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A Randomized Effectiveness Trial of Collaborative Care for Patients With Panic Disorder in Primary Care
Peter P. Roy-Byrne, MD;
Wayne Katon, MD;
Deborah S. Cowley, MD;
Joan Russo, PhD
Arch Gen Psychiatry. 2001;58:869-876.
ABSTRACT
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Background Effectiveness studies have tested interventions to improve quality of
care for depression in primary care, but none, to our knowledge, have been
completed for panic disorder (PD) in this setting. This study sought to test
the clinical effectiveness of PD pharmacotherapy embedded in a disease management
framework of "collaborative care" (CC).
Methods One hundred fifteen patients with PD from 3 primary care clinics were
randomized to CC or "usual care" (UC). Patients in CC (n = 57) received educational
videotapes and pamphlets; pharmacotherapy with the selective serotonin reuptake
inhibitor paroxetine; 2 psychiatrist visits and 2 telephone calls in the first
8 weeks; and up to 5 telephone calls between 3 and 12 months' follow-up. Usual
care patients (n = 58) were treated by their primary care physician. Telephone
assessments of panic, anxiety sensitivity, depression, and disability variables
were performed at 3, 6, 9, and 12 months' follow-up. Adequacy of pharmacotherapy
was assessed with an algorithm based on a review of efficacy studies.
Results Patients in CC were more likely to receive adequate (type, dose, duration)
medication and more likely to adhere to this medication at 3 and 6 months.
Random regression analyses showed that CC patients improved significantly
more over time compared with UC patients on anxiety, depression, and disability
measures, with the greatest effects at 3 and 6 months.
Conclusions Compared with UC, CC interventions significantly improved both quality
of care and clinical and functional outcomes in primary care PD patients.
Clinical differences were greatest in the first 6 months, corresponding to
the greater quality of care and the greater intensity of intervention.
INTRODUCTION
PANIC DISORDER (PD) is a prevalent1 and
disabling2 psychiatric condition affecting
3% of the US population at some point during a lifetime. Because the dramatic
physical manifestations of a panic attack often mimic a variety of cardiorespiratory,3 gastrointestinal,4
and otoneurologic5 illnesses, a large proportion
of PD patients (80% according to one estimate6)
initially receive treatment in the general medical setting.7, 8
The current prevalence of PD in primary care is estimated at 4% to 6%.9 These patients use primary care services at several
times the rate of other patients, including those with depression10 and those with comparable medical illness severity,11 and are overrepresented among cohorts of distressed
patients who frequently use health care services.12
Despite this pattern of frequent utilization and expensive health care cost,
PD is often not recognized9 by primary care
physicians and, even when recognized, is inadequately treated. The few available
studies suggest that fewer than 1 in 4 patients receives adequate pharmacotherapy,
and only 1 in 8 receives adequate psychotherapy.13, 14
These rates are lower than rates recently reported for depressed patients
in primary care.15, 16
Throughout the past decade, several studies have addressed the gap between
scientific knowledge of antidepressant treatment and the quality of care that
patients with depression receive in primary care by developing and testing
a variety of approaches to improving primary care treatment for depression.
Using strategies that seek to overcome patient, physician, and process-of-care
barriers to mental health treatment, along with judicious use of specialty
consultation and close and sustained follow-up of patients, these approaches
have demonstrated superior clinical care and greater cost-effectiveness compared
with care as usual in the primary care setting.15, 17, 18, 19
More recently, a quality improvement strategy, using principles derived from
these approaches to change the care process in primary care systems on a larger
scale, has been shown to improve depression outcomes compared with care as
usual.20 In contrast to the progression from
efficacy studies to effectiveness studies to system-wide quality improvement
studies in primary care depressive illness, there have been no attempts to
adapt proven efficacious PD treatments to the primary care setting using an
effectiveness treatment model.
To address this gap, a study tested the clinical effectiveness of PD
pharmacotherapy embedded in a disease management framework of "collaborative
care" (CC), a model shown to improve primary care outcomes for major depression.15, 17, 18 The following questions
were addressed: (1) Will CC patients have greater utilization of "adequate"
pharmacotherapy (ie, correct drug type, dose and duration of treatment) compared
with patients receiving care as usual? (2) Can this program improve clinical
and functional outcomes compared with "usual care" (UC), acutely and over
the longer-term 12-month period? (3) Will patients involved in this program
be more satisfied with their care than patients treated with care as usual
by primary care physicians?
SUBJECTS AND METHODS
SUBJECTS
Settings for this study were 3 Seattle, Wash, primary care clinics.
Two university-associated internal medicine clinics cared for 8000 and 6000
patients, respectively (50%-60% with private insurance) with 30 attending
physicians providing 70% of care and rotating medical residents providing
the rest. The third clinic, a community family medicine clinic, part of a
multisite health care system, cared for 10 000 patients (80%-90% with
private insurance), with 8 attending physicians.
Patients had to be between age 18 and 65 years and meet DSM-IV criteria for PD, with at least 1 panic attack in the past month.
We accepted all psychiatric and physical comorbidities except those that were
potentially life-threatening (eg, active suicidal ideation or terminal medical
illness) or those that would limit patient participation or adherence (psychosis,
current substance abuse, dementia, and pregnancy). Patients had to be English-speaking
and have a telephone to participate in follow-up assessments. We excluded
patients currently receiving psychiatric treatment and patients currently
receiving or applying for disability benefits. All physicians were informed
about the study, and referrals from physicians were encouraged. However, we
also recruited patients in the waiting room using a highly sensitive 2-question
PD screen.21 All positive screens and referrals
received a telephone diagnostic interview to determine final eligibility.
The study procedure was approved by the Institutional Review Board of the
University of Washington Medical School, Seattle.
Before participating in the randomized trial, physicians received a
1-hour didactic on the recognition and treatment of PD and a medication algorithm22 detailing medication types and dosing strategies
for PD to improve knowledge and reduce an overfocus on medical problems. Previous
CC studies15, 17, 18
showed intervention-UC differences despite provision of this type of information
to all physicians.
Patients were randomized using a random number table either to the CC
model or to UC treatment. Because randomization was by patient, the same physician
could have patients in CC and UC arms of the study. Randomization was stratified
according to whether patients had been referred or screened, based on greater
panic severity in referred patients,23 and
whether they had an additional comorbid axis I diagnosis. Medications were
provided free to all patients and were obtained at hospital pharmacies (2
university clinics) or in the clinic (family medicine clinic).
INTERVENTION
A multifaceted intervention targeted patient, physician, and process-of-care
variables. Patients were provided with an initial psychiatric visit (one psychiatrist
covered each clinic), at which time they were prescribed the selective serotonin
reuptake inhibitor (SSRI) paroxetine based on prior agreement with SmithKline
Beecham Pharmaceuticals, Philadelphia, Pa, who funded the study, unless they
had shown previous nonresponse or intolerance to this medication, in which
case another SSRI was prescribed. Paroxetine was started at 10 mg daily, increased
to 20 mg as tolerated in the second week, and, if no response was reported
by the fourth week and the patient was able to tolerate it, 40 mg. On the
day of randomization, CC patients were also mailed an educational videotape
describing the nature of PD, its ability to mimic other medical illnesses,
the time course and effectiveness of medication treatment, and a model of
how medications work in the brain,24 along
with an educational pamphlet about the medication and its adverse effects.
These points were systematically reemphasized during psychiatrist visits at
which psychiatrists also addressed negative attitudes toward taking medications
in general, receiving treatment for panic in particular, or having the PD
diagnosis. Two follow-up psychiatric telephone calls and a second visit were
offered to address problems with adverse effects or further address clinical
issues. Although no formal cognitive therapy was offered, patients were encouraged
to expose themselves, as tolerated, to any feared and avoided situations.
A schedule of extended care aimed to overcome the usual lack of planned
follow-up and monitoring that occurs in acute care–oriented primary
care19 (1-hour psychiatric visit during week
1; 10- to 15-minute telephone call, week 2; 30-minute visit, week 4; telephone
call between weeks 6 and 8). Selected patients were occasionally seen for
extra sessions. The primary care physician received a typed consultation note
after each psychiatric visit. Between months 3 and 12, psychiatrists attempted
to telephone patients 5 times at equal intervals to reinforce the importance
of medication adherence and address any other pertinent issues. The psychiatrist
throughout the course of this study made all medication adjustments (P.P.R.-B.,
D.S.C., W.K.).
USUAL CARE
Usual care patients received treatment as usual (ie, pharmacotherapy)
from their primary care physician in the clinic, who received the results
of the initial diagnostic telephone assessment to eliminate nonrecognition
of panic and associated disorders as a factor in outcome. Usual care patients
could also be referred to university or community mental health practitioners,
although only a small proportion, about 25%, were referred during the study.
ASSESSMENTS
Patients were assessed at 3-month intervals by BA psychologist telephone
interviewers blind to randomization status. Interviewers were trained using
videotapes, manuals, and practice interviews monitored by an experienced interviewer
to check for reliability. The interview included portions of the Composite
International Diagnostic Interview (CIDI), modified for DSM-IV,25 which has acceptable reliability
for mood and anxiety disorder diagnoses.26, 27, 28
Telephone structured psychiatric interviews have high concordance with in-person
interviews.29, 30 The interview
also included the Panic Disorder Severity Scale (PDSS), a reliable and valid
scale that rates a spectrum of PD symptoms31
and is sensitive to treatment effects32; the
Anxiety Sensitivity Inventory (ASI), a core measure of PD apprehension and
discomfort with psychological and physical symptoms of anxiety,33
which predicts risk for panic, maintenance of panic in the absence of treatment,
and long-term outcomes34 and is about 40% heritable35; the Fear Questionnaire,36
which measures phobia symptoms; the Center for Epidemiological Studies Depression
Scale (CES-D),37 a reliable and valid measure
of depression; the 36-Item Short Form Health Survey (SF-36),38
a widely used health status inventory; a single 1-5 Likert scale item from
a previous study15 that measured patient satisfaction
with recent care for personal and emotional problems; the NEO (Neuroticism,
Extroversion, Openness) Inventory Scale,39
which measures a neurotic trait that predicted poor outcome in previous CC
studies40; and the Cumulative Illness Rating
Scale (CIRS),41 which uses medical record review
to measure degree of medical comorbidity. The CIRS ratings were completed
independently and then jointly (resolving disagreements) by a board-certified
internist and a psychiatrist (P.P.R.-B., D.S.C., W.K.).
Adequacy of antipanic medication (appropriate type, dose, and duration
of 6 weeks) was rated from patient self-reports during the assessments using
a previously published algorithm based on a review of PD efficacy studies.22 We elected to use a threshold of 20 mg as an adequate
dose for paroxetine because our CC protocol allowed psychiatrists to stop
at 20 mg if patients had responded (consistent with recent data42)
or had dose-limiting adverse effects. Patients were classified as "adherent"
if they reported taking medication at least 25 days in the month prior to
assessment. This self-report measure has high concordance with automated pharmacy
refill data.16
STATISTICAL ANALYSIS
Baseline diagnostic, symptom severity, and functional status variables
were compared between patients completing the study and those missing at least
1 follow-up interview using t tests for continuous
data and  2 analyses with corrections for continuity for categorical
data. Baseline demographic and diagnostic data were compared between CC and
UC patients using t tests for continuous data and 2 analyses with corrections for continuity for categorical data. Analyses
of covariance (ANCOVA) using age, sex, ethnicity, NEO Inventory Scale score,
clinic site, and medical comorbidity were used to compare baseline symptom
severity and functional status variables between the treatment groups. Treatment
group differences in the quality of care with respect to medication and satisfaction
with care were examined using 2 analyses with corrections
for continuity at 3-, 6-, 9-, and 12-month assessments.
To evaluate panic severity and functional impairment, we chose 6 primary
outcomes: PDSS total score, ASI total score,33
the Agoraphobia subscale from the Fear Questionnaire,36
the CES-D scale, and the Social Functioning and Role Impairment subscales
from the SF-36. The latter subscale was created to increase sensitivity by
combining the role impairment owing to physical and emotional problems subscales.43 In the event of a significant result for the PDSS
total scores, 7 post hoc analyses were performed on the individual ratings
owing to their theoretical importance. Mixed-effects random regression analysis
procedures were used44 because this procedure
permits inclusion of patients with 1 or more missing data points (45 of the
115 in the study) and allows for individual varying slopes and intercepts
over time.45 Clinic site, age, sex, NEO Inventory
Scale score, ethnicity, and medical comorbidity scores were used as covariates.
Site and ethnicity by treatment interaction terms were tested for each outcome.
These interactions were not significant, so they were excluded from the final
regression analyses to increase power. The procedure uses maximum likelihood
estimates to evaluate group, time, and group x time interaction effects.
In the event of a significant group x time interaction, post hoc ANCOVAs
on each follow-up assessment (3, 6, 9, and 12 months) were computed with clinic
site, age, sex, NEO Inventory Scale score, baseline scale scores, and medical
comorbidity scores used as covariates. For significant findings (  .05),
changes between the groups over each 6-month period were also examined using
similar ANCOVAs. As a final measure of response, we compared the proportion
of responders in each group by 2 distinct measures. We defined patients who
were "recovered" from anxiety sensitivity as those who scored lower than a
commonly reported mean posttreatment score of 20, cited in a recent review
of treated samples.35 In addition, we used
a 40% reduction in PDSS total score to define a "partial" response to treatment,
as done in the recently published multicenter efficacy study in panic.32
RESULTS
Of 7875 patients (7765 encountered in the waiting room; 110 referrals),
3797 were eligible, and 3035 agreed to be screened. Of those, 479 (429, waiting
room; 50, referrals) were positive for PD, and 115 (71, waiting room; 44,
referrals) were ultimately enrolled. Only 21 (5%) of 479 waiting room subjects
who were positive for PD and later qualified refused enrollment into the study
(Figure 1). The 115 patients enrolled
were randomized to either intervention (n = 57) or care as usual (n = 58)
groups. Of the 115 patients, 99 (86%), 92 (80%), 81 (70%), and 91 (79%) completed
the 3-, 6-, 9-, and 12-month assessments, respectively. Seventy (61%) completed
all assessments, 17 (15%) completed 3 of the 4 assessments, and 10 (9%), 12
(10%), and 6 (5%) completed 2, 1, or no assessments, respectively. The 45
patients missing at least 1 follow-up interview were equally distributed between
the treatment and UC groups (37% and 41%) and did not differ from the 70 patients
completing all follow-ups on any of the demographic or clinical variables
listed in Table 1.
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Figure 1. Flow diagram depicting patient
process at each step and reasons for ineligibility or nonparticipation. PD
indicates panic disorder.
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Table 1. Baseline Demographic and Clinical Characteristics*
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PATIENT CHARACTERISTICS
Table 1 depicts patient
characteristics, which were similar in intervention and UC groups. No differences
reached statistical significance. The group was demographically heterogeneous
with representative proportions of ethnic minority (37%) and indigent/unemployed
(36%) patients. Average medical comorbidity was moderate, with patients having
1 to 3 medical illnesses requiring medication, but few had serious medical
illnesses. Half the patients had a comorbid major depression, and one-third
to one-half had a comorbid generalized or social anxiety disorder. Panic attack
frequency was low, with patients averaging 1 to 2 panic attacks per week,
although attacks were usually intense enough to stop activity (3 on the 4-point
PDSS). Anticipatory anxiety was often present, and patients reported that
it affected their lifestyle. However, they had only mild levels of phobic
avoidance. Social and work impairment was rated to be moderate but manageable.
PARTICIPATION IN THE INTERVENTION PROGRAM
Of 57 patients assigned to the CC arm, 49 (86%) made at least 1 psychiatrist
visit, and 43 (75%) made at least 2 visits in the initial 3-month period.
Intervention patients were seen an average of 1.77 ± 0.95 visits (mean
± SD; range, 0-5 visits). During the first 3 months, patients also
received an average of 2.25 ± 1.53 follow-up telephone calls (range,
0-6 calls), with 81% receiving at least 1 telephone call. The mean ±
SD number of calls for the last 3 quarters of the year were 1.40 ±
0.96, 1.12 ± 1.10, and 0.81 ± 0.85, with 77%, 67%, and 53% receiving
at least 1 call during these time periods. The number of telephone calls decreased
significantly over the course of the year (F3,168 = 26.48; P<.001).
QUALITY OF CARE WITH RESPECT TO MEDICATION
Table 2 contains percentages
for appropriate type, dose/duration, and adherence to antipanic medication
during the 12-month study period. Compared with UC patients, significantly
more CC patients reported receiving an appropriate type (3 months) and adequate
dose duration (3 and 6 months) of evidence-based antipanic medication, and
self-administering them for 25 or more days in the last month (3 and 6 months).
At 9 and 12 months, these differences were no longer significant owing to
declining rates over the course of the year in CC patients and continued steady
but lower rates in UC patients. Throughout the year, 85% of CC patients self-administering
medication received paroxetine; 10%, sertraline; and the remainder, a tricyclic
or benzodiazepine. Throughout the year, 65% of the medicated UC patients received
various SSRIs (including paroxetine); 20%, benzodiazepine medications; and
15%, tricyclic medications. Only 3 of 57 CC patients changed medication type
during the year.
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Table 2. Quality of Care With Respect to Medication*
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PANIC SEVERITY AND FUNCTIONING INTERVENTION OUTCOMES
The mixed-effects random regression procedure revealed a significant
treatment group x time interaction for the PDSS total score, ASI, SF-36
Role Function, and CES-D scales (Table 3). Although CC patients scored lower at all time points, on the
PDSS, the difference was only significant at 6 months (F1,83 =
9.31; P = .003) (Figure 2). Post hoc random regression analyses of the individual
PDSS items showed that the significant treatment group x time interaction
was owing to a significant interaction on the item-assessing severity of anticipatory
anxiety. In contrast, for the ASI total score, the CC group scored significantly
lower than the UC group at the 3-month (F1,90 = 5.32; P = .002), 6-month (F1,80 = 11.10; P<.001),
and 12-month follow-ups (F1,82 = 4.60; P
= .035) (Figure 3). Similarly, for
the CES-D, the CC group had significantly decreased depression severity at
all follow-up assessments.
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Table 3. Panic and Functioning Outcomes*
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Figure 2. Adjusted means based on covariates
of age, sex, clinic, NEO (Neuroticism, Extroversion, Openess) Inventory Scale
score, and medical comorbidity in both groups over time. Sample sizes at baseline,
3, 6, 9, and 12 months, respectively: collaborative care patients—57,
51, 45, 43, and 45; usual care patients—58, 48, 47, 38, and 46.
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Figure 3. Adjusted means based on covariates
of age, sex, clinic, NEO (Neuroticism, Extroversion, Openness) Inventory Scale
score, and medical comorbidity in both groups over time. Sample sizes at baseline,
3, 6, 9, and 12 months, respectively: collaborative care patients—57,
51, 45, 43, 45; usual care patients—58, 48, 47, 38, and 46.
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Finally, for SF-36 role functioning, the CC group only showed significantly
greater improvements at 12 months (F1,81 = 6.16; P = .015). The Agoraphobia subscale from the Fear Questionnaire and
the Social Functioning scale from the SF-36 did not show any significant effects.
In all the outcomes with significant time x group interactions, the
rate of change was significantly greater for the CC group compared with the
UC group from baseline to 6 months but not from 6 months to 1 year. The effect
sizes for CC vs UC for the decrease in severity during the first 6-month period
were 1.01 for the ASI, 0.69 for the PDSS total, 0.57 for the CES-D, and 0.42
for the SF-36 Role Functioning scale. This indicates that, despite an overall
improvement with time in each group, there was a significant intervention
effect. There were no sex or racial differences in outcome.
Another test of treatment effectiveness is whether patients meet a predefined
level of clinical recovery or improvement. At 3 months, the higher proportion
of CC patients reaching these levels was only significantly different using
the ASI recovery criteria (40% vs 15%) but not the PDSS improvement criteria
(61% vs 42%). However, by 6-months' follow-up, the rate of both recovery and
improvement in the CC group was more than twice the rate in the UC group (ASI,
49% vs 17%; PDSS, 76% vs 38%). At 9 months the differences in the rate of
recovery on the ASI (33% vs 24%) and PDSS (82% vs 60%) were no longer significant.
At the 12-month assessment, significantly more CC patients were both improved
and recovered on the PDSS (80% vs 59%) and the ASI (47%
vs 20%).
SATISFACTION WITH TREATMENT
At the 6- and 12-month follow-up interviews, more CC than UC patients
were satisfied or very satisfied with the quality of care they received for
emotional problems (6 months: 82% vs 43%, 21 =
13.71, P<.001; 12 months: 76% vs 52%, 21 = 4.28, P = .039).
COMMENT
Our findings indicate that compared with care as usual, CC approaches,
previously shown to be effective for depressed primary care patients,15, 17, 18 improved the symptomatic
and functional outcomes of patients with PD in primary care. These differences
were most consistent and pronounced over the initial 6-month period of the
study, corresponding to both the more intensive nature of the disease management
intervention during this period, as well as the greater rates of utilization
of and adherence to "effective" antipanic medication regimens during this
same time. Patients in the CC group were also significantly more satisfied
with the care they received for their mental and emotional problems.
Although both groups improved over time (as seen in most clinical trials),
patients receiving the CC intervention had greater improvements over the 6-month
period in overall panic severity on the PDSS, largely owing to significant
changes in anticipatory anxiety. Differences between CC and UC patients were
most consistent and pronounced for anxiety sensitivity, with statistical significance
at 3 of 4 assessment points. The 10-point difference in improvement in this
measure at 6 months is particularly noteworthy, since this core underlying
feature of PD is an important determinant of the transition from nonclinical
sporadic panic attacks to PD,35 where the fear
of internal bodily sensations often results in hypochondriacal preoccupation.
More than twice as many CC as UC patients reached "normal" levels of this
measure, a clinically important finding. These pronounced effects and the
absence of effects on panic attack frequency (which decreased substantially
in both groups) may be related to the absence of any disease management in
UC patients but the presence of some, albeit lower quality, pharmacotherapy
(which would preferentially affect panic frequency more than anticipatory
anxiety). Sustained effects on depressive symptoms were also consistently
noted. Intervention patients also had significant improvements in work (SF-36)
disability compared with UC patients.
Because UC physicians received patient diagnosis at baseline, these
intervention effects are not owing to improved screening or recognition. The
provision of a panic medication algorithm and 1-hour didactic at baseline
for all physicians also suggests that differences in physician knowledge about
panic treatment were not a factor. Instead, the most likely factor is improved
quality of care defined as adequacy of, and adherence to, antipanic medication,
facilitated by disease management focusing on improving patient education
and PD monitoring and follow-up. Primary care physicians received no feedback
about UC patient adherence, employed no specific adherence strategies, and
had little time for psychoeducation. Although CC patients received paroxetine,
any other SSRI would likely be equally effective. Patients in the UC arm of
the study showed slower, but detectable, improvement on a number of measures.
Partial response rates at 3 months in this group are similar to the 40% response
rates for depression in previous CC studies. The changes that occurred in
the UC group may represent spontaneous improvement, fluctuations in the ordinary
course of PD, or, in the patients receiving and adhering to appropriate treatment,
a true treatment response. Unlike 8- to 12-week efficacy studies, this year-long
study allows more time for both natural symptom improvement and continual
care seeking and active medication treatment in UC subjects.
The effect sizes for certain core measures such as anxiety sensitivity
and anticipatory anxiety, as well as full recovery using the ASI, seemed to
increase slightly at 6 vs 3 months. Although intensity of the intervention
was greatest between 0 and 3 months, studies suggesting that anxious patients
respond more slowly to treatment provides a possible explanation for this
delayed effect. Consistent with several previous studies of this approach
in depression, which showed that beneficial effects of acute 3-month interventions
seemed to decrease between 4 and 7 months,18, 20
the robust CC vs UC differences noted at 6 months gradually began to narrow
between 6 and 12 months.
This study has a number of limitations. First, generalizability is compromised
by the use of a small number of sites. However, the ethnic, socioeconomic,
and health care financing mix was far broader than in previous CC studies
that focused on middle class, working, white patients in health maintenance
organizations, and the absence of site and racial differences suggests that
beneficial effects were generalized to the entire group. Second, all subjects
were provided medication free of charge, which differs from the "real world"
of primary care. Third, the use of anxiety disorder specialists and university
sites (in 2 of the 3 settings) may suggest it would be difficult to implement
this intervention in certain rural and urban inner-city settings owing to
a lack of specialists. However, this simple intervention might be carried
out by well-trained physician extenders (such as nurses) with psychiatric
supervision, as is being done for depression in the Kaiser Health System (Oakland,
Calif).46 Fourth, it is not possible to determine
which components of the intervention were responsible for the beneficial effects
since no systematic assessment of the treatment process was made. Nonetheless,
it seems that the provision of skilled assessment and treatment explanations,
the scheduling of regular patient-clinician contact, and the ongoing monitoring
of treatment tolerance, adherence, and outcomes were most important in possibly
allowing better management of medication adverse effects and dose adjustments.
Finally, this effectiveness study, by nature, lacked certain methodologic
controls common to more internally valid efficacy studies. The PDSS has not
been validated for use via the telephone or by lay interviewers, and the ASI
has been infrequently used as a pharmacotherapeutic outcome measure,35 though its content is unusually well suited for primary
care PD. Efficacy studies have established that 40 mg of paroxetine is the
efficacious dose,43 while our modal paroxetine
dose was 20 mg, the most common dose in primary care clinics47
(Risa B. Weisberg, PhD, Martin Keller, MD, e-mail communication, March 2001)
and an effective dose for some patients.43
Although our protocol allowed psychiatrists to stop at 20 mg, it is possible
that pushing the dose higher could have increased response in CC patients.
These limitations are balanced by some important strengths not seen
in efficacy studies. First, our long-term retention rate was almost 75% at
12 months, substantially higher than the approximate 40% long-term retention
rate in the recent collaborative PD efficacy study by Barlow et al.32 Second, the high level of psychiatric and medical
comorbidity in our sample more accurately reflects the real world of primary
care. Third, even though our comparison group received, at low but steady
rates throughout the 1-year study, active medication rather than placebo,
and their physicians received reports of their diagnosis and education about
a potential antipanic treatment, we were still able to show that our intervention
made a significant difference. Finally, related to this, we had no differential
dropout in our comparison group compared with our intervention group, something
that is often seen in the placebo cell of efficacy studies.
These findings demonstrate that a CC intervention for patients with
PD in primary care increases patients' use of and adherence to guideline-recommended
pharmacotherapy and results in greater clinical and functional improvements
and greater patient satisfaction with care compared with care as usual in
this setting. This "carved in" collaborative model has now been adopted to
treat multiple psychiatric disorders by both university clinics in this study,
and is being used by Group Health Cooperative (Seattle), Kaiser Permanente
(Oakland, Calif), and the VA Hospitals primary care clinics, which collectively
care for more than 20 000 patients. Now that this intervention has been
shown to be effective, future studies in this setting should consider employing
the "stepped care" approach recently reported to be effective in depression.18 In this approach, patients would first be treated
by their primary care physician, and only incomplete responders or patients
at high risk for relapse and or a chronic condition would receive a second
"step" of CC. This mode of care would be potentially more cost-effective than
the approach reported here and could address the reluctance of primary care
clinics to adopt these models because of concerns about added cost,47 despite demonstrated cost-effectiveness in depression.19
AUTHOR INFORMATION
Accepted for publication April 3, 2001.
Data analytic and manuscript preparation time were supported by grants
MH 57858 (Dr Roy-Byrne) and MH 01643 (Dr Katon). This study was supported
by an investigator-initiated grant from SmithKline Beecham Pharmaceuticals,
Philadelphia, Pa.
The authors gratefully acknowledge the skilled intervening of Emily
Cohen, BA, Erin Michelson, BA, and Tamara Parrot, BA; the overall study coordination
efforts of Ms Michelson; and the collaborative efforts of D. C. Dugdale, MD,
and Daniel Lessler, MD, who served as medical clinic liaisons at the 2 university
clinics and determined medical comorbidity scores for patients using the CIRS.
We are also grateful to Providence Green Lake Family Medicine Clinic, University
of Washington General Internal Medicine Clinic, and Harborview Medical Center
Adult Medicine Clinic, Seattle, for participating in this study.
From the Department of Psychiatry and Behavioral Sciences, University
of Washington School of Medicine (Drs Roy-Byrne, Katon, Cowley, and Russo),
and Harborview Medical Center (Drs Roy-Byrne and Russo), Seattle.
Corresponding author and reprints: Peter P. Roy-Byrne, MD, Department
of Psychiatry and Behavioral Sciences, Harborview Medical Center, 325 9th
Ave, Box 359911, Seattle, WA 98104 (e-mail: roybyrne{at}u.washington.edu).
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