Download Depression Following Spinal Cord Injury

816
REVIEW ARTICLE
Depression Following
Spinal Cord Injury
Timothy R. Elliott, PhD, Robert G. Frank, PhD
ABSTRACT. Elliott TR, Frank RG. Depression following
spinal cord injury. Arch Phys Med Rehabil 1996;77:816-23.
Although depression has been widely studied among persons
with spinal cord injury, the ubiquitous and unsophisticated use
of the term and presumtions about its manifestations in the
rehabilitation setting have needlessly encumbered the understanding and treatment of depression. Major themes and issues
in the study, measurement, and treatment of depression among
persons with spinal cord injury are reviewed. Greater precision
is recommended in distinguishing diagnosable depression from
displays of negative affect, anxiety, distress, and dysphoria.
Correlates of depressive behavior among persons with SC1 are
surveyed, and guidelines for research and practice in the SC1
setting are explicated.
0 1996 by the American Congress of Rehabilitation
Medicine
and the American Academy of Physical Medicine and Rehabilitation
EPRESSION is probably the most frequently studied psyD
chological variable among persons with spinal cord injury
(SCI).’ In the 8 years since Frank and colleagues’ reviewed the
existing literature, 36 additional studies addressing depression
after SC1 have appeared in MEDLINF and 28 studies are cited
in PSYLIT. Despite the addition of 64 studies, many of the
problems identified in the articles cited in 1987 still characterize
the literature on SC1and depression.‘,’ Methodologic issuesthat
continue to constrain the study of depression following SC1
include: (1) unclear or inconsistent use of diagnostic criteria;
(2) use of imprecise and ambiguous definitions of depression;
(3) inaccurate measurement of depression; (4) lack of cogent,
testable theoretical approaches regarding depression after SCI;
(5) failure to integrate models of depression after SC1 with
the extant literature on depression; and (6) a lack of rigorous
longitudinal research on the development, course, resolution,
and treatment of depression among persons with SCI. Researchers in this area have too often conducted work without regard
to history, ignoring substantial findings and commentary in previous research.4,5These recurrent problems have contributed to
a general lack of integration and progress in this area.
In this article, we review the clinical aspects of depression
and briefly describe the historical view of depression in SC1
rehabilitation prior to 1987, then we addressissuesin the definition, measurement, and description of depression, depressive
behavior, and distress following SCI. We survey empirical research to date concerning clinical correlates of depression and
distress among persons with SCI, with particular attention to
From the Department of Rehabilitation
Medicine, University
of Alabama at
Birmingham
(Dr. Elliott) and the College of Health Professions, University
of
Florida, Gainesville (Dr. Frank).
Submitted for publication August 15, 1995. Accepted in revised form January
2, 1996.
No commercial party having a direct financial interest in the subject matter of
this article has or will confer a benefit upon the authors or upon any organization
with which the authors are associated.
Reprint requests to Timothy Elliott, PhD, Department of Rehabilitation Medicine, Spain Rehabilitation
Center, 1717 Sixth Avenue South, Birmingham,
AL
35233.7330.
0 I996 by the American Congress of Rehabilitation Medicine and the American
Academy of Physical Medicine and Rehabilitation
0003-9993/96/7708-3836$3.00/O
Arch
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personal, environmental, and psychophysiological factors. Finally, we summarize the major unresolved issues concerning
measurement and treatment of depression after SC1and provide
specific recommendations for future research.
CLINICAL
ASPECTS OF DEPRESSION:
AN OVERVIEW
Depressed mood or affect refers to a state of dysphoria that
occurs routinely and is a normal process. Depressed mood accompanied by persistent and pervasive loss of emotional
involvement with other people, objects, or activities distinguishes a normal mood state of sadness, demoralization, or
other negative affects such as anxiety from the syndrome of
depression. A diagnosable depressive syndrome refers to a constellation of observable symptoms that may encompass tearfulness, apathy, irritability, loss of appetite, disturbed sleep, lack
of energy, death thoughts, etc, in addition to depressed mood.
For an individual, a depressive syndrome is recognized when
the behavioral characteristics deviate from the norm in several
realms of functioning. Depressive disorders are categorized according to specific criteria constituting psychiatric diagnoses in
Diagnostic and Statistical Manual of Mental Disorders (DSMIV) ?
In general, the incidence of depressive disorders is increasing
(see Fombonne7 for a comprehensive review). Several studies
of families have shown increased incidence of new-onset depressive disorders in the youngest cohort (younger than 40
years) who had rates 3 times as high as the oldest cohort.’ At
any age the youngest birth cohorts completing a period at risk
have higher rates of disorders than the older cohorts and have
progressively earlier age of onset.8 Surprisingly, the lifetime
rate of any depressive disorder declines with age, with lower
rates found among elderly people.’ Although most evidence
continues to suggest that women have twice the risk of a depressive disorder, among the younger cohorts the gap between
the two genders may be diminishing.8
Depression is a disabling syndrome. Hays and associates’
recently found that depressed individuals were less able to perform activities of daily living than patients with chronic medical
conditions such as diabetes and arthritis. After 2 years, patients
with dysthymia were significantly more limited in physical and
role functioning than patients with hypertension despite significant deterioration of functioning for the hypertensive patients
relative to their baseline.’ Outcome data indicate that individuals
who recover from depressive episodes tend to be employed,
have a lower intake of alcohol, use active coping strategies, and
have higher levels of physical activity and social support in
comparison with persons who do not recover over time.’
Depression is a major public health problem associatedwith
excessive mortality and morbidity.” Impairment and disability
associated with depression is equal to that attributed to cardiovascular disease, and greater than that caused by other chronic
physical disorders such as hypertension, diabetes mellitus, and
arthritis.’ ’ Although 6% to 10% of medical patients have Major
Depressive Disorder, depression is often undetected and untreated among these persons.’ ’
The advances in the pharmacotherapy of affective disorders
over the last four decades have helped illuminate the psychobiology of depressive disorders. Beginning in the 1950s tricyclic
DEPRESSION
FOLLOWING
antidepressants (TCAs) replaced monoamine oxidase inhibitors
(MAOs) as the treatment of choice for unipolar depression.
TCAs have a relatively high affinity for muscarinic, histaminergic, and adrenergic receptors causing the side effects and toxicity associated with this class of drugs. In 1987, the new selective
serotonin reuptake inhibitors (SSRIs) were introduced. More
recently, dual action serotonin-norepinephrine
reuptake inhibitors have been introduced. These two classes of drugs have
supplanted TCAs. Adoption of SSRIs reflects their improved
ease of administration
and the reduced side effects experienced
by patients using the drugs. Despite these advantages, as many
as 30% to 40% of patients fail to respond satisfactorily to an
adequate trial of SSRIs and a significant number of patients fail
to achieve long-term remission.
The development of antidepressant medications has underscored the role of neurotransmitters
in the pathophysiology
of
depression. It is now well accepted that serotonin (5HT) neuronal systems are involved in many episodes of depression. It
is unlikely, however, that only a single neurotransmitter
system
underlies the neurochemical basis of all depressions. Other neurotransmitters systems likely to be involved in the pathogenesis
of depression include norepinephrine
(NE), dopamine, and a
variety of neuropeptides, most prominently corticotropin-releasing factor (CRF).”
More than 75 neurotransmitters
have been identified to date.
Two of the identified transmitters, NE and 5HT, are especially
important in the pathogenesis of depression.‘3 NE is a catecholamine neurotransmitter
synthesized from l-tyrosine, while 5HT
is an indoleamine synthesized from I-tryptophan. Both of these
amino acids are derived from dietary sources, although tyrosine
can be synthesized from phenylalanine in vivo. Norepinephrine
is inactivated by the degradative enzymes monoamine oxidase
(MAO) and catechol-0-methyltransferase
(COMT), whereas
5HT is inactivated only by MAO. After neurotransmitter release
from the presynaptic terminal, 5HT and NE are taken into the
presynaptic terminal and recycled into storage vesicles or are
degraded by MAO in the nerve terminal. Reuptake is the principle mechanism for terminating noradrenergic
and serotonergic
transmission. Enzymatic degradation provides a secondary route
for inactivation.
DEPRESSION
AND SCI: A HISTORICAL
BACKDROP
Before 1987, much of the work concerning depression after
SC1 was embedded in nonempirical
models preoccupied with
a direct relationship between the SC1 and psychological adjustment. Individual and environmental characteristics of the patient
were largely ignored; presumed mechanisms that drive human
behavior were generally disregarded or deemed superfluous.
The presence of SC1 was essentially considered the most salient,
distinguishing
feature-and
the most powerful predictor-of
the individual’s
subsequent behavior and experience. Classically defined stage models-derived
loosely from psychoanalytic conceptions of loss-posited
that a person with recentonset SC1 should be expected to pass through several stages of
psychological
adjustment. A depressive phase was to be expected-if
not encouraged-and
the experience of depression
was basically construed as a therapeutic prerequisite for optimal
adjustment. In contrast, the absence of depression was arguably
maladaptive and indicative of an unhealthy denial of the concomitants and finality of the injury (for a synopsis of these, see
our earlier reviews*,“).
To a great extent, these assumptions may have been influenced by the stereotypical expectation that people with SC1
are consumed with the trauma of physical disability.14 Such
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Elliott
assumptions could also reflect gross extrapolations
from personal experience with distressed patients in rehabilitation
units,
or reckless generalizations from studies with small sample sizes
and inadequate measures. Consequently,
the association between depression and SC1 was rarely questioned in the rehabilitation clinic prior to 1987.
Nevertheless, our earlier critiques melded a disjointed yet
developing empirical literature that converged to contradict the
basic tenets of stage of model mentality. In sum, these databased studies systematically demonstrated a lack of objective,
empirical support for stage models in our understanding of psychological adjustment following SCI. We found the empirical
evidence warranted a greater clinical and theoretical appreciation of the individual differences, environmental characteristics,
and physiological
parameters associated with depression in this
population.
DEFINING
AND
ASSESSING
DEPRESSION
IN SC1
REHABILITATION
A major depressive episode is categorized as one of four
different types of mood disorder. A diagnosis of Major Depressive Disorder must involve either the presence of a depressed mood or loss of pleasure or interest over a 2-week span
and at least five of the following
symptoms “...most of the
day, nearly every day” within the same time frame: significant
weight loss or gain, decreased or increased appetite, insomnia
or hypersomnia, psychomotor agitation or retardation, fatigue
or energy loss, feelings of worthlessness, excessive or inappropriate guilt, diminished ability to think or concentrate, indecisiveness, and recurrent thoughts of death or suicide. These
symptoms must also cause significant impairment
in social,
occupational, or other roles; they must not be due to a “general
medical condition”
(eg, hyperthyroidism),
bereavement, or the
physiological
effects of a mood-altering
substance.’
Despite the refinements in diagnosis and understanding of
depression, clinical practice in the rehabilitation
of individuals
with SC1 and depression has been historically guided by anecdotal and impressionistic notions of “depression.”
Rehabilitation professionals are particularly
reactive to displays of depressed mood and dysphoria.‘5,‘6 Nevertheless, depressed mood
alone does not warrant a diagnosis of Major Depressive Disorder; it may only represent a transient experience of negative
affect in reaction to a wide array of personal or environmental
circumstances, of which SC1 might be but one. As such, this
behavior might reflect symptomology
subsumed under other
diagnoses. For example, when fewer than five symptoms are
observed, the appropriate diagnosis might be Depressive Disorder Not Otherwise Specified (eg, Minor Depressive Disorder).7
The presence of a downcast mood and corresponding behaviors
within 3 months of injury onset might be best described as an
Adjustment Disorder with Depressed Mood, if other criteria
for Major Depressive Disorder or Dysthymic Disorder are not
satisfied.
Studies relying on DSM-III criteria using relatively small
samples of recently injured individuals and stringent interview
systems have found that the rate of major depressive episodes
among persons with SC1 ranges from 22.7%” to over 30%.“.”
Lower rates have been observed in studies utilizing less stringent interview methods (13.7%; total sample N = 227),*” and
with self-report measures based on DSM-IIIR criteria with a
sample varying considerably in time since injury onset (1 1%).2’
Recent data suggest that many among newly injured persons
who have diagnosed problems with Major and Minor Depressive Disorders may remit within 3 months of injury onset,
but these studies have yet to be replicated.‘2,‘3
These findings have several implications.
First, depressive
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DEPRESSION
FOLLOWING
syndromes, as defined by standardized psychiatric criteria, are
not universal and inevitable sequelae after SCI. This appears to
be true among newly injured and community residing persons.
Yet a significant minority of persons with SC1 do meet criteria
for a major depressive episode at some point following the
injury. Examination of the extant literature does not clarify if
a higher rate of depressive syndromes occurs in the immediate
period after SCI, or if this rate diminishes among those who
have been injured for longer periods of time.
It is unclear if the differences in depression frequency are a
function of the different diagnostic and interview systems or
possible differences between samples. It may be possible that
structured and semistructured interview methods are more sensitive to the salient and multifaceted features of depression and
have greater specificity in diagnosing depression. Unfortunately, interview systems can be clinically cumbersome and
time consuming. Many rehabilitation clinicians apparently rely
on unstructured interview methods in their assessment practicesz4
In contrast, much of the extant literature utilizes self-report
measures of depression. Most of these instruments do not measure depression according to standardized criteria for diagnostic
disorders; rather, these instruments provide an index of the relative intensity of certain behaviors that often accompany a depressive episode. Several of these measures have cutoff scores
or algorithms that suggest clinical severity resembling a depressive syndrome. Self-report measures are convenient, easily
adapted, and easily administered to persons with mobility impairments. The most popular self-report measures are fairly
reliable and valid. Measures commonly used in the current literature include the Beck Depression Inventory,25 the Zung SelfRating Depression Scale,26 the Center for Epidemiological
Studies Depression Scale,27and the Inventory to Diagnose Depression.*’ Although these instruments are suitable for use in
research and practice with persons who have physical disability,’ the use of self-report measures of depression calls attention
to two major issuesin defining and assessingdepression following SCI.
What
To Do With
Vegetative
Symptoms?
Acute SC1 is typically marked by weight loss, disruptions in
appetite, sleep cycles, physical sensations, energy levels, and
mobility problems. These symptoms are also symptomatic of
depressive conditions.2329This overlap has prompted some to
advocate for revision of diagnostic criteria and self-report items
that are confounded by the physical sequelae of acute SCI?
Sleep disturbance, disruptions in weight and appetite, and
dramatic fluctuations in energy level and activity have been
found to reflect the severity of the mood disturbance in everyday
life. Research to date has not clarified symptom differences for
persons with recent-onset SC1and others who have been injured
for many years. If SC1 affects vegetative/somatic symptoms
that parallel depression, items assessingthese symptoms should
be elevated among newly injured individuals. Available research indicates that vegetative/somatic symptoms are not inflated on self-report depression measures among persons with
general medical conditions.“’ Despite longstanding concern that
vegetative and somatic items taint the diagnosis of depression,
a series of studies has found that vegetative/somatic items may
be less of a confound in the diagnosis of depression among
persons with SC1 than often suspected. It now appears that
dysphoria-represented by symptoms of negative self-evaluations, depressedmood, and suicidal ideation-constitutes a core
element of depression common to persons with SCI, individuals
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with rheumatoid arthritis, college students, and community-residing adults.*’ Symptoms uniquely predictive of Major Depressive Disorder for persons with SC1 include psychomotor
disturbance, appetite change, and sleep disturbance.29
Deleting items that assesssleep disturbance may deprive a
clinician of potentially valuable information. Sleep disturbance
may reflect a sleep cycle disrupted by initial trauma, medical
intervention, or transitions from intensive care units to the rehabilitation center. Such disruptions can adversely affect patient
mood, motivation, and cognition.” Despite systematic research
demonstrating the efficacy of behavioral interventions for insomnia among medical patients generally,” this work has not
yet been extended to the rehabilitation setting.
The clinical interpretation and recognition of vegetative/somatic symptoms varies between patients. Many patients recognize these symptoms are normal reactions to the trauma and
sudden changes in physical functioning and may in turn experience less overall distress.” Interpretation of vegetative symptoms has been correlated with general cognitive style. For example, individuals with adaptive reality negotiation strategies may
experience less distress by refusing to acknowledge certain aspects of their injury until they can find appropriate goals to
pursue.” In contrast, those persons who lack goal-directed energy are more likely to acknowledge somatic symptoms and
demonstrate elevated levels of distress regardless of the time
since the onset of injury. Clearly, it is important to understand
how the patient recognizes, understands, interprets, and experiences vegetative/somatic symptoms.
Although somatic criteria for depression may bias the prevalence of estimates of depression among patients with chronic
physical conditions, correlations between depression scoresand
other psychological variables are not likely to be affected.“’
Reidy and Caplan,” for example, found self-blame for the incident culminating in SC1 significantly correlated with the cognitive/affective and the total score of the Beck Depression Inventory (which contained the vegetative/somatic items).*’ When
evaluating mood after catastrophic injury, it is important for
clinicians to examine reported problems from the patient’s perspective. Systematic evaluations of the separatedomains of cognitive (low self-worth, hopelessness),affective (sad mood, loss
of pleasure, irritability), and somatic (sleep disturbance, appetite
disruption) symptoms are vital for planning effective interventions in SC1rehabilitation. Cognitive aspects of depression are
typically less amenable to pharmacological strategies and warrant psychological interventions. Sleep disturbance in the period
following injury may be treated with psychopharmacological
agents, then with behavioral strategies.
The use of self-report depression scaleshas been common in
rehabilitation settings. As has been described, these scales reflect a confluence of variables which may affect their reliability.
Clinicians must scrutinize symptom patterns on any depression
measure and rely less on any total score. Studies that examine
separate symptom patterns and their relation to other variables
will undoubtedly expand our understanding of this general issue.
Diagnosable
Distress
Depression,
Depressive
Behavior,
and
The basic assumptions guiding the use of self-report depression measures in SC1 rehabilitation need to be examined. Too
often data from these scales are considered synonymous with
diagnosable
depression,
ie, depression defined and diagnosed
according to existing nosological criteria (eg, DSM-IV).
Thoughtful researchersand clinicians have recently pointed out
the many flaws that negate this assumption.
Self-report depression measures are susceptible to a host of
DEPRESSION
FOLLOWING
negative affects including transitory distress in reaction to stress
and life events, mood changes attributable to alcohol or drug
use, or displays of anxiety, tension, or fear.36-‘8 A total score
on a self-report depression measure may reflect a “...summary
of feelings, symptoms, and attitudes” tangentially
related to
diagnosable depression.i6 Furthermore,
practically all self-report measures lack adequate time parameters and referents to
determine duration necessary to diagnose depression, and they
inadequately sample salient features crucial to a diagnosis.“6-‘8
Self-report
depression instruments
are best construed as
measures of distress, unhappiness, dysphoria, or depressive behavior.‘6-‘8 Of these terms, distress and depressive behavior
describe with greater accuracy what is being measured by selfreport measures. Scores on the Beck Depression Inventory, for
example, can reflect a cluster of behaviors that might be associated with diagnosable depression or another condition, such as
an anxiety disorder.”
The term dysphoric is somewhat misleading because it implies a sense of sadness, hopelessness, or
helplessness; a high score can be attained on any self-report
depression measure without endorsement of any of these symptoms.‘* Unfortunately,
many who are aware of the distinctions
between diagnosable depression and scores from a self-report
instrument still lapse into “depression”
terminology.‘9
This
regrettable imprecision
limits clinical and theoretical understanding of depression and distress in rehabilitation
and in the
larger scientific community.‘6 In this article, we distinguish between studies that address depression as a diagnosable condition, and those using a self-report measure as a proxy of depression. In this way, the measurement of depressive behavior or
distress will be differentiated
from a diagnosable depression
syndrome.
CLINICAL CORRELATES OF DEPRESSIVE
BEHAVIOR AND DISTRESS AFTER SC1
Empirical studies have supplied information that contradicts
stage-model anecdotes about depression that extol1 the beneficial properties of “depression”
soon after injury onset.“’ In
contrast to these models, depressive behavior has been associated with increased hospital stays and fewer functional improvements in SC1 rehabilitation:’
Patients who exhibit more depressive behavior tend to expect a longer hospitalization
and
in turn evidence lower levels of functional independence and
mobility at discharge than those without these problems.42 In
comparison, those with the highest expectancies for recovery
of functional abilities report less depressive behavior and subsequently demonstrate a greater change in activities of daily living
after rehabilitation.4’
Cross-sectional research has also painted an equally dismal
view of depressive behavior among those injured for longer
periods of time. Depressive behavior has been associated with
the occurrence of secondary complications
(eg, pressure sores,
urinary tract infections),44 and poor self-assessed health status.45
Depressive behavior is a powerful predictor of decreased spare
time activities.46 Community-residing
adults with SC1 who report problems with depressive symptoms also demonstrate decreased mobility, poor social integration, and a dearth of meaningful social pursuits, generally.47,48 In the most extensive
documentation to date, Tate and coworkers’” found that persons
with higher self-report depression scores spent more days in
bed, fewer days outside the home, and had greater use of paid
personal care attendants and greater general medical expenses
than those with lower levels of depression.
These studies suggest that depressive behavior does not appear to signal “acceptance”
of disability. Depressive behavior
has been consistently associated with an array of psychosocial
and medical complications. These complications occur at high
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SCI, Elliott
cost to the person, the rehabilitation
nity,
program,
and the commu-
THEORETICAL EXPLANATIONS OF DEPRESSION
AND DISTRESS AFTER SC1
The findings concerning the correlates of depressive behaviors do not clarify why some individuals develop problems with
depression and distress. In the study of behavioral disorders, of
which depression is but one, there is a tendency to develop
explanatory models that are unique to a given population but
divorced from contemporary perspectives of behavior and behavioral disorders. For example, impressionistic
stage models
have historically guided clinical judgements in absence of cogent, testable, theoretical frameworks. The weaknesses of these
impressionistic
models have been addressed in earlier reviews.2,4 Elliott” argued that theoretical explanations of behavioral phenomena in general apply to individuals with SCI, theoretical models are ultimately superior to others in guiding
interventions, and theoretical explanations provide potentially
testable hypotheses necessary to advance science.” Ideally, contemporary theories of adjustment to physical disability take into
account the interactive effects of disability parameters, psychosocial stressors, and person/environment
factors that culminate in the prediction of depression and other aspects of adaptation.5’
A biopsychosocial perspective appears to be the most relevant
model of adjustment after SCI.’ From this perspective, unique
features of the individual, the environment, and the spinal cord
injury-its
physical concomitants and other medical conditions-are
taken into consideration to understand a given behavior. Accumulating
evidence has supported such a view at
each separate domain.
Personal Factors
Some individuals are more likely to exhibit depressive behavior following SC1 than others for a variety of reasons. Individuals with preinjury histories of social maladjustment, psychological disorders, and alcohol/substance
abuse have particular
difficulties adjusting to SCI, and depressive behavior is often
manifested in these cases.52.53These data imply that individuals
who have exhibited difficulties coping with the general demands
of life will have greater difficulty coping after SCI. It logically
follows that those with greater personal resources and those
who have demonstrated an optimal level of adjustment before
injury would be less likely to display depressive behaviors after
SCI. Although this latter hypothesis has not been tested directly,
several cross-sectional
studies lend indirect support. Self-appraised skills in solving everyday problems are inversely related
to depressive behavior among people in general.54 Elliott and
colleagues”
found effective skills in solving problems and a
greater confidence in problem solving were significantly associated with lower scores on a self-report depression measure
among persons with SCI, and this relationship was not mediated
by time since injury onset. This study suggests that those with
planful, goal-directed strategies may be less likely to have problems with depression and distress. It has also been found that
depressive behavior after SC1 is associated with a heightened
and haphazard use of many situation-specific
coping efforts.56
Those who maintained internal expectancies for control over
reinforcers and outcomes for their behavior were less distressed,
however. Other studies indicate that higher levels of hope and
goal-directed energy are associated with less distress, regardless
of time since injury onset.3’ Social-cognitive
characteristics
such as problem solving, hope, and locus of control are particularly valuable to clinicians; these variables are embedded in a
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FOLLOWING
learning tradition and are thus theoretically amenable to psychological interventions in the medical setting.57
Environmental
Factors
Several studies have documented that a lack of social support
is associated with depressive behavior.58,59Unfortunately, the
mechanisms by which social support is enhanced or eroded after
SC1 are not well understood. It is possible, for example, that
chronic strain following SC1 has a deteriorating effect on the
quality of intimate relationships (ie, the deterioration hypothesis).60Preliminary research indicates that many family caregivers of persons with SC1 encounter difficulties in helping with
activities of daily living, personal hygiene, and self-care regimens!’ Other data indicate that unique characteristics of the
person with SC1 might moderate the effectiveness of social
support. Those with more assertive mannerisms might be able
to marshal1 available social support in certain situations; others
may actually alienate otherwise supportive relationships.62
A series of laboratory studies suggest that displays of depressive behavior can have aversive ramifications for a person
with SCI. Persons appearing to have SC1 and who emit depressed mood and dysfunctional cognition elicit greater rejection, interpersonal avoidance, and stereotypic attitudes toward
persons with physical disability. 61,64Rehabilitation staff members feel greater hostility and decline interaction with a person
with SC1 who acts in a depressed fashion’$ persons with SC1
are also inclined to reject and devalue a depressed peer.65Conversely, persons with SC1 who are not depressed and who display socially appropriate behaviors engender more positive attitudes and cognitions.6’@ Interpersonal displays of depressive
behavior might contribute to subsequent social isolation and
strains on intimate relationships, and culminate in chronic problems with depression.@
Person and environment variables can also interact with deleterious effects. Frank and Elliott67 found persons with SC1 differed considerably in their recent experience of major life
events. Participants who reported a higher level of life stress
from such events as death of a loved one, death of a close
friend, loss of finances, etc, reported more depressive behavior
than other patients regardless of time since injury onset. Other
data have confirmed that the subjective perception of stressand
setbacks are related to patient distress.68The need to consider
phenomenological stressors other than the SC1 is crucial in
appreciating the nature of depressive behavior in SC1rehabilitation.
Psychoimmunological
and Physiological
Factors
Many attempts have been made to explain possible psychophysiological consequences of SC1 that may moderate depression after SCI. For example, it has long been assumed that
persons with SC1have a decreased ability to experience intense
emotions, presumably due to “physiological suppression” that
diminishes the physical experience of emotion.“z.68Contemporary research has not supported this position. Chwalisz and
colleagues69found that persons with SC1reported many intense
experiences of emotion regardless of their level of autonomic
feedback. Their ratings of positive and negative emotions were
basically equivocal to those culled from a group of participants
with other physical disabilities and a group with no physical
conditions. These researchers concluded that autonomic and
visceral feedback was not crucial for the experience of emotion
after SCI, and noted that cognitive arousal theories may hold
more promise for understanding emotion after SCI.
Palmer7’ reasoned that presumed disruptions in adrenocortical functions following SC1 could affect the experience of depression among these patients. Biochemical indicators like the
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dexamethasone suppression test (DST) were recommended for
clinical trials. Yet Frank and coworkers’* found the DST was
not a sensitive indicator of depression among 32 patients with
SCI. DST results were unrelated to level of lesion or time since
injury. These authors speculated that continued study of the
hypothalamic-pituitary-adrenal axis might eventually elucidate
our understanding of depression following SCI. Few have attended to these issues; efforts to continue this line of inquiry
have failed to establish a relationship between patient depressive
behavior and circulating plasma levels of beta-endorphin and
cortisol.”
Recent developments in the psychopharmacology of depressivedisorders have received scantattention in the SC1literature. The SSRIs were the first classof drugs developed to target
the 5HT reuptake carrier. These drugs have few if any effects
on histaminergic, muscarinic, and (Y,-adrenergic receptors and
sodium fast channels, thereby avoiding the side effects that
plague use of TCAs (eg, sedation anticholingeric affects, orthostatic hypotension and cardiotoxicity).” These side effects
are especially problematic for persons with SCI. Because of
these favorable side effects profiles, SSRIs have replaced TSAs
as the drug of choice in the treatment of major depression.
Indeed, clinical anecdotes suggest that these drugs have gained
popularity in the treatment of depression associated with SCI,
although there does not appear to be any clinical outcome research to verify this assumption. Despite advances associated
with the introduction of SSRIs, drugs that act on 5HT and other
transporters may be even more advantageous in the treatment
of depression. These dual action serotonin-norepinephrine reuptake inhibitors include venlafaxine, duloxetine, and milnacripran. Venlafaxine is a unique inhibitor of both 5HT and NE
reuptake. This class of drugs retains the safety profile of the
SSRIs while possibly offering more antidepressant advocacy
including increased onset of action and dosage flexibility. Unfortunately, the lack of applicable research in SC1rehabilitation
limits our understanding of the relation of these neurotransmitters to the occurrence of diagnosable depression among persons
with SCI.
Other lines of research have expanded into areas that were
previously ignored before our 1987 articles. Initial evidence
indicates that neuropsychological concomitants sustained in
trauma that resulted in SC1 are unrelated to self-report depression scores.73However, patients who report a persistent experience of pain exhibit more depressive behavior than those who
report no pain.74,75Complaints of pain among newly injured
patients can be a significant predictor of distress 2 years after
injury onset.76Chronic pain following SC1 is not well understood, but it is clearly emerging as a major correlate of wellbeing and adjustment that will likely require an array of intervention strategies.77
SUMMARY
Despite frequent discussion in the literature, little effort has
been directed toward systematically assessingtreatment of depression and distress associated with spinal cord injury. In a
recent review of the literature, no documented study of the
treatment of depression or distress following SC1 with either
behavioral or psychopharmacological strategies was found. The
outcome researchthat has been conducted has generally focused
on skill-building (eg, assertion training)78 or well-being (eg,
acceptance of disability).79In light of our knowledge about the
detrimental concomitants of depressivebehavior following SCI,
it is imperative that the next wave of research focus on the
prevention and treatment of depression and distressamong these
patients.
DEPRESSION
FOLLOWING
In order to conduct this work, it is important to test assumptions gleaned from clinical practice and available theory. For
example, do antidepressants that regulate the sleep cycle prove
more efficacious in the treatment of diagnosable depression
among acute injuries in SC1 rehabilitation? Do these agents
have a therapeutic effect on subclinical displays of dysphoria
and distress? Are these agents ably supplemented or replaced
by behavioral strategies designed to develop adaptive sleep habits? Are other agents more efficacious among outpatients who
have been injured for longer periods of time and who might have
more recurrent, chronic problems with dysfunctional moods and
cognition? Are these patients better served by interventions that
attempt to improve interactions with the environment in terms
of relationships, meaningful leisure activities, or other pursuits
that might heighten a sense of competence?”
From a behavioral standpoint, it is important to know if cognitive-behavioral strategies (eg, problem solving training)8’ are
helpful in preventing and alleviating depressive behavior among
persons with recent-onset SCI. Are psychoeducational and support groups equally effective in working with family members
and identified caregivers during acute SC1 rehabilitation? Do
group approaches offer the most efficacious format for treating
depression and distress after SCI? Available evidence conceming the social aspects of depressive behavior imply that strategies that reconstruct and promote a therapeutic milieu might be
a potent agent of change for these persons.78-80It seems that
coping strategies and cognitive beliefs vary in effectiveness at
different times following SCI1’,“; it may be necessaryto train
patients with a more flexible repertoire of available strategies.
We need to clarify relations between depression and other
variables crucial to quality of life and potentially amenable to
therapeutic interventions. For example, we have only a cursory
understanding of hopelessnessand suicidal ideation among persons with SCI.8”,84Similarly, little is known about anxiety disorders and social phobias in this area. The mechanisms by which
dysphoria and distress exert a detrimental influence on health
status, secondary complications, immune functioning, and intimate relationships over time have not been explicated.
The development and treatment of depression and distress
among children and adolescents who acquire SC1 is also poorly
understood.” It is probable that family dynamics are salient in
this particular arena; unfortunately, researchers have neglected
this challenging area of inquiry. SC1 might increase an overall
vulnerability to life’s routine stressesand strains. Families that
have more adaptive and expansive strategies in coping with
stressmight be more adaptive following pediatric SCI, resulting
in a more optimal outcome for the child. In this scenario, it
seems more profitable to study family, rather than individual,
reactions to SCI, taking into account family dynamics, division
of tasks, and the experience of strain and stresson the system.
Despite several interesting studies,‘8*7o,7’
little is known about
alterations in the hypothalamic-pituitary-adrenal axis after SCI.
Changes in neuroendocrine function after SC1 warrant further
investigation. The new classesof SSRIs offer a method of elucidating the action of receptors after SCI. Along the same line
symptomatic assessmentof efficacy of SSRIs in the treatment
of major depression after SC1 is justified.
Measures that cull from the patient’s perspective and that of
a significant other are definitely preferred over staff ratings,
which are undoubtedly contaminated by staff issues about adjustment following SCI. Studies that insist on examing presumed symptom patterns piecemeal may be more convenient
academically and clinically. Intervention studies and investigations of the mechanisms of depression and distress on daily
function and the treatment of these problems are ultimately
more demanding, worthwhile, and deserving of high priority
821
SCI, Elliott
from funding agencies. Research of this nature is of greater
potential value at this juncture.
Specific
Recommendations
for Research
and Practice
It is important that rehabilitation professionals dispense with
pseudodiagnostic language and use precise descriptions of behavior.86 Research participants and patients who fail to meet
diagnostic standards for depression may be best described as
distressed; dysphoric may be the best available adjective to
describe those who emit downcast or sad mood, hopelessness,
or helplessnessin absence of other symptomology necessary
for diagnosis. Practitioners should carefully consider the presence of behaviors characteristic of anxiety (eg, worry, dread,
tension) that might differentiate the clinical picture from a diagnosable depression.
It is time for us to establish standards for the measurement
of depression in SC1 research congruent with contemporary
diagnostic criteria and nomenclature. If diagnosable depression
is to be the focus of inquiry, then studies at a minimum should
(1) articulate clear diagnostic parameters (2) by established and
accepted criteria (3) using standard interview systems. Furthermore, (4) evidence of interrater reliability should be provided
and (5) efforts should be conducted to differentiate depression
from other conditions (eg, generalized anxiety disorder) and
rule out mood-related changes attributable to drug or alcohol
use, or to the general medical condition. Makeshift or “homegrown” interview systemsare fundamentally inadequate to this
task, popular systems such as the SCID” or the DISs8 are preferred.
Self-report depression measures should be used with certain
caveats. In clinical practice, clinicians should take care to describe endorsed items that approximate depressive symptomatology and those that could be associatedwith other syndromes
(eg, sleep disturbance, worry, restlessness,irritability, anxiety).
Patients should not be categorized as depressed on the basis of
self-report measures alone. If a self-report measure of depression is to be used to classify participants for study, then researchers should comply with recommended procedures and
corresponding terminology to prevent erroneous and misleading
interpretations. For example, if the Beck Depression Inventory
is to be used to classify participants the recommendations from
Kendall and colleagues”’ should be employed. Interested researchers should also consider the Inventory to Diagnose Depression. This scale provides information essential for the diagnosis of major depression and dysthymia, and it has been
used successfully in recent studies of depression following
scI.2’,29 This instrument can also be administered as a semistructured interview. ’
Research projects that examine the predicted relation of a
theoretically derived variable to self-report depression measures
can be enlightening.89 However, the report should not lapse into
language reserved for a diagnosable depression condition, and
the explicit focus and language of the study should be confined
to the distress and/or depressive behavior.‘” It is important that
we identify precursors of distress, anxiety, and depression to
guide prevention and intervention strategies. Whenever possible, it would be advantageous to include measuresof trait negative affectivity, trait anxiety, or neuroticism to examine and
partial out the confounding effects of these variables on depressive behavior.
Critics of the depression literature have lamented the overreliante on samples of convenience (eg, college students) and from
the mental health clinic.” Results from these studies do not
readily generalize to the community in general, nor do they
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822
DEPRESSION
FOLLOWING
accurately capture the nature of depression observed in the medical setting. In our opinion, the SC1 rehabilitation
setting provides a fertile laboratory for studying the course, correlates, and
treatment of depression in a rigorous yet stimulating environment. Increasing our precision and sophistication in the study
and treatment of depression following
SC1 could potentially
enrich our understanding of this disorder in other contexts.
22.
23.
24.
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