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Am J Psychiatry 154:1, January 1997
Special Article
CHRISTINA SOBIN AND HAROLD A. SACKEIMPSYCHOMOTOR SYMPTOMS OF DEPRESSION
Psychomotor Symptoms of Depression
Christina Sobin, Ph.D., and Harold A. Sackeim, Ph.D.
Objective: The authors summarize current knowledge regarding the psychomotor symp-
toms of depression.
Method: Findings from the objective quantification of psychomotor symp-
toms are reviewed, and methodological issues are considered. The contemporary empirical
literature regarding the diagnostic, prognostic, and potential pathophysiologic significance of
psychomotor symptoms is summarized.
Results: It has been repeatedly shown that depressed
patients differ from normal and psychiatric comparison groups with regard to objectively
quantified gross motor activity, body movements, speech, and motor reaction time. Course of
illness, diurnal variation, medication status, sex, and age are associated with agitation and
retardation and should be controlled when one is studying psychomotor symptoms. Psycho-
motor symptoms in depression may have unique significance. They have high discriminative
validity, may be the only symptoms of depression that distinguish depression subtypes, and
are predictive of good response to tricyclic antidepressants. Results of brain imaging and
biochemical studies link depression and motor symptoms to abnormalities in the basal ganglia
and basal ganglia/thalamo-cortical circuits.
Conclusions: The investigation of psychomotor
disturbance in depression is specifically consistent with neo-Kraepelinian standards for the
study of psychiatric disorders. Our current knowledge of psychomotor symptoms is concep-
tually obscure, yet a large body of evidence specifies their manifestation and supports their
significance. Identifying the incidence of abnormal motor behaviors in depressed patients and
assessing the component processes that accompany and determine their manifestation may be
important advances in the study of psychomotor symptoms in depression.
(Am J Psychiatry 1997; 154:4–17)
He is apparently unable to move and express himself
freely. This very circumstance, that the answers come
slowly, even on matters of indifference, shows that in this
patient we have not to deal with a fear of expressing himself
but with some general obstacle to the utterance of speech.
Indeed, not only speech but all action of the will is extremely
difficult to him . . . . The disturbance must be essentially
confined to the accomplishment of voluntary movements.
This constraint is by far the most obvious clinical feature of
the disease and compared with this, the sad, oppressed
mood has but little prominence.
—Kraepelin (1)
K
raepelin’s evocative description of his patient’s psy-
chomotor symptoms echoed the observations of
the earliest psychiatric writers, including Aretaeus of
Cappadocia, Hippocrates, Caelius Aurelianus, and Plu-
tarch (2, 3), and psychomotor disturbance continues to
be regarded as an essential feature of major depressive
disorder. Objectively measured motor behavior, includ-
ing gross motor activity, discrete body movements,
speech, and motor reaction time, have been shown to re-
liably differentiate depressed patients from psychiatric
and normal comparison groups. From a nosologic per-
spective, psychomotor disturbance remains a principal
symptom category in contemporary classification sys-
tems. Of 16 symptom domains, only psychomotor dis-
turbance was included in all of the 10 diagnostic systems
that defined criteria for the melancholic subtype (4). Fur-
thermore, evidence suggests that psychomotor symptoms
may have unique prognostic and, perhaps, pathophysi-
ologic significance. However, explicit definitions of psy-
chomotor phenomena remain elusive. The term is com-
Received Feb. 5, 1996; revision received June 17, 1996; accepted
July 1, 1996. From the Department of Psychiatry, College of Physi-
cians and Surgeons, Columbia University, and the New York State
Psychiatric Institute, New York. Address reprint requests to Dr. So-
bin, The Rockefeller University, 1230 York Ave., Box 313, New
York, NY 10021.
Supported in part by grants from the National Association for Re-
search on Schizophrenia and Depression Young Investigators Pro-
gram and NIMH grants MH-35636 and MH-47739.
4 Am J Psychiatry 154:1, January 1997
monly applied to virtually any observable manifestation
of slowing (retardation) or increased activity (agitation)
during a depressed state (DSM-IV), and many have ob-
served that our knowledge of psychomotor symptoms is
seriously limited and awaits major methodologic and
theoretical development (5–8). Thus, a central purpose of
this review is to examine our accumulated knowledge
and promote the development of an informed definition
of psychomotor symptoms in depression.
We begin with a review of studies that have objec-
tively quantified the manifestation of psychomotor
symptoms in the domains of gross motor activity, dis-
crete body movements, speech, and motor reaction
time. These results provide an empirical foundation for
considering the nature of psychomotor symptoms and
raise important issues regarding their measurement. Us-
ing results of studies that have assessed psychomotor
functioning in depression through clinical ratings, we
review the diagnostic, prognostic, and possible patho-
physiologic significance of psychomotor symptoms. We
conclude with a summary of alternative strategies for
expanding our understanding of the significance of psy-
chomotor symptoms in depression.
MANIFESTATIONS OF PSYCHOMOTOR SYMPTOMS
Studies that have objectively measured the individual
manifestations of psychomotor symptoms in depressed
patients have found that depressed patients differ from
psychiatric and normal comparison groups with regard
to gross motor activity level, movements of the limbs,
trunk, and head, speech, and motor reaction time (table
1). These studies provide a foundation for conceptualiz-
ing the manifestation of motor symptoms in depression.
Gross Motor Activity
Among the methods of quantifying psychomotor re-
tardation and agitation, perhaps none is as intuitively
TABLE 1. Summary of Key Findings From Unidimensional Studies of the Manifestations of Psychomotor Abnormalities in Depressed Patients
Variable Finding for Subjects Compared Reference for Study
Gross motor activity
Amount of 24-hour activity Bipolar, depressed < normal comparison 9, 10
Bipolar, manic > normal comparison 10
Amount of activity between midnight and 7:00 a.m. Depressed, unipolar/bipolar > schizophrenic 11
Percent of total activity between midnight and 7:00 a.m. Depressed, unipolar/bipolar > schizophrenic 11
Activity level variability Depressed, unipolar/bipolar < schizophrenic 11
Amount of 24-hour activity Bipolar, depressed < unipolar, depressed 9, 12
Body movements
Duration and frequency
Self-touching Depressed > normal comparison 13
Eye contact Depressed < normal comparison 13
Smiling Depressed < normal comparison 13
Eyebrow movement Depressed < normal comparison 13
Self-touching Depressed > schizophrenic 13
Small head movements Depressed > schizophrenic 13
Frequency of large head movements Depressed > schizophrenic 13
Duration of eye contact Depressed < schizophrenic 13
Speech
Speech pause time Depressed > normal comparison 14–17
Depressed with retardation > normal comparison 11
Depressed without retardation ≅ normal comparison 11
Pause time at speech initiation Depressed > normal comparison 17
Fundamental frequency change rate Depressed < normal comparison 18
Fundamental frequency variability Depressed < normal comparison 14, 16–20
Rate of diphthong production (articulation) Depressed < normal comparison 5
Parkinson’s disease < normal comparison 5
Depressed ≅ Parkinson’s disease 5
Speech pause time Depressed > psychiatric comparison 5
Unipolar > bipolar 15
Motor response time
Decision time and motor response time Depressed > normal comparison 21–28
Central processing component of decision time
a
Depressed > normal comparison 21–28
Simple reaction time Psychotically depressed > normal comparison 29
Nonpsychotically depressed ≅ normal comparison 29
Decision time and motor response time Depressed with retardation > normal comparison 21
Motor response time Depressed with retardation > depressed with agitation 21
Depressed with agitation > normal comparison 21
Melancholic depressed > normal comparison 30
Nonmelancholic depressed > normal comparison 30
Decision time Melancholic depressed > normal comparison 30
Nonmelancholic depressed ≅ normal comparison 30
Total reaction time variability Depressed < schizophrenic 29
a
Through peripheral initiation of motor response.
CHRISTINA SOBIN AND HAROLD A. SACKEIM
Am J Psychiatry 154:1, January 1997 5
apparent as continuous activity monitoring. Unlike
other techniques, measurement of motor activity over a
24-hour period captures the diurnal variation that is
fundamental to human behavior. Motor activity has
been measured with telemetric and nontelemetric wrist-
watch-like devices that transform large arm movements
into electronic impulses for storage in solid-state mem-
ory. High correspondence of the activity data with
changes in patients’ activities, as well as with staff ob-
servations of activity levels and ratings of mood state,
has substantiated the validity of this method (31, 32).
High between-patient variability and differences in ac-
tivity regimentation across inpatient wards led to the
recommendation that the relative distribution of activ-
ity during a 24-hour period be examined also (11).
Thus, variables in the studies of gross motor activity
include the total number of movements in a 24-hour
period and ratios of daytime activity levels to levels dur-
ing nighttime hours as well.
Depressed bipolar inpatients have manifested low ac-
tivity levels relative to normal comparison groups (9,
10), whereas patients in the manic phase have shown
elevated levels (10). In the only comparison of 24-hour
motor activity in which a psychiatric comparison group
was used (11), drug-free schizophrenic inpatients and
depressed inpatients (12 unipolar and five bipolar)
differed in the absolute amount and distribution of
their activity levels. The depressed patients exhibited a
greater amount of activity between midnight and 7:00
a.m. and had a greater percentage of their total 24-hour
activity during these nighttime hours. Furthermore, the
schizophrenic patients had greater temporal variability
in their activity levels.
Research that compared the activity levels of pa-
tients with subtypes of depression demonstrated that
unipolar patients had higher motor activity levels than
bipolar depressed patients (9, 12). Studies have also
shown that 24-hour activity levels covaried with changes
in clinical state. Kupfer and Foster (33) reported
that as the mood of a 54-year-old psychotic woman
with unipolar depression resolved, her gross motor ac-
tivity decreased by 25% during daytime hours and by
50% during nighttime hours. In contrast, Post et al.
(32), in a single-case study of a rapid-cycling bipolar
patient, found that motor changes occurred primarily
during daytime hours and preceded gradually the more
abrupt onset of mood change, suggesting the potential
clinical value of tracking shifts in motor activity in bi-
polar patients. In one of the largest studies completed
to date (9), 25 bipolar patients had less motor activity
in their depressed state than in their euthymic and
manic states. These changes were found to occur during
daytime but not nighttime hours.
Thus, bipolar depressed patients have been found to
differ from normal comparison groups in absolute lev-
els of 24-hour motor activity. During depressed phases,
their activity is decreased, and during manic phases it is
increased. The 24-hour gross motor activity of unipolar
depressed inpatients is greater than that of schizo-
phrenic patients and bipolar depressed patients, and
unipolar depressed inpatients are more active during
nighttime hours. Furthermore, 24-hour motor activity
may be a sensitive measure of mood change within cy-
cling and recovering mood disorder patients. Unipolar
depressed patients may have increased gross motor ac-
tivity, the resolution of which is most apparent during
nighttime hours, while bipolar patients have decreased
gross motor activity, the resolution of which may be
most apparent during daytime hours.
Movements of the Head, Torso, and Limbs
Naturalistic observation through videotaped ratings
offers a method for determining the individual move-
ments that together may constitute agitation or retarda-
tion in depressed patients. In one of the only studies of
its kind, Jones and Pansa (13) videotaped medication-
free depressed and schizophrenic patients (ICD-9 crite-
ria) and a normal comparison group during a 10-min-
ute interview session and during the presentation of
visual stimuli with moderate emotional content. They
examined facial gestures, head movements, looking be-
havior, and self-touching behavior. The depressed pa-
tients were found to differ from the normal comparison
group in the duration and frequency of self-touching
(increased), direct eye contact with the interviewer (de-
creased), smiling (decreased), and eyebrow movement
(decreased). When compared to the schizophrenic pa-
tients, the depressed patients had more frequent and
longer small movements of the head, more frequent
large movements of the head, more frequent body
touching, and shorter duration of eye contact with the
interviewer and toward visual stimuli. Thus, the behav-
iors that differentiated the depressed patients from both
the psychiatric group and the normal comparison
group included increased frequency of body touching
and diminished eye contact.
Results from one of the only studies to examine mul-
tiple manifestations of psychomotor symptoms within de-
pressed patients suggested that motor retardation and
agitation are likely to be multidimensionally manifested.
Ulrich and Harms (8) factor analyzed the videotape-based
ratings of nonverbal behaviors of 47 patients with endo-
genous depression (ICD-9 criteria). A retardation factor
and two agitation factors emerged. The loadings of 0.75
and above on the retardation factor included those for
reduced eye movements, reduced facial expression, con-
stricted posture, low voice amplitude, diminished pros-
ody, and shortened speaking time. The first agitation fac-
tor was characterized as “gross motor restlessness” and
included postural restlessness, brief repetitive body
touching, and continuous hand-to-head touching. The
second agitation factor was characterized as “constricted
restlessness” and included constricted posture, postural
restlessness, and continuous hand-to-hand movements.
As with any factor analytic results, high factor loadings
do not necessarily indicate the behaviors that will co-oc-
cur within individual patients (34, 35). These findings
await replication and determination of their covariation
with clinical judgments of agitation and retardation.
PSYCHOMOTOR SYMPTOMS OF DEPRESSION
6 Am J Psychiatry 154:1, January 1997
Speech
The complex motor act that results in speech has long
been considered a valuable objective measure of psycho-
motor retardation in depression (14, 15). In addition to
paucity of speech, the motor-retarded depressed pa-
tient may show slowed responses, monotonic phrases,
and poor articulation. Among the temporal characteristics
of speech, the amount of time between utterances (speech
pause time) while a person is engaged in a simple counting
task has been shown to correlate with global psychomotor
retardation, as measured by the Widlocher Retardation
Rating Scale (36). It has been shown that depressed pa-
tients have increased speech pause time during an auto-
matic counting task (14–16) and during a clinical inter-
view (17) when compared to normal comparison groups.
Greden et al. (16) contrasted the speech pause time of 36
unipolar and bipolar depressed subjects with that of 19
nondepressed psychiatric control subjects (eight schizo-
phrenic, three demented, two phobic, one with Briquet’s
disorder, three with other psychiatric disorder as defined
by the Research Diagnostic Criteria [RDC], and two with
no psychiatric diagnosis). Speech pause time was longer
only among the depressed patients, regardless of subtype.
Inconsistent results have emerged, however, in the
comparison of bipolar and unipolar depressed patients.
While Greden et al. (16) reported that the speech pause
time of unipolar and bipolar patients did not differ,
Hoffman et al. (15) reported that only unipolar, and
not bipolar, depressed patients had increased speech
pause time relative to a normal comparison group. This
is the opposite of what would be predicted by results
from gross motor activity studies and could suggest that
the mechanisms underlying speech delay are inde-
pendent of those responsible for reduced gross motor
activity. In the only demonstration of the association
between clinically rated motor retardation and speech,
these same unipolar and bipolar patients were re-
grouped according to their retardation scores on the
Widlocher scale (36). Only those with retardation dif-
fered from the normal comparison group in speech
pause time (15). Nilsonne (17) has further suggested
that the speech delay characteristic of depressed pa-
tients may occur specifically in the initiation of re-
sponses to interviewers’ questions.
Differences between depressed and normal compari-
son groups have also been shown in the variables meas-
uring aspects of fundamental frequency (mean vocal
pitch). In one study (18), depressed patients had a re-
duced rate of change and less variability in mean vocal
pitch when compared to a group of normal subjects.
Flint et al. (5) compared the articulation characteristics
of 30 motor-retarded depressed patients, 30 nonde-
pressed and nondemented patients with Parkinson’s
disease, and 31 normal subjects. Second formant tran-
sition (speed of diphthong production) and voice onset
time (time between consonant production and the fol-
lowing vowel) were decreased, while spirantization
(voice noise or “leakage”) was increased in the patients
with major depression compared to the normal group.
The patients with Parkinson’s disease had similarly de-
creased second formant transition and voice onset time,
but they did not differ from the normal comparison
group on spirantization. There were no significant dif-
ferences between the patients with major depression
and those with Parkinson’s disease on any of the articu-
lation measures.
Alterations in speech among depressed patients have
been repeatedly shown to be externally valid. Both
speech slowing and reduced prosody have been found
to have a high correlation (14, 19) with a validated psy-
chomotor retardation rating scale (36). Nilsonne (17)
reported a high correlation between clinical ratings of
retardation and both slowed speech initiation and re-
duced pitch variability. Global depression scores also
have been found to be associated with these same
speech measures (14, 16, 19). The predictive validity of
increased speech pause time and decreased pitch var-
iability has been suggested by their change to more
normal values when depressed patients return to a eu-
thymic state (14, 16, 20, 37). At the same time, data
indicating the discriminative validity of pause time,
pitch variability, and altered articulation for retarded
and nonretarded depressed patients are limited.
Motor Speed
The speed with which patients execute a discrete mo-
tor act has also been used as an objective measure of
psychomotor retardation. Earlier investigators simply
timed the completion of a task, such as card sorting,
with a stopwatch (38). However, reaction time repre-
sents a combination of cognitive and motor processes.
The attempt to assess evaluative or decision processes
before the execution of a motor response separately
from motor speed is unique to the field of reaction time
research, and in this way, researchers have tried to iden-
tify the “functional basis” of motor retardation in de-
pression (39). Thus, while some researchers have used
a simple key press task, many have used the “fixed
foreperiod” paradigm. In this method, a trial begins
when the subject presses a “home” key with the domi-
nant index finger. A timer starts as a visual, auditory,
or tactile stimulus is presented and stops when the sub-
ject lifts his or her finger from the home key en route to
the appropriate “choice” key. When the first timer
stops, a second timer starts, and it stops when the sub-
ject presses the choice key. The time between stimulus
presentation and release of the home key has been in-
terpreted as decision time, and the time required to
reach the decision key has been considered the motor
response time. Decision time, motor response time, and
total reaction time, assessed with the fixed foreperiod
paradigm, decrease after pharmacologic treatment of
depression and subsequent symptom remission (40),
suggesting that these measures are an objective gauge of
depression-related phenomena.
The separation of decision and motor response com-
ponents has been advantageous. In the one study to
compare clinically assessed, medication-free, retarded
CHRISTINA SOBIN AND HAROLD A. SACKEIM
Am J Psychiatry 154:1, January 1997 7
and agitated depressed inpatients and a normal com-
parison group (21), only motor response time distin-
guished the agitated depressed patients from the re-
tarded depressed patients and the normal comparison
group. The retarded depressed patients were found to
be slower than the normal comparison group with re-
gard to both decision time and motor response time.
Another valuable finding to emerge from the separation
of response components concerns the relationship be-
tween them. Within normal comparison groups, deci-
sion and motor response times are independent (22–24,
41), while for female depressed subjects, decision and
motor response times were found to be correlated, sug-
gesting that these processes may become linked during
depression (25). However, the separation of decision
and motor response components has added little to our
understanding of the differences in motor speed be-
tween depressed patients and normal comparison
groups. Both components are slower in depressed pa-
tients, as compared to normal groups, in response to
visual, auditory, and tactile stimuli in both simple and
choice paradigms (21–28). Similarly perhaps, the sepa-
ration of decision and motor reaction times has not en-
hanced the differentiation of depressed and schizo-
phrenic patients with regard to motor speed (42–44),
although patients with depressive disorder have been
shown to be less variable in their total reaction time
than schizophrenic patients (29).
The separation of decision and motor response times
by means of the fixed foreperiod paradigm has also
been criticized for its underlying assumption that cog-
nitive and motor processes are distinct, sequentially oc-
curring components of performance (30). The instruc-
tion to subjects that movement should not occur until a
final choice has been made is fundamental in this
method, and low mean error rates are typically re-
ported as confirmation that a final choice decision was
made before movement. In fact, a decision process that
continues during the initiation and execution of move-
ment may not necessarily result in error, and it may
accurately reflect an efficient interaction of cognitive
and motor processes. Borrowing from the cognitive
psychology literature (45), Cornell et al. (30) assessed
cognitive slowing during a reaction time task by hold-
ing constant the motor demand while varying the cog-
nitive complexity; motor slowing was assessed by hold-
ing constant the cognitive complexity and varying the
motor demand. It was suggested that comparisons of
the reaction times of patients and a group of normal
subjects under low and high demand conditions could
potentially reveal deficits in each component process
among the patient groups. Cornell et al. found that mel-
ancholic and nonmelancholic depressed patients dif-
fered from the normal comparison group with regard
to motor slowing, while only the melancholic depressed
patients differed from the normal subjects with regard
to cognitive slowing.
While the reaction time literature offers one strategy
for controlling cognitive factors in the study of motor
disturbance in depression, ultimately, new strategies
will be needed to assess the central processing deficits
associated with motor agitation and retardation. Infor-
mation-processing models that accommodate the inter-
play of motor and cognitive functions have been pro-
posed (46) and may provide a useful direction for
further study.
CHARACTERISTICS OF PSYCHOMOTOR SYMPTOMS
AND METHODOLOGIC CONSIDERATIONS
Studies of the individual manifestations of psycho-
motor disturbance in depression offer many interesting
clues to their nature. From an experimental perspective,
these results also suggest comparisons for future studies
and factors that should be controlled in examining mo-
tor agitation and retardation. Several manifestations of
psychomotor disturbance in depression have been
shown to differentiate depressed patients from normal
subjects. These include amount of 24-hour gross motor
activity; duration and frequency of body movements
such as self-touching, eye contact, smiling, and eyebrow
movement; speech pause time, voice pitch, and articu-
lation; and reaction time. Fewer studies, however, have
demonstrated the specificity of these motor distur-
bances to depressed patients. Results to date suggest
that depressed patients have increased self-touching, in-
creased head movements, and decreased eye contact
when compared to schizophrenic patients. Depressed
patients have been shown to have increased speech
pause time as compared to a mixed group of nonde-
pressed psychiatric control subjects, and depressed pa-
tients have been shown to have less variability in their
total reaction time across trials. However, motor dis-
turbance is known to occur in many psychiatric disor-
ders. Motor deficits have been a key feature in studies
of negative-symptom schizophrenia (47, 48), and mo-
tor restlessness has been described in studies of anxiety
disorder (49, 50). Whether the retardation in depres-
sion is behaviorally equivalent to the retardation char-
acteristic of negative-symptom schizophrenia, however,
has not been studied. Similarly, the nervous restlessness
that is clinically observed in anxious patients may or
may not mimic the agitation observed in patients with
agitated depression. Studies that compare the specific
motor components of clinically assessed retardation
and agitation in different psychiatric groups are needed
before the specificity of psychomotor disturbance to de-
pression can be understood.
The data reviewed suggest that whether a patient is
retarded or agitated or both may depend on whether
the lifetime course of illness is unipolar or bipolar. In
addition, the high rates of overlap in depression and
anxiety syndromes (51, 52) and the possible influence
of this comorbidity on the manifestation of motor
symptoms suggest that the presence of secondary disor-
ders and lifetime course of illness should also be ascer-
tained when one is studying psychomotor symptoms.
Retardation and agitation are not mutually exclusive.
Reduced looking and decreased facial expression are
PSYCHOMOTOR SYMPTOMS OF DEPRESSION
8 Am J Psychiatry 154:1, January 1997
often coupled with gross motor restlessness and in-
creased hand movements (8, 13), especially in patients
with severe depression. Thus, instruments used for
identifying and measuring retardation and agitation
must be designed to accommodate the presence of
either or both, and clinical raters must be trained to
consider them independently.
Research on the abnormalities of circadian rhythms
in depressed patients suggests that controlling the time
of day of testing is also essential in studies of the psy-
chomotor symptoms in depression. Peaks and lows in
motor activity, as well as in urinary norepinephrine me-
tabolites (3-methoxy-4-hydroxyphenylglycol [MHPG])
and oral temperature, were found to be advanced by
1–3 hours in bipolar patients when compared to normal
subjects (10). More recently, Piletz et al. (53) suggested
that the phase advance phenomenon was associated
more strongly with agitated than retarded depression,
and with first as compared to subsequent depressive
episodes. Furthermore, the variability of circadian
peaks and lows was found to be increased in depressed
patients as compared to normal subjects. In a demon-
stration of the profound effect of diurnal variation on
motor reaction time, Moffoot et al. (54) reported that
the decision time and movement time of melancholic
depressed patients were slower than the times in a nor-
mal comparison group during morning but not evening
hours, and while the afternoon performance of the mel-
ancholic patients improved, the performance of the
comparison group diminished.
In addition, both sex and age may be determinants of
the manifestation of psychomotor symptoms. Males
have been found to have more retardation than females,
while females have been found to have more agitation
than males (55–57). With regard to age, depressed pa-
tients under 40 years are more likely to have motor re-
tardation, while patients over age 40 are more likely to
have motor agitation (55, 57). This association may
warrant special examination. The loss of subcortical
neurons and subsequent reduction of dopamine-synthe-
sizing enzymes, which are characteristic of normal ag-
ing (58), might predict the opposite. Because sedation
can be a side effect of heterocyclic antidepressants, and
agitation can be a side effect of the unicyclics and selec-
tive serotonin reuptake inhibitors, controlling medica-
tion status is essential in the design of motor behavior
studies.
Finally, the significance of psychomotor symptoms
across the full spectrum of depressive disorders, and
their association with illness severity, must eventually
be addressed. The only study to examine the association
between severe depressive symptoms and motor distur-
bance (55) reported that in three groups of depressed
inpatients stratified according to the presence of motor
agitation or motor retardation or the absence of motor
symptoms, those with motor retardation were more
likely to be psychotic than were those with motor agi-
tation. This may indirectly suggest that global sever-
ity is associated with motor-retarded but not motor-
agitated depression. Obviously, however, the question
awaits further analysis. Methods for objectively meas-
uring minor manifestations of endogenous depression
have rarely been applied in nosologic studies. Psycho-
motor disturbance, one of the only objectively measur-
able symptoms of endogenous depression, may be a
reasonable starting point for such an endeavor. While
particular features of endogenous depression, such as
psychomotor disturbance, have long been recognized as
features of psychotic depression (59, 60), it has not yet
been determined whether these features occur only in
cases of severe depression. The possibility of a mild
form of endogenous depression with psychomotor dis-
turbance, similar to the “endogenomorphic” depres-
sion described by Klein (61), should not be ruled out.
DIAGNOSTIC SIGNIFICANCE OF PSYCHOMOTOR
SYMPTOMS
Despite the many advances in the objective assess-
ment of psychomotor symptoms in depression, studies
examining their diagnostic significance derive from
clinical judgment and single-item ratings. In these stud-
ies, psychomotor disturbance was evaluated with items
describing global agitation and/or retardation. As sug-
gested above, objective assessment has indicated that
motor agitation and retardation can be manifested in
multiple motor domains. It is not known which mani-
festations of psychomotor disturbance result in a posi-
tive single-item clinical rating of agitation or retarda-
tion, whether most patients simultaneously experience
more than one motor disturbance, and whether the dif-
ferent manifestations of motor disturbance are equally
apparent to observing clinicians.
Historically, psychomotor symptoms contributed im-
portantly to the evolving nosology of depression sub-
types. Early studies sought to isolate the clinical differ-
ences between psychotic and neurotic patients. Linear
discriminant function analysis was used to optimize
separation of these “known” subgroups, and it was re-
peatedly found that psychomotor symptoms provided
the strongest differentiation. In a study of 391 psychotic
and 250 neurotic depressed patients diagnosed accord-
ing to ICD-7 criteria (62), discriminant function analy-
sis indicated that of 60 symptoms and course descrip-
tors, delusions and psychomotor symptoms were the
most robust subtype discriminators. In a later study of
115 psychotic and 63 neurotic inpatients (63), the high-
est loadings of the 32 symptoms assessed were for audi-
tory hallucinations (0.92), agitation (0.77), and delu-
sions (0.70). Feeling motorically slowed (as assessed on
the Present State Examination [PSE]) had the next high-
est loading (0.50), but it is interesting that observed mo-
tor retardation (PSE behavior rating) had one of the low-
est loadings. In another comparison of psychotic (N=
65) and neurotic (N=39) inpatients, Fleiss (64) found
that motor retardation, agitation, and somatic com-
plaints best discriminated the psychotic group. In the
only analysis to include a rating of global symptom se-
verity, Bhrolchain et al. (65) found that global severity
CHRISTINA SOBIN AND HAROLD A. SACKEIM
Am J Psychiatry 154:1, January 1997 9
and motor retardation best distinguished 73 psychotic
female inpatients from 41 neurotic female outpatients.
The presumption in earlier studies was that a particu-
lar subtyping distinction, psychotic versus neurotic,
was valid, and the most discriminating symptom fea-
tures were identified. Later studies did not precategor-
ize patient subgroups and instead attempted to identify
depression subtypes by analyzing the factor structure of
presenting symptoms. These studies suggested that psy-
chomotor symptoms were among the strongest indica-
tors of the melancholic/endogenous subtype. In a com-
prehensive review of factor analytic studies, Nelson and
Charney (7) observed that 11 of 12 reports that evalu-
ated psychomotor retardation found that this symptom
loaded on the melancholic/endogenous factor at 0.50 or
higher, with the exception reporting a factor loading of
0.40. Of the 20 depressive symptoms considered, psy-
chomotor retardation had the highest and the most con-
sistent (positive) loadings on the melancholic/endo-
genous factor. More recent reviews of this literature (4,
66) concluded the same.
The frequency with which a given symptom occurs
within patients can further indicate its diagnostic sig-
nificance relative to other aspects of a given syndrome.
The close examination of a symptom that rarely occurs
may add little to our understanding of a diagnostic syn-
drome, while a symptom that occurs in virtually every
case will not contribute to the differentiation of syn-
drome subtypes. Unfortunately, relatively few recent
studies have reported and compared symptom rates
within depressed patients. A literature search revealed
only six such studies, and in these, the presence or ab-
sence of symptoms was determined by clinical interview
and the rating of single-symptom items (table 2). In gen-
eral, the frequency of psychomotor symptoms falls ap-
proximately within the range of the frequency of other
symptoms of depression, suggesting that they are not so
rare as to be nosologically insignificant. Perhaps not
surprisingly, “marked” psychomotor symptoms have
been found to occur with considerably less frequency
than moderate manifestations. Young et al. (69), in an
analysis of the symptoms of a mixed unipolar/bipolar
group of 788 patients meeting definite RDC for major
depressive disorder found that marked psychomotor
symptoms (agitation or retardation) occurred in only
11.8% of the patients. However, in contrast to the
more moderate psychomotor symptoms, the discrimi-
native sensitivity of marked psychomotor symptoms to
DSM-III-defined melancholia was high, although their
absence did not always indicate a nonmelancholic sub-
type. Accurately assessing the severity of psychomotor
symptoms may be critical in determining their diagnos-
tic discriminative power.
In two studies that examined symptom rates across
diagnostic subtypes, large differences were indicated.
One pre-DSM-III study that used the psychotic/neurotic
distinction (65) suggested that psychotic patients were
more likely to manifest retardation than were neurotic
depressed patients. When bipolar, unipolar, and reac-
tive depressed patients were compared (71), the bipolar
patients appeared to manifest more psychomotor dys-
function than the unipolar and reactive patients. Retar-
dation was more common among the depressed bipolar
patients than the depressed unipolar patients, while the
unipolar patients were more likely than the bipolar pa-
tients to manifest agitation. The rates of no other de-
pressive symptoms differed as greatly across subtypes
of depression. In a study that was designed to examine
TABLE 2. Symptom Rates in Studies of Depression
Patients With Major Depression
Buchwald
and
Rudick-
Davis
Miller
and
Nelson
Young
et al. Mendels
Nelson and Charney (71)
(N=76)
e
Bhrolchain et al.
(65) (N=114)
f
(67)
(N=107)
a
(68)
(N=95)
b
(69)
(N=788)
c
(70)
(N=50)
d
Bipolar
(N=7)
Unipolar
(N=29)
Reactive
(N=40)
Psychotic
(N=62)
Neurotic
(N=49)
Symptom N % N % N % N % N % N % N % N % N %
Any psychomotor disturbance 62 58 531 67 7 100 20 69 14 35
Retardation 44 46 25 50 6 86 10 34 10 25 45 73 15 31
Agitation 44 46 2 29 11 38 4 10
“Marked” motor symptoms 93 12
Sleep disturbance 98 92 55 58 590 75 32 64 5 71 29 100 33 83 43 69 27 55
Appetite disturbance 86 80 49 52 555 70 7 100 28 97 36 90 50 81 31 63
Decreased energy 93 87 71 75 3 43 14 48 13 33
Loss of interest/pleasure 75 70 78 82 763 97 7 100 29 100 32 80
Guilt/self-reproach 29 31 601 76 25 50 0 0 13 45 2 5
Concentration disturbance 78 73 71 75 6 86 26 90 14 35
Suicidal ideation/intent 74 69 55 58 5 71 15 52 33 83
a
DSM-III-R diagnosis; mean age=33 years (SD=10); 67% female; 100% psychiatric emergency room intake patients.
b
DSM-III diagnosis; mean age=49 years (SD=19); 72% female; 100% inpatients; 3% bipolar, 3% schizoaffective.
c
DSM-III/RDC diagnosis; mean age=38.7 years (SD=14.5); 59% female; 77% inpatients; 66% endogenous/melancholic.
d
Clinical diagnosis; 100% inpatients; 38% endogenous.
e
RDC diagnosis; mean age=37 years; 82% female; 100% acute inpatients.
f
Present State Examination diagnosis; age range=18–65 years; 100% female; 59% inpatients.
PSYCHOMOTOR SYMPTOMS OF DEPRESSION
10 Am J Psychiatry 154:1, January 1997
the frequency of depressive symptoms and their diag-
nostic value (67), unlike other neurovegetative symp-
toms (including appetite loss, sleep disturbance, and
loss of energy), psychomotor symptoms were reported
least frequently (19%) by patients not meeting criteria
for a major depressive episode, suggesting that psycho-
motor symptoms may have high discriminative validity.
Determining the specificity of these symptoms to major
depression, however, will require studies that examine
and compare their specific manifestations within differ-
ent diagnostic groups.
Thus, psychomotor symptoms, as judged by clinical
ratings, are among the most frequently occurring symp-
toms associated with the melancholic subtype. They are
infrequently reported by patients not meeting criteria
for major depressive disorder, and unlike other neuro-
vegetative symptoms, they appear to discriminate among
depression subtypes. Evidence suggests that bipolar de-
pressed patients may be more likely to manifest retar-
dation than unipolar depressed patients, while unipolar
patients may be more likely to manifest agitation than
bipolar patients. At the same time, the specificity of re-
tardation and agitation to depressive disorder awaits
further examination.
PROGNOSTIC SIGNIFICANCE OF PSYCHOMOTOR
SYMPTOMS
Of the symptoms associated with depression, psycho-
motor retardation may be the most consistently predic-
tive of good response to tricyclic antidepressants (72).
Overall et al. (73) reported that among 77 psychotically
depressed inpatients subtyped as either anxious, hos-
tile, or motor-retarded, only the motorically disturbed
patients responded to imipramine. Downing and Rick-
els (74) reported that among 95 moderately depressed
outpatients treated with amitriptyline by general prac-
titioners, psychomotor symptoms were predictive of re-
sponse. White and White (75) found that psychomotor
retardation, as well as depressed mood and weight loss
as assessed by the Hamilton Depression Rating Scale,
predicted superior response to tranylcypromine in 58
depressed inpatients.
The results of studies that have objectively measured
specific manifestations of psychomotor symptoms also
lend support for their predictive value. Ranelli and Mil-
ler (76) compared the baseline speech and motor move-
ments of unipolar depressed inpatients, diagnosed ac-
cording to the RDC, who were responders (N=8) and
nonresponders (N=10) to amitriptyline and of a normal
comparison group (N=18). Speech pause time and du-
ration of head aversions were greater in the unipolar
depressed patients who responded to amitriptyline as
compared to the nonresponders and the normal sub-
jects. Depressed nonresponders had increased body
touching and postural changes as compared to the nor-
mal group. Global clinical ratings of agitation and re-
tardation were not examined. However, to the extent
that the objective measures of delayed speech and in-
creased body movement were a manifestation of retar-
dation and agitation, respectively, the results of clinical
rating and objective studies together suggest that mo-
tor-retarded depressed patients may have a superior re-
sponse, and motor-agitated depressed patients may
have an inferior response, to at least some forms of anti-
depressant treatment.
In contrast, the results of studies that examined the
predictive value of motor symptoms in depression with
regard to outcome after ECT have been inconsistent.
Early studies reported strong positive associations be-
tween psychomotor symptoms in the context of melan-
cholic depression and good response to ECT (70, 77).
More recently, Avery and Silverman (55) examined the
response to ECT of depressed inpatients subgrouped
according to the presence of either agitation or retarda-
tion or the absence of motor symptoms. While all of the
patients with motor impairment had a superior re-
sponse to ECT when compared to the patients with no
motor symptoms, the patients with retardation alone
had a slower and poorer response to ECT than the pa-
tients with agitation alone. Strian et al. (78) also re-
ported superior response to ECT in agitated depressed
patients as opposed to retarded depressed patients.
Results from studies comparing real and sham ECT
are inconsistent regarding the prognostic value of psy-
chomotor symptoms in ECT. Brandon et al. (79) in-
itially reported that among 77 depressed inpatients, re-
tardation and/or delusions predicted increased efficacy
of real as opposed to sham ECT. Agitation was not con-
sidered. Buchan et al. (80) combined the reported data
from the Northwick Park study (81, 82) and the Leices-
tershire study (79) and found that the combination of
delusions and retardation led to the greatest response to
ECT. It was concluded that real ECT was not more ef-
fective than simulated treatment for patients without
retardation or delusions. Again, the role of agitation
was not considered. In contrast, O’Leary et al. (83) re-
ported that in a group of 44 depressed inpatients, real
ECT was of greater benefit than sham treatment for all
patients, including those without retardation and delu-
sions. Similarly, in a recent analysis comparing the
treatment response of 148 patients meeting the RDC
and DSM-IV criteria for major depressive disorder (84),
neither agitation, retardation, nor psychosis predicted
superior response to effective versus ineffective forms of
ECT. Thus, there is evidence to suggest that motor re-
tardation may predict superior response, and agitation
may predict poorer response, to some types of anti-
depressant medication, but that the prognostic value of
these symptoms with regard to ECT is uncertain.
POTENTIAL PATHOPHYSIOLOGIC SIGNIFICANCE
OF PSYCHOMOTOR SYMPTOMS
A collection of provocative findings suggest that mo-
tor symptoms in major depression may indicate con-
comitant abnormalities in specific structures and path-
ways of the brain. It has frequently been reported that
CHRISTINA SOBIN AND HAROLD A. SACKEIM
Am J Psychiatry 154:1, January 1997 11
patients with basal ganglia diseases, characterized by
motor dysfunction and dopaminergic abnormalities,
such as Parkinson’s disease (85), supranuclear palsy
(86), Huntington’s disease (87), Meige’s disease (88,
89), Wilson’s disease (90, 91), and basal ganglia calci-
fication (92), manifest high rates of mood disorders.
These findings are not intuitive and have led some
authors to propose that the well-defined neuropathol-
ogy of specific basal ganglia diseases may provide a use-
ful model for investigating the pathophysiology of
mood disorders (93).
The results of other investigations have linked both
behavioral apathy, or “frontal lobe” syndrome, and de-
pression to abnormalities in the structures of the basal
ganglia and in the parallel segregated circuits that con-
nect the basal ganglia to the prefrontal and anterior cin-
gulate cortex (94). For example, a review of case re-
ports of 240 patients with lesions of the caudate,
putamen, and/or globus pallidus (95) revealed that an
apathy syndrome—characterized by the loss of initia-
tive, spontaneous thought, and emotional responsiv-
ity—was the most common behavioral disturbance,
with particular overrepresentation in patients with cau-
date lesions. Dystonia was the most frequent motor
syndrome reported among all of the patients and was
most prominent in patients with lesions of the putamen
and globus pallidus. Starkstein et al. (96) reported that
poststroke mood disorders were more frequent and se-
vere among patients with left-side caudate lesions, as
compared to poststroke patients with right-side caudate
or thalamic lesions. Citing the finding that lesions in the
basal ganglia/anterior cingulate circuit are strongly as-
sociated with the clinical presentation of poststroke
mania, these authors suggested that the functioning of
this pathway may be both negatively influenced by le-
sions of the caudate through which it passes and funda-
mental to the modulation of mood. Similarly, a review
of findings from patients with specific basal ganglia/
thalamo-cortical circuit damage (97) suggested that be-
havioral syndromes unique to each pathway were iden-
tifiable. In particular, while disordered movement was
indicative of lesions in the caudate nucleus, apathy syn-
dromes were linked to lesions of the basal ganglia/ante-
rior cingulate circuit. Finally, Laplane et al. (98) studied
eight patients with bilateral basal ganglia lesions re-
stricted to the area of the lentiform nucleus (putamen
and globus pallidus). PET findings revealed hypo-
metabolism of the lateral prefrontal cortex, the cortical
area innervated by the dorsolateral prefrontal basal
ganglia/thalamo-cortical circuit. More generally, the
parallel, segregated circuits of the basal ganglia, each
with connectivity to distinct brain areas, may explain
the fact that comparable basal ganglia lesions result in
different clinical manifestations, including either motor
symptoms, an apathy or mood syndrome, or both.
Laplane et al. hypothesized that psychiatric disorders
such as major depression may be associated with struc-
tural or functional anomalies of the dorsolateral pre-
frontal basal ganglia circuit.
Brain imaging studies provide supporting evidence
for basal ganglia and basal ganglia/thalamo-cortical
circuit abnormalities in major depression. Magnetic
resonance imaging studies in depressed inpatients have
revealed an increase in basal ganglia lesions among eld-
erly depressed patients (99) and an excess of hyperin-
tensities in the basal ganglia, as well as in deep white
matter regions containing basal ganglia/thalamo-corti-
cal circuit fibers, among both elderly and nonelderly
depressed patients (100–104). Depressed patients have
been found to have decreased volume of the putamen
nuclei (105) and caudate nucleus (106) when compared
to control subjects matched on age and sex. While Ayl-
ward et al. (107) did not replicate these volumetric find-
ings, in their data there was a trend toward reduced
caudate, putamen, and globus pallidus volumes among
female bipolar subjects as compared to female control
subjects.
Functional imaging studies also lend support for ab-
normalities in basal ganglia structures and in brain ar-
eas innervated by basal ganglia/thalamo-cortical pro-
jections in depressed patients. A decreased metabolic
rate in the caudate nucleus (108–111) and a left-side
decrease in caudate blood flow (112) have been re-
ported. Decreased regional cerebral blood flow (CBF)
in the anterior cingulate region (113, 114) and de-
creased glucose metabolism in the left dorsolateral pre-
frontal cortex (113–117) have been reported. Reduced
glucose metabolism in the temporal cortex of depressed
patients (114, 118), an area innervated by the same ba-
sal ganglia/thalamo-cortical loop as that which projects
to the anterior cingulate region, has also been reported.
Surprisingly few studies have attempted to relate
symptom features of major depression—in particular,
motor disturbance—to the patterns of functional defi-
cits. Thus, a link between specific areas of deficit and
symptom expression has not been clearly established.
One exception has been the work of Mayberg et al.
(119). Using single photon emission computed to-
mography, they compared subjects with severe depres-
sion to an age-matched normal group. Decreases in
CBF were found in paralimbic regions, including the
inferior frontal, anterior cingulate, and anterior tempo-
ral cortex. When the associations between psychiatric
symptoms and perfusion were examined, only clinically
rated psychomotor slowing was correlated with perfu-
sion levels, and this occurred in all three regions of hy-
poperfusion. Another exception has been the work of
Bench et al. (120). High scores on a symptom-derived
psychomotor retardation factor were associated with
reduced regional CBF in the left dorsolateral prefrontal
cortex and left angular gyrus. Increased blood flow in
the cingulate cortex and inferior parietal lobe corre-
lated with a psychomotor agitation factor. Similarly,
Liddle et al. (121) found a reduction of regional CBF in
the dorsolateral prefrontal cortex of schizophrenic pa-
tients with psychomotor poverty. Studies of response
selection in the absence of extrinsic information have
suggested that activation of the dorsolateral prefrontal
cortex is associated with intrinsically generated, willful
behavior (122), and it has been proposed that psycho-
PSYCHOMOTOR SYMPTOMS OF DEPRESSION
12 Am J Psychiatry 154:1, January 1997
motor retardation reflects a volitional disturbance com-
mon to both schizophrenia and depression that results
from dorsolateral prefrontal cortex dysfunction (123).
Given that segregated basal ganglia projections inner-
vate the dorsolateral prefrontal cortex, the anterior cin-
gulate region, and the lateral temporal lobe, this propo-
sition is consistent with a theory of depression which
posits that abnormalities in basal ganglia/thalamo-cor-
tical circuitry may underlie some of its clinical manifes-
tations (119).
It is well established that the striatum receives a pri-
mary serotonergic projection from the dorsal raphe nu-
cleus (124). In addition, more than 80% of the dopa-
mine in the brain is produced in the basal ganglia (125).
Thus, despite the fact that psychobiological studies of
depression have focused primarily on noradrenaline
and serotonin abnormalities, it is not surprising that
preclinical studies of atypical antidepressants have
aroused new interest in the complex interdependency
between the serotonergic and dopaminergic systems
(126–128). These studies might also suggest that abnor-
malities of the basal ganglia or basal ganglia/thalamo-
cortical circuitry in some depressed patients indicate
dopaminergic dysfunction modulated by concomitant
serotonergic abnormalities. Several studies have sug-
gested that abnormal dopamine levels occur in some
depressed patients (129). Studies have reported in-
creased CSF dopamine levels in depressed patients as
compared to normal groups (130, 131). It has also been
reported that CSF homovanillic acid (HVA), a dopa-
mine metabolite, is lowered in depressed patients com-
pared to normal groups (132) and, more specifically, in
melancholic as compared to nonmelancholic depressed
patients and a normal group (133). Furthermore, it has
been suggested that the nature of abnormalities in pe-
ripheral catecholamine concentrations may be a func-
tion of symptom features. Decreased HVA levels have
been shown to be associated with increased motor re-
tardation (134), while reduced plasma HVA has been
shown to be related to increased extrapyramidal symp-
toms in a mixed group of patients with Alzheimer’s dis-
ease, Parkinson’s disease, or major depressive disorder
(135). MHPG, a norepinephrine metabolite, has been
reported to have a curvilinear relationship with psycho-
motor retardation and anxiety in depressed patients
(136). Finally, Maes et al. (137) reported that the 24-
hour urinary excretion of norepinephrine, adrenaline,
and dopamine was positively correlated with middle in-
somnia, while MHPG excretion was negatively associ-
ated with somatic anxiety and hypochondriasis. To the
extent that the latter symptoms are associated with psy-
chomotor agitation, these findings may suggest that in-
creased catecholamine turnover contributes to the de-
pressive symptoms of motorically agitated patients. In
contrast, decreased dopamine turnover may be associ-
ated with psychomotor retardation.
Positive findings regarding the catecholamine meta-
bolites have been described here; however, many stud-
ies have failed to replicate these results. In addition, the
metabolite research has been criticized for focusing on
presynaptic and synaptic action, while giving little at-
tention to postsynaptic events (138). Ultimately, the
conclusions that can be drawn from metabolite studies
may be limited. Treatment efficacy studies with de-
pressed patients, however, may offer collateral evidence
of an association between dopaminergic abnormalities
and depressive symptom manifestation. Rampello et al.
(139), testing a dopaminergic hypothesis for retarded
depression, used a double-blind, placebo-controlled de-
sign and found that the clinical improvement in psycho-
motor-retarded depressed patients paralleled the dopa-
minetic specificity of the antidepressants administered,
which included amineptine, minaprine, and clomipra-
mine. Furthermore, double-blind, placebo-controlled
studies examining the antidepressant effects of dopa-
mine agonists, including
L-deprenyl (140), bupropion
(141, 142), and nomifensine (143, 144), have demon-
strated substantial antidepressant effects.
Interpretation of these provocative findings awaits
further research. Results of studies in the 1990s (126–
128) suggest that exclusive focus on either the seroto-
nergic or dopaminergic transmitter system will neces-
sarily lead to incomplete and misleading conclusions.
Furthermore, enhanced delineation and improved as-
sessment of psychomotor symptoms will undoubtedly
strengthen the investigation of their pathophysiologic
significance.
SUMMARY AND CONCLUSIONS
Use of psychomotor symptoms as a focus of research
is specifically consistent with neo-Kraepelinian stand-
ards for the study of psychiatric disorders (145). These
symptoms are objectively observable and are measur-
able with the use of advanced technology that yields
data appropriate for statistical analysis, and substantial
progress has been made in identifying the complex
neuroanatomical pathways and processes that combine
to produce motor acts (146). Depressed patients have
been shown to differ from normal and psychiatric com-
parison groups in gross motor activity, discrete body
movements, speech characteristics, and motor speed.
Studies of psychomotor symptoms have demonstrated
that course of illness, time of day, medication status,
sex, and age are factors that influence the expression of
psychomotor symptoms. Furthermore, it has been sug-
gested that agitation and retardation are not mutually
exclusive and should be measured as independently
varying phenomena. Evidence also suggests that psy-
chomotor symptoms have special diagnostic, prognos-
tic, and possibly pathophysiologic significance.
At the same time, a consideration of these results il-
luminates gaps in our understanding of psychomotor
phenomena in depression. Historical and contempo-
rary descriptions have suggested that motor retardation
and agitation are manifested in multiple motor do-
mains, yet studies that objectively measure psychomo-
tor symptoms tend to focus on only a single manifesta-
tion of agitation or retardation, and diagnostic studies
CHRISTINA SOBIN AND HAROLD A. SACKEIM
Am J Psychiatry 154:1, January 1997 13
have been based primarily on the presence or absence
of single-symptom items. Unidimensional studies can
incorrectly subgroup patients whose motor dysfunction
is not manifested in the measured domain. Clinical rat-
ings can miss patients whose psychomotor manifesta-
tions occur over time (24-hour gross motor activity) or
at a particular time of day (motor reaction time) or are
too subtle to rate reliably (diminished pitch variability
in the speaking voice). Few studies have objectively
measured these multiple manifestations within de-
pressed patients. Thus, we do not know which of these
abnormalities constitute the necessary and sufficient
components of motor retardation or motor agitation in
depression. Determining the extent to which motor be-
havior per se contributes to psychomotor phenomena
in depression will also be essential to the further study
of these symptoms.
As research on the psychomotor symptoms of depres-
sion progresses, many additional issues will inform our
understanding of their nature. For example, very little
is known regarding the course of psychomotor symp-
toms within and across episodes of depression. Few
studies have examined psychomotor symptoms in de-
pression from a developmental perspective, and rates
of motor symptoms in depressed children have not
been reported. Furthermore, while normal aging results
in altered dopamine production and motor system
changes, the interaction of age and depressive illness is
not obvious, as suggested by the increased rates of agi-
tation among elderly depressed persons (55).
Thus, while psychomotor symptoms have been stud-
ied intensively from unidimensional and symptom-
based perspectives, there remains substantial concep-
tual uncertainty regarding the nature of the deficits that
give rise to psychomotor symptoms. The term “psycho-
motor” itself reflects our lack of knowledge regarding
the contribution of component processes that we sus-
pect may be involved (30, 46). Identifying the incidence
of psychomotor symptoms within depressed patients,
in addition to assessing the component processes that
precede and accompany motor disturbance, may yield
the methods necessary for the identification of more ho-
mogeneous subgroups of patients, a fuller interpreta-
tion of past studies of psychomotor manifestations in
depression, and, perhaps, new hypotheses regarding the
pathophysiologic significance of psychomotor symp-
toms in depression.
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