Standing on the edge
Kicking me off my bed
Dragging to the grave
Loud voices in my head
Sinking my judgement
I can see through
Heart drowning
Impossible to breathe
Too proud to give up
Too weak to carry on
Keep on fighting
It’s a never ending war
JmaC
It’s not everyday that we catch a glimpse of the sun waking up
Or going to bed.
There is beauty all around us
That we don’t often see
We just focus on misery.
JmaC
An insane person invented time
It’s the only way to either
Measure out pain
Or endure it
JmaC
Anxiety can be a symptom of bipolar disorder. This was recognized by the fellow who originally described bipolar disorder as such, Dr. Emil Kraepelin, back in 1921. He described “anxious mania”, and also “excited depression”, which included a “great restlessness”. He specifically named anxiety as one of the components of this illness. All that requires saying, because “anxiety” is not generally regarded as a bipolar symptom. Yet it clearly is, as summarized in an excellent review by Freeman, Freeman and McElroy.Freeman
The International Society for Bipolar Disorders (ISBD) further strengthened the view that anxiety can be part of bipolar disorder in a Task Force report detailed below. That ought to be enough to put any remaining controversy about this to rest.
The International Society for Bipolar Disorders assembled committees of bipolar specialists to prepare reports on several aspects of bipolar diagnosis.
One particular report deserves attention here: first, because the authors are very well-regarded bipolar experts. Second, because it was published in a top psychiatric journal. And most importantly, because their statements are firm and clear.ISBD
Their paper was on “mixed states” in bipolar disorder, which is the primary setting in which anxiety makes sense as a bipolar symptom. For basics on “mixed states”, see that section of the Diagnosis page. Reviewing briefly:
can be part of bipolar disorder. In fact, the ISBD report states that anxiety is “a core symptom of mixed states”. Here the ISBD is not alone.Kauer-Sant’anna
That ought to be enough to put to rest any controversy about this. Unfortunately, however, several of the “anxiety disorders” in the diagnostic manual (the DSM) can look like “mixed states”. So confusion is the norm. One ought to be confused. As you’ll see below, it’s almost impossible to separate some of these diagnoses.
There are basically two ways you can have anxiety with bipolar disorder. First, it can be a symptom of the bipolar disorder itself. Secondly, you can have a separate anxiety condition in addition to bipolar disorder. In medical lingo, that is called a “co-morbid” condition (in case you run across that term). It means both conditions are present, and thus implies that anxiety is a separate condition, not coming from the bipolar disorder itself.
These two ways of looking at anxiety have important implications. If the symptoms are coming from bipolar disorder itself, then they should get better when the bipolar disorder gets better. But if they are coming from a separate condition, they could persist even when the bipolar disorder improves.
If your anxiety is really a separate condition, it’s going to require a separate treatment. And that really complicates things, because very often the recommended treatment for the anxiety condition could be an antidepressant medication — and antidepressant medications can make bipolar disorder worse! (see the section on treatment for details on that problem; or the controversy over use of antidepressants in bipolar disorder).
What is the anxiety of bipolar disorder like? Patients describe it as “agitation”, and sometimes that is quite obvious: their foot bounces on the floor while we talk; they pick at their nails; sometimes they can’t even bear to sit still and will get up and pace around the office during our interview. But sometimes the agitation is only “inside”: patients experience “too much energy inside my skin”, like they’re going to “explode”, and usually their thoughts are going very fast (sometimes called “racing thoughts”). However, when this is severe, people may not experience that fast thinking, but instead just an extremely disorganized thinking — not being able to keep their mind on one thing for more than a few seconds, not being able to accomplish anything. Of course that can make “anxiety” worse as people recognize that they are really ill with something that is not obvious to anyone else, yet they are not really functioning either. How do you explain that to someone?
When this kind of anxiety is present with other manic symptoms like irritability, it can create an awful experience people feel desperate to get out of. (Very often they discover that alcohol can help settle this down for an hour or two. Unfortunately when it wears off, the symptoms come back, very often worse than before. If a person responds to that by drinking more, that can cause a worsening of the condition over several days or weeks — but because they get brief relief from drinking, they keep doing it and often have to drink more over time to keep their symptoms controlled. This is a dangerous spiral which is statistically associated with successful suicide attempts, so represents a clear reason to get help as soon as possible.) Fortunately there are very good medication approaches to this which can help within an hour.Olanzapine/Zyprexa has a special role here, in my view.
When this kind of anxiety is present with depression, this may be the worst combination of all. Anxiety is a very strong risk factor for suicide when people are depressed. The future looks hopeless and pointless because of the depression; and the present feels unbearable. Again, it’s important to know that this combination is very treatable. If you find yourself feeling and thinking like this, and you don’t have a doctor or therapist to help you manage it in the short and long term, you should take specific steps to keep yourself safe, including going to an emergency room if necessary.
Now we’ll have to be more specific about “what kind of anxiety are we talking about?”. There are several specific forms of anxiety which appear to be clearly separate from bipolar disorder (e.g. there are people with these conditions who clearly do not have any bipolar symptoms). Here’s a list, and then we’ll look at specific symptoms that identify each one. After that we’ll look at the treatment implications of having one of these. Jump to each by the link below.
Most of these have been shown to occur more often than you would expect in people with bipolar disorder (more often than the percentage found when thousands of people identified at random from the phone book were interviewed). We’ll look at each one or you can use the link above to jump to the one you’re interested in.
There is a lot of overlap in the diagnostic criteria for GAD and bipolar II. We need to look at this in some detail because they may be actually the same thing, at least in some people (as opposed to the rest of the list below, which are somewhat more “separate”). If you’ve read about GAD and think you have it; or if you’re curious about anxiety and bipolar disorder generally (pardon the pun); please read this essay on GAD and BPII.
This condition is well described, including its treatment with a psychotherapy approach (in addition to or instead of antidepressants), on the useful HelpGuide.org site. Go there to learn much more about social phobia.
For our purposes here, you should also know that social phobia is common in people with bipolar disorder. Starting with “how many people with bipolar disorder have social phobia?”, findings range from 15% to almost 50% in one study. Looking at it the other way, “how many people with social phobia have bipolar disorder?”, one recent study found 21%. These numbers come from the review on anxiety and bipolar disorder by Freeman and colleagues.Freeman
However, some of my patients with bipolar disorder have clearly had “cycling” in their social phobia symptoms, that goes right along with their bipolar cycling. They get much more socially anxious at some times than others. Or rather, on some occasions, which can be rare but seem always to coincide with their hypomanic phases, their social phobia virtually disappears. They can talk freely, even in a group, even with strangers. They can walk up and introduce themselves to people they have never met. They can speak up in front of others, which they normally would strictly avoid. Then, when their mood and energy cycle back down again, their social anxiety returns. They avoid social circumstances, and all the anxiety they usually get if in the center of attention, even dealing with the check-out guy in a grocery store line, comes back.
This “cycling” of social phobia symptoms along with bipolar symptoms suggests that these conditions are not just co-occurring, but are connected somehow. However, unlike the anxiety of GAD which seems to go away when bipolar cycling is controlled, some degree of social phobia symptoms seems to hang around when bipolar disorder is controlled. This is extremely frustrating for a person who knows that once in a while they don’t have to be like this.
However, the usually offered treatment for social phobia — e.g. antidepressants like paroxetine/Paxil — can make bipolar disorder worse. But fortunately, there is an excellent treatment for social phobia that does not rely on medications at all. This therapy is described well on the HelpGuide site, here. Usually this treatment is best done with the help of a therapist who knows “cognitive behavioral therapy”. If you can’t get such a therapist, some people have had some success on their own using a basic online anxiety treatment program (free). It works great, but very few people can do this on their own and get through it: “e-couch” from Australia.
In my experience when people have their bipolar cycling controlled, they stop having panic attacks in almost all cases (there are surely some exceptions). So rather than focus on the panic symptoms, I almost always go after the bipolar symptoms first.
Note that if for some reason panic symptoms persisted after bipolar symptoms were treated, there is a non-medication approach that works better in most people than pills.
This condition too is described well by a HelpGuide page. About 40% of people with bipolar disorder also have PTSD.Freeman The converse appears to be relevant as well: growing up in an environment of trauma appears to raise the risk of getting bipolar disorder, if one is genetically susceptible.Post
I see these two conditions together all the time. Sometimes it’s very difficult to tell them apart from one another. This has implications for treatment, as discussed below.
For more information on OCD, there is a comprehensive website by the OCD Foundation. Their page on “What is OCD?” is a good starting place.
OCD has a complex relationship with bipolar disorder. I’ve seen some patients start out looking like they have classic OCD and end up looking like they have definite bipolar disorder without OCD. These two conditions might be part of the same thing somehow, at least in some people. At least we know they are found together very often, much more so that one would expect. In one study, 20% of people with bipolar disorder had OCD, twice the number seen in unipolar depression (which is also higher than people with no diagnosis).Chen
A group of researchers has looked at how OCD and bipolar relate. They found that whereas unipolar depression was “incidental”, i.e. not clearly related to the OCD (although common), by contrast bipolar disorder seemed to be more directly related to the OCD. For example, people with religious and sexual obsessions as part of their OCD were more likely than those with other obsessions to have bipolar disorder. The authors specifically recommend that bipolar disorder take precedence over the OCD in terms of which is treated first.Perugi
These include snake, spider and height phobias, which are common. They are also extremely treatable using the “behavioral” approaches (i.e. not medications) described for some of the anxiety disorders above (success rates exceed 80%). There is no specific association with bipolar disorder, to my knowledge.
Antidepressants can make bipolar disorder worse. Eventhough antidepressants are a standard treatment for anxiety problems (e.g. OCD,PTSD; and to a lesser extent Social Phobia, Panic Disorder and GAD), mostexperts agree: treat the bipolar disorder first, then if anxiety symptoms remain, treat them.
I would go a bit further. If symptoms remain, “treat them” with a psychotherapy if at all possible rather than an antidepressant. There are excellent therapies with results equal to or better than medications for panic and social phobia. There are therapies which get good results, though often only with medications, for PTSD and OCD. If after the therapy has been tried, an antidepressant still must be considered, it should be added to mood stabilizers already underway (per theexpert recommendation cited above).
In my opinion, when a diagnosis of GAD is made, the patient should be informed about the extent of overlap with bipolar disorder and an effort made to determine if the patient might have bipolar disorder. (At minimum, use the screening questionnaire called the MoodCheck ). If after that the patient prefers to start with an antidepressant (versus psychotherapy, if available; or a mood stabilizer trial), don’t forget to look for hypomania or cycling of mood and energy in the first few months.
If you have anxiety symptoms, or if you have an anxiety condition in addition to your bipolar symptoms, make sure your doctor and/or therapist know about these because even with bipolar disorder they are treatable. The trick is to make sure the treatment for the one doesn’t make the other worse. That can be done.
An international group of expertsISBD described anxiety in bipolar disorder thus:
These symptoms are not generally regarded as symptoms of bipolar disorder. Unfortunately, the very name “bi-polar” is misleading. As noted above by Dr. Jamison, mania can be negative as often as it is positive. The “racing thoughts” can have a very negative focus, especially self-criticism. The high energy can be experienced as a severe agitation, to the point where people feel they must pace the floor for hours at a time. Sleep problems can show up as insomnia: aninabilityto sleep, a desperate wish to be able to sleep to get out of the agitated state.
One way to understand these symptoms is called “mixed states”. Bipolar disorder is an unfortunate name, as it implies a North/South Pole experience. A better picture looks like this graph:
Both manic symptoms and depressive symptoms at the same time? Sure enough. Not intuitive, if you think North/South pole. But these symptoms can vary independently or occur together (For more on that, see mixed states as waves of depression, anxiety, and normal time.)
This is not controversial. Mixed states were officially recognized in the 1994 version of the DSM, and expanded to look more like the graph above in the 2013 version.
What’s the difference between “anxious depression” and a bipolar mixed state? Not enough to easily be able to tell them apart, unfortunately. The same group of experts quoted above also said: “some but not all agitated depressed states are bipolar.”ISBD
Worst of all, mixed states can be caused by antidepressants.ISBD Yet antidepressants are what depressed patients commonly receive, of course.right? But some of those depressed folks have bipolar depression. The antidepressants can take them from pure depression to agitated depression. The good news is that slowly coming off the antidepressant is one way to address anxiety.Phelps Don’t do that on your own, of course. Here are some guidelines on stopping antidepressants in bipolar disorder.
Recent work suggests that a broad clinical spectrum of bipolar disorder is more common than previously thought and that the disorder may affect up to 5% of the population. The correct definition and diagnosis of hypomania is central to the identification of bipolar disorder. In this review we focus on recent diagnostic and clinical advances relating to bipolar disorder, with particular reference to hypomanic states. We also highlight some of the controversies in this field and discuss ways in which clinicians might improve their detection of bipolar disorders.
‘When you’re high it’s tremendous. The ideas and feelings are fast and frequent … Shyness goes, the right words and gestures are suddenly there, the power to captivate others a felt certainty … Sensuality is pervasive and the desire to seduce and be seduced irresistible’ (Jamison, 1995: p. 67).
‘In hypomania, there is an increased pressure of speech with prolixity, an abnormal liveliness of expressive movements, superficial bustling activity and a tendency to be argumentative and irritable if thwarted in any way. The patient is interested in everything, starts many projects, and finishes none … the elated mood leads to faulty judgement and a lack of consideration for others … hypersexuality may lead to venereal disease in men and pregnancy in women … the mental illness may be obvious only to the relatives and doctors, and other outside observers may merely regard the patient as a cheerful chap or somewhat of a “card” ’ (Fish, quoted by Hamilton, 1974: p. 73).
Although Kay Jamison’s evocative description of the early stages of mania contrasts with the phenomenological account provided by Frank Fish (writing in the 1960s), these two quotations illustrate a fundamental point about the presentation and diagnosis of hypomanic states. People with mild manic symptoms rarely complain about feeling unwell (indeed, many enjoy their ‘supernormal’ levels of functioning), whereas family members and psychiatrists will usually be quick to recognise the behavioural manifestations of the illness. In this review, we focus on some of the recent advances in our understanding of the presentation and detection of hypomania.
The study of less severe forms of bipolar disorder has been neglected for many years, but developments in clinical phenomenology, nosology and epidemiology have given rise to renewed interest in the correct definition and diagnosis of hypomania.
Many of the diagnoses used in psychiatry, including those described in ICD–10 (World Health Organization, 1992) and DSM–IV (American Psychiatric Association, 1994), are categorical in nature and based on a checklist approach that specifies an arbitrary number of symptoms as a threshold for diagnosis. Although these classifications have been of considerable value, they fail to reflect the clinical reality that psychiatric presentations are often dimensional rather than all-or-nothing phenomena.
For mood disorders, one of the consequences of this has been the proliferation of a large collection of diagnoses, ranging from major (unipolar) depression through to severe psychotic disorders such as schizoaffective disorder. Not surprisingly, the dividing line between what might be considered normal temperament and full-blown mood disorder can often appear blurred. A good illustration of this is the retention of sub-threshold disorders such as dysthymia and cyclothymia in ICD–10 and DSM–IV. For bipolar disorder, the accurate detection of hypomania is of pivotal diagnostic importance and has considerable implications for treatment.
Although ICD–10 and DSM–IV are generally in agreement over what constitutes a core manic symptom, there are important differences in the guidance that they provide for the diagnosis of hypomania. In ICD–10, hypomania is considered to be a lesser degree of mania lasting ‘several days’ and causing ‘considerable interference with work or social activity’. In contrast, DSM–IV stipulates that hypomania occurs ‘without [my italics] marked social or occupational dysfunction’ (leading to a diagnosis of bipolar II disorder). Full-blown mania in DSM–IV refers to any persistent elevation of mood lasting more than 1 week that causes functional impairment (and leads to a diagnosis of bipolar I disorder).
Thus, many patients with ICD–10-defined hypomania may actually satisfy DSM–IV criteria for mania. This confusion is compounded in the UK by an apparent overuse of the term ‘hypomania’. It is not uncommon for a patient who has been hospitalised for weeks with severe mania to be given a discharge diagnosis of hypomania (Goodwin, 2002).
Some of the core manic symptoms of hypomania may be more common than others. For example, ‘increased activity’ and ‘increased energy’ are almost universal, whereas ‘increased talkativeness’ does not feature in over a quarter of hypomanic presentations (Fig. 1⇓) (Wicki & Ansgt, 1991).
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Frequency of core manic symptoms in hypomania (data from Wicki & Angst, 1991).
Prevalence rates for bipolar disorders depend on the diagnostic criteria applied to people with recurrent major depression, and central to this issue is the correct definition of the boundaries of hypomania. The minimum duration required for a diagnosis of hypomania in the DSM has changed significantly over the years. In the Research Diagnostic Criteria it was 2 days (Spitzer et al, 1978), in DSM–III (1980) and DSM–III–R (1987) it was not specified, and in DSM–IV it has been set arbitrarily at 4 days. Within the past few years, a group of experts on bipolar disorder have recommended reverting to the threshold of 2 days, for two reasons. First, most people with bipolar disorder report a median duration of hypomanic symptoms of 1–3 days (rather than 4 or more) (Benazzi & Akiskal, 2003). Second, several longitudinal studies have reported that people who experience brief hypomanic periods do not differ from those with longer periods in terms of features age at illness onset, family history of mania and lifetime illness chronicity (Akiskal et al, 2000; Angst et al, 2003; Benazzi & Akiskal, 2003; Judd et al, 2003).
The traditional view of hypomania as a predominantly euphoric mental state is challenged by recent studies. Many people with bipolar disorder experience ‘dysphoric’ or ‘mixed’ hypomanic periods that can be diagnostically challenging (Akiskal et al, 2003a). Some studies have estimated that at least half of all mood episodes in bipolar disorder are mixed presentations (Cassidy & Carroll, 2001).
In a recent 7-year naturalistic study of 908 people with bipolar disorder within the Stanley Bipolar Treatment Network, Suppes et al(2005) found that out of 1044 visits in which the patients met DSM–IV criteria for hypomania, in 57% of cases they also met criteria for ‘mixed hypomania’ (defined as a Young Mania Rating Scale score ≥12 and an Inventory of Depressive Symptomatology score ≥15). Mixed hypomania was much more likely in women than in men, supporting previous findigns of an overrepresentation of mixed states in female patients with bipolar disorder (Arnold et al, 2000; Benazzi, 2003).
The diagnosis of hypomania can also be more difficult because hypomanic symptoms can feature prominently in a number of other conditions. A commonly encountered difficulty is the differentiation of hypomania from periods of elevated mood, overactivity and grandiosity that can occur in individuals with extrovert or cyclothymic personalities. Similarly, people with DSM–IV cluster B personality disorders (particularly borderline personality disorder) who do not have a mood disorder can present with high levels of affective arousal that can mimic hypomania. Diagnosis in these patients is often made even more difficult by their concurrent use of drugs such as cannabis, amphetamine and cocaine.
Leaving aside concerns about the clinical validity of a diagnosis of adult attention-deficit hyperactivity disorder (ADHD) (Asherson, 2004; Zwi & York, 2004), some individuals presenting with hyperactivity, disinhibition and inattention may be misdiagnosed as being hypomanic. However, the differentiation of ADHD from hypomania should usually be straightforward if based on a systematic assessment for other hypomanic features such as elevated or irritable mood, inflated self-esteem and decreased need for sleep.
As with all psychiatric diagnoses, care should be taken to eliminate a clear organic cause for hypomanic symptoms, such as the use of stimulant drugs or an endocrine abnormality like hyperthyroidism. Box 1⇓ shows the most common differential diagnoses for hypomania. A key issue in its differential diagnosis is that the psychiatric assessment should focus not only on the present mental state but also on the longitudinal history and temporal pattern of recurrent mood episodes (be they depressive, manic or mixed).
Levels of elevated mood and overactivity that lie within normal limits
Drug misuse: cannabis, amphetamine, methylenedioxymethamphetamine (MDMA, ecstasy) and cocaine
Cyclothymia
Cluster B personality disorder (e.g. borderline personality disorder)
Attention-deficit hyperactivity disorder
Endocrinopathy such as hyperthyroidism (rare)
A large body of evidence has now accumulated to support the assertion that bipolar disorder is under-recognised in everyday clinical practice. When the duration criterion for hypomania is reduced from 4 to 2 days, the prevalence of bipolar disorder rises from 1% to at least 5% (Angst, 1998; Akiskal et al, 2000). This rise occurs at the expense of recurrent unipolar depression, suggesting that between 25% and 50% of all people with recurrent depression may in fact be part of a bipolar group (Hantouche et al, 1998; Angst & Gamma, 2002; Benazzi & Akiskal, 2003).
Using the Zurich cohort of 4547 young adults, who were formally assessed six times between 1978 and 1999, Angst et al(2003) tested the diagnostic criteria of DSM–IV hypomania and attempted to develop and validate criteria for softer expressions of bipolar II disorder. They used the standard DSM–IV definition of hypomania in addition to ‘Zurich strict’ and ‘Zurich broad’ criteria (Box 2⇓). They found the prevalence of bipolar II disorder to be 2% under DSM–IV criteria, 5% under Zurich strict criteria and 11% under Zurich broad criteria. Interestingly, the clinical validity of diagnoses using both sets of Zurich criteria was supported by data on family history, illness course and clinical characteristics. Under the Zurich broad criteria, up to half of those with recurrent major depression in this cohort could be considered to have bipolar II disorder.
Strict criteria
Euphoria, irritability or overactivity
At least three of the seven DSM–IV symptoms of hypomania
Hypomanic symptoms of at least 1 day’s duration
Experience of negative consequences of hypomanic periods
Broad criteria
Euphoria, irritability or overactivity
At least two of the seven DSM–IV symptoms of hypomania
No minimum duration of hypomanic symptoms
No requirement to have experienced negative consequences of hypomania
(Angst et al, 2003, with permission)
Several additional reports support a higher prevalence and clinically significant spectrum of bipolar disorders (Angst, 1998; Akiskal et al, 2000; Judd et al, 2003). For example, when people with a diagnosis of recurrent major depression are systematically assessed for a past history of hypomanic symptoms, 45% satisfy the diagnostic criteria for a bipolar disorder, suggesting that the detection of hypomania in everyday practice is deficient, even when using criteria that are overly restrictive (Allilaire et al, 2001).
Although the concept of a broadened bipolar spectrum has gained some prominence in recent years, it must be noted that this area remains controversial. Baldessarini (2000) has argued that classic bipolar disorder is probably as close to a ‘disease’ as we have in modern psychiatry and that widespread acceptance of broadened definitions of bipolarity run the risk of trivialising the core concept. This view has important implications for biological research into bipolar (and unipolar) disorder, including neuropsychological, imaging and genetic studies. It would also affect the future design of treatment trials for depression and bipolar disorder. If one accepts that a proportion of people with recurrent depression may indeed have a bipolar disorder (even if broadly defined), this raises the uncomfortable possibility that much of the data on the efficacy of antidepressants in unipolar depression may have been derived from clinical populations that contain a significant proportion of people with bipolar depression.
Several factors contribute to the underdiagnosis of hypomania in clinical practice.
Bipolar disorder is characterised by oscillations between depression and hypomania and/or mania. For many years it was believed that mood symptoms and levels of functioning returned to normal between episodes of illness, but recent work has challenged this idea. Long-term follow-up studies of the symptomatic status of people with bipolar disorder have demonstrated that clinically relevant symptoms are extremely common and can have a major impact on psychosocial functioning.
Judd et al(2003) prospectively followed 86 individuals with bipolar II disorder for a mean duration of 13.4 years and found that depressive symptoms were reported in 50.3% of the weeks studied. Hypomanic symptoms were reported in only 3.6% of the weeks studied. In a similar study of 146 people with bipolar I disorder followed over 12.8 years, individuals were symptomatic for 47% of the study time (Judd et al, 2002). As with bipolar II disorder, depressive symptoms predominated over manic or hypomanic symptoms (31.9% v. 14.8% of total follow-up weeks) (Judd et al, 2002). The clinical course of bipolar disorders is therefore dominated by depression rather than hypomania. This is especially true for bipolar II disorder, where the ratio of time spent with depressive symptoms relative to time with hypomanic symptoms is about 30:1 (Judd et al, 2003).
Traditionally, we have been trained to diagnose bipolar disorder on the basis of manic presentations against a background of recurrent depression rather than taking into account other, more subtle clinical variables. Unsurprisingly, most people with bipolar disorder do not seek help during hypomanic periods. As a result, both primary care physicians and psychiatrists usually come into contact with them only during depressive episodes. Furthermore, patients recollection of previous hypomanic symptoms at this time is often poor. Depressive cognitive distortions tend to make their recall of elevated periods less likely and some patients may consciously (and unconsciously) withhold information about hypomanic symptoms, for example because of a reluctance to take mood-stabilising medication. Most clinicians are also much better at assessing depressive symptoms than hypomanic symptoms (Sprock, 1988).
The individual’s lack of insight during hypomanic and manic episodes is a major factor in the under-detection of bipolar disorder. Although impaired insight is well documented as a core feature of psychosis, it has been much less studied in mood disorders. Insight has been shown to be significantly more impaired during hypomania and mania than during depression, and impaired insight appears to be almost as prominent a feature in mania as in psychosis (Ghaemi et al, 1995). A meta-analysis of studies found that impaired insight is a state-dependent feature of mania and should probably, as with psychosis, form part of the diagnostic picture (Ghaemi & Rosenquist, 2004).
For these reasons, it is essential that a corroborative history be obtained from a first-degree relative, partner or close friend during any assessment of possible bipolar disorder. Including family members in the assessment significantly increases the detection rate of bipolar disorder. In a study of the prodromal features of depression and mania, families reported behavioural manifestations of mania more than twice as frequently as patients (47% v. 22%) (Keitner et al, 1996). In our own clinical experience, we often observe a striking disparity between the account of hypomanic features provided by patients and by their close relatives.
Although this kind of assessment may be time-consuming, it can significantly alter the long-term prognosis for many patients. Clinicians’ time can be saved by a brief informative telephone call to a family member rather than hours of inaccurate or evasive interviews with the patient. Involving family members in assessment also has a number of less obvious advantages. It may bring to light a previously unknown family history of bipolar disorder or psychosis and can help some patients to engage more fully in their treatment plans.
A more systematic search for previous symptoms of hypomania may be prompted by a clinical suspicion that a depressed patient is presenting with bipolar rather than unipolar depression. Although it is widely held that people with bipolar depression are indistinguishable on clinical grounds from those with unipolar depression, a number of recent studies challenge this idea.
In a 3-year prospective follow-up study of 206 consecutive out-patients with depression and no prior history of bipolar disorder, 41 (20%) developed an episode of mania (Akiskal et al, 1983). Several variables were associated with bipolar outcome: depressive episodes of acute onset, frequent recurrence and brief duration; a family history of bipolar disorder; post-partum depression; psychomotor retardation or atypical features; and antidepressant-associated hypomania. The strongest associations with bipolar outcome were a family history of bipolar disorder and antidepressant-associated hypomania, with positive predictive values of 94% and 100% respectively (Akiskal et al, 1983).
In a small study of 27 individuals with unipolar depression and 27 age- and gender-matched people with bipolar depression, Mitchell et al(1992) found that those with bipolar depression tended to exhibit less psychomotor slowing, more agitation, more atypical symptoms and had shorter depressive episodes. Atypical depressive features (including mood reactivity, overeating, oversleeping, excessive fatigue, so-called leaden paralysis in the limbs and sensitivity to interpersonal rejection) appear to be at least twice as common in bipolar as in unipolar depression (Angst et al, 2005).
A comparison of 39 depressed patients with bipolar I disorder with age- and gender-matched depressed patients with unipolar depression found that the former were significantly more likely to have experienced an episode of psychotic depression in the past (Mitchell et al, 2001).Goldberg et al(2001) conducted a 15-year follow-up of 74 young adults hospitalised for severe unipolar depression and found that 27% subsequently developed hypomania, with an additional 19% experiencing at least one episode of full-blown mania. The presence of mood-congruent psychotic symptoms during the index depressive episode was strongly predictive of bipolar disorder, with 8 out of 10 patients with psychotic depression eventually becoming bipolar during the 15-year follow-up period.
A number of other variables have been associated with bipolar outcome in those with apparent unipolar disorder, although the evidence for these is weaker. These include hyperthymic personality, which in some studies (Akiskal et al, 2000) but not in others (Cassano et al, 1999) has been associated with a family history of bipolar disorder. Studies of the natural history of mood disorders suggest that bipolar depressive episodes tend to be shorter than unipolar depressive episodes (with a median duration of 3–6 months compared with 6–12 months) (Goodwin & Jamison, 1990). Acute but not prophylactic response to antidepressants (often referred to as ‘antidepressant wear-off’) and a history of non-response to multiple courses of antidepressants might also be predictive of bipolar outcome (Goodwin & Jamison, 1990). Possible indicators of bipolarity in apparently unipolar depression are listed in Box 3⇓.
First-degree relative with bipolar disorder
Antidepressant-induced mania or hypomania
Multiple family members with major depression
Early age at onset of depression (less than 25 years old)
Psychotic features (before age 35)
Atypical features
Post-partum illness
Brief recurrent episodes of depression (less than 6 months’ duration)
As noted above, the apparent ‘bipolarity’ of mood episodes in bipolar disorder (a clear manic polev. a clear depressive pole) may be a reflection of different proportions of manic and depressive symptoms within any given episode, rather than the occurrence of discrete ‘pure manic’ and ‘pure depressive’ episodes. Just as depressive symptoms occur during hypomanic periods of bipolar disorder, so hypomanic symptoms seem to occur during depressive episodes of the disorder.
In a cross-sectional analysis of both depressive and manic symptoms in a treated sample of 441 people with bipolar disorder, Bauer et al(2005) found that 68 (15.4%) met DSM–IV criteria for a current hypomanic or manic episode and that most of these (64/68, 94.1%) also had clinically significant depressive symptoms.
This idea that mood episodes in bipolar disorder can often present as admixtures of depressive and hypomanic symptoms is supported by evidence that mixed depression may represent a clinical marker for bipolar disorder. In a consecutive sample of 226 individuals with bipolar II disorder and 151 with unipolar depression, Akiskal & Benazzi (2003) assessed the prevalence of mixed depression during an index depressive episode. They defined mixed depression as DSM–IV major depression plus three or more concurrent hypomanic symptoms. Mixed depression was present in 58.4% of those in the bipolar II group and in 23.1% of those in the unipolar group. Those with mixed depression in the two groups shared similar clinical variables such as age at illness onset, atypical features and family history of bipolar disorder, suggesting that they might have a bipolar-spectrum disorder.
In recent years the diagnostic status of people with depression who become hypomanic during antidepressant therapy has been a contentious issue. Many psychiatrists believe that in patients with no previous history of hypomania, brief periods of hypomania occurring within weeks of starting antidepressants should not necessarily lead to a diagnosis of bipolar illness. In DSM–III–R, antidepressant-associated hypomania was considered part of ‘the bipolar spectrum’, whereas in DSM–IV it is categorised as a ‘substance-induced mood disorder’. However, a consensus is re-emerging that people with depression who experience antidepressant-associated hypomania are truly bipolar.
This is a difficult area because many of the original descriptions of antidepressant-induced hypomania did not distinguish between patients with pre-existing diagnoses of unipolar or bipolar disorder. In addition, most treatment trials of antidepressants for depression do not systematically assess patients for hypomanic symptoms during the recovery period. To address these deficiencies, Chun & Dunner (2004) reviewed 98 trials of antidepressants for depression where a systematic effort was made to separate participants with bipolar or unipolar disorder. Most of these studies (89%) reported no cases of antidepressant-associated hypomania or mania, suggesting that antidepressants do not make individuals with correctly diagnosed unipolar disorder bipolar. In other words, when hypomania occurs as an adverse event following antidepressant therapy, it is because the patient has bipolar disorder. This is supported by evidence that individuals with unipolar depression who have antidepressant-associated hypomania and individuals with bipolar disorder who experience spontaneous hypomanias have very similar rates of mania in their family histories (Akiskal et al, 2003b).
The issue of whether antidepressants are helpful in both the short and long term in the treatment of bipolar depression is unresolved. In a recent meta-analysis of the short-term outcome of antidepressant treatment for bipolar depression, Gijsman et al(2004) found that antidepressants were effective in resolving depressive symptoms and did not appear to lead to more manic switches than did placebo. Conversely, in a literature review of hypomania or mania associated with recent antidepressant use in bipolar disorder, Goldberg & Truman (2003) concluded that between 20% and 40% of all people with bipolar disorder were inherently susceptible to antidepressant-induced manias. They found this to apply to all classes of antidepressant, although selective serotonin reuptake inhibitors (SSRIs) may be less likely to cause hypomania or mania in bipolar disorder than are tricyclics or dual-action antidepressants such as venlafaxine.
It is likely that bipolar disorder represents a collection of heterogeneous disorders, some of which may be more sensitive to antidepressant-induced switching than others (Wehr et al, 1988). It also seems likely that a minority of people with bipolar disorder will require longer-term antidepressant therapy in combination with mood stabilisers to protect against depressive relapse (Altshuler et al, 2003).
Goldberg & Truman (2003) have suggested that factors such as a strong genetic loading for bipolar illness, an early onset of illness, a history of multiple previous antidepressant trials and a history of antidepressant-induced manias should signal caution in the use of antidepressants for bipolar depression.
Psychiatric comorbidity in bipolar disorder is extremely common and exerts a significant influence on the presentation, course and outcome. Comorbid conditions such as drug and alcohol misuse can mask the presentation of bipolar disorder, especially in the early stages of illness.
In the USA, McElroy et al(2001) evaluated 288 out-patients with bipolar disorder and found that 187 (65%) also met DSM–IV criteria for at least one comorbid lifetime Axis I disorder, the most common being substance misuse (n = 78, 42%). Alcohol misuse was present in 96 individuals (33% of the total sample). There were also significant levels of marijuana (16%), cocaine (9%), stimulant drug (9%), sedative drug (8%) and opiate (7%) misuse. Anxiety disorders were very common: 20% of the sample had a lifetime history of panic disorder; 16% social phobia; 9% obsessive–compulsive disorder; and 6% had a history of eating disorder. Current Axis I comorbidity was associated with an earlier age at onset of affective symptoms and the development of both cycle acceleration and more severe episodes over time.
DSM–IV Axis II comorbidity is also common in bipolar disorder and may exert an even greater influence on misdiagnosis and prognosis. Around one-third of people with bipolar disorder have a comorbid diagnosis of at least one personality disorder, and by far the most common of these is borderline personality disorder (Vieta & Colom, 1999; Benazzi, 2000; Joyce et al, 2004). As many clinicians will recognise, mood episodes and affective instability are extremely common in borderline personality disorder. When individuals with borderline personality disorder are systematically assessed for the presence of bipolar features, rates of previously undiagnosed bipolarity of up to 69% have been reported (Deltito et al, 2001).
Although the relationship between bipolarity and borderline pathology is undoubtedly complex (for a review of this area see Paris, 2004, and Smith et al, 2004), many people with a diagnosis of borderline personality disorder may in fact have an undiagnosed bipolar-spectrum disorder and, as a result, may be denied effective treatments for their mood disorder. Conversely, some patients diagnosed with bipolar disorder will inevitably be more appropriately managed as patients with a borderline personality disorder (Bolton & Gunderson, 1996).
We have already mentioned a number of straightforward measures for improving the detection of bipolar disorder (Box 4⇓). Within the past few years, several assessment instruments have been developed to aid the detection of hypomanic symptoms.
Involving a reliable witness in the assessment of the patient
Having a greater awareness of the natural history of bipolar disorder
Recognising clinical features of bipolar depression and mixed affective states
Having a greater awareness of subtle hypomanic symptoms and the impact of comorbidity
Recognising the importance of bipolar disorder in a first-degree relative
Recognising the likely bipolar status of antidepressant-associated hypomania
One of us (S.N.G.) with colleagues has suggested structured diagnostic criteria for bipolar-spectrum disorder that describe patients who do not meet the strict DSM–IV criteria for bipolar disorder but who none the less have a number of important bipolar features (Ghaemi et al, 2001). These criteria, shown in Box 5⇓, give priority to a first-degree family history of bipolar disorder and a personal history of antidepressant-associated hypomania (Ghaemi et al, 2004). They also suggest that clustering of more subtle bipolar features may be used to aid diagnosis.
At least one major depressive episode
No spontaneous DSM–IV hypomanic or manic episodes
first-degree relative with bipolar disorder
antidepressant-associated mania or hypomania
hyperthymic personality
more than three depressive episodes
brief major depressive episodes (of less than 3 months’ duration)
atypical depressive symptoms
psychotic major depressive episodes
early age at onset (less than 25 years old)
post-partum depression
antidepressant wear-off (acute but not prophylactic response)
lack of response to more than two antidepressant trials
The Mood Disorder Questionnaire (MDQ) is perhaps the best known screening instrument for bipolar disorder (Hirschfeld et al, 2000; available to patients at http://www.bipolar.com/mdq.htm). It is a brief form filled in by patients that can be easily incorporated into routine practice. In psychiatric out-patient settings, a positive response to 7 of the 13 core manic symptom questions (all occurring at the same time and associated with at least ‘minor’ functional impairment) gives a sensitivity for bipolar disorder of 0.73 and a specificity of 0.90 (Hirschfeld et al, 2000).
However, in general population settings this instrument has a much lower sensitivity, of only 0.28, and a specificity of 0.97 (Hirschfeld et al, 2003). Miller et al(2002) tested the sensitivity of the MDQ in a population of individuals with bipolar disorder and found that it was much better at detecting bipolar I disorder (with a sensitivity of 0.70) than bipolar II disorder (sensitivity 0.30). Despite this, in the clinical setting, many psychiatrists have found the MDQ to be useful in the overall assessment of bipolar features.
(From Ghaemi et al, 2001, with permission)
The Bipolar Spectrum Diagnostic Scale (BSDS) is a narrative-based scale that has been developed to target symptoms of bipolar II disorder (Ghaemi et al, 2005). As it is a relatively little-known instrument we show it in Box 6⇓. With a team of colleagues one of us (S.N.G.) compared the sensitivity and specificity of this scale with those of the MDQ for 73 people with bipolar disorder and 20 with unipolar depression (Ghaemi et al, 2005). We found the MDQ to be better at correctly detecting bipolar I than bipolar II disorder (confirming Miller et al’s findings mentioned earlier), whereas the BSDS was just as good at identifying both bipolar I and bipolar II disorder. This suggests that the BSDS may be particularly useful at detecting the broader spectrum of bipolar disorders.
InstructionsFirst, please read through the passages below, without filling in any blanks. Then read them again and put a tick in the box at the end of any sentences that you think fit you. Finally, tick one of the four boxes at the end of the passages.
Some individuals notice that their mood and/or energy levels shift drastically from time to time □. They notice that their mood and/or energy levels are sometimes very low and at other times, very high □.
During their low phases, these individuals often feel a lack of energy, a need to stay in bed or get extra sleep, and little or no motivation to do things they need to do □. They often put on weight during these periods □. During their low phases, these individuals often feel blue, sad all the time or depressed □. Sometimes, they feel hopeless or even suicidal □. Their ability to function at work or socially is impaired □. Typically, these low phases last for a few weeks, but sometimes they last only a few days □.
In between mood swings these individuals may experience a period of normal mood, during which their mood and energy level feel right and their ability to function is not disturbed □.
They may then notice a marked shift or switch in the way they feel □. They enter into a high period, when their energy increases above what is normal for them, and they often get many things done they would not ordinarily be able to do □. During these high periods, these individuals sometimes feel as if they have too much energy or feel ‘hyper’ □. Some feel irritable, on edge or aggressive □. Some take on too many activities at once □. Some spend money in ways that cause them trouble □. They may be more talkative, outgoing or sexual during high periods □. Sometimes, their behaviour during these high periods seems strange or annoying to others □. Sometimes, these individuals get into difficulty with co-workers or the police at this time □. Sometimes, they increase their alcohol or non-prescription drug use □.
Now that you have read the passages and ticked the boxes, please tick one of the following four boxes
□ This story fits me very well, or almost perfectly
□ This story fits me fairly well
□ This story fits me to some degree, but not in most respects
□ This story does not really describe me at all
Scoring the BSDS
Each sentence ticked is worth 1 point. Add 6 points for ‘fits me very well,’ 4 points for ‘fits me fairly well’ and 2 points for ‘fits me to some degree’.
Optimum threshold for positive diagnosis: score of 13 or more.
When using instruments such as the MDQ and BSDS, due consideration should be given to clinical context. These screening tools should obviously be used to complement, rather than replace, careful clinical assessment.
We have tried to provide a useful summary of recent advances in the clinical presentation and diagnosis of hypomania. This area is not simply of academic interest but has implications for the way in which we assess and treat patients with recurrent mood disorders. Correctly identifying hypomania (using universally accepted criteria) will also influence many strands of mood disorder research, from animal models and genetics through to neuroimaging studies and the design of treatment trials of new medications.
S.N.G has been involved in the development and testing of the Bipolar Spectrum Diagnostic Scale.
manic episodes always last longer
manic episodes can be associated with normal levels of social and occupational functioning
hypomania can be regarded as a normal psychopathological state
dysphoric hypomania is rare in bipolar disorder
most hypomanic episodes in bipolar II disorder last at least 4 days.
clinicians fail to ask about brief periods of elevated mood and activity
clinicians do not consider brief periods of elevated mood to be diagnostically important
many assessments of recurrent depression do not include taking a history from first-degree relatives or spouses
people with bipolar disorder tend to present for help only when depressed
the diagnosis of bipolar disorder has traditionally focused on the identification of mania rather than more subtle bipolar features of recurrent depression.
there are no significant phenomenological differences
atypical symptoms are more common in unipolar depression
where hypomania occurs as an adverse event in the treatment of unipolar depression, this probably means the patient has bipolar disorder
psychotic depression in earlier adulthood is strongly suggestive of bipolar disorder
a family history of bipolar disorder is more common in bipolar depression.
recent antidepressant therapy
substance misuse
borderline personality disorder
symptoms of attention-deficit hyperactivity disorder
thyrotoxicosis.
seeking accounts of behaviour from family members
taking a comprehensive family history for mood disorders
recognising the potential diagnositic significance of antidepressant-associated hypomania
probing for a past history of hypomanic symptoms in recurrent depression
not using the MDQ or BSDS.
| Dimension | 20 points | 15 points | 10 points | 5 points | 2 points |
| Episode Characteristics | Manicsymptoms with “prominenteuphoria, grandiosity or expansiveness”. | Manic symptoms withdysphoria, irritability | Hypomanic symptoms; or mania following an antidepressant | Hypomanic symptoms following an antidepressant; or hypomania below DSM threshold; or major soft signs: atypical or postpartum depression | Psychosis, without other signs of mania |
| Age of Onset | 15-19 | <15 or 20-29 | 30-45 | > 45 | — |
| Illness Course (and Other Features) | Manic episodes separated by periods of full recovery | Incomplete recovery between manic episodes; or hypomania with full recovery between episodes | Mania, incomplete recovery, but also substance use; or psychosis only during mood episodes; or legal problems associated with mania | Repeated episodes of unipolar depression, no hypomania (3 or more); or hypomania with incomplete recovery between episodes; or any of several other features: borderline; anxiety disorder; ADHD as a child; gambling or other risk behaviors without mania per se; or PMS | Hyperthymictemperament; >3 marriages, or two jobs in two years; or two advanced degrees (seeAkiskal reference on these latter features) |
| Response to Medications | Fullrecoverywithin 4 weeks of treatment with mood stabilizers | Full recovery within 12 weeks of treatment; orrelapse within 12 weeks of stopping mood stabilizers; orswitch to mania within 12 weeks of starting antidepressant | Worsening dysphoria or mixed state symptoms during antidepressant; or partial response to mood stabilizers; or antidepressant induced rapid cycling or worsening thereof | Lack of response to 3 or more antidepressants; or mania / hypomania when antidepressant stopped | Immediate response, almost complete, to antidepressant within 1 week or less |
| Family History | 1st degree relative (brother / sister, parent, or child) with clear bipolardisorder | 2nd degree relativewith bipolar diagnosis; or 1st degree relative with recurring unipolardepression andfeatures suggestive of bipolar disorder | 1st degree relative with recurring unipolar depression orschizoaffective disorder; or any relative with clear bipolar diagnosis; or any other relative with unipolar depression and symptoms suggestive of bipolar | 1st degree relative has clear problem with drugs or alcohol | 1st degree relative has repeated episodes of depression; or has an anxiety disorder, an eating disorder, or ADHD |
| Dimension | 20 points | 15 points | 10 points | 5 points | 2 points |
| Episode Characteristics | Manicsymptoms with “prominenteuphoria, grandiosity or expansiveness”. | Manic symptoms withdysphoria, irritability | Hypomanic symptoms; or mania following an antidepressant | Hypomanic symptoms following an antidepressant; or hypomania below DSM threshold; or major soft signs: atypical or postpartum depression | Psychosis, without other signs of mania |
| Age of Onset | 15-19 | <15 or 20-29 | 30-45 | > 45 | — |
| Illness Course (and Other Features) | Manic episodes separated by periods of full recovery | Incomplete recovery between manic episodes; or hypomania with full recovery between episodes | Mania, incomplete recovery, but also substance use; or psychosis only during mood episodes; or legal problems associated with mania | Repeated episodes of unipolar depression, no hypomania (3 or more); or hypomania with incomplete recovery between episodes; or any of several other features: borderline; anxiety disorder; ADHD as a child; gambling or other risk behaviors without mania per se; or PMS | Hyperthymictemperament; >3 marriages, or two jobs in two years; or two advanced degrees (seeAkiskal reference on these latter features) |
| Response to Medications | Fullrecoverywithin 4 weeks of treatment with mood stabilizers | Full recovery within 12 weeks of treatment; orrelapse within 12 weeks of stopping mood stabilizers; orswitch to mania within 12 weeks of starting antidepressant | Worsening dysphoria or mixed state symptoms during antidepressant; or partial response to mood stabilizers; or antidepressant induced rapid cycling or worsening thereof | Lack of response to 3 or more antidepressants; or mania / hypomania when antidepressant stopped | Immediate response, almost complete, to antidepressant within 1 week or less |
| Family History | 1st degree relative (brother / sister, parent, or child) with clear bipolardisorder | 2nd degree relativewith bipolar diagnosis; or 1st degree relative with recurring unipolardepression andfeatures suggestive of bipolar disorder | 1st degree relative with recurring unipolar depression orschizoaffective disorder; or any relative with clear bipolar diagnosis; or any other relative with unipolar depression and symptoms suggestive of bipolar | 1st degree relative has clear problem with drugs or alcohol | 1st degree relative has repeated episodes of depression; or has an anxiety disorder, an eating disorder, or ADHD |
First, before treatment actually starts, you and your doctor must be sure that you don’t have thyroid changes causing your mood problem. This can be done with a simple test called “TSH”, which measures the level of “thyroid stimulating hormone”. Usually your doctor will also order other tests at this time, if you have not had a recent check of cell counts and blood chemicals, to make sure you don’t have other potential medical causes for your mood problems. Because it is not very common to find a problem using these tests, treatment can start even before the results are back. The doctor is just making sure she/he doesn’t miss something unusual. (Thyroid hormone has also been shown to act as a treatmentfor bipolar disorder in some cases, so it is important to know just where your “TSH” is).
Now, the three most important principles, in my view, of bipolar treatment:
Read through the rest of this page first, for an overview of treatment. Then skim through again and take some of the links in each section for more details on concepts of particular interest to you.
Brace yourself. The good news: here come lots of non-medication options for treatment. The bad news: they all take at least a little work on your part. Some take a lot. But almost all are virtually risk free and cheap. Hard to beat that. I wish they were easier for most people. Some are hard for people without symptoms to do! But if you maximize these, you’ll almost certainly need less medication; and — importantly — the opposite is also true: if you don’t, you’re likely to need more medication.
| TREATMENT COMPONENT | OFFICIAL THERAPY | WHERE TO FIND MORE INFORMATION |
|---|---|---|
| Regular daily schedule | Social rhythm therapy | Treating Bipolar Disorder, by Ellen Frank; or chapter 11 from my book(just read it while standing in the bookstore!); or my web-essay: Light and darkness in bipolar disorder |
| Minimize alcohol | Behavioral therapy | Helpful treatment overall, for most people, if you need it: www.AA.org |
| Regular exercise | Behavioral therapy | Exercise and Mood: not the usual rap |
| Making sure your thoughts are helping, not setting you back | Cognitive Therapy | The Bipolar Workbook: Tools for Controlling Your Mood Swings, by Monica Basco |
| Accepting the illness | Interpersonal therapy | Treating Bipolar Disorder, by Ellen Frank |
| Learning about bipolar disorder | PsychoEducation | (this website); or for therapists, The Psychoeducation Manual for Bipolar Disorder, by Eduard Vieta and Francesc Colom |
| Light therapy for depression | dawn simulator | Dawn simulators; and with caution, light and chronotherapies |
| Making sure your family is on board, and helping |
Family-focused therapy | Bipolar Disorder: Family-Focused Treatment Approach (for therapists) The Bipolar Disorder Survival Guide: What You and Your Family Need to Know (for patients and families) |
| Helping your significant others cope | Interpersonal therapy | Loving Someone With Bipolar Disorder, by Julie Fast |
Here are a few details for some of the not-obvious treatment components above. One approach that is crucial for most patients with bipolar disorder is to maintain a regular daily schedule, especially regular patterns of sleep. An entire therapy for bipolar disorder is organized around this daily schedule idea (“social rhythm therapy”) — especially around having a regular time to go to sleep, and a regular time to wake up and get out of bed. Yes, sorry to say, it would be best to do that same routine even on weekends.
Talk about lifestyle change! This idea of a regular sleep schedule could be very difficult for some people. Unfortunately, the most important steps you can take, without medications, can seem quite restrictive. Many people resist these restrictions, which is understandable. But that often means they will have to rely more heavily on medications, which can mean having to deal with more side effects or risks.
For many people, a very important part of bipolar disorder treatment is getting help coming to terms with having the illness at all. Accepting the illness, and accepting some limitations in order to deal with it — sometimes getting some help with this makes a huge difference. Call it “psychotherapy”, or just call it getting some help: either way, it can make this important step much easier. I hope this is obvious: if you are still spending all your energy trying to resist the fact that you have a mood problem, you won’t be able to accept some of the lifestyle changes that could make your mood problem much easier to manage.
In fact, multiple research studies have shown that using a therapist to help you with this acceptance stage, and then with making some of the necessary changes in your routines, leads to much better long-term outcomes. Three major forms of bipolar-specific psychotherapy emphasize this process of acceptance and change. All of them are variations on techniques which have been around for a long time: cognitive behavioral therapy, interpersonal therapy, and family therapy. Most therapists you can find will be familiar with one or several of these techniques. The bipolar-specific versions simply incorporate some special features pertinent to people with bipolar disorder.
Unfortunately, most psychotherapists (as of 2008) are not specifically trained in the bipolar-specific versions of these therapies. Unless you live near one of the training centers for these methods, you may not be able to find a therapist who who has had specific training on using such an approach. Worse yet, the training manuals for these therapies, which are easily obtained, tend to focus on Bipolar I. The emphasis is on preventing subsequent severe episodes of mania or depression. For people with Bipolar II, these psychotherapies require some adaptation. For now, the easiest way to do this is to work closely with a good therapist, emphasizing the following (you can even point out to your therapist where to find more information on these, using the resources in the right-hand column):
The research behind these approaches has been summarized on a separate page on this website, Psychotherapies for Bipolar Disorder.
In addition to these non-medication approaches, most people with bipolar disorder also need to use medications — although if more people were really rigorous about the non-medication approaches, and I mean really rigorous, perhaps we’d be able to use less medications. But that’s really tough, especially since motivation goes missing during bipolar depression, and most of those approaches require either motivation or a really good system of habits.
The main medications for bipolar disorder are called “mood stabilizers”. There are at least 5 options, and the list continues to grow. Your doctor will choose, or help you choose, based on her/his sense of what will work best for your set of symptoms; or what has worked for others in your family, which is often a huge clue; or based on your preferences, looking at the potential side effects and risks.
You might think “whoa, I’m being offered medications they use for people with serious mental illnesses — look, there’slithium!” But you didn’t know that lithium is commonly used as a booster for antidepressants in plain old depression. It even works by itself as an antidepressant. So taking lithium is not a marker for “serious” mental illnesses (whatever that means. See my little essay about “Normal — or Mentally Ill?” in Treatment FAQ). But what about side effect risks from mood stabilizers? Are they worse than antidepressants?
Some mood stabilizer options carry significant risks, unfortunately. Many doctors shy away from talking about bipolar disorder as a possible diagnosis because the think the risks of the treatments are much greater than the risks of antidepressants, for example. But if you read Prozac Backlash, which offers an extreme view of the possible risks of antidepressants, you’d probably think at least some of the mood stabilizers look better, by comparison. If you include the risk of antidepressants making bipolar disorder worse, then the risks of the mood stabilizers could be regarded as roughly in the same realm as the risks of antidepressants. Update 7/2006 : when I wrote that last sentence, this view was pretty radical. But listen to this statement from one of the most widely respected bipolar experts in the world, Dr. Fred Goodwin, who said that doctors and patients tend to think of antidepressants:
“…as light, easy uncomplicated drugs; and mood stabilizers as heavy drugs that should be reserved for use as a last resort. But in fact, recent data suggest that we may have to reverse that order of preference, or at least put them on an equal plane.” (interview, Primary Psychiatry, 2005)
Dr. Goodwin is saying the same thing I’ve been saying for over 5 years — but neither of us has very solid data to go on, unfortunately. We’re worrying, more than we’re saying we know.
Ahem, back to the mood stabilizer options. While your mind may leap to considering the risks, you should step back first and consider the evidence for effectiveness, of any treatment you’re considering. Will it work? If that evidence isn’t very strong, then the risk side of the equation may not matter much — unless the treatment is cheap, harmless, and may have other benefits. There are several such options, it turns out. But you won’t like the sound of them, when described. Too bad. Wait a minute, wait a minute. What is he talking about: cheap, harmless, other benefits? Okay, try this: “exercise” (it’s like invoking the name of the devil, in some circles, to say that). Or this: “sleep” (ah, that wasn’t so bad, was it) Well, “about 8 hours of sleep on a regular schedule”, that’s the hard part. Even good old fish oil has remarkably good evidence for a “mood stabilizer” effect, but you have to take a lot. So it’s not entirely “cheap”. But it does appear to be nearly harmless and have other benefits.
Ahem again (why is this so hard to stay on track here? Well, there is just so much to say about all this. You won’t see them all but this website now has about 300 pages, many on very specific topics with only a single path that will take you there. So I’ve buried a lot of information. Let’s get back to the basics, shall we?)
My main point about choosing a medication: become familiar with at least some of the evidence for the options you’re being offered, or should be offered. Some doctors don’t keep up with that evidence; or are too swayed by pharmaceutical company pitches; or just use what they are comfortable with. The more you learn the more you’ll be in a position to help determine your own treatment. (Not that it will be an easy negotiation with your doctor all the time. Read my hints about Talking with Doctors.)
Depression is the big problem in non-manic versions of bipolar disorder (these versions include Bipolar II, and “softer” versions, as described in the Diagnosis section of this website). Thus many people with bipolar mood problems are offered antidepressants at some point. Seems logical, yet research does not strongly support this approach. Worse yet, antidepressants can make some people with bipolar disorder worse. Therefore most mood experts recommend using antidepressants only when one or several of the mainstay medications, the “mood stabilizers” discussed below, have not been able to prevent or relieve a bipolar depression. In other words, there is general agreement that antidepressants are not the first thing to turn to in the treatment of bipolar depression.
However, beyond that general agreement, controversy abounds. Some experts think that antidepressants do not have a role at all in treating bipolar depression, except perhaps as a maneuver of last resort. Such experts point either to the lack of evidence for sustained benefit, or the several lines of evidence that they can do harm. More details about the role of antidepressants in bipolar disorder treatment, including links to relevant articles that form the basis of my view, and a summary of an alternative point of view, can be found on the Antidepressant Controversies page.
Because antidepressants are so widely used, I will take this opportunity here to make sure that you are familiar with the concerns about antidepressants. First let us look at the generally agreed upon risks of antidepressants– although even these are somewhat controversial, because some doctors think they are not common; and some think that if they occur, then one simply treats them and continues the antidepressant.
Secondly, here are the more controversial risks.
- Antidepressants may cause “mood destabilizing” — increasing cycle frequency over a longer period of time; in other words, having more mood episodes than before, or more rapid switches from one mood state to another. This is regarded as worsening the mood condition overall, making it less stable. This is one of the main concerns expressed by one of the lead experts on this issue, Dr. Ghaemi, whose work is cited extensively in the Antidepressant Controversiesessay.
- Finally, could antidepressants cause kindling”, in which the illness worsens more quickly with time than it might have if antidepressants weren’t there? I don’t hear too many other experts fretting about this as I do, so I won’t worry you with it here. If you’d like to hear some more of my concerns, there is a section on “kindling” in the Antidepressant Controversies essay.
Whatever you do with antidepressants, you really need to work closely with your doctor on this. DO NOT STOP your antidepressant. It must be tapered at minimum, if you’re going off, or you could — for sure; I’m not making this up — actually end up quickly worse. You have to plan this out with your doctor. If you have trouble getting your concerns or ideas heard, here are some ideas on talking with doctors.
Meanwhile, however, the good news is that we have at least ten different ways of treating depression in bipolar disorder, without using antidepressants. These are summarized on the page entitled Antidepressants That Aren’t “Antidepressants”. Most of these are ingredients in basic treatment, outlined in the next two sections B and C below.
There are several options, shown by generic name in the diagram below. How do you decide which to use? Here’s a very simplified view to start; then we’ll look at some other ways to choose; and finally, we will look in detail at the most commonly used medications.
(For women of child-bearing age: I am sorry to say, all of these medication approaches carry significant risks in pregnancy. It is generally recommended that women take very effective precautions against becoming pregnant while taking these medications. It is possible to have a child, but it must be a planned pregnancy. Before stopping your birth control methods, you should have a very solid treatment relationship developed with a competent psychiatrist. With her or him you will work out a detailed plan, including: how you will taper off your current medications; how your symptoms will be controlled during the pregnancy, if they return; how those medications will be adjusted as you near the end of your pregnancy; and what medications you’ll either be taking, or resume, after delivery. Guys can help out here: use condoms, they’re effective and she doesn’t get side effects — as long as you don’t grumble about using them.)
After I show patients the whole “menu” of mood stabilizers, they almost always end up choosing one based on some combination of these factors:
However, some of these medications have been around longer, so we know much more about their benefits and risks (those whose role is in some doubt have a question mark in the figure above). We’ll start by looking at what mood experts have suggested.
Expert agreement: “first line” medications
Lithium and valproate/divalproex/Depakote used to be the first line” options according to expert consensus”. This means that mood experts agree these are the best choices as a place to start if you’ve never taken a mood stabilizer before. Basic information on using lithium and valproate follows below. But since those consensus guidelines were written up, most of the new recommendations focus on the non-medication options above. There is little new, in terms of medications; except a lot more controversy about the role of antidepressants. You’re welcome to see for yourself: here’s an introduction to international guidelines.
It Depends On Where You’re Starting From
For people whose predominant symptom is depression, as is almost always the case in Bipolar II, then their “mood stabilizer” ought to have plenty of antidepressant “oomph” (a peculiar American term meaning clout, or ability to knock the air out of your lungs, reflecting our peculiar passion for violent versions of football). Here are some mood stabilizers that have well-accepted antidepressant “oomph”, yet are not antidepressants themselves.
Careful now — you will soon discover that olanzapine and quetiapine are new-generation “antipsychotics”. Wow, the idea of lithium was freaky enough, and now we’re talking antipsychotics? Aren’t those the big guns”? If that worries you, see my little essay about the term antipsychotic; it might reassure you a little bit.
But as you can see, I emphasize lithium and lamotrigine over the rest. This helps avoid the “atypical antipsychotic” group, which includes olanzapine/Zyprexa and quetiapine/Seroquel, as well as risperidone and aripiprazole/Abilify, and now the new guy, lurasidone/Latuda. My patients usually don’t like to stay on those medications long-term, for two reasons. First, even the new “second generation” or “atypical” antipsychotics still feel like antipsychotics to a lot of people: they slow down thinking, especially. Sometimes that’s a very good thing, and when that effect is necessary, these are great options. But I generally prefer to use medications that when they are working well are still basically “invisible” to the person taking the medication: you feel “normal”, not “drugged” in the least.
Secondly, all of these medications sometimes cause weight gain and can raise the risk of diabetes. Olanzapine is worst in this respectLeslie and risperidone and quetiapine are thought to be intermediate. Aripiprazole causes less weight gain, but it can still cause this problem just like the rest; and ziprasidone perhaps least, maybe only rarely doing so (unfortunately ziprasidone is the trickiest to use; after years of fooling with it I still have trouble prescribing it, so don’t expect your primary care doctor to be suggesting it, despite the better risk profile regarding weight). Lurasidone/Latuda, we don’t really know yet about the weight gain; it’s looking pretty good so far (11/2014).
Not first line but worth a serious look in some cases
Omega-3 fatty acids from fish oil have several studies supporting their use (too bad there’s no company going to make millions by studying this more closely, as that would move the research on O-3’s along faster). The reason for looking closely at fish oil is not the great results in research trials, although there are some; but rather the complete lack of any risk known at this point. In fact, there’s even a potential for lowering cholesterol levels. So, it’s cheap; it has no long term risk; it has almost no side effects; it’s available without a prescription — hey, if it actually worked, that would be sort of a bonus!
(That’s a joke, mind you. Usually we start by looking at benefits of medications, since if they have no evidence for benefit, the evidence about risks doesn’t matter much, right? I’d like to hear a resounding “RIGHT” there, folks…) Here are theresearch studies showing it may indeed work, at least to some degree, and links to more detail about fish oil. Even if it does work, though, it appears to take over a month, probably closer to two. So if you have symptoms that are really getting in your way now, don’t rely on fish oil alone. (For sure do not go off some other medication and onto fish oil instead; that must be discussed with your doctor.)
Finally, there are add-on medications as well (not mood stabilizers themselves, as such). These include benzodiazepines(alprazolam/Xanax, lorazepam/Ativan, diazepam/Valium), which work well at first but usually lose some of their effectiveness over time, with the possible exception of clonazepam/Klonopin.
Thyroid hormone has a specific role, especially when a person’s thyroid hormone is already low, or on the low side of normal — and perhaps especially if there are a lot of people in the family who have both thyroid and mood problems. Recent research suggests that thyroid hormone, which is very inexpensive, may be both an antidepressant and a mood stabilizer, at least in women (2010); this has been under study for years, but with recent emerging evidence has climbed much higher on my list of options. For details, first read basics about thyroid and bipolar disorder; then see my page onhigh-dose thyroid hormone.
Another add-on: verapamil has been around for a long time but has received renewed interest as an option during pregancyWisner, and for women at risk of weight gain and metabolic changes from other mood stabilizers; it may only work when added to lithium, though.Mallinger
In any case, you can see there are a lot of medications you might consider. Here’s a master list with several other waysof looking at the options. You might end up trying quite a few looking for the best one for you. And you’ll need to be keeping track of your symptoms to know how you’re doing on each one. So you may as well start right now with the tracking. Options include paper/pencil and electronic. Parents and significant others can keep such a chart, if the patient her/himself is not doing so, even if there are a lot of missing data-days. I strongly recommend that, at least at first.
If you are currently on an antidepressant:
Please note the emphasis on talking with your doctor. Some of my colleagues have expressed their concern to me that their patients will read this website and stop their antidepressants. If that was really happening very often, I’d have to consider shutting down the site. The intent here is not to undermine other doctors, just to educate those who wish to learn more than their doctors have time to teach.
There is strong consensus that antidepressants can — in some people — make bipolar disorder worse.The depression gets better, but the “manic” side symptoms (remember, this can include sleep problems, anxiety/agitation, irritability, and difficulty concentrating) get worse. The whole mess can start to “cycle” more frequently, even though the depression is better. In many people, eventually a full depression episode occurs again, despite being on an antidepressant, even one that “worked” before! For some people, you can even say that the antidepressant is causing depression, by making the cycling continue, including cycling into depression.
In that case, even if a mood stabilizer does not have antidepressant effects by itself (there is debate about valproate and carbamazepine in this respect, compared to lithium) it can “work” as an antidepressant very well, by stopping the cycling. I have seen this happen many, many times: so many, in fact, that I routinely rely on the mood stabilizers to help depressed people, and taper off their antidepressants, even while they are depressed. Many times it’s the only way out of the problem (though usually I’ll start the mood stabilizer along with their antidepressant, then taper off the antidepressant when it’s clear the person is getting better).
Gary Sachs, the Harvard bipolar expert, jokes that he tell bipolar patients who experience a very strong antidepressant response: “great, let’s celebrate, let’s lower the dose of your antidepressant!” Note how different an approach this is than in unipolar depression, where continuing an effective antidepressant for 6 months is the standard advice .
I advise patients that they have not had an adequate trial of mood stabilizers if they were simultaneously on an antidepressant at the time. If we try almost everything and the patient still does not improve, eventually she/he will need to try the same mood stabilizers again without an antidepressant on board.
Should I show you that link to controversies regarding antidepressant use one more time? (the language is more complex but I hope you’ll find the concepts fairly clear). Yeesh, this Phelps guy really seems to have a thing about antidepressants, doesn’t he?
Most people ask: “will I have to take this for the rest of my life?” I generally answer this by suggesting that first we should see whether the medication seems to work; later, if it does, we’ll discuss how long to continue it. People often seem to grasp intuitively that if they have had symptoms for many years, they will probably require medications to “normalize their brain chemistry” for many years.
Bipolar I is a long-term illness that usually requires lifelong preventive strategies, at least after several manic or depressed phases have occurred. Bipolar II is less well defined but intuition is generally correct: the longer people have had symptoms, the longer it makes sense to continue the medication before a trial of tapering it off. In any case, “taper” is the most important concept. There are several studies in Bipolar I which seem to indicate that rapidly discontinuing lithium leads to rapid relapse, where tapering off does not present that risk. For lithium at least, stopping should take months, decreasing by 150mg increments all the way to zero; and this probably applies, by extension (for the moment, at least, until we have some data to go on), to other mood stabilizers.
However, you obviously have ultimate control over how your medication is managed — you’re the one that has to put the pills in your mouth every day. If you decided to, you could just stop doing that. So you really ought to know about any risks that might come with doing that, and there are some. At minimum, if your symptoms have been severe in the past, you should have some sort of a “safety net” if you’re going to stop the medications: a partner, or parent, or several close friends and a work acquaintance. Somehow there should be a group who’s going to easily notice if you’re “slipping”, including someone who can take charge of getting you help, if you are not able to do so yourself.
Be aware that you cannot expect the medications will “work” again if you stop taking them, then start again. Bipolar disorder in many cases seems to progress, as though each cycle was increasing the likelihood and the severity of yet more cycles. Left uncontrolled for a period of time, it can worsen so that previously effective treatments are no longer adequate.
The thoughtful reader may have wondered: “is there any evidence that starting mood stabilizers then stopping them is worse than never having started them at all?” There is no evidence of this that I know of. We should worry about it, though. I have seen about three patients where it looked to me as though this might have occurred (out of more than two thousand), but there are so many variables involved it is impossible to be at all certain. The fact that I have yet to encounter other experts writing about this possibility is somewhat reassuring.
I have seen mood stabilizers seem to make people more depressed than they were before they started, so that is worth watching for (we stopped the medication and things got better; then tried other approaches). This has occurred particularly with divalproex/Depakote, oxcarbazepine/Trileptal, and carbamazepine/Tegretol, though it’s very uncommon, perhaps 1 in 50 or so by my estimate. I’ve not seen other mood experts describe this problem. Nor have I seen it with lithium or lamotrigine or thyroid, all of which have some “built-in” antidepressant potential.
You should do this with a psychiatrist who knows about bipolar II if you can. But if it is impossible for you to find a psychiatrist, obviously you and your primary care provider may be stuck trying whatever you can. Hopefully this website will help you decide if “bipolarity” should be considered, and help with trying some basic treatments if you decide bipolarity has the power to explain your experience.
Primary care providers are being bombarded with material from the internet. They don’t have time to read it all. If you think your doctor needs to know some of the kinds of things you are learning here, you can gently suggest she read this page you’re on now. You might be able to convince her if you say something like:
“I know you’re trying to help me, and I wish I had a simpler problem to deal with. I found a site on the internet that made a lot of sense to me, and might help us help me. Here’s a letter from the doctor who wrote it.”
Then hand her a Dear Doctor letter — or use any approach you think might work to get her here!
But please remember: most primary care providers have not been well-trained in this area. Asking them to do something outside their training will make many providers very anxious. They may resist this, and in some cases they may resist in odd ways. If they are frustrated at not being able to help you, which is probably true, their frustration can sometimes seem like it’s aimed at you. It should be aimed at the symptoms, of course. Give him room to “say no” gracefully — which may save both of you some discomfort. After that, if you need it, here are those thoughts about how to talk to doctors.
Congratulations, that’s it for the basics of treatment. From here you can go back to the Table of Contents (always up there, top right) , or I’d particularly recommend more treatment details.
Used by permission of Dr. Nassir Ghaemi
and developer Dr. Ron Pies
The BSDS is a test for subtle versions of bipolar disorder. Before you start this test, you should know that it will not give you a “yes or no” answer as to whether you have bipolar disorder. See the scoring essay for more details about that. There is another test, called the MDQ, that you may run into which gives a “yes or no” answer, but is thus capable of giving a “wrong” answer. In fact, both of these tests have a serious problem with potential “false positives.”
If you are having some doubts about “how bipolar am I?”, continue your education (on this site, for example) about Bipolar II and less prominent versions of bipolar disorder. Then if you can, see a mental health professional, either a skilled therapist like an MSW, or Ph.D. psychologist, or a psychiatrist. If she/he gives you a diagnostic opinion that differs from your self-educated impression, you can discuss the differences in your points of view. If the difference is not resolved, you could try to hunt around for a second opinion.
Somewhere in that process you might take this “test” for bipolar disorder. It is similar to another well-known “test” called the MDQ (Mood Disorders Questionnaire), maybe just slightly better for detecting subtle bipolarity — which is why I’m posting it here instead of the MDQ. (Besides, the MDQ was copyrighted, for unclear reasons). However, make sure to read very carefully about scoring the BSDS after you take it.
Finally, if you would like a paper-and-pencil version of this test which you can easily take to your doctor; which also includes a paper-and-pencil summary of the “soft signs” of bipolar disorder, then use this version..
Here is the test. Read the following paragraph all the way through first, then follow the instructions which appear belowit.
Some individuals noticed that their mood and/or energy levels shift drastically from time to time ______ . These individuals notice that, at times, they are moody and/or energy level is very low, and at other times, and very high______.
During their “low” phases, these individuals often feel a lack of energy, a need to stay in bed or get extra sleep, and little or no motivation to do things they need to do______ .
They often put on weight during these periods______ . During their low phases, these individuals often feel “blue,” sad all the time, or depressed______ .
Sometimes, during the low phases, they feel helpless or even suicidal _____ . Their ability to function at work or socially is impaired ______ . Typically, the low phases last for a few weeks, but sometimes they last only a few days ______ . Individuals with this type of pattern may experience a period of “normal” mood in between mood swings,
during which their mood and energy level feels “right” and their ability to function is not disturbed ______ . They may then noticed they marked shift or “switch” in the way they feel ______ . Their energy increases above what is normal for them, and they often get many things done they would not ordinarily be able to do ______ . Sometimes during those “high” periods, these individuals feel as if they had too much energy or feel “hyper” ______ . Some individuals, during these high periods, may feel irritable, “on edge,” or aggressive ______.
Some individuals, during the high periods, take on too many activities at once ______. During the high periods, some individuals may spend money in ways that cause them trouble______ .They may be more talkative, outgoing or sexual during these periods ______ . Sometimes, their behavior during the high periods seems strange or annoying to others ______ . Sometimes, these individuals get into difficulty with co-workers or police during these high periods ______ .
Sometimes, they increase their alcohol or nonprescription drug use during the high periods ______ .
After you have read this passage, please decide which of the following is most accurate:
Now please go back and put a check after each sentence in the paragraph above that accurately describes you. Print this page, or just keep track of your “checks” on a blank page). When you are done, total the number of check marks.
Click here to score your test.
Bipolar Support Groups.com blog 
