Schizoaffective Disorder: A Case Study

Kathleen LeClear O’Connell MSN, ANP

Journal of Psychosocial Nursing and Mental Health Services

October 1995 - Volume 33 · Issue 10: 35-40

A review of medical and nursing literature provides little background on schizoaffective

disorder as a diagnosis different from schizophrenia. For the client and family members
involved, however, schizoaffective disorder means a chronic roller coaster ride of symptoms
and problems that may be more difficult to cope with than either of its "parent" diseases,
schizophrenia or mood disorders. The nurse, in collaboration with the psychiatrist, can help
the client and family cope with this severe and chronic mental illness.

Two subtypes of schizoaffective disorder have been identified: bipolar type and depressive
type. Bipolar type is associated with the presence of manic or mixed episodes within the
illness. Depressive type is associated with clients who display only major depressive
episodes within the illness (American Psychiatric Association [APA], 1994).

Schizoaffective disorder, like schizophrenia, usually begins in early adulthood. Although

research on schizoaffective disorder is scarce, it appears to occur more often in women
(APA, 1994). Despite efforts to classify this disorder separately from schizophrenia, Torrey
(1995) likens this argument among psychiatrists as futile as an effort to determine "how
many angels can dance on the head of a pin" (p. 91).

Clients with schizoaffective disorder presenting in psychosis with manic symptoms may be
inaccurately diagnosed with bipolar disorder (manic depression). A careful history obtained
from the client and family is critical in providing a more accurate assessment of the full
range of client symptoms (APA, 1994).

Neuroanatomical and Physiological Pathology

Psychiatric and psychiatric-mental health nursing references usually discuss schizoaffective

disorder by referring to their schizophrenia and mood disorders chapters. Little is found in
the literature that identifies the specific neuroanatomical and physiological changes that
might be unique to schizoaffective disorder, the assumption being that schizoaffective
clients must have some of each. Lapensée (1992) identifies that while some clients with
schizoaffective disorder may have illnesses that are just variations of schizophrenia or
Bipolar disorder, others have a different and unrelated psychosis.

In the 1970s, computerized axial tomography scanning provided us with a look at the
differences in the brains of people with schizophrenia, finding larger ventricles and
corresponding brain atrophy throughout areas of the brain that help us synthesize and
analyze sensory input. Decreased blood flow to the prefrontal cortex also has been
demonstrated (Berman, 1987; Johnstone, 1976; Rabins, 1987). Mood disorders are thought
to be caused by imbalances in brain neurotransmitters, specifically deficiencies of
norepinephrine and serotonin (Keltner & Folks, 1993).

Klein (1989) hypothesizes that we all are constantly undergoing reality testing and that we
have a regulator in the brain (Klein refers to it as a "comparator") that compares incoming
data with known data. This is usually on an unconscious level unless the data do not fit
together at which time, Klein says, we start thinking consciously about the mismatch. In
psychotics, the comparator "strips its gears" and results in the person forming inaccurate
conclusions, even when the data do not fit. They have a "psychotic illumination" that helps
them organize all of their disordered ideas into a larger disordered idea, but one that makes
sense to them. Disorders of cognition and information processing have long been
recognized in the client population diagnosed with schizophrenia (Braff, 1993; Strauss,
1993).

Klein further postulates that genetics are responsible for regulating our psychomotor rates
and that bipolar disorder is caused by abnormalities in this regulation. In some people, an
autointoxicating agent, such as 6-hydroxydopamine or 5-7 dihydroxytryptamine, also may
cause their "comparator" to go awry, resulting in a progression from mood change into
psychosis. Klein cites evidence that long periods of psychosis may have toxic effects on the
brain that cause chronic psychotic conditions. He also cites other research that found an
excessive number of people with bipolar disorder in families of persons diagnosed with
schizophrenia (Klein 1989).

Clients with schizoaffective disorder present a special challenge to the physician, clinical
nurse specialist (CNS), or psychiatric nurse practitioner managing their care, especially if
they are elderly. Antipsychotics may help control the psychotic, but not the affective
symptoms. Mania may be regulated to some extent with lithium, but antidepressant use for
the depressive cycle may trigger mania. The following is a case history of a client with
chronic schizoaffective disorder that illustrates not only the complexity of pharmacological
treatment for this illness, but also points out the need for effective case management to
closely monitor therapy effectiveness and identify adverse reactions.

Treatment: Case Description of "Maria"

"Maria" is a 73-year-old white female with a history of diagnosed mental illness dating back
34 years to age 39. Maria had an apparently unremarkable psychological history throughout
childhood, adolescence and early adulthood. At one point in early adulthood, she was the
featured singer at many local civic affairs. She was born to immigrant Italian parents in a
city in Pennsylvania that was largely an Italian settlement. After graduating from high
school, she worked as a secretary for a group of lawyers and then her father's construction
firm. At age 29, she married and at age 3 1 had her first child. At age 32, she, her husband,
and child moved several hundred miles away from Maria's hometown. She had four more
pregnancies between age 32 and age 37, resulting in three live births. In her new
surroundings, Maria lacked family support systems and, as was common in the 1950s, did
not work outside the home or drive a car, adding to her isolation. Shortly after the birth of
her last child, Maria's father, with whom she had a close relationship, died suddenly. Over
the next year, grief turned into a severe, chronic depression. She was treated by the family
physician for "early menopause." Her mood deteriorated into profound depression then
suddenly elevated into mania, manifested by little sleep, high energy, hysterical laughter,
and bizarre behavior. Her symptoms were witnessed by her children, but her ability to
control the worst aspects of her behavior around her husband resulted in his assumption
that she was "better" and, therefore, the mania was not diagnosed or treated. The mania
eventually subsided and the deep depression returned. Finally, she was referred to a
psychiatrist who diagnosed Major Depression, and a series of Electroconvulsive therapy
were given that brought her into remission.

Over the next several years, Maria functioned fairly well, but was prone to paranoid
ideation, social isolation, and became severely anxious when stressed. A source of strength
for her was her religion and she eventually agreed to become a member of the church choir.
Maria's second episode of severe depression followed her dismissal from this choir after the
choirmaster determined her strong voice to be a "distraction." This depression was resolved
with antidepressants and psychotherapy.

The next period of depression was associated with a manic episode that resulted from
antidepressant treatment and occurred during hospitalization. Lithium was initiated and the
diagnosis of manic depressive (bipolar, mixed) disorder was made. Lithium helped control
her mania, but she was occasionally hospitalized over the next several years for recurrent
depression. Maria's social isolation continued and her behavior and mood became more
unpredictable.

At age 67, Maria's husband divorced her, citing her chronic mental illness. Shortly after their
initial separation, she began calling her children in panic over the "voices" she was hearing
in her bedroom. She admitted that she had been hearing "pleasant" voices and music for
several years, but now they were frightening - motorcycle noises, angry voices, sounds of
rushing water. Maria's longtime psychiatrist refused to acknowledge the significance of
these auditory hallucinations for Maria. The psychiatrist blamed the auditory hallucinations
on her poor hearing, tried to talk her out of them, and refused to change her medication.
Unfortunately, the psychiatric nurse generalist who worked for the psychiatrist and with
Maria agreed with his assessment and advised Maria to "get out more." As Maria became
desperate, another psychiatrist was consulted and she was started on an antipsychotic
medication (haloperidol) for the first time in addition to her lithium.

Within weeks of beginning haloperidol, the voices had decreased in both intensity and
content. However, Maria began showing many extrapyramidal symptoms, including
akathisia (severe, subjective restlessness) and pseudoparkinsonism. The dose of
haloperidol was decreased and benztropine added, but the side effects of the drug
persisted. In addition, she developed a severe depression and was hospitalized. The
haloperidol was stopped by the admitting psychiatrist and she was started on an
antidepressant and eventually dismissed. Following a short period of relative stability (1
month), Maria became severely manic with psychosis, and was rehospitalized under the
care of another psychiatrist. Despite her earlier difficulties, but because of her severe
symptoms, haloperidol was restarted and again brought her out of the acute mania and
controlled her hallucinations and delusions. However, again the side effects began, this time
with akathisia so severe she was unable to sleep despite antiparkinsonian medication. The
psychiatrist, and his nurse therapist, advised the family to place her in a nursing home and
have her assessed for Alzheimer's disease. Finally, when Maria began exhibiting symptoms
of tardive dyskinesia with lip smacking, the haloperidol was stopped and her "Alzheimer's
disease" was cured. The family consulted another psychiatrist, this time one who
specialized in geriatric clients.

Maria's next episode of psychosis was marked by severe paranoid delusions and command
hallucinations. Due to her inability to tolerate traditional antipsychotics, clozapine was
initiated. Shortly after clozapine was initiated, Maria experienced an episode of
unresponsiveness that over a period of three days ranged from lethargic to deeply
comatose. No explanation for this was ever found, but her clozapine was held during this
time and restarted at a lowered dose.

Discussion

An extreme change in level of consciousness is not normally found as a side effect of

clozapine and may indicate an overdose; however, drowsiness, dizziness, headache, sleep
disturbance, tachycardia, dry mouth and constipation are some of the more frequent side
effects experienced. Agranulocytosis resulting in death also has occurred, necessitating
weekly monitoring of the white blood cell (WBC) count in association with the distribution of
only a week's supply at a time of the drug. If the WBC count drops below 3,000/mm3 with
granulocytes less than 1,500/mm3, the medication should be held and the client watched
for signs of infection. When the WBC count returns to 3500/mm3 and the client is free from
signs of infection, therapy may be cautiously restarted, although the risk for adverse
reactions is now increased. Clients in whom the WBC count dropped below 2,000/mm3, or
whose granulocyte counts dropped below 1 ,000/mm3 should not be further treated with
clozapine (Keltner & Folks, 1993; Springhouse, 1992).

At the time that clozapine was initiated, a re-evaluation of the chronicity of Maria's
hallucinations, delusions, and other schizophrenic-type symptoms, along witfi her persistent
mood swings, resulted in a new diagnosis of schizoaffective disorder, bipolar type. Also, at
this time, Maria's care was referred for case management to the CNS who worked with her
psychiatrist.
With clozapine, Maria has had better control of her schizophrenic symptoms, but has
continued to have unstable moods with a fairly persistent depression and chronic auditory
and occasional visual hallucinations. Her hallucinations vary in quality and quantity, but do
not ever go away completely. For the last year, she has "heard" a radio station, Studio One,
which brings her music and "news." She has great difficulty discriminating fact versus fiction
despite reassurance that "Studio One" does not exist. She also has persistent somatic and
paranoid delusions. Her clozapine dose is low (175 mg a day) due to her age and the
unexplained neurological episode that occurred after initial administration. Risperidone is
being considered for the future, if the clozapine does not continue to control her symptoms
or if she shows any evidence of agranulocytosis. At times, she seems more depressed as
her psychosis subsides and she must face the reality of her illness. Other times, the
depression brings on acute psychosis. She has approximately 10 days per year in which
she exhibits no affective symptoms and few schizophrenic symptoms except for
hallucinations.

Since being on clozapine, Maria's only hospitalizations have been for one episode of acute
mania precipitated by attempted therapy for depression with the antidepressant, Wellbutrin
(buproprion hydrochloride) and for lithium toxicity, which unfortunately occurred despite
close monitoring and resulted in chronic mild dementia. In the summer of 1992, Maria
began complaining of chronic diarrhea and anorexia. She was assessed and treated by her
family practitioner for a gastrointestinal virus. Over several weeks, she became increasingly
confused and lethargic. She also began refusing fluids. Throughout this entire episode, her
lithium levels stayed within "normal" limits. She was watched closely by her family and the
staff of the assisted living apartment in which she lived; however, she eventually became
lethargic and was admitted to an acute care hospital with dehydration. On admission, her
lithium level was 1.2 mEq/L, but elevated to 1.5 mEq/L over the next 24 hours. Lithium was
held and she was rehydrated.

Clients on lithium need frequent lithium levels drawn at the initiation of therapy and then
maintenance levels drawn at approximately every 2 to 3 months and as needed thereafter
to check for laboratory signs of lithium toxicity. Early lithium toxicity may be manifested by
symptoms, such as nausea with vomiting, severe diarrhea, tinnitus, dizziness, ataxia,
increasing tremor, and sleepiness, and may be confused with symptoms of a physical
illness, especially in an elderly person. Severe toxicity may present with visual or auditory
hallucinations, impaired consciousness, confusion, oliguria or anuria, and progress to coma
and death (Moller, 1990). Lithium toxicity also may cause cardiac arrhythmias and
hypotension (Keltner & Folks, 1993).
Table E

A desirable range of therapeutic levels for maintenance on lithium is between 0.6 mEq/L to
1.2 mEq/L. Lithium becomes toxic at a level of 1 .5mEq/L, but older clients may have a
relative toxicity at lower lithium levels. Serum lithium levels are more safely kept at 0.4
mEq/L to 0.8 mEq/L in this population (Keltner & Folks, 1993). In elderly or chronically
psychotic clients, lithium toxicity may be difficult to identify in the absence of increased
lithium levels.

Lithium, even at therapeutic levels, may cause thyroid dysfunction and renal damage
(Keltner & Folks, 1993). Maria has taken lithium for more than 20 years. Maria was
diagnosed with hypothyroidism secondary to lithium treatment in 1980 and was placed on
thyroid replacement therapy. She has shown no signs of renal damage with assessment by
periodic BUN and serum creatinine.
Lithium continues to be one of the drugs of choice in the treatment of schizoaffective
disorder and has been shown to benefit clients diagnosed with schizophrenia, as well as
bipolar clients. However, research has shown that clients with schizoaffective disorder who
have predominantly affective symptoms do better on lithium than clients with predominantly
symptoms of schizophrenia (Klein, 1989). Clients refractory to lithium have shown
improvement with anticonvulsants, such as carbamazepine (Tegretol) (Lapensée 1992).
Maria was placed on carbamazepine at one point to attempt to gain better control of her
bipolar symptoms, but it was not as effective for her as lithium.

Neuroleptics are usually combined with lithium in the treatment of schizoaffective clients to
control the schizophrenic symptoms. Maria is presently taking clozapine and has taken
haloperidol in the past. In schizodepressive clients, a combination of neuroleptics and
antidepressants may be more effective; however, various research studies have shown that
schizoaffective clients have a poorer response to antidepressants than bipolar clients,
especially if they also suffer from delusions (Lapensée, 1992).

Electroconvulsive therapy (ECT) has been shown to be more effective than antidepressants
in the treatment of depressed schizoaffective clients (Lapensée, 1992). Maria has
undergone ECT in the past. ECT may be required in clients whose depressive symptoms
are refractory to medication or who cannot take antidepressants (Keltner & Folks, 1993).

The CNS sees Maria on a monthly or bimonthly basis and more often if needed. The CNS
closely evaluates her symptoms, coping level, and response to medications. In addition, she
assesses her for adverse reactions to treatment, monitors Maria's weekly WBC, in
conjunction with her clozapine treatment, and recommends changes in the treatment plan
as necessary in collaboration with Maria's psychiatrist.

The CNS has worked closely with the Maria's family, as well as the staff, at the intermediate
care facility where Maria now lives to help them identify significant symptoms in Maria and
to build more positive coping skills for Maria and themselves. Caregivers, whether they are
family or health care workers, may be familiar, through the lay media, with some of the
symptoms of schizophrenia and bipolar disorder. Because schizoaffective disorder is so
rarely discussed as a separate disorder, caregivers may require education on the unique
symptoms and course that this disease may present, as well as the reasons for and side
effects of the various medications the client may be taking. They also need to know which
symptoms must be reported early in order to help provide early intervention and decrease
hospitalizations.

Families should be referred to organizations, such as local Mental Health Associations and
the Alliance for the Mentally 111, for additional information and support. Esser & Lacey ( 1
989) provide practical information for families in their book, Mental Illness: A Homecare
Guide. Other helpful books for caregivers are Surviving Schizophrenia: A Manual for
 Families, Consumers and Providers by E. Fuller Torrey (1995) and The Family Face of
Schizophrenia by P. Backlar(1994).

Maria represents a complex client with schizoaffective disorder who has received a variety
of treatments. In this day of "managed care," a CNS or psychiatric nurse practitioner can
provide a critical link between the short period of time clients, like Maria, receive "intensive"
inpatient care and the long periods of time when they are cared for by self, family members
or others.

Interventions that focus on the client's strengths versus illness and include the use of
psychoeducation to assist clients and families in learning about the illness and identify and
cope with distressing symptoms will help empower clients and families to work more
collaboratively with health care providers in order to decrease hospitalizations and increase
quality of life (Montgomery & Webster, 1993).

References

 American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th
ed). Washington, DC: Author.
 Backlar, P. (1994). The family face of schizophrenia. New York: Putman.
 Berman, K., Weinberger, D.R., Shelton, R.C., & Zee, R. F. (1987). A relationship between
anatomical and physiological brain pathology in schizophrenia: Lateral cerebral ventricular size
predicts cortical blood flow. American Journal of Psychiatry, 144, 1277.
 Braff, D. (1993). Information processing and attention dysfunctions in schizophrenia. Schizophrenia,
79(2), 59-86.
 Esser, A., & Lacey, S. (1989). Mental illness: A homecare guide. New York: John Wiley & Sons.
 Johnstone, E., Craw, T.J., Frith, CD., Huband, J., & Kreel, L. (1976). Cerebral ventricular size and
cognitive impairment in chronic schizophrenia. Lancet, 2, 924.
 Keltner, N., & Folks, D. (1993). Psychotropic drugs. St. Louis, MO: CV. Mosby Books.
 Klein, D. (1989). Schizophrenia and Bipolar affective disorders: Likenesses and differences. Journal
of Clinical Psychiatry, 17(1), 3-15.
 Lapensée, M. (1992). A review of schizoaffective disorder: Somatic treatment. Canadian Journal of
Psychiatry, 37, 347-349.
 Moller, M. (1990). Understanding and communicating with a person who is experiencing mania.
Videotape study guide. Omaha: NursSeminars, Inc.

 Montgomery, C1 & Webster, D. (1993). Caring and nursing's metaparadigm: Can they survive in
the era of managed care? Perspectives in Psychiatric Care, 29(A), 5-12.
 Rabins, P., Pearlson, G., Jayaram, G., Steele, C, & Tune, L. (1987). Increased ventricle-to-brain
ratio in late onset schizophrenia. American Journal of Psychiatry, 144, 1216.
 Springhouse Corp. (1992). Handbook of psychotropic drugs. Springhouse, PA: Springhouse Corp.
 Strauss, M. (1993). Relations of symptoms to cognitive deficits in schizophrenia. Schizophrenia,
19(2), 41-58.
 Torrey, E.F. (1995). Surviving schizophrenia: A manual for families, consumers, and providers (3rd
ed.). New York: Harper Perennial.