A Preliminary Model for Posttraumatic Brain Injury Depression

1087

ORIGINAL ARTICLE

A Preliminary Model for Posttraumatic Brain Injury Depression James F. Malec, PhD, ABPP-Cn, Rp, Allen W. Brown, MD, Anne M. Moessner, RN, MSN, CRRN, Timothy E. Stump, MA, Patrick Monahan, PhD ABSTRACT. Malec JF, Brown AW, Moessner AM, Stump TE, Monahan P. A preliminary model for posttraumatic brain injury depression. Arch Phys Med Rehabil 2010;91:1087-97. Objective: To develop, based on previous research, and evaluate a model for depression after traumatic brain injury (TBI). Design: Cross-sectional structural equation modeling (SEM) of data from consecutively recruited patients. Setting: Acute hospital and inpatient rehabilitation units. Participants: Adult patients (N⫽158) after hospital admission for moderate to severe TBI. Interventions: Not applicable. Main Outcome Measures: External appraisal of ability in participants was measured by the Mayo-Portland Adaptability Inventory (MPAI-4) Ability Index completed by a TBI clinical nurse specialist. Patient self-appraisal of post-TBI ability and depression were measured by the Awareness Questionnaire and Beck Depression Inventory-II. Functional outcome 1 year after injury was assessed with the MPAI-4 Participation Index. Results: Successive SEM resulted in a parsimonious model with excellent fit. Consistent with prior research, a moderately strong association between self-appraisal of post-TBI ability and depression was found. Injury severity, as measured by the duration of posttraumatic amnesia (PTA), was not significantly associated with post-TBI depression. The 1-year functional outcome was associated with depression and TBI severity. Conclusions: The strong association between self-appraisal of post-TBI ability and depression is consistent with the cognitive-behavioral model of depression and recommends consideration and further study of cognitive-behavioral therapy for post-TBI depression. The lack of association between TBI severity and depression may represent the indirect and proxy nature of current measures of TBI severity such as PTA. Emerging neuroimaging techniques (eg, diffusion tensor imaging, magnetic resonance imaging spec-

troscopy) may provide the more direct measures of disruption of brain function after TBI that are needed to advance this line of research. Key Words: Brain injuries; Depression; Rehabilitation. © 2010 by the American Congress of Rehabilitation Medicine EPRESSION IS ESTIMATED to affect the majority of D people who sustain moderate to severe TBI. Previous have shown that post-TBI depression has a negastudies 1-5

2,6-13

tive effect on long-term functional outcome and community participation. Among a relatively comprehensive array of major personality features, depression alone contributed to the prediction of outcome 1 to 2 years after injury in a consecutive series of patients admitted to the hospital after TBI.14,15 The mechanisms of post-TBI depression are not well understood. TBI may cause changes in brain function that mimic or reproduce a clinical presentation similar to depression as displayed by a primary psychiatric population.4,16 Jorge et al17,18 have contributed substantially to understanding neurophysiologic effects that may contribute to post-TBI depression including neuronal and glial loss in the prefrontal and hippocampal regions. These researchers have also pointed to genetic, developmental, and psychosocial factors19 and alcohol misuse20 as contributing factors in the development of post-TBI depression. Other drugs including prescription medications may also contribute to depression although research is very limited in this area. Losses caused by activity limitations after brain injury or associated physical injuries and pain as well as other psychologic and environmental factors have also been implicated.21-28 Current theory highlights the temporal evolution and interaction of physiologic, psychologic, and social factors in the development of depression after TBI.7,29-33 Two prior studies have documented a strong association between self-appraisal of severity of disability and depression List of Abbreviations

From the Rehabilitation Hospital of Indiana (Malec); Department of Physical Medicine and Rehabiliation (Malec) and Division of Biostatistics (Stump, Monahan), Indiana University School of Medicine, Indianapolis, IN; and Departments of Physical Medicine and Rehabilitation (Brown) and Nursing (Moessner), Mayo Clinic, Rochester, MN. Presented to the International Brain Injury Association, April 9 –12, 2008, Lisbon, Portugal; World Federation of NeuroRehabilitation, September 24 –27, 2008, Brazilia, Brazil; and North American Brain Injury Association, October 2– 4, 2008, New Orleans, LA. Supported by the National Institute for Disability and Rehabilitation Research (TBI Model System grant no. H133A020507). No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit on the authors or on any organization with which the authors are associated. Correspondence to James F. Malec, PhD, ABPP-Cn, Rp, Rehabilitation Hospital of Indiana, 4141 Shore Dr, Indianapolis, IN 46077, e-mail: [email protected]. Reprints are not available from the author. 0003-9993/10/9107-00959$36.00/0 doi:10.1016/j.apmr.2010.04.002

AQ BDI BDI-II BIC CFI CNS DSM-IV MPAI-4 NFI PTA RMSEA SEM SRMR TBI

Awareness Questionnaire Beck Depression Inventory Beck Depression Inventory-II (2nd edition) Bayesian Information Criterion Comparative Fit Index clinical nurse specialist Diagnostic and Statistical Manual of Mental Disorders, 4th. Edition Mayo-Portland Adaptability Inventory (4th edition) Neurobehavioral Functioning Inventory posttraumatic amnesia root mean square error of approximation structural equation modeling standardized root mean residual traumatic brain injury

Arch Phys Med Rehabil Vol 91, July 2010

1088

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

after TBI. In the first study34 of patients admitted to a single midwestern hospital after mild to severe TBI, self-report of perceived physical and cognitive disabilities using the NFI at hospital discharge was highly correlated with self-report of depression on the NFI Depression scale at discharge (r⫽.83) and 1 to 2 years after injury (r⫽.59). Depression was most prevalent among those who overestimated the severity of their disability relative to family or significant others. The severity of TBI as indicated by the duration of PTA did not predict postinjury depression. In this sample, depression was no more prevalent among those with TBI than among orthopedic controls, suggesting that psychologic and environmental factors may be more significant in the development of post-TBI depression than alteration of brain function directly caused by trauma to the brain. A second study35 examined data for 745 individuals with generally moderate to severe TBI admitted to inpatient rehabilitation at multiple medical centers contributing to the National Institute for Disability and Rehabilitation Research TBI Model System Database. This sample showed a similar association between overestimates of disability by the patient (relative to assessment by research staff) and increased prevalence of depression as measured by the NFI. In this study, TBI severity, as measured by the duration of PTA, showed a weak association with severity of depression. Sliwinski et al36 have also reported a moderately strong correlation (r⫽.67) between depression as measured by the BDI and non– depression-related problems post-TBI reported on The Institute for Rehabilitation and Research Symptom Checklist. These investigators, however, also noted a low correlation (r⫽.30) between the BDI and a diagnosis of depression based on the Structured Clinical Interview for DSM-IV Diagnosis. They concluded that, in a TBI population, the BDI represents general distress and hyperreactivity to negative stimuli rather than psychiatric depression per se. Nonetheless, their findings are very similar to our own34,35 in showing a moderately strong correlation between self-assessment of disability after TBI and self-reported symptoms of depression. Our prior studies also mirror other research in this area in identifying an inconsistent and weak relationship between TBI severity and post-TBI depression.2,3,37-39 Our previous studies show that the overestimation of disability, rather than the lack of awareness of disability, is the primary factor in the strong relationship between self-appraisal of post-TBI ability and post-TBI depression. Consistent with

this, Evans et al40 reported that post-TBI depression was not diminished in a group of patients with reduced self-awareness as defined by the difference between self and staff ratings on the AQ. However, these researchers did not report the relative incidence of depression among those who may have overestimated their level of impairment and disability. DEVELOPING A MODEL Based on previous research including our own, we began to develop a model for post-TBI depression. This report represents an intermediate step in model building. Figure 1 describes the initial model that was specified a priori before fitting SEM to the data. This initial model was developed with a high degree of parsimony by focusing on several major and important constructs of the model. Variable selection and initial hypotheses about relationships that comprise the initial model were based on our own and others’ prior research. The rationale for variable selection and these initial hypotheses are described in detail in the section that follows. In the long run, a comprehensive model of post-TBI depression would presumably specify greater detail. For instance, TBI severity may ultimately be specified more precisely by measuring the extent and nature of actual structural and neurochemical brain disruption caused by TBI. External appraisal of post-TBI ability would describe interrelationships of more specific factors, such as physical and cognitive limitations and pain, that are currently represented by this more global concept. In the model, post-TBI depression is broadly defined to include a number of syndromes characterized by dysphoria, anhedonia, and other symptoms as described by measures of depression, such as the BDI, NFI Depression, and the Patient Health Questionnaire-9 depression measure. Post-TBI depression, as defined for the model, includes disorders with symptom arrays that are typical of a range of DSM-IV depression diagnoses, such as major depression, adjustment disorder with depressed mood, dysthymia, and mood disorder due to TBI (depressed subtype). Self-appraisal of Post-TBI Ability and Post-TBI Depression The strongest relationship identified in prior research is that between self-reported perception of ability and post-TBI depression. In the model, self-appraisal of post-TBI ability is defined as self-report of abilities (eg, mobility, speech, cogni-

Fig 1. Initial model: standardized path coefficients for postTBI depression. Estimatorⴝ MLR; Nⴝ158; ␹2ⴝ31.64; Pⴝ .0002; CFIⴝ.832; TLIⴝ.663; BICⴝ4904.067; RMSEAⴝ.126; 95% confidence intervalⴝ.080 – .175; SRMRⴝ.067. *P<.05, †P<.01, ‡P<.001. Abbreviations: MLR, robust maximum likelihood estimator; TLI, TuckerLewis Index.

Arch Phys Med Rehabil Vol 91, July 2010

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

tion) by the person with TBI on measures such as the NFI scales other than Depression or Hostility, the AQ, or The Institute for Rehabiliation and Research Symptom Checklist. Our prior studies and that of Sliwinski et al36 have found the correlations between these 2 variables to be in the range of .65 to .80. We assumed, as we began model development, that the association is mutually enhancing and therefore bidirectional (ie, perceptions of more severe disability lead to more severe depression, which, in turn, potentiates more negative selfappraisal). External Appraisal and Self-appraisal of Post-TBI Ability External appraisal of post-TBI ability is defined in this model as the assessment of abilities by a person other than the person with TBI who arguably can be more objective in this assessment. Ideally, this construct is based on evaluation by a rehabilitation professional or team. However, some prior studies have based this assessment on the report of significant others. We hypothesized that an external assessment of postTBI ability would be associated with self-appraisal of post-TBI ability with a weak positive correlation between these 2 variables. Greater externally assessed limitations in ability would be expected to be associated with self-perceptions of more limited ability. However, cognitive impairment because of TBI that causes ability limitations is also expected to interfere with accurate self-appraisal, mitigating the strength of the positive relationship between external appraisal and self-appraisal of post-TBI ability. Pre-TBI and Post-TBI Depression Pre-TBI depression is difficult to assess because depression is often undiagnosed, misdiagnosed, or unrecognized in the general population. Consequently, self-report of pre-TBI depression is likely to be only partially accurate. Prior studies34,35 have shown a weak positive relationship between evidence of depression before TBI and post-TBI depression. For this reason, we included this relationship in the model and hypothesized a positive relationship between these 2 variables (ie, the presence of pre-TBI depression would be associated with the presence of post-TBI depression). The assumption in the model that pre-TBI depression may be a particularly salient factor in the evolution of post-TBI depression is not intended to suggest that other preinjury psychologic factors and personality features may not also be relevant. As this model develops, investigations at this level of detail would be desirable. It is also possible that, as a result of more detailed investigations, a few key indicators such as “pre-TBI depression” may be discovered that represent a variety of associated traits but allow for parsimony to be retained in the model. TBI Severity and External Appraisal of Post-TBI Ability Based on the work of Bush,41 Novack,42 and colleagues, we hypothesized that greater TBI severity (as defined by measures, such as the duration of PTA, length of unconsciousness, or the initial Glasgow Coma Scale score) would be inversely associated with external appraisal of post-TBI ability. Pre-TBI Education and External Appraisal of Post-TBI Ability Based on evidence of a weak relationship between these 2 variables in prior research,34 we hypothesized a weak positive relationship between pre-TBI education and external appraisal of post-TBI Ability.

1089

TBI Severity and Post-TBI Depression TBI severity has not been consistently associated with severity of post-TBI depression.2,27,28,32,34,43 Nonetheless, this relationship was evaluated in the initial model. External Appraisal of Post-TBI Ability and Post-TBI Functional Outcome In the proposed model, functional outcome is defined as the level of activity and community participation at long-term follow-up (ie, 1 or more years after injury). Measures of functional outcome, as broadly defined in this model, include the Disability Rating Scale, independent living status, vocational status, and, as measured in the present study, the MPAI-4. A positive relationship between external appraisal of post-TBI ability and post-TBI functional outcome was expected. Post-TBI Depression and Functional Outcome Previous research2,6-15 has identified an inverse relationship between post-TBI depression and functional outcome, and this was hypothesized in the initial model. Impaired Self-Awareness of Disability, Post-TBI Depression, Mediation, and Moderation In our own previous reports of the relationship between self-appraisal of post-TBI ability and post-TBI depression, we have focused on the construct of impaired self-awareness of disability. In prior studies, impaired self-awareness of disability post-TBI has typically been operationalized as the difference between external appraisal of post-TBI ability and selfappraisal of post-TBI ability. Research in this area has focused on those individuals with TBI who tend to underestimate their level of disability relative to an external assessment, presumably because of cognitive impairment. On closer consideration, the concept of impaired self-awareness appears to represent types of cognitive impairments that have not been precisely operationalized in the literature. Cognitive impairment underlying impaired self-awareness appears to have at least 2 dimensions. One dimension represents the inability to accurately perceive or, more likely, conceptualize post-TBI changes in the self, resulting in an overestimate of ability relative to the assessments of others. A second dimension represents the tendency to focus attention on disability to the exclusion of context, temporal, or other mitigating factors resulting in an underestimate of ability relative to the assessment of others. Ownsworth et al44 present results of a cluster analysis and a thorough review of the available literature describing distinct groups of individuals who tend to overestimate or underestimate problems after brain injury as well as a third group who appears to accurately perceive their situation. She further subdivides the group that underreports symptoms into those whose under-reporting may be caused by neuropsychological impairment as evidenced on neuropsychologic testing and a group without such executive cognitive dysfunction whose underreporting may be psychologically based (ie, representing a cognitive personality style). Even though the viewpoint of a family member is incorporated in completing the Self-Awareness of Deficits Interview used in this study, Ownsworth’s multidimensional characterization of these groups improves on the methodology of contrasting the report of the person with brain injury with a presumably more “objective” observer because it reduces the bias of the observer. Overall, previous methods used to characterize impaired self-awareness serve as a proxy measure for the specific types of impairment in executive cognitive functions (which may translate into Arch Phys Med Rehabil Vol 91, July 2010

1090

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

overprocessing vs underprocessing new information about acquired disability). More direct measures of these kinds of cognitive impairments would be preferable. However, such measures are not currently available. At this point in model building, we did not attempt to distinguish whether a reduced ability to perceive personal limitations is a consequence of brain injury or a more longstanding cognitive style because well-established methods for making this distinction are not available. Arguably, both could be caused by cerebral dysfunction or injury of recent, remote, or genetic origin. As it is currently operationalized, impaired self-awareness of disability is not distinct from self-appraisal of post-TBI ability and external appraisal of post-TBI ability because it is derived as the difference between the 2 latter measures (impaired self-awareness of disability ⫽ self-appraisal of post-TBI ability ⫺ external appraisal of post-TBI ability). Consequently, we did not include impaired self-awareness of disability as a separate factor in the model because it would be redundant with selfappraisal of post-TBI ability and external appraisal of post-TBI ability when the latter are both in the model. The current study was conducted to test a priori–specified relationships described in the initial model (see fig 1) through a confirmatory SEM of a dataset that has not been examined previously in this line of research. An advantage of SEM over regression is that all paths in the model can be (and were in the present study) assessed simultaneously, including tests of mediation and indirect effects. Another advantage, the ability to model latent variables, was not implemented in the present study because of the modest sample size; instead, a future larger study will account for measurement error in covariates with SEM by specifying multiple indicators of latent constructs in a more comprehensive model. (See Results section for SEM power analysis). Previous studies have shown a strong relationship between self-appraisal of abilities and depression both early (at discharge from inpatient rehabilitation)34 and late (at 1 or more years after injury).35,36 This and other relationships among variables in the proposed model may vary over time after injury. However, prior research has shown that the relationship between self-appraisal and depression, which was of particular interest, as well as depression itself emerges relatively early after injury. With this in mind, an acute sample was chosen for initial evaluation and further development of the model. In doing so, we recognized that, if a viable model could be determined, it would need to be further assessed and refined at time points more distal to injury. METHODS Participants This study included 158 patients admitted to the hospital with moderate to severe TBI. This sample was part of a larger sample of 230 patients consecutively recruited for participation in a study of factors in medical decision making and functional outcome after TBI. All of the 72 patients who were not included had missing data on all or almost all of the variables; in most cases, these were patients who were discharged from the hospital soon after admission. Because this group very likely represented a distinct subset of admissions for TBI and because of extensive missing data in these cases, imputation procedures to estimate missing data were not attempted and appeared inappropriate. However, an imputation procedure was used to estimate missing data for 37 participants within the sample of 158 who were missing information on the most distal outcome variable in the model (functional outcome). Specifically, we used the Mplusa method of maximum likelihood estimation Arch Phys Med Rehabil Vol 91, July 2010

while imputing missing data using all available data; this imputation method performs an adjustment to the bias of the sample statistics for the complete data under the assumption that data are missing at random and produce parameter estimates and standard errors that are consistent and efficient. The present sample consisted of those who consented to participation and for whom relevant measures were available. All participants were adults (over age 18) admitted to the hospital with moderate to severe TBI as defined by meeting 1 or more of the following 3 conditions: (1) Glasgow Coma Scale less than 13, (2) PTA more than 24 hours, or (3) the presence of injury-related abnormalities on neuroimaging (ie, all participants had evidence of definite TBI as described by the Mayo Classification System for Traumatic Brain Injury Severity45). Although we wished to restrict the sample to those with clear evidence of brain injury (ie, definite TBI), data for PTA show that the sample represented a wide range of severity. PTA was 1 hour or less for 18%, between 1 and 24 hours for 18%, 1 to 7 days for 19%, 1 to 2 weeks for 11%, 2 to 4 weeks for 18%, and greater than 4 weeks for 16%. Those with PTA less than 1 day were admitted to the study based on the presence of another indicator of definite TBI, most often, the presence of neuroimaging abnormalities. The participants in the study sample were 122 men (77%) and 36 women (23%). Mean age ⫾ SD was 48.11⫾20.48 years. Mean years of education ⫾ SD was 12.87⫾2.29 years with 18% completing less than 12 years of formal education, 66% completing high school or high school and some college, and 16% with a college education or advanced degree. Individuals with an identified history of preinjury depression constituted 15% of the sample. The mean score ⫾ SD on the BDI-II completed after injury was 9.81⫾8.57). Sixty percent of the participants scored less than 10 on the BDI-II, 30% between 10 and 20 (mild depression), and 10% over 20 (moderate-severe depression). The average score for the AQ was 2.63⫾.50, indicating that, on average, participants felt they were “a little worse” to “about the same” since their injuries. The average score ⫾ SD for the MPAI-4 Ability Index was 34.65⫾20.11. Compared with national norms,46 this score indicates relatively severe and pervasive impairments and, taken together with the AQ average score, suggests that individuals in the sample may have tended to underestimate their level of initial disability. The average score ⫾ SD on the MPAI-4 Participation Index for the 121 completing follow-up was 3.65⫾5.67) suggesting, with reference to national norms,46 that the sample as a whole generally experienced good return to community participation. Measures In this study, constructs in the proposed model were operationalized in the following manner. Years of formal education completed before TBI represented pre-TBI education. Pre-TBI depression (1⫽present, 0⫽absent) was assessed conservatively and recorded as positive only if there was evidence in the medical record or a reported history of psychiatric or psychological treatment or hospitalization. We adopted a conservative approach because of the difficulty of evaluating the reliability self-reports of prior experiences of “depression.” Although raising the risk of false-negatives, requiring an external indication of a diagnosis of depression presumably enhanced the reliability of this data point. TBI severity was represented by PTA duration. External appraisal of post-TBI ability was measured by the MPAI-4 Ability Scale completed by a TBI CNS. Self-appraisal of post-TBI ability was assessed by the patient’s responses to the AQ and post-TBI depression by the patient’s responses to the BDI-II. Although in a previous study34 we

1091

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

used the same measure (NFI) to assess both external and self-appraisal of post-TBI ability, we elected to use different measures of the same construct (ability) for this study to reduce the potential for method invariance (ie, inflated correlation between measures because of structural similarity between measures). Functional outcome was represented by the MPAI-4 Participation Index completed by telephone follow-up about 1 year after TBI. Greater detail about these measures is provided later. Posttraumatic amnesia. Previous research47 has shown PTA to be as or more reliable than other measures of TBI severity, such as the Glasgow Coma Scale, in predicting longterm outcome. The duration of PTA was determined by the TBI CNS through clinical follow-along or, in cases of short hospital stays, by chart review after hospital discharge. For some patients included in the TBI Model System National Database, the resolution of PTA was determined by serial administration of the Galveston Orientation and Amnesia Test. For others, PTA was determined when the patient was oriented to person, time, and place on 2 consecutive days. This latter approach was also used to determine the resolution of PTA through chart review. All these approaches to assessing PTA are considered valid and equivalent in the TBI Model Systems research program. In this study, PTA was recorded on an ordinal scale as follows: (1⫽⬍1 hour, 2⫽1 to 24 hours, 3⫽1 to 7 days, 4⫽1 to 2 weeks, 5⫽2 to 4 weeks, and 6 ⫽ ⬎4 weeks). Ability Index. The MPAI-4 Ability Index48 includes 13 items to assess mobility, use of hands, vision, audition, dizziness, motor speech, verbal communication, nonverbal communication, attention/concentration, memory, fund of information, novel problem solving, and visuospatial abilities. These items are rated on a 5-point scale: (0) none; (1) mild problem, which does not interfere with activities, and may use assistive device or medication; (2) mild problem, which interferes with activities 5% to 24% of the time; (3) moderate problem, which interferes with activities 25% to 75% of the time; and (4) severe problem, which interferes with activities more than 75% of the time. Participation Index. The MPAI-4 Participation Index includes 8 items measuring initiation, social contact, leisure and recreational activities, self-care, independent living, employment, transportation, and money management. These items are also rated on a 5-point scale, which is similar to the scale for the Ability Index for most items. Ratings for the employment item are more specific (ie, representing variations of full-time, part-time, unpaid, and supported work, and unemployment). Recommended scoring conventions for both MPAI-4 indices were followed. For clarity, we reversed the scoring on the MPAI-4 measures so that higher scores on these indices represented greater ability and greater participation, respectively. Both these indices have satisfactory internal consistency and

correlate moderately well with the full-scale MPAI-4, which, in turn, has well-established reliability and validity.48-51 Beck Depression Inventory. The BDI-II includes items that assess common symptoms of depression and dysphoria, such as feeling sad, having a low opinion of self, guilt, selfblame, hopelessness, discouragement, fatigue, sleep disturbance, and appetite disturbance. The BDI is frequently used to measure depression in research and clinical practice and has been used widely in previous studies to measure depression in individuals with brain injuries.27,52,53 Awareness Questionnaire. The patient version of the AQ consists of a series of Likert scales on which the person with TBI is asked to rate their abilities from “much worse” to “much better” than before their injury. The AQ has been carefully studied and validated.54 Procedure The entire MPAI-4, which includes the Ability Index, was rated by a TBI CNS who followed all individuals with TBI from hospital admission through discharge. MPAI-4 ratings were based on her assessment and experience with study participants during acute hospital medical treatment before hospital discharge or transfer to the inpatient rehabilitation unit. She completed MPAI-4 ratings as early as possible after hospital admission, in most cases within the first week of hospital admission, and in many cases with proxy consent for study participation provided by a family member or significant other. Only the Ability Index of the MPAI-4 collected at this time was used to measure external appraisal of abilities. The TBI CNS collected injury-related and demographic data, including education and psychiatric history, at about the same time. Patients with TBI were asked to complete the BDI-II and the AQ by the TBI CNS as soon as possible after the resolution of PTA. The MPAI-4 Participation Index obtained through telephone follow-up about 1 year after injury was used to represent longterm functional outcome. Statistical Analysis SEM was performed by using the Mplus software.55 Goodness of fit was assessed with the chi-square test and with the fit indices of CFI, RMSEA, and SRMR. Maximum likelihood estimation robust to nonnormality was performed. A CFI greater than .95, RMSEA less than .06, and SRMR less than .08 were considered indicators of a good-fitting model.56 The Mplus software provides a variety of estimators. Maximum likelihood estimation robust to nonnormality was chosen because it uses a sandwich estimator to produce standard errors that are robust to nonnormality.55 Indirect effects were also tested.

Table 1: Spearman (Lower Left) and Pearson (Upper Right) Correlations Among Variables in Post-TBI Depression Model

Variables

Pre-TBI education Pre-TBI depression PTA MPAI Ability Index AQ BDI-II Functional outcome

Pre-TBI Education (y)

Pre-TBI Depression

TBI Severity (PTA)

.09 (.28) .10 (.22) .09 (.27) .00 (.97) .05 (.51) .00 (.96) .13 (.10) .09 (.27) ⫺.23 (.003) ⫺.04 (.61) ⫺.21 (.009) ⫺.12 (.12) ⫺.16 (.04) .18 (.02) .06 (.42) .17 (.06) ⫺.06 (.49) ⫺.23 (.01)

External Appraisal of Post-TBI Ability (MPAI Ability Index)

.11 (.17) .09 (.27) ⫺.23 (.004) .21 (.009) ⫺.08 (.29) .22 (.01)

Self-appraisal of Post-TBI Ability (AQ)

.01 (.92) ⫺.20 (.01) .10 (.22) .19 (.02) ⫺.69 (⬍.0001) .23 (.01)

Post-TBI Depression (BDI-II)

⫺.20 (.01) .18 (.02) .06 (.44) ⫺.05 (.51) ⫺.66 (⬍.0001)

Functional Outcome (MPAI Participation Index 1 Year Post-TBI)

.18 (.05) ⫺.01 (.88) ⫺.29 (.001) .21 (.02) .29 (.001) ⫺.36 (⬍.0001)

⫺.22 (.01)

NOTE. Values inside parentheses are P values. Arch Phys Med Rehabil Vol 91, July 2010

1092

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

RESULTS Table 1 shows the Spearman and Pearson correlation coefficients among the variables in the model. Testing Fit of the Initial Model A confirmatory SEM was fit to the a priori theoretic model in figure 1. The standardized coefficients are shown along with an indication of statistical significance. Although 5 paths were statistically significant, the overall fit of the model could be improved, namely, although the SRMR (.07) indicated adequate fit, the CFI (.83) was not close to the .95 cut point, and the lower bound (.08) of the 95% CI for RMSEA was above the .06 cut point. Model Revision Therefore, the model was revised by using the following steps based on statistical and clinical rationale. (Note that the final revised model no longer represents a confirmatory model but rather a model-generating approach that must be confirmed by a future study.) From the statistical standpoint, an examination of the Mplus modification index at the .01 alpha level showed that only 3 regression paths were estimated to be significant if added to the model, and no other paths were significant if the more relaxed .05 alpha were used. Two of these paths involved the path from education to self-appraisal of post-TBI ability and from education to post-TBI depression. The third path (a direct path from TBI severity to functional outcome) was also of high clinical relevance. A fourth path from self-appraisal of post-TBI ability to functional outcome was judged by our team to be clinically relevant. Therefore, those 4 paths were added to the model. The result of adding these 4 paths (fig 2) represents an intermediate model. Although this intermediate model provided great improvement by yielding a reasonably good fit to the data (CFI⫽.95, RMSEA⫽.08, SRMR⫽.05), it is more complicated. Furthermore, according to the chi-square goodness of fit test, the null hypothesis of good fit should be rejected at the .05 significance level (P⬍.05). To simplify the model, we decided to drop the pre-TBI education variable. Its path to objective appraisal of post-TBI ability was not significant in the initial model and is not as strongly supported in the literature34 as paths among other

variables in the model. Furthermore, after discussion among our team, the path from self-appraisal of post-TBI ability to functional outcome was dropped because of its nonsignificance and medium clinical relevance. The path from pre-TBI depression to postinjury depression was retained, despite its nonsignificance in the initial model, because of its high clinical relevance. The final revised model is much more parsimonious (fig 3). The overall fit of the model was very good. Specifically, the chi-square goodness of fit test was no longer significant (P⫽.33), and the fit indices showed excellent fit. The CFI was near 1.0 (.99), RMSEA (.031) was well below the .06 cut point, and SRMR (.04) was well below its cut point of .08. The Bayesian Information Criterion statistic, which is useful for comparing the fit of different SEM models, showed that the final revised model had the best fit (ie, lowest BIC). It should be noted that postinjury depression much more strongly predicted self-appraisal of post-TBI ability (⫺.76) than the reverse; however, there is likely a bidirectional relationship between these variables. Furthermore, because of the high degree of variance shared between these 2 variables, it is difficult to tease out the unique variance from one of these variables to the other, a goal made even more elusive in the absence of an experimental design. Sensitivity Analyses The SEMs were also estimated by modeling the post-TBI ability variable using censored and negative binomial distributions. The reason for this was to adjust for the nonnormality in post-TBI ability and to determine if it had any effect on the parameter estimates. The magnitude and significance of the path coefficients and values for the BIC statistic were very similar to those found in figures 1 through 3. Relationships Among Variables Following is a more specific discussion of relationships among variables in the examined models. Self-appraisal of Post-TBI Ability and Post-TBI Depression The standardized coefficients between these 2 variables were moderately strong and in the same range as correlations ob-

Fig 2. Intermediate model: standardized path coefficients for post-TBI depression. EstimatorⴝMLR; Nⴝ158; ␹2ⴝ14.09; Pⴝ.0496; CFIⴝ.947; TLIⴝ.864; BICⴝ4898.72; RMSEAⴝ.080; 95% confidence intervalⴝ .003–.141; SRMRⴝ.052. *P<.05, †P<.01, ‡P<.001. Abbreviations: MLR, robust maximum likelihood estimator; TLI, TuckerLewis Index.

Arch Phys Med Rehabil Vol 91, July 2010

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

1093

Fig 3. Final model: standardized path coefficients for post-TBI depression. EstimatorⴝMLR; N ⴝ 158; ␹2ⴝ6.93; Pⴝ.3271; CFIⴝ.992; TLIⴝ.981; BICⴝ4195.019; RMSEAⴝ.031; 95% CIⴝ0 –.111; SRMRⴝ.040. *P<.05, †P<.01, ‡P<.001. Abbreviations: MLR, robust maximum likelihood estimator; TLI, Tucker-Lewis Index.

tained between these 2 variables in previous studies.34-36 As predicted, the relationship for the significant path had a negative valence, indicating that those who reported higher levels of depressive symptoms tended to perceive more limited ability post-TBI, with a likely bidirectional causal relationship between these 2 variables that is difficult to tease apart in crosssectional nonexperimental studies. External Appraisal and Self-appraisal of Post-TBI Ability These 2 variables appeared weakly associated. The positive valence of the coefficient indicates that those with fewer externally assessed deficits, in fact, were more likely to perceive fewer deficits (ie, more preserved ability). Pre-TBI and Post-TBI Depression The relationship between pre-TBI depression and post-TBI depression was not significant in the final model. However, as simple correlations indicate (see table 1), those with pre-TBI depression generally perceived their post-TBI ability as lower than those without a history of depression. The possibility of an interaction was explored (ie, we examined whether those with a pre-TBI history of depression would show a stronger relationship between self-appraisal of post-TBI ability and postTBI depression than those without a pre-TBI history of depression. However, the SEM using Mplus showed this interaction to be nonsignificant. This nonsignificance was also verified with bivariate statistics, namely, almost identical (and strong) correlations between self-appraisal of post-TBI ability and depression were obtained for both the group with pre-TBI depression (r⫽⫺.64) and the group without pre-TBI depression (r⫽⫺.65). The possibility that self-appraisal of post-TBI ability mediates the effect of pre-TBI depression on post-TBI depression was also explored by using the Mplus option to estimate indirect effects. This analysis revealed an indirect effect of pre-TBI depression through aelf-appraisal to post-TBI depression (standard coefficient⫽.13, P⫽.012). In the absence of a direct relationship between pre- and post-TBI Depression, this finding suggests that self-appraisal mediates this relationship. TBI Severity and External Appraisal of Post-TBI Ability A significant relationship was apparent between these 2 variables in the predicted direction (ie, greater injury severity as measured by PTA was associated with reduced ability post-TBI).

Pre-TBI Education and External Appraisal of Post-TBI Ability The coefficient between these 2 variables was positive but not significant, and education was eliminated from the final model. Examination of table 1 reveals that preinjury education may have a weak but significant association with post-TBI depression. However, because the relationship appeared marginal and with no clear mediational path for this variable, we could not justify reintroducing pre-TBI education into the model in a different role. TBI Severity and Post-TBI Depression Contrary to prediction, there was no evidence of a relationship between PTA and post-TBI Depression; consequently, this association was eliminated from the final model. External Appraisal of Post-TBI Ability and Post-TBI Depression There was no evidence of a substantial relationship between the external appraisal of post-TBI ability and post-TBI depression (see table 1). We explored the possibility of a moderating relationship (or interaction) between self-appraisal and external appraisal of ability in the relationship of these variables to depression. Mplus showed no statistical significance for such an interaction, and this was verified with bivariate statistics by dividing participants into those with low external (MPAI-4 Ability Index) ability scores (⬍.5 SD below the mean) and high external ability scores (⬎.5 SD above the mean). The distribution tended to be bimodal with 55% in the low external ability group and 41% in the high external ability group and only 4% close to the mean. Both groups showed moderately strong and similar correlations between self-appraisal of ability and post-TBI depression (r⫽⫺.69 for the low external ability group and r⫽⫺.63 for the high external ability group), arguing against a moderating relationship. External Appraisal of Post-TBI Ability and Post-TBI Functional Outcome; Post-TBI Depression and Functional Outcome Consistent with prediction, functional outcome, as measured by the Participation Index, had a weak association with external appraisal of post-TBI ability (significant in the initial model but not significant in the final model) and a weak to moderate significant relationship with post-TBI depression. Inspection also reveals weak but significant correlations of functional Arch Phys Med Rehabil Vol 91, July 2010

1094

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

outcome to TBI severity (see figs 2 and 3, see table 1) and self-appraisal of post-TBI ability (see table 1, but not significant in fig 2). Associations of both TBI severity and external appraisal of post-TBI ability to functional outcome raise the possibility that the former variables have a mediational relationship. This mediation effect was tested; however, Mplus showed that the indirect effect was not significant. A possible mediational relationship to functional outcome was also explored between post-TBI depression and self-appraisal of postTBI ability. This mediation effect was tested for both variables (ie, self-appraisal of post-TBI ability as a mediator in depression¡self-appraisal of post-TBI ability¡outcome and depression as a mediator in self-appraisal of post-TBI ability¡ depression¡outcome); however, Mplus showed that the indirect effect through the potential mediator was not significant for either variable on functional outcome. Power Analysis of Final SEM Model A power analysis was performed of the final SEM model using the MPlus software; the analysis accounted for missing data using the PATMISS and PATPROBS options. The observed coefficients, intercepts, residual variances, and means and variances of independent variables were entered as parameters in the simulation program. Parameters were accurately recovered, indicating that the simulation results were accurate. The results showed that for an alpha of .05 and 2-sided Wald z tests, the power was very high (.96 –1.00) for 5 of the paths, and power was low for 3 paths: functional outcome on external appraisal of post-TBI ability (power⫽.46), functional outcome on postinjury depression (power⫽.42), and external appraisal of post-TBI ability on post-TBI ability (power⫽.36). However, 2 of these paths were found to be significant despite the lower power, which eliminates the concern regarding type II error for those 2 paths. Only the path of functional outcome on external appraisal of post-TBI ability had low power and was also not significant (P⫽.114), but this path had the smallest effect size of all the paths (standardized coefficient⫽.11). Therefore, the SEM analysis appears to have had adequate power to detect differences as small as a .20 magnitude in a standardized coefficient, with the exception that the standardized coefficient of .11 for the path of functional outcome on external appraisal of post-TBI ability. Future studies of this specific relationship may benefit from a larger sample size and increased power. DISCUSSION Results of this study provide additional evidence of a moderately strong association between self-reported symptoms of depression and self-appraisal of ability after TBI and extend previous research by showing this relationship using statistical modeling that incorporated all variables in the model (SEM) and using a measure (AQ) that was specifically designed to assess self-appraisal after TBI. This study also used a more objective measure of ability post-TBI than we have used in previous studies. The abilities of the participant with TBI were assessed by a TBI CNS based on direct observation of the patient rather than by a significant other or over the telephone as in prior studies. The relationship between self-appraisal of more impaired abilities and greater depression has been previously interpreted to indicate general distress or neurotic personality traits.36 However, a more straightforward interpretation may be that post-TBI depression is much like psychiatric depression as originally described by Beck.57 That is, depression is associated with negative appraisal of the self, which may become sufficiently exaggerated to represent cognitive distortions. Arch Phys Med Rehabil Vol 91, July 2010

These negative, sometimes distorted, self-appraisals engender and reinforce feelings and symptoms of depression. As defined in the proposed model, depression may range from a mild adjustment disorder to a major depressive disorder. A direct effect of pre-TBI depression on post-TBI depression was not confirmed by analyses. To some degree, this may be caused by imprecise measurement of pre-TBI depression. However, exploratory mediation analysis suggests the possibility that self-appraisal mediates the relationship between preand post-TBI depression (ie, those with a prior history of depression may tend to make more negative self-appraisals of the effects of TBI, resulting in greater depression post-TBI). The lack of experimental evidence cautions us against definitive directional claims; however, statistically, it is clear, from these data, that pre-TBI depression has an association with post-TBI depression indirectly through self-appraisal. A more comprehensive model may reveal other direct and indirect associations. Somewhat surprisingly, limitations in ability, which are externally assessed, are not significantly associated with level of depression. In other words, those who appear to have more impairment and potentially more reason to be depressed are not necessarily more depressed. The MPAI-4 Ability Index includes ratings of cognitive impairment that may interfere with accurate self-appraisal. Perhaps because of cognitive impairment interfering with accurate self-appraisal, externally assessed ability and perceived ability were only weakly correlated. Methods to precisely characterize and assess cognitive deficits that may interfere with accurate self-appraisal are not currently available. A potential interaction between cognitive impairments of various types and the capacity for accurate self-appraisal is of particular relevance to modeling processes involved in post-TBI depression. Presumably, underestimates of current ability may be caused by either the overprocessing of information about deficits or underprocessing of information about abilities. Overestimates of current ability may conversely be caused by overprocessing of information indicating enhanced ability or underprocessing of information regarding deficits. Prior research has identified a tendency for those with more severe injuries to more commonly underprocess information about their deficits and thus appear unaware of these deficits. Hypothetically, milder TBI may reduce the capacity of those who tend to overprocess (ie, ruminate) about deficits to mitigate these tendencies through a more logical internal dialogue. As implied in the preceding discussion, types of cognitive deficits may be associated with TBI severity, thus also mitigating the relationship between TBI severity and depression. Better identification and operationalization of specific cognitive impairments that are associated with either reduced or exaggerated self-appraisal of disability and their relationship to TBI severity are appropriate goals of future research in this area. Increased TBI severity (as measured by variables such as PTA) resulted in poorer functional outcomes in the long-term. Analyses conducted in this study do not support the mediation of TBI severity on functional outcome by external appraisal of post-TBI ability, whereas Bush41 and Novack’s42 work suggests a mediational relationshp (ie, TBI severity is associated with post-TBI disability but does not add to the prediction of functional outcome when post-TBI disability is included in the model). The timing of the ability assessment may explain the variation in findings. In the present study, an external assessment of ability was performed very early in the recovery process during acute hospital care. In the Bush and Novack studies, the ability assessment was performed at discharge from

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

inpatient rehabilitation when patients’ ability profiles were likely more stable. Study Limitations Clear identification of these relationships is, to some degree, compromised by the proxy nature of current measures of TBI severity. The current, widely used and accepted proxy measures of injury severity, such as, PTA, GCS, or time to follow commands, are behavioral measures. Although believed to represent the severity of brain trauma, these measures are gross and indirect indicators of actual structural and neurochemical changes resulting from TBI. Emerging neuroimaging techniques, such as diffusion tensor imaging or magnetic resonance imaging spectroscopy, may provide more direct measures of the extent and location of brain damage. Imaging techniques that record these structural and chemical changes with greater precision than proxy behavioral measures are essential to the advancement of this line of research and to the study of TBI generally. Such direct measures of TBI severity would offer valuable, more reliable estimates of the correlation of TBI severity to other variables in the proposed model. A physiologic measure of TBI severity would also allow more definitive study of the effect of cerebral damage on depression. The current study and prior research does not establish a direct relationship between TBI severity and postTBI depression. TBI severity may affect depression through its impact on cognitive abilities, which, in turn, affect self-appraisal of abilities. However, this is contrary to conventional wisdom that organic brain dysfunction caused by TBI does, in fact, directly contribute to post-TBI depression by disrupting neurochemical systems involved in mood and motivation. A more direct physiologic measure of TBI severity is required to further clarify these relationships. Other limitations of this study are the use of a self-report measure for depression and the relatively small number of participants. The power analysis suggests that the SEM model had generally adequate power for confirming the fit of the paths in the a priori model. Therefore, any lack of fit would appear to be primarily the result of the model needing modification rather than inadequate sample size. However, the modest sample cannot be entirely dismissed as a contributing factor to model lack of fit, imprecision, misspecification, and unavoidable sampling error. In particular, the nonsignificance for the path from external appraisal of post-TBI ability to functional outcome may have been caused by the model being underpowered to detect significance for that path if the true effect size is as small as a standardized coefficient of .11. An objective, symptom-based assessment of depression, such as the Structured Clinical Interview for DSM-IV Disorders, to confirm the reliability of self-report of both current and past depression would be of value in future research. The relationship between self-appraisal and post-TBI depression has been shown in several studies34-36 conducted at various times after injury. However, other relationships apparent in the proposed model may reflect the early time point in recovery at which assessments were made. As noted previously, relationships among variables in the model may change over time post-injury. Examination of such shifts in the model over the course of recovery awaits further research. Implications for Future Research and Clinical Practice The proposed model for post-TBI depression is in an early stage of development and requires additional research for verification and elaboration. Future research should also be directed at further expanding the model to include other factors

1095

that may affect post-TBI depression, such as those identified in the literature reviewed in this article (eg, genetic, developmental, and psychosocial factors; alcohol and other drug use including prescription drug use; and associated physical injuries and pain, other comorbid or premorbid psychologic conditions and environmental factors). Nonetheless, the relationship between post-TBI depression and poor outcome specified in the proposed model has been consistently shown in the current study and previous research.34-36 This underscores the importance of recognizing and treating post-TBI depression. PostTBI depression not only is a treatable condition but also has significant secondary negative effects on quality of life and community participation. As noted previously,34,35 the relationship between self-appraisal of abilities and depression invites consideration of cognitive-behavioral therapy as a modality in the treatment of depression post-TBI. CONCLUSIONS Despite its parsimony, the final model presented here shows several relationships of importance in the care of individuals with TBI: (1) negative self-appraisal is a strong correlate of depression consistent with a cognitive-behavioral model of depression; (2) self-appraisal of disability is associated with depression, whereas external appraisal of disability is not; and (3) depression has a significant relationship to functional outcome independent of injury severity and disability. This model is at an early stage of development. Further examination and elaboration of the model and the development of more precise measurement technologies for assessing a number of factors in the model (such as, the organic effects of TBI and cognitive processes affecting self-appraisal after TBI) will be required to arrive at a more comprehensive and validated model of postTBI depression. Nonetheless, this preliminary model appears consistent with other research on post-TBI depression in focusing on the importance of addressing post-TBI depression and the consideration of a cognitive-behavioral approach to treatment. Perhaps the greatest value of preliminary attempts at model building, such as this one, is the questions that the process raises and the resulting impetus and direction for future investigation and development of assessment technologies. In this spirit, we propose this preliminary model to provide a framework for future research that may profitably focus on a variety of samples at various time points post-TBI. References 1. Kreutzer JS, Seel RT, Gourley E. The prevalence and symptom rates of depression after traumatic brain injury: a comprehensive examination. Brain Inj 2001;15:561-2. 2. Seel RT, Kreutzer JS, Rosenthal M, Hammond FM, Corrigan JD, Black K. Depression after traumatic brain injury: a National Institute on Disability and Rehabilitation Research Model Systems multicenter investigation. Arch Phys Med Rehabil 2003;84:177-84. 3. Seel RT, Kreutzer JS. Depression assessment after traumatic brain injury: An empirically based classification method. Arch Phys Med Rehabil 2003;84:1621-8. 4. Jorge RE, Robinson RG, Moser D, Tateno A, Crespo-Facorro B, Arndt S. Major depression following traumatic brain injury. Arch Gen Psychiatry 2004;61:42-50. 5. Fann JR, Burington B, Leonetti A, Jaffe K, Katon WJ, Thompson RS. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry 2004;61:53-61. 6. Jorge RE, Robinson RG, Arndt SV, Forrester AW, Geisler F, Starkstein SE. Comparison between acute- and delayed-onset depression following traumatic brain injury. J Neuropsychiatry Clin Neurosci 1993;5:43-9. Arch Phys Med Rehabil Vol 91, July 2010

1096

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

7. Jorge RE, Robinson RG, Arndt SV, Starkstein SE, Forrester AW, Geisler F. Depression following traumatic brain injury: a 1 year longitudinal study. J Affect Disord 1993;27:233-43. 8. Gomez-Hernandez R, Max JE, Kosier T, Paradiso S, Robinson RG. Social impairment and depression after traumatic brain injury. Arch Phys Med Rehabil 1997;78:1321-6. 9. Sander AM, Kreutzer JS, Rosenthal M, Delmonico R, Young ME. A multicenter longitudinal investigation of return to work and community integration following traumatic brain injury. J Head Trauma Rehabil 1996;11:70-84. 10. Morton M, Wehman P. Psychosocial and emotional sequelae of individuals with traumatic brain injury: a literature review and recommendations. Brain Inj 1995;9:81-92. 11. Witol AD, Sander AM, Seel RT, Kreutzer JS. Long term neurobehavioral characteristics after brain injury: Implications for vocational rehabilitation. J Vocational Rehabil 1996;7:159-167. 12. Levin HS, Goldstein FC, MacKenzie EJ. Depression as a secondary condition following mild and moderate traumatic brain injury. Semin Clin Neuropsychiatry 1997;2:207-15. 13. Hoofien D, Gilboa A, Vakil E, Donovick PJ. Traumatic brain injury (TBI) 10-20 years later: a comprehensive outcome study of psychiatric symptomatology, cognitive abilities and psychosocial functioning. Brain Injury 2001;15:189-209. 14. Malec JF, Brown AW, Moessner AM. Personality factors and injury severity in the prediction of early and late TBI outcomes. Rehabil Psychol 2004;49:55-61. 15. Rush BK, Malec JF, Brown AW, Moessner AM. Personality and functional outcome following traumatic brain injury. Rehab Psychol 2006;51:257-64. 16. Fedoroff JP, Starkstein SE, Forrester AW, et al. Depression in patients with acute traumatic brain injury. Am J Psychiatry 1992; 149:918-23. 17. Jorge RE, Acion L, Starkstein SE, et al. Hippocampal volume and mood disorders after traumatic brain injury. Biol Psychiatry 2007; 62:332-8. 18. Jorge RE, Robinson RG, Moser D, et al. Major depression following traumatic brain injury. Arch Gen Psychiatry 2004;61:42-50. 19. Jorge RE, Starkstein SE, Jorge RE, Starkstein SE. Pathophysiologic aspects of major depression following traumatic brain injury. J Head Trauma Rehabil 2005;20:475-87. 20. Jorge RE, Starkstein SE, Arndt S, et al. Alcohol misuse and mood disorders following traumatic brain injury. Arch Gen Psychiatry 2005;62:742-9. 21. Wallace CA, Bogner J. Awareness of deficits: emotional implications for persons with brain injury and their significant others. Brain Inj 2000;14:549-62. 22. Godfrey HPD, Partridge FM, Knight RG, Bishara S. Course of insight disorder and emotional dysfunction following closed head injury: a controlled cross-sectional follow-up study. J Clin Exp Neuropsychol 1993;15:503-15. 23. Hibbard MR, Ashman TA, Spielman LA, Chun D, Charatz HJ, Melvin S. Relationship between depression and psychosocial functioning after traumatic brain injury. Arch Phys Med Rehabil 2004;85(Suppl 2):S43-53. 24. Rowland SM, Lam CS, Leahy B. Use of the Beck Depression Inventory-II (BDI-II) with persons with traumatic brain injury: analysis of factorial structure. Brain Inj 2005;19:77-83. 25. Groom KN, Shaw TG, O’Connor ME, Howard NI, Pickens A. Neurobehavioral symptoms and family functioning in traumatically brain-injured adults. Archives of Clinical Neuropsychology 1998;13:695-711. 26. Leach LR, Frank RG, Bouman DE, Farmer J. Family functioning, social support and depression after traumatic brain injury. Brain Inj 1994;8:599-606. Arch Phys Med Rehabil Vol 91, July 2010

27. Curran CA, Ponsford JL, Crowe S. Coping strategies and emotional outcome following traumatic brain injury: a comparison with orthopedic patients. J Head Trauma Rehabil 2000;15:1256-74. 28. Moore AD, Stambrook M. Cognitive moderators of outcome following traumatic brain injury: a conceptual model and implications for rehabilitation. Brain Inj 1995;9:109-30. 29. Rosenthal M, Christensen BK, Ross TP. Depression following traumatic brain injury. Arch Phys Med Rehabil 1998;79:90-103. 30. Ownsworth TL, Oei TPS. Depression after traumatic brain injury: conceptualization and treatment considerations. Brain Inj 1998; 12:735-51. 31. Moldover JE, Goldberg KB, Prout MF. Depression after traumatic brain injury: A review of evidence for clinical heterogeneity. Neuropsychol Rev 2004;14:143-54. 32. Dikmen SS, Bombardier CH, Machamer JE, Fann JR, Temkin NR. Natural history of depression in traumatic brain injury. Arch Phys Med Rehabil 2004;85:1457-64. 33. Babin PR. Diagnosing depression in persons with brain injuries: a look at theories, the DSM-IV and depression measures. Brain Inj 2003;17:889-900. 34. Malec JF, Testa JA, Rush BK, Brown AW, Moessner AM. Selfassessment of impairment, impaired self-awareness, and depression after traumatic brain injury. J Head Trauma Rehabil 2007;22:156-66. 35. Phatak VS, Malec JF, Cicerone K, et al. Patient perception of disability and post-injury depression in traumatic brain injury (TBI). Thirty-Fifth Annual Meeting of the International Neuropsychological Society. Portland, OR; February 7–10, 2007. 36. Sliwinski M, Gordon WA, Bogdany J. The Beck Depression Inventory: is it suitable as a measure of depression for individuals with TBI? J Head Trauma Rehabil 1998;13:40-6. 37. Levin HS, Grossman RG. Behavioral sequelae of closed head injury. Arch Neurol 1978;35:720-7. 38. Satz P, Zaucha K, Forney DL, et al. Neuropsychological, psychosocial and vocational correlates of the Glasgow Outcome Scale at 6 months post-injury: a study of moderate to severe traumatic brain injury patients. Brain Inj 1998;12:555-67. 39. Satz P, Forney DL, Zaucha K, et al. Depression, cognition, and functional correlates of recovery outcome after traumatic brain injury. Brain Inj 1998;12:537-53. 40. Evans CC, Sherer M, Nick TG, Nakase-Richardson R, Yablon SA. Early impaired self-awareness, depression, and subjective well-being following traumatic brain injury. J Head Trauma Rehabil 2005;20:488-500. 41. Bush BA, Novack TA, Malec JF, Stringer AY, Millis S, Madan A. Validation of a model for evaluating outcome after traumatic brain injury. Arch Phys Med Rehabil 2003;84:1803-7. 42. Novack TA, Bush BA, Meythaler JM, Canupp K. Outcome following traumatic brain injury: contributions from premorbid, injury severity, and recovery variables. Arch Phys Med Rehabil 2001;82:300-5. 43. Jorge RE, Starkstein SE. Pathophysiologic aspects of major depression following traumatic brain injury. J Head Trauma Rehabil 2005;20:475-87. 44. Ownsworth T, Fleming J, Strong J, et al. Awareness typologies, longterm emotional adjustment and psychosocial outcomes following acquired brain injury. Neuropsychol Rehabil 2007;17:129-50. 45. Malec JF, Brown AW, Leibson CL, et al. The Mayo Classification System for Traumatic Brain Injury Severity. J Neurotrauma 2007; 24:1417-24. 46. Malec JF, Lezak MD. Manual for the Mayo-Portland Adaptability Inventory 2008. Available at: www.tbimis.org/combi/mpai. Accessed January 2, 2010. 47. Brown AW, Malec JF, McClelland RL, Diehl NN, Englander J, Cifu DX. Clinical elements that predict outcome after traumatic brain injury: a prospective multicenter recursive partitioning (decision-tree) analysis. J Neurotrauma 2005;22:1040-51.

POSTTRAUMATIC BRAIN INJURY DEPRESSION, Malec

48. Malec JF, Kragness M, Evans RW, Finlay KL, Kent A, Lezak MD. Further psychometric evaluation and revision of the MayoPortland Adaptability Inventory in a national sample. J Head Trauma Rehabil 2003;8:479-92. 49. Malec JF. Comparability of Mayo-Portland Adaptability Inventory ratings by staff, significant others and people with acquired brain injury. Brain Inj 2004;18:563-76. 50. Malec JF. The Mayo-Portland Participation Index (M2PI): a brief and psychometrically-sound measure of brain injury outcome. Arch Phys Med Rehabil 2004;85:1989-96. 51. Malec JF, Moessner AM, Kragness M, Lezak MD. Refining a measure of brain injury sequelae to predict postacute rehabilitation outcome: rating scale analysis of the Mayo-Portland Adaptability Inventory (MPAI). J Head Trauma Rehabil 2000;15:670-82. 52. Glenn MB, O’Neil-Pirozzi T, Goldstein R, Burke D, Jacob L. Depression amongst outpatients with traumatic brain injury. Brain Inj 2001;15:811-8.

1097

53. Perlesz A, Kinsella G, Crowe S. Psychological distress and family satisfaction following traumatic brain injury: injured individuals and thier primary, secondary, and tertiary carers. J Head Trauma Rehabil 2000;15:909-29. 54. Sherer M, Bergloff P, Boake C, High WJ, Levin E. The Awareness Questionnaire: factor structure and internal consistency. Brain Inj 1998;12:63-8. 55. Muthén LK, Muthén BO. Mplus user’s guide. 5th ed. Los Angeles, CA: Muthén & Muthén; 1998-2007. 56. Hu L-T, Bentler PM. Cutoff criteria for fit indexes in covariance structure analysis: conventional criteria versus new alternatives. SEM 1999;6:1-55. 57. Beck AT. Depression: causes and treatment. Philadelphia: University of Pennsylvania Press; 1967. Supplier a. Muthén & Muthén, 3463 Stoner Ave, Los Angeles, CA 90066.

Arch Phys Med Rehabil Vol 91, July 2010