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Bipolar disorder is the medical name
for manic depression. The terms may be used interchangeably. Bipolar disorder is a mental illness, but it' s more appropriately described
as a neurobiological brain disorder involving extremes in mood.
It's 1 of the 3 major affective (mood) disorders. Most medical researchers believe that bipolar disorder has genetic roots.
The diagnosis of bipolar disorder is recognized thru at least one, but usually more, manic episodes
or mixed
episodes. It's common for those
experiencing bipolar disorder to have experienced major depressive disorder as well.
Bipolar
Disorder a Misunderstood Disease
Few Americans think it's a mental illness, know its symptoms
THURSDAY, Oct. 9 (HealthDayNews) A new survey found 78% of Americans polled failed to name bipolar disorder as a mental illness & 38% couldn't name a single symptom associated w/the disease.
The survey was released Oct.
9 by The Nation's Voice on Mental Illness (NAMI) & Abbott Laboratories to mark the first national Bipolar Disorder Awareness Day.
The day includes free mental
health screenings & referrals for treatment of bipolar disorder, along w/efforts to
provide people with info about bipolar disorder, also known as manic-depressive
illness.
Bipolar disorder affects more than 2.3 million people in the US. The biochemically based mood disorder features mood swings from mania to depression to normal mood.
"The impact of untreated bipolar disorder on a person's life is huge," Richard C. Birkel, NAMI executive director, says
in a prepared statement.
"Early detection & treatment
can prevent years of illness-driven choices that produce devastating individual losses. Bipolar Awareness Day offers screening, education, information, hope for the millions of Americans living with bipolar disorder," Birkel says.
Among the survey findings:
- Women aged 35 - 54 have the
greatest awareness (39%) of bipolar disorder, followed by college-aged students at 35%. Awareness of bipolar disorder in the average population is 22%.
- People age 55 & older
have an awareness rate of 12%.
- Awareness about bipolar disorder among whites is 24%, among Hispanics it's 23% & among blacks
it's 10%.
More information
Here's where you can learn more about bipolar disorder. And here's a list of the free screening sites across the country.
Robert Preidt
SOURCE:
NAMI, news release, Oct. 9, 2003 Last updated 10/9/2003.
click here to access this article:
click here to access our additional page
concerning Bipolar Disorder
  
Criteria for Determining Manic Episodes
A distinct period
of, abnormally & persistently elevated, expansive, or irritable mood, lasting at least 1 week (or any duration if hospitalization is necessary.)
During the period
of mood disturbance, 3 (or more) of the following symptoms have persisted (4 if the mood is only irritable) & have been present to a significant degree:
- decreased need for sleep (i.e., feels rested after only 3 hours of sleep)
- more talkative than usual or pressure to keep talking
- flight of ideas or subjective experience that thoughts are racing
- distractibility (i.e., attention
too easily drawn to unimportant or irrelevant external stimuli)
- increase in goal-directed activity (either
socially, at work or school, or sexually) or psychomotor agitation
- excessive involvement in pleasurable activities that
have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual
indiscretions, or foolish business investments - important consideration for other disorders as well)
(minor or temporary depression)
Depressive Reaction involves the normal depressed feelings that arise because of a specific life situation or life transition. Depressive reaction is also called an "adjustment disorder w/depressed mood."
The symptoms can
be severe, but they usually don't need treatment & will slowly disappear over time, anywhere between 2 weeks & 6 months.
Dysthymia:(a minor form of longer-term depression)
(click above to read a more in depth description of
Dysthymia)
Similar to depressive
reaction in its symptoms & degree of suffering, it lasts longer though, at least 2 years. Dysthymia presents a chronic feeling of ill being or lack of interest in activities that were formerly enjoyable,
but to a lesser level than that required for Major depression.
Unipolar Major Depressive Disorder
Introduction
Major depressive disorder
(MDD) is a painful, chronic,
debilitating & potentially lethal condition that can
be effectively managed with several safe & relatively
easy to use, forms of treatment. Current data suggest that MDD is a syndrome, originating
from complex interactions between vulnerability genes, stressful & traumatic life events & general health status.
It's believed that all current treatments for depression assist in regaining function, but don't eliminate or reverse underlying vulnerability factors, explaining why treatment often needs to be administered
chronically to avoid relapse & to prevent recurrence.
Treatment options
for MDD include various forms
of psychotherapy, a wide array of medications, electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation (rTMS) & vagal nerve stimulation
(VNS).
First-line treatment
can be initiated with antidepressant
agents, or psychotherapy alone. A large number of factors can influence the selection of treatment for MDD;
therefore, the choice should be made on an individual basis.
For example, a recent study by Nemeroff et al suggested that individuals
with a history of early parental loss, or childhood abuse, may require concomitant psychotherapy, with or without medication treatment.1
The most pragmatic approach
is to choose the safest available treatment with the side effect profile most compatible with the patient’s specific symptoms.
The clinical factors
that can influence choice of treatment include:
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the presence of psychosis or atypical features
-
general health status
-
age
-
prior treatment history (in particular, nonresponse to, or intolerance of, prior treatments)
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current severity of illness
-
symptom profile
For example, individuals with MDD & psychotic features may respond more favorably to
either ECT, or the combination of an antidepressant & an antipsychotic,
rather than to an antidepressant drug alone.
Guidelines for treatment
of MDD suggest that a
staged approach be taken, with each step building on prior
steps & taking into account the degree of improvement or tolerability associated with a prior step.
Figure 1 presents published guidelines from the British National Institute for
Clinical Excellence (NICE).2
Most
guidelines suggest careful assessment, including
a review of systems, with physical examination preceding
treatment selection. For mild
depression, the NICE guidelines suggest the possibility
of “watchful waiting” for 2 weeks, or the use of psychological approaches.
First-line treatment includes either psychotherapy, or the combination of an antidepressant & psychotherapy.
Figure 1. The Stepped Care Model *
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Step 5: Inpatient
care, crisis teams
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Risk to life, severe self-neglect
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Medication, combined treatments, ECT
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Step 4: Mental
health specialists, including crisis teams
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Treatment-resistant, recurrent, atypical & psychotic depression
& those at significant risk
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Medication, complex psychological interventions, combined
treatments
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Step 3: Primary care team, primary care mental
health worker
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Moderate or severe depression
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Medication, psychological interventions, social support
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Step 2: Primary
care team, primary care mental health worker
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Watchful waiting, guided self-help, computerized CBT, exercise, brief psychological interventions
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Step 1: GP,
practice nurse
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*Reproduced with permission of the National Institute for Health and Clinical Excellence. Adapted from NICE.
2004, Clinical Guideline 23.
Cognitive Behavior Therapy
Cognitive therapy
is the most extensively researched psychological treatment
for unipolar depression.
Cognitive therapy, focused on dysfunctional beliefs, when
incorporated with components of behavior therapy, is cognitive behavior therapy (CBT).
Gloaguen et al
examined 48 randomized controlled trials that included 2765
patients with MDD or dysthymia.3
The treatment of patients receiving CBT was reported to be superior to wait-listed or placebo-control subjects & other therapies, including
supportive & nondirective psychotherapies, interpersonal
psychotherapy (IPT) & relaxation therapy; CBT wasn't better than simple behavior therapy.
Combined psychological & pharmacological therapies may be useful in minimizing
relapse & recurrence.
Concurrent therapy is only as effective as monotherapy for the treatment of mild to moderate depressive
disorder, but may show a potential treatment advantage when
depression is severe. Sequencing of pharmacotherapy
& psychotherapy shows some benefit in the prevention of relapses & recurrence.
Variants of cognitive
therapy that have been modified to specifically address
residual symptoms in patients appear to be the most effective.4
Interpersonal Therapy
Interpersonal psychotherapy (IPT) was developed in the 1970’s by Klerman
et al as a time-limited, weekly outpatient treatment for MDD.5 IPT
proved more effective than placebo, but there
were no differences between the efficacy of IPT & medication.
Combined therapy
(IPT plus antidepressant medication) & medication alone aren't different. Thus, there's no adjunctive effect for IPT in major depression.6
Antidepressants
Antidepressant drugs tend to be grouped based on pharmacological properties,
although the historical distinction between monoamine oxidase inhibitors (MAOI's) & tricyclic antidepressants (TCA's) tends to
still be employed in describing these older compounds. Newer
drugs tend to be grouped based on their relative effects
on blocking the reuptake of the monoamine neurotransmitters norepinephrine (NE), serotonin
(5-HT) & dopamine (DA).
Table 1 lists common TCA's & Table 2 lists newer drugs.
Monoamines are
released from the terminals of nerves that modulate emotion
circuits in the limbic system. When these neurotransmitters
are released into the synapse, they're rapidly taken back up into the monoamine
nerve cell via proteins called transporters or reuptake
pumps. When the reuptake is blocked by a drug, the neurotransmitter stays in the synapse longer, increasing some of their effects on target limbic-system neurons.
Transporters for
NE, 5-HT, and DA are structurally distinct proteins &
certain drugs are capable of blocking the ability of one or more of these transporters to take back the monoamine intrinsic to that neuron.
Drugs that are
called “selective reuptake inhibitors” tend
to be much more powerful in blocking one transporter &
are less likely to block other transporters, unless very high doses are used.
For example, escitalopram blocks only the 5-HT transporter, even at very high doses,
while paroxetine blocks the 5-HT transporter at low- to
mid-dose levels; at high-dose levels, paroxetine may also
begin to block the NE transporter.7
Venlafaxine & duloxetine are often described as “dual action” drugs because they are both likely to block both the 5-HT & NE transporters
at commonly used doses. Another characteristic that defines
a drug as a “selective” reuptake inhibitor is
the absence of pharmacological effects on various monoamine receptors. This is the reason
why the older TCAs are not described as “selective,”
even though some of them only block NE reuptake (see Table 1).
As presented in Table 3, TCAs block histamine, acetylcholine,
and NE receptors, leading to side effects such as sedation, dry mouth & orthostatic hypotension that aren't present with newer,
truly selective agents.
While NE, 5-HT,
and DA neurons overlap considerably in the brain areas they
modulate, there are well established differences in their distribution. The full significance of this isn't currently understood, but this knowledge has led investigators to search for differences
in therapeutic profile of drugs that are selective serotonin
reuptake inhibitors (SSRIs) & those that have “dual action” on both 5-HT and NE (selective norepinephrine and serotonin reuptake inhibitors – SNRIs).
While levels of monoamines increase within hours of ingestion of the first dose of an antidepressant, the therapeutic response doesn't begin in most patients
until several weeks later.
Current theory
suggests that increased synaptic levels of monoamines
is the first step in a cascade of effects that may ultimately result in alterations in a variety of cellular functions of limbic circuit
neurons; as these circuits begin to function more normally,
there is a corresponding improvement in the symptoms of depression.8
Similar to the selection
of treatment in general, a large number of factors
can influence the choice of an antidepressant. Selection should be based on safety, tolerability, comorbid medical & psychiatric conditions,
cost, ease of administration & an assessment of any
drug-drug interactions.
While the TCA's are as effective as newer drugs, as a class, TCAs are associated
with moderate rates of side effects, often limiting the ability to achieve a therapeutic dose due to their many receptor-blocking properties.
Because TCA's & MAOI's are comparably effective as SSRI's,
NICE guidelines recommend that first-line antidepressant treatment use an SSRI, as
SSRI's have fewer safety concerns.
TCA side effects are listed in Table 3 & those of SSRI's in Table 4.
There are some data
suggesting that SSRI's aren't as effective in the treatment of neuropathic pain.9,10 Meta-analysis of treatment studies in chronic pain suggest that SNRI's & TCA's are more effective than SSRI's; therefore, this should be considered when
treating a patient with MDD & cooccurring neuropathic pain.
The onset of clinically evident antidepressant effect may take 2 weeks or longer after the treatment is begun. An adequate trial of an antidepressant is defined as an adequate dose, over an adequate time period (8-12 weeks), with an adequate blood
level.
When stopping treatment,
tapering off the medication is preferable to reduce the risk of discontinuation syndromes,
especially for those antidepressants with short half-lives.
Long-term prophylactic / maintenance antidepressant therapy is indicated
when depression is recurrent.
NICE guidelines
suggest that patients who've had 2 or more depressive episodes in the recent past & who have experienced significant functional
impairment during the episodes, should continue antidepressant
treatment for 2 years.
For instance, suddenly discontinuing SSRI's can lead to somatic & psychological withdrawal symptoms, “SSRI discontinuation syndrome.” This is more common in shortacting SSRI's than those
with a long half-life, such as fluoxetine.
Seasonal
Affective Disorder
Seasonal Affective Disorder is an extreme form of the "winter blues" depression that occurs at the same time each year. This disorder was only recently recognized as a specific disorder. Since 1982 much has been learned about it & how to treat it.
Those experiencing Seasonal Affective Disorder undergo extreme differences in mood, as if they were split between a summer person & a winter person.
Identifying symptoms
are:
-
Sluggishness
-
Trouble functioning normally
- Impaired functioning
-
-
Difficulty enjoying life
-
-
Loss of energy
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Inertia
-
-
-
Difficulty getting up in
the Morning
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Carbohydrate cravings
-
-
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Decreased sex drive
-
Vague physical complaints
-
Marked cravings
for Junk Food
Although a different kind of Seasonal Affective Disorder can occur in the summer, its most common form, winter depression, begins gradually in late August or early September & continues through March or early
April.
Sufferers have been known to
increase their sleep by as much as 4 hours a night & gain more than 20 pounds as they attempt to hibernate the winter away.
Researches suggest that Seasonal Affective Disorder may affect as many as 11 million
people in the US each year. An additional 25 million suffer a milder form, referred to as the winter blues. 4 times as many women experience this disorder
than men & it does seem to run in families.
Causes for Season Affective Disorder
The Chemical or Neurotransmitter, "serotonin" is produced less & less in the body, when the sun doesn't shine as much. Serotonin helps to control moods & sleep.
Geographical location plays
a role in susceptibility - People in Canada & the Northern US are 8 times more likely to fall victim to Seasonal Affective Disorder than those in the sunny southern areas, like Florida.
Seasonal Affective Disorder usually develops in those that are in their early 20's w/the risk
for developing it decreasing w/age.
 Treatment
for Seasonal Affective Disorder
Other forms of treatment
- Taking a walk at lunchtime when the sun is
high. Being outdoors as often as possible
- Exercise as much as possible
- Take winter vacations in places w/sunny longer
days
- Increase the natural light in your home by
trimming low-lying branches near the house & hedges around windows
- Paint your walls w/lighter colors
- Keep warm & enjoy the fun aspects of
winter, such as fires, books & music
- If all else fails, moving to a sunnier climate may be a consideration
- Massage can be a helpful therapy
Electrical emissions
into the atmosphere, negative ions, improve a persons mood & health.
In the last 30 years, scientists have developed small devices that emit negative
ions into the atmosphere of a room. The negative ionizer seems particularly helpful for people w/Seasonal
Affective Disorder (one study showed a 58% reduction in depression) & may be a good supplement to light therapy & medications.
Nutrition & Diet
People with Seasonal Affective Disorder are apt to overeat in the winter, w/special cravings for sweets & starches.
One Seasonal Affective Disorder expert recommends that patients avoid snacking on carb rich
foods & trying to balance their diets as much as possible.
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