1. health and fitness
2. disorders

Date of Release: October 1, 2010
Date of Credit Expiration: September 30, 2011
Supplement to
Faculty Chair
Free
1.0 CME
credit
Henry A. Nasrallah, MD
Professor of Psychiatry and Neuroscience
University of Cincinnati College of Medicine
Cincinnati, Ohio
N o v e m b e r 2 0 1 0 / VO L 2 2 , N O 4
Faculty
Joseph F. Goldberg, MD
Associate Clinical Professor of Psychiatry
Mount Sinai School of Medicine
New York, New York
CME Reviewer
Christoph U. Correll, MD
Medical Director
Recognition and Prevention (RAP) Program
The Zucker Hillside Hospital
Associate Professor of Psychiatry
Albert Einstein College of Medicine
Bronx, New York
Disclosures
Joseph F. Goldberg, MD: AstraZeneca (Speaker’s
Bureau); Cephalon, Inc. (Consultant); Eli Lilly
and Company (Speaker’s Bureau, Consultant);
GlaxoSmithKline (Speaker’s Bureau); Janssen-Cilag
(Lecture); Merck & Co., Inc. (Speaker’s Bureau); Pfizer
Inc. (Speaker’s Bureau)
Henry A. Nasrallah, MD: AstraZeneca (Speaker’s
Bureau, Consultant); Forest Pharmaceuticals (Grants/
Research); Janssen (Speaker’s Bureau, Consultant,
Grants/Research); Merck & Co., Inc.(Speaker’s
Bureau, Consultant); Novartis (Speaker’s Bureau,
Consultant); Otsuka Pharmaceuticals (Grants/
Research); Pfizer Inc. (Speaker’s Bureau, Consultant);
Sepracor/Sunovion (Speaker’s Bureau, Consultant);
Shire Pharmaceuticals (Grants/Research)
Christoph U. Correll, MD: Consultant and/
or advisor to or received honoraria from Actelion
Pharmaceuticals; AstraZeneca; Boehringer Ingelheim;
Bristol-Myers Squibb; Cephalon, Inc.; Eli Lilly and
Company; GlaxoSmithKline; Hoffmann- La Roche;
Intra-Cellular Therapeutics; Janssen; Lundbeck
Inc.; Medicure; Otsuka Pharmaceuticals; Pfizer Inc.;
Schering-Plough; Sepracor/Sunovion; Supernus
Pharmaceuticals; Takeda; Vanda Pharmaceuticals Inc.
Christopher Ontiveros, PhD (Medical Writer): Has
no conflict of interest(s) to report
co n t i n u e d o n pa g e S 2
Jointly sponsored by Albert Einstein College
of Medicine, Montefiore Medical Center, and
Asante Communications, LLC.
This activity is supported by an educational
grant from Janssen, Division of Ortho-McNeilJanssen Pharmaceuticals, Inc., administered by
Ortho-McNeil-Janssen Scientific Affairs, LLC.
It was peer reviewed by Annals of Clinical
Psychiatry.
Copyright © 2010 Quadrant HealthCom Inc.
Available at aacp.com
Differential Diagnosis and
Therapeutic Management of
Schizoaffective Disorder
Introduction
An estimated 1 of 4 inpatient psychiatry admissions is attributed to
schizoaffective disorder (SAD).1,2 Lifetime prevalence of this important
yet poorly understood disorder ranges between 0.5% and 0.8%. Despite
its common presentation, few studies with selectively enriched SAD patient populations have been conducted; therefore, information about
the phenomenology and treatment of SAD derives more from observational studies or small, post hoc analyses, than from large-scale randomized studies.
SAD is a heterogeneous clinical construct marked by mixed psychotic
and affective symptoms, the inter-relationships of which vary considerably between and within individuals, presenting formidable challenges
even to experienced psychiatrists.3,4 The bipolar and depressive subtypes
of SAD exert different influences on perception, cognition, affect, mood,
and physiological functioning. Knowledge about the clinical features,
differential diagnosis, clinical course, and management of SAD has been
shaped by diversity of opinion more than by consensus within the field,
precluding even the most rudimentary definitions for standard of care. In
the American nosology, diagnostic inclusion and exclusion criteria were
not specified prior to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV). International Classification of Diseases and
Related Health Problems 10th revision (ICD-10) criteria for SAD differ in
several fundamental respects from those of DSM-IV (Table 1, page S4)3,5
and likely contribute to variations in diagnostic practice in the United
States and abroad. The paucity of established treatments for SAD, particularly with agents approved by the U.S. Food and Drug Administration,
may further diminish the ability of clinicians to diagnose and treat SAD
with confidence.
Until established norms and rigorous treatment standards for SAD
are developed, discussion about what constitutes optimal care is premature. Although additional well-designed studies would provide much
needed insights into SAD, their enormous cost and length make it unlikely that robust data will be available in the near future. Until a more
extensive evidence base emerges to better inform clinical decision making, expert guidance and practice parameters, which help to fill the gaps
in knowledge, are critically needed. Accordingly, psychiatrists highly
skilled in SAD management convened to foster debate and to exchange
their own best practices. Utilizing a modified Delphi process, the SAD
Working Group deliberated over their own observations and experience with SAD patients, while comparing and contrasting their views on
published studies, which vary considerably by experimental design and
rigor. Although initial efforts have included psychiatrists from across the
c o n t i n u e d o n pa g e S 3
Supplement to Annals of Clinical Psychiatry | Vol 22, No 4 | November 2010
S1
Schizoaffective disorder
Activity Goal
Learners Gap
The goal of this activity is to educate psychiatrists
and other health care professionals on best
practices in the assessment, diagnosis, treatment,
and ongoing care of patients with schizoaffective
disorder.
Patients with SAD meet criteria for schizophrenia,
while also meeting criteria for major depressive
disorder or mania, and will have periods of
psychosis without mood disorder symptoms.
SAD remains underdiagnosed in part because
it is frequently confused with other psychiatric
disorders with overlapping diagnostic criteria—
chiefly schizophrenia, bipolar disorder, and
major depressive disorder. Understanding the
collaborative management of patients with
SAD is an important educational imperative for
psychiatrists and other health care professionals.
Considerable gaps in level-1 evidence mirror
the need for psychiatrists to exchange insights
into this heterogeneous clinical construct and its
clinical management.
Learning Objectives
t the conclusion of this program, participants will
A
be better prepared to:
1.Conduct initial and ongoing assessment of
patients with schizoaffective disorder (SAD),
identifying comorbidities, current and prior
medical history, and treatment goals
2.Diagnose SAD, differentiating it from
schizophrenia, bipolar disorder, and major
depressive disorder
3.Design and implement an appropriate
multimodal treatment plan tailored to
the patient’s SAD subtype and medical
comorbidities
4.Implement psychosocial and
psychopharmacologic interventions shown
to improve treatment outcomes in patients
with SAD
5.Utilize psychosocial and pharmacologic
strategies to improve treatment adherence
among patients with SAD
Intended Audiences
Accreditation Statement
This activity has been planned and implemented
in accordance with the Essential Areas and Policies
of the Accreditation Council for Continuing
Medical Education (ACCME) through the joint
sponsorship of Albert Einstein College of Medicine
and Montefiore Medical Center and Asante
Communications, LLC. Albert Einstein College of
Medicine is accredited by the ACCME to provide
continuing medical education (CME) for physicians.
Credit Designation
This activity is intended for psychiatrists and
other health care professionals interested
in improving their knowledge base and skill
sets in the individualized assessment and
management of patients with schizoaffective
disorder.
Albert Einstein College of Medicine designates
this educational activity for a maximum of 1.0
AMA PRA Category 1 Credit™. Physicians should
only claim credit commensurate with the extent
of their participation in the activity.
Statement of Need
The Conflict of Interest Disclosure Policy of
Albert Einstein College of Medicine requires
that faculty participating in any CME activity
disclose to the audience any relationship(s)
with a pharmaceutical, product, or device
company. Any presenters whose disclosed
relationships prove to create a conflict of
interest with regard to their contribution to the
activity will not be permitted to present.
Patients with SAD must satisfy the criteria
for both schizophrenia and either a major
depressive episode or a manic/mixed
episode.3 The prevalence of SAD has
been estimated at nearly 1% of the US
population.3 Although first characterized
nearly 80 years ago, the evidence base
supporting differential diagnosis and
therapeutic management is limited.
Clinical studies have frequently evaluated
heterogeneous patient populations.
Consequently, much of the guidance for
diagnostic and therapeutic management
derives from studies of schizophrenia, a similar
but nevertheless distinct disorder.7
Schizoaffective disorder remains
difficult to define, monitor, and treat.
Long-term evaluation of patients with SAD,
in particular, presents distinct challenges,
not least because of its often evolving
symptomatology.4 Diagnostic changes
are not unusual and require tight clinical
management. The paucity of peer-reviewed
evidence specifically addressing this clinical
construct confounds treatment, however.
Recent scientific and clinical advances
in our understanding of SAD risk factors,
pathogenesis, and management highlight
an important need among psychiatrists for
peer-to-peer education.
S2
Conflict of Interest Statement
Albert Einstein College of Medicine also requires
that faculty participating in any CME activity
disclose to the audience when discussing
any unlabeled or investigational use of any
commercial product or device not yet approved
for use in the United States.
Joseph F. Goldberg, MD: AstraZeneca
(Speaker’s Bureau); Cephalon, Inc.
(Consultant); Eli Lilly and Company (Speaker’s
Bureau, Consultant); GlaxoSmithKline
(Speaker’s Bureau); Janssen-Cilag (Lecture);
Merck & Co., Inc. (Speaker’s Bureau); Pfizer
Inc. (Speaker’s Bureau).
Henry A. Nasrallah, MD:
AstraZeneca (Speaker’s Bureau, Consultant);
Forest Pharmaceuticals (Grants/Research);
Janssen (Speaker’s Bureau, Consultant,
Grants/ Research); Merck & Co., Inc. (Speaker’s
Bureau, Consultant); Novartis (Speaker’s
November 2010 | Vol 22, No 4 | Supplement to Annals of Clinical Psychiatry
Bureau, Consultant); Otsuka Pharmaceuticals
(Grants/Research); Pfizer Inc.(Speaker’s Bureau,
Consultant); Sepracor/Sunovion (Consultant);
Shire Pharmaceuticals (Grants/Research).
Christoph U. Correll, MD: Consultant and/
or advisor to or has received honoraria from
Actelion Pharmaceuticals; AstraZeneca;
Boehringer Ingelheim; Bristol-Myers Squibb;
Cephalon, Inc.; Eli Lilly and Company;
GlaxoSmithKline; Hoffmann- La Roche; IntraCellular Therapeutics; Janssen; Lundbeck Inc.;
Medicure; Otsuka Pharmaceuticals; Pfizer
Inc.; Schering-Plough; Sepracor/Sunovion;
Supernus Pharmaceuticals; Takeda; Vanda
Pharmaceuticals Inc.
Christopher Ontiveros, PhD (Medical
Writer): Has no conflict of interest(s) to report.
Albert Einstein College of Medicine and
Montefiore Medical Center, Center for
Continuing Medical Education (CCME) staff,
and the staff of Asante Communications, LLC,
have no conflicts of interest with commercial
interests related directly or indirectly to this
educational activity.
The staff at Albert Einstein College of Medicine
has no disclosures to report other than the
following:
Steven Jay Feld, or a member of his
household, owns securities in Bioheart, Inc.;
Chelsea Therapeutics, Inc.; and Pharmacopeia,
Inc.
Method of Participation
There are no fees for participating in and
receiving credit for this activity. Participants
should complete the activity, the self-report
credit form, posttest, and activity evaluation form
on pages S11 and S12 and mail to CCME, 3301
Bainbridge Avenue, Bronx, NY 10467, or fax to
(718) 798-2336. A score of at least 70% is required
to successfully complete this activity. Certificates
will be mailed approximately 6 to 8 weeks after
receipt of mailed submissions and verification
of a passing grade. Online participation is also
available via www.psychclinician.com/education
(availability may be delayed from original print
date). Enter the activity title in the search field
to access the activity directly. Credit is available
through September 30, 2011.
Copyright Information
Copyright ©2010 Albert Einstein College of
Medicine and Montefiore Medical Center and
Asante Communications, LLC. All rights reserved.
No part of this monograph may be used or
reproduced in any manner whatsoever without
written permission except in the case of brief
quotations embodied in articles or reviews.
c on t in ued from page S1
United States, the SAD Working Group hopes to expand
the consensus conference globally, underscoring the need
for improved therapeutic management of this prevalent
and complex disorder.
Methods
The SAD Working Group was convened as a continuing
medical education activity accredited by the Albert Einstein Medical Center. Chaired by Henry A. Nasrallah, MD,
the Working Group comprises a diverse group of thought
leaders with expert insights into the etiology of SAD,
strengths and limitations of screening and assessment
tools, and current pharmacotherapy and psychosocial interventions. Members of the SAD Working Group utilized
a modified Delphi process to draft and refine consensus
statements on key issues relevant to the assessment and
management of patients with SAD (Appendix, page S8).
First, the SAD Working Group explored the phenomenology of SAD, consolidating seminal studies on its diagnostic and clinical correlates. Second, evidence-based studies
and clinical experience provided the substrate for a clinical
framework, outlined by consensus statements of threshold
importance and designed to operationalize the recognition, differential diagnosis, and initial and ongoing management of patients with SAD. Third, the clinical utility of
the Delphi consensus statements were evaluated at a series
of regional workshops, where academic and communitybased psychiatrists discussed salient issues in a series of
case studies. Feedback from these workshops helped inform the final consensus statements.
Phenomenology
Variations in diagnostic criteria for SAD (DSM-IV TR
vs. ICD-10) (Table 1, page S4), low inter-rater diagnostic
reliability, and limited understanding of the factors that
govern its onset, progression, and pathogenesis seriously hinder recognition, diagnosis, and treatment of this
complex disorder.3,5,8 Current diagnostic systems divide
psychotic disorders into subtypes, directly conflicting
with Kraepelin’s dichotomous classification. Additionally, DSM-IV TR defines SAD as an uninterrupted illness, whereas ICD-10 considers SAD as episodic. Such
confounding diagnostic criteria present clinicians with a
nosological dilemma, and undermine perceptions of SAD
as a unified clinical entity. To date, several classification
schemas for SAD have been proffered, reflecting the limited scientific and clinical data. The scope of this report
precludes in-depth comparisons of the merits and limitations of these varying descriptions.
SAD has been variously described as a heterogeneous disorder comprising elements of both schizophrenia and bipolar disorders9,10; a distinct clinical construct
unrelated to bipolar disorder or schizophrenia7; schizophrenia with mood symptoms11; a mood disorder with
psychosis12; comorbid schizophrenia and mood disorder13; and finally a heterogeneous phenomenon situated
on a middle point in a continuum between schizophrenia and mood disorders14,15 (Table 2, page S5). Additional studies are needed to better understand its place in
the psychiatric nomenclature, as well as to provide practical knowledge about its recognition and treatment.
Etiology/pathophysiology
Based on empirical observations and varying levels of
evidence from clinical studies, the SAD Working Group
identified core concepts that define SAD etiopathophysiology. First, the SAD Working Group supports SAD as
a clinical construct best described as situated on a continuum between schizophrenia and bipolar disorder.
Among authorities in the field—including psychiatrists,
clinical researchers, and scientists—there is considerable
uncertainty about the relationship of SAD to schizophrenia and mood disorders. Some primarily view SAD as
schizophrenia or a psychotic disorder, whereas others
argue it is a mood disorder variant. The questions constitute a still emerging area of research, with investigators evaluating genetic, neuroanatomic, and physiologic
differences across different patient populations. For example, inherited susceptibility to SAD is attributed to
risk alleles. Mansour and coworkers have reported that
a variety of genes and risk alleles may be associated
with SAD susceptibility and etiology.16 Genes involved
in circadian rhythm and retinoic acid receptor systems,
for example, have been linked with SAD.16 Importantly,
variants of these genes are also associated with schizophrenia and bipolar disorder.16,17 Although incomplete,
the data support SAD as a genetic intermediary between
bipolar disorder and schizophrenia.
The SAD Working Group identified distinct neuroanatomic and physiologic abnormalities in patients with
SAD. Several published studies have reported abnormal
saccades, altered evoked potentials, and cognitive impairments in patients with SAD. Computerized measures of
memory are significantly different in schizophrenia and
SAD patient populations.18, 19 For example, while patients
with schizophrenia exhibit pronounced verbal and visuomotor working memory impairments, patients with SAD
maintain normal verbal working memory.18 As SAD is an
illness that may change over time, it is important to understand the possible differential diagnostic utility of neurocognitive assessment over extended periods. One study
found significant differences between patients with schizophrenia and SAD on motor screening and explicit memory
tests during 3 office visits over a period of 19 months.19
While sufficient studies have not been conducted on the
diagnostic utility of neurocognitive and similar discriminative tests, it is hoped that such batteries may eventually
serve as clinical assessment tools that facilitate a more accurate diagnosis. Further research will inform clinical recognition and assessment of patients with SAD, promising
to optimize differential diagnosis and treatment success.
Assessment and diagnosis
SAD is a psychiatric illness characterized by schizophrenia co-occurring with prominent affective symptomatology consistent with a major mood episode. In addition to
cross-sectional symptoms that may be evident on acute
presentation, an accurate diagnosis of SAD requires a longitudinal assessment of patient history, particularly psychiatric information, to determine temporal overlap and
relative distribution of psychotic and mood symptoms over
at least one month. To this end, it is necessary to rely on
accurate personal reports of symptoms and behaviors, col-
Supplement to Annals of Clinical Psychiatry | Vol 22, No 4 | November 2010
S3
Schizoaffective disorder
Table 1
DSM-IV TR and ICD-10 diagnostic criteria for SAD
Diagnostic Criteria
Affective
DSM-IV
ICD-10
Major depressive, manic, or
mixed episode
Prominent
manic, depressive, or mixed
symptoms
Schizophrenic
Duration
Meeting Criterion
A for schizophrenia
(presence of ≥2 delusions, hallucinations,
disorganized speech,
behavioral disturbances, or negative
symptoms)
Major depressive
episode 2 weeks;
mixed or manic
1 week
One, preferably 2 of
(a)-(d) symptoms for
schizophrenia*
Mania ≥1 week;
depression ≥2
weeks
Simultaneity
During the same
period of the illness
Psychotic symptoms 1 month to
meet Criterion A
for schizophrenia
Additional
Delusions or hallucinations for ≥2 weeks
without prominent
mood symptoms
Mood symptoms as a
substantial portion of
the total illness duration
Simultaneous, or at
least within a few
days of each other
* Symptoms include (a) thought echo, thought insertion or withdrawal, or thought broadcasting; (b) delusions of control, influence or passivity, clearly referred to body
or limb movements or specific thoughts, actions, or sensations; delusional perception; (c) hallucinatory voices giving a running commentary on the patient’s behavior, or discussing him between themselves, or other types of hallucinatory voices coming from some part of the body; (d) persistent delusions of other kinds that are
culturally inappropriate and completely impossible (eg, being able to control the weather, being in communication with aliens from another world).
Source: References 3,5
lateral information, and medical and mental health records.
Comprehensive multiaxial physical and neurological examinations can provide important information as well.
Timely recognition and appropriate differential diagnosis of SAD helps individualize treatment. Initial assessment includes consideration of risk factors such as
family history and age. Despite the limited data, the SAD
Working Group recognizes a family history of psychotic or
mood disorders as an important risk factor predictive of
SAD. According to results from a recent large-scale study,
the relative risk of SAD was 2.76 if a first-degree relative
had a history of mental illness compared with control subjects with no with no such family history.20 More precisely,
the relative risk of SAD was 3.23, 2.57, or 1.92 if the firstdegree relative had bipolar disorder, schizophrenia, or
SAD, respectively. Age is another risk factor, especially for
the recognition of SAD subtype. Although empirically derived data are lacking, the SAD Working Group concluded
that depressive symptoms generally predominate with increasing age, as with bipolar disorder. Long-term studies
demonstrating this age-related phenomenon are needed to
substantiate the consensus. Conversely, younger patients
are more likely to present with manic features, although
here, too, the data are largely empirical.
The timing and duration of psychotic and mood
symptoms are the most important determinants for an accurate SAD diagnosis. The temporal relationship of psychotic and affective symptoms and proportion of affective
symptoms relative to the entire duration of the illness must
be ascertained. In addition, clinicians must differentiate
negative symptoms from depression and mania from agitation. Whether mood symptoms are of sufficient duration
and severity to warrant a diagnosis of SAD in contradistinction to schizophrenia is a common challenge. Further,
it is often difficult to determine whether the psychosis occurs only within the context of a mood episode, in which
case the diagnosis would be mood disorder with psychotic
features rather than SAD. The complex differential diagnosis should address psychosis due to a medical condition,
S4
delirium, or dementia; mood symptoms in schizophrenia;
mood disorders with psychotic features; and substanceinduced psychotic disorder.
Longitudinal history-taking and multiaxial examination are critical determinants for accurate SAD diagnosis.
A variety of patient-administered tools are available. Some
practitioners may find self-report or clinician-rated assessment tools as useful adjuncts to supplement their clinical
interviews. Structured questionnaires, interviews, and rating scales are available to help differentiate SAD subtypes,
measure the severity of illness and its impact on patient
function, and monitor treatment responsiveness. Although
no assessment methods and resources have as yet been validated specifically for SAD, the SAD Working Group nevertheless recommends a variety of tools (Table 3, page S6).
Comprehensive assessment provides important
biopsychosocial data critical for understanding the SAD
patient. Several studies have reported high rates of comorbidity, impaired social, vocational and/or occupational
function, and associated reduction in overall quality of
life.21, 22 Patients with SAD, for example, have a high prevalence of metabolic syndrome and chronic pulmonary disease.23, 24 Higher rates of coexisting psychiatric morbidities
have been reported as well. According to work by Cosoff
and Hafner, nearly one-half of all SAD patients (45%; 9/20)
had symptoms consistent with comorbid anxiety disorder.25 The SAD Working Group stressed the importance
of recognizing and managing medical and psychiatric comorbidities, especially metabolic dysregulation or weight
gain, which can be causally related to the illness itself,
sedentary lifestyle, unhealthy diet, medication side effects,
or a combination of these factors. Medication-related morbidity warrants careful assessment of current and prior
medication history. Adjustments to diet, exercise, and/or
medications should be considered consistent with patient
preferences, goals, and needs.26
For good treatment outcomes, patient assessment is
necessarily longitudinal. At times, mood state changes
across the life cycle of SAD patients may be particularly
November 2010 | Vol 22, No 4 | Supplement to Annals of Clinical Psychiatry
dramatic, warranting a change in diagnosis from the depressive to manic subtype, with important implications for
multimodal treatment. For some patients, the lability of the
mood and psychotic features may manifest across different
episodes of the illness separated by a recovery period. For
example, an individual may have SAD depressive subtype,
fully recover, and after several months develop hallucinations and delusions without prominent mood symptoms
for an extended period (eg, 7 months), warranting a change
of diagnosis to schizophrenia. This evolution of symptomatology in patients initially diagnosed with SAD is not uncommon. According to a seminal 2-year study, only 36%
(12/33) of patients initially diagnosed with SAD continued
to meet DSM-IV diagnostic criteria for the illness.27 After
2 years, the predominant diagnostic changes were to major depressive disorder (26%, 27/103), followed by bipolar disorder (17%; 24/141) and finally schizophrenia (8%;
12/145). In a separate, 5-year, retrospective study, 61% of
patients initially diagnosed with SAD (37/61) were subsequently diagnosed with bipolar disorder.28 In addition
to the age-related instability of subtypes, SAD is the most
commonly revised diagnosis in patients with psychotic features. One large-scale study found that 22.4% (112/500) of
patients had a different diagnosis 2 years after their initial
diagnosis; SAD represented the most changed-to diagnosis
(53.6%; 60/112).29 The results of these studies are consistent
with the instability of an SAD diagnosis and highlight the
benefits of longitudinal assessment and need to restructure
treatment accordingly
Treatment/ongoing care
Reflecting an inadequate understanding of the biologic basis and clinical correlates of SAD, treatment strategies have
received little attention in the peer-reviewed literature and
evidence-based guidelines. Only a handful of well-controlled studies have investigated the efficacy of pharmacologic or psychotherapeutic approaches in well-defined
SAD patient populations. Clinicians necessarily draw
tentative conclusions from studies of mixed patient populations—including, for instance, SAD and schizophrenia—
that demonstrate significantly improved outcomes.
The primary objective of pharmacotherapy is to
achieve symptomatic control. As with virtually all psychiatric disorders, best patient outcomes are achieved
by multimodal therapy, usually a combination of pharmacologic agents with psychotherapeutic or psychosocial modalities. Atypical antipsychotics are currently the
mainstay of pharmacotherapy for SAD, although more
studies are needed to establish their efficacy, particularly in patients with complex, evolving symptomatology.
Acute and maintenance therapy are guided by results
from longitudinal, multiaxial assessment, from experience in managing this sometimes difficult-to-treat patient
population, and from good clinical judgment. Accompanying this monograph is an evidence-based conceptual
framework and consolidated resource that will, when
applied on a patient-by-patient basis, help structure the
decision making process for patients with SAD.
Selecting an appropriate atypical antipsychotic requires adequate physician-patient dialogue, patient and
family education, treatment adherence, and thoughtful
Table 2 Comparative symptom severity of
schizoaffective disorder, schizophrenia, and
mood disorder comparator
Variable
Pattern of characteristics
Demographic data
• Female
• Never married
• Unemployed
SCH≤SAD≤MD
SCH≥SAD≥MD
SCH>SAD>MD
Family morbidity
• SCH risk
• MD risk
SCH≥SAD≥MD
SCH≤SAD≤MD
Complementary exams
• Dexamethasone suppression test
• Structural neuroimage
SCH<SAD<MD
SCH=SAD≥MD
Symptomatology
• Global evaluation
• Psychotic
• Negative
• Affective
• Cognitive deficit
• Insight deficit
SCH=SAD=MD
SCH≥SAD≥MD
SCH>SAD>MD
SCH≤SAD≤MD
SCH>SAD>MD
SCH≥SAD≤MD
Other clinical variables
• Social premorbid adaptation
• Age of illness onset
• Total number of episodes
• Total number of hospitalizations
• Suicidal behavior
• Comorbidity with substance abuse
• Clinical evolution
• Response to drug treatment
SCH<SAD<MD
SCH≤SAD≤MD
SCH<SAD≤MD
SCH≤SAD≥MD
SCH≤SAD≥MD
SCH≤SAD≤MD
SCH≤SAD≤MD
SCH≤SAD≤MD
SCH: schizophrenia; SAD: schizoaffective disorder; MD: mood disorder
Source: Reference 15
assessment and management of adverse events. Careful
review of the available evidence provides essential, albeit
limited, guidance. For example, randomized controlled
trials of atypical antipsychotic monotherapy in mixed
samples of SAD and schizophrenia patients have shown
significant improvements in symptoms, social rehabilitation, and quality of life when compared to patients treated
with typical antipsychotics.21,30 Only 2 randomized, doubleblind, placebo-controlled studies of an atypical antipsychotic (paliperidone extended-release, now FDA-approved
for the treatment of SAD), have been conducted in a welldefined SAD patient population (Figure, page S7).31 Treatment was well-tolerated and conferred significant benefits
across numerous psychiatric, functional, mood, and quality
of life domains as measured by the Positive and Negative
Syndrome Scale (PANSS), Clinical Global Impressions Scale
(CGI-S), Young Mania Rating Scale (YMRS), and Hamilton
Depression Rating Scale (HAM-D).31-35 In a randomized,
placebo-controlled study in patients with SAD, Keck and
coworkers reported improved mean scores in ziprasidonetreated patients as per the Brief Psychiatric Rating Scale
(BPRS) total, BPRS core, BPRS manic, and mean CGI-S
scales.36 Reflecting the infancy of comparative effectiveness
research in general, few studies with SAD patients have
utilized active controls. In 2 older studies, olanzapine demonstrated superior efficacy when compared to haloperidol,
Supplement to Annals of Clinical Psychiatry | Vol 22, No 4 | November 2010
S5
Schizoaffective disorder
Table 3
Scale
Assessment questionnaires
Administration (time)
Domains of assessment
Psychosis
PANSS
Clinician-rated (20-30 min)
Severity of common symptoms in patients with schizophrenia and other psychotic
disorders, delineation of target symptoms, and monitoring of treatment response
BPRS
Clinician-rated (20-30 min)
Response to treatment in patients with moderate to severe
psychotic disorders
BDI-II
Self-report or clinician-report
(5-10 min)
Severity of depressive symptoms in patients diagnosed with depressive illness
and monitoring of treatment effects
GDS
Self-report (10-15 min)
Depressive illness and monitoring changes with treatment in geriatric patients
HAM-D
Clinician-reported (15-20 min)
Severity of depressive symptoms in patients with primary depressive
illness and monitoring changes with treatment
MADRS
Clinician-reported (5-10 min)
Severity of depressive symptoms
PHQ-9
Self-report, clinician-reported
(<2 min)
DSM-IV depressive disorder diagnoses and grading of depressive symptom
severity
QID-SR
Self-report (5-7 min)
Depressive symptom severity and symptomatic changes in a time-efficient
manner to gauge effects of treatment
YMRS
Clinician-reported (15-30 min)
Severity of mania and evaluation of changes in mania symptoms with treatment
over time
Mood
PANSS: Postive and Negative Syndrome Scale; BPRS: Brief Psychiatric Rating Scale; BDI-II: Beck Depression Inventory II; GDS: Geriatric Depression Scale;
HAM-D: Hamilton Depression Rating Scale; MADRS: Montgomery-Åsberg Depression Rating Scale; PHQ-9: Patient Health Questionnaire-9; QID-SR: Quick Inventory
of Depressive Symptomatology—Self-Report; YMRS: Young Mania Rating Scale
Source: References 36,54-57
while another study showed significantly improved sideeffect profiles in risperidone-treated patients compared
with those receiving haloperidol.37-39
Other published studies supporting the safety and efficacy of atypical antipsychotics in SAD patients are limited by their focus on patients with schizophrenia and/
or bipolar disorder, and by their post hoc analyses of SAD
subgroups. Available data are limited also by the heterogeneity of SAD itself; studies often included patients with
established bipolar and depressive subtypes without prospectively defined and subtype-specific endpoints. Still
other variations in experimental design—including study
duration, size, methodology, and outcome measures—also
limit the conclusions (and recommendations) that the SAD
Working Group can make.40 Consensus on important treatment issues did emerge, nonetheless.
Among the clear points of consensus is that acute management of psychotic symptoms in SAD patients should include antipsychotic therapy. The SAD subtype influences
pharmacologic approaches to maintenance treatment,
however. Although all patients with SAD are generally
prescribed an antipsychotic, there is debate about the value
of adjunctive antidepressants or mood stabilizers such as
lithium or divalproex.30,41-43 Nevertheless, based at least in
part on their experience managing patients with bipolar
disorder, the SAD Working Group recommends addition of
a mood stabilizer in patients with SAD bipolar subtype, at
least when manic symptoms do not adequately respond to
antipsychotic treatment alone.
Randomized controlled trials have evaluated rational
multi-drug therapy, with inconclusive findings, although
most viewed atypical antipsychotics as first-line treatment
S6
for SAD, particularly during acute episodes.30,44,45 Two randomized controlled trials have shown measurable benefits
of mood stabilizers in patients with SAD. In an older trial,
fluphenazine proved superior to lithium in patients with
SAD depressive subtype, and carbamazepine demonstrated superior prophylactic efficacy when compared to
lithium in patients with SAD bipolar subtype.46,47 Limited
evidence precludes definitive conclusions regarding the
role of antidepressants, yet the SAD Working Group concluded that the addition of an antidepressant is reasonable
when depressive symptoms persist following stabilization
of psychosis.
Most of the psychiatrists in the SAD Working Group
emphasized that non-pharmacologic therapies should generally be used in combination with pharmacologic agents to
achieve the greatest benefit, although the notion of additive
and potentially supra-additive effects is based on empirical
observations alone. Psychosocial interventions, which often include the patient with select family members, friends,
partners, and caregivers, can enhance patient insight into
the illness, teach appropriate social skills, and restore vocational functioning. Cognitive-behavioral therapy (CBT) can
help patients understand the relationship between their feelings, maladaptive patterns of thinking, and distress. Over
time, CBT helps patients develop adaptive behaviors and
routines that improve adherence to the prescribed regimen,
a linchpin for sustained efficacy. Along these lines, psychoeducation can help raise patient awareness about the illness
and appropriate treatment options. Patients are educated,
for instance, about treatment-related side effects, timing of
dosing, and other particulars that can prove daunting to patients with impaired cognition and executive function.
November 2010 | Vol 22, No 4 | Supplement to Annals of Clinical Psychiatry
ADelphi-BAseDResouRce
DSM-IV TR Criteria for
Schizoaffective Disorder (SAD)a
• An uninterrupted period of illness during which there is a
major depressive episode, a manic episode, or a mixed
episode, concurrent with symptoms that meet criterion A for
schizophreniab
• During the same period of illness, delusions or hallucinations
persisting for >2 weeks in the absence of prominent mood
symptoms
• Symptoms meeting criteria for a mood episode are present
for a substantial portion of the total duration of the active and
residual periods of the illness
• The disturbance is not due to the direct physiological effects of
a drug of abuse, a medication, or a general medical condition
• Bipolar subtype: if the disturbance includes a manic or a
mixed episode (or a manic or a mixed episode and major
depressive episodes)
• Depressive subtype: if the disturbance includes only a major
depressive episode
DSM-IV TR, Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition,
Text Revision; ICD-10, International Classification of Diseases-10th Revision.
a
DSM-IV TR diagnostic criteria are not consistent with ICD–10 criteria, and genetic,
neurophysiologic, and psychological benchmarks of schizoaffective disorder are
not unequivocal.1,2
b
Includes delusions, hallucinations, disorganized speech, grossly disorganized or
catatonic behavior, and negative symptoms. Does not include symptoms due to a
general medical condition.3
Jointly sponsored by Albert Einstein College of Medicine and Montefiore Medical Center, and
Asante Communications, LLC.
This activity is supported by an educational grant from Janssen, Division of Ortho-McNeil-Janssen
Pharmaceuticals, Inc., administered by Ortho-McNeil-Janssen Scientific Affairs, LLC.
Behavior Therapy
Family Therapy
Group Therapy
Supportive Psychotherapy
Bipolar
Depressive
Prominent psychotic
component9,10
Non-Pharmacologic
3
1
6
Depressive
Anxiolytics and
Anticonvulsants
Mood Stabilizers
Antidepressants
Antipsychotics
2
Bipolar
Pharmacologic
Minimal psychotic
component9,10
5
SAD constitutes a heterogeneous clinical construct encompassing both schizophrenia and mood
disorders and forming a continuum between the 2 conditions.4 DSM-IV TR defines SAD as a longitudinal,
uninterrupted disorder but ICD-10 classes it as episodic. Nevertheless, it is generally agreed that
duration, and relative proportion of psychotic vs affective symptoms can enable accurate SAD diagnosis
and treatment optimization.5 To date, treatment of SAD is largely symptomatic and predicated on
the management of other psychotic and/or mood disorders. This algorithm summarizes best-practice
parameters derived from the literature.6
Assessment and Diagnosis
• Determine whether patient meets criteria for SAD
– Conduct diagnostic interview
– Obtain history and self-report, including current medications
– Use structured diagnostic questionnaires and rating scales such as Hamilton Depression Rating Scale (HAM-D),
Montgomery-Åsberg Depression Rating Scale (MADRS), Positive and Negative Syndrome Scale (PANSS), Personal and
Social Performance (PSP) scale, Young Mania Rating Scale (YMRS)
• Obtain physical exam and laboratory panel
• Rule out symptoms secondary to a substance-induced or general medical condition
• Assess psychiatric and physical comorbidities (eg, anxiety disorder, migraine, substance-use disorder, Axis II
disorder, metabolic syndrome7,8)
• Evaluate need for and components of multimodal treatment plan
4
The selection of medications used to treat SAD depends on whether the depressive or bipolar subtype is present. When there is good
premorbid function, early treatment frequently improves outcomes. In the depressive subtype, an antipsychotic is used sometimes in
combination with an antidepressant. In the bipolar subtype, an antipsychotic can be used in combination with a mood stabilizer.
When psychosis is not prominent, psychotherapy can be very effective.
Circled numbers in this flow chart are expanded upon in the corresponding numbered boxes. Assessment and diagnostic recommendations run
from top down in this schematic.
SAD Tool R9.indd 2
Faculty Chair
Henry A. Nasrallah, MD
Professor of Psychiatry and Neuroscience
University of Cincinnati
College of Medicine
Cincinnati, Ohio
Joseph F. Goldberg, MD
Associate Clinical Professor of Psychiatry
Mount Sinai School of Medicine
New York, New York
CME Reviewer
Christoph U. Correll, MD
Medical Director, Recognition and
Prevention (RAP) Program
The Zucker Hillside Hospital
Associate Professor of Psychiatry
Albert Einstein College of Medicine
Bronx, New York
This and other resources are available at
SAD Treatment Algorithm
•Annals of Clinical Psychiatry, Vol 22. No 4, November 2010
Thisresourceispartofaneducationalprogram,componentsofwhichinclude:
•Webcast on Medscape via http://cme.medscape.com/viewprogram/31497
•Additional resources made available at PSYCHClinician.com
12. Greil W, Ludwig-Mayerhofer W, Erazo N, et al. Lithium vs
carbamazepine in the maintenance treatment of schizoaffective disorder: a randomised study. Eur Arch Psychiatry Clin
Neurosci. 1997;247(1):42-50.
References
1. Mental and behavioural disorders. In: World Health Organization. International Statistical Classification of Diseases and
Related Health Problems. 10th rev, version for 2007. Geneva,
Switzerland: World Health Organization; 2007:chap V.
13. Bechdolf A, Knost B, Nelson B, et al. Randomized comparison of group cognitive behaviour therapy and group
psychoeducation in acute patients with schizophrenia:
effects on subjective quality of life. Aust N Z J Psychiatry.
2010;44(2):144-150.
1
2
3
4
5
6
SAD with prominent psychotic component9,10
• Assess proportionality of depressive vs bipolar components
SAD with minimal psychotic component9,10
• Assess proportionality of depressive vs bipolar components
SAD with prominent psychotic component—bipolar
• Initiate immediate antipsychotic pharmacotherapy 11
• Assess probable need for and responsiveness to mood stabilizers12
• Consider addressing manic elements with mood stabilizer
• Initiate psychotherapy tailored to patient and family needs13
SAD with prominent psychotic component—depressive
• Initiate immediate antipsychotic pharmacotherapy14
• Assess probable need for and responsiveness to an antidepressant12,15,16
• Initiate psychotherapy tailored to patient and family needs13
SAD with minimal psychotic component—bipolar
9/24/10 1:30:43 PM
• Assess pharmacotherapeutic approach to treating psychotic component15,16
• Consider mood-stabilizing pharmacotherapy17
• Enhance patient insight into the illness; include family, friends, partners, and caregivers
• Teach appropriate social skills, focusing on vocational functioning13
• Use cognitive behavioral therapy to help patients understand relationships between feelings,
thinking patterns, and distress
• Consider behavioral tailoring to help develop a routine for taking medication
• Educate patients about treatment and the illness13 (eg, psychoeducation focused on medication effects,
timing of dosing, etc)
SAD with minimal psychotic component—depressive
• Assess pharmacotherapeutic approach to treating psychotic component
• Consider antidepressant pharmacotherapy
• Assess current quality of life and use cognitive behavioral therapy to help patients understand relationship
between feelings, thinking patterns, and distress
• Address social/vocational functioning with individual/family counseling
Need for adjunctive antidepressants or mood stabilizers is not universally agreed upon, given the mood-stabilizing properties of the newest
generation antipsychotic medications.16,18,19
This and other resources are available at
19. Perlis RH, Welge JA, Vornik LA, et al. Atypical antipsychotics in the treatment of mania: a meta-analysis of
randomized, placebo-controlled trials. J Clin Psychiatry.
2006;67(4):509-516.
18. Levinson DF, Umapathy C, Musthaq M. Treatment of schizoaffective disorder and schizophrenia with mood symptoms.
Am J Psychiatry. 1999;156(8):1138-1148.
17. Bowden CL, Grunze H, Mullen J, et al. A randomized,
double-blind, placebo-controlled efficacy and safety study
of quetiapine or lithium as monotherapy for mania in bipolar
disorder. J Clin Psychiatry. 2005;66(1):111-121.
16. Kempf L, Hussain N, Potash JB. Mood disorder with psychotic features, schizoaffective disorder, and schizophrenia
with mood features: trouble at the borders. Int Rev Psychiatry. 2005;17(1):9-19.
15. Cosoff SJ, Hafner RJ. The prevalence of comorbid anxiety in
schizophrenia, schizoaffective disorder and bipolar disorder.
Aust N Z J Psychiatry. 1998;32(1):67-72.
14. Keck PE Jr, Reeves KR, Harrigan EP, Ziprasidone Study
Group. Ziprasidone in the short-term treatment of patients
with schizoaffective disorder: results from two double- blind,
placebo-controlled, multicenter studies. J Clin Psychopharmacol. 2001;21(1):27-35.
2. Maj M, Pirozzi R, Formicola AM, et al. Reliability and validity
of the DSM-IV diagnostic category of schizoaffective disorder: preliminary data. J Affect Disord. 2000;57(1-3):95-98.
3. American Psychiatric Association. Diagnostic and Statistical
Manual of Mental Disorders. 4th ed, text rev. Washington,
DC: American Psychiatric Association; 2000.
4. Cheniaux E, Landeira-Fernandez J, Lessa Telles L, et al.
Does schizoaffective disorder really exist? A systematic
review of the studies that compared schizoaffective disorder
with schizophrenia or mood disorders. J Affect Disord.
2008;106(3):209-217.
5. Nardi AE, Nascimento I, Freire RC, et al. Demographic and
clinical features of schizoaffective (schizobipolar) disorder—
a 5-year retrospective study. Support for a bipolar spectrum
disorder. J Affect Disord. 2005;89(1-3):201-206.
6. Azorin JM, Kaladjian A, Fakra E. Current issues on schizoaffective disorder [in French]. Encephale. 2005;31(3):359-365.
7. Basu R, Brar JS, Chengappa KN, et al. The prevalence of
the metabolic syndrome in patients with schizoaffective
disorder–bipolar subtype. Bipolar Disord. 2004;6(4):314-318.
8. Olfson M, Marcus SC, Wan GJ. Treatment patterns for
schizoaffective disorder and schizophrenia among Medicaid
patients. Psychiatr Serv. 2009;60(2):210-216.
9. Levitt JJ, Tsuang MT. The heterogeneity of schizoaffective disorder: implications for treatment. Am J Psychiatry.
1988;145(8):926-936.
10. Evans JD, Heaton RK, Paulsen JS, et al. Schizoaffective
disorder: a form of schizophrenia or affective disorder?
J Clin Psychiatry. 1999;60(12):874-882.
11. Canuso CM, Lindenmayer JP, Kosik-Gonzalez C, et al. A
randomized, double-blind, placebo-controlled study of
paliperidone ER in the treatment of subjects with schizoaffective disorder [poster]. Paper presented at: US Psychiatric
and Mental Health Congress; October 30-November 2,
2008; San Diego, CA.
This and other resources are available at
FolDheRe
FolDheRe
Side Effect Profile
• Assess antipsychotic and mood-stabilizer pharmacotherapy for early nonresponse (<20% PANSS
reduction) and adjust treatment plan accordingly
• Continue pharmacotherapy in partial responders for 8-12 weeks with dose optimization to
determine efficacy
• Monitor for changes in the balance between psychotic symptoms and affective/mood symptoms.
Initial SAD subtype diagnosis is frequently unstable and may progress to schizophrenia or major
depression/mania with psychotic features
• Watch for rapid switch from depression to mania and/or a mixed state after treatment with an
antidepressant; may suggest SAD with bipolar symptoms
• Initiate other therapeutic options, such as electroconvulsive therapy or clozapine if
patient is consistently unresponsive to multiple pharmacotherapy trials or other targeted,
individualized interventions
• Utilize a multimodal approach, combining pharmacotherapy with psychotherapy and psychosocial/
vocational intervention, such as individual and family counseling
• Combine ≥1 psychotropic drugs (an antipsychotic with a mood-stabilizing or antidepressant
medication) based on SAD subtype, medical/psychiatric comorbidities, and psychosocial variables,
including medication adherence
• Initiate antipsychotic therapy with an atypical agent first in SAD with bipolar symptoms; subsequently
add a mood stabilizer if needed
• Initiate antipsychotic therapy first in SAD with depressive symptoms, to limit
frequency/severity of psychoses. After stabilization of psychosis, antidepressant
therapy should be considered
• Monitor symptoms longitudinally to ensure optimal assessment and treatment response
• Perform physical exam, laboratory panel, medical/psychiatric history, and assessment of
comorbidities (eg, obesity, diabetes, anxiety, substance-induced syndromes)
• Inquire about suicidal/homicidal ideation, evidence of self-neglect/disability, and any history of
admission to inpatient psychiatric facilities
• Use rating scales including HAM-D, MADRS, PANSS, PSP, and YMRS, to quantify affective/
psychiatric symptoms
• Risk factors include female sex and familial/genetic predisposition to psychosis and
mood disorders
• Neuroanatomic abnormalities likely present in striatum, corpus callosum, and
neocortical volume
• Neurophysiologic abnormalities likely present in signal processing, cognitive impairment
(eg, memory and executive functions), saccadic eye movements, and altered evoked potentials,
which mirror bipolar disorder and schizophrenia
• Symptoms that meet criterion A for schizophrenia (delusions, hallucinations, disordered
thoughts/speech or behavior, or negative symptoms) concurrent with significant manic or
depressive symptoms
• Delusions, hallucinations, or disordered thoughts without significant manic/depressive symptoms
persisting for >2 weeks
• Manic or depressive phase duration significant in comparison to total duration of psychotic illness
• Two subtypes: SAD with bipolar symptoms and SAD with depressive symptoms, with latter more
prevalent with increasing age of patient population
• Clinical studies reporting pharmacotherapeutic success in SAD are limited
SAD Diagnosis and Treatment Quick Reference
SAD Tool R9.indd 3
Boxed
Warnings
1
Neuroleptic malignant syndrome, QTc
prolongation, tardive dyskinesia, and
hyperprolactinemia
Relevant Indications
1,2
Somnolence, dizziness, dry mouth,
constipation, and weight gain
Intervention
1
Cerebrovascular events in
elderly patients with dementiarelated psychosis, neuroleptic
malignant syndrome, tardive
dyskinesia, hyperglycemia, and
hyperprolactinemia
Paliperidone
1
QTc prolongation, neuroleptic
malignant syndrome, tardive
dyskinesia, and rash
• Major depressive disorder
Adjunctive Medications
Ziprasidone
Risperidone
Quetiapine
2
Agitation, dry mouth, insomnia,
headache/migraine, nausea/vomiting,
and tremor
Drowsiness, headache, motor coordination impairment, and upset stomach
• SAD (Note: only medication currently
approved for SAD)
• Acute and/or maintenance treatment of
patients with schizophrenia
• Available as extended-release oral and
long-acting injectable formulations
• Schizophrenia
• Acute treatment of manic episodes
associated with BD I, both as monotherapy
and as an adjunct to lithium or divalproex
• Acute treatment of depressive episodes
associated with bipolar disorder
• Maintenance treatment of BD I
• Available as oral and extended-release
oral formulations
• Schizophrenia
• Acute mania or mixed episodes
associated with BD I
• Maintenance treatment of BD I
• Available as oral and long-acting
injectable formulations
• Schizophrenia
• Acute manic or mixed episodes
associated with BD I
• Maintenance treatment of BD I
• Acute agitation in schizophrenia
• Available as oral and injectable formulations
Bupropion
4
Drowsiness, headache, dizziness,
motor coordination impairment,
upset stomach, liver enzyme
elevation, thrombocytopenia, hair
loss, and possible teratogenicity
during pregnancy
Nausea, somnolence, dry mouth,
headache, and dizziness
Note: Side effect incidence is reduced
compared with first-generation tricyclic
antidepressants
Dry mouth, anorexia, sedation,
constipation, and increased appetite
Note: Frequently used for bipolar-prominent
SAD cases
Carbamazepine • Acute manic and mixed episodes
associated with BD I
5
2
• Acute manic and mixed episodes
associated with bipolar disorder
• Depression
Divalproex/
Valproic Acid
2
Desipramine
Duloxetine
• Major depressive disorder
• Generalized anxiety disorder
FolDheRe
FolDheRe
Phenomenology
Assessment and
Etiology/
Differential Diagnosis Pathophysiology
Initial Treatment
Ongoing Care
Relevant Indications
Boxed
Warnings
1
Side Effect Profile
Note: Depot fluphenazine injections used in
cases of poor compliance
Tardive dyskinesia, akathisia, acute
dystonia, EPS, and neuroleptic
malignant syndrome
1
1,2
Somnolence, insomnia, EPS, headache,
akathisia, and dizziness
Akathisia, EPS, sedation, restlessness,
and tremor
Note: Depot haloperidol injections used in cases
of poor compliance
3
1
1
Continued
Neuroleptic malignant syndrome,
weight gain, hyperlipidemia,
hyperglycemia, anticholinergic effects,
and cognitive/motor impairment
Hypotension, dizziness, somnolence,
tachycardia, and QTc prolongation
Neuroleptic malignant syndrome,
weight gain, hyperglycemia,
hyperlipidemia, and suicidality
1
Akathisia, tardive dyskinesia, Rabbit
syndrome, extrapyramidal symptoms
(EPS), neuroleptic malignant syndrome,
and, rarely, hypothermia and blood
pressure fluctuations
Select Pharmacologic Interventions for SAD
Intervention
• Prolonged and parenteral therapy
for schizophrenia
• Available as oral, injectable, and
long-acting injectable formulations
Typical Antipsychotics
Fluphenazine
Haloperidol
• Schizophrenia
• Severe behavioral problems in children
• Available as oral, injectable, and
long-acting injectable formulations
Atypical Antipsychotics
Aripiprazole
Asenapine
Clozapine
Iloperidone
Olanzapine
• Schizophrenia
• Manic/mixed episodes associated with
bipolar I disorder (BD I), adjunctive with
lithium or valproate
• Maintenance treatment of BD I
• Major depressive disorder (adjunctive)
• Agitation associated with schizophrenia
or BD I
• Available as oral and injectable formulations
• Acute treatment of schizophrenia
• Acute treatment of mixed or manic episodes
associated with BD I, with or without
psychotic features
• Available as an oral formulation
• Treatment-resistant schizophrenia
• Reducing the risk of recurrent suicidal
behavior in patients with schizophrenia or SAD
• Available as an oral formulation
• Acute treatment of schizophrenia
• Available as an oral formulation
• Schizophrenia
• Acute or mixed mania episodes
associated with BD I
• Maintenance treatment of BD I
• Acute agitation in patients with
schizophrenia or bipolar mania
• Depressive episodes associated with BD I
(in conjunction with fluoxetine)
• Treatment-resistant depression
(in conjunction with fluoxetine)
• Available as oral and long-acting
injectable formulations
Nausea, insomnia, somnolence,
anorexia, and anxiety
9/24/10 1:30:43 PM
2
Nausea, vomiting, insomnia,
somnolence, dizziness, and anxiety
Side Effect Profile
• Major depressive disorder
• Obsessive-compulsive disorder
• Panic disorder
2
Nausea, vomiting, insomnia,
somnolence, dizziness, and anxiety
Boxed
Warnings
Fluoxetine
• Obsessive-compulsive disorder
• Social anxiety disorder
2
Dizziness/nausea, headache, diplopia,
ataxia, and blurred vision
Relevant Indications
Fluvoxamine
• Symptoms of depression
6
Intervention
Imipramine
• Maintenance treatment of BD I
Dizziness, blurred vision, sedation,
somnolence, and malaise/lassitude
Lamotrigine
2
7
• Major depressive disorder
Nausea, asthenia, dizziness,
somnolence, and headache
• Acute manic episodes associated with
bipolar disorder
• Maintenance treatment of bipolar disorder
Mirtazapine
2
Nausea, sexual dysfunction, insomnia,
diarrhea, and dry mouth
Lithium
carbonate
Paroxetine
• Major depressive disorder
• Obsessive-compulsive disorder
• Panic disorder
• Social anxiety disorder
• Generalized anxiety disorder
2
Anxiety, weakness, dizziness,
dry mouth, and nausea
Possible teratogenicity during
pregnancy, nephrogenic diabetes
insipidus. At higher dosages:
possible diarrhea, motor coordination
impairment, vomiting, and
muscular weakness
Sertraline
• Major depressive disorder
• Obsessive-compulsive disorder
• Panic disorder
• Social anxiety disorder
2
Amnesia, confusion, hypesthesia,
trismus, and vertigo
Tranylcypromine • Major depressive episode without
melancholia
2
Venlafaxine
• Major depressive disorder
• Generalized anxiety disorder
• Social anxiety disorder
• Panic disorder
Complete prescribing information is available at PSYCHClinician.com
Boxed Warnings
1. Increased mortality in elderly patients with dementia-related psychosis. 2. Increased risk of suicidality in children, adolescents, and young
adults with major depressive disorder and other psychiatric disorders. 3.Agranulocytosis, seizures, myocarditis, and cardiovascular/respiratory
adverse events, especially in elderly patients with dementia-related psychoses. 4.Serious dermatologic reactions including Stevens-Johnson
syndrome, HLA-B1502 allele, aplastic anemia, and agranulocytosis. 5.Hepatotoxicity and hepatic failure resulting in fatalities. Valproate can
produce teratogenic effects, such as neural tube defects, in a developing fetus. Cases of life-threatening pancreatitis have been reported in both
children and adults. 6. Life-threatening serious rashes, including Stevens-Johnson syndrome, toxic epidermal necrolysis, and/or rash-related
death. The rate of serious rash is higher in pediatric patients than in adults. 7.Lithium toxicity is closely related to serum lithium levels, and can
occur at doses close to therapeutic levels.
Drs. Christoph Correll, Joseph Goldberg and Henry Nasrallah selected the screening tools, medications and related information for this
educational resource.
This and other resources are available at
FIGURE
Differences in PANSS
total change scores
with paliperidone ER
vs placebo
Subjects were randomly assigned to
paliperidone ER lower dose (6 mg/d,
option to reduce to 3 mg/d), higher
dose (12 mg/d, option to reduce to
9 mg/d), or placebo. Higher-dose
paliperidone ER demonstrated
significant improvement in PANSS
score 6 weeks following treatment.
Source: Canuso CM, Lindenmayer
JP, Kosik-Gonzalez C, et al. A randomized, double-blind, placebocontrolled study of 2 dose ranges of
paliperidone extended-release in the
treatment of subjects with schizoaffective disorder. J Clin Psychiatry.
2010;71(5):587-598. Copyright 2010
Physicians Postrgraduate Press.
Reprinted by permission.
Overall Population
Placebo (n = 107) vs
Higher-dose paliperidone ER (n = 98)
Lower-dose paliperidone ER (n = 105)
-8.3 (95% Cl, -13.8 to -2.9)
-3.6 (95% Cl, -9.0 to 1.8)
With antidepressants/mood stabilizers
Placebo (n = 40) vs
Higher-dose paliperidone ER (n = 39)
Lower-dose paliperidone ER (n = 38)
-5.3 (95% Cl, -14.1 to 3.4)
-0.9 (95% Cl, -9.7 to 7.9)
Without antidepressants/mood stabilizers
Placebo (n = 67) vs
Higher-dose paliperidone ER (n = 59)
Lower-dose paliperidone ER (n = 67)
-10.2 (95% Cl, -17.1 to -3.3)
-5.2 (95% Cl, -12.1 to 1.6)
US subjects
Placebo (n = 39) vs
Higher-dose paliperidone ER (n = 35)
Lower-dose paliperidone ER (n = 39)
-6.4 (95% Cl, -15.6 to 2.7)
-3.3 (95% Cl, -12.3 to 5.7)
Non-US subjects
Placebo (n = 68) vs
Higher-dose paliperidone ER (n = 63)
Lower-dose paliperidone ER (n = 66)
-9.4 (95% Cl, -16.3 to -2.6)
-3.6 (95% Cl, -10.4 to 3.2)
YMRS ≥ 16 at baseline
Placebo (n = 90) vs
Higher-dose paliperidone ER (n = 79)
Lower-dose paliperidone ER (n = 88)
-9.0 (95% Cl, -15.0 to -3.0)
-3.9 (95% Cl, -9.8 to 2.0)
HAM-D ≥ 16 at baseline
Placebo (n = 64) vs
Higher-dose paliperidone ER (n = 61)
Lower-dose paliperidone ER (n = 76)
-6.3 (95% Cl, -13.2 to 0.6)
-6.1 (95% Cl, -12.7 to 0.5)
YMRS and HAM-D ≥ 16 at baseline
Placebo (n = 47) vs
Higher-dose paliperidone ER (n = 42)
Lower-dose paliperidone ER (n = 59)
-6.7 (95% Cl, -15.0 to 1.5)
-7.0 (95% Cl, -14.7 to 0.6)
-20
-10
-5
0
LS Mean Difference in PANSS Total Score
5
10
Favors Placebo
CI: confidence interval; ER: extended-release; HAM-D: Hamilton Depression Rating Scale, 21-item version; ITT: intent to treat;
LS: least squares; PANSS: Positive and Negative Syndrome Scale; YMRS: Young Mania Rating Scale
Patients with SAD tend to respond to treatment better than those with schizophrenia, although SAD is associated with significantly worse outcomes compared
with bipolar disorder or major depression.15 As with all
psychiatric disorders, maximizing treatment adherence
in patients with SAD is a critical determinant of treatment
success.48 For reasons only partly understood, SAD and
schizophrenia patients have similarly low treatment adherence rates. In 1 study, only 59% (8,557/16,570) of SAD
patients were at least moderately adherent to antipsychotic therapy as indicated by their medication possession ratio, defined as the number of days of medication
dispensed as a percentage of the 180-day study period.24,49
These adherence data are consistent with previously published studies of patients with schizophrenia.50 Strategies
designed to promote treatment adherence in patients
with psychiatric disorders include psychoeducation,
motivational interviewing, simplification of prescribed
regimens, the use of calendars to self-monitor treatment
adherence, maintenance of routines such as dosing times,
and supervised medication intake.48 Antipsychotic pharmacokinetic and pharmacodynamic profiles also play an
important role. Poor tolerability may discourage patients
from taking medications. Finally, studies have demonstrated improved adherence and patient outcomes with
simplified medication regimens and long-acting injectable antipsychotic formulations.51-53
Conclusion
-15
Favors Treatment
Although significant advances have been made in our understanding of the biopsychosocial basis of SAD, little is
known about this clinical construct, and evidence-based
approaches to the assessment, diagnosis, and treatment
of patients with SAD are limited. Patients with SAD often
present with a complex combination of psychotic and affective symptoms. Differential diagnosis of SAD and its
subtypes is challenging, reflecting inconsistent diagnostic
criteria; a paucity of clearly demarcated genetic, neuropsychological, or neurophysiological determinants; and an often-evolving clinical presentation that shares features with
schizophrenia and bipolar disorder. Evidence supporting
diagnosis and treatment is limited and clinicians rely largely on a handful of well-designed studies, experience, and
case study reports. Accordingly, the SAD Working Group
has formulated consensus statements (Appendix) that define the current state of knowledge and practice consistent
with the available evidence and expert opinion. Diagnosis
is aided by numerous assessment tools, none of which has
been specifically validated for the SAD patient population. Treatment with atypical antipsychotics is generally
considered necessary for symptomatic control, with less
uniform agreement on the role and duration of therapy
with traditional mood stabilizers or antidepressants. A
variety of adjunctive nonpharmacologic modalities may
help to foster medication adherence and improve overall
outcomes. Many patients struggle to maintain adherence
to their multimodal regimens, owing in part to the nature
of the illness and intolerability to the pharmacotherapy.
Switching compounds within the atypical class to improve
tolerability and/or reduce the frequency of daily dosing,
or choosing long-acting injectable formulations may, on a
patient by patient basis, further help improve adherence.
Supplement to Annals of Clinical Psychiatry | Vol 22, No 4 | November 2010
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Schizoaffective disorder
APPENDIX
Schizoaffective Disorder (SAD) Working Group Consensus Delphi Statements
Phenomenology
1. SAD is a chronic and debilitating psychotic/mood disorder characterized by delusions,
hallucinations, formal thought disorder, or negative symptoms that co-occur with depressive and/or manic symptoms and persist
for at least 2 weeks in the absence of prominent mood symptoms meeting criteria for a major mood episode.a
2. Although the temporal patterns of symptoms vary among patients with SAD, the duration of the depressive and/or manic
episode(s) is significant when compared with the total uninterrupted period of psychotic illness.
3. SAD bipolar subtype includes manic or mixed manic symptoms.
4. SAD depressive subtype includes only depressive symptoms.
Diagnostic and Statistical Manual of Mental Disorder, 4th edition, text revision diagnostic criteria state that symptoms must meet Criterion A for schizophrenia (delusions,
hallucinations, disorganized speech, grossly disorganized or catatonic behavior, negative symptoms)
a
Etiology/pathophysiology
1. SAD is a lifelong psychiatric illness encompassing clinical features found in both mood disorders and schizophrenia.
2. Inherited susceptibility to SAD is thought to involve multiple risk alleles for psychosis and mood disorders.
3. Some SAD patients exhibit abnormal saccades, altered evoked potentials, processing impairments, and cognitive
impairments similar to those found in schizophrenia, while other SAD patients display neurophysiologic abnormalities
indistinguishable from those seen in bipolar disorder.
4. Neuroanatomic abnormalities in this patient population include reduced grey and white matter and overall brain volume, as well
as morphologic changes in the striatum and corpus callosum.
Assessment and differential diagnosis
1. Optimal assessment of SAD patients is longitudinal and addresses medical, psychiatric, and social/vocational functioning.
2. A
review of historical, mental status, and physical exam findings should exclude general medical conditions, substance-induced
syndromes, and psychiatric comorbidities that may confound SAD diagnosis.a
3. SAD patients often have comorbid medical conditions such as obesity and type II diabetes.b
4. Significant risk factors for SAD include female gender and a family history of psychiatric disease, especially psychotic and mood
disorders.
5. The age of onset of SAD is similar to that of schizophrenia and bipolar disorder.
6. The relative prominence of mood symptoms and psychotic features in patients suspected of having SAD can be quantified using
appropriate rating scales.
7. Measurement tools such as the Positive and Negative Syndrome Scale (PANSS), Hamilton Depression Rating Scale (HAM-D),
Young Mania Rating Scale (YMRS), or Personal and Social Performance (PSP) scale facilitate determination of the severity of an
SAD subtype.
8. The relative proportion of mood to psychotic symptoms may change over the course of the disorder, warranting ongoing assessment and a possible change in diagnosis from SAD to schizophrenia with secondary depression, or to a psychotic mood disorder
such as major depression with psychotic features.
9. S
AD evolves into more depressive features with aging, even in early-onset patients. Older adults are more likely to have the SAD
depressive subtype, whereas younger people tend to have the SAD bipolar subtype with more manic episodes.c,d
10. Patients with suspected SAD should be evaluated for suicidal/homicidal ideation or grave self-neglect/disability, and admitted to
an inpatient psychiatric unit as necessary.
a
Pertinent laboratory findings were highlighted by some SAD Working Group members as an important part of the assessment of medical conditions
b
Comorbidities may or may not be caused by medication
c
Long-term studies are limited
d
Based on extrapolation of data from studies in patients with bipolar disorder
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November 2010 | Vol 22, No 4 | Supplement to Annals of Clinical Psychiatry
Treatment/ongoing care
1. SAD requires ongoing and concurrent multimodal treatment that includes pharmacologic therapy to stabilize mood and to alleviate psychotic symptoms and thought disorders, and psychotherapeutic approaches to enhance insight into the illness, teach
appropriate social skills, and restore vocational functioning.
2. In patients with SAD depressive subtype, adherence to antipsychotic therapy can help achieve symptomatic control, stabilizing
mood and limiting the frequency and severity of psychotic episodes.
3. Selection of the optimal antipsychotic is based in part on SAD subtype, signs and symptoms, coexisting psychiatric and medical
disorders, and patient adherence.
4. In patients with SAD depressive subtype, antidepressant therapy may be used in combination with antipsychotic
maintenance after psychosis is stabilized and depressive symptoms persist.
5. In patients with SAD bipolar subtype, an antipsychotic and a mood stabilizer are recommended.
6. Selective serotonin reuptake inhibitors may have a favorable clinical profile in patients with SAD depressive subtype,
but their use is evidence-based in major depression, not in SAD per se.
7. Antidepressant-induced switching from depression to mania in a patient with SAD may warrant changing the SAD
diagnosis to the bipolar subtype.a
8. A trial that achieves an optimal dose of antipsychotic may require up to 8 to 12 weeks before full efficacy is realized.
9. Evidenceb supporting pharmacotherapy in SAD patients is largely empirical and level-one evidence is limited to 2
randomized, double-blind, placebo-controlled studies.
10. For patients with SAD bipolar subtype exhibiting severe or persistent psychotic symptoms, clozapine, which is approved for
refractory schizophrenia and for suicidality in patients with chronic schizophrenia, is a legitimate option.
11. The persistence of severe depressive or manic symptoms, despite trials of multiple mood stabilizing agents, warrants
consideration of electroconvulsive therapy.
12. Psychosocial interventions include cognitive-behavioral therapy, as well as individual and family therapy, either alone or in
combination with appropriate pharmacotherapy.c,d
13. Longitudinal assessment with appropriate scales—including PANSS, HAM-D, YMRS, and PSP, among others—may be
particularly helpful in gauging treatment response.
a
ntidepressant-induced switching from depression to mania in a patient with SAD is a substance-induced mood disorder that may portend a greater risk for future
A
spontaneous manias/hypomanias; such future spontaneous manias or hypomanias would then warrant changing the SAD diagnosis to the bipolar subtype
b
Placebo-controlled monotherapy studies
c
Behavioral tailoring was also deemed important for some SAD patients by some SAD Working Group members
d
The majority of SAD patients will benefit from a combinaton of psychosocial and pharmacotherapeutic interventions
Supplement to Annals of Clinical Psychiatry | Vol 22, No 4 | November 2010
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Schizoaffective disorder
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November 2010 | Vol 22, No 4 | Supplement to Annals of Clinical Psychiatry
Schizoaffective Disorder Posttest Questions
1. Which of the following statements regarding
Diagnostic and Statistical Manual of Mental
Disorders, 4th edition, Text Revision (DSM-IV-TR)
diagnostic criteria for schizoaffective disorder
is incorrect?
a. Patients with schizoaffective disorder may
experience major depressive, manic, or mixed
episodes
b. Delusions or hallucinations must be present for at
least 2 weeks in the absence of prominent mood
symptoms
c. A schizoaffective disorder diagnosis cannot be given
if the disturbance is due to the effects of medication
d. Affective symptomatology does not co-occur with
psychosis
2. Increasing age is associated with __________
symptomatology in patients with schizoaffective
disorder.
a. Physical
b. Depressive
c. Aggressive
d. Manic
3. Schizoaffective disorder depressive subtype
includes psychosis and which of the following
symptoms?
a. Depression
b. Mania
c. Mix of depression and mania
d. Bipolar depression
4. The relative proportion of mood to psychotic
symptoms __________.
a. Can only be determined in patients with
schizoaffective disorder bipolar subtype
b. Is generally stable in patients with schizoaffective
disorder
c. Decreases with increasing age
d. May change during the course of schizoaffective
disorder
5. Which of the following treatment regimens is the
most reasonable for a patient with schizoaffective
disorder bipolar subtype?
a. Antidepressant and psychotherapy
b. Atypical antipsychotic alone
c. Atypical antipsychotic, mood stabilizer, and
psychotherapy
d. Psychotherapy alone
6. Psychotic patients with a family history of mental
illness compared to psychotic patients without a
family history of mental illness __________.
a. Have a greater risk of developing schizoaffective
disorder
b. Are more treatment responsive
c. Are at no greater risk of developing schizoaffective
disorder
d. Are less treatment responsive
7. Which of the following is an appropriate
psychosocial intervention for the treatment of
patients with schizoaffective disorder?
a. Psychoeducation
b. Behavioral tailoring
c. Cognitive-behavioral therapy
d. All of the above
8. Which of the following is false about the
treatment of schizoaffective disorder?
a. A patient’s prescribed treatment may change with
change of diagnosis
b. In patients with schizoaffective disorder depressive
subtype, antidepressant therapy may be initiated
after psychosis is stabilized and depressive
symptoms persist
c. A 1-month antipsychotic trial is sufficient to realize
full efficacy
d. The choice of antipsychotic should also be based
on the risk of patient nonadherence to treatment
9. A change in diagnosis from schizoaffective
disorder depressive subtype to bipolar subtype
with manic symptoms and persistent psychosis
would warrant a modification of treatment.
Which of the following best describes the most
appropriate approach?
a. Antipsychotic discontinuation only
b. Antipsychotic continuation, antidepressant
discontinuation
c. Antipsychotic discontinuation, antidepressant
continuation
d. Antipsychotic discontinuation, mood stabilizer
initiation
10. Which of the following is true regarding the
relationship between psychotic and affective
symptoms in patients with schizoaffective disorder?
a. Psychotic symptoms and affective symptoms never
occur simultaneously
b. Psychotic symptoms simultaneously present with
affective symptoms
c. Psychotic symptoms may simultaneously present
with depressive symptoms but never with mania
d. Psychotic symptoms may simultaneously present
with manic symptoms but never with depressive
symptomatology
Supplement to Annals of Clinical Psychiatry | Vol 22, No 4 | November 2010
S11
Schizoaffective disorder
Schizoaffective Disorder Evaluation Form & Self-Report Credit Form
Your frank and considered evaluation will be helpful in improving our CME activities. We urge you to rate the following areas and return this
form along with the completed Self-Report Credit Form. You can mail your forms to CCME, 3301 Bainbridge Avenue, Bronx, NY 10467, or
fax to (718) 798-2336. Your CME certificate will be mailed approximately 6 to 8 weeks after receipt of mailed submissions and verification of a
passing grade. Please print clearly.
1Did the activity meet the following learning objectives?
Objective 1: Conduct initial and ongoing assessment of patients with schizoaffective disorder
(SAD), identifying comorbidities, current and prior medical history, and treatment goals
Objective 2: Diagnose SAD, differentiating it from schizophrenia, bipolar disorder, and major depressive disorder
Objective 3: Design and implement an appropriate multimodal treatment plan for a patient with SAD, tailored to the patient’s SAD subtype and medical comorbidities
Objective 4: Implement psychosocial and psychopharmacologic interventions shown to
improve treatment outcomes in patients with SAD
Objective 5: Utilize psychosocial and pharmacologic strategies to improve treatment adherence among patients with SAD
Yes
No
☐
☐
☐
☐
☐
☐
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☐
☐
2
3This activity provided evidence-based information that will be useful to me in my job or practice.
☐
☐
4Did the information received today confirm how you treat/manage patients?
☐
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5Will you make changes that will benefit patient care as a result of the information received today? If yes, please describe. _____________________________________________________________________
☐
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6What subject matter not presented in this activity do you think should be included in future activities?
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7Was this CME activity “free of commercial bias for or against any product”?
☐
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What percentage of this activity was effective in teaching you something new?
☐ 90% ☐ 70% ☐ 50% ☐ 30% Optional Questions
☐ 10%
Superior
Excellent
Satisfactory
Unsatisfactory
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8
Compared with other similar activities, how would you rate this activity?
9
And please take a moment… Hand washing saves lives. I wash my hands before and after each patient encounter.
☐ Always ☐ Most of the time ☐ Sometimes ☐ Never ☐ N/A
If you did not answer “Always,” please list any factors that, in your opinion, act as barriers:
10
As of today, I will wash my hands before and after each patient encounter.
☐ Always ☐ Most of the time ☐ Sometimes ☐ Never ☐ N/A ☐
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Completion of this form is necessary to obtain credit for this activity. Please complete this form and mail to CCME, 3301
Bainbridge Avenue, Bronx, NY 10467, or fax to (718) 798-2336. All requests for credit should be submitted no later than
September 30, 2011. Please print.
First Name: Accreditation Statement
This activity has been planned and implemented in accordance with the
Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of Albert
Einstein College of Medicine and Montefiore Medical Center, and Asante
Communications, LLC. Albert Einstein College of Medicine is accredited by
the ACCME to provide continuing medical education (CME) for physicians.
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Albert Einstein College of Medicine designates this educational activity for
a maximum of 1.0 AMA PRA Category 1 Credit™. Physicians should only
claim credit commensurate with the extent of their participation in the activity.
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this CME activity
Signature (required):
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Are you willing to participate in a future survey to assess outcomes for this course?
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November 2010 | Vol 22, No 4 | Supplement to Annals of Clinical Psychiatry
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