Bipolar Support Groups.com blog

The “bottom line” of diagnosis

If your depressions are complicated; if you have mood swings, but not “mania”, you can still be “bipolar enough” to need a treatment that’s more like the treatments we use in more easily recognized Bipolar Disorder. You’ll read here about forms of depression  which do not have “mania” to make them stand out as different, yet are not plain depression either. For these people, Depression is  by far the main symptom, including especially sleeping too much, extreme fatigue, and lack of motivation. What makes bipolar depression different is the presence of something else as well.
But that “something else” often does not look anything like mania. “Hypomania”, which you’ll learn about here, can show up as extreme insomnia, irritability, agitation/anxiety, and difficulty concentrating.  And finally, some people can have some bipolarity without any hypomania at all. Really. You’ll see references to mood experts who have shown all these things as you go.
Wait a minute: isn’t there concern about overdiagnosis of bipolar disorder? Yes, we’ll talk about that too, after you’ve learned some basics.

What happened to “manic-depressive”? What’s “Bipolar II”?

Somewhere along the way you probably learned about manic-depressive illness: episodes of mania, and episodes of severe depression. Here are the symptoms of “mania”.  Not that you have these, as such; the lack of them is the main point here. Hang on.

• Mood much better than normal
• Rapid speech
• Little need for sleep
• Racing thoughts, trouble concentrating
• Continuous high energy
• Overconfidence
• Delusions (often grandiose, but including paranoid)

What happened to “manic-depressive”? As our understanding of bipolar disorder has grown, the naming system has changed as well. Recently the concept of a “mixed state” of bipolar disorder, in which manic symptoms and depressive symptoms are found at the same time, was added. Obviously this changes the understanding of manic-depressive illness from one in which the two mood states alternate, to one in which they can co-occur! Things are getting more complicated.
Psychiatry has a diagnostic “rule book” that lists the symptoms people must have in order to meet the definition of a particular “disorder”, called the Diagnostic and Statistical Manual. The most recent edition came out in 2013, the “DSM 5”. If much of what you read below seems to describe you well, but someone tells you “you don’t have bipolar disorder”, it could be that they are using a strict interpretation of the DSM rules. This is a highly controversial area in psychiatry. Even the validity of the DSM itself is now controversial. (For examples of this, see my page on DSM SPECTRUM DIAGNOSIS).
Technically Bipolar II describes a pattern in which patients experience “hypomania” (to be discussed in detail below), alternating with episodes of severe depression. However, one of the most experienced professionals in this field, who has bipolar disorder herself, has criticized the DSM as too limited:

“The clinical reality of manic-depressive illness is far more lethal and infinitely more complex than the current psychiatric nomenclature, bipolar disorder, would suggest. Cycles of fluctuating moods and energy levels serve as a background to constantly changing thoughts, behaviors, and feelings. The illness encompasses the extremes of human experience. Thinking can range from florid psychosis, or “madness,” to patterns of unusually clear, fast and creative associations, to retardation so profound that no meaningful mental activity can occur. Behavior can be frenzied, expansive, bizarre, and seductive, or it can be seclusive, sluggish, and dangerously suicidal. Moods may swing erratically between euphoria and despair or irritability and desperation. The rapid oscillations and combinations of such extremes result in an intricately textured clinical picture.” (Kay Jameson p.h.d.)

I arrived at the same conclusion from listening to patients describe their symptoms. When I used this broader conception to guide treatment, people who had struggled for years often got much better.
Yet when I tried to explain this to some of my colleagues, they thought I was a “bipolar wacko”. That’s how this website got started, and why you’ll see so many reference links. I needed to show that these were not my ideas alone, but rather those of mood experts around the world (it also seemed like a handy way to explain all this to my patients without saying the same thing over and over!) For example, everything you will read below can be found in a review by two mood experts, except that their version is written in full medical jargon.
Even the International Society for Bipolar Disorders has advocated a change in diagnostic procedure, moving beyond the DSM, using what we’ve learned in the last decade.  See Ghaemi and collegues; if you look closely you’ll see that my name is on the list of co-authors. I was honored to be invited to participate and write for this 2008 update on bipolar diagnosis guidelines. I was the lead author on the “Bipolar Spectrum” paper. Its content is reflected below.

What’s “Bipolar II”?

Depression for sure. Depression far more than anything else. And then there’s this other little part.  The technical name is misleading, and causes all sorts of trouble, so careful, don’t get thrown off by it.  We’re talking about a very small amount (sometimes larger) of manic-side symptoms:

• Mood better than normal
• Rapid speech
• Dramatically reduced sleep
• Racing thoughts, trouble concentrating
• Continuous high energy
• Overconfidence

People with Bipolar II don’t have mania. They don’t have “psychosis” (loss of contact with reality). They don’t have extreme behaviors that people think are “crazy”.  They do have phases that their family and friends recognize as “not your usual self”:  something unusual along the lines of the bullets above.  Notice that “delusions” are gone from the earlier list.
Another variation less severe than Bipolar II is the combination of hypomanic phases with separate phases of mild depression.  This is called “cyclothymia”. Getting confused? I certainly was, until I began to think of these variations as points on a continuous spectrum. I hope the following discussion will impress you as simpler.

What is the “mood spectrum?”

Until very recently, depression and “manic-depressive illness” were understood as completely independent: a patient either had one or the other. Now the two are seen by most mood specialists as two extremes on a continuum, with variations found at all points in between, even though only some points have names (e.g. Ghaemi; Pies; Moller; BirMaer; SKeppar; Mackinnon; Angst  Cassano; my ISBD in 2008; and 2014 updates.)

On the left, the “unipolar” extreme represents straightforward depression with no complications. There are many forms of depression, of course (see  “What kinds of Depressions are there“). The depressions discussed further below are of a more genetic, or “chemical” nature; versus those of a more situational type, like losing a loved one. Situational depressions may respond well to time or therapy and not require “bipolar” thinking.
On the right, the “manic-depressive” extreme is defined by the presence of manic episodes, just the kind that most people have seen or heard of:  full delusional mania. But in between these extremes is a large area which some mood experts think might be the most common form of bipolar disorder: the green zone below.Angst

Got all that?  It gets trickier yet.  Consider the points A and B on this spectrum:
Point A on the continuum describes people who have a complex depression but who still respond well to antidepressant medication or psychotherapy. Around point B, however, there is some sort of threshold where these approaches are no longer completely or continuously effective: either they don’t work at all, offer only partial relief, or help for a while then “stop working” (which may account for some or much of “Prozac poop-out”, now regarded as a non-manic marker of bipolar disorder, described below).
Until 1994 and the publication of the DSM-IV, there was no official name for all the variations betweenB and the “manic-depressive” extreme. It was as though these variations did not exist. In the minds of a few, they still don’t, including some psychiatrists who have not adopted this new “spectrum” way of thinking about diagnosis. The DSM does not describe this “spectrum” concept. In it, the entire span between blue and green is still “Major Depression”, the same as the violet end to your left. Only the orange and red zones are clearly “bipolar”.
Light green and yellow is BP NOS, Bipolar Not Otherwise Specified (or in the DSM5: BP-NEC, Not Elsewhere Classified). That diagnosis means you have something that looks like bipolar disorder but does not meet the criteria for BP II or BP I. Isn’t it simpler just to think of it as a continuum? That is much closer to reality. We see all sorts of variations in between these named points on the graph above.

What do “bipolar variations” look like?

Warning: this is controversional territory. Ironically, your diagnosis could be determined more by the professional whom you see than the symptoms you have. Really. Read that again. This happens all the time. If your therapist or nurse practitioner or doctor uses a DSM framework, and you don’t meet criterial for bipolar disorder, then you just don’t have bipolar disorder at all. Period.
On the other hand, if your therapist/NP/etc thinks in terms of a “spectrum” of bipolarity, then you could get a bipolar label that someone else might think was “overdiagnosis”. Starts to sound kind of ridiculous, doesn’t it?  But a lot of energy becomes focused here. “Bipolar” carries more stigma than “depression”. Many believe that antidepressants are less risky than mood stabilizers (that’s not so clear either, in my view). So the “yes-or-no” view is still very powerful. You could easily be told “you don’t have bipolar disorder” when someone else has said you do.  The solution is to learn more. Read on.
Roller coaster depression
Many people have forms of depression in which their symptoms vary a lot with time: “crash” into depression, then up into doing fine for a while, then “crash” again — sometimes for a reason, but often for no clear reason at all. They feel like they are on some sort of mood “roller coaster”. They wonder if they have “manic-depression”. But, most people know someone or have heard of someone who had a “manic” episode: decreased need for sleep, high energy, risky behaviors, or even grandiose delusions (“I can make millions with my ideas”; “I have a mission in space”; “I’m a special representative for God”). So they think “well, I can’t have that — I’ve never had a manic episode”.
However, a spectrum view of mood disorders  invites you to reconsider. Hypomania doesn’t look or feel at all like full delusional mania in some patients. Sometimes there is just a clear sense of something cyclic going on. (For a striking version of this, read a patient’s count).
Some mood disorder experts consider depression that occurs repeatedly to have a high likelihood of having a manic phase at some point Fawcet, especially if the first depression occurred before age twenty. Geller, Rao These two features–repeated recurrence, and early onset–are also included among the non-manic markers below: not enough to make a diagnosis, but suggestive, especially if they occur with several other such signs  (even if “hypomania” is not detectable at all).
Depression with profound anxiety
Many people live with anxiety so severe, their depression is not the main problem. They seem to handle the periods of low energy, as miserable as they are. Often they sleep for 10, 12, even 14 hours a day during those times. But the part they can’t handle is the anxiety: it isn’t “good energy”. Many say they feel as though they just have too much energy pent up inside their bodies. They can’t sit still. They pace. And worst of all, their minds “race” with thoughts that go over and over the same thing to no purpose. Or they fly from one idea to the next so fast their thoughts become “unglued”, and they can’t think their way from A to C let alone A to Z.
When this is severe, people who enjoy books can find themselves completely unable to read: they just go over and over the same paragraph and it doesn’t “sink in”. They will get some negative idea in their head and go around and around with it until it completely dominates their experience of the world. Usually these “high negative energy” phases come along with severely disturbed sleep (see Depression with Severe Insomnia, below). Thoughts about suicide are extremely common and the risk may be high.Fawcett
Depressive episodes with irritable episodes
Many people with depression go through phases in which even they can recognize that their anger is completely out of proportion to the circumstance that started it. They “blow up” over something trivial. Those close to them are very well aware of the problem, of course. Many women can experience this as part of “PMS“. As their mood problems become more severe, they find themselves having this kind of irritability during more and more of their cycle. Similarly, when they get better with treatment, often the premenstrual symptoms are the “last to go”. Others can have this kind of cyclic irritability without any relationship to hormonal cycles. Many men with bipolar variations say they have problems with anger or rage.
Depression that doesn’t respond to antidepressants (or gets worse, or “poops out”)
Many people have repeated episodes of depression. Sometimes the first several episodes respond fairly well to antidepressant medication, but after a while the medications seem to “stop working”. For others, no antidepressant ever seems to work. And others find that some antidepressants seem to make them feel terrible: not just mild side effects, but severe reactions, especially severe agitation. These people feel like they’re “going crazy”. Usually at this time they also have very poor sleep. Many people have the odd experience of feeling the depression actually improve with antidepressants, yet overall —perhaps even months later —they somehow feel worse overall. In most cases this “worse” is due to agitation, irritability, and insomnia.
In some cases, an antidepressant works extremely well at first, then “poops out”.Byrne The benefits usually last several weeks, often months, and occasionally even years before this occurs. When this occurs repeatedly with different antidepressants, that may mark a “bipolar” disorder even when little else suggests the diagnosis.SHarma
Depression with periods of severe insomnia
Finally, there are people with depression whose most noticeable symptom is severe insomnia. These people can go for days with 2-3 hours of sleep per night. Usually they fall asleep without much delay, but wake up 2-4 hours later and the rest of the night, if they get any more sleep at all, is broken into 15-60 minute segments of very restless, almost “waking” sleep. Dreams can be vivid, almost real. They finally get up feeling completely unrested. Note that this is not “decreased need for sleep” (the Bipolar I pattern). These people want desperately to sleep better and are very frustrated.

Non-manic markers of bipolarity? Even with no hypomania at all?

You have probably figured it out by now: making a diagnosis of bipolar disorder can be pretty tricky sometimes!  You’re about to read a list of eleven more factors that have been associated with
bipolar disorder. None of these factors “clinches” the diagnosis. They are suggestive of bipolarity, but not sufficient to establish it. They are best regarded as markers which suggest considering bipolar disorder as a possible explanation for symptoms. They are not a scoring system, where you might think “the more I have of these, the more likely it is that I have bipolar disorder.” That way of thinking about these factors has not been tested.
Here’s the list of items which are found with bipolar disorder more often than you would expect by chance alone. The particular list below is adapted from a landmark article by Drs. Ghaemi and Goodwin and Ko.  (Drs. Goodwin and Ghaemi are among the most respected authorities on bipolar diagnosis in the world.
[list=”border: 0px; font-family: Lato, sans-serif; font-size: 16px; margin: 16px 0px 16px 20px; outline: 0px; padding-right: 0px; padding-left: 0px; vertical-align: baseline; color: rgb(43, 43, 43); line-height: 24px; background-color: rgb(255, 255, 255);”]
[*]The patient has had repeated episodes of major depression (four or more; seasonal shifts in mood are also common).

[*]The first episode of major depression occurred before age 25 (some experts say before age 20, a few before age 18; most likely, the younger you were at the first episode, the more it is that bipolar disorder, not “unipolar”, was the basis for that episode).

[*]A first-degree relative (mother/father, brother/sister, daughter/son) has a diagnosis of bipolar disorder.

[*]When not depressed, mood and energy are a bit higher than average, all the time (“hyperthymicpersonality”).

[*]When depressed, symptoms are “atypical”: extremely low energy and activity; excessive sleep (e.g. more than 10 hours a day); mood is highly reactive to the actions and reactions of others; and (the weakest such sign) appetite is more likely to be increased than decreased.  Some experts think that carbohydrate craving and night eating are variants of this appetite effect.

[*]Episodes of major depression are brief, e.g. less than 3 months.

[*]The patient has had psychosis (loss of contact with reality) during an episode of depression.

[*]The patient has had severe depression after giving birth to a child (“postpartum depression“).

[*]The patient has had hypomania or mania while taking an antidepressant (remember, severe
irritability, difficulty sleeping, and agitation may — but do not always — qualify for “hypomania”).

[*]The patient has had loss of response to an antidepressant (sometimes called “Prozac Poop-out”):  it worked well for a while then the depression symptoms came back, usually within a few months.

[*]Three or more antidepressants have been tried, and none worked.

[/list]

Bipolarity with no hypomania at all? (!)

There is a very radical idea buried in the above 11 items, which we should look at before going on. But be aware that this idea is likely be dismissed with a “hmmmph” by many  practicing psychiatrists. The idea is this: Dr. Ghaemi and colleagues propose that there might be a version of “bipolar disorder” that does not have any mania at all, not even hypomania. They call it “bipolar spectrum disorder”.
This is strange, you are saying to yourself. “Don’t you have to have some hypomania in order to be bipolar?  How could it be ‘bi’ – polar if there is no other pole!?”
But Dr. Ghaemi and colleagues assert that there are versions of depression that end up acting more like bipolar disorder, even though there is no hypomania at all that we can detect (or, as in item #9, only when an antidepressant has been used). These conditions often do not respond well, in the long run, to antidepressant medications (which “poop out” or actually start making things worse). They respond better to the medications we routinely rely on in bipolar disorder, the “mood stabilizers” you’ll be introduced to in the Treatment section of this website (including several non-medication approaches). And these patients have other folks in their family with bipolar disorder or something that looks rather more like that (e.g. dramatic “mood swings”, even if the person never really gets ill enough to need treatment).
In Dr. Ghaemi’s description, then, there are people whose depression looks so “unipolar” that even a “fine-toothed comb” approach to looking for hypomania will not identify their depression as part of the “bipolar spectrum”. According to Ghaemi and colleagues, these people should be regarded as “bipolar”,in a sense, because of the way they will end up responding to treatment. In other words, there is something in these people which doesn’t look like our old idea of bipolar disorder, or even our newer idea of bipolar disorder (bipolar II, etc.), but will still better describe their future and the medications that are most likely to help them.
Remember that this is the very purpose of “diagnosis”, to describe the likely outcomes with and without treatment, and to identify effective treatments. So, on that basis, it seems reasonable to include these patients on the “bipolar spectrum”, like this:

The idea that someone can “have” bipolar disorder and yet not have any hypomania at all is not widely understood. You probably would get blank looks from most psychiatrists if you mention it, and frank disbelief from nearly all primary care doctors, who don’t have time to read the literature on the diagnosis of bipolar disorder. So, if you mention this idea to anyone, be prepared for some serious resistance.
Here’s some ammunition for you (nice soft paper bullets…) . As of 2005 the Harvard-associated Mood Disorder program started using this approach to diagnosis. They call it the Bipolar Index.
More:  Other researchers are also beginning to use the same framework of thought. For example, one research group just reported that patients with migraine headaches are much more likely to have these bipolar spectrum traits.Odegaard (Migraines are much more common in patients with unipolar and Bipolar II than in Bipolar I, interestingly.Fasmer) One recent summary article for primary care doctors, about bipolar disorder, discusses these “soft signs” in considerable detail.SWANN
More: The concept of a bipolar “spectrum” is supported by work from a research group calling themselves the Spectrum Project.

More?  Consider the sources.  Dr. Ghaemi was the chairman of the Committee on Diagnosis for the International Society for Bipolar Disorder. His co-author is Dr. Frederick Goodwin, who wrote the “bible” of bipolar disorder for our lifetime (Manic-Depressive Illness, with Dr. Kay Jamison). These are highly respected researchers amongst mood experts.   Dr. Ghaemi emphasizes the need to rely onevidence in all his papers on diagnosis and treatment and is very frequently cited by other authors on this topic.  You’ll see quite a few references to him on this website. But he is certainly not the only such voice, as I hoped you’ve noticed from all the references linked so far.

Bipolarity Index Table

The Bipolarity Index: a 5-dimension, 100-pt. system

Sometimes referred to as Psychiatric or Psychological Disorders, Mental Health Disorders are caused by complex interactions between physical, Psychological, social, cultural, and hereditary influences. They involve disturbances in thinking, emotion, and/or behavior. Small disturbances in these aspects of life are common, but when such disturbances distress the person greatly, interfere with daily life, or both, they are considered Mental Illness or a Mental Health disorder. The effects of Mental Illness may be long-lasting or temporary.
Bipolar or Manic Depressive Disorder as well as other Mental Health Diagnosis cause Radical Emotional changes and Mood Swings, from Manic Highs to Depressive Lows. The majority of individuals experience alternating episodes of Mania, Depression, and etc. are from a minor state of life, to lifelong disability.

MENTAL HEALTH DIAGNOSIS:

Mental health (psychiatric or psychological) disorders involve disturbances in thinking, emotion, and/or behavior. Small disturbances in these aspects of life are common, but when such disturbances distress the person greatly and/or interfere with daily life, they are considered mental illness or a mental health disorder. The effects of mental illness may be long-lasting or temporary. These disorders are caused by complex interactions between physical, Psychological, Social, Cultural, and Hereditary Influences.

OVERVIEW OF MOOD DISORDERS:
Mood disorders are mental health disorders that involve emotional disturbances consisting of long periods of excessive sadness (depression), excessive joyousness or elation (mania), or both. Depression and mania represent the two extremes, or poles, of mood disorders.

Mood disorders are emotional disturbances consisting of prolonged periods of excessive sadness, excessive joyousness, or both. Mood disorders are categorized as depressive or bipolar. Anxiety and related disorders.
Sadness and joy (elation) are part of everyday life. Sadness is a universal response to defeat, disappointment, and other discouraging situations. Joy is a universal response to success, achievement, and other encouraging situations. Grief, a form of sadness, is considered a normal emotional response to a loss. Bereavement refers specifically to the emotional response to death of a loved one.

A mood disorder is diagnosed when sadness or elation is overly intense and persistent, is accompanied by a requisite number of other mood disorder symptoms, and significantly impairs the person’s capacity to function. In such cases, intense sadness is termed depression, and intense elation is termed mania. Depressive disorders are characterized by depression; bipolar disorders are characterized by varying combinations of depression and mania.
Lifetime risk of suicide (see Suicidal Behavior) for people with a depressive disorder is 2 to 15%, depending on severity of the disorder.

Risk is further increased in the following cases:

At the start of treatment, when psycho-motor activity is returning to normal but mood is still dark
During mixed bipolar states
At personally significant anniversaries
By severe anxiety
By alcohol and substance use

Other complications include disability ranging from mild to complete inability to function, maintain social interaction, and participate in routine activities; impaired food intake; severe anxiety; alcoholism; and other drug dependencies.

Bipolar Disorder and other serious “Brain Diseases” are an extreme challenge for the individual and the entire family. Depression is an Illness that involves the body, mood, and thoughts. It affects how one eats, and sleeps, the way one feels about oneself, and the way one thinks about things!
The information here should not be used as a substitute for seeking medical care for diagnose or treatment.

Borderline personality disorder is characterized by a pervasive pattern of instability and hypersensitivity in interpersonal relationships, instability in self-image, extreme mood fluctuations, and impulsivity. Diagnosis is by clinical criteria. Treatment is with psychotherapy and drugs.

Patients with borderline personality disorder have an intolerance of being alone; they make frantic efforts to avoid abandonment and generate crises, such as making suicidal gestures in a way that invites rescue and caregiving by others.

Reported prevalence of borderline personality disorder varies but is probably between 1.7 to 3% in the general population, but up to 15 to 20% in patients being treated for mental health disorders. In clinical settings, 75% of patients with this disorder are female, but in the general population, the ratio of men to women is 1:11

Etiology

Stresses during early childhood may contribute to the development of borderline personality disorder. A childhood history of physical and sexual abuse, neglect, separation from caregivers, and/or loss of a parent is common among patients with borderline personality disorder.

Certain people may have a genetic tendency to have pathologic responses to environment life stresses, and borderline personality disorder clearly appears to have a heritable component. First-degree relatives of patients with borderline personality disorder are 5 times more likely to have the disorder than the general population. Disturbances in regulatory functions of the brain and neuropeptide systems may also contribute but are not present in all patients with borderline personality disorder.

Symptoms and Signs

When patients with borderline personality disorder feel that they are being abandoned or neglected, they feel intense fear or anger. For example, they may become panicky or furious when someone important to them is a few minutes late or cancels an engagement. They think that this abandonment means that they are bad. They fear abandonment partly because they do not want to be alone.

These patients tend to change their view of others abruptly and dramatically. They may idealize a potential caregiver or lover early in the relationship, demand to spend a lot of time together, and share everything. Suddenly, they may feel that the person does not care enough, and they become disillusioned; then they may belittle or become angry with the person. This shift from idealization to devaluation reflects black-and-white thinking (splitting, polarization of good and bad).

Patients with borderline personality disorder can empathize with and care for a person but only if they feel that another person will be there for them whenever needed.

Patients with this disorder have difficulty controlling their anger and often become inappropriate and intensely angry. They may express their anger with biting sarcasm, bitterness, or angry tirades, often directed at their caregiver or lover for neglect or abandonment. After the outburst, they often feel ashamed and guilty, reinforcing their feeling of being bad.

Patients with borderline personality disorder may also abruptly and dramatically change their self-image, shown by suddenly changing their goals, values, opinions, careers, or friends. They may be needy one minute and righteously angry about being mistreated the next. Although they usually see themselves as bad, they sometimes feel that they do not exist at all—eg, when they do not have someone who cares for them. They often feel empty inside.

The changes in mood (eg, intense dysphoria, irritability, anxiety) usually last only a few hours and rarely last more than a few days; they may reflect the extreme sensitivity to interpersonal stresses in patients with borderline personality disorder.

Patients with borderline personality disorder often sabotage themselves when they are about to reach a goal. For example, they may drop out of school just before graduation, or they may ruin a promising relationship.

Impulsivity leading to self-harm is common. These patients may gamble, engage in unsafe sex, binge eat, drive recklessly, abuse substances, or overspend. Suicidal behaviors, gestures, and threats and self-mutilation (eg, cutting, burning) are very common. Although many of these self-destructive acts are not intended to end life, risk of suicide in these patients is 40 times that of the general population; About 8 to 10% of these patients die by suicide. These self-destructive acts are usually triggered by rejection by, possible abandonment by, or disappointment in a caregiver or lover. Patients may self-mutilate to compensate for their being bad or to reaffirm their ability to feel during a dissociative disorder.

Dissociative episodes, paranoid thoughts, and sometimes psychotic-like symptoms (eg, hallucinations, ideas of reference) may be triggered by extreme stress, usually fear of abandonment, whether real or imagined. These symptoms are temporary and usually not severe enough to be considered a separate disorder.

Symptoms lessen in most patients; relapse rate is very low. However, functional status does not usually improve as dramatically.

Diagnosis:

Clinical criteria ( Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition [DSM-5])

For a diagnosis of borderline personality disorder, patients must have persistent pattern of unstable relationships, self-image, and emotions (ie, emotional dysregulation) and pronounced impulsivity, as shown by ≥ 5 of the following:

• Desperate efforts to avoid abandonment (actual or imagined)
• Unstable, intense relationships that alternate between idealizing and devaluing the other person
• An unstable self-image or sense of self
• Impulsivity in ≥ 2 areas that could harm themselves (eg, unsafe sex, binge eating, reckless driving)
• Repeated suicidal behavior, gestures, or threats or self-mutilation
• Rapid changes in mood, lasting usually only a few hours and rarely more than a few days
• Persistent feelings of emptiness
• Inappropriately intense anger or problems controlling anger
• Temporary paranoid thoughts or severe dissociative symptoms triggered by stress

Also, symptoms must have begun by early adulthood but can occur during adolescence.

Differential diagnosis

Borderline personality disorder is most commonly misdiagnosed as bipolar disorder because of the wide fluctuations in mood, behavior, and sleep. However, in borderline personality disorder, mood and behavior change rapidly in response to stressors, especially interpersonal ones, whereas in bipolar disorder, moods are more sustained and less reactive.

Other personality disorders share similar manifestations. Patients with histrionic personality disorder or narcissistic personality disorder can be attention-seeking and manipulative, but those with borderline personality disorder also see themselves as bad and feel empty. Some patients meet criteria for more than one personality disorder.

Borderline personality disorder can be distinguished from mood and anxiety disorders based on the negative self-image, insecure attachments, and sensitivity to rejection that are prominent features of borderline personality disorder and are usually absent in patients with a mood or anxiety disorder.

Differential diagnosis for borderline personality disorder also includes substance abuse disorders and posttraumatic stress disorder; many disorders in the differential diagnosis of borderline personality disorder coexist with it.

 
Treatment

• Psychotherapy
• Drugs

General Treatment of borderline personality disorder is the same as that for all personality disorders.

Identifying and treating coexisting disorders is important for effective treatment of borderline personality disorder.

Psychotherapy

The main treatment for borderline personality disorder is psychotherapy.

Many psychotherapeutic interventions are effective in reducing suicidal behaviors, ameliorating depression, and improving function in patients with this disorder.

Cognitive-behavioral therapy focuses on emotional dysregulation and lack of social skills. It includes the following:

• Dialectical behavioral therapy (a combination of individual and group sessions with therapists acting as behavior coaches and available on call around the clock)
• Systems training for emotional predictability and problem solving (STEPPS)

Other interventions focus on disturbances in the ways patients emotionally experience themselves and others. These interventions include the following:

• Mentalization-based treatment
• Transference-focused psychotherapy
• Schema-focused therapy

Mentalization refers to people’s ability to reflect on and understand their own state of mind and the state of mind of others. Mentalization is thought to be learned through a secure attachment to the caregiver. Mentalization-based treatment helps patients do the following:

• Effectively regulate their emotions (eg, calm down when upset)
• Understand how they contribute to their problems and difficulties with others
• Reflect on and understand the minds of others

It thus helps them relate to others with empathy and compassion.

Transference-focused psychotherapy centers on the interaction between patient and therapist. The therapist asks questions and helps patients think about their reactions so that they can examine their exaggerated, distorted, and unrealistic images of self during session. The current moment (eg, how patients are relating to their therapist) is emphasized rather than the past. For example, when a timid, quiet patient suddenly becomes hostile and argumentative, the therapist may ask whether the patient noticed a shift in feelings and then ask the patient to think about how the patient was experiencing the therapist and self when things changed. The purpose is

• To enable patients to develop a more stable and realistic sense of self and others
• To relate to others in a healthier way through transference to the therapist

Schema-focused therapy is an integrative therapy that combines cognitive-behavioral therapy, attachment theory, psychodynamic concepts, and emotion-focused therapies. It focuses on lifelong maladaptive patterns of thinking, feeling, behaving and coping (called schemas), affective change techniques, and the therapeutic relationship, with limited reparenting. The purpose is help patients change their schemas. Therapy has 3 stages:

• Assessment: Identifying the schemas
• Awareness: Recognizing the schemas when they are operating in daily life
• Behavioral change: Replacing negative thoughts, feelings, and behaviors with healthier ones

Some of these interventions are specialized and require specialized training and supervision. However, some interventions do not; one such intervention, which is designed for the general practitioner, is

• General (or good) psychiatric management

This intervention uses individual therapy once a week and sometimes drugs.

Supportive psychotherapy is also useful. The goal is to establish an emotional, encouraging, supportive relationship with the patient and thus help the patient develop healthy defense mechanisms, especially in interpersonal relationships.

Drugs

Drugs work best when used sparingly and systematically for specific symptoms.

SSRIs are usually well-tolerated; chance of a lethal overdose is minimal. However, SSRIs are only marginally effective for depression and anxiety in patients with borderline personality disorder.

The following drugs are effective in ameliorating symptoms of borderline personality disorder:

• Mood stabilizers such as lamotrigine: For depression, anxiety, mood lability, and impulsivity
• Antipsychotics: For anxiety, anger, and cognitive symptoms, including transient stress-related cognitive distortions (eg, paranoid thoughts, black-and-white thinking, severe cognitive disorganization)

Benzodiazepines and stimulants also may help relieve symptoms but are not recommended because dependency and drug diversion are risks.

Last full review/revision January 2016 by Lois Choi-Kain, MD

Drugs Mentioned In This Article
Drug Name

• Select Brand Names
• lamotrigine
  LAMICTAL

Bipolar disorders are characterized by episodes of mania and depression, which may alternate, although many patients have a predominance of one or the other. Exact cause is unknown, but heredity, changes in the level of brain neurotransmitters, and psycho social factors may be involved. Diagnosis is based on history. Treatment consists of mood-stabilizing drugs, sometimes with psychotherapy.

Bipolar disorders usually begin in the teens, 20s, or 30s. Lifetime prevalence is about 4%. Rates of bipolar I disorder are about equal for men and women.

Bipolar disorders are classified as

• Bipolar I disorder: Defined by the presence of at least one full-fledged (ie, disrupting normal social and occupational function) manic episode and usually depressive episodes
• Bipolar II disorder: Defined by the presence of major depressive episodes with at least one hypo manic episode but no full-fledged manic episodes
• Unspecified bipolar disorder: Disorders with clear bipolar features that do not meet the specific criteria for other bipolar disorders

In cyclothymic disorder, patients have prolonged (> 2-yr) periods that include both hypo manic and depressive episodes; however, these episodes do not meet the specific criteria for a bipolar disorder.

Etiology

Exact cause is unknown. Heredity plays a significant role. There is also evidence of dys-regulation of serotonin and norepinephrine. Psycho social factors may be involved. Stressful life events are often associated with initial development of symptoms and later exacerbations, although cause and effect have not been established.

Certain drugs can trigger exacerbations in some patients with bipolar disorder; these drugs include sympathomimetics (eg, cocaine, amphetamines), alcohol, and certain antidepressants (eg, tricyclics, MAOIs).

Symptoms and Signs[/size]

Bipolar disorder begins with an acute phase of symptoms, followed by a repeating course of remission and relapse. Remissions are often complete, but many patients have residual symptoms, and for some, the ability to function at work is severely impaired. Relapses are discrete episodes of more intense symptoms that are manic, depressive, hypomanic, or a mixture of depressive and manic features. Episodes last anywhere from a few weeks to 3 to 6 mo. Cycles—time from onset of one episode to that of the next—vary in length among patients. Some patients have infrequent episodes, perhaps only a few over a lifetime, whereas others have rapid-cycling forms (usually defined as ≥ 4 episodes/yr). Only a minority alternate back and forth between mania and depression with each cycle; in most, one or the other predominates to some extent.

Patients may attempt or commit suicide. Lifetime incidence of suicide in patients with bipolar disorder is estimated to be at least 15 times that of the general population.

Mania

A manic episode is defined as ≥ 1 wk of a persistently elevated, expansive, or irritable mood and persistently increased goal-directed activity or energy plus ≥ 3 additional symptoms:

• Inflated self-esteem or grandiosity
• Decreased need for sleep
• Greater talkativeness than usual
• Flight of ideas or racing of thoughts
• Distractibility
• Increased goal-directed activity
• Excessive involvement in activities with high potential for painful consequences (eg, buying sprees, foolish business investments)

Manic patients may be inexhaustibly, excessively, and impulsively involved in various pleasurable, high-risk activities (eg, gambling, dangerous sports, promiscuous sexual activity) without insight into possible harm. Symptoms are so severe that they cannot function in their primary role (occupation, school, housekeeping). Unwise investments, spending sprees, and other personal choices may have irreparable consequences.

Patients in a manic episode may be exuberant and flamboyantly or colorfully dressed and often have an authoritative manner with a rapid, unstoppable flow of speech. Patients may make clang associations (new thoughts that are triggered by word sounds rather than meaning). Easily distracted, patients may constantly shift from one theme or endeavor to another. However, they tend to believe they are in their best mental state. Lack of insight and an increased capacity for activity often lead to intrusive behavior and can be a dangerous combination. Interpersonal friction results and may cause patients to feel that they are being unjustly treated or persecuted. As a result, patients may become a danger to themselves or to other people. Accelerated mental activity is experienced as racing thoughts by patients and is observed as flights of ideas by the physician.

Manic psychosis is a more extreme manifestation, with psychotic symptoms that may be difficult to distinguish from schizophrenia. Patients may have extreme grandiose or persecutory delusions (eg, of being Jesus or being pursued by the FBI), occasionally with hallucinations. Activity level increases markedly; patients may race about and scream, swear, or sing. Mood liability increases, often with increasing irritability. Full-blown delirium (delirious mania) may appear, with complete loss of coherent thinking and behavior.

Hypomania

A hypo manic episode is a less extreme variant of mania involving a distinct episode that lasts ≥ 4 days with behavior that is distinctly different from the patient’s usual non depressed self and that includes ≥ 3 of the additional symptoms listed above under mania. During the hypo manic period, mood brightens, the need for sleep decreases, and psycho motor activity accelerates. For some patients, hypo manic periods are adaptive because they produce high energy, creativity, confidence, and super normal social functioning. Many do not wish to leave the pleasurable, euphoric state. Some function quite well, and in most, functioning is not markedly impaired. However, in some patients, hypo mania manifests as distractabilty, irritability, and labile mood, which the patient and others find less attractive.

Depression

A depressive episode has features typical of major depression (see Depressive Disorders); the episode must include ≥ 5 of the following during the same 2-wk period, and one of them must be depressed mood or loss of interest or pleasure:

• Depressed mood most of the day
• Markedly diminished interest or pleasure in all or almost all activities for most of the day
• Significant (> 5%) weight gain or loss or decreased or increased appetite
• Insomnia (often sleep-maintenance insomnia) or hyper somnia
• Psycho motor agitation or retardation observed by others (not self-reported)
• Fatigue or loss of energy
• Feelings of worthlessness or excessive or inappropriate guilt
• Diminished ability to think or concentrate or indecisiveness
• Recurrent thoughts of death or suicide, a suicide attempt, or specific plan for suicide

Psychotic features are more common in bipolar depression than in uni polar depression.

Mixed features

An episode of mania or hypo mania is designated as having mixed features if ≥ 3 depressive symptoms are present for most days of the episode. This condition is often difficult to diagnose and may shade into a continuously cycling state; the prognosis is worse than that in a pure manic or hypo manic state.

Risk of suicide during mixed episodes is particularly high.

Diagnosis

• Clinical criteria ( Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition)
• Thyroxine (T 4 ) and TSH levels to exclude hyperthyroidism
• Exclusion of stimulant drug abuse clinically or by urine testing

Diagnosis is based on identification of symptoms of mania or hypo mania as described above, plus a history of remission and relapse. Symptoms must be severe enough to markedly impair social or occupational functioning or to require hospitalization to prevent harm to self or others. Some patients who present with depressive symptoms may have previously experienced hypo mania or mania but do not report it unless they are specifically questioned. Skillful questioning may reveal morbid signs (eg, excesses in spending, impulsive sexual escapades, stimulant drug abuse), although such information is more likely to be provided by relatives. All patients must be asked gently but directly about suicidal ideation, plans, or activity.

Similar acute manic or hypo manic symptoms may result from stimulant abuse or physical disorders such as hyperthyroidism or pheochro mocytoma. A review of substance use (especially of amphetamines and cocaine) and urine drug screening can help identify drug causes. However, because drug use may simply have triggered an episode in a patient with bipolar disorder, seeking evidence of symptoms (manic or depressive) not related to drug use is important. But thyroid function testing (T 4 and TSH levels) is a reasonable screen for new patients. Patients with pheochromo cytoma are markedly hypertensive; if they are not, testing is not indicated.

Some patients with schizoaffective disorder (see Schizoaffective Disorder) have manic symptoms, but such patients rarely return to normal between episodes, and they, unlike most patients with mania, do not show interest in connecting with other people.

Patients with bipolar disorder may also have anxiety disorders (eg, social phobia, panic attacks, obsessive-compulsive disorders), possibly confusing the diagnosis.

Treatment

• Mood stabilizers (eg, lithium, certain anticonvulsants), a 2nd-generation antipsychotic, or both
• Support and psychotherapy

Treatment usually has 3 phases:

• Acute: To stabilize and control the initial, sometimes severe manifestations
• Continuation: To attain full remission
• Maintenance or prevention: To keep patients in remission

Although most patients with hypomania can be treated as outpatients, severe mania or depression often requires inpatient management.

Drugs for bipolar disorder include

• Mood stabilizers
• 2nd-generation antipsychotics

These drugs are used alone or in combination for all phases of treatment, although at different dosages.

Mood stabilizers consist of lithium and certain anticonvulsants, especially valproate, carbamazepine, andlamotrigine. Second-generation antipsychotics include aripiprazole, lurasidone, olanzapine, quetiapine,risperidone, and ziprasidone.

Specific antidepressants (eg, SSRIs) are sometimes added for severe depression, but their effectiveness is controversial; they are not recommended as sole therapy for depressive episodes.

Electroconvulsive therapy (ECT) is sometimes used for depression refractory to treatment and is also effective for mania. Phototherapy can be useful in treating seasonal bipolar I or bipolar II disorder (with autumn-winter depression and spring-summer hypomania). It is probably most useful as augmentative therapy.

Drug selection and use

Choice of drug can be difficult because all drugs have significant adverse effects, drug interactions are common, and no drug is universally effective. Selection should be based on what has previously been effective and well-tolerated in a given patient. If there is no prior experience (or it is unknown), choice is based on the patient’s medical history (vis-à-vis the adverse effects of the specific mood stabilizer) and the severity of symptoms.

For severe manic psychosis, in which immediate patient safety and management is compromised, urgent behavioral control usually requires a sedating 2nd-generation antipsychotic, sometimes supplemented initially with a benzodiazepine such as lorazepam or clonazepam 2 to 4 mg IM or po tid.

For less severe acute episodes in patients without contraindications (eg, renal disorders), lithium is a good first choice for both mania and depressive episodes. Because its onset is slow (4 to 10 days), patients with significant symptoms may also be given an anticonvulsant or a 2nd-generation antipsychotic. For those with depression, lamotrigine may be a good choice of anticonvulsant.

For bipolar depression, the best evidence suggests using quetiapine or lurasidone alone or the combination offluoxetine and olanzapine.

Once remission is achieved, preventive treatment with mood stabilizers is indicated for all bipolar I patients. If episodes recur during maintenance treatment, clinicians should determine whether adherence is poor and, if so, whether nonadherence preceded or followed recurrence. Reasons for nonadherence should be explored to determine whether a change in mood stabilizer type or dosing would render treatment more acceptable.

Lithium

As many as two thirds of patients with uncomplicated bipolar disorder respond to lithium, which attenuates bipolar mood swings but has no effect on normal mood. Whether lithium or another mood stabilizer is being used, breakthroughs are more likely in patients who have mixed states, rapid-cycling forms of bipolar disorder, comorbid anxiety, substance abuse, or a neurologic disorder.

Lithium carbonate is started at 300 mg po bid or tid and titrated, based on steady-state blood levels and tolerance, to a range of 0.8 to 1.2 mEq/L. Levels should be drawn after 5 days at a stable dose and 12 h after the last dose. Target drug levels for maintenance are lower, about 0.6 to 0.7 mEq/L. Higher maintenance levels are more protective against manic (but not depressive) episodes but have more adverse effects. Adolescents, whose glomerular function is excellent, need higher doses; elderly patients need lower doses.

Lithium can cause sedation and cognitive impairment directly or indirectly (by causing hypothyroidism) and often exacerbates acne and psoriasis. The most common acute, mild adverse effects are fine tremor, fasciculation, nausea, diarrhea, polyuria, polydipsia, and weight gain (partly attributed to drinking high-calorie beverages). These effects are usually transient and often respond to decreasing the dose slightly, dividing the dose (eg, tid), or using slow-release forms. Once dosage is established, the entire dose should be given after the evening meal. This dosing may improve adherence. A β-blocker (eg, atenolol 25 to 50 mg po once/day) can control severe tremor; however, some β-blockers (eg, propranolol) may worsen depression.

Acute lithium toxicity is manifested initially by gross tremor, increased deep tendon reflexes, persistent headache, vomiting, and confusion and may progress to stupor, seizures, and arrhythmias. Toxicity is more likely to occur in elderly patients, in patients with decreased creatinine clearance, and in those with Na loss (eg, due to fever, vomiting, diarrhea, or use of diuretics). Thiazide diuretics, ACE inhibitors, and NSAIDs other thanaspirin may contribute to hyperlithemia. Lithium blood levels should be measured every 6 mo and whenever the dose is changed.

Long-term effects include hypothyroidism, particularly when there is a family history of hypothyroidism, and renal damage involving the distal tubule (mainly in patients with a history of renal parenchymal disease). Therefore, TSH levels should be monitored when lithium is started and annually thereafter if there is a family history of thyroid dysfunction or every other year for all other patients. Levels should also be measured whenever symptoms suggest thyroid dysfunction (including when mania recurs) because hypothyroidism may blunt the effect of mood stabilizers. BUN and creatinine should be measured at baseline, 2 or 3 times during the first 6 mo, and then once or twice a year.

Anticonvulsants

Anticonvulsants that act as mood stabilizers, especially valproate and carbamazepine, are often used for acute mania and for mixed states (mania and depression). Lamotrigine is effective for mood-cycling and for depression. The precise mechanism of action for anticonvulsants in bipolar disorder is unknown but may involve γ-aminobutyric acid mechanisms and ultimately G-protein signaling systems. Their main advantages over lithium include a wider therapeutic margin and lack of renal toxicity.

For valproate , a loading dose of 20 mg/kg is given, then 250 to 500 mg po tid (extended-release formulation can be used); target blood levels are between 50 and 125 μg/mL. This approach does not result in more adverse effects than does gradual titration. Adverse effects include nausea, headache, sedation, dizziness, and weight gain; rare serious effects include hepatotoxicity and pancreatitis.

Carbamazepine should not be loaded; it should be started at 200 mg po bid and be increased gradually in 200-mg/day increments to target levels between 4 and 12 μg/mL (maximum, 800 mg bid). Adverse effects include nausea, dizziness, sedation, and unsteadiness. Very severe effects include aplastic anemia and agranulocytosis.

Lamotrigine is started at 25 mg po once/day for 2 wk, then 50 mg once/day for 2 wk, then 100 mg/day for 1 wk, and then can be increased by 50 mg each week as needed up to 200 mg once/day. Dosage is lower for patients taking valproate and higher for patients taking carbamazepine. Lamotrigine can cause rash and, rarely, the life-threatening Stevens-Johnson syndrome (see Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)), particularly if the dosage is increased more rapidly than recommended. While taking lamotrigine, patients should be encouraged to report any new rash, hives, fever, swollen glands, sores in the mouth and on the eyes, and swelling of the lips or tongue.

Antipsychotics

Acute manic psychosis is being increasingly managed with 2nd-generation antipsychotics, such as risperidone(usually 4 to 6 mg po once/day), olanzapine (usually 10 to 20 mg po once/day), quetiapine (200 to 400 mg po bid), ziprasidone (40 to 80 mg po bid), and aripiprazole (10 to 30 mg po once/day). In addition, evidence suggests that these drugs may enhance the effects of mood stabilizers after the acute phase.

Although any of these drugs may have extrapyramidal adverse effects and cause akathisia, risk is lower with more sedating drugs such as quetiapine and olanzapine. Less immediate adverse effects include substantial weight gain and development of the metabolic syndrome (including weight gain, excess abdominal fat, insulinresistance, and dyslipidemia); risk may be lower with the least sedating 2nd-generation antipsychotics,ziprasidone and aripiprazole. For extremely hyperactive psychotic patients with poor food and fluid intake, an antipsychotic given IM plus supportive care in addition to lithium or an anticonvulsant may be appropriate.

Precautions during pregnancy

Lithium use during pregnancy has been associated with an increased risk of cardiovascular malformations (particularly Ebstein anomaly). However, the absolute risk of this particular malformation is quite low. Takinglithium during pregnancy appears to increase the relative risk of any congenital anomaly by about 2-fold, a risk similar to the 2- to 3-fold increased risk of congenital anomalies associated with use of carbamazepine orlamotrigine and is substantially lower than the risk associated with use of valproate. Valproate appears to increase risk of neural tube defects and autism spectrum disorders.

Extensive study of the use of 1st-generation antipsychotics and tricyclic antidepressants during early pregnancy has not revealed causes for concern. The same appears to be true of SSRIs,  Data about the risks of 2nd-generation anti psychotics to the fetus are sparse as yet, even though these drugs are being more widely used for all phases of bipolar disorder.

Use of drugs before parturition may have carry-over effects on neonates.

Treatment decisions are complicated by the fact that with unplanned pregnancy, teratogenic effects may already have taken place by the time practitioners become aware of the issue. Consultation with a perinatal psychiatrist should be considered. In all cases, discussing the risks and benefits of treatment with patients is important.

Education and psychotherapy

Enlisting the support of loved ones is crucial to preventing major episodes. Group therapy is often recommended for patients and their partner; there, they learn about bipolar disorder, its social sequelae, and the central role of mood stabilizers in treatment. Individual psychotherapy may help patients better cope with problems of daily living and adjust to a new way of identifying themselves.

Patients, particularly those with bipolar II disorder, may not adhere to mood-stabilizer regimens because they believe that these drugs make them less alert and creative. The physician can explain that decreased creativity is relatively uncommon because mood stabilizers usually provide opportunity for a more even performance in interpersonal, scholastic, professional, and artistic pursuits.

Patients should be counseled to avoid stimulant drugs and alcohol, to minimize sleep deprivation, and to recognize early signs of relapse. If patients tend to be financially extravagant, finances should be turned over to a trusted family member. Patients with a tendency to sexual excesses should be given information about conjugal consequences (eg, divorce) and infectious risks of promiscuity, particularly AIDS.

Support groups (eg, the Depression and Bipolar Support Alliance [ DBSA } can help patients by providing a forum to share their common experiences and feelings.

Key Points

Bipolar disorder is a cyclic condition that involves episodes of mania with or without depression (bipolar 1) or hypomania plus depression (bipolar 2).

• Bipolar disorder markedly impairs the ability to function at work and to interact socially, and risk of suicide is significant; however, mild manic states (hypomania) are sometimes adaptive because they can produce high energy, creativity, confidence, and supernormal social functioning.
• Length and frequency of cycles vary among patients; some patients have only a few over a lifetime, whereas others have ≥ 4 episodes/yr (rapid-cycling forms).
• Only a few patients alternate back and forth between mania and depression during each cycle; in most cycles, one or the other predominates.
• Diagnosis is based on clinical criteria, but stimulant abuse and physical disorders such as hyperthyroidism or pheochromocytoma must be ruled out by examination and testing.
• Treatment depends on the manifestations and their severity but typically involves mood stabilizers.

Last full review/revision November 2013 by William Coryell, MD