic disorders. 

While mania and depression are related to the metabolism of the cerebral monoamines and to changes in water balance and sodium ion concentration, no specific biochemical correlation has yet been demonstrated for the schizophrenic s visions and voices. The report suggests that the only rational approach for the biochemist in the study of schizophrenia is drug induced psychosis. Large single doses of LSD have been shown to effect metabolic changes (increase in serotonin and decrease in norepinephrine). 

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. 

Patients whose depression has apparently been resistant to standard antidepressant treatment often have had inadequate trials of antidepressants or have been nonadherent with drug therapy. Depression in a patient who has failed to complete an adequate trial of an antidepressant drug does not constitute treatment-resistant depression. A patient who reports a history of robust but short-lived responses to several antidepressants may be manifesting a medication-induced rapid-cycling course. Mild episodes of hypomania during the course of treatment may be overlooked, especially in a productive patient with a high level of functioning and a premorbid history of hyperthymic personality, defined as a chronic state of mild hypo-mania. In these cases, treatment with a mood stabilizer is indicated (see Chapter 5). 

Oxcarbazepine is a keto derivative of carbamazepine but offers several advantages over carbamazepine. Oxcarbazepine does not require blood cell count, hepatic, or serum drug level monitoring. It causes less cytochrome P450 enzyme induction than does carbamazepine (but may decrease effectiveness of oral contraceptives containing ethinyl estradiol and levonorgestrel). As opposed to carbamazepine, oxcarbazepine does not induce its own metabolism. These properties, combined with its similarity to carbamazepine, led many clinicians to use this medication for the treatment of bipolar disorder. Randomized controlled trials suggested efficacy in the treatment of acute mania compared with lithium and haloperidol, but these trials were quite small and did not include a placebo control (Emrich 1990). 

An episode of mania/depression is drug- or alcohol-induced. 

The depressive phase of manic-depressive disorder often requires concurrent use of an antidepressant drug (see Chapter 30). Tricyclic antidepressant agents have been linked to precipitation of mania, with more rapid cycling of mood swings, although most patients do not show this effect. Selective serotonin reuptake inhibitors are less likely to induce mania but may have limited efficacy. Bupropion has shown some promise but—like tricyclic antidepressants—may induce mania at higher doses. As shown in recent controlled trials, the anticonvulsant lamotrigine is effective for many patients with bipolar depression. For some patients, however, one of the older monoamine oxidase inhibitors may be the antidepressant of choice. Quetiapine and the combination of olanzapine and fluoxetine has been approved for use in bipolar depression. 

The authors commented that the manic symptoms had probably been caused by glucocorticoids or glucocorticoid withdrawal. They concluded that patients with cluster headache and a history of affective disorder should not be treated with glucocorticoids, but with valproate or lithium, which are effective in both conditions. Lamotrigine, an anticonvulsive drug with mood-stabilizing effects, may prevent glucocorticoid-induced mania in patients for whom valproate or lithium are not possible (101). 

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