Beruflich Dokumente
Kultur Dokumente
HYPOMANIA
DYSTHYMIA
CME INFORMATION
Overview
This monograph is a summary of the bipolar disorder sessions previously presented at the 2007 NEI Psychopharmacology 2-Day Academies,
with a discussion of the neurobiology, diagnosis, and treatment of bipolar spectrum disorders.
Target Audience
This activity was designed for healthcare professionals, including psychiatrists, neurologists, primary care physicians, clinical psychologists,
pharmacists, psychotherapists, nurses, nurse practitioners, addiction counselors, social workers and others, who treat patients with psychiatric
conditions.
Statement of Need
The content of this educational activity was determined by rigorous assessment, including activity feedback, expert faculty assessment, literature
review, and new medical knowledge, which revealed the following unmet needs:
Thirty percent of bipolar patients are misdiagnosed. Four key areas are important for discerning if a patient may have a bipolar
spectrum disorder: sleep, treatment-response history, family history, talking to a relative. In addition, bipolar spectrum disorders are
progressive illnesses making tracking of symptoms and treatment responses necessary.
Because efcacy and tolerability of mood stabilizers, particularly atypical antipsychotic mood stabilizers, may vary depending on the
phase of illness, treatment selection and dosing may need to be state-dependent in bipolar spectrum disorders.
Evidence-based and/or rational polypharmacy techniques for treating bipolar spectrum disorders are lacking, since most of the studies
focus on monotherapy.
Learning Objectives
Upon completion of this activity, you should be able to:
Track history and progression of symptoms and treatment responses for patients with mood/behavioral symptoms
Select mood stabilizers and their doses based on patient presentation
Use neurobiologic and mechanistic rationale when combining medications to treat bipolar spectrum disorders
Activity Instructions
This CME activity is in the form of a printed monograph and incorporates instructional design to enhance your retention of the information and
pharmacological concepts that are being presented. You are advised to go through this activity from beginning to end and then complete the
posttest and activity evaluation. The estimated time for completion of this activity is 2 hours.
-1-
Content Editors
Meghan Grady
Director, Content Development
Neuroscience Education Institute, Carlsbad, CA
No other nancial relationships to disclose.
Stephen M. Stahl, MD, PhD
Adjunct Professor, Department of Psychiatry
University of California, San Diego School of Medicine, San Diego, CA
Board Member: Cypress Bioscience; NeuroMolecular; Pierre Fabre; Tetragenix
Grant/Research: Alkermes; AstraZeneca; Bristol-Myers Squibb; Cephalon; Cyberonics; Eli Lilly; GlaxoSmithKline; Janssen; Jazz; Neurocrine
Biosciences; Novartis; Organon; Pzer; Sepracor; Shire; Somaxon; Takeda; Wyeth
Consultant/Advisor: Acadia; Amylin; AstraZeneca; Avera; Azur; Biovail; Boehringer Ingelheim; Bristol-Myers Squibb; Cephalon; CSC;
Cyberonics; Cypress Bioscience; Eli Lilly; Epix; Forest; GlaxoSmithKline; Janssen; Jazz; Labopharm; Neurocrine Biosciences; NeuroMolecular;
Neuronetics; Novartis; Organon; Pamlab; Pzer; Pierre Fabre; sano-aventis; Schering-Plough; Sepracor; Shire; Solvay; Somaxon; Tethys;
Tetragenix; Vanda; Wyeth
Speakers Bureau: AstraZeneca; Cephalon; CSC; Eli Lilly; Pzer; Wyeth
Peer Reviewer
Meera Narasimhan, MD
Professor, Department of Psychiatry
Director of Biological Research, Ofce of Biological Research
Department of Neuropsychiatry and Behavioral Science
University of South Carolina School of Medicine, Columbia, SC
Grant/Research: AstraZeneca Pharmaceuticals LP; Bristol-Myers Squibb Company; Forest Laboratories, Inc.; Janssen Pharmaceutica Inc.
Consultant/Advisor: Bristol-Myers Squibb Company; Eli Lilly and Company
Speakers Bureau: AstraZeneca Pharmaceuticals LP; Bristol-Myers Squibb Company; Eli Lilly and Company; Janssen Pharmaceutica Inc.
Jahon Jabali
Interactive Designer
Neuroscience Education Institute, Carlsbad, CA
No other nancial relationships to disclose.
Jaime Derringer
Project Manager
Neuroscience Education Institute, Carlsbad, CA
No other nancial relationships to disclose.
Nancy Muntner
Director, Medical Illustrations
Neuroscience Education Institute, Carlsbad, CA
No other nancial relationships to disclose.
Stacey L. Hughes
Director, Program Development
Neuroscience Education Institute, Carlsbad, CA
No other nancial relationships to disclose.
Steve Smith
President and COO
Neuroscience Education Institute, Carlsbad, CA
No other nancial relationships to disclose.
Disclosed nancial relationships have been reviewed by the Neuroscience Education Institute CME Advisory Board to resolve any potential
conicts of interest. All faculty and planning committee members have attested that their nancial relationships do not affect their ability to
present well-balanced, evidence-based content for this activity.
Disclaimer
Participants have an implied responsibility to use the newly acquired information from this activity to enhance patient outcomes and their own
professional development. The information presented in this educational activity is not meant to serve as a guideline for patient management.
Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this educational activity should not be used by
clinicians without evaluation of their patients conditions and possible contraindications or dangers in use, review of any applicable
manufacturers product information, and comparison with recommendations of other authorities. Primary references and full prescribing information should be consulted.
-2-
1. Introduction
The family history of patient X reveals a history of mental illnesses. His maternal grandfather had suffered from
depression and died in a psychiatric hospital; his mother
was once hospitalized for depression and was treated
with amitriptyline for most of her life; and his fraternal
twin brother suffered from situational depression. As a
child, patient X experienced episodes where his thoughts
and reactions seemed magnied and was plagued with
behavioral problems such as impulsivity, distractibility
and hyperactivity. He was intelligent but never excelled
in school. Since he was a child, he thought that things
would grow bigger and become dangerous. The current
state of mind of patient X is that he wants to be pleasing, accepted, loved, admired, and special, and he suffers from self-esteem issues, which could uncover signs of
narcissistic personality traits. When he preaches, patient
X transcends sickness and reaches a high; at the same
time he thinks that his role as a preacher has diminished
in todays society and he feels worthless.
Patients with bipolar disorder (BPD) will often be misdiagnosed for many years, resulting in an escalation of symptoms and leading to an increased burden on the patient,
their family and society.1 In worst cases, treatment based
on an erroneous diagnosis can actually exacerbate the
state and symptoms of the patients. An early and correct
diagnosis, on the other hand, can substantially increase
quality of life and lead to a productive social life. This
monograph aims to educate the reader about the intricacies of diagnosing BPD and about the preferred use of
different medications.
2. What is Bipolar Disorder?
In the Diagnostic and Statistical Manual of Mental Disorders Version IV, Text Revision (DSM-IV-TR), BPD encompasses four distinct disorders, i.e. bipolar I (BP-I), bipolar II
(BP-II), cyclothymic disorder, and bipolar disorder not otherwise specied (BP-NOS). The lifetime prevalence of BPD
is approximately 1%2 but if the denition of the disease is
widened to include all illnesses within the spectrum, the
prevalence can be as high as 2.6% to 6.5%.3 Almost a
third (31%) of patients with BPD have been misdiagnosed
with unipolar depression, and about 35% of BPD patients
have waited 10 or more years to be accurately diagnosed.4
In general, BPD can be difcult to differentiate from other
psychiatric conditions especially unipolar depression,
and until recently it has been widely underdiagnosed.5
-5-
the WHO ICD-107 have substantially different denitions of bipolar disorder leading to discrepancies in
diagnosis and treatment between both systems.
ii. WHO ICD-10 criteria for the diagnosis of bipolar affective disorder (BAD).
To be diagnosed with
BP II, patients need to have experienced at least one episode of hypomania and at least one episode of major
depression
Figure 1: Graphic representation of the different stages seen in BP-I (A) and BP-II (B).
-6-
% Time (hypo)manic
% Time depressed
% Time cycling/mixed
%Time asymptomatic
BP- I
9.3%
31.9%
5.9%
52.7%
BP-II
2.3%
46.1%
A study by Serretti and Olgiati challenged the notion of the DSM-IV-TR which describes manic episode
as being similar to hypomanic episode except more
severe.11 Additionally it is common for manic patients to undertake reckless activities due to psychomotor agitation and poor judgment,13 and uncommon for hypomanic patients to do so.14 The major
depressive episodes seen in BP-II are often mixed
with hypomanic symptoms, such as irritability, mood
liability, racing thoughts, increased sexuality and
distractibility, leading to a misdiagnosis as depressive mixed states.14 When compared to BP-I, more
than half of BP-II patients exhibit their rst symptoms
before the age of 19,8 and there is a much higher
prevalence of family history, i.e. a rst-degree relative suffering from the same illness, in BP-II compared
to BP-I (6.1% versus 1.8% respectively).15, 16
-7-
cycling lasts at least three days with at least four cycles per month and 3) ultra ultra rapid or ultradian
cycling lasts less than twenty-four hours.22, 23 About
1030% of BP patients exhibit a rapid cycling pattern and 7090% of rapid cycling patients are women.24 There is also a higher risk in women (29.6%)
than in men (16.5%) to develop rapid cycling.25 In
general, BP-II patients have a higher risk (30.3%) of
developing rapid cycling compared to BP-I patients
(6%), especially if a depressive episode presented
rst.26, 27 In some patients, the rapid cycling pattern
can subside after a few years.28, 29 In summary, the
usual clinical prole of BP-II patients with rapid cycling
includes 1) being a woman, 2) presenting rst with a
depressive episode, 3) exhibiting a sequence of cycles
such as depression-mania-euthymia, 4) having a premorbid cyclo- or hyperthymic temperament and 5) in
E.
Diagnosing BPD in adolescents can be especially difcult due to the high comorbidity rate (87%) with attention decit disorder.37 Additionally, children and
adolescents often present with short and frequent episodes of mania and/or depression as well as subsyndromal symptoms.38 As children exhibit less discrete
episodes of mania and depression,37 clinicians need
to look for higher rates of mixed mania (55%) and
rapid cycling (87%). Many studies have shown that
even though recovery is quite high in this population
of patients, there is also a high rate of recurrence,
despite the presence of pharmacotherapy, including many suicide attempts or completed suicides.38
Compared to adults, children and adolescents with
BP-I spend more time symptomatic, have more mixed
episodes and cycling occurrences and present with
more subsyndromal symptoms.38 There is also a higher rate of conversion between BP-I and BP-II in youth
compared to adults.38 Children will often be wrongly
characterized as temperamental and explosive with
a high degree of irritability, and non-treatment or mistreatment can be devastating to their future clinical
history.
The clinical consequences resulting from misdiagnosing BPD include the risk of suicide, substance abuse and
iatrogenic complications.15 It has been shown that of
-8-
A very important aspect in treating BPD is to ascertain that the patients recover functionally and not
only syndromally. Functional recovery is the restoration of normal functioning at work, at home, and
with family and friends.40 A recent study has found
that compared to non-depressed patients, subsyndromally depressed BP patients are signicantly more
likely to be impaired at work and at home, both
in relationships with family members and with respect to home duties.41 The degree of impairment is
also signicantly correlated with the intensity of the
subsyndromal symptoms and close to that of syndromally depressed patients.41 In general, subsyndromal
depression is more common than subsyndromal mania
and there is an association between the rst subsyndromal symptoms and the subsequent mood episode
of the same polarity.16, 42 The global impact that impairment in functionality has on society16 in addition to
the poor quality of life of the patients supports the need
to assess functional recovery in patients who have subsyndromal symptoms and to consider long-term treatment of these patients.
F.
ii.
The diagnosis of BP-II is improved when semistructured interviews are given to patients by
trained clinicians who focus on the symptoms
of hypomania.44 A systematic evaluation of hypomanic symptoms and the use of more elaborate checklists and alternative rating scales
-9-
Acute Mania or
Mixed Episodes (ME)
Acute Depression
Maintenance Treatment
APA
BAP
If mania predominates:
1) Li, Val, OLZ; 2) CBZ; 3) combo
If depression predominates:
1) La; 2) Li; 3) combo
CANMAT
Table 2: Treatment recommendations for BPD. AD=antidepressant; AP=antipsychotic; APA=American Psychiatric Association; ARI=aripiprazole; BAP= British Association of Psychopharmacology; CANMAT=Canadian Network for Mood and Anxiety Treatments; CBZ=carbamazepine; Cloz=clozapine; ECT=electroconvulsive
therapy; FGA=1st generation AP; La=lamotrigine; Li=lithium; ME=mixed episodes; OLZ=olanzapine; QUE=quetiapine; RIS=risperidone; SGA=2nd generation AP;
SSRI=selective serotonin reuptake inhibitor; TCA=tricyclic antidepressant; Val=valproate; ZIP=ziprasidone.
-10-
5HT2A
D2
5H
M1
A
T1
M3
H
1
1
2
5HT1D
SRI
atypical
antipsychotic
NRI
5HT2C
D1
3
5HT
5HT
7
D2
D4
D3
clinical
actions
pharmacologic
actions
NE and DA
disinhibition
mood and
cognition
antihistamine
NE and DA
disinhibition
H1
5HT2A
5HT
disinhibition
H1
5HT2A
mood
2
SRI
NRI
SERT
inhibition
2C
mood
2
1D
SRI
NRI
mood
2C
NET
inhibition
mood
mood and
cognition
NE and DA
disinhibition
trophic
factors
insomnia
1A
-11-
5HT2A
1D
blocks DA
hyperactivity
reduces glutamate
hyperactivity
1A
5H
T6
neurogenesis?
circadian
rhythms
sleep, mood?
FDA-Approval *
(Non FDA-Approval)
Dosing
Maintenance Tx of BP-I
- 200-800 mg/day
- low dose may have more sedative effects
- ampuls and vials contain sultes that could cause allergic reactions; one
of the few AP available as suppository
- 15-30 mg/day
- lower doses may be needed to avoid akathisia/activation and for max
tolerability
- if patient is switched from another AP to ARI, consider adding a full dose
of ARI to the maintenance dose of 1st AP for several days prior to a slow
down-titration of the 1st drug
K+
Na+ channel
unit
glu
glu
GABA
GABA
Na+ channel
unit
H1
1
D2
5HT2A
5HT1D
SRI
NRI
5HT2C
D2
5HT
D3
MOA: blocks D2 and 5-HT2A receptors; interactions at 5-HT2C; 5-HT1A and 1D receptors may
contribute to efcacy in cognitive and affective
symptoms
5HT2A
D2
D3
PA
M1
M3
5HT2A
5HT2C
D2
5H
T6
5HT
D1
D4
D3
A
X?
PA
M1
M3?
H
5HT2A
1
2
5H
5HT
7
T6
D2
5HT2A
1
2
5HT7
D2
(BPD)
Table 3: Drugs used in the treatment of BPD, their mechanism of action, FDA-approved doses, and side effects and special considerations.
*these drugs have additional FDA-approved uses not mentioned in the table. For additional information please refer to Stahl SM (2005) Essential Psychopharmacolgy. The Prescriber's Guide. Cambridge:
Cambridge University Press.
(1) Risk categories in Pregnancy -- Risk Category C: some animal studies show adverse effect, no controlled studies available in humans; Risk Category D: positive evidence of risk to human fetus, during
1st trimester may increase risk of neural tube defects or congenital anomalies
-12-
Most common: dizziness, insomnia, akathisia, activation, nausea, vomiting, occasional orthostatic hypotension, theoretical risk of TD
Life-threatening: rare neuroleptic malignant syndrome, rare seizures
SC: dose adjustment not necessary in patients with renal and hepatic impairment; use in patients with cardiac impairment not studied; not ofcially recommended for
patients under 18, but clinical experiences suggest it is safe and effective; risk category C in pregnancy(1), probably found in breast milk, best to discontinue drug or
bottle feed; well accepted in clinical practice especially as it results in less weight gain, and leads to less sedation as most AP; may not have diabetes or dyslipidemia
risk; favorable tolerability prole
Most common: risk for diabetes mellitus and dyslipidemia, dizziness, sedation, dry mouth , constipation, weight gain, joint, back and chest pain, abnormal gait,
peripheral edema, tachycardia, rare orthostatic hypotension, rare TD, rare rash due to sunlight exposure
Life-threatening: hyperglycemia, rare cases associated with ketoacidosis or hyperosmolar coma and death, increased incidence of cerebrovascular event, increased
incidence of mortality in elderly patients with dementia-related psychosis, rare neuroleptic malignant syndrome, rare seizures
SC: women have decreased clearance of OLZ; lower dose for patients with hepatic impairment and monitor liver function tests; no adjustment for patients with renal
impairment; use with caution in patients with cardiac impairment due to orthostatic hypotension; lower dose in elderly; increased risk of stroke in elderly; not ofcially
recommended for children under 18, but clinical experience suggests it is safe for Tx of behavioral disturbances in children and adolescents, if monitored closely; risk
category C in pregnancy(1); may be preferable to anticonvulsants during pregnancy; best to discontinue drug or bottle feed, monitor infants closely if breast-fed; useful
in Tx-resistant cases, efcacious as augmenting agent to SSRI (uoxetine) in BP depression; causes more weight gain than other AP; less sedation; cigarette smoking
decreases OLZ levels; 1 of only 2 AP with a short-acting IM formulation
Most common: may increase risk of diabetes and dyslipidemia, dizziness, sedation, dry mouth, constipation, dyspepsia, abdominal pain, weight gain, tachycardia,
orthostatic hypotension
Life-threatening: hyperglycemia, in some case with associated ketoacidosis or hyperosmolar coma and death, rare neuroleptic malignant syndrome, rare seizures
SC: no dose adjustment in patients with renal impairment; downward dose adjustment in patients with hepatic impairment; use with caution in patients with cardiac
impairment due to orthostatic hypotension; lower doses used in elderly; not ofcially recommended in children under 18; but safe for Tx of behavioral disturbances in
children and adolescents, if monitored closely; risk category C in pregnancy(1); may be preferable to anticonvulsants during pregnancy; best to discontinue drug or
bottle feed, monitor infants closely if breast fed; preferred AP for psychosis in Parkinsons disease and Lewy Body dementia; efcacious in Tx-resistant patients, efcacy
often underestimated as it is often underdosed; induces more sedation than other APs, no motor SE or prolactin elevation
Most common: may increase risk for diabetes and dyslipidemia, dose-dependent EPS, dose-related hyperprolactinemia, rare TD, dizziness, insomnia, headache,
anxiety, sedation, nausea, constipation, weight gain, rare orthostatic hypotension, tachycardia, sexual dysfunction
Life-threatening: hyperglycemia, sometimes associated with ketoacidosis or hyperosmolar coma and death, increased incidence of cerebrovascular event, increased
incidence of mortality in elderly patients with dementia-related psychosis, rare neuroleptic malignant syndrome, rare seizures
SC: oral solution not compatible with cola/tea; in patients with renal or hepatic impairment and in elderly start drug at 0.5 mg/day 2X/day for 1 wk, increase to 1
mg/day 2X/day during 2nd wk; look for orthostatic hypotension in patients with cardiac impairment; most frequent AP used in children/adolescents; safe for Tx of
behavioral disturbances in children and adolescents, if monitored closely; risk category C in pregnancy(1); may be preferable to anticonvulsants during pregnancy;
best to discontinue drug or bottle feed, monitor infants closely if breast-fed; well accepted for Tx of agitation and aggression in elderly demented patients and for
behavioral symptoms in children/adolescents; useful in Tx-resistant patients; only AAP to raise prolactin levels; hyperprolactinemia in women with low estrogen could
accelerate osteoporosis; monitor sedation and weight gain in pediatric patients; problematic in Parkinsons disease or Lewy Body dementia; the only AAP with longacting depot formulation
Abbreviations:
5-HT=serotonin; 5-HT(1A, 2A, 2C, 1D)=specic serotonin receptors; AAP=atypical antipsychotics; AP=antipsychotic; ARI=aripiprazole; CBZ=carbamazepine; Chlor=chlorpromazine; DA=dopamine;
D(2,3)=specic dopamine receptors; EPS=extrapyramidal side effects; GABA=gamma-aminobutyric acid; Glu=glutamate; H1=histamine receptor; hrs=hours; IM=intramuscular; La=lamotrigine;
Li=lithium; M1=muscarinic receptor; MOA=mechanism of action; NT=neurotransmitter; OLZ= olanzapine; QUE=quetiapine; RIS=risperidone; SC=special consideration; SE=side effects;
SIADH=syndrome of inappropriate antidiuretic hormone secretion; TD=tardive dyskinesia; Tx=treatment; Val=valproate; VSSCs=voltage-sensitive sodium channels; Wk(s)=week(s); ZIP=ziprasidone.
-13-
-14-
-15-
The study showed that the use of bupropion or paroxetine in conjunction with a mood stabilizer was as efcacious as a mood stabilizer alone when treating BP
depression, and that neither treatment option led to an
increase in switches to mania. Unfortunately, though,
the study did not look at the use of antidepressants without mood stabilizer.73 In general, patients on an antidepressant in addition to a mood stabilizer or an atypical
antipsychotic were more likely to respond and reach
remission, supporting a positive efcacy for antidepressants in BPD.70 Finally the selegiline transdermal system
might be an interesting choice in the treatment of BP depression, as it does not lead to manic switches at low
doses. There are however various drug-drug interactions
to be aware of with the patch formulation.74 Thus it has
become accepted that when an antidepressant is
to be used, it is best to rst start patients on a mood
stabilizer and then add the antidepressant as this
might reduce the risk, if any, of a manic switch,
and because the mood stabilizer itself can prove to
have antidepressive action.75 Additionally the switch
rate is much lower in BP-II than in BP-I patients,
suggesting that antidepressant treatment in BP-II patients
may be accepted, especially in light of the fact that BP-II
patients spend more time in the depressed state.75 Figure 3 exemplies the most common, but certainly not
the only, combinations of drugs used by clinicians that have both evidence- and practicebased rationales, and that have been the most
efcacious.9 Rationale differences between
various drug combinations might also exist
depending on the geographical location of
physicians and patients (Boston Bipolar Brew;
California Careful cocktail or Tennessee mood
shine).9
Finally, various other agents need to be mentioned, as studies are currently underway to
determine their efcacy in the treatment of
BPD. These include memantine and amantadine, both NMDA glutamate receptor antagonists, with amantadine having the additional
property of releasing DA. Consistent data
however are still required to ascertain their efcacy in BPD. The anesthetic ketamine might
be an interesting drug for treatment-resistant
depression in BPD, as it shares the NMDA receptor antagonism of the two previous drugs,
and has also proven benecial in treatmentresistant unipolar depression.76 By blocking
phosphokinase C activity, omega-3 fatty acids share their mechanism of action with valproate. Despite a high heterogeneity in results,
omega-3 fatty acids have shown to be efcacious in unipolar and BP depression and they
have additional health benets important for
psychiatric patients.77 Inositol might be useful
as an augmenting agent to an antidepressant,
especially as this product is also linked to the
signal transduction cascade of 5-HT2A receptors; one of the main receptors of atypical
antipsychotics. L-methylfolate, the active form
of the folate vitamin, can increase levels of
5-HT, DA and NE and has shown to enhance
the therapeutic efcacy of antidepressants.78
Additionally some patients may lack folate
vitamin, as anticonvulsants can interfere with
both the absorption and the metabolism of
folate, thus adding it to anticonvulsants
might be a good idea. Finally the T3 thyroid hormone has shown mood stabilizing
properties in some patients but should be
studied in more detail. The DA D2/D3 agonist pramipexole, currently FDA-approved
for the treatment of Parkinsons disease and
Restless Leg Syndrome, has been tested in the
treatment of BPD, because its mechanism of
action of enhancing DA release and having
neurotrophic effects could potentially be very
useful in BPD. When added to mood stabilizers, such as lithium and valproate, pramipexole (at a dose between 0.3754.5 mg/day)
signicantly reduces depressive symptoms
+
atypical-lithium
combo
atypical
lithium
DPA
+
atypical-valproate combo
atypical
valproate
divalproex
DPA
+
Li-Do
divalproex
lithium
+
La-Do
lamotrigine
caution
divalproex
+
La-Li
lamotrigine
lithium
+
La-Li-Do
lamotrigine
divalproex
lithium
caution
antidepressant
antidepressant
caution
+
Tennessee mood shine
(atypical + antidepressant)
atypical
antidepressant
lamotrigine
monotherapy
stealth treatment
+
lami-quel
Lamictal/
lamotrigine
Seroquel/
quetiapine
quel kit
(any combo containing
quetiapine)
quetiapine
+
modafinil lamotrigine
+
modafinil
modafinil combo
+
lamotrigine/Quetiapine
antidepressant
reluctant combo
-16-
quetiapine
Psychosocial therapies
It can be very tricky to impossible to treat manic patients with psychotherapy, as they might not be receptive to it. Psychotherapy is most efcacious when
patients are euthymic or depressed. There are different types of psychosocial therapies available and the
main goal is to educate the patients about how their
lifestyle can impact their disorder. For some patients,
psychotherapy can be a good alternative to polypharmacy as it does not have any side effects. It is
important to note, though, that psychosocial therapy
requires trained clinicians and can be expensive.
rate of relapses, of both manic and depressive episodes, and had fewer hospitalizations than patients in the control group.86
Interestingly, when PE is given to the family and
caregivers, it not only allows the family to understand and support the patient, but this added
support also translates into better outcomes for
the patients, such as lower rate of relapse, longer inter-episodes intervals and better treatment
adherence.87 Finally, suicide attempts are signicantly reduced in patients on pharmacotherapy,
especially lithium, when it is coupled with PE, as
the patients can better recognize the beginning of
a relapse and they feel supported by the environment providing this education.88
ii.
Cognitive-behavior therapy
i.
Psychoeducation
-17-
increasing awareness of mood, recognizing subsyndromal symptoms and signs of upcoming episodes, and preventing the escalation to full blown
episodes.88, 89 Adding CBT to pharmacotherapy
results in better adherence to medical treatment,
fewer hospitalizations and relapses and less uctuations in mood.90, 91
iii.
Family-focused treatment
iv.
Reference List
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
BPD is difcult to diagnose and treat, but better diagnostic tools, more awareness and more studies investigating
different treatment regimens, such as real-life combination therapies, in different patient populations (the young,
the elderly) should enhance treatment outcomes. Systematic monitoring can also help in the treatment of patients, as
the more often the patient is seen by a physician, the better
picture the doctor will have to adequately adjust treatment
plans. BPD has a devastating impact on the patient, their
36.
37.
38.
39.
40.
41.
42.
-18-
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
88.
89.
90.
91.
92.
93.
94.
95.
96.
97.
Abbreviations:
5-HT=serotonin; 5-HT(1A, 2A, 2C, 1D)=specic serotonin receptors; AAP=atypical
antipsychotics; AD=antidepressants; AP=antipsychotic; APA=American
Psychiatric Association; ARI=aripiprazole; BAD=Bipolar Affective Disorder;
BAP=British Association of Psychopharmacology; BPD=Bipolar Disorder;
BSP=Bipolar Spectrum Disorder; BP-I=Bipolar I disorder; BP-II=Bipolar II
disorder; BP-NOS=Bipolar disorder not otherwise specied;
CANMAT=Canadian Network for Mood and Anxiety Treatments;
CBT=Cognitive-Behavior Therapy; CBZ=carbamazepine; Chlor=chlorpromazine;
Cloz=clozapine; DA=dopamine; D(2,3)=specic dopamine receptors; DSM-IV
(TR)=Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text
revision; ECT=electroconvulsive therapy; EPS=extrapyramidal side effects;
FDA=Food and Drug Administration; FFT=Family-Focused Treatment; FGA=rst
generation antipsychotic; GABA=gamma-aminobutyric acid; Glu=glutamate;
H=histamine; H1=histamine receptor; IM=intramuscular; IPSRT=Interpersonal
and Social Rhythm Therapy; La=lamotrigine; Li=lithium; M1=muscarinic
receptor; ME=mixed episodes; MOA=mechanism of action; Na=sodium;
NE=norepinephrine; NMDA=N-methyl-d-aspartate; NIMH-LCM-p=National
Institute of Mental Health daily prospective Life-Chart Method;
NT=neurotransmitter; OLZ=olanzapine; PE=Psychoeducation; QUE=quetiapine;
RIS=risperidone; SC=special consideration; SE=side effects; SGA=second
generation antipsychotics; SIADH=syndrome of inappropriate antidiuretic
hormone secretion; SSRI=selective serotonin reuptake inhibitor; TD=tardive
dyskinesia; Tx=treatment; Val=valproate; VSSCs=voltage sensitive sodium
channels; Wk=week; WHO ICD-10=World Health Organization International
Classication of Diseases Version 10; ZIP=ziprasidone.
-19-
A.
B.
C.
D.
E.
Being a woman
Having a manic episode at onset
Hyperthymic temperament
A and C
A, B and C
disorder?
10. Which 2 antipsychotics have intramuscular
A. Unipolar depression
B. Bipolar I
C. Bipolar II
formulations?
A.
B.
C.
D.
receptor?
A.
B.
C.
D.
E.
F.
-20-
Olanzapine
Aripirazole
Risperidone
Ziprasidone
A and C
B and D
Posttest
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Activity Evaluation
Please rate the following, using a scale of:
1-poor
2-fair
3-good
4-very good
5-excellent
1.
1 2 3 4 5
2.
1 2 3 4 5
3.
The level at which the learning objective was met of teaching me to track history and progression of symptoms and treatment
responses for patients with mood/behavioral symptoms
1 2 3 4 5
4.
The level at which the learning objective was met of teaching me to select mood stabilizers and their doses based on patient
presentation
1 2 3 4 5
5.
The level at which the learning objective was met of teaching me to use neurobiologic and mechanistic rationale when combining
medications to treat bipolar spectrum disorders
1 2 3 4 5
6.
The level at which this activity was objective, scientically balanced, and free of commercial bias was
1 2 3 4 5
7.
1 2 3 4 5
8.
9.
Basic
Appropriate
Complex
Too Complex
Change my practice
Seek additional information on this topic
Do nothing as current practice reects activitys recommendations
Do nothing as the content was not convincing
10. What barriers might keep you from implementing changes in your practice youd like to make as a result of participating in this activity?
11. The following additional information about this topic would help me in my practice:
Name:
Credentials:
Specialty:
Address:
City, State, Zip:
Email:
Phone: