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Diagnosing depression in persons with brain
injuries: a look at theories, the DSM-IV and
depression measures
PATRICIA ROGERS BABIN
Charlotte Institute of Rehabilitation, Charlotte, NC, USA
(Received 3 June 2002; accepted 13 January 2003 )
There have been numerous articles published on the incidence of depression after brain injury.Unfortunately, the studies have shown the incidence of depression varies widely depending on multi-ple factors: definition of ‘depression’, time of assessment post-injury and type of measure used. It is wellknown that traumatic brain injury (TBI) sequelae and depressive symptoms overlap, contributingfurther to measurement error and ultimately epidemiologic report of depression. This paper reviewsdifferent theories of depression, the DSM-IV depression diagnoses, the overlap in depression and TBIsymptoms and depression measures and how they contribute to possible diagnostic error. This paperalso discusses evaluation and treatment considerations when assessing depression in a person with aTBI.
Introduction
Depression is a relatively common diagnosis affecting at least 20% of people in thegeneral population at some point in their lives [1]. Persons surviving traumatic braininjury (TBI) may be even more susceptible to depression. The incidence rate forpersons with TBI ranges from less than 10% to 77% [2, 3]. Other authors have notedthat TBI is a risk factor for subsequent psychiatric disabilities, notably depression andanxiety disorders. Prevalence rates for comorbid diagnoses may be as high as 44%[4].
Obviously, there is a wide range of variability in the report of psychiatricdisorders—namely depression—after TBI. The disparity in report of depressivedisorders is the result of multiple factors. One problem has been that previousstudies have not been epidemiologic and have been limited by small, unrepresen-tative samples [5]. Another problem has been how a clinician or researcher makes adifferential diagnosis between depression and other depressive-like disorders associ-ated with TBI i.e. how interpretation of symptoms contributes to diagnostic error.The diagnosis of depression is further complicated by the number of DSM-IVdiagnostic categories from which a clinician can choose to diagnose depression[6]. Lastly, measurement error plays a large role in diagnosing depression. Manydepression inventories contain items that overlap with TBI sequelae—making thetests sensitive, but not specific. In addition, time of assessment post-injury affectsresponse patterns on tests of depression [7].
Brain Injury ISSN 0269–9052 print/ISSN 1362–301X online # 2003 Taylor & Francis Ltdhttp://www.tandf.co.uk/journals
DOI: 10.1080/0269905031000088595
Correspondence to: Patricia Rogers Babin, PhD, Charlotte Institute of Rehabilitation, 1100Blythe Blvd, Charlotte, NC 28203, USA. e-mail: [email protected]
BRAIN INJURY, VOL. 17, NO. 10 (OCTOBER 2003), 889–900
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This article will briefly discuss the neurological underpinnings of emotion anddepression: namely the limbic system. A number of theories of depression will belisted in order to provide a foundation and direction for making a differentialdiagnosis. The differential diagnosis between depression and dementia will beaddressed since a diagnosis of TBI can have some similarity with a dementia diag-nosis. This article also seeks to help the clinician clarify the distinction between braininjury sequelae and mood disorders—specifically depression and depression-likedisorders—as well as to help tease out the differential diagnosis among the variouscategories of depression-like disorders. A brief discussion of depression measures willbe included with comments about their strengths and weaknesses when used withpersons with TBI. The ultimate goal of the following discussion is to provide aframework for clinicians to diagnose and develop appropriate treatment plans forthe patient with a TBI.
Emotion, mood and the limbic system
Emotion has been defined as a reaction, both psychological and physiological,subjectively experienced as strong feelings, many of which prepare the body forimmediate action [8]. Certain emotions are considered primary emotions and arethought to be innate. They include happiness/joy, anger, sadness, fear, disgust and,more equivocally, love and surprise [8, 9]. Depression is considered a ‘mood state’and is generally more enduring than an emotion. Mood states are thought tofunction as moderators of emotional experience [9].
Emotions and moods are under the control of the brain. The limbic system,located in the dorsolateral frontal and medial temporal lobes of the brain, plays amajor role in the production of emotions and, ultimately moods. The limbic systemincludes the hypothalamus, which affects emotional responses through its control ofthe endocrine and autonomic systems; the amygdala, which is best known for itsrole in fear and aggressive behaviour; the hippocampus, which plays a critical role inmemory formation; and parts of the thalamus, which receives sensory input and actsas a relay station by sending messages to various parts of the brain.
There are major connections between the limbic system and the frontal lobes.The frontal lobes are employed to monitor and manage emotional input.Unfortunately, the frontal lobes are most susceptible to injury in acceleration/deceleration brain injuries. In addition, the limbic system—namely the hippo-campus—sustains numerous cellular changes resulting in neurotoxic injury as aresult of even mild brain injury. As such, emotions frequently become volatileand unpredictable in persons who have sustained a TBI with frontal-lobe injury[10].
Possible diagnoses
The rehabilitation specialist working with a patient with TBI has a number ofDSM-IV TR diagnostic categories from which to choose when assessing depressivesymptoms [6] (see table 1).
(1) Major depressive disorder is by far the most studied of these listed diagnosticoptions. Their specific diagnostic criterion lends itself to be readily measuredand, therefore, more easily diagnosed. The DSM-IV clearly delineates
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criteria, which must be experienced more times than not over a 2-weekperiod. To be diagnosed with a major depressive disorder, one must experi-ence either a depressed mood or loss of interest/pleasure plus at least four ofthe following symptoms: weight loss or gain; insomnia or hypersomnia;psychomotor agitation or retardation; fatigue or loss of energy; feelings ofworthlessness or guilt; diminished ability to think/concentrate or indecisive-ness; and/or recurrent thoughts of death or dying.
(2) Depressive disorder NOS is a general catchall category to diagnose a depressionthat does not meet the criteria for a major depressive episode, but clearlycauses the subject distress. Examples of this diagnosis are minor depression ordepression related to PMS.
(3) Mood disorder due to TBI with depressive features or with a major depressive-likeepisode is diagnosed when a medical condition—in this case, TBI—fullyaccounts for the depressive symptoms.
(4) Adjustment disorder with depressed mood is a diagnostic category used todescribe a depression that occurs after a major psychosocial stressor, butdoes not meet the criteria for a major depressive episode.
(5) Dementia due to head trauma with or without behavioural disturbance is diagnosedwhen the predominate feature of the presenting symptomatology is demen-tia, as defined by ‘significant memory impairment and one or more of thefollowing cognitive deficits: aphasia, apraxia, agnosia or a disturbance inexecutive functioning.’ It is not rare to find that a survivor of a severeTBI who has damage to the frontal and limbic structures will demonstratemany vegetative symptoms that ‘look’ like depression, but are more closelyrelated to a significant dementia.
Evaluating and diagnosing depression after TBI presents a diagnostic puzzle.Although the exercise may be academic, making the ‘best’ diagnosis is frequentlyuseful when considering treatment options.
Depression and dementia
Numerous articles have been written about research into the incidence and diag-nosis of depression in progressive dementias [11]. Many studies have looked at theoverlap of depressive and dementia symptoms, and there have been efforts todevelop measures and ways of assessing depression in patients with dementia toassist with making the differential diagnosis [12, 13]. If a person with a TBI sustains asevere enough injury and deficits are demonstrated in a number of cognitive areas(using the DSM-IV TR as a reference), the person may be diagnosed with a
Diagnosing depression in brain injuries 891
Table 1. DSM-IV TR diagnostic categories
296.2x Major depressive disorder
311 Depressive disorder NOS293.83 Mood disorder due to TBI with depressive features OR with major depressive-like disorder309.0 Adjustment disorder with depressed mood294.1 Dementia due to head trauma with or without behavioural disturbance.
Note that substance-induced mood disorders will not be addressed as they are beyond the purview of this paper.
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‘dementia due to head trauma.’ If a person also demonstrates symptoms consistentwith a major depressive disorder, which can’t be better accounted for by a dementia,depression can be diagnosed [6]. As many clinicians and researchers working withthe elderly know, making a differential diagnosis between depression and dementiacan be difficult. ‘Pseudodementia’ can present very similar to dementia. In theperson with TBI, the differential diagnosis can be just as difficult—the personwith a TBI is in a dynamic state of recovery and symptoms seen and/or reportedchange throughout recovery, making the diagnosis of depression perhaps a bit moreelusive.
Theories of depression
Some of the most common behaviours and symptoms seen in persons with acuteTBIs are flat affect, irritability, sleep and appetite disturbance, impaired concentra-tion and lability—all of which are ‘hallmarks’ of depression [6]. However, is itdepression that one is seeing? Hundreds, if not thousands, of articles and bookshave been published on the aetiology of depression. In order to diagnose depression,one must have some type of conceptual framework to guide the evaluation process.Throughout the years, if not centuries, many theories of depression have beenproposed: A few theories of depression are summarized below.
� Psychodynamic theories. Based on Freudian concepts, psychodynamic theoriessuggest that trauma or object loss early in a person’s childhood predisposes thatperson to developing depression later on. In other words, when a personexperiences loss through adult trauma, they re-experience their earlier traumaand become depressed [14].
� Learned Helplessness theory. Seligman [15] proposed that people becomedepressed when they experience recurrent failures or stressors they believethey cannot control. In addition, people may attribute external or internalevents incorrectly, making them more susceptible to depressive disorders. Forexample, if a person consistently attributes mistakes made on the job to someinternal consistent personal flaw, he or she will likely experience low self-esteem and subjective dysphoria.
� Cognitive theory. This theory purports that when people think in maladaptiveways, they assign negatively valenced interpretations to their perceptions.These distorted perceptions of the world and of self lead to stuck patternsof negative thought and behaviour [16].
� Physiological/biological theories. These theories suggest there are genetic and/orphysiological components to depression. For instance, some people mighthave a physiologically based impaired ability to generate important mood-related neurotransmitters such as serotonin and norepinephrine [17].
� Contemporary models. Contemporary models of depression argue that classifi-cations such as ‘reactive depression’ or ‘endogenous vs. exogenous’ depressionare no longer appropriate as they are deconstructive and simplistic.Depression, then, can be both reactive and physiological. Persons under agreat deal of stress release an excessive quantity of neurotoxic substances suchas corticotropin releasing factor (CRF), which affects hippocampal function-ing. Specifically, CRF is released during physical trauma, e.g., injury to thecortex or any other part of the body. Dysfunction of the hippocampus likely
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underlies some of the vegetative symptoms and cognitive deficits seen indepressed patients [18]. Chronic stress, biological predisposition and/or injurycan also trigger alterations in the norepinephrine, serotonin and dopaminecircuitry. Depletion of any one of these neurotransmitters is associated withany number of depressive symptoms [19, 20]. Additionally, functionalneuroimaging and post-mortem studies on persons with depression withouta history of TBI implicate dysfunction and reduced cortical volume in themedial orbitofrontal cortex as well as sub-cortical areas [21, 22].
Diagnosing depression after TBI
Traumatic brain injuries are commonly classified using initial Glasgow ComaScores: GCS of � 8 is severe, 9–12 is moderate and � 13 is mild. The types ofdeficits experienced by persons who have sustained brain injuries are, of course,multiple and varied. It is very common to see frontal lobe or executive dysfunctionand temporal lobe dysfunction after TBI from acceleration/deceleration events orblunt trauma, e.g., motor-vehicle accidents or falls. The mechanism of injury maybe manyfold, e.g., contusion, diffuse-axonal injury, shearing or haemorrhage. Injuryto the frontal and temporal lobes may be associated with deficits in attention,concentration, memory, problem-solving, organization, reasoning, social judge-ment, inhibition, initiation, pragmatics, awareness of deficits and emotion manage-ment. Emotion-management deficits may include increased irritability, lability,lowered frustration tolerance, disinhibition, anger dyscontrol and problems withaffect (namely flat affect) [23, 24].
In addition, sleep and appetite disturbances are frequently demonstrated afterTBI. A person’s sleep-wake cycle may be disturbed due to changes in neurotrans-mitters and/or damage to the brain stem and arousal regulating systems. Increasedsleep or need for sleep may be the result of the overwhelming fatigue and exhaus-tion frequently experienced by persons with TBI. Appetite disturbances may resultfrom olfactory bulb damage, hypothalamic damage or damage to taste receptors.Alterations to the olfactory and gustatory senses may serve to increase or decreaseeating and result in corresponding weight gain or loss. Damage to arousal andattention-regulating centres may correspond with difficulties focusing on and com-pleting the eating task, resulting in possible weight loss. Lastly, injury to thehypothalamus and certain areas of the frontal lobes may result in an increase ordecrease in food intake and result in weight changes [23, 24].
As previous research on the differential diagnosis of depression and dementia hasshown, brain injury sequelae—frontal lobe deficits in particular—overlap to a largedegree with symptoms of depression and, therefore, create a diagnostic differentialdilemma. Except for subjective feelings of guilt, feelings of worthlessness andthoughts of death or dying, the symptoms of a major depressive episode are con-sistent with many aspects of a TBI.
Consider the following case example: A 20-year-old female is admitted to arehabilitation hospital after sustaining a TBI in a motor-vehicle collision. Initial CTscan of the head reveals bilateral frontal hygromas and diffuse axonal injury. Inaddition to cognitive deficits, she has a fractured clavicle and ankle. Six weekspost-initial injury, she presents with flat affect, decreased initiation, wakefulnessduring sleep, irritability and lability. She is oriented in all spheres, but continuesto demonstrate decreased attention, concentration, memory and decision-making.
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She refuses some therapies complaining of pain and fatigue. The staff is concernedthat she is depressed. Your evaluation shows clear deficits in memory storage andretrieval and significant executive dysfunction. She is able to tell you what happenedto her and acknowledges post-traumatic amnesia for � 3 weeks. She denies prob-lems with any aspect of cognitive functioning. She has no awareness of her deficitsand demonstrates safety and judgement deficits. She is restless, but denies and doesnot demonstrate problems with tearfulness. Her affect is flat. She denies feeling sador anxious. She denies low self-esteem, guilt or feelings of worthlessness. She isoptimistic about her recovery and the future in general. She acknowledges problemswith sleep and appetite, indicating the nurses wake her up and the food has noflavour.
And so the question: Is she ‘depressed’ or not? As with many medical andpsychiatric conditions, the diagnosis cannot be made without a thorough evaluationof neurological impairment and mood status. If she is consistently denying andnot demonstrating emotional distress, from a DSM-IV mood-disturbance diagnosisstandpoint, she is probably not experiencing a mood disorder. This patient is likelydemonstrating symptoms consistent with injury to the frontal lobes and perhaps theolfactory bulbs and medial temporal areas of the brain. Of course, another major orleast intriguing issue that arises when assessing a mood disturbance such as depressionis whether or not the patient is aware of his or her own internal thoughts and moodstates. Certainly, there are persons without brain injury who deny depressive symp-toms and distress although they may appear depressed. Awareness of deficits, aware-ness of self and awareness of internal states is beyond the scope of this paper.However, awareness post-TBI can play a major role in how and when a diagnosisof depression can be made [25, 26].
Regardless of whether the patient in question is aware of her deficits andinternal mood states, the therapists working with her say she’s resistant, labile andlacks initiation. In this case, individual insight-oriented psychotherapy is not likelyto prove fruitful. This patient could better benefit from a structured treatment/behaviour programme. Education about the patient’s symptoms, differential diag-nosis and behavioural interventions should be offered to the treatment team, familyand, of course, the patient. The treating physician may want to consider medica-tions such as Ritalin or Amantadine to help with initiation and attention. Also, ananti-depressant, e.g., an SSRI, may be warranted for the treatment of symptomssuch as sleep and appetite disturbance, lability and irritability. It is not unusualpractice for physicians to prescribe medications ‘off label,’ that is, medications aresometimes prescribed to treat particular symptoms of one condition with medica-tions FDA approved for another diagnosis. In the case of TBI, medications FDAapproved for ‘depression’ are used to treat impaired initiation, lability, pathologiccrying, sleep disturbance and appetite disturbance, without a definitive diagnosis of aDSM-IV depressive disorder.
The previous case scenario highlights the difficulty in making a differentialdiagnosis. A consideration is whether the depression in patients with TBI is primary(or idiopathic) vs. secondary (or neurologic) [27, 28]. In other words, is the depres-sion truly a mood disturbance accompanied by subjective feelings of sadness and lowself-esteem, or does it arise from neurophysiological changes in brain functioning?Obviously, this is a dichotomous way of thinking and does not account for thecoexistence of a primary and neurologic depression. That is, a person can have
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neurological impairment and experience subjective feelings of loss and distress, i.e.depression in response to the neurological impairment.
Another issue that must be taken into account is the possible temporal relation-ship between the type of depression that develops after TBI. For example, Jorge etal. [7] suggest depressive symptoms that develop acutely are associated with neuro-physiological changes in the brain and late-onset depressions are associated withpsychosocial factors.
One should also consider another argument proposed—or at least implied—by anumber of authors and researchers: Making a distinction between endogenous(neurological or biochemical) and exogenous (reactive or psychosocial stress-related)depression is artificial and simplistic, as both ‘types’ of depression can lead toneurochemical changes in the brain [18, 29, 30]. With regard to persons withTBI, some studies have found that depression is associated with lesion location—specifically, damage to the left dorsolateral frontal and/or left basal ganglia, lefthemisphere in general, or frontal and temporal lobes in general, is associated withgreater incidence of depression [31–34]. As previously noted, time of assessment,type of measure and definition of depression have varied greatly among the studies,which contributes to the problem of accurately diagnosing depression and,ultimately, administering the appropriate treatment.
Measures of depression
Assessment of depression by standard depression instruments has contributed to theinconsistency and variability in diagnosis of depression in persons with TBI. Evendepression measures that were developed to account for symptoms found in medicaland aged populations, such as the Geriatric Depression Scale (GDS) and the HospitalAnxiety and Depression Scale (HAD Scale), contain items that may potentiallyconfound depression measurement. For example, the GDS queries memory,energy, crying, concentration and the HAD Scale asks about being ‘sloweddown’ and ‘restless.’ The Beck Depression Inventory (BDI and BDI-II) is a verycommon measure used to assess depression. Kathol et al. [35] summarized anumber of studies that used the BDI to assess depression in medical populations(not specifically TBI populations). The authors found that a substantial number ofpatients that scored above the cut-off scores were not, in fact, clinically depressed.The authors also explored the positive predictive value of the BDI and found thatlowering the cut-off score to account for an overlap in medical symptoms didnot significantly improve depression predictability. Kathol et al. [35] posited thatperhaps they were over-diagnosing depression in their medical populations.Interestingly, Kathol et al. [35] also suggested that using DSM-III R criteria, aswould be used during a Structured Clinical Interview for DSM-IV Axis IDisorders (SCID), is actually too restrictive and may lead to type II errors. Ofcourse, under-diagnosing depression using the DSM can easily occur if one doesnot consider that somatic or neurological complaints may not be due solely tomedical issues, but to very ‘real’ subjective feelings of distress. The issues discussedin depression measurement serve to highlight the problems of measurement errorwhen assessing mood disturbance in persons with TBI. Common instruments arelisted in table 2.
The goal in assessment is to find an instrument that is both sensitive and specificin diagnosing depression. As can be seen by viewing table 1, only one instrument to
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date—the NFI-R—has a depression scale that deals with the problems in measuringdepression in persons with TBI by including mostly subjective feelings associatedwith depression and avoiding somatic and neurological items that contribute todiagnostic confound. The depression and TBI item overlap of the more traditionaldepression measures makes the instruments sensitive, but not specific, in diagnosingdepression. In short, they ‘find’ depression in persons with TBI using traditionaldepressive diagnostic criteria, but they likely over-diagnose depression in this samepopulation.
Discussion
Persons with TBI may (or may not) report and/or demonstrate more depressivesymptoms as measured by traditional depression measures. Given this ambiguity, is
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Table 2. Common depression measures used with persons with TBI
Measure References Description and possible item confound
Beck DepressionInventory-II
(BDI-II)
[36, 37] 21 items; scored 0, 1, 2 or 3. At least 10 items overlapwith TBI sequelae: Crying, Agitation, Loss of Interest,Indecisiveness, Loss of Energy, Sleep, Irritability,Appetite, Concentration, Fatigue.
Center for EpidemiologicalStudies—DepressionScale (CES—D)
[38] 20 items; rated on 4-point likert-type scale. At least sevenitems overlap with TBI sequelae: Lowered frustrationtolerance, appetite, cognitive, fatigue/energy,restlessness, initiation, lability.
Hospital Anxiety andDepression Scale(HADS)
[39] Seven depression items; scored 0, 1, 2 or 3. At least twoitems overlap with TBI sequelae: ‘I can enjoy a goodbook or radio or TV programme’ and ‘I feel as if I amslowed down.’
Hamilton Rating Scalefor Depression(HRSD)
[40, 41] 21 items; scored 0, 1, 2; 0, 1, 2, 3; or 0, 1, 2, 3, 4.At least nine items overlap with TBI sequelae:Sleep (three items); Fatigue; Cognition (two items);Agitation; Appetite/Weight (two items).
HAM-D 17 items; scored 0, 1, 2; 0, 1, 2, 3; or 0, 1, 2, 3, 4.At least seven items overlap with TBI sequelae:Sleep (three items); Psychomotor Retardation;Agitation; Weight; Work.
Minnesota MultiphasicPersonalityInventory—2(MMPI-2)
[42] 57 depression items. At least 40 items overlap withTBI sequelae: Psychomotor retardation (14 items);Physical Malfunctioning (11 items); Mental Dullness(15 items).
NeurobehaviouralFunctioning Inventory-R(NFI-R)
[43] 83 items; rated on 5-point likert scale. 13 depressionitems—all subjective feeling states. NFI-R developedto reduce TBI and Depression diagnosis confound.
Structured ClinicalInterview for DSM-IVAxis-I Disorders (SCID)
[44] 62-page structured interview based on DSM-IV decisiontrees: multiple confounds due to variability ininterpretation and presumed aetiology of patientsymptoms.
Symptom Checklist-90-Revised (SCL-90-R)
[45] 90 items; rated on 5-point likert scale. 13 depressionitems. At least six overlap with TBI symptoms:Sleep, Appetite, Fatigue/Energy, Initiation, Cognitive.
Zung Depression Scale [46] Crying, Sleep, Appetite, Fatigue, Cognition, TaskCompletion, Restlessness, Indecisiveness.
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one getting an accurate reading on depression in persons with TBI? With mostcurrent depression measures, one might get the impression that depression isrampant in persons with TBI. This is not to say that they don’t have a ‘right’ tobe depressed. Their lives have changed. They’ve been through trauma. They mayhave physical changes. They may have significant cognitive challenges. They mayhave incurred financial loss. They may have lost their jobs. They may have lost theirindependence, their sense of self—the list goes on. This author argues it is notwhether they have clinically elevated scores on standard depression instruments;instead, evaluators need to look more closely at the quality of their responses.
High scores on any depression measure tend to indicate ‘something’ is up.Referring back to theories of depression, high scores could mean the person isfeeling out of control and has developed a learned helplessness. Perhaps the personhas a biological or genetic predisposition to develop depression. Perhaps the personhas always been struggling with a psychodynamic ‘loss’ and his or her currentsituation creates an even stronger need to have this loss replace or void filled. Inthese cases, one might create a treatment plan that emphasizes psychotherapy.
However, high scores could also represent symptoms consistent with damage tothe fronto-temporal cortex and/or neurotransmitter circuitry. For the sake of argu-ment, let’s say the person has a high depression score because of a significant cortexinjury (and, therefore, significant neurological symptoms) and he or she subjectivelyfeels his or her losses and feels distressed. In this case, the high depression scoredoesn’t give the evaluator any guidance regarding medical intervention or psycho-logical treatment. The person with both neurological deficits (consistent withDementia due to TBI) and subjective distress (consistent with a diagnosis of depres-sion) may require therapy, psychosocial support, and, possibly, medication.
What about persons with TBI who have clinically elevated scores on depressionmeasures, but deny—or at least fail to report—distress, sadness, low self-esteem and/or loss of pleasure? Are they depressed and simply unaware of how bad things reallyare? Possibly—awareness may have a lot to do with subjective distress. Do they havesignificant injury to their fronto-temporal and/or neurotransmitter circuitry andsimply do not ‘feel’ distressed or upset? Unfortunately, a depression measure maynot provide insight into the aetiology of an elevated depression score. The personwith an elevated depression score may benefit from medication and a behavioural/environmental intervention—it is up to the astute clinician to determine the diag-nosis and best plan of treatment.
Regardless, the issue, this author argues, is that high scores on traditional depres-sion measures don’t give enough information. One needs to come up with bettermeasures of depression for persons with TBI and dementia in general. The NFI-R isa great start. Normed on persons with TBI, the NFI-R attempts to distinguishamong somatic symptoms, cognitive symptoms and subjective distress.
A colleague once argued that trying to make a distinction between vegetative/neurological symptoms of depression and subjective feelings of distress associatedwith depression was simply an academic exercise. This author believes making adistinction is not a frivolous waste of neurochemical energy. If health-care profes-sionals can be more specific in their diagnosis, more appropriate medications can beprescribed to target specific symptoms, and psychotherapeutic interventions can bebetter tailored to meet the needs of the patient. For example, providers can deter-mine whether or not a patient would benefit from insight-oriented psychotherapy,cognitive-behavioural psychotherapy or a behaviour-management plan.
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Recommendations
When a healthcare professional is asked to evaluate a person with a TBI for depres-sion, the professional should keep in mind the issues listed in table 3.
References
1. ROBIN, L. N. and REGIER, D. A.: Psychiatric Disorders in America: the epidemiologic catchment areastudy (New York: The Free Press), 1991.
2. RUTHERFORD, W. H., MERRETT, J. D. andMCDONALD, J. R.: Sequelae of concussion causedby minor head traumas. Lancet, 1: 1–4, 1977.
3. VARNEY, N. R., MARTZKE, J. S. andROBERTS, R. J.: Major depression in patients with closedhead injury. Neuropsychology, 1: 7–9, 1987.
4. HIBBARD, M. R., UYSAL, S., KEPLER, K. et al.: Axis I psychopathology in individuals withtraumatic brain injury. Journal of Head Trauma Rehabilitation, 13: 24–39, 1998.
5. ROSENTHAL, M., CHRISTENSEN, B. K. and ROSS, T. P.: Depression following traumatic braininjury. Archives of Physical Medicine and Rehabilitation, 79: 90–103, 1998.
6. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4thedn—Text Revision (Washington, DC: American Psychiatric Association), 2000.
7. JORGE, R. E., ROBINSON, R. G. and ARNDT, S. V.: Are depressive symptoms specific for adepressed mood in tbi? Journal of Nervous and Mental Disorders, 181: 91–99, 1993.
8. GALE ENCYCLOPEDIA OF PSYCHOLOGY: Emotions (Gale Group, Inc) (website), 1–2, 2002.9. STARRATT,C.: Emotional disorders associated with neurological disease. In: P. J. Snyder and P. D.
Nussbaum (editors) Clinical Neuropsychology: A pocket handbook for assessment (Washington, DC:American Psychological Association), pp. 613–628, 1998.
10. BUSCH, C. R. andALPERN, H. P.: Depression after mild traumatic brain injury: a review of thecurrent literature. Neuropsychology Review, 8: 95–108, 1998.
11. ROSENSTEIN, L. D.: Differential diagnosis of the major progressive dementias and depression inmiddle and late adulthood: a summary of the literature of the early 1990s. Neuropsychology Review,8: 109–167, 1998.
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Table 3. Assessment considerations
(1) Time of assessment:(a) Is the person very early in his recovery and still severely impaired from a cognitive standpoint?
Is the person aware of his surroundings and/or deficits? Are the symptoms more consistentwith neurological injury and brain-injury recovery?
(b) Is the person being evaluated later in his recovery and is he experiencing significantpsychosocial stress of internal distress?
(2) History of depression: A TBI survivor with a history of depression may be at higher risk fordeveloping a depressive disorder.
(3) Type of measure: Is the measure loaded with vegetative or neurological items that could beattributed to TBI sequelae and not just depression?
(4) Type of measure: Can subjective depression and neurological symptoms be qualitatively analysed?(5) DSM-IV diagnosis: Is there one diagnosis that fits the symptoms better than others? If not, should a
depression diagnosis be deferred?(6) Treatment plan (medical): Regardless of whether or not the TBI survivor reports or demonstrates
vegetative/neurological symptoms of depression or feels subjectively depressed, could the patientbenefit from a particular medication?
And lastly:
(7) Treatment plan (psychological/behavioural): If the survivor expresses emotional distress, sadness, lowself-esteem, etc., could he benefit from insight-oriented psychotherapy?
(8) If the patient lacks insight, denies sadness or distress, could he benefit from a systematic behaviourprogramme?
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