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VOL22.NO. 3, 1996
Schizophrenia and HIV
by Daniel D. Sewell
Abstract
There is very little published information regarding the co-occurrence
of human immunodeficiency virus
(HlV)-spectrum illness and psychotic illnesses, including schizophrenia, even though their coexistence in the same patient may
severely affect the course of both illnesses. Estimates of the frequency
of HIV infection in patients with
preexisting mental illness range
between 5 and 7 percent. Estimates
of new-onset psychosis in patients
with HIV-spectrum illness range
between 0.2 and 15 percent and may
increase as the stage of HIV illness
progresses. Regardless of which illness camefirst,their occurrence
together appears to be associated
with more morbidity and mortality
than would be expected with either
illness alone. Patients with newonset psychosis respond to and tolerate relatively low doses of antipsychotic medication. Whether the
presence of HIV decreases the effective daily dose of neuroleptic medication in patients with preexisting
psychosis is not yet known. A
clearly superior neuroleptic medication for patients with both psychosis and HIV infection has not yet
been identified. Further systematic
exploration is needed.
Schizophrenia Bulletin, 22(3):
465-473,1996.
Patients with schizophrenia or other
psychotic illnesses and human immunodeficiency virus (HIV)-spectrum illness may be differentiated
based on the temporal relationship
between the onset of psychotic symptoms and the discovery of infection
with HIV. One group is composed of
patients who have a psychotic disorder and then become infected with
HIV (preexisting psychosis), and the
465
second group consists of patients
who have no past history of psychotic disorder but who develop a
psychotic disorder after infection
with HIV (new-onset psychosis).
There are a number of reasons why
the overlap of schizophrenia and
other psychotic illnesses with HIVspectrum illness deserves discussion
and study. First, those who have
cared for patients with psychosis and
HIV-spectrum illness generally agree
that regardless of which came first,
co-occurrence of these disorders
leads to greater morbidity (and perhaps greater mortality) than would
be associated with either disorder
alone. Second, due to the everincreasing prevalence of HIV-spectrum illness, it appears that co-occurrence of these illnesses is likely to
increase steadily. Last, the study of
the co-occurrence of these illnesses
has the potential to increase our
understanding of the etiopathologic
basis of psychosis in general and of
schizophrenia in particular.
Preexisting Psychotic Illness
and HIV Infection
Prevalence. Currently, there is a
paucity of information about the
prevalence of HIV-spectrum illness
among patients with preexisting psychotic illness. Although there have
been some studies of HIV infection
among psychiatric patients, there
appear to be no published studies
that focus exclusively on patients
with psychotic illness, including
schizophrenia. Table 1 lists the seroprevalence of HIV antibodies in
patients with psychiatric illness as
Reprint requests should be sent to Dr.
D.D. Sewell, Medical Director, Mission
Valley Mental Health Clinic, San Diego
Veterans Affairs Medical Center, 2022
Camino Del Rio North, San Diego, CA
92108.
SCHIZOPHRENIA BULLETIN
466
Table 1. Prevalence of human immunodeficiency virus (HIV)
infection in populations of psychiatric inpatients
Study
Cournos et al. (1991)
Empfield et al. (1993)
Sacks et al. (1992)
Zamperetti et al. (1990)
Location
New York City
New York City
New York City
Milan, Italy.
Number of
patients
451
203
350
475
Percent with
HIV(n)
5.5 (25)
6.4(13)
7.1 (25)
6.5(31)
reported in the four published studies on the topic. Although these studies were conducted by a variety of
scientists in two countries, they all
share a common methodology. The
subjects in each study were patients
consecutively admitted to psychiatric
hospitals. The prevalence of HTV
infection in these studies ranged
from 5.5 to 7.1 percent. Because the
Empfield et al. (1993) study included
only homeless patients, it is very
likely that the study population had
a high proportion of patients with
schizophrenia and other psychotic illnesses. The work by Cournos et al.
(1991) may most closely estimate the
frequency of HIV in patients with
preexisting psychotic illness: 81.8
percent of the patients in their sample had some type of psychotic illness (45.2% were diagnosed with
schizophrenia).
severe mental illness may exhibit
more risk behavior due to hypersexuality, poor impulse control, selfdestructive behavior, casual sexual
relationships, lack of awareness of
risks, impaired judgment, substance
abuse, and potential for sexual victimization. A study of risk behavior
among chronically mentally ill
patients (Kelly et al. 1992) found that
62 percent had been sexually active
during the 1-year period before entry
into the study and that 42 percent of
the men and 19 percent of the women
reported multiple sexual contacts
and infrequent use of condoms during intercourse. These findings indicate that a significant proportion of
chronically mentally ill patients,
including patients with psychosis,
have either already been infected
with HIV or may be likely to become
infected due to high-risk behaviors.
Risk Behavior in Patients With Preexisting Psychosis. Behaviors that
place an individual at risk for acquiring HIV include needle-sharing and
unprotected sex, except that which
occurs within a monogamous relationship in which both individuals
are known to be seronegative. Tynes
et al. (1993) reviewed the literature
regarding risk of HIV infection
among patients with chronic mental
illness, including patients with preexisting psychotic illness, and concluded that patients with chronic
Impact on Course of Illness. No
systematically obtained information
is currently available regarding the
impact of HTV infection on the course
of illness in patients with a preexisting psychotic disorder. Anecdotal
information suggests that, if there is
an impact, it is generally negative.
Patients with psychotic illnesses such
as schizophrenia may be more vulnerable to the numerous stresses
associated with HTV infection and
may have less personal, financial,
and social resources for addressing
the problems associated with HIVspectrum illness. Altamura et al.
(1991) studied a group of 25 HIVpositive schizophrenia patients and
found that neuroleptic treatment was
associated with reduction in psychiatric symptoms but may also have
been associated with more marked
immune-system changes and a
higher incidence of infectious diseases. In addition, these researchers
found a deterioration in the cognitive
performance of patients with schizophrenia and HIV.
There appear to be no systematic
published studies on the effect schizophrenia has on progression of HIVspectrum illness. Nonetheless, it is
widely accepted that diseases generally tend to be more serious in
patients with schizophrenia and that
deaths from most causes are more
frequent among persons with schizophrenia than among the general public (Torrey 1988). In the absence of
data to the contrary, it seems reasonable to assume that both these generalizations apply to patients with
schizophrenia and HTV-spectrum illness. The reasons for this higher morbidity and mortality are varied and
include (1) the difficulty the patients
have in complying with medical care,
(2) a decreased ability to explain
symptoms to medical personnel, (3) a
tendency for medical personnel to
pay less attention to the physical
complaints of patients with schizophrenia, and (4) the presence in some
patients with schizophrenia of an
elevated pain threshold, which results in patients not complaining of
symptoms until the disease has progressed to a critical stage.
New-Onset Psychosis
Associated With HIV Infection
Although a causal relationship
VOL22.NO. 3, 1996
467
between the presence of HIV in the
central nervous system (CNS) and
the development of psychosis has not
been established with certainty, a
growing body of scientific information supports this possibility (Masdeu et al. 1991; Masliah et al. 1992).
Prevalence. The frequency of newonset psychosis in HTV-infected
patients is not well established but
may vary according to stage of illness. Table 2 summarizes results
from a number of studies that have
attempted to estimate the frequency
of new-onset psychosis in HIVinfected patients. Although there
were methodological differences
among the studies, including the use
of different HIV illness classification
systems, it is notable that the highest
reported frequency of psychosis
(15.2%) occurred in a population of
46 patients with acquired immunodeficiency syndrome (AIDS) dementia
(Navia et al. 1986). In their study, ElMallakh et al. (1993) compared 60
individuals who were HlV-seropositive with 20 patients who met diagnostic criteria for AIDS and found
that patients with AIDS had not only
a higher incidence of AIDS-related
dementia, as expected, but also a
higher incidence of psychosis.
Characteristics of the Psychosis.
Sewell et al. (1994a) reported a systematic study of 20 HIV-infected men
who had noniatrogenic new-onset
psychosis and who were not currently abusing drugs or alcohol. The
researchers found that all 20 men had
delusions, and two-thirds had more
than one type of delusion. The most
common types were paranoid,
grandiose, and bizarre delusions.
Auditory (n = 12) and visual (n - 9)
hallucinations were also frequently
present. They also found that mood
symptoms (depression, euphoria,
and mixed-mood symptoms) tended
to occur prominently and frequently
(65%). Classifying the patients according to criteria of DSM-IH-R
(American Psychiatric Association
1987) proved challenging. When psychiatric diagnoses were made with
the assumption that HTV was not etiologically related to the psychiatric
symptoms, the following diagnoses
were obtained: psychotic disorder
not otherwise specified (n = 8); bipolar disorder, manic (n = 5); major
depression with psychotic features
(n = 4); schizoaffective disorder (n =
2); and schizophrenia, subchronic,
undifferentiated type (n = 1).
With regard to the stage of HIVspectrum illness, 12 of the patients
Table 2. Prevalence of new-onset psychosis in patients with
human immunodeficiency virus (HIV)-spectrum illness
Study
Stage of HIV1
Illness
El-Mallakh et al. (1993)
All stages
80
Halstead et al. (1988)
All stages
2,200
0.23 (5)
Harris etal. (1991)
Stages A and B
124
3.2 (4)
Navia etaJ. (1986)
Stage C (AIDS)
46
15.2 (7)
Prieretal. (1991)
All stages
573
1.2 (7)
Number of
patients
'Classification system for HIV (Centers for Disease Control [CDC] 1986,1992).
Includes two cases of 'secondary mania* and two cases of psychosis.
Percent with
psychosis (n)
5.0 (4)2
with new-onset psychosis were in
Centers for Disease Control (CDC;
1986,1992) Stage IV, 6 were in CDC
Stage III, and 2 were in CDC Stage II
at the time of onset of psychotic
symptoms.
The clinical course of these patients
was variable. In 11 patients, attempts
to discontinue treatment with antipsychotic medication were unsuccessful because of recurrence or
worsening of psychotic symptoms.
Six patients had one discrete episode
of psychosis with complete recovery.
Three patients had multiple discrete
episodes (range = 2-4). El-Mallakh
(1992) reported on the course of illness of four patients with HTV-associated psychosis. In two patients, it
appeared that worsening of dementia
was associated with remission of the
psychotic symptoms. Based on this
observation, El-Mallakh proposed a
window of vulnerability to psychosis
in patients with HIV infection that
occurs in the setting of mild to moderate brain damage from HIV.
In Sewell et al. (1994o), patients
with new-onset psychosis were compared to 20 nonpsychotic HTVinfected men matched with respect to
age, race, years of education, and
CDC HIV stage. It was found that the
psychotic subjects had a higher lifetime prevalence of stimulant and
sedative-hypnotic abuse or dependence and a trend toward greater
global neuropsychological impairment than did the nonpsychotic subjects. The psychotic patients also had
a higher mortality rate. During the 3
years of the study, 11 psychotic
patients and 3 nonpsychotic patients
died. The mean survival time was
22.6 months for the psychotic
patients and 50.8 months for the
nonpsychotic patients.
Etiopathology of New-Onset Psychosis. The etiopathology of new-
468
onset psychosis in individuals infected with HIV remains unclear;
however, a number of hypotheses
have been proposed (Harris et al.
1991). One hypothesis maintains that
the psychosis is a direct effect of HIV
infection of the brain, that is, the psychosis is secondary to HIV encephalopathy (Halstead et al. 1988). This
theory is derived in part from a
growing body of the literature suggesting that HIV can cause an array
of nervous system disorders such as
HIV dementia complex (Ostrow et al.
1988). Results of a study using singlephoton emission computed tomography also suggested that new-onset
depression or psychosis in individuals infected with HIV might be associated with HIV encephalopathy
(Masdeu et al. 1991).
In the previously described study
of 20 HIV-infected men who had
noniatrogenic new-onset psychosis,
the psychotic subjects had greater
neuropsychological impairment, suggesting an association of encephalopathy with psychotic symptoms.
Similarly, the work by El-Mallakh et
al. (1993) points to an association
between cognitive deterioration and
severe brain dysfunction such as psychosis, mania, or dementia. The only
available autopsy results from
patients with new-onset HlV-associated psychosis (Sewell et al. 1994<J)
tend to support this theory only partially, as three of the autopsied subjects had no detectable virus in their
brains. It is possible that the quantity
of the virus in the brain may vary
over time and that the divergent
findings are related to temporal sampling error. In addition, once the
virus or its sequela (cytokine activation) has "damaged* the brain,
symptoms could persist even without continued viral presence in the
CNS. Lower cerebrospinal fluid
(CSF) protein and white blood count
SCHIZOPHRENIA BULLETIN
values in the psychotic patients
(Sewell et al. 1994a) suggest that the
psychotic patients may have a less
robust immune response in the CNS,
which would then allow more damage from the HIV or from some other
infectious pathogen to occur and
would thus predispose the psychotic
patient to an encephalopathy and
subsequent psychosis, followed by
death.
El-Mallakh (1991) speculates that
intracellular free calcium accumulation may be responsible for newonset psychosis in patients infected
with HIV, at least when the psychosis
occurs along with manic symptoms.
His idea is based on the work of
Dubovsky et al. (1989), Dreyer et al.
(1990), and El-Mallakh and Jaziri
(1990). Dreyer et al. (1990) found that
purified HIV coat protein, gpl20,
increased intraneuronal free calcium
in vitro in a dose-dependent manner.
El-Mallakh and Jaziri (1990) hypothesize that increases in intracellular free
calcium bring about increased and
inappropriate neurotransmitter
release, which may then lead to the
production of manic and psychotic
symptoms.
Interestingly, Sierra-Honigmann et
al. (1995) approached the relationship
between psychosis and HIV, as well
as other viruses, by studying patients
with well-established schizophrenia
rather than those with new-onset
psychosis. They used viral-detection
methods to test the viral etiology of
schizophrenia. Specifically, they used
polymerase chain reaction (PCR) to
search for cytomegalovirus, HIV, influenza A, and several other viruses
in the hippocampus (n = 3) or CSF
(n = 48) or mononuclear cells (n = 9)
of patients with well-documented
schizophrenia. They found no virusspecific nucleic acids in any of the
samples tested.
Another theory to explain new-
onset psychosis in HIV-infected individuals is that it results from brain
damage from some other "opportunistic" infectious agent such as herpes simplex virus or cytomegalovirus. The findings by Sewell et al.
(1994a) did not support this hypothesis. In general, their patients had
onset of psychotic symptoms while
medically stable. One would expect
that a patient with an opportunistic
infection of the CNS might show systemic symptoms of illness, such as
fever. In addition, one would expect
evidence of infection to be apparent
on magnetic resonance imaging
(MRI) scans. This, however, was not
the case for the psychotic patients
studied. Last, although autopsy findings of Sewell et al. (1994a) revealed a
variety of opportunistic pathogens,
there was no association of a specific
opportunistic infection with psychiatric or neuropsychological findings
in their small sample.
Still another theory proposes that
the psychosis in these patients may
result from one or more events that,
singly or together, would be
markedly stressful to almost anyone
in similar circumstances in the person's culture (i.e., brief reactive psychosis). A case report by Boast and
Coid (1994) supports this possible etiology. These authors conclude that
the study of the psychodynamic
aspects of acute psychotic disorders
without evidence of cognitive impairment in HIV-infected patients has
been neglected. Although the patients
Sewell et al. (1994a) studied did experience multiple significant stresses, in
all cases the symptoms lasted for
more than a month and thus did not
meet the DSM-Hl-R criteria for brief
reactive psychosis. In addition, there
was no evidence that the psychotic
patients had more stresses or more
severe stresses than the nonpsychotic
comparison patients.
VOL. 22, NO. 3, 1996
One intriguing finding is that HIVinfected patients with new-onset psychosis may have a more frequent past
history of stimulant and sedativehypnotic abuse or dependence than
HIV-infected patients who are not
psychotic (Sewell et al. 1994a). It is
conceivable that such drug abuse
increases a patient's susceptibility of
developing psychosis when he or she
is later infected with HIV.
Other possible explanations exist
for new-onset psychosis. The development of psychosis in HIV-infected
individuals could simply be due to
the coincidental occurrence of newonset schizophrenia or a psychotic
mood disorder. Finally, a number of
separate etiological factors mentioned above may act jointly and lead
to psychosis in HIV-infected patients.
Evaluation of Psychosis in
Patients With HIV Infection
The first step in the evaluation of
HIV-infected patients with psychosis
is to rule out known causes of psychosis such as a primary psychiatric
illness (preexisting or new-onset),
medical illness, or adverse reaction to
medication. Table 3 lists many of the
possible causes of psychosis in an
HIV-infected patient. The causes are
numerous and varied. For example,
Daif et al. (1992) published a case
report of a patient with AIDS and
tuberculous meningitis who presented with paranoid psychosis.
Evaluation should include a comprehensive history and a physical
examination. In many instances,
sources of history other than the
patient will be needed. In addition to
determining the onset and course of
the patient's symptoms, information
regarding a possible preexisting psychotic illness should be sought. Signs
of medical illness, drug intoxication,
or medication toxicity may be evi-
469
Table 3. Possible causes of psychosis in human
immunodeficiency virus (HIV)-infected patients
Primary psychiatric illnesses (preexisting or new-onset)
Bipolar affective disorder with psychosis
Brief psychotic disorder
Delusional disorder
Major depression with psychosis
Schizoaffective disorder
Schizophrenia
Schizophreniform disorder
Shared psychotic disorder
Substance-induced psychotic disorder (amphetamine)
Medical illnesses
Autoimmune disorder
Systemic lupus erythematosus
Endocrine disorders
Hyper- or hypoparathyroidism
Hyper- or hypothyroidism
Hypoadrenocorticism
Hepatic diseases
Neurological disorders
Auditory nerve injury/deafness
Central nervous system infections (e.g., tuberculous meningitis or cryptococcal infection)
Central nervous system neoplasm (e.g., lymphoma)
Cerebrovascular accidents
Epilepsy
Huntington's disease
Migraine
Renal diseases
Medications
Acyclovir
Azidothymidine
Buspirone
Cydoserine
Ganciclovir
Interferons
Isoniazid
Predrusone
Trimethoprim-sulfamethoxazole
Vincristine
dent on physical examination. The
possibility that new-onset psychotic
symptoms may result from medications deserves special consideration
due to the number of prescribed
medications and self-administered
remedies that are often part of a
patient's survival strategy. For example, Smith et al. (1994) described two
patients with HIV-associated
nephropathy who were treated with
60 mg of predrusone daily for 2-6
weeks and who subsequently developed psychosis, and Chen et al.
470
(1992) reported a case of ganciclovirinduced visual hallucinations. In
addition, a patient with HTV and
severe anxiety developed psychosis
after one 5-mg dose of buspirone
(Trachman 1992).
Focal neurologic deficits may herald the presence of stroke or CNS
neoplasm. Lesions in certain brain
regions such as the anterior frontal
lobes may not cause focal deficits
and, therefore, even in the absence of
focal deficits, computed tomography
(CT) or MRI scan is an important part
of the evaluation of an HIV-infected
patient with new-onset psychosis.
With strict assessment criteria, it
seems that electroencephalograms
(EEGs) are normal in HIV-infected
patients who have unimpaired neuropsychological status (Binnie and
Prior 1994). In patients with AIDS
dementia, 65 percent will have diffuse slowing, 22 percent will have
focal slowing, and 11 percent will
have paroxysmal slow and sharp
activity. In the absence of cognitive
deficits or signs and symptoms of
delirium, EEGs probably are not a
necessary part of the evaluation of
new-onset psychosis; however, quantitative EEG assessment methods in
longitudinal studies may provide a
sensitive warning of impending neurological disease in asymptomatic
patients (Binnie and Prior 1994).
The evaluation of new-onset psychosis in patients infected with HIV
should also include a general admission panel of laboratory tests, including electrolytes, a complete cell count,
liver function tests, thyroid function
tests, urinalysis, and some form of
drug screening (urine or blood).
Treatment of Psychosis in
Patients With HIV Infection
If the evaluation uncovers any under-
SCHIZOPHRENIA BULLETIN
lying causes or contributing factors,
then initial treatment efforts should
be geared toward eliminating them.
Frequently, addressing the underlying cause may result in resolution of
the psychosis.
Regardless of the etiology of the
psychotic symptoms, symptomatic
treatment with neuroleptic medication is usually necessary, at least initially. In their review of case reports,
Harris et al. (1991) found that almost
all commonly used neuroleptic medications have been prescribed to treat
psychosis. Clinicians with experience
treating new-onset psychosis in HTVinfected patients generally agree that
these patients are unusually sensitive
to both the benefits and the side
effects associated with neuroleptic
medications. Whether the presence of
HIV increases this sensitivity is not
known. Ostrow et al. (1988) recommends that low doses of highpotency neuroleptics be used because
of the lower risk of anticholinergic
side effects. Numerous reports suggest that HIV-infected patients may
be especially vulnerable to extrapyramidal symptoms, including neuroleptic malignant syndrome and tardive dyskinesia (YD) (Shedlack et al.
1994).
Fernandez and Levy (1993) reported a series of four patients with
HIV infection and psychosis from
various etiologies who had developed severe extrapyramidal symptoms from fluphenazine, haloperidol,
perphenazine, thioridazene, and
thiothixene. Each patient was ultimately switched to molindone, and
each experienced significant therapeutic benefits without extrapyramidal side effects (EPS). Fernandez and
Levy (1993) note that molindone does
not appear to have the same propensity to induce side effects as do other
neuroleptic agents (Markowitz and
Brown 1987; Owen and Cole 1989);
this may be the result of its weak
affinity to bind centrally to D, (Owen
and Cole 1989) and D2 receptors
(Richelson 1984) as well as to H,
muscarinic and a, adrenergic receptors. Singh and Catalan (1994) successfully treated four psychotic male
AIDS patients with risperidone. They
found that low doses of risperidone
(1 or 2 mg twice daily) were effective
and did not cause EPS, even though
two of the patients had previously
developed EPS from haloperidol,
chlorpromazine, and thioridazine.
A rater-blind randomized study of
the efficacy and side effects of
haloperidol and thioridazine in the
treatment of new-onset psychosis in
HIV-positive individuals was
reported by Sewell et al. (1994i>). The
study included 13 men in whom the
development of psychosis could not
be attributed to delirium or to nonHlV-related organic factors such as
recent drug or alcohol abuse or
dependence. Patients who entered
the study were evaluated with a
number of rating scales of psychopathology and medication side
effects and then were randomly
assigned to treatment with haloperidol or thioridazine.
The mean (± standard deviation
[SD]) starting dose in chlorpromazine
equivalents (CPZE) for patients
treated with haloperidol was 48 (±
41) mg, and the mean (± SD) starting
dose for patients treated with thioridazine in CPZE was 86 (± 46) mg.
The optimal dose was established
clinically by balancing maximum
possible reduction in psychotic
symptoms against minimal possible
side effects. In general, each patient's
dose was gradually increased over
the 6-week study period. Patients
were not treated prophylactically
with an anti-EPS medication. Eight
patients who were treated with
haloperidol completed the study, and
VOL. 22, NO. 3, 1996
the mean maximum daily dose for
these eight patients was 120 (± 61)
mg CPZE. Five patients who were
treated with thioridazine completed
the study, and the mean maximum
daily dose for these five patients was
131 (± 68) mg CPZE. The difference in
mean maximum daily dose between
the two groups was not significant.
Both neuroleptics produced modest but significant reductions in overall level of psychosis and in positive
symptoms, but not in negative symptoms. In terms of side effects, none of
the patients experienced symptomatic orthostasis. All the haloperidoltreated patients developed EPS and
required treatment with anticholinergic medication. One patient treated
with haloperidol developed TD, and
another patient experienced sedation.
Three of the five patients treated with
thioridazine had problematic side effects. One patient developed EPS,
and another had noticeable sedation.
A third patient experienced weight
gain, dry mouth, and retrograde ejaculation and developed TD.
Because of the risk of side effects,
including TD, before beginning treatment patients should be educated
about the risks and benefits of the use
of neuroleptic medication, should
have an opportunity to ask questions,
and should indicate in writing their
agreement with the treatment plans,
including the use of neuroleptic medication. Of course, in emergency situations when patients are extremely
agitated, neuroleptic treatment may
have to be initiated before obtaining
the patient's consent. In this case,
written consent should be obtained
as soon as the patient is clinically
able to cooperate with the process.
When a patient is initially too agitated to provide consent for neuroleptic medication, it is helpful to
471
determine if the patient has designated someone to make decisions on
his or her behalf in the event that he
or she is unable to do so (e.g., durable
power of attorney for health care). If
such a person exists, then consent for
the use of neuroleptic medication
should be obtained from this person.
If no such person has been designated, then obtaining the approval
from a partner or family member is
recommended. Although obtaining
the approval of a family member may
not provide legal immunity, it seems
ethically reasonable and helps
achieve two important goals: establishing rapport with key individuals
in the patient's support system and
educating these individuals.
Nonpharmacological treatment
approaches are extremely important
for patients with HIV-spectrum illness and psychosis. While the
patient's symptoms are acute, it is
usually helpful to include at least one
member of the individual's support
system for at least part of each
appointment. Many patients with
HIV-associated psychosis may benefit from participation in a support
group for patients with HIV-spectrum illness and serious psychiatric
illness. If a patient has drug or alcohol abuse or dependence, then participation in an active recovery program
is essential. Once the psychosis has
been effectively treated, some
patients may benefit from couples'
therapy to resolve issues such as the
impact of HIV on the relationship.
Patients with psychosis who are in
the later stages of HIV-spectrum illness may benefit from an array of
supportive services, including home
meal delivery, day treatment center
participation, or relocation to a
board-and-care home for patients
infected with HTV.
Summary
The amount of published systematic
information about preexisting psychosis and HIV-spectrum illness and
about new-onset HIV-associated psychosis is limited. This article summarizes what is known and what is suspected about both of these conditions. Although neither condition is
especially common, when they cooccur, they appear to be associated
with more morbidity and mortality
than would be expected if either condition was present alone. It appears
that no matter which illness develops
first, the combination may hasten a
patient's death. The etiopathology of
new-onset psychosis in patients infected with HTV remains unclear but
seems likely to be possible sequela of
HTV encephalopathy.
The first and most important task
in the evaluation of an HIV-infected
patient with psychosis is to rule out
known causes of psychosis. If an
underlying reversible condition is
discovered, then the initial treatment
should attempt to treat this condition. Regardless of the etiology of the
psychotic symptoms, neuroleptic
medication is often needed. Neither
the systematic studies by Sewell et al.
(1994b) nor any of the other published reports dearly identify a preferred neuroleptic medication for this
group of patients, although molindone and risperidone may ultimately
prove to be superior to other neuroleptic medications. Patients with
psychosis and HIV-spectrum illness
appear to be unusually sensitive to
both the therapeutic benefits and the
side effects associated with neuroleptic medication. Further systematic
exploration of these issues hopefully
will lead to more effective interventions and may potentially shed light
on the etiopathological basis of psy-
472
chosis in general and of schizophrenia in particular.
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The Author
Daniel D. Sewell, M.D., is Assistant
Clinical Professor, Department of
Psychiatry, University of California,
San Diego, and Medical Director,
Mission Valley Mental Health Clinic,
San Diego Veterans Affairs Medical
Center, San Diego, CA.