Delusional Disorders Pakistani hought Processes BACKGROUND The client is a 34-year-old Pakistani female who moved to the United States in her late teens/early 20s. She is currently in an “arranged” marriage (her husband was selected for her since she was 9 years old). She presents to your office today following a 21 day hospitalization for what was diagnosed as “brief psychotic disorder.” She was given this diagnosis as her symptoms have persisted for less than 1 month. Prior to admission, she was reporting visions of Allah, and over the course of a week, she believed that she was the prophet Mohammad. She believed that she would deliver the world from sin. Her husband became concerned about her behavior to the point that he was afraid of leaving their 4 children with her. One evening, she was “out of control” which resulted in his calling the police and her subsequent admission to an inpatient psych unit. During today’s assessment, she appears quite calm, and insists that the entire incident was “blown out of proportion.” She denies that she believed herself to be the prophet Mohammad and states that her husband was just out to get her because he never loved her and wanted an “American wife” instead of her. She tells you that she knows this because the television is telling her so. She currently weighs 140 lbs, and is 5’ 5” SUBJECTIVE Client reports that her mood is “good.” She denies auditory/visual hallucinations, but believes that the television does talk to her. She believes that Allah sends her messages through the TV. At times throughout the clinical interview, she becomes hostile towards the PMHNP, but then calms down. You reviewed her hospital records and find that she has been medically worked up by a physician who reported her to be in overall good health. Lab studies were all within normal limits. Client admits that she stopped taking her Risperdal about a week after she got out of the hospital because she thinks her husband is going to poison her so that he can marry an American woman. MENTAL STATUS EXAM The client is alert, oriented to person, place, time, and event. She is dressed appropriately for the weather and time of year. She demonstrates no noteworthy mannerisms, gestures, or tics. Her speech is slow and at times, interrupted by periods of silence. Self-reported mood is euthymic. Affect constricted. Although the client denies visual or auditory hallucinations, she appears to be “listening” to something. Delusional and paranoid thought processes as described, above. Insight and judgment are impaired. She is currently denying suicidal or homicidal ideation. The PMHNP administers the PANSS which reveals the following scores: -40 for the positive symptoms scale -20 for the negative symptom scale -60 for general psychopathology scale Diagnosis: Schizophrenia, paranoid type RESOURCES § Kay, S. R., Fiszbein, A., & Opler, L. A. (1987). The Positive and Negative Syndrome Scale (PANSS) for schizophrenia. Schizophrenia Bulleti ...

1. Delusional Disorders
Pakistani hought Processes
BACKGROUND
The client is a 34-year-old Pakistani female who moved to the
United States in her late teens/early 20s. She is currently in an
“arranged” marriage (her husband was selected for her since she
was 9 years old). She presents to your office today following a
21 day hospitalization for what was diagnosed as “brief
psychotic disorder.” She was given this diagnosis as her
symptoms have persisted for less than 1 month.
Prior to admission, she was reporting visions of Allah, and over
the course of a week, she believed that she was the prophet
Mohammad. She believed that she would deliver the world from
sin. Her husband became concerned about her behavior to the
point that he was afraid of leaving their 4 children with her.
One evening, she was “out of control” which resulted in his
calling the police and her subsequent admission to an inpatient
psych unit.
During today’s assessment, she appears quite calm, and insists
that the entire incident was “blown out of proportion.” She
denies that she believed herself to be the prophet Mohammad
and states that her husband was just out to get her because he
never loved her and wanted an “American wife” instead of her.
She tells you that she knows this because the television is
telling her so.
She currently weighs 140 lbs, and is 5’ 5”
SUBJECTIVE
Client reports that her mood is “good.” She denies
auditory/visual hallucinations, but believes that the television
does talk to her. She believes that Allah sends her messages
through the TV. At times throughout the clinical interview, she

2. becomes hostile towards the PMHNP, but then calms down.
You reviewed her hospital records and find that she has been
medically worked up by a physician who reported her to be in
overall good health. Lab studies were all within normal limits.
Client admits that she stopped taking her Risperdal about a
week after she got out of the hospital because she thinks her
husband is going to poison her so that he can marry an
American woman.
MENTAL STATUS EXAM
The client is alert, oriented to person, place, time, and event.
She is dressed appropriately for the weather and time of year.
She demonstrates no noteworthy mannerisms, gestures, or tics.
Her speech is slow and at times, interrupted by periods of
silence. Self-reported mood is euthymic. Affect constricted.
Although the client denies visual or auditory hallucinations, she
appears to be “listening” to something. Delusional and paranoid
thought processes as described, above. Insight and judgment are
impaired. She is currently denying suicidal or homicidal
ideation.
The PMHNP administers the PANSS which reveals the
following scores:
-40 for the positive symptoms scale
-20 for the negative symptom scale
-60 for general psychopathology scale
Diagnosis: Schizophrenia, paranoid type
RESOURCES
§ Kay, S. R., Fiszbein, A., & Opler, L. A. (1987). The Positive
and Negative Syndrome Scale (PANSS) for schizophrenia.
Schizophrenia Bulletin, 13(2), 261-276.
§ Clozapine REMS. (2015). Clozapine REMS: The single shared
system for clozapine. Retrieved from
https://www.clozapinerems.com/CpmgClozapineUI/rems/pdf/res
ources/Clozapine_REMS_A_Guide_for_Healthcare_Providers.p
df

3. § Paz, Z., Nalls, M. & Ziv, E. (2011). The genetics of benign
neutropenia. Israel Medical Association Journal. 13. 625-629.
Decision Point One
Select what the PMHNP should do:
Start Zyprexa 10 mg orally at BEDTIME
Start Invega Sustenna 234 mg intramuscular X1 followed by
156 mg intramuscular on day 4 and monthly thereafter
Start Abilify 10 mg orally at BEDTIME
Delusional Disorders
Pakistani Female With Delusional Thought Processes
Decision Point One
Start Zyprexa (olanzapine) 10 mg po orally at BEDTIME
RESULTS OF DECISION POINT ONE
· Client returns to clinic in four weeks
· Client's PANSS decreases to a partial response (25%)
· Client comes in today with a reported weight gain of 5
pounds. When questioned further on this point, she states that
she can never seem to get full from her meals so she is snacking
constantly throughout the day.
Decision Point Two
Select what the PMHNP should do next:
Decrease Zyprexa to 7.5 mg BEDTIME
Change medication to Geodon 40 mg orally BID with meals

4. Add-on Wellbutrin XL 150 mg orally in the MORNING
Delusional Disorders
Pakistani Female With Delusional Thought Processes
Decision Point One
Start Invega Sustenna 234 mg intramuscular X1 followed by
156 mg intramuscular on day 4 and monthly thereafter
RESULTS OF DECISION POINT ONE
· Client returns to clinic in four weeks
· A decrease in PANSS score of 25% is noted at this visit
· Client seems to be tolerating medication
· Client's husband has made sure she makes her appointments
for injections (one thus far)
· Client has noted a 2 pound weight gain but it does not seem to
be an important point for her
· Client complains of injection site pain telling the PMHNP
that she has trouble siting for a few hours after the injections
and doesn’t like having to walk around for such a long period of
time
Decision Point Two
Select what the PMHNP should do next:
Continue same decision made but instruct administering nurse
to begin injections into the deltoid at this visit and moving
forward
Discontinue Invega Sustenna and start Haldol Decanoate
(haloperidol decanoate ) 50 mg IM q2weeks with oral Haldol 5
mg BID for the next 3 months

5. Continue Invega Sustenna. Begin injections into the deltoid and
add on Abilify Maintena 300 mg intramuscular monthly with
oral Abilify 10 mg in the MORNING for 2 weeks
Delusional Disorders
Pakistani Female With Delusional Thought Processes
Decision Point One
: Start Abilify (aripiprazole) 10 mg orally at BEDTIME
RESULTS OF DECISION POINT ONE
· Client returns to clinic in four weeks
· Client returns and looks disheveled. Upon questioning, her
husband states that she has not been sleeping at night. He states
she is up and down all night and has also been disrupting his
sleep
· Clientis unable to participate in the PANSS rating tool
because she continually is nodding off (sleeping) during the
appointment
· The appointment is not productive for assessing how she is
responding to the Abilify started 4-weeks ago
Decision Point Two
Select what the PMHNP should do next:
Change Abilify administration time to AM dosing
Reduce Abilify dose to 7.5 MG orally at BEDTIME
Discontinue Abilify and start Geodon (ziprasidone ) 40 mg
orally BID with meals

6. MGMT8110–Global Business
Perspectives
Professor Name: Rupinder Sodhi
email:[email protected]
Winter2020
Final Essay Writing Assignment
(Worth 25% of Course Grade)
Delivery Method: Uploaded to Assignments Section of
eConestoga, under category Final Essay Submission
Due Date: Tuesday, April 14, 2020 not later than 11:59 PM
Late Submissions: After Class deadline: 10% loss in marks for
per day late
After 3 days: The final essay
automatically receives a zero mark
Essay Requirements:
The essay is a well-structured research paper that opens with an
introduction (introduces the Thesis Statement), well-

7. researched arguments (minimum 2-3) with a clear conclusion in
support of your Thesis Statement.
Based on your approved topic write and submit an essay which
has the following elements:
1) Introduction: An introductory paragraph that catches the
reader’s attention and states the relevance of your topic (any
background or current issues), identifying your Thesis
Statement.
2) Body: The body should be formatted with arguments which
support and defend the Thesis Statement. These
arguments need to:
i. Be well organized and flow from a logical start to a strong
conclusion.
ii. It also needs to demonstrate the significance of your topic
from a global business perspective.
mailto:[email protected]
iii. Clearly support, defend or justify the thesis as present.
IV. Be analytical and show your abilities to develop clear
ideas with originality of thought.
V. Include evidence to demonstrate width/depth of research.
VI. To be written in descriptive form by not inserting any

8. image, graph or table etc.
3) Have good quality writing:
i. Grammar, punctuation & spelling are virtually flawless.
ii. Language and word choice are appropriate throughout.
4) Be well formatted and pleasant to read:
i. Has an opening and concluding sentence.
ii. The essay follows scholarly conventions including proper
formatting, citation methods and is virtually flawless.
5) Be original:
i. Your paper can use quotes from your research, but cannot
comprise more than 10% of your
paper.
ii. Make sure you take advantage of the Originality Check
available on eConestoga.
iii. During Originality Check on Turntin if it is found that essay
content has been put in without using
appropriate citations or referencing then a case of Academic
Dishonesty will be filed.
iv. Before the due date in order to conduct Originality Check,
you may make a multiple number of essay submissions
into the assignment folder. However, your latest submission
will be treated as your final submission.

9. 6) Have the following length and format:
i. Between 10 to12 pages excluding title page and reference
pages in
Times New Roman or Ariel, 12 points font & double-spaced
ii. Title Page must include:
tion
– Winter2020
7) Create a thread:
Starting from the Thesis Statement, create a thread of logic that
will follow throughout the essay. This thread will be
built on your research findings.
i. The thread needs to be directly related to your thesis.
ii. Creating a thread means it will have an introduction, body,

10. conclusion – all focused on supporting the Thesis
Statement.
8) Wrap up your essay with a strong concluding paragraph that
summarizes your essay with a strong concluding paragraph
that summarizes your arguments and affirm your Thesis
Statement. In references use the APA standard formatting (sixth
edition).
Your Essay will be evaluated using the following rubric:
Excellent 9-10pts Good 7-8 pts Average 5-6 pts Poor 1-4 pts
Essay Arguments (50%)
Organization
Essay proceeds logically from
start to finish and is coherent
throughout.
Essay includes some logical
inconsistencies, but they hardly
detract from the overall
coherence of the
argument

11. Significant logical
inconsistencies in parts of the
paper make the
overall credibility of the
argument somewhat
dubious.
The essay is illogical, incoherent,
and as a result completely
unconvincing.
Thesis Quality
Thesis, whether implicit or
explicit, is absolutely clear
and highly original.
Thesis, whether implicit or
explicit, is clear and
deliberate. Essay
effectively recognizes a
variety of
points of view.

12. Thesis is identifiable in
some form, with effort.
Essay does not contain–either
implicitly or explicitly-a thesis.
Objectivity
Essay demonstrates a
masterful grasp of all
sides of the issue.
Essay effectively recognizes
a variety of points of view.
Essay is clearly, albeit
unintentionally, partial. It
either fails to deal with
contrary points of view out
of ignorance or deals
with them unfairly.

13. Essay is deliberately not
impartial. The author has used
the paper as a pulpit instead of as
a framework for rigorous critical
analysis.
Analysis
Analytical abilities on display
are clearly superior and
reflect an originality of
thinking.
Analytical abilities on display
demonstrate an ability to
separate ideas into their
component parts.
Analytical abilities on
display are inconsistent.
Some ideas are clear and
fully understood; others are

14. not.
Paper reproduces arguments
from other sources without any
evidence of understanding.
Evidence supporting arguments and Thesis Statement (35%)
Depth
Essay draws from sources
that represent the best
information on the subject.
Quantity exceeds
expectations.
Essay draws from a legitimate
variety of information. Quantity
of sources meets or exceeds
expectations.
While the essay might draw
from a number of sources,

15. but the information obtained
is largely surface level.
Essay is drawn largely, if not
exclusively, from
inappropriate material.
Breadth
Essay draws from an
impressive variety of
sources and perspectives.
Essay draws from an
acceptable variety of
sources and
perspectives.
Sources either come from
a single perspective or are
insufficient to meet the
demands of the
assignment.

16. Sources are both
excessively limited in
quantity and
Represent an excessively
limited point of view.
Synthesis
Presentation of the
evidence demonstrates a
masterful understanding
of its themes, both specific
and general.
Presentation of the
evidence demonstrates
a clear understanding of
its themes, both specific
and general.
Presentation of the
evidence demonstrates

17. a flawed
understanding of either its
specific or general
themes.
Presentation of the evidence
demonstrates a flawed
understanding of both its
specific and general themes.
Relevance
Evidence is directly
applicable to the analysis
throughout
Evidence is largely
applicable to the
analysis throughout.
Some of the evidence is
clearly tangential and
detracts from the

18. credibility of the argument.
Evidence does not
contribute to a fulfillment of
the goals of the assignment.
Quality of Writing (10%)
Grammar &
Language
Grammar, punctuation,
spellings are virtually
flawless. Language and
word choice are
appropriate throughout.
Limited flaws in grammar,
punctuation, and/or spelling
do not detract from the
overall message of the
essay. Some minor

19. problems with language and
word choice are noted, but
not problematic.
Significant flaws in some
of grammar, punctuation,
spelling, language and/or
word choice.
Paper is incoherent because
of flaws in grammar,
punctuation, spelling, language,
and/or word choice.
Quality of
Format
(5%)
Essay follows scholarly
conventions including
proper formatting & citation
methods which are virtually

20. free from flaw.
Only minor flaws in terms of
scholarly conventions
including formatting & citation
methods.
Significant flaws in terms of
formatting & scholarly
conventions (likely
including problems with
citation methods).
Paper displays a blatant
disregard for proper formatting
& scholarly conventions.
Final Essay Writing Assignment(Worth 25% of Course
Grade)Delivery Method: Uploaded to Assignments Section of
eConestoga, under category Final Essay SubmissionAfter 3
days: The final essay automatically receives a zero mark
Antipsychotic agents

21. This chapter will explore antipsychotic drugs, with an emphasis
on treatments for schizophrenia.
These treatments include not only conventional antipsychotic
drugs, but also the newer atypical
antipsychotic drugs that have largely replaced the older
conventional agents. Atypical antipsychotics
are really misnamed, since they are also used as treatments for
both the manic and depressed
phases of bipolar disorder, as augmenting agents for treatment-
resistant depression, and "off-label"
for various other disorders, such as treatment-resistant anxiety
disorders. The reader is referred to
standard reference manuals and textbooks for practical
prescribing information, such as drug doses,
because this chapter on antipsychotic drugs will
Figure 5-1. . ThroughoutQualitative and semi-quantitative
representation of receptor binding properties
this chapter, the receptor binding properties of the atypical
antipsychotics are represented both graphically and
semi-quantitatively. Each drug is represented as a blue sphere,
with its most potent binding properties depicted
along the outer edge of the sphere. Additionally, each drug has
a series of colored boxes associated with it.
Each colored box represents a different binding property, and
binding strength is indicated by the size of the box
and the number of plus signs. Within the colored box series for
any particular antipsychotic, larger boxes with
more plus signs (positioned to the left) indicate stronger
binding affinity, while smaller boxes with fewer plus
signs (positioned to the right) represent weaker binding affinity.
The series of boxes associated with each drug
are arranged such that the size and positioning of a box reflect
the binding potency for a particular receptor. The
vertical dotted line cuts through the dopamine 2 (D ) receptor

22. binding box, with binding properties that are more2
potent than D on the left and those that are less potent than D
on the right. All binding properties are based on2 2
the mean values of published K (binding affinity) data ( ). The
semi-quantitative depictioni http://pdsp.med.unc.edu
used throughout this chapter provides a quick visual reference
of how strongly a particular drug binds to a
particular receptor. It also allows for easy comparison of a
drug's binding properties with those of other atypical
antipsychotics.
emphasize basic pharmacologic concepts of mechanism of
action and not practical issues such as
how to prescribe these drugs (for that information see for
example Stahl's Essential
, which is a companion to this textbook).Psychopharmacology:
the Prescriber's Guide
Antipsychotic drugs exhibit possibly the most complex
pharmacologic mechanisms of any drug class
within the field of clinical psychopharmacology. The
pharmacologic concepts developed here should
help the reader understand the rationale for how to use each of
the different antipsychotic agents,
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All rights reserved. Not for commercial use or unauthorized
distribution.
based upon their interactions with different neurotransmitter

23. systems ( ). Such interactionsFigure 5-1
can often explain both the therapeutic actions and the side
effects of various antipsychotic
medications and thus can be very helpful background
information for prescribers of these therapeutic
agents.
Conventional antipsychotics
What makes an antipsychotic "conventional"?
In this section we will discuss the pharmacologic properties of
the first drugs that were proven to
effectively treat schizophrenia. A list of many conventional
antipsychotic drugs is given in .Table 5-1
These drugs are usually called antipsychotics, but they are
sometimes also called conventional
antipsychotics, or antipsychotics, or antipsychotics. The
earliestclassical typical first-generation
effective treatments for schizophrenia and other psychotic
illnesses arose from serendipitous clinical
observations more than
Table 5-1 Some conventional antipsychotics still in use
60 years ago, rather than from scientific knowledge of the
neurobiological basis of psychosis, or of
the mechanism of action of effective antipsychotic agents. Thus,
the first antipsychotic drugs were
discovered by accident in the 1950s when a drug with
antihistamine properties (chlorpromazine) was
serendipitously observed to have antipsychotic effects when this
putative antihistamine was tested in
schizophrenia patients. Chlorpromazine indeed has
antihistaminic activity, but its therapeutic actions

24. Downloaded from http://stahlonline.cambridge.org
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All rights reserved. Not for commercial use or unauthorized
distribution.
in schizophrenia are not mediated by this property. Once
chlorpromazine was observed to be an
effective antipsychotic agent, it was tested experimentally to
uncover its mechanism of antipsychotic
action.
Early in the testing process, chlorpromazine and other
antipsychotic agents were all found to cause
"neurolepsis," known as an extreme form of slowness or
absence of motor movements as well as
behavioral indifference in experimental animals. The original
antipsychotics were first discovered
largely by their ability to produce this effect in experimental
animals, and are thus sometimes called
"neuroleptics." A human counterpart of neurolepsis is also
caused by these original (i.e.,
conventional) antipsychotic drugs and is characterized by
psychomotor slowing, emotional quieting,
and affective indifference.
Figure 5-2. . Conventional antipsychotics, also called first-
generation antipsychotics or typicalD antagonist2
antipsychotics, share the primary pharmacological property of D
antagonism, which is responsible not only for2
their antipsychotic efficacy but also for many of their side
effects. Shown here is an icon representing this single
pharmacological action.

25. D receptor antagonism makes an antipsychotic conventional2
By the 1970s it was widely recognized that the key
pharmacologic property of all "neuroleptics" with
antipsychotic properties was their ability to block dopamine D
receptors ( ). This action has2 Figure 5-2
proven to be responsible not only for the antipsychotic efficacy
of conventional antipsychotic drugs,
but also for most of their undesirable side effects, including
"neurolepsis."
The therapeutic actions of conventional antipsychotic drugs are
hypothetically due to blockade of D2
receptors specifically in the mesolimbic dopamine pathway ( ).
This has the effect ofFigure 5-3
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distribution.
reducing the hyperactivity in this pathway that is postulated to
cause the positive symptoms of
psychosis, as discussed in ( and ). All conventional
antipsychotics reduceChapter 4 Figures 4-12 4-13
positive psychotic symptoms about equally well in
schizophrenia patients studied in large multicenter
trials if they are dosed to block a substantial number of D
receptors there ( ).2 Figure 5-4
Unfortunately, in order to block adequate numbers of D

26. receptors in the mesolimbic dopamine2
pathway to
Figure 5-3. . In untreated schizophrenia, the
mesolimbicMesolimbic dopamine pathway and D antagonists2
dopamine pathway is hypothesized to be hyperactive, indicated
here by the pathway appearing red as well as by
the excess dopamine in the synapse. This leads to positive
symptoms such as delusions and hallucinations.
Administration of a D antagonist, such as a conventional
antipsychotic, blocks dopamine from binding to the D2 2
receptor, which reduces hyperactivity in this pathway and
thereby reduces positive symptoms as well.
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All rights reserved. Not for commercial use or unauthorized
distribution.
Figure 5-4. . All known antipsychoticsHypothetical thresholds
for conventional antipsychotic drug effects
bind to the dopamine 2 receptor, with the degree of binding
determining whether one experiences therapeutic
and/or side effects. For most conventional antipsychotics, the
degree of D2 receptor binding in the mesolimbic
pathway needed for antipsychotic effects is close to 80%, while
D2 receptor occupancy greater than 80% in the
dorsal striatum is associated with extrapyramidal side effects
(EPS) and in the pituitary is associated with
hyperprolactinemia. For conventional antipsychotics (i.e,. pure
D2 antagonists) it is assumed that the same
number of D2 receptors is blocked in all brain areas. Thus, there
is a narrow window between the threshold for

27. antipsychotic efficacy and that for side effects in terms of D2
binding.
quell positive symptoms, one must simultaneously block the
same number of D receptors2
throughout the brain, and this causes undesirable side effects as
a "high cost of doing business" with
conventional antipsychotics ( through ). Although modern
neuroimaging techniquesFigures 5-5 5-8
are able to measure directly the blockade of D receptors in the
dorsal (motor) striatum of the2
nigrostriatal pathway, as shown in , for conventional
antipsychotics it is assumed that theFigure 5-4
same number of D receptors is blocked in all brain areas,
including the ventral limbic area of2
striatum known as the nucleus accumbens of the mesolimbic
dopamine pathway, the prefrontal
cortex of the mesocortical dopamine pathway, and the pituitary
gland of the tuberoinfundibular
dopamine pathway.
Neurolepsis
D receptors in the mesolimbic dopamine system are postulated
to mediate not only the positive2
symptoms of psychosis, but also the normal reward system of
the brain, and the nucleus accumbens
is widely considered to be the "pleasure center" of the brain. It
may be the final common pathway of
all reward and reinforcement, including not only normal reward
(such as the pleasure of eating good
food, orgasm, listening to music) but also the artificial reward
of substance abuse. If D receptors are2
stimulated in some parts of the mesolimbic pathway, this can
lead to the experience of pleasure.
Thus, if D receptors in the mesolimbic system are blocked, this

28. may not only reduce positive2
symptoms of schizophrenia, but also block reward mechanisms,
leaving patients apathetic,
anhedonic, lacking motivation, interest, and joy from social
interactions, a state very similar to that of
negative symptoms of schizophrenia. The near shutdown of the
mesolimbic dopamine pathway
necessary to improve the positive symptoms of psychosis ( )
may contribute to worseningFigure 5-4
of anhedonia, apathy, and negative symptoms, and this may be a
partial explanation for the high
incidence of smoking and drug abuse in schizophrenia.
Antipsychotics also block D receptors in the mesocortical DA
pathway ( ), where DA may2 Figure 5-5
already be deficient in schizophrenia (see through ). This can
cause or worsenFigures 4-14 4-16
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distribution.
negative and cognitive symptoms even though there is only a
low density of D receptors in the2
cortex. An adverse behavioral state can be produced by
conventional antipsychotics, and is
sometimes called the "neuroleptic-induced deficit syndrome"
because it looks so much like the
negative symptoms produced by schizophrenia itself, and is
reminiscent of "neurolepsis" in animals.

29. Extrapyramidal symptoms and tardive dyskinesia
When a substantial number of D receptors are blocked in the
nigrostriatal DA pathway, this will2
produce various disorders of movement that can appear very
much like those in Parkinson's disease;
this is why these movements are sometimes called drug-induced
Figure 5-5. . In untreated schizophrenia, theMesocortical
dopamine pathway and D antagonists2
mesocortical dopamine pathways to dorsolateral prefrontal
cortex (DLPFC) and to ventromedial prefrontal cortex
(VMPFC) are hypothesized to be hypoactive, indicated here by
the dotted outlines of the pathway. This
hypoactivity is related to cognitive symptoms (in the DLPFC),
negative symptoms (in the DLPFC and VMPFC),
and affective symptoms of schizophrenia (in the VMPFC).
Administration of a D antagonist could further reduce2
activity in this pathway and thus not only not improve such
symptoms but actually potentially worsen them.
parkinsonism. Since the nigrostriatal pathway is part of the
extrapyramidal nervous system, these
motor side effects associated with blocking D receptors in this
part of the brain are sometimes also2
called extrapyramidal symptoms, or EPS ( and ).Figures 5-4 5-6
Worse yet, if these D receptors in the nigrostriatal DA pathway
are blocked chronically ( ),2 Figure 5-7
they can produce a hyperkinetic movement disorder known as
tardive dyskinesia. This movement
disorder causes facial and tongue movements, such as constant
chewing, tongue protrusions, facial
grimacing, and also limb movements that can be quick, jerky, or
choreiform (dancing). Tardive

30. dyskinesia is thus caused by long-term administration of
conventional antipsychotics and is thought
to be mediated by changes, sometimes irreversible, in the D
receptors of the nigrostriatal DA2
pathway. Specifically, these receptors are hypothesized to
become supersensitive or to "upregulate"
(i.e., increase in number), perhaps in a futile attempt to
overcome drug-induced blockade of D2
receptors in the striatum ( ).Figure 5-7
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distribution.
About 5% of patients maintained on conventional antipsychotics
will develop tardive dyskinesia every
year (i.e., about 25% of patients by 5 years), not a very
encouraging prospect for a lifelong illness
starting in the early twenties. The risk of developing tardive
Figure 5-6. . The nigrostriatal dopamine pathway isNigrostriatal
dopamine pathway and D antagonists2
theoretically unaffected in untreated schizophrenia. However,
blockade of D receptors, as with a conventional2
antipsychotic, prevents dopamine from binding there and can
cause motor side effects that are often collectively
termed extrapyramidal symptoms (EPS).
dyskinesia in elderly subjects may be as high as 25% within the
first year of exposure to conventional
antipsychotics. However, if D receptor blockade is removed
early enough, tardive dyskinesia may2

31. reverse. This reversal is theoretically due to a "resetting" of
these D receptors by an appropriate2
decrease in the number or sensitivity of them in the nigrostriatal
pathway once the antipsychotic drug
that had been blocking these receptors is removed. However,
after long-term treatment, the D2
receptors apparently cannot or do not reset back to normal, even
when conventional antipsychotic
drugs are discontinued. This leads to tardive dyskinesia that is
irreversible, continuing whether
conventional antipsychotic drugs are administered or not.
Is there any way to predict those who will be harmed with the
development of tardive dyskinesia after
chronic treatment with conventional antipsychotics? Patients
who develop EPS early in treatment
may be twice as likely to develop tardive dyskinesia if
treatment with a conventional antipsychotic is
continued chronically. Also, specific genotypes of dopamine
receptors may confer important genetic
risk factors for developing tardive dyskinesia with chronic
treatment using a conventional
antipsychotic. Risk of new cases of tardive
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Figure 5-7. . Long-term blockade of D receptors in the
nigrostriatal dopamine pathway canTardive dyskinesia 2
cause upregulation of those receptors, which may lead to a
hyperkinetic motor condition known as tardive

32. dyskinesia, characterized by facial and tongue movements (e.g.,
tongue protrusions, facial grimaces, chewing)
as well as quick, jerky limb movements. This upregulation may
be the consequence of the neuron's futile attempt
to overcome drug-induced blockade of its dopamine receptors.
dyskinesia, however, can diminish considerably after 15 years
of treatment, presumably because
patients who have not developed tardive dyskinesia despite 15
years of treatment with a
conventional antipsychotic have lower genetic risk factors for
it.
A rare but potentially fatal complication called the "neuroleptic
malignant syndrome," associated with
extreme muscular rigidity, high fevers, coma, and even death,
and possibly related in part to D2
receptor blockade in the nigrostriatal pathway, can also occur
with conventional antipsychotic agents.
Prolactin elevation
Dopamine D receptors in the tuberoinfundibular DA pathway
are also blocked by conventional2
antipsychotics, and this causes plasma prolactin concentrations
to rise, a condition called
hyperprolactinemia ( ). This is associated with conditions called
galactorrhea (i.e., breastFigure 5-8
secretions) and amenorrhea (i.e., irregular or lack of menstrual
periods). Hyperprolactinemia may
thus interfere with fertility, especially in women.
Hyperprolactinemia might lead to more rapid
demineralization of bones, especially in postmenopausal women
who are not taking estrogen
replacement therapy. Other possible problems associated with
elevated prolactin levels may include

33. sexual dysfunction and weight gain, although the role of
prolactin in causing such problems is not
clear.
The dilemma of blocking D dopamine receptors in all dopamine
pathways2
It should now be obvious that the use of conventional
antipsychotic drugs presents a powerful
dilemma. That is, there is no doubt that conventional
antipsychotic medications exert dramatic
therapeutic actions upon positive symptoms of schizophrenia by
blocking hyperactive dopamine
neurons in the mesolimbic dopamine pathway. However, there
are dopamine pathways in theseveral
brain, and it appears that blocking dopamine receptors in of
them is useful ( ),only one Figure 5-3
whereas blocking dopamine receptors in the remaining pathways
may be harmful (Figures 5-4
through ). The pharmacologic5-8
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Figure 5-8. . The tuberoinfundibular
dopamineTuberoinfundibular dopamine pathway and D
antagonists2
pathway, which projects from the hypothalamus to the pituitary
gland, is theoretically "normal" in untreated
schizophrenia. D antagonists reduce activity in this pathway by
preventing dopamine from binding to D2 2

34. receptors. This causes prolactin levels to rise, which is
associated with side effects such as galactorrhea (breast
secretions) and amenorrhea (irregular menstrual periods).
quandary here is what to do if one wishes simultaneously to
dopamine in the mesolimbicdecrease
dopamine pathway in order to treat positive psychotic symptoms
theoretically mediated by
hyperactive mesolimbic dopamine neurons and yet dopamine in
the mesocortical dopamineincrease
pathway to treat negative and cognitive symptoms, while
leaving dopaminergic tone unchanged in
both the nigrostriatal and tuberoinfundibular dopamine
pathways to avoid side effects. This dilemma
may have been addressed in part by the atypical antipsychotic
drugs described in the following
sections, and is one of the reasons why the atypical
antipsychotics have largely replaced
conventional antipsychotic agents in the treatment of
schizophrenia and other psychotic disorders
throughout the world.
Muscarinic cholinergic blocking properties of conventional
antipsychotics
In addition to blocking D receptors in all dopamine pathways (
through ), conventional2 Figures 5-3 5-8
antipsychotics have other important pharmacologic
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35. Figure 5-9. . Shown here is an icon representing a conventional
antipsychoticConventional antipsychotic
drug. Conventional antipsychotics have pharmacological
properties in addition to dopamine D antagonism. The2
receptor profiles differ for each agent, contributing to divergent
side-effect profiles. However, some important
characteristics that multiple agents share are the ability to block
muscarinic cholinergic receptors, histamine H1
receptors, and/or -adrenergic receptors.1
properties ( ). One particularly important pharmacologic action
of some conventionalFigure 5-9
antipsychotics is their ability to block muscarinic M -
cholinergic receptors ( through ).1 Figures 5-9 5-11
This can cause undesirable side effects such as dry mouth,
blurred vision, constipation, and
cognitive blunting ( ). Differing degrees of muscarinic
cholinergic blockade may alsoFigure 5-10
explain why some conventional antipsychotics have a lesser
propensity to produce extrapyramidal
side effects (EPS) than others. That is, those conventional
antipsychotics that cause more EPS are
the agents that have only anticholinergic properties, whereas
those conventional antipsychoticsweak
that cause fewer EPS are the agents that have anticholinergic
properties.stronger
How does muscarinic cholinergic receptor blockade reduce the
EPS caused by dopamine D2
receptor blockade in the nigrostriatal pathway? The reason
seems to be based on the fact that
dopamine and acetylcholine have a reciprocal relationship with
each other in the nigrostriatal

36. pathway ( ).Figure 5-11
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Figure 5-10. . In this diagram, the icon of aSide effects of
muscarinic cholinergic receptor blockade
conventional antipsychotic drug is shown with its M
anticholinergic/antimuscarinic portion inserted into1
acetylcholine receptors, causing the side effects of constipation,
blurred vision, dry mouth, and drowsiness.
Figure 5-11
A. . Dopamine and acetylcholine have a reciprocalReciprocal
relationship of dopamine and acetylcholine
relationship in the nigrostriatal dopamine pathway. Dopamine
neurons here make postsynaptic connections with
the dendrite of a cholinergic neuron. Normally, dopamine
suppresses acetylcholine activity (no acetylcholine
being released from the cholinergic axon on the right).
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B. . This figure shows what happens to acetylcholine

37. activityDopamine, acetylcholine, and D antagonism2
when dopamine receptors are blocked. As dopamine normally
suppresses acetylcholine activity, removal of
dopamine inhibition causes an increase in acetylcholine
activity. Thus if dopamine receptors are blocked at the
D receptors on the cholinergic dendrite on the left, then
acetylcholine becomes overly active, with enhanced2
release of acetylcholine from the cholinergic axon on the right.
This is associated with the production of
extrapyramidal symptoms (EPS). The pharmacological
mechanism of EPS therefore seems to be a relative
dopamine deficiency and a relative acetylcholine excess.
C. . One compensation for the overactivity that occurs whenD
antagonism and anticholinergic agents2
dopamine receptors are blocked is to block the acetylcholine
receptors with an anticholinergic agent (M1
receptors being blocked by an anticholinergic on the far right).
Thus, anticholinergics overcome excess
acetylcholine activity caused by removal of dopamine inhibition
when dopamine receptors are blocked by
conventional antipsychotics. This also means that
extrapyramidal symptoms (EPS) are reduced.
Dopamine neurons in the nigrostriatal dopamine pathway make
postsynaptic connections with
cholinergic neurons ( ). Dopamine normally acetylcholine
release fromFigure 5-11A inhibits
postsynaptic nigrostriatal cholinergic neurons, thus suppressing
acetylcholine activity there (Figure
). If dopamine can no longer suppress acetylcholine release
because dopamine receptors are5-11A
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38. Stahl Online © 2020 Cambridge University Press.
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distribution.
being blocked by a conventional antipsychotic drug, then
acetylcholine becomes overly active (
).Figure 5-11B
One compensation for this overactivity of acetylcholine is to
block it with an anticholinergic agent (
). Thus, drugs with anticholinergic actions will diminish the
excess acetylcholine activityFigure 5-11C
caused by removal of dopamine inhibition when dopamine
receptors are blocked ( and Figures 5-10
). If anticholinergic properties are present in the same drug with
D blocking properties, they5-11C 2
will tend to mitigate the effects of D blockade in the
nigrostriatal dopamine pathway. Thus,2
conventional antipsychotics with potent anticholinergic
properties have lower EPS than conventional
antipsychotics with weak anticholinergic properties.
Furthermore, the effects of D blockade in the2
nigrostriatal system can be mitigated by co-administering an
agent with anticholinergic properties.
This has led to the common strategy of giving anticholinergic
agents along with conventional
antipsychotics in order to reduce EPS. Unfortunately, this
concomitant use of anticholinergic agents
does not lessen the ability of the conventional antipsychotics to
cause tardive dyskinesia. It also
causes the well-known side effects associated with
anticholinergic agents, such as dry mouth,

39. blurred vision, constipation, urinary retention, and cognitive
dysfunction ( ).Figure 5-10
Other pharmacologic properties of conventional antipsychotic
drugs
Still other pharmacologic actions are associated with the
conventional antipsychotic drugs. These
include generally undesired blockade of histamine H receptors
( ) causing weight gain and1 Figure 5-9
drowsiness, as well as blockade of -adrenergic receptors causing
cardiovascular side effects such1
as orthostatic hypotension and drowsiness. Conventional
antipsychotic agents differ in terms of their
ability to block these various receptors represented in . For
example, the popularFigure 5-9
conventional antipsychotic haloperidol has relatively little
anticholinergic or antihistaminic binding
activity, whereas the classic conventional antipsychotic
chlorpromazine has potent anticholinergic
and antihistaminic binding. Because of this, conventional
antipsychotics differ somewhat in their
side-effect profiles, even if they do not differ overall in their
therapeutic profiles. That is, some
conventional antipsychotics are more sedating than others, some
have more ability to cause
cardiovascular side effects than others, some have more ability
to cause EPS than others.
A somewhat old-fashioned way to subclassify conventional
antipsychotics is "low potency" versus
"high potency" ( ). In general, as the name implies, low-potency
agents require higher dosesTable 5-1
than high-potency agents, but, in addition, low-potency agents
tend to have more of the additional

40. properties discussed here than do the so-called high-potency
agents: namely, low-potency agents
have greater anticholinergic, antihistaminic, and antagonist
properties than high-potency agents,1
and thus are probably more sedating in general. A number of
conventional antipsychotics are
available in long-acting depot formulations ( ).Table 5-1
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Psychosis and schizophrenia
Psychosis is a difficult term to define and is frequently misused,
not only in the media but
unfortunately among mental health professionals as well.
Stigma and fear surround the concept of
psychosis, and sometimes the pejorative term "crazy" is used for
psychosis. This chapter is not
intended to list the diagnostic criteria for all the different
mental disorders in which psychosis is either
a defining feature or an associated feature. The reader is
referred to standard reference sources
such as the DSM ( ) of the American Psychiatric Association
and theDiagnostic and Statistical Manual
ICD ( ) for that information. Although schizophrenia
isInternational Classification of Diseases
emphasized here, we will approach psychosis as a syndrome
associated with a variety of illnesses
that are all targets for antipsychotic drug treatment.

41. Symptom dimensions in schizophrenia
Clinical description of psychosis
Psychosis is a syndrome - that is, a mixture of symptoms - that
can be associated with many different
psychiatric disorders, but is not a specific disorder itself in
diagnostic schemes such as the DSM or
ICD. At a minimum, psychosis means delusions and
hallucinations. It generally also includes
symptoms such as disorganized speech, disorganized behavior,
and gross distortions of reality.
Therefore, psychosis can be considered to be a set of symptoms
in which a person’s mental
capacity, affective response, and capacity to recognize reality,
communicate, and relate to others is
impaired. Psychotic disorders have psychotic symptoms as their
defining features; there are other
disorders in which psychotic symptoms may be present, but are
not necessary for the diagnosis.
Those as a feature of the diagnosisdisorders that require the
presence of psychosis defining
include schizophrenia, substance-induced (i.e., drug-induced)
psychotic disorders, schizophreniform
disorder, schizoaffective disorder, delusional disorder, brief
psychotic disorder, and psychotic
disorder due to a general medical condition ( ). Table 4-1
Disorders that may or may not have
as features include mania and depression as well as
severalpsychotic symptoms associated
cognitive disorders such as Alzheimer’s dementia ( ).Table 4-2

42. Psychosis itself can be paranoid, disorganized/excited, or
depressive. Perceptual distortions and
motor disturbances can be associated with any type of
psychosis. includePerceptual distortions
being distressed by hallucinatory voices; hearing voices that
accuse, blame, or threaten punishment;
seeing visions;
Table 4-1 Disorders in which psychosis is a defining feature
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reporting hallucinations of touch, taste or odor; or reporting that
familiar things and people seem
changed. are peculiar, rigid postures; overt signs of tension;
inappropriate grinsMotor disturbances
or giggles; peculiar repetitive gestures; talking, muttering, or
mumbling to oneself; or glancing around
as if hearing voices.
In , the patient has paranoid projections, hostile belligerence
and grandioseparanoid psychosis
expansiveness. includes preoccupation with delusional beliefs;
believing thatParanoid projection
people are talking about oneself; believing one is being
persecuted or being conspired against; and
believing people or external forces control one’s actions. is
verbal expression ofHostile belligerence
feelings of hostility; expressing an attitude of disdain;
manifesting a hostile, sullen attitude;

43. manifesting irritability and grouchiness; tending to blame others
for problems; expressing feelings of
resentment; complaining and finding fault; as well as expressing
suspicion of people. Grandiose
is exhibiting an attitude of superiority; hearing voices that
praise and extol; believingexpansiveness
one has unusual powers or is a well-known personality, or that
one has a divine mission.
In a there is conceptual disorganization, disorientation,
anddisorganized/excited psychosis
excitement. can be characterized by giving answers that are
irrelevant orConceptual disorganization
incoherent, drifting off the subject, using neologisms, or
repeating certain words or phrases.
is not knowing where one is, the season of the year, the
calendar year, or one’s ownDisorientation
age. is expressing feelings without restraint; manifesting
speech that is hurried; exhibitingExcitement
an elevated mood; an attitude of superiority;
Table 4-2 Disorders in which psychosis is an associated feature
dramatizing oneself or one’s symptoms; manifesting loud and
boisterous speech; exhibiting
overactivity or restlessness; and exhibiting excess of speech.
Depressive psychosis is characterized by psychomotor
retardation, apathy, and anxious
self-punishment and blame. and are manifested by slowed
speech;Psychomotor retardation apathy
indifference to one’s future; fixed facial expression; slowed
movements; deficiencies in recent
memory; blocking in speech; apathy toward oneself or one’s

44. problems; slovenly appearance; low or
whispered speech; and failure to answer questions. is
theAnxious self-punishment and blame
tendency to blame or condemn oneself; anxiety about specific
matters; apprehensiveness regarding
vague future events; an attitude of self-deprecation, manifesting
as a depressed mood; expressing
feelings of guilt and remorse; preoccupation with suicidal
thoughts, unwanted ideas, and specific
fears; and feeling unworthy or sinful.
This discussion of clusters of psychotic symptoms does not
constitute diagnostic criteria for any
psychotic disorder. It is given merely as a description of several
types of symptoms in psychosis to
give the reader an overview of the nature of behavioral
disturbances associated with the various
psychotic illnesses.
Schizophrenia is more than a psychosis
Although schizophrenia is the commonest and best-known
psychotic illness, it is not synonymous
with psychosis, but is just one of many causes of psychosis.
Schizophrenia affects 1% of the
population, and in the US there are over 300 000 acute
schizophrenic episodes annually. Between
25% and 50% of schizophrenia patients attempt suicide, and
10% eventually succeed, contributing to
a mortality rate eight times greater than that of the general
population. Life expectancy of a patient
with schizophrenia may be 20-30 years shorter than the general
population, not only due to suicide,
but in particular due to premature cardiovascular disease.
Accelerated mortality from premature
cardiovascular disease in patients with schizophrenia is caused

45. not only by genetic and lifestyle
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factors, such as smoking, unhealthy diet, and lack of exercise
leading to obesity and diabetes, but
also - sorrily - from treatment with some antipsychotic drugs
which themselves cause an increased
incidence of obesity and diabetes, and thus increase cardiac
risk. In the US, over 20% of all social
security benefits are used for the care of patients with
schizophrenia. The direct and indirect costs of
schizophrenia in the US alone are estimated to be in the tens of
billions of dollars every year.
Schizophrenia by definition is a disturbance that must last for
six months or longer, including at least
one month of delusions, hallucinations, disorganized speech,
grossly disorganized or catatonic
behavior, or negative symptoms. are listed in and shown in
Positive symptoms Table 4-3 Figure
. These symptoms4-1
Table 4-3 Positive symptoms of psychosis and schizophrenia
of schizophrenia are often emphasized, since they can be
dramatic, can erupt suddenly when a
patient decompensates into a psychotic episode (often called a
psychotic "break," as in break from

46. reality), and are the symptoms most effectively treated by
antipsychotic medications. areDelusions
one type of positive symptom, and these usually involve a
misinterpretation of perceptions or
experiences. The most common content of a delusion in
schizophrenia is persecutory, but it may
include a variety of other themes including referential (i.e.,
erroneously thinking that something refers
to oneself), somatic, religious, or grandiose. are also a type of
positive symptom (Hallucinations
) and may occur in any sensory modality (e.g., auditory, visual,
olfactory, gustatory, andTable 4-3
tactile), but auditory hallucinations are by far the most common
and characteristic hallucinations in
schizophrenia. Positive symptoms generally reflect an of
normal functions, and in addition toexcess
delusions and hallucinations may also include distortions or
exaggerations in language and
communication (disorganized speech), as well as in behavioral
monitoring (grossly disorganized or
catatonic or agitated behavior). Positive symptoms are well
known because they are dramatic, are
often the cause of bringing a patient to the attention of medical
professionals and law enforcement,
and are the major target of antipsychotic drug treatments.
Negative symptoms are listed in and and shown in .
Classically, there areTables 4-4 4-5 Figure 4-1
at
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47. Figure 4-1. . The syndrome of schizophrenia consists of
aPositive and negative symptoms of schizophrenia
mixture of symptoms that are commonly divided into two major
categories, positive and negative. Positive
symptoms, such as delusions and hallucinations, reflect the
development of the symptoms of psychosis; they
can be dramatic and may reflect loss of touch with reality.
Negative symptoms reflect the loss of normal
functions and feelings, such as losing interest in things and not
being able to experience pleasure.
least five types of negative symptoms all starting with the letter
A ( ):Table 4-5
alogia - dysfunction of communication; restrictions in the
fluency and productivity of thought
and speech
affective blunting or flattening - restrictions in the range and
intensity of emotional expression
asociality - reduced social drive and interaction
anhedonia - reduced ability to experience pleasure
avolition - reduced desire, motivation or persistence;
restrictions in the initiation of
goal-directed behavior
Table 4-4 Negative symptoms of schizophrenia
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Negative symptoms in schizophrenia, such as blunted affect,
emotional withdrawal, poor rapport,
passivity and apathetic social withdrawal, difficulty in abstract
thinking, stereotyped thinking and lack
of spontaneity, commonly are considered a reduction in normal
functions and are associated with
long periods of hospitalization and poor social functioning.
Although this reduction in normal
functioning may not be as dramatic as positive symptoms, it is
interesting to note that negative
symptoms of schizophrenia determine whether a patient
ultimately functions well or has a poor
outcome. Certainly, patients will have disruptions in their
ability to interact with others when their
positive symptoms are out of control, but their degree of
negative symptoms will largely determine
whether patients with schizophrenia can live independently,
maintain stable social relationships, or
re-enter the workplace.
Although formal rating scales can be used to measure negative
symptoms in research studies, in
clinical practice it may be more practical to identify and
monitor negative symptoms quickly by
observation alone ( ) or by some simple questioning ( ).
Negative symptoms areFigure 4-2 Figure 4-3
not just part of the syndrome of schizophrenia - they can also be
part of a "prodrome" that begins
with subsyndromal symptoms that do not meet the diagnostic
criteria of schizophrenia and occur

49. before the onset of the full syndrome of schizophrenia.
Prodromal negative symptoms are important
to detect and monitor over time in high-risk patients so that
treatment can be initiated at the first
signs of psychosis. Negative
Table 4-5 What are negative symptoms?
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Figure 4-2. . Some negative symptoms of schizophrenia -
suchNegative symptoms identified by observation
as reduced speech, poor grooming, and limited eye contact - can
be identified solely by observing the patient.
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Figure 4-3. . Other negative symptoms of schizophrenia can
beNegative symptoms identified by questioning
identified by simple questioning. For example, brief questioning
can reveal the degree of emotional
responsiveness, interest level in hobbies or pursuing life goals,
and desire to initiate and maintain social
contacts.

50. symptoms can also persist between psychotic episodes once
schizophrenia has begun, and reduce
social and occupational functioning in the absence of positive
symptoms.
Current antipsychotic drug treatments are limited in their ability
to treat negative symptoms, but
psychosocial interventions along with antipsychotics can be
helpful in reducing negative symptoms.
There is even the possibility that instituting treatment for
negative symptoms during the prodromal
phase of schizophrenia may delay or prevent the onset of the
illness, but this is still a matter of
current research.
Beyond positive and negative symptoms of schizophrenia
Although not recognized formally as part of the diagnostic
criteria for schizophrenia, numerous
studies subcategorize the symptoms of this illness into five
dimensions: not just positive and negative
symptoms, but also cognitive symptoms, aggressive symptoms,
and affective symptoms ( ).Figure 4-4
This is perhaps a more sophisticated, if complicated, manner of
describing the symptoms of
schizophrenia.
Aggressive symptoms such as assaultiveness, verbally abusive
behaviors, and frank violence can
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51. Figure 4-4. . The different symptom domains of schizophrenia
areLocalization of symptom domains
hypothesized to be regulated by unique brain regions. Positive
symptoms of schizophrenia are hypothetically
modulated by malfunctioning mesolimbic circuits, while
negative symptoms are hypothetically linked to
malfunctioning mesocortical circuits and may also involve
mesolimbic regions such as the nucleus accumbens,
which is part of the brain’s reward circuitry and thus plays a
role in motivation. The nucleus accumbens may also
be involved in the increased rate of substance use and abuse
seen in patients with schizophrenia. Affective
symptoms are associated with the ventromedial prefrontal
cortex, while aggressive symptoms (related to
impulse control) are associated with abnormal information
processing in the orbitofrontal cortex and amygdala.
Cognitive symptoms are associated with problematic
information processing in the dorsolateral prefrontal cortex.
Although there is overlap in function among different brain
regions, understanding which brain regions may be
predominantly involved in specific symptoms can aid in
customization of treatment to the particular symptom
profile of each individual patient with schizophrenia.
occur with positive symptoms such as delusions and
hallucinations, and be confused with positive
symptoms. Behavioral interventions may be particularly helpful
to prevent violence linked to poor
impulsivity by reducing provocations from the environment.
Certain antipsychotic drugs such as
clozapine, or very high doses of standard antipsychotic drugs,
or occasionally the use of two
antipsychotic drugs simultaneously, may also be useful for

52. aggressive symptoms and violence in
some patients.
It can also be difficult to separate the symptoms of formal
cognitive dysfunction from the symptoms of
affective dysfunction and from negative symptoms, but research
is attempting to localize the specific
areas of brain dysfunction for each symptom domain in
schizophrenia in the hope of developing
better treatments for the often-neglected negative, cognitive,
and affective symptoms of
schizophrenia. In particular, neuropsychological assessment
batteries are being developed to
quantify cognitive symptoms, in order to detect cognitive
improvement after treatment with a number
of novel psychotropic drugs currently being tested. Cognitive
symptoms of schizophrenia are
impaired attention and impaired information processing
manifested as impaired verbal fluency (ability
to produce spontaneous speech), problems with serial learning
(of a list of items or a sequence of
events), and impairment in vigilance for executive functioning
(problems with sustaining and focusing
attention, concentrating, prioritizing, and modulating behavior
based upon social cues).
Important cognitive symptoms of schizophrenia are listed in .
These do not includeTable 4-6
symptoms of dementia and memory disturbance more
characteristic of Alzheimer’s disease, but
cognitive symptoms of schizophrenia emphasize "executive
dysfunction," which includes problems
representing and maintaining goals, allocating attentional
resources, evaluating and monitoring
performance, and utilizing these skills to solve problems.
Cognitive symptoms of schizophrenia are

53. important to recognize and monitor because they are the single
strongest correlate of real-world
functioning, even stronger than negative symptoms.
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Table 4-6 Cognitive symptoms of schizophrenia
Symptoms of schizophrenia are not necessarily unique to
schizophrenia
It is important to recognize that several illnesses other than
schizophrenia can share some of the
same five symptom dimensions as described here for
schizophrenia and shown in . Thus,Figure 4-4
disorders in addition to schizophrenia that can have include
bipolar disorder,positive symptoms
schizoaffective disorder, psychotic depression, Alzheimer’s
disease and other organic dementias,
childhood psychotic illnesses, drug-induced psychoses, and
others. can alsoNegative symptoms
occur in other disorders and can also overlap with cognitive and
affective symptoms that occur in
these other disorders. However, as a primary deficit state,
negative symptoms are fairly unique to
schizophrenia. Schizophrenia is certainly not the only disorder
with . Autism,cognitive symptoms
post-stroke (vascular or multi-infarct) dementia, Alzheimer’s
disease, and many other organic
dementias (Parkinsonian/Lewy body dementia,

54. frontotemporal/Pick’s dementia, etc.) can also be
associated with cognitive dysfunctions similar to those seen in
schizophrenia.
Affective symptoms are frequently associated with
schizophrenia but this does not necessarily mean
that they fulfill the diagnostic criteria for a comorbid anxiety or
affective disorder. Nevertheless,
depressed mood, anxious mood, guilt, tension, irritability, and
worry frequently accompany
schizophrenia. These various symptoms are also prominent
features of major depressive disorder,
psychotic depression, bipolar disorder, schizoaffective disorder,
organic dementias, childhood
psychotic disorders, and treatment-resistant cases of depression,
bipolar disorder, and
schizophrenia, among others. Finally, occur in numerous
otheraggressive and hostile symptoms
disorders, especially those with problems of impulse control.
Symptoms include overt hostility, such
as verbal or physical abusiveness or assault, self-injurious
behaviors including suicide, and arson or
other property damage. Other types of impulsiveness such as
sexual acting out are also in this
category of aggressive and hostile symptoms. These same
symptoms are frequently associated with
bipolar disorder, childhood psychosis, borderline personality
disorder, antisocial personality disorder,
drug abuse, Alzheimer’s and other dementias, attention deficit
hyperactivity disorder, conduct
disorders in children, and many others.
Brain circuits and symptom dimensions in schizophrenia
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55. Stahl Online © 2020 Cambridge University Press.
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The various symptoms of schizophrenia are hypothesized to be
localized in unique brain regions (
). Specifically, the positive symptoms of schizophrenia have
long been hypothesized to beFigure 4-4
localized to malfunctioning mesolimbic circuits, especially
involving the nucleus accumbens. The
nucleus accumbens is considered to be part of the brain’s
reward circuitry, so it is not surprising that
problems with reward and motivation in schizophrenia,
symptoms that can overlap with negative
symptoms and lead to smoking, drug and alcohol abuse, may be
linked to this brain area as well.
The prefrontal cortex is considered to be a key node in the
nexus of malfunctioning cerebral circuitry
responsible for each of the remaining symptoms of
schizophrenia: specifically, the mesocortical and
ventromedial prefrontal cortex with negative symptoms and
affective symptoms, the dorsolateral
prefrontal cortex with cognitive symptoms, and the orbitofrontal
cortex and its connections to
amygdala with aggressive, impulsive symptoms ( ).Figure 4-4
This model is obviously oversimplified and reductionistic,
because every brain area has several
functions, and every function is certainly distributed to more
than one brain area. Nevertheless,
allocating specific symptom dimensions to unique brain areas
not only assists research studies, but
has both heuristic and clinical value. Specifically, every patient

56. has unique symptoms, and unique
responses to medication. In order to optimize and individualize
treatment, it can be useful to consider
which specific symptoms any given patient is expressing, and
therefore which areas of that particular
patient’s brain are hypothetically malfunctioning ( ). Each brain
area has uniqueFigure 4-4
neurotransmitters, receptors, enzymes, and genes that regulate
it, with some overlap, but also with
some unique regional differences, and knowing this can assist
the clinician in choosing medications
and in monitoring the effectiveness of treatment.
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distribution.
Assessing and Treating Adult Clients with Mood Disorders
A mood disorder describes a psychological disorder which is
characterized as a fluctuation of one’s mood, such as a major
depressive or bipolar disorder. An estimated 20 million
individuals in the United States have depression which
comprises of symptoms such as a loss of pleasure in activities,
sadness, weight changes, feelings of hopelessness, fatigue as
well as suicidal ideation; all of which can significantly impact
daily functioning (Mental Health.gov, 2017). According to Park
and Zarate (2019) onset of depression in adulthood continues to
flourish where an estimated 30 percent of adults have a lifetime
risk of experiencing a major depressive episode with a median
age of 32.5. The author further indicates screening for
depression, a thorough evaluation, and monitoring is necessary
to ensure safety and wellbeing (Park & Zarate, 2019).
Pharmacotherapy, along with psychotherapy are first-line

57. therapies for effective outcomes (Park & Zarate, 2019). The
purpose of this paper is to review a case study, choose the
appropriate selection utilizing research, and discuss ethical
considerations.
Case Study
A 32-year-old Hispanic American client presents to the initial
appointment with depression. Health history, along with
medical workup, appears to be unremarkable except for the
slight back and shoulder pain due to his occupation. The clinical
interview reveals past feelings of being an “outsider” and has
few friends (Laureate Education, 2016). There is a decline in
daily activities, a weight increase of 15 pounds over two
months, along with diminished sleep and the inability to fully
concentrate (Laureate Education, 2016). The results of the
depression screening administered by the psychiatric mental
health nurse practitioner (PMHNP), indicates severe depression
with a score of 51 (Montgomery & Asberg, 1979).
Decision Point One
The selections include Zoloft 25 mg orally daily, Effexor 37.5
XR mg orally daily, or Phenelzine 15 mg orally TID. As a
healthcare professional treating a client, Zoloft (sertraline) 25
mg is the first choice at decision point one. Selective serotonin
reuptake inhibitors (SSRIs) impede the reabsorption of this
neurotransmitter; thus, increasing the serotonin levels of the
nerve cells in the brain to allow for improvement in mood
(Stahl, 2013). SSRIs have been utilized as first-line therapy to
treat major depressive disorder due to efficacy, fewer side
effects, cost-effectiveness as well as a wider availability
(Masuda et al., 2017). The therapeutic dosing range is typically
50 mg-200 mg (Stahl, 2017). However, beginning at 25 mg and
gradually titrating the dose, depending on tolerability, is an
appropriate health care decision (National Alliance on Mental
Illness, 2018b). Therefore, a low dose of Zoloft appears to be
the best option in caring for this client.
Effexor (venlafaxine) is classified as a selective serotonin-
norepinephrine reuptake inhibitor (SNRI) which impedes the

58. reabsorption of the neurotransmitters serotonin and
norepinephrine changing the chemistry in the brain to regulate
mood (Stahl, 2013). Bhat and Kennedy (2017) describe
antidepressant discontinuation syndrome (ADS) as a
“medication-induced movement disorder” along with various
adverse reactions such as intense sadness and anxiety; periods
of an “electric shock” sensation; sights of flashing lights; and
dizziness upon movement (Bhat & Kennedy, 2017, p. E7).
These symptoms are often experienced a few days after sudden
discontinuation of an antidepressant with a shorter-life (3-7
hours) such as venlafaxine or paroxetine (Bhat & Kennedy,
2017; Stahl, 2017). Moreover, Stahl (2017) indicates
venlafaxine is one of the drugs with more severe withdrawal
symptoms in comparison to other antidepressants. It may take
some clients several months to taper off of this medicine;
therefore, Effexor is not the optimal selection at this time.
Phenelzine is classified as an irreversible monoamine oxidase
inhibitor (MAOI) which impedes the monoamine oxidase from
deconstructing serotonin, dopamine, as well as norepinephrine.
Thus, boosting the levels of neurotransmitters in the brain to
regulate mood (Stahl, 2017). Park and Zarate (2019) purport
the use of monoamine oxidase inhibitors have a higher risk
profile; therefore, are not typically utilized unless a newer
antidepressant is considered ineffective. Bhat and Kennedy
(2017) indicate there is a need for a long taper with MAOIs.
Further, this medication may lose effectiveness after long-term
use, and it is considered to have habit-forming qualities for
some individuals (Stahl, 2017). The initial dose for phenelzine
is taken three times a day which research suggests medication
adherence is often tricky when the administration is more than
once a day (Goette & Hammwöhner, 2016). Stahl (2017)
describes certain risk factors comprising of frequent weight
gain, interference of certain food products containing tyramine,
drug interactions (serotonin syndrome), as well as a
hypertensive crisis. When utilizing this medication for
treatment-resistant depression, the advance practitioner is aware

59. of the detrimental adverse reactions which may occur.
Therefore, phenelzine is not the safest option for this client.
The overarching goal for this male client is to reduce the
symptoms related to his major depressive disorder and to
eventually achieve remission without relapse where he can
maintain normalcy in his life. After four weeks, his depressive
symptoms decrease by 25 percent which is progress; however,
he has a new onset of erectile dysfunction (Laureate Education,
2016). Sexual dysfunction is a notable side effect of sertraline
(Stahl, 2017). Therefore, the clinician will reevaluate the plan
of care given this new information. The outcomes were to be
expected as the client was started on a low dose of sertraline,
and treatment is typically 50 mg to 200 mg. A continuation in
progress may require more time, approximately six to eight
weeks in total (Stahl, 2017).
Decision Point Two
The present selections include decrease dose to 12.5 daily
orally, continue same dose and counsel client, or augment with
Wellbutrin 150 IR in the morning. The preference for decision
point two is Wellbutrin (bupropion) 150 IR, which is considered
a norepinephrine dopamine reuptake inhibitor (SDRI). An
SDRI elevates the neurotransmitters dopamine, noradrenaline,
and norepinephrine in the brain to achieve an improvement in
depressive symptoms (Stahl, 2017). The purpose of utilizing
this agent is three-fold: (1) To boost mood (2) To treat the new
onset of sexual dysfunction (3) To aid in weight-loss.
According to the National Alliance on Mental Illness [NAMI]
(2018a), Wellbutrin is a medication administered for major
depressive disorder often in conjunction with an SSRI (NAMI,
2018a).
Further, Wellbutrin may be prescribed with an SSRI to reverse
the effects of SSRI-induced sexual dysfunction (Stahl, 2017).
Dunner (2014) purports combining antidepressants are safe and
may enhance efficacy; however, the combination of medications
may also be utilized as an approach to reduce the effects of
antidepressant pharmacotherapy. Dunner (2014) concurs that

60. bupropion is frequently used with an SSRI or SNRI to alleviate
sexual dysfunction. Stahl (2017), findings indicate the most
common side effects of bupropion consist of constipation, dry
mouth, agitation, anxiety, improved cognitive functioning, as
well as weight loss. The client in this scenario has gained 15
pounds over two months; thus, this medication may aid in his
desire to lose weight (Laureate Education, 2016). Further, this
agent typically is not sedating as it does not have
anticholinergic or antihistamine properties yet have a mild
stimulating effect (Guzman, n.d).
Decreasing the Zoloft dose from 25 mg daily to 12.5 mg would
not prove feasible as the client has reached a 25 percent
reduction in symptomology. The treatment for adults is 50 mg-
200 mg, taking an approximate six to eight weeks to see the
results in some individuals (Stahl, 2017). If the provider is
tapering the medication as part of the client's plan of care,
reducing the dose to 12.5 mg would prove beneficial. Research
finds that when taking an antidepressant, the neurons adapt to
the current level of neurotransmitters; therefore, if
discontinuing an SSRI too quickly some of the symptoms may
return (Harvard Health Publishing, 2018). Under some
circumstances, discontinuation signs may appear, such as sleep
changes, mood fluctuations, unsteady gait, numbness, or
paranoia (Harvard Health Publishing, 2018). However, the
client is experiencing slow and steady progress on his current
dose of Zoloft, so no adjustments are warranted.
At this point, positive results have been verbalized with the
current dose of Zoloft 25 mg daily, with the exception of the
onset of erectile dysfunction, which is a priority at this time.
One study finds that comorbid depression and anxiety disorders
are commonly seen in adult males with sexual dysfunction
(Rajkumar & Kumaran, 2015). An estimated 12.5 percent of
participants experienced a depressive disorder before the
diagnosis of sexual dysfunction. The author’s findings suggest a
significant increase in suicidal behaviors with this comorbidity.
Moreover, the study indicates, some men experienced a sexual

61. disorder while taking prescribed medication such as an
antidepressant (Rajkumar & Kumaran, 2015). According to Li
et al. (2018), cognitive-behavioral therapy (CBT) is a beneficial
tool utilized with clients experiencing mood disorders. The
implementation of CBT may increase the response and
remission rates of depression. However, the option of
continuing the same dose and engaging in counseling services is
not the priority at this time. It is essential to address this side
effect to enhance his current pharmacotherapy and prevent an
increase in depressive symptoms.
The continued goal of therapy is to achieve “full” remission of
this individual’s major depressive disorder and to enhance his
wellbeing. After four weeks, the client returns to the clinic
with a significant reduction in depressive symptoms along with
the dissipation of erectile dysfunction. However, he reports
feelings of “jitteriness” and on occasion “nervousness”
(Laureate Education, 2016). This course of treatment has
proven successful thus far, and the outcomes are to be expected
due to the medication trials.
Decision Point Three
The present selections are to discontinue Zoloft and continue
Wellbutrin, change Wellbutrin to XL 150 mg in the morning, or
add Ativan 0.5 mg orally TID/PRN for anxiety. The selection
for decision point three is to change the Wellbutrin from IR to
XL 150 mg in the morning. The first formulation is immediate-
release (IR) and the recommended dosing is divided beginning
at 75 mg twice daily increasing to 100 mg twice daily, then 100
mg three times a day with the maximum of 450 mg (Stahl,
2017). The second formulation is extended-release (XL),
where the administration for the initial dose is once daily taken
in the morning; the maximum is 450 mg in a single dose (Stahl,
2017). The peak level of bupropion XL is approximately five
hours; therefore, the side effects reported may subside as the
absorption rate is slower than the IR dose (U.S. Food and Drug
Administration, 2011a). The immediate-release peak level is
approximately two hours which may account for the client’s

62. notable feelings of being jittery and at times nervous (U.S. Food
and Drug Administration, 2011b). Furthermore, clients are
switched to extended-release to improve tolerance and treatment
adherence to once-daily treatment (Guzman, n.d). As a mental
health provider, caring for this client, changing the formulation
is the best decision at this point as well as to continue to
monitor side effects.
As mentioned above, Zoloft, an SSRI, can be utilized as a first-
line agent for major depressive disorder (Masuda et al., 2017).
Using Wellbutrin as an adjunct to the regimen has continued to
reduce his symptoms of depression and has alleviated one of his
primary concerns which is sexual dysfunction. Therefore,
discontinuing Zoloft and maintaining the use of Wellbutrin is
not an appropriate option at this time.
Ativan (lorazepam) is a benzodiazepine with anxiolytic, anti-
anxiety, and sedative properties. It provides short-term relief of
anxiety symptoms or insomnia (U.S. National Library of
Medicine [NLM], n.d.). Lorazepam works by enhancing the
effect of the inhibitory neurotransmitter GABA, which inhibits
the nerve signals, in doing so, reducing the “nervous excitation”
(NLM, n.d., para. 1). In some instances, a low dose, 0.5 mg,
may be administered short-term to reduce side effects from
another medication. Stahl (2017), indicates many side effects
will not improve with an augmenting drug. Common side effects
consist of confusion, weakness, sedation, nervousness, and
fatigue (Stahl, 2017). Further, Ativan has an increased risk for
abuse potential as it is known to have habit-forming properties
(Stahl, 2017). As a result, administering Ativan would not be in
the best interest of the client.
The ultimate goal is to achieve remission of his mood disorder.
The medication regimen has proven effective; thus, considering
this to be a successful plan of care. Taking both the sertraline
and bupropion can exhibit side effects of jitteriness; however,
changing to the extended-release may aid in the dissipation of
these feelings. The addition of Ativan to relieve side effects,
that are perhaps temporary, is against better judgment without

63. first making an effort to change or modify the medication
regimen (Laureate Education, 2016).
Summary with Ethical Considerations
Mood disorders affect millions of individuals in the United
States on an annual basis. The prevalence of mental illness
continues to flourish, impacting one’s quality of life. Initiating
treatment, under the guidance of a healthcare professional, is of
the utmost importance. Further, an individualized plan of care
comprising of education, therapy, medication, and support is
crucial for overall health and wellbeing.
The client is a Hispanic American male employed as a laborer
in a warehouse (Laureate Education, 2016). It is essential to
assess his financial means before prescribing medications.
Although one cannot assume the client has financial hardships,
having this knowledge will guide in the process of treatment. If
the client is without insurance and has to pay out-of-pocket,
medication adherence may not be sustainable. Therefore, as a
psychiatric nurse practitioner, providing a cost-effective means
whether, through generic prescriptions, discount pharmacies, or
prescribing a larger quantity may be a necessary option (Barker
& Guzman, 2015). Further, the partnership among clients and
practitioners is essential; to establish trust and respect as well
as understanding cultural preferences while avoiding
stereotypes is vital.