What is Bipolar Disorder?

Bipolar disorder, also known as manic depression, is a mental illness that brings severe high and low
moods and changes in sleep, energy, thinking, and behavior.
People who have bipolar disorder can have periods in which they feel overly happy and energized
and other periods of feeling very sad, hopeless, and sluggish. In between those periods, they usually
feel normal. You can think of the highs and the lows as two "poles" of mood, which is why it's called
"bipolar" disorder.
The word "manic" describes the times when someone with bipolar disorder feels overly excited and
confident. These feelings can also involve irritability and impulsive or reckless decision-making.
About half of people during mania can also have delusions (believing things that aren't true and that
they can't be talked out of) or hallucinations (seeing or hearing things that aren't there).
"Hypomania" describes milder symptoms of mania, in which someone does not have delusions or
hallucinations, and their high symptoms do not interfere with their everyday life.
The word "depressive" describes the times when the person feels very sad or depressed. Those
symptoms are the same as those described in major depressive disorder or "clinical depression," a
condition in which someone never has manic or hypomanic episodes.
Most people with bipolar disorder spend more time with depressive symptoms than manic or
hypomanic symptoms.

Types of Bipolar Disorder

There are a few types of bipolar disorder, including:
Bipolar I disorder: With this type, you have extreme erratic behavior, with manic “up” periods that
last at least a week or are so severe that you need medical care. There are also usually extreme
“down” periods that last at least 2 weeks. 
Bipolar II disorder: With this type, you also have erratic highs and lows, but it isn’t as extreme as
bipolar I.
Cyclothymic disorder: This type involves periods of manic and depressive behavior that last at least
2 years in adults or 1 year in children and teens. The symptoms aren’t as intense as bipolar disorder I
or bipolar disorder II.
With any type of bipolar disorder, misuse of drugs and alcohol use can lead to more episodes.
Having bipolar disorder and alcohol use disorder, known as “dual diagnosis,” requires help from a
specialist who can address both issues. 

Symptoms
In bipolar disorder, the dramatic episodes of high and low moods do not follow a set pattern.
Someone may feel the same mood state (depressed or manic) several times before switching to
the opposite mood. These episodes can happen over a period of weeks, months, and sometimes
even years.
How severe it gets differs from person to person and can also change over time, becoming more
or less severe.
Symptoms of mania ("the highs"):
 Excessive happiness, hopefulness, and excitement
 Sudden changes from being joyful to being irritable, angry, and hostile
 Restlessness
 Rapid speech and poor concentration
 Increased energy and less need for sleep
 Unusually high sex drive
 Making grand and unrealistic plans
 Showing poor judgment
 Drug and alcohol abuse
 Becoming more impulsive
 Less need for sleep
 Less of an appetite
 Larger sense of self-confidence and well-being
 Being easily distracted
During depressive periods ("the lows"), a person with bipolar disorder may have:
 Sadness
 Loss of energy
 Feelings of hopelessness or worthlessness
 Not enjoying things they once liked
 Trouble concentrating
 Forgetfulness
 Talking slowly
 Less of a sex drive
 Inability to feel pleasure
 Uncontrollable crying
 Trouble making decisions
 Irritability
 Needing more sleep
 Insomnia
 Appetite changes that make you lose or gain weight
 Thoughts of death or suicide
 Attempting suicide

Causal Factors in Bipolar Disorders

As for unipolar disorders, a host of causal factors for bipolar disorder have been posited over the
past century. However, biological causal factors are clearly dominant, and the role of
psychological causal factors has received significantly less attention. The majority of research
has focused on bipolar I disorder, which is what we focus on here.

Biological Causal Factors

Genetic Influences
There is a greater genetic contribution to bipolar I disorder than to unipolar disorder. A summary
of studies using refined diagnostic procedures suggests that about 8 to 10 percent of the first-
degree relatives of a person with bipolar I illness can be expected to have bipolar disorder,
relative to 1 percent in the general population. The first-degree relatives of a person with bipolar
disorder are also at elevated risk for unipolar major depression (especially atypical depression),
although the reverse is not true.

Although family studies cannot by themselves establish a genetic basis for the disorder, results
from twin studies dating back to the 1950s also point to a genetic basis because the concordance
rates for these disorders are much higher for identical than for fraternal twins. For example, one
review found that the average concordance rate was about 60 percent for monozygotic twins and
about 12 percent for dizygotic twins. The best study to date found that 67 percent of
monozygotic twins with bipolar disorder had a co-twin who shared the diagnosis of bipolar or
unipolar disorder (60 percent of these concordant co-twins had bipolar disorder, and 40 percent
had unipolar disorder). The concordance rate in dizygotic twins was 19 percent. This and other
studies suggest that genes account for about 80 to 90 percent of the variance in the liability to
develop bipolar I disorder. This is higher than heritability estimates for unipolar disorder or any
of the other major adult psychiatric disorders, including schizophrenia. Moreover, genetic
influences are even stronger in early- as opposed to late-onset bipolar disorder. Efforts to locate
the chromosomal site(s) of the implicated gene or genes in this genetic transmission of bipolar
disorder suggest that it is polygenic. Although a great deal of research has been directed at
identifying candidate genes through linkage analysis and association studies, no consistent
support yet exists for any specific mode of genetic transmission of bipolar disorder, according to
several comprehensive reviews.

Neurochemical Factors
The early monoamine hypothesis for unipolar disorder was extended to bipolar disorder, the
hypothesis being that if depression is caused by deficiencies of norepinephrine or serotonin, then
perhaps mania is caused by excesses of these neurotransmitters. There is good evidence for
increased norepinephrine activity during manic episodes and less consistent evidence for lowered
norepinephrine activity during depressive episodes. However, serotonin activity appears to be
low in both depressive and manic phases. As noted earlier, norepinephrine, serotonin, and
dopamine are all involved in regulating our mood states. Evidence for the role of dopamine
stems in part from research showing that increased dopaminergic activity in several brain areas
may be related to manic symptoms of hyperactivity, grandiosity, and euphoria. High doses of
drugs such as cocaine and amphetamines, which are known to stimulate dopamine, also produce
manic-like behavior.

Abnormalities of Hormonal Regulatory Systems

Some neurohormonal research on bipolar disorder has focused on the HPA axis. Cortisol levels
are elevated in bipolar depression (as they are in unipolar depression), but they are usually not
elevated during manic episodes. Similarly, bipolar depressed patients show evidence of
abnormalities on the dexamethasone suppression test (DST) described earlier at about the same
rate as do unipolar depressed patients, and these abnormalities persist even when the patients
have been fully remitted and asymptomatic for at least 4 weeks. During a manic episode,
however, their rate of DST abnormalities has generally (but not always) been found to be much
lower. Research has also focused on abnormalities of the hypothalamic-pituitarythyroid axis
because abnormalities of thyroid function are frequently accompanied by changes in mood.
Many bipolar patients have subtle but significant abnormalities in the functioning of this axis,
and administration of thyroid hormone often makes antidepressant drugs work better. However,
thyroid hormone can also precipitate manic episodes in patients with bipolar disorder.

Neurophysiologic and Neuroanatomic Influences

With positron emission tomography (PET) scans, it is possible to visualize variations in brain
glucose metabolic rates in depressed and manic states, although there is far less evidence
regarding manic states because of the great difficulties studying patients who are actively manic.
Several summaries of the evidence from studies using PET and other neuroimaging techniques
show that, whereas blood flow to the left prefrontal cortex is reduced during depression, during
mania it is increased in certain other parts of the prefrontal cortex. Thus there are shifting
patterns of brain activity during mania and during depressed and normal moods.
Other neurophysiological findings from patients with bipolar disorder have shown both
similarities to and differences from patients with unipolar disorder and normal controls. For
example, several recent reviews suggest that there are deficits in activity in the prefrontal cortex
in bipolar disorder. These seem related to neuropsychological deficits that people with bipolar
disorder show in problem solving, planning, working memory, shifting of attention, and
sustained attention on cognitive tasks. This is similar to what is seen in unipolar depression, as
are deficits in the anterior cingulate cortex. However, structural imaging studies suggest that
certain subcortical structures, including the basal ganglia and amygdala, are enlarged in bipolar
disorder but reduced in size in unipolar depression. The decreases in hippocampal volume that
are often observed in unipolar depression are generally not found in bipolar depression. Some
studies using fMRI also find increased activation in bipolar patients in subcortical brain regions
involved in emotional processing, such as the thalamus and amygdala, relative to unipolar
patients and normal. Overall, it is hard to draw firm conclusions in this area yet because there are
so many inconsistencies in results across studies. However, there is initial metaanalytic support
for dysregulation in frontal-limbic activation in individuals with bipolar disorder compared to
controls. Hopefully more definitive findings will follow when much-needed technological
innovations unfold.

Sleep and Other Biological Rhythms

There is considerable evidence regarding disturbances in biological rhythms such as circadian
rhythms in bipolar disorder, even after symptoms have mostly remitted. During manic episodes,
patients with bipolar disorder tend to sleep very little (seemingly by choice, not because of
insomnia), and this is the most common symptom to occur prior to the onset of a manic episode.
During depressive episodes, they tend toward hypersomnia (too much sleep). Even between
episodes people with bipolar disorder show substantial sleep difficulties, including high rates of
insomnia. Bipolar disorder also sometimes shows a seasonal pattern in the same way unipolar
disorder does, suggesting disturbances of seasonal biological rhythms, although these may be the
result of circadian abnormalities in which the onset of the sleep–wake cycle is set ahead of the
onset of other circadian rhythms. Given the cyclic nature of bipolar disorder itself, this focus on
disturbances in biological rhythms holds promise for future integrative theories of the biological
underpinnings of bipolar disorder. This is particularly true because patients with bipolar disorder
seem especially sensitive to, and easily disturbed by, any changes in their daily cycles that
require a resetting of their biological clocks.

Psychological Causal Factors

Although biological factors play a prominent role in the onset of bipolar disorder, psychosocial
factors have also been found to be involved in the etiology of the disorder. In particular, stressful
life events, poor social support, and certain personality traits and cognitive styles have been
identified as important psychological causal factors.

Stressful Life Events

Stressful life events appear to be as important in precipitating bipolar depressive episodes as they
are in triggering unipolar depressive episodes. There is also some evidence that stressful life
events are sometimes involved in precipitating manic episodes as well. The stressful life events
are thought to influence the timing of an episode, perhaps by activating the underlying
vulnerability. One study also found that patients who experienced severe negative events took an
average of three times longer to recover from manic, depressive, or mixed episodes than those
without a severe negative event. Even minor negative events were found to increase time to
recovery. It has long been argued that as the illness unfolds, the manic and depressive episodes
become more autonomous and do not usually seem to be precipitated by stressful events. Some
of these conclusions may be premature, however, given that most studies addressing this issue
have relied on patients’ memories of events before episodes, which may be unreliable. In several
good prospective studies using more sophisticated stress measurement techniques, Ellicott and
colleagues did not find that stress played a less important role in precipitating episodes for
people who had had more episodes. How might stressful life events operate to increase the
chance of relapse? One hypothesized mechanism is through the destabilizing effects that stressful
life events may have on critical biological rhythms. Although evidence in support of this idea is
still preliminary, it appears to be a promising hypothesis, especially for manic episodes.

Other Psychological Factors in Bipolar Disorder

Other social environmental variables may also affect the course of bipolar disorder. For example,
one study found that people with bipolar disorder who reported low social support showed more
depressive recurrences over a 1-year follow-up, independent of the effects of stressful life events,
which also predicted more recurrences. There is also some evidence that personality and
cognitive variables may interact with stressful life events in determining the likelihood of
relapse. For example, the personality variable neuroticism has been associated with symptoms of
depression and mania, and two studies have found that neuroticism predicts increases in
depressive symptoms in people with bipolar disorder just as it does in unipolar disorder.

Moreover, personality variables and cognitive styles that are related to goal-striving, drive, and
incentive motivation have been associated with bipolar disorder. For example, two personality
variables associated with high levels of achievement striving and increased sensitivity to rewards
in the environment predicted increases in manic symptoms—especially during periods of active
goal striving or goal attainment such as studying for an important exam and then doing very well
in it. Another study found that students with a pessimistic attributional style who also had
negative life events showed an increase in depressive symptoms whether they had bipolar or
unipolar disorder. Interestingly, however, the bipolar students who had a pessimistic attributional
style and experienced negative life events also showed increases in manic symptoms at other
points in time.