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book |
Introduction
Neuroimaging
approaches have been used to investigate neurobiological
changes in depressive patients in studies that address
remission after psychotherapy or antidepressant medication [1–2].
The majority of these studies focused on the effect of
treatment
on brain metabolism or perfusion at rest. A more recent series
of functional neuroimaging (fMRI) studies has turned to the use
of experimental tasks to examine processes that may be more directly
involved in emotional appraisal and control processes [3–6].
To date, studies examining the functional neuroanatomy of psychotherapy
in depressed patients have applied interpersonal therapy
or cognitive behavioural therapy [7–8]. The present research
reports on the first fMRI study with recurrently depressed patients
treated with psychodynamic psychotherapy. Long-term
psychodynamic
psychotherapy has been shown to be associated with
larger improvement in these difficult forms of depression than shorter
treatments [9–10].
The interest aroused
by neuroimaging studies of treatment of depression
is in part due to their potential importance in shedding light on the
mechanism of therapy. There is considerable evidence for
increased activation in limbic areas in depression, especially the amygdala,
under exposure to emotional stimuli [5–8,11–12]. This limbic
activation may be related to an increased reactivity of depressed
patients to emotional stimuli of negative valence [13]. It has
been proposed that antidepressant medication acts directly on this
abnormal reactivity [1], since amygdalar activation normalizes in
medicated remission [5–6]. However, changes associated with depression
have also been reported for prefrontal regions during the
execution of cognitive tasks [14]. Because of the regulatory nature
of many processes mapped onto the prefrontal cortex, these changes
may refer to mechanisms involved in emotional regulation during
the acute depressive episode, or reflect deficits in cognitive control
[15–16]. Different interpretations of signal changes in the prefrontal
cortex in depression or after therapy may be given [17].
Given
that emotion regulation may either have adverse or protective
roles in mental health, depending on the mechanism through
which it operates [18–19], it may be important to determine
not only if, but also how emotions are regulated [20].
Psychodynamic
approaches propose that depression, besides its biological
and social underpinnings, may be meaningfully conceived
as a specific organization of an individual’s conscious or
unconscious beliefs and feelings. The resulting mental operations
constitute defensive strategies that aim at avoiding negative
feelings arising out of conflict in order to maximize a subjective
sense of safety [21]. The objective of long-term psychodynamic
psychotherapy is a stable modification of these strategies
that allows the patient to work through, achieve insight, and
reappraise experiences that are related to depressive pathology.
Therefore, in our study we would expect neural patterns
of appraisal of sensitive material to change during therapy and
move from emotion regulation styles characterized by unfavourable
strategies to more integrated acceptance and awareness.
The identification of these neural patterns was the general
aim of our study.
To
date, only one fMRI study has investigated the effect of psychotherapy
(cognitive behavioural therapy) on major depression using
a standardized experimental task (Fu et al., [22]). In this study,
participants were exposed to faces portraying different degrees
of sadness. This study detected changes in the amygdalaanterior hippocampus
and posterior cingulate-precuneus regions as
well as the superior frontal gyrus, suggesting that areas
associated
in previous studies with increased reactivity to emotional
stimuli and mechanisms of control are also relevant for
psychotherapy effects.
In
the present study, patients with recurrent unipolar depression underwent
functional neuroimaging scans at the beginning of treatment
and after 15 months, during which they were treated with
psychodynamic psychotherapy by experienced therapists. A matched
healthy control group without psychotherapy was scanned
at the same time points. The stimulus materials were attachment-related
pictures from the Adult Attachment Projective Picture
System (AAP [23]), a measure that has been shown to be valid
for use in an fMRI environment [24–25]. These pictures are designed
to elicit mental engagement with attachment-related experiences
such as separation, illness, danger, and loss. The fundamental
ability to form attachment is indispensable for human social
relationships. Since Bowlby’s seminal contributions [26], attachment
and separation have become essential theoretical components
of developmental psychology, and psychodynamic theory
[27]. One key feature of interpersonal problems in depressed
patients is their feelings of helplessness and fear of losing
the love of a significant other [28]. Internal representations of
the self as unlovable and of attachment figures as unloving are a central
dimension of Beck’s cognitive triad of depression [29].
To
increase the capacity of the signal to elicit a response related to
the emotional processes of each individual, material was here prepared
using personalized content [11,30–32] derived from AAP
interviews with each participant. In the personally relevant
condition
the AAP attachment scenes were accompanied by individually
tailored descriptions containing core sentences from the
patient’s own narrative previously elicited by each picture (see Material
and methods for details). The same series of attachment scenes
accompanied by a standard factual, non-emotional description
for all participants was used as control condition.
In
addition to the detection of a neural signature of treatment, we
were interested to see the extent in which the pattern of change corresponded
or differed from the one described by Fu et al. [22].
On
the basis of this study, we formulated specific hypotheses relative
to the general aim of the study of characterizing changes in neural
patterns of appraisal and emotion regulation occurring after therapy.
Our first hypothesis was the normalization of emotional reactivity
indexed by changes in the amygdala-anterior hippocampus region,
as found by Fu et al. [22]. Our second hypothesis was
the existence of changes in prefrontal areas detected in previous
studies [22,31,33] as possible markers of the specific effect of
psychodynamic psychotherapy on styles of emotion regulation[1,8].
The
present design differed from that of previous studies in several
further respects. As mentioned before, neuroimaging studies
have examined the effects of short time psychotherapy (e.g.
12–20 weeks), applying cognitive-behavioural or interpersonal therapy
[7–8]. We examined depressed patients with a history of several
previous depressive episodes during psychodynamic treatment
providing a longer observation window (15 months of therapy)
than in previous studies.
The
present investigation therefore complements the existing emerging
picture of changes associated with the therapy of depression
emerging from neuroimaging studies. In meta-analyses of
neuroimaging studies of the effect of psychopharmacological intervention
[34], decreased activation following treatment was reported
in the anterior hippocampus and parahippocampal cortex,
in the subgenual and pregenual cingulus, in the insula, and the
putamen. In the prefrontal cortex, decreased activation was reported
in the middle and superior left frontal gyrus. The frontal lobes,
however, were also the seat of several meta-analytic foci of increased
activation following treatment (in the middle frontal gyri bilaterally
and the dorsal anterior cingulate cortex). Further increased
activation was found in the posterior cingulate cortex and
in temporo-parietal regions on both sides. With the exception of
Fu et al. [22], neuroimaging studies of psychotherapy of depression
have examined only resting state metabolism (for reviews,
see [7–8,35]). Here, therapy outcomes were associated primarily
with changes in the prefrontal cortex (dorsolateral, ventrolateral,
and medial) [36–38], but the direction of changes was
not entirely consistent. Some studies reported reduced rest metabolism
or perfusion that normalized at endpoint [37–38]. In other
studies, however, this finding was reversed [36]. When both psychotherapy
and pharmacotherapy were compared [37], there was
limited overlap between changes found in these two therapy modalities.
While all these studies appear to be broadly compatible with
the involvement of limbic and prefrontal areas, more studies of
task-related activation are needed to provide a comprehensive picture
of changes associated with remission.
Materials
and Methods
The
study protocol was approved by the ethical committee of the
University of Ulm and was in compliance with national legislation,
the principles expressed in the Declaration of Helsinki, and
the Code of Ethical Principles for Medical Research Involving Human
Subjects of the World Medical Association. All participants gave
written informed consent.
Participants
Patients
were recruited from the outpatient departments of two psychoanalytic
institutes in Bremen, Germany, and diagnosed by two
trained clinicians using the Structured Clinical Interview for DMS-IV
Diagnosis (SCID, German version, [39]). Eight patients
were
diagnosed with double depression (dysthymia and former major
depression episodes); in the remaining patients, degree of depression
was severe. Ten patients had a comorbid anxiety disorder.
Patients reported 3–10 previous depressive episodes (mean
6 episodes, standard deviation 3.4). Age at first occurrence of
depression was between 8 and 37 years (mean 20 years, standard
deviation 9.2). All patients reported previous unsuccessful psychopharmacological
and/or psychotherapeutic treatment (none
of which was psychodynamic). Exclusion criteria were other psychiatric
conditions as main diagnosis, substance abuse, significant
medical or neurological conditions (including medical causes
of depression) and psychotropic medication. Inclusion criteria
were a long history of recurrent major depression as an appropriate
indication for psychodynamic treatment. Nondepressed controls
were recruited from the community, matched for
age, sex and education; control participants had no history of previous
depressive episodes or other psychiatric conditions (SCID).
Ethical considerations precluded the recruitment of a depressed
group left untreated for the duration of the study. All participants
were right-handed.
Depression
severity and general psychological symptoms were assessed
using the Beck Depression Inventory (BDI, [40], German version
[41]) and the Global Severity Index (GSI) from the revised Symptom
Check List (SCL-90-R [42], German version [43]). Of
the
initial sample of 38 participants, 5 dropped out of the study (3 controls
and 2 patients). The final sample of 33 consisted of 16 patients
and 17 controls (7 males, mean age 38.9 years, standard devaition
12.4, range 20–64). Patients and controls in the final
sample
did not differ in age (logistic multiple regression, z
= 0.41, p
=0.68), sex (z
=0.49, p=
0.62), and education (z =
0.56, p=
0.57).
Treatment
Patients
were treated with long-term psychodynamic psychotherapy by
16 formally trained psychoanalysts (mean years of experience
22.4, standard deviation 7.9). Training as a psychodynamic psychotherapist
is certified by the German state and regulated
by laws specifying the hours of theory, psychotherapy under
supervision, and self-awareness training. Patients underwent 2
to 4 hours of therapy weekly (2 patients had 4 hours, 7 had 3
hours, and 7 had 2 hours per week). At the end of the study period
of 15 months, patients had received from 90 to 210 hours of
psychotherapy (mean 129 hours, standard deviation 37). Psychotherapy
formally qualified as psychodynamic on the basis of
two criteria. The first was observance of the ‘‘couch setting’’
in which
the patient talks while lying on a couch with no visual contact
with the therapist. The second were the core features of psychodynamic
thinking and therapeutic technique, which include interventions
focusing on the interpretation of the patient’s unconscious
conflicts as they emerge in the transference relationship
[21], and the focus on affect as it emerges in
relationships,
in attempts to avoid distressing thoughts, in memory of
past events, and in recurring patterns of interactions [44]. Adherence
to these principles was assured by a regular casediscussion group
led by one co-author (GB) in which all participating
therapists presented their patients and interventions. Participants
to this group had no access to the material produced by
patients during the AAP interview and its results used to create personalized
stimuli in the scanner.
All
patients were free of psychotropic medication throughout the
entire 15 months of the study by their own choice. After the end
of the study, therapy continued for varying periods of time, for total
therapy lengths ranging between 24 and 48 months in accordance
to individual therapeutic contracts, course of treatment, and
health insurance allowance.
Experimental
design
Stimuli
were derived from the Adult Attachment Projective Picture
System (AAP, [23]), an established and validated interview to
assess attachment patterns. The AAP consists of 7 picture stimuli,
designed to activate the attachment system [25]. Two to four
weeks prior to the fMRI experiment, one trained judge (ST) conducted
a standard AAP interview. Administration involves asking
participants in a semi-structured format to describe the scene
in the picture, including what characters are thinking or feeling,
and what they think might happen next. Three core sentences
that represented the attachment pattern of the participants
were extracted from the audiotaped responses to
each
AAP picture stimulus by two independent certified judges (e.g.,
‘‘A girl is incarcerated in that big room’’, ‘‘My mother suffered
until the end and the ambulance came often’’). These sentences
were paired to the respective picture to constitute the
‘‘personally
relevant’’ trials tailored to each participant (Figure 1).
The
same pictures, paired to sentences describing only the environment
of the depicted situation (e. g. ‘‘There is a window with
curtains on the left and right’’, ‘‘There is a bed with a big blanket’’)
constituted the ‘‘neutral’’ trials, and were identical for all
participants.
Each trial consisted of the presentation of the picturesentence pair
for 5 seconds, followed by a fixation cross between 7.5
and 12.5 seconds. Participants were instructed to mentally engage
with the attachment scene in the picture and its textual description.
Stimuli
were presented in two blocks of six trials each. Each block
contained three different sets of personally relevant sentences and
neutral sentences for each picture stimulus. Trials alternated between
the personally relevant and neutral in groups of seven AAP
picture stimuli. In total, there were 84 trials resulting in a scanning
time of about 21 min. After scanning, participants filled out
a questionnaire that asked to rate on a 7-point Likert scale the degree
of emotional arousal and relevance of the personally related sentences
(emotional arousal is here a construct referring to the degree
to which participants rated personal sentences emotionally involving,
not the degree of depressive symptoms associated with them).
There were no significant differences in the ratings of patients
and controls (t31 = 0.31, p= 0.38), thus suggesting that differences
in neural activation levels between patients and controls
were not driven by higher emotional valence of the stimuli.
Image acquisition
MRI
data were obtained with a 3-T Magnetom Allegra head scanner
(Siemens, Erlangen, Germany), equipped with a standard quadrature
head coil. To reduce anxiety levels, anatomical images were
acquired first (3D high resolution T1-weighted volume, MPRAGE-sequence;
TR/TE/TI = 2300/4.38/900 ms, flip angle =8u,
FOV= 25662566176 mm, isotropic voxel size 1 mm, total
acquisition time 7.5 min). A total of 508 EPI T2*-weighted whole
brain volumes were acquired (TR/TE = 2500/30 ms, flip
angle
90u, FOV 192 mm, matrix 64664, voxel size 363 mm, slice thickness
3 mm, 44 slices, interleaved acquisition order, standard AC-PC
orientation).
Statistical
analysis
Data
were analyzed and visualized using Brain Voyager QX1.10
(Brain Innovation, Maastricht, Netherlands). Volumes were
slice-time corrected and realigned to the first volume, normalized
into standard Talairach space with parameters obtained
from the co-registered high-resolution structural volumes, and
smoothed with a Gaussian isotropic kernel (8 mm full width-half
maximum). To remove low frequency drifts, data were high-pass
filtered (3 cycles, 3 sine waves within the extent of the data)
and z-transformed in each voxel separately. The BOLD response
function was modeled by convolving the trial onsets with a
standard hemodynamic response function. Motion-correction parameters
were included in the model as confounding covariates at
the first level. Effects of interest were estimated in each subject separately
and brought to the second level to account for a random effect
of subjects. Data were analyzed using a 2 (participant
group)62
(time)62 (sentence) factorial design. The main effect of interest
of the study was the interaction between the main effects of group
(patients vs. healthy control subjects) and time (baseline month
1 vs. endpoint month 15) on the activation detected by the
contrast
personally relevant vs. neutral. To identify regions associated
with changes we performed a whole-brain estimation of
the model voxel by voxel, considering a priori clusters larger than
20 voxels. Because effect sizes obtained in an interaction may be
expected to be small, we relied on the results of Fu et al. [22] to support
inference and considered the extent to which our result confirmed
findings of this previous study. The region of interest emerging
from this study, and from the comparison with the existing
literature on depression and its therapy, were the amygdala-anterior
hippocampus region, and prefrontal areas as markers
of emotion regulation processes [22,31,33], and more specifically
on the medial surface [22], given the inconsistency of reports
on the lateral surface/dorsolateral prefrontal cortex [45]. We
report on additional findings with explorative intent. Anatomical
identification of foci relied on publicly available
empirical
cytoarchitectonic maps [46–47] where these maps exist (amygdala
and hippocampus). In the regressions of clinical response
on signal changes, confounding by initial conditions was
avoided by including baseline scores (BDI or GSI) and signal
as
covariates in the model (as in ref. [31]).
Results
Clinical
Response
We
first looked at changes in depressive symptoms to ensure that
patients had responded to therapy. BDI scores refer to the level
of depressive symptoms, whereas GSI scores reflect general symptomatic
distress. At baseline, BDI score mean was 24.4 (standard
deviation 9.5, range 10 to 40). BDI scores from 10 to 18 suggest
mild to moderate depression; from 19 to 29 moderate to severe
depression [48]. At endpoint (i.e. at the time of the second scan),
the mean BDI score was 12.9 (standard deviation 8.2, range 2.5
to 35). Mean reduction in scores was 11.47 (paired t15
=4.99, p,0.001).
Mean GSI score at baseline was 1.35 (standard deviation
0.57, range 0.19 to 2.52), at endpoint 0.69 (standard
deviation
0.36, range 0.16 to 1.41). Mean GSI score reduction was 0.66
(paired t15
= 5.99, p,0.001).
Clinically, five patients still fulfilled
diagnostic criteria for major depressive disorder at endpoint.
All patients were planning at the end of the study to continue
psychotherapy.
At
baseline, controls showed scores in the healthy range in both GSI
(mean score 0.18, standard deviation 0.13) and BDI (mean score
2.17, standard deviation 2.48). GSI and BDI scores did not change
in controls. At endpoint, mean GSI score was 0.13 (standard
deviation 0.11) and mean BDI score was 1.94 (standard deviation
2.36; GSI: paired t16
=2.11, p=
0.052; BDI: paired t17
= 1.07, p=
0.299).
Neuroimaging
data
The
main effect of interest of the study was given by the interaction
between group (patients and controls) and time (pre vs. post)
for the contrast relevant vs. irrelevant, as this interaction directly
detects changes intervening during therapy that affected patients
but not controls in the appraisal of personalized material. In
this interaction an effect in the left amygdala was detected ([46], Talairach
coordinates x,
y, z:
233, 211,
224, F1,32
=9.00, p=
0.005), extending laterally into the anterior hippocampus where
it reached its peak in Brodmann area (BA) 36 (x,
y, z:
233, 214,
225, F1,32
=12.11, p =0.001,
Figure 2A, red circle), and towards
the middle temporal gyrus. On the right, the interaction failed
to reach significance (x,
y, z:
24, 210, 227,
F1,32
=3.24, p=
0.08), but this was consistent with the general left-lateralized pattern
of activation elicited by the task. Post-hoc analysis revealed this
effect to be due to patients showing more activity than control
subjects
at baseline (x,
y, z:
233, 214,
225, t32
= 2.81, p=
0.008), which
equalized or partially reversed at endpoint (t32
=22.41, p
=0.01).
An
interaction effect was also present in the ventral anterior cingulate
cortex (vACC, x,
y, z:
0, 23, 4, BA25, F1,32
= 6.91, p
=0.013, Figure 2B, blue circle).
Post-hoc analysis identified this interaction
as being mainly due to patients activating less when exposed
to self-referential material at endpoint than controls (t32
=22.1, p=
0.02), while at baseline the relation was partially inverted,
with patients activating more than controls (t32
= 1.74, p
=0.05). A fairly large area of
interaction involved the medial prefrontal
cortex in a much more dorsal position (x,
y, z:
3, 44, 49, BA8-9,
F1,32 =
13.47, p,0.001,
Figure 2B, yellow circle), which extended
onto the lateral aspect in the superior frontal gyrus and posteriorly
reached the middle frontal gyrus. This interaction was due
to cortical activation in patients at baseline relative to controls (t32
= 3.00, p=
0.003) that equalized at endpoint (t32
=21.6, n.s.).
No
other clusters of interaction in either direction were present with
a size larger than 150 mm3 (about 20 voxels), even when selected
at the liberal threshold p,0.05,
uncorrected.
Correlation
of clinical response and cerebral activity
To
verify that the areas detected by the interaction were related with
changes in depressive symptoms, we regressed changes in the signal
of the contrast personally relevant vs. neutral on the improvement
in BDI scores, adjusting for initial levels to avoid
confounding
for initial severity. In the hippocampal/amygdalar cluster,
the association was only at trend level (t12
= 1.29, p=
0.11), accounting
for only 12% of the change in the signal from baseline to
endpoint. A stronger association was found in the ventral ACC
(t12
= 2.19, p=
0.02, explained variance 29%, Figure 3A, blue), which
did not change when age and sex were included as covariates
in the analysis (28%). In the medial prefrontal cortex the
association between the interaction effect and clinical response
was
not significant (t14
=0.92, p =0.19).
Long-term
psychodynamic psychotherapy is indicated for the treatment
of chronic depression [9], and may be expected to address
a wide range of issues that may complicate the depressive illness
and contribute to chronicity. For this reason, we extended our
analysis of the association of changes with response to the Global
Severity Index (GSI [42]), a more general index of psychic well
being than BDI. GSI and BDI scores were moderately associated
at baseline (r= 0.32, z = 1.80, p =0.04, 11% explained variance),
but strongly correlated at endpoint (r= 0.87, z =7.04, p,0.001,
76% of explained variance), suggesting effective treatment
of initial non-depressive symptoms captured by the GSI
score (interaction of the BDI/GSI association with time, t28
= 2.36, p= 0.01).
As
in the previous analysis with BDI scores, there was no significant
association between GSI improvement and the change in
the contrast signal in the hippocampal/amygdalar cluster (t12
= 1.08, n.s.). However, a significant association was found in the
ventral ACC cluster (t12 = 1.77, p= 0.05, explained variance 21%),
which was not changed by including sex and age as covariates
(20%). As one can see in Figure 3A, the association with GSI
improvement (in red) did not differ much from that of BDI (in blue).
Also in the medial prefrontal cortex there was an association between
the change in the contrast signal and clinical response measured
by GSI (t12 = 2.05, p= 0.03, explained variance 26%), which
remained after including age and sex as confounding covariates
(28%). As shown in Figure 3B, changes in the contrast signal
were more strongly associated with the general improvement measured
by GSI (in red) than with recovery from depression
as reflected by the BDI scores (in blue).
Discussion
When
exposed to personally attachment-relevant material, patients
undergoing long-term psychodynamic psychotherapy showed
changes in brain activation that were not observed in a sample
of control participants. The significant association of the changes
in the subgenual cingular and medial prefrontal cortex with
symptom improvement supported the hypothesis of their relevance
to the changes intervened during therapy.
Among
the areas involved by these changes, the anterior hippocampus/amygdalar
complex has been shown to be implicated in
the detection of emotional stimuli [49–52]
and displays
enhanced reactivity in depression [4–8,11–12,16] and anxiety [53–56].
The hippocampal/amygdalar correlate of change of the present
study fell within 5–10 mm of the anterior hippocampal area
associated with therapy change by Fu et al. [22] using cognitive
behavioral therapy. Changes in the ventral ACC were located
in the subgenual area reported by previous studies [36–37,57–59]
that provided converging evidence of its critical involvement
in both mood dysregulation and its resolution [60–61].
Changes over time in both areas consisted of a reduction in the
reactivity of these areas in response to personally relevant material
in patients. This pattern was not observed in controls.
A
third area, located anteriorly and superiorly in the medial prefrontal
cortex, was found in the present study to change from baseline
to endpoint in patients and not in controls. This area has been
associated with voluntary emotion regulation [19,62–63]. In
the
present study, this area displayed increased activation when exposed
at baseline to personally relevant material in patients, and equalized
at endpoint. Furthermore, changes in this area were associated
with changes in general symptom severity rather than with
changes in depressiveness specifically. This finding is consistent
with research showing this area’s general role in emotion
regulation and control processes.
It
is interesting that the prefrontal areas in which changes were detected
in the present study correspond to those associated with emotion
regulation [19,62–63]. Studies of emotional appraisal and regulation
have associated intentional avoidant and emotion
suppression
styles with increased psychiatric morbidity and vulnerability
to depression [19]. Because the material in the present
study was carefully chosen to represent personally relevant attachment
themes, we consider the associated emotional appraisal
to reflect the style of affect regulation.
There
were several aspects of this study that are worth commenting.
Among its strengths was the extension of neuroimaging approaches
to the investigation of changes during therapy in conditions
not investigated in previous studies: the recurrent type of
the depression from which patients suffered, the length of therapy,
and the psychodynamic nature of treatment. There were also
several limitations. First, while the personalized design may have
allowed an increase in validity and sensitivity of the stimuli used
in the scanner [11,30–32], it also introduces a possible confound
due to the existence of systematic differences in the material
produced by patients and controls. However, the absence of
differences in the rating of the emotional arousal of these personalized
sentences between patients and controls makes the existence
of this confound less likely. Second, the study lacked a natural
course control group composed by depressed patients on a waiting
list. Given the length of time during which the study was conducted,
keeping recurrent depressive patients on a waiting list would
have been unethical.
The
pattern of changes in prefrontal areas found in the present study
may be specifically associated with mechanisms of emotional appraisal
and control, suggesting reduced recourse to styles characterized
by suppression and avoidance after long-term therapy.
This interpretation outlines a possible mechanism for the
understanding of emotional appraisal and regulation in the psychodynamic
psychotherapy of depression. The relevance of these
finding for future studies rests in the possibility of documenting
specific mechanisms of action of depression therapy by
systematically collating results from different studies and comparing
different psychotherapeutic approaches, such as
psychodynamic,
behavioral, interpersonal, and psychopharmacological.
This
would be a first step towards monitoring progress of therapy
in individual patients.
|
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