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Address for correspondence: Dr Amanda Lane-Brown, Rehabilitation Studies Unit, c/– Royal Rehabilitation CentreSydney, PO Box 6, Ryde NSW 1680, Australia. E-mail: amandal@med.usyd.edu.au

Apathy After Traumatic Brain Injury: An Overview of the Current State of Play

Amanda T. Lane-Brown1,2 and Robyn L. Tate1,2

1 Rehabilitation Studies Unit, Northern Clinical School, Sydney Medical School, University of Sydney,Australia

2 Royal Rehabilitation Centre Sydney, Australia

Apathy is a decrease in behavioural, cognitive and emotional components ofgoal-directed behaviour. Clinically, it is characterised by diminished initiation,

reduced concern, and decreased activity. Apathy is a common occurrence follow-ing traumatic brain injury (TBI), occurring in around 60% of people.Consequences are widespread, negatively impacting independence, social inte-gration, rehabilitation outcome, vocational outcome, coping and caregiver burden.The current knowledge base on apathy following TBI is presented, with implica-tions for clinical practice. This includes a review of clinical presentations, neu-roanatomical and neurochemical substrates associated with apathy, anddifferential diagnoses. Instruments to measure apathy are presented, highlightingthose with demonstrated reliability and validity for the TBI population. Current evi-dence for pharmacological and non-pharmacological methods of treatment isdescribed, with a model for non-pharmacological interventions provided and dis-cussion of challenges faced by clinicians when treating the patient with apathy. Inthe TBI arena, greater understanding of apathy and methods of treatment is piv-otal given the frequency of occurrence and widespread negative consequences.

Keywords: apathy, traumatic brain injury, goal, motivation, activity, drive

Of the executive dysfunctions ‘perhaps the mostserious … (is) the impaired capacity to initiateactivity, decreased or absent motivation, anddefects in planning and carrying out the activitysequences that make up goal-directed behaviours’(Lezak, Howieson, & Loring, 2004, p. 36). Thisproblem, termed apathy, has been referred to inneurological literature for many years (e.g.,Bianchi, 1895, cited in Benton, 1991). However,over the last 20 years it has attracted increasinginterest following the landmark work of Marin(1990, 1991). In the traumatic brain injury (TBI)arena, greater understanding of apathy and meth-ods of treatment is pivotal because it occurs fre-quently and has numerous and widespreadnegative consequences.

Apathy is a common occurrence followingTBI. Published prevalence rates range from 46.4%(Andersson, Krogstad, & Finset, 1999) to 71.1%(Kant, Duffy, & Pivovarnik, 1998). Van Reekum

Stuss, and Ostrander (2005) undertook an exten-sive literature review to collate data regarding theprevalence of apathy following TBI and found apoint prevalence of 61.4%. The variability inprevalence rates among studies results from a lackof consensus in definitions, difficulties in mea-surement, and differences in clinical samples.Irrespective of the precise prevalence, when itoccurs apathy is a significant source of disabilityand an obstacle to improving functional ability.Disorders of behavioural excesses, such as disin-hibition, aggression or impulsivity may be morestriking, however, the behavioural deficiencies,such as apathy, are equally disabling withwidespread effects. Gray, Shepherd, and McKinley(1994) investigated the impact of apathy on 53TBI patients one year post-discharge. This studyindicated that apathy negatively affected numer-ous areas, including rehabilitation status, indepen-dence, activity and social integration. Presence of

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AMANDA T. LANE-BROWN AND ROBYN L. TATE

apathy (specifically, loss of initiative) is a predic-tor of employment status (Crepeau & Scherzer,1993), compounded by the patient with apathybeing less willing to look for employment(Prigatano, 1992), thereby negatively impactingvocational outcome (Gray et al., 1994). Mazaux etal. (1997) demonstrated that apathy also negativelyaffects social autonomy. Apathy impacts copingskills, with patients with apathy adopting passivecoping strategies characterised by a lack of active,approach-oriented coping behaviour (Finset &Andersson, 2000). The impact of apathy may beexaggerated by the patient with apathy not receiv-ing treatment either because he/she withdraws fromtreatment or because the behavioural excesses, dueto their often confronting nature, are the primaryfocus of clinical attention. Furthermore, apathy notonly affects the patient, it also increases strain onthe relative (Gray et al., 1994) and creates caregiverburden (Marsh, Kersel, Havill, & Sleigh, 1998). Tocompound matters, long-term outcome studieshave reported a statistically significant increase inapathy over time (Thomsen, 1984). These numer-ous consequences suggest apathy can have devas-tating effects on rehabilitation and outcome.

This article presents the current knowledge onapathy following TBI, with implications for clini-cal practice. It includes a review of clinical pre-sentations, neuroanatomical and neurochemicalsubstrates associated with apathy, and differentialdiagnoses. Instruments to measure apathy are pre-sented, highlighting those with demonstrated reli-ability and validity for use within the TBIpopulation. Current evidence for pharmacologicaland non-pharmacological methods of treatment isdescribed, with a model for non-pharmacologicalinterventions provided and discussion of chal-lenges faced by clinicians when treating thepatient with apathy.

Clinical Presentations and Clinico-Pathological CorrelatesIn Stoic philosophy, apathy refers to an absence ofpathe, or emotions and passions (EncyclopaediaBrittanica, 2002). This was considered a positivetrait and something for which to strive. Today, theterm has more negative connotations, with mostEnglish language dictionaries defining apathy asdiminished interest, emotion or concern. Withinthe neurological literature excellent headway wasmade towards creating an operational definitionthrough the work of Marin (1991) and Stuss, vanReekum, & Murphy (2000). The most commonlyused definition is a decrease in behavioural, cog-nitive and emotional components of goal-directed

behaviour (Marin, 1991), which will be used forthe remainder of this article. It is noted, however,that in a recent review paper on the nosologicalposition of apathy, Starkstein and Leentjeens(2008) conclude that there is currently no consen-sus on definitions and that research is being ham-pered by a lack of universally accepted diagnosticcriteria. This fundamental issue is being addressedby a working party lead by Marin (Wongpakaran& van Reekum, 2007) and ‘Apathy Syndrome’ isnow being considered for inclusion in the fifthedition of the American Psychiatric Association’sDiagnostic and Statistical Manual (AmericanPsychiatric Association, 2010). Clarificationregarding definition and diagnostic criteria will beinvaluable to the field and future research.

Apathy falls at the milder end of a continuumof severity (Marin, 1997). As apathy increases inseverity, it becomes abulia, characterised bypoverty of speech and behaviour, with corre-sponding lack of initiation, emotional responses,psychomotor slowing and inability to regulatepurposeful behaviour (Marin, 1990; Marin &Wilkosz, 2005). As abulia worsens, it is classed asakinetic mutism, a total absence of speech ormovement in the presence of visual tracking(American Congress of Rehabilitation Medicine,1995). Clinically, apathy is characterised bydiminished initiation, concern and goal-directedbehaviour, as described below:

Behavioural components of apathy refer to aperson’s engagement or performance in goal-directed activities (Andersson & Bergedalen,2002). The patient with apathy has impaired self-initiated activity or responsiveness to stimuli(Stuss et al., 2000). Clinically, this may be seen asa difficulty in commencing activity towards agoal. Other characteristics include diminishedeffort or productivity (Resnick, Zimmerman,Magaziner, & Adelman, 1998), observed as diffi-culty sustaining effort and activity in order tocomplete a goal. A common change followingbrain injury is the diminished ability to translateplans into goal-directed activity (Goldstein &Levin, 1989), viewed as anergia, or social with-drawal. Consequently, people with apathy can bedescribed as sluggish and disengaged.

Cognitive components of apathy, as described byMarin (1991), refer to goal-directed cognition(later termed ‘thought content’; Marin & Wilkosz,2005) operationalised as interest, concern andimportance placed in goal-related domains.Apathy is placed within the realm of executivefunctioning (Cummings, 1985) and correlateswith tests of executive functioning (Andersson &

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Bergedalen, 2002; Crowe, 1992). Thus it is sug-gested that cognitive functions are integral togoal-directed activity and therefore should beincluded in the cognitive components of apathy.The cognitive components required for achievinga goal can be framed as the thinking skills neces-sary to create a plan, start and sustain the requiredaction, and cease action when the goal is met. Thisprocess requires generativity, volition, initiation,ability to sustain activity, and ability to stay ontask.

Emotional components of apathy refer to thelevel of emotional responsivity and excitementinduced by negative or positive events (Marin,1991). Clinically, the patient with apathy presentswith flattened, shallow or unchanging affect, emo-tional blunting, or reduced emotional responsivity(Marin, 1990; Marin & Wilkosz, 2005; Resnick etal., 1998).

Neuroanatomical and NeurochemicalSubstrates of ApathyThere are a number of potential causes of apathy;for example, side-effects of medication (such asselective serotonin-reuptake inhibitors; Barnhart,Makela, & Latocha, 2004; Hoehn-Saric, Lipsey,& McLeod, 1990). The subject of this article,however, is apathy resulting from cerebraldamage, the candidate functional systems beingthe frontal lobes and/or limbic system (Stuss et al.,2000). Frontal dysfunction, particularly in the pre-frontal cortex, leads to adynamia and inertia(Luria, 1973; Stuss et al., 2000). Dysfunction ofdifferent areas of the prefrontal cortex have beenlinked to slightly varying clinical presentations ofapathy: the convexity of the lateral surface of theanterior frontal lobes are linked to indifference,psychomotor slowing, impersistence, cognitiverigidity, and decreased generativity (Cummings,1985); the dorsolateral surface leads to a decreasein generativity and active selection of behaviours,whereas lateral orbitofrontal areas result in per-sonality and affective blunting (Stuss et al., 2000).Medial frontal dysfunction leads to paucity ofspontaneous movement and reduced verbal output(Cummings, 1985).

The limbic system is also implicated in apathy.The anterior cingulate gyrus plays a role in goal-directed behaviours such as reward-based deci-sion-making (Bush et al., 2002). The broadconnectivity of the cingulate gyrus with theremainder of the limbic system connects thesestructures to the frontal lobes (Lezak et al., 2004).Studies of people with Alzheimer’s diseasedemonstrate that damage to the anterior cingulate

leads to apathy (Migneco et al., 2001). Morespecifically, damage to the anterior cingulate gyrusleads to diminished initiation, emotional respon-sivity, behavioural regulation, along with affectiveplacidity and disrupted ability to assess internaland external stimuli for motivational information(Stuss et al., 2000). Disruption to neural circuitsthat lead to apathy include circuits linking thefrontal lobes to the thalamus, striatum, globus pal-lidus and substantia nigra (Cummings, 1993; Mega& Cummings, 1994). Bhatia and Marsden (1994)report that apathy was the most commonbehavioural effect in 240 (mainly) stroke caseswith lesions to the basal ganglia, particularly thecaudate nucleus. Cummings (1993) also describeda ‘globus pallidus syndrome’, where all reviewedreports of globus pallidus lesions resulted inmarked apathy.

Neurochemically, dopamine is the neurotrans-mitter most commonly linked to apathy.Abnormal functioning in dopaminergicfrontal/subcortical pathways is related to changesin goal-directed activities and apathy (Masterman& Cummings, 1997). Pharmacological studiesalso support a link between apathy and dopamine.There is evidence suggesting that dopaminelargely mitigates the reward properties of stimuli,thereby increasing or decreasing the likelihood ofgoal-directed behaviour (Nader, Bechara, & vander Kooy, 1997). A decrease in passivity isobserved through treatment with dopamine ago-nists acting on dopaminergic projections linkingthe prefrontal cortex with the limbic system(Muller & von Cramon, 1994). Other neurotrans-mitters play smaller roles in apathy. Glutamate hasbeen linked with goal-directed behaviour: Whiledopamine ‘directs’ behaviour, glutamate controlsthe ‘intensity’ of behaviour (Duffy, 2006).Similarly, the cholingeric system has been incor-porated into the neurochemistry of apathy becauseit has a stimulatory influence on dopamine efflux(Duffy, 2006).

Subtypes of ApathyThe varying clinical presentations of patientswith apathy, along with the neuroanatomical/neu-rochemical specificity, suggest heterogeneitywithin the apathy construct, consistent with thesubtypes of apathy (Duffy, 2006; Levy & Dubois,2006; Marin, 1996; Stuss et al., 2000). The sub-types vary in terms of the emphasis given to eachof the behavioural, cognitive and emotional com-ponents.

Marin (1996) suggests four subtypes ofapathy, as follows: cognitive apathy (associatedwith executive dysfunction), motor apathy (asso-

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AMANDA T. LANE-BROWN AND ROBYN L. TATE

ciated with extrapyramidal motor dysfunction),sensory apathy (following corticosensory impair-ment) and affective apathy (apathy occurring inthe absence of associated symptoms of cognitive,motor or sensory apathy). Duffy (2006) also refersto four subtypes very similar to Marin’s (1996),with corresponding neural subcircuitry linked toeach subtype (see Figure 1). However, in Duffy’ssubtypes, sensory apathy has been replaced by‘arousal’ apathy. Disruption to these different sub-circuits results in slightly varying clinical presen-tations of apathy. The ‘cognitive’ subcircuitassists in coordinating the cognitive functions fora motivational response. The ‘motor’ subcircuit,on the other hand, acts as the working memory formotivational responses, thus allowing prioritisa-tion and facilitation of motivational responses.The ‘arousal’ subtype refers to the autonomicresponse to motivational stimulus and the ‘emo-tional’ subcircuit acts to integrate the memory ofreward potential with the behavioural response.

In developing these subtypes, both Marin(1996) and Duffy (2006) emphasise the importanceof motivation to the apathy construct. Other authors(Levy & Dubois, 2006; Stuss et al., 2000) arguethat this creates confusion because of the numerousinterpretations for the psychological construct of‘motivation’. These authors suggest apathy shouldbe based on observable behaviours (rather than psy-chological constructs) that can then be linked toneural substrates and circuitry. This method yieldsthree subtypes. The work of Levy and Dubois(2006) extensively and convincingly builds on theinitial proposal from Stuss et al. (2000) for threesubtypes. This division into subtypes links closelywith the operational definition of apathy; namelybehavioural, cognitive and emotional componentsof goal-directed behaviour. Regions of the basal

ganglia located within limbic territories, particu-larly the globus pallidus, are linked to the ‘auto-activation’ subtype (termed ‘behavioural’ subtypeaccording to Stuss et al., 2000). This subtype isassociated with difficulties in self-initiatingthoughts and behaviours. The ‘cognitive’ subtype isassociated with dysfunction of the lateral prefrontalcortex and dorsal basal ganglia, particularly thecaudate nucleus. This subtype is typified by deficitsin generativity, maintenance of set, sustaining, cog-nitive flexibility and planning. The third subtype,the ‘emotional-affective’ subtype, is associatedwith dysfunction of the orbital-medial prefrontalcortex and is characterised by impaired ability todecode emotional content and diminished ability toassociate emotion with behaviour leading to emo-tional blunting and loss of interest in day-to-dayactivities.

Differential DiagnosisApathy is distinguished from decreased levels ofconsciousness (such as a minimally consciousstate) and extremely severe global cognitiveimpairment (Marin, 1990). Additionally, apathy isdifferentiated from fatigue, substance abuse andemotional distress (Duffy, 2006; Marin, 1990).The differential diagnosis between apathy andemotional distress, specifically depression, is thesubject of considerable investigation. Symptomsof apathy overlap with those of depression, suchas flattened affect, reduced responsivity and iner-tia (American Psychiatric Association, 2000;Marin, 1991). However, Marin, Firinciogullari,and Biedrzycki (1993) argue that these two con-structs are distinct and discernable despite theconceptual overlap. This distinction can be illus-trated with reference to emotional concern; the

Cognitive apathy Motor apathy Arousal apathy Emotional apathy

Ventral pallidum Ventral tegmental area Ventral pallidum Ventral tegmental area

Mediodorsal nucleus Nucleus accumbens Pedunculopontine nucleus Amygdala

Pre-frontal cortex Ventral pallidum Ventral tegmental area Nucleus accumbens

Nucleus accumbens

Ventral tegmental area

FIGURE 1Neural subcircuitry corresponding to varying subtypes of apathy.

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patient with apathy displays diminished concernwhereas the depressed patient suffers from emo-tional distress. There is strong empirical supportfor a differential diagnosis in the dementia popu-lation and following stroke (e.g., Levy et al., 1998;Marin, Biedrzycki, & Firinciogullari, 1991;Starkstein et al., 1992). Within the TBI popula-tion, investigators have also examined the abilityto differentially diagnose apathy from depression,the majority indicating dissociation between thetwo constructs (Al-Awadi, Powell, & Greenwood,1998; Kant et al., 1998; Lane-Brown & Tate,2009a).

Measurement of ApathyDespite the number of scales that have been devel-oped to measure apathy, only two have been vali-dated in the TBI populations, the ApathyEvaluation Scale (AES; Marin et al., 1991) andthe Frontal Systems Behavior Scale, Apathy sub-scale (FrSBe-A; Grace & Malloy, 2001). Themost commonly used scale to measure apathy isthe AES. There are three versions available: clini-cian, informant and self-rated. This rating scalewas developed based on Marin’s (1991) defini-tion: diminished behavioural, cognitive and emo-tional components of goal-directed activity due toreduced motivation. The 18 items were selectedwith reference to pertinent literature, consultationwith colleagues, clinical knowledge and statisti-cal analysis on items following a trial of 40patients with dementia or depression. A thoroughpsychometric study on 123 participants between55 to 85 years old from four groups (stroke,Alzheimer’s disease, depression and healthyolder people) revealed this was a psychometri-cally sound measure. The AES has recently beenvalidated in the TBI population (Lane-Brown &Tate, 2009a), with findings indicating this is areliable and valid measure for use within thispopulation. Internal consistency is high(Cronbach α = .89), and concurrent validitybetween the AES and FrSBe-A is moderate (r =.71, p = .00). Discriminant validity is demon-strated by differentiating apathy from bothdepression and fatigue. A cut-off score of 37 orhigher to indicate presence of apathy within theTBI population was identified with reasonablediagnostic accuracy (83% sensitivity and 67%specificity). The FrSBe-A (Grace & Malloy,2001) has two versions available, family and self-rated. It is reliable and valid for use within theTBI population, and is able to dissociate apathyfrom depression and fatigue (Lane-Brown &Tate, 2009a).

A number of other scales developed to mea-sure apathy in neurological populations other thanTBI have been published. Starkstein et al. (1992)abridged the AES for people with Parkinson’s dis-ease to the 14-item Apathy Scale. The ApathyScale is valid and reliable in the Parkinson’s dis-ease population (Starkstein et al., 1992) and hashigh intra- and inter-rater reliability withinAlzheimer’s disease and stroke populations(Peyser & Fedoroff, personal communication,cited in Starkstein et al., 1992). The Lille ApathyRating Scale (Sockeel et al., 2006), like the AES,used Marin’s (1991) operational definition. It wasdeveloped to overcome the criticism that the AESsuffers from a lack of standardisation in theadministration instructions and scoring method.This scale comprises 33 items falling into one ofnine domains corresponding to a clinical manifes-tation of apathy. Subgroups of these nine domainscores are combined to produce four factorial sub-scores: intellectual curiosity, emotion, action initi-ation and self-awareness. The self and caregiverversions of this scale are reliable and valid for usewith patients with Parkinson’s disease (Dujardin,Sockeel, Delliaux, Destee, & Defebvre, 2008;Sockeel et al., 2006).

The Apathy Inventory (Robert et al., 2002)was developed to measure apathy in observable,behavioural terms. Three dimensions assessed inthis scale were chosen with reference to the litera-ture, Marin’s (1991) operational definition ofapathy, and diagnostic criteria utilised in the AES(Marin et al., 1991). These three dimensions com-prise emotional blunting, lack of initiative and lackof interest. The caregiver or patient is interviewedabout the presence of behaviour changes relevantto apathy, and if behaviour change is reported, thefrequency and severity of the behaviour isassessed. This scale is validated for use with theAlzheimer’s disease, Parkinson’s disease, mildcognitive impairment, and healthy elderly popula-tions (Robert et al., 2002). Finally, theNeuropsychiatric Inventory (Cummings, 1994)was developed to measure 10 neurobehaviouraldisorders present in dementia, including apathy.Administration consists of a caregiver being inter-viewed about patient behaviours. This scale is wellvalidated in the dementia population. A recentpilot study utilised the Neuropsychiatric Inventoryto assess the possibility of using this instrumentwith the TBI population (Kilmer et al., 2006), withpreliminary results suggesting this measure maybe suitable. However, this scale also incorporatesmeasures of some behaviours relevant to dementiathat are not common following TBI, such as hallu-cinations and aberrant motor behaviours.

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To date, only questionnaires and interviewshave been validated for use in the diagnosis ofapathy. These measures may be included within abroader assessment of cognitive, emotional andbehavioural functioning to confirm findings andassist in the differential diagnosis of conditionswith overlapping symptomatology, such asdepression. In addition, given that previousresearch indicates discrepancies between self, rel-ative and clinician report in brain injury popula-tions, particularly when the person with braininjury has diminished insight (Malec, Machulda& Moessner, 1997), it is suggested that ratingsshould be obtained from multiple sources and incombination with other objective measures wherepossible.

Treatments for ApathySome evidence is available on which to base treat-ment practice in the TBI literature, although it issparse and hampered by limited high-quality stud-ies. Interventions can be conveniently divided intopharmacological and non-pharmacological inter-ventions, with the focus of this review on non-pharmacological interventions.

Pharmacological Treatments These treatments act by targeting neurotransmit-ters known to be associated with apathy, namelydopamine and acetylcholine. There is, however,no high-quality evidence evaluating pharmacolog-ical treatments for apathy following TBI, as indi-cated by a Cochrane systematic review searchingfor randomised, controlled trials (RCT) of treat-ments for apathy (Lane-Brown & Tate, 2009b). Tothe best of the authors’ knowledge, lower levels ofevidence have not been systematically reviewed todate, although there are a number of non-system-atic reviews (e.g., Campbell & Duffy, 1997; Kant& Smith-Seemiller, 2002; Marin & Wilkosz,2005; Roth, Flashman, & McAllister, 2007; Stusset al., 2000). These reviews have highlighted therole of dopamine agonists, such as amantadine,bromocriptine and selegline, in increasingtalkativeness and activity level (Roca, Santmyer,Gloth, & Denman, 1990), and decreasing apathyin individuals with TBI (Newburn & Newburn,2005; van Reekum et al., 1995) and in mixed neu-rological populations (Barrett, 1991; Powell, Al-Adawi, Morgan, & Greenwood, 1996).Psychostimulants, such as methylphenidate (apotent dopaminergic releaser) also show promisein the treatment of apathy (Chatterjee & Fahn,2002). Acetylcholinesterase inhibitors, such asdonepezil, galantamine and rivastigmine, have

demonstrated ability to improve apathy in the TBIpopulation (Masanic, Bayley, van Reekum, &Simard, 2001; Tenovuo, 2005).

Non-Pharmacological Treatments These treatments for apathy were the subject oftwo systematic reviews (Lane-Brown & Tate,2009b; Lane-Brown & Tate, 2009c). The afore-mentioned Cochrane review (Lane-Brown & Tate,2009b) demonstrated a scarcity of evidence fortreatments of apathy following TBI. Given thisfinding, in conjunction with the knowledge thattreatments can successfully be utilised across neu-rological populations (Glisky & Schacter, 1988), abroader systematic review (Lane-Brown & Tate,2009c) was conducted incorporating a range ofmethodological designs and neurological groups.Results of this review identified 28 trials, three-quarters of which were conducted in the dementiapopulation. Five empirical studies examined theTBI population, providing varying levels of evi-dence. One RCT was identified (Smith, Tiberi, &Marshall, 1994), investigating cranial electrother-apy stimulation to decrease inertia, a componentof apathy. Although cranial electrotherapy stimu-lation improved fatigue/inertia, no between-groupanalysis was conducted and thus it was not possi-ble to determine if the treatment was more effec-tive than control group treatments. A non-RCT(von Cramon, Matthes-von Cramon, & Mai,1991) treated, inter alia, the generation of goal-directed ideas using problem-solving training.Similarly, no between-group statistical analysiswas conducted and therefore it is unknown if theproblem-solving training was more effective thanthe memory-training control. Three single-partici-pant designs also investigated treatments forapathy after TBI. Burke, Zencius, Wesolowski,and Doubleday (1991), in a well-designed study,introduced checklists with tasks in sequentialorder to improve self-initiation. The three partici-pants with TBI improved self-initiation, withimprovements maintained after withdrawal oftreatment. Sohlberg, Sprunk, and Metzelaar(1988) used external cueing to successfullyprompt verbal initiation in a patient followingsevere TBI, with maintained increased initiationpost-treatment. DePoy, Maley, and Stanraugh(1990) utilised computerised cognitive retrainingand paper-and-pencil cognitive retraining to treatinitiation with inconsistent results. Additional tothe above systematic review findings, a multiple-baseline, single-case experimental design (Lane-Brown & Tate, 2010) indicated that motivationalinterviewing and external compensation effec-

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tively decreased apathy, and increased initiationand sustained activity for cumulative goals.

Findings from the previously mentionedbroader systematic review (Lane-Brown & Tate,2009c) suggested that treatment for apathyshould differ depending upon the patient’s levelof functional impairment. Marin and Wilkosz(2005) suggest a series of steps for the pharma-cological treatment of apathy. This model can beadapted and combined with current empiricalevidence to provide a model of best practice fornon-pharmacological interventions for apathy inpatients with TBI. This treatment model is sum-marised in Figure 2.

Diagnosis: Ease of diagnosing the presence ofapathy is enhanced by routine assessment ofapathy symptomatology with a standardised andvalid measure that is quick to administer andscore. The AES and the FrSBe-A are good candi-dates for this purpose. When choosing a cut-off

score to indicate presence of apathy, given thewidespread impact and likelihood of patients withapathy to withdraw from treatment, underestima-tion is of greater concern than overestimation. Inother words, sensitivity is of great clinical impor-tance, even if it is at the expense of specificity.Simultaneously the clinician should assess thepatient for depression and fatigue, given the highrates of co-morbidity and the differing treatmentapproaches used depending upon on the conditionidentified.

Access to reward potentials within the environ-ment: Apathy resulting from environmentalcauses can be decreased or rectified by modifyingthe environment. This can be done by makingrewarding stimuli accessible; for example, provid-ing devices to overcome impairments such as awheelchair for increased mobility (Marin, 1996),or by increasing the sources of interest, stimula-tion and pleasure in the environment (Kant &

Yes

Present

No

Yes

Stand-aloneactivity

Cumulativegoal

No

Yes

FIGURE 2Non-pharmacological treatment model for apathy.

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AMANDA T. LANE-BROWN AND ROBYN L. TATE

Smith-Seemiller, 2002). However, if the patient isable to access the reward potential within the envi-ronment, but is prevented from doing so becauseof the impairment of apathy, then other causesneed to be assessed.

Aetiology of apathy: The clinician needs to inves-tigate if apathy is resulting from a neurologicalcause (e.g., damage to the frontal systems) or if itis caused by a non-neurological cause, such asmedication effects — for example, selective sero-tonin reuptake inhibitors (Barnhart et al., 2004). Ifthe cause of apathy is suspected to be non-neuro-logical then this cause should be addressed first(e.g., adjust medication). However, if the cause issuspected to be neurological, then assessment ofthe level of functional impairment would follow.The patient’s level of functional impairment canbe determined by reviewing functional ability,their current residential requirements and amountof caregiver support needed.

• Severe ranges of functional impairment: Currentevidence indicates the most effective method ofintervention is music therapy, preferably withlive musicians (Holmes, Knights, Dean,Hodkinson, & Hopkins, 2006), or use of struc-tured activity kits (Politis et al., 2004).

• Milder ranges of functional impairment:Treatment will differ depending on the type ofgoal the patient is trying to achieve; a goal thatrequires a stand-alone action that is to be initi-ated daily or a goal that requires cumulativeaction where goal mastery is dependent on theactivity being initiated and sustained over aprotracted time period. The goal choice willdepend on factors such as necessity, interestand severity of other impairments. For exam-ple, if a patient does not take his/her medicationat the correct time, then a stand-alone goalwould be the most appropriate. However, if thepatient is working toward a goal such as returnto work at a level above repetitive labour, thena cumulative goal is relevant. For stand-aloneactivity goals, evidence suggests treatment withexternal compensation techniques to promptinitiation of goal-directed activity. Examples ofsuccessful external compensation techniquesinclude NeuroPage, a mnemonic cueing system(Evans, Emslie, & Wilson, 1998), checklists(Burke et al., 1991), or a person-promptingaction (Sohlberg et al., 1988). For goals thatrequire cumulative activity to be sustained overa protracted period of time, a combination ofmotivational interviewing and external com-pensation has demonstrated efficacy (Lane-Brown & Tate, 2010).

Challenges in Treating ApathyThe first challenge in treating apathy is beingaware of the presence of the condition. Given thatapathy presents clinically as a behavioural deficit,as with other negative symptoms, it may not be asstriking as the behavioural excesses. Furthermore,because patients with apathy are less likely toremain involved in the rehabilitation process(Gray et al., 1994), it follows that clinicians mayno longer be actively treating a number of patientswho have apathy, and therefore may not be awareof the prevalence of the condition. In order toincrease awareness and improve detection ofapathy, it is recommended that assessment forapathy be routinely conducted, preferably startingin the inpatient phase before the likelihood ofwithdrawal from treatment increases.

Treatment of patients with apathy can be a dif-ficult and frustrating undertaking for the clinician.Considerable time and effort is required on thepart of the clinician to engage and maintain a ther-apeutic relationship with a patient who has dimin-ished concern about their current situation, is notactively enthusiastic about being involved in reha-bilitation and may withdraw from treatment with-out distress. Thus, even greater effort thannormally applied is required when working withpatients with apathy. Working in collaborationwith the patient’s family can also assist treatmentadherence. Given that these patients can be diffi-cult to engage, commencement of therapy withinthe inpatient rehabilitation phase that continuespost-discharge could be of benefit, and one-on-one therapy is recommended rather than grouptherapy. Given that patients with apathy oftenhave difficulty initiating and sustaining goal-directed activity, it is suggested that treatment beof sufficient length to ensure the activity is contin-ued to goal mastery. To assist with sustaining,‘booster’ sessions may be of use after formal ther-apy has ceased. Finally, given that apathy is char-acterised by indifference (Marin, 1991), theimportance of individually tailoring therapy toeach patient is paramount: therapy goals must bein line with the patients interests.

Despite these challenges, we hope the clini-cian/researcher is not deterred. Research to dateshows some initial promise for the developingmethods of measuring and treating apathy follow-ing TBI; however, there is a need for moreresearch, particularly trials of high methodologi-cal quality. When good quality evidence for thetreatment of apathy is available, investigation intotreatments dependent on subtypes of apathywould be beneficial. Given the widespread conse-quences of apathy, further work in this area is vital

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to assist improving outcomes for the large numberof people with TBI who have apathy.

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