Management of acute bipolar disorder

In 1854, Jean Pierre Falret and Jules Baillarger independently described a bipolar disorder in which affected individuals cycled between periods of elation or mania and depression. This was variously called folie circulaire or folie de deux périodes. It forms the basis for what later became manic-depressive disorder and is now often called bipolar disorder. 1 and 2 In 1896, Emil Kraepelin divided the major psychiatric illnesses into manic-depressive illness and schizophrenia. The former was primarily a disorder of mood, the latter a disturbance of cognitive functions. The former usually followed an episodic course with individuals recovering to normal between episodes. The latter was more likely to become a chronic illness, with a majority of affected individuals never fully recovering. These distinctions held through to the mid-1990s when a number of pharmaceutical companies began to promote mood-stabilisers for bipolar disorder. ¹

Within the manic-depressive group, Kraepelin included all mood disorders, whether or not the person oscillated between manic and depressive poles. For this reason, until recently many individuals who only had recurrent depressive moods were diagnosed as having manic-depressive illness. But since the 1980s there has been an increasing tendency to distinguish between bipolar and unipolar mood disorders. In bipolar mood disorders, individuals present with episodes of both mania and depression, in contrast to unipolar disorders in which there appear to be only depressive episodes. Unipolar mania is rare.

At present there is little to distinguish bipolar disorders from unipolar disorders other than episodes of mania. When they are depressed, both groups look indistinguishable, both arguably respond to the same treatments – although this is a matter of dispute – and there are at present no biological markers that reliably pick out the one group from the other. In part the problem may be that, in practice, one never knows whether one is dealing with a true unipolar disorder or a bipolar disorder that has hitherto presented only with depressive episodes.

There are claims that between one-third and one-half of depressions are associated with an episode of mania at some point during a subject’s lifetime. The difficulties in being precise lie in the fact that many episodes of ‘biological’ depression may be so mild as to go largely unnoticed. In addition depending on the patient for an accurate history of either manic or depressive episodes has problems and the patient’s partner, parents or children may have a more accurate view of how serious or sustained periods of overactivity and disinhibition were, or of depression. Some episodes of hypomania can be diagnosed retrospectively based on a clear history of a sustained period of several weeks during which the subject was elated, overactive and perhaps somewhat disinhibited, but during which the individual’s behaviour led neither to a diagnosis nor to hospitalisation.

Distinctions are now also drawn between bipolar 1 disorders, where an individual has been hospitalised or severely incapacitated by a manic episode at some point, and bipolar 2 disorders, where there is a history suggestive of a period of elation but the person may not have been admitted to hospital for either a depression or mania. There is increasing talk of bipolar 3, 4, 5 and 6, as well as bipolar spectrum disorders, with some data suggesting that up to 5% of the population may have a bipolar disorder. Whether the patient has a traditional diagnosis of manic-depressive illness or one of the newer fashionable bipolar illnesses, treatment is increasingly likely to be with so-called mood-stabilisers rather than antidepressants.

This chapter deals with drugs used to treat mania, now typically called mood-stabilisers; the issue of the possible prophylactic effects of these drugs is picked up in Chapter 7.

While the majority of people affected with mania present with an elated and euphoric mood, or with disinhibited behaviour, not all do. Others may be irritable rather than elated and euphoric, and paranoid rather than grandiose. Common to both groups is an increased level of activity, so that hyperactivity is perhaps the most consistent diagnostic feature of mania. In addition, there is typically an increase in appetites and a decrease in time spent asleep.

In the case of a single manic episode, the Diagnostic and Statistical Manual (DSM) requires a diagnosis of bipolar disorder. However, other systems such as the International Classification of Diseases (ICD) do not and in fact a number of free-standing manic episodes show a great deal of overlap with the acute and transient psychoses (Ch. 2). They do not recur. Furthermore, some patients may show recurrent manic episodes with many years between episodes, without any indication they have a recurrent bipolar disorder. Finally it is far from clear that patients who are ordinarily depressive but have a ‘manic’ reaction to an antidepressant should be regarded as bipolar.

For these reasons the treatment of mania and the possibility of mood stabilisation should be separated but they rarely are. In the case of an episode of possible mania, there is a default toward putting patients on mood-stabilisers to ward off future episodes of what is presumed to be a bipolar disorder that will entail future depressions and manias. As we shall see, however, the supposedly prophylactic treatments probably all bring about withdrawal syndromes, and this clouds the interpretation of what they actually do. Given these factors, while the treatment of mania very commonly slides into prophylaxis, the attempt to ward off future episodes may do more harm than good.

LITHIUM

Lithium is used both as a specific treatment for mania and as a mood-stabiliser in the prophylaxis (prevention) of further episodes of either mania or depression. The issues of lithium’s dosage and side effects are covered in Chapter 7. In terms of managing acute episodes, many claim that lithium is the most specific treatment for mania, bringing about a cleaner resolution of manic episodes than treatment with antipsychotic drugs. According to this view, patients will sometimes need to be controlled with antipsychotics for the first days in hospital but, if they are prescribed lithium also, the mania will resolve much more specifically and cleanly than it would on antipsychotics alone – usually somewhere around day 10 after therapeutic blood levels have been reached. ³

There have been great disputes about whether lithium is prophylactic or not but what is not in dispute is that it can produce responses in mania. This is sometimes lost sight of and patients are treated with antipsychotics instead. The reasons for this probably lie in the fact that using lithium involves a physical screen of the patient beforehand, which takes some days. In addition, the effects of lithium are slower in onset than those of antipsychotics and the use of lithium is usually seen as involving a commitment to ongoing therapy, which the patient may not be able to make in the acute stage of a manic illness.

Whether lithium is more specific to mania than other drugs remains uncertain. In addition, it is worth considering exactly what lithium does that is beneficial in mania. It is clear that the sedative and anti-impulsive effects of anticonvulsants and antipsychotics (see below) might be useful. Lithium is much less sedative than these other drugs, making the responses to it look at times as though they are in some way a more specific treatment for mania than the responses obtained from non-specific sedation. However, it has anti-impulsive or anti-irritability effects that have been relatively poorly characterised to date.

This returns us to the theme of this book – what we might find out if we asked people taking the different drugs what their drug was doing for them that they found useful. At present, the idea that drugs are mood-stabilisers acts as barrier to questions and to thought. Such drugs are supposedly correcting some physiological tendency to mania and to mood instability and asking whether they also do something useful is close to irrelevant. When a first mood-stabiliser fails to work, the response then is to add further mood-stabilisers so that the treatment of mania and the prophylaxis of bipolar disorder can end up with the patient on five or six drugs, with all the attendant risks of indiscriminate combination therapy.

ANTIPSYCHOTICS FOR MANIA

In practice, antipsychotics are often the first line of treatment for mania. In part this stems from the often pressing need to contain the behaviour of individuals with mania, and antipsychotics in moderate to large doses do this relatively quickly. Some of the largest clinical doses of antipsychotics are used for just this purpose.

However, while obviously useful to gain control of the clinical picture, antipsychotics are often the only treatment given for an episode of mania – commonly neither lithium nor an anticonvulsant will be needed. Recovery on treatment with antipsychotics only has therefore led to suggestions that these antipsychotics are specific treatments for mania. And, because antipsychotics are helpful in manic states, it is also argued that mania must involve a disturbance of dopamine neurotransmission. But this argument is clearly a circular one.