The Neurocognitive Basis of Compromised Autonomy AfterTraumatic Brain Injury: Clinical and Ethical Considerations

Warren E. Lux

Program in Human Research Ethics, Office of the Science Advisor, U.S. Environmental Protection Agency, Washington, DC,and Center for Clinical Bioethics, Georgetown University, Washington, DC

Summary: It is widely accepted, based on the principle ofrespect for autonomy, that there are ethical constraints on therange of tactics that persons may use to influence the decisionsand behaviors of others. However, accurate ascriptions of au-tonomy to either persons or acts may vary considerably, de-pending on properties of the person, the situation, or both.Traumatic brain injury affects cognitive domains that are crit-ical for the effective exercise of autonomy, and so offers acontext for further examination of this variability. Analysis of

the neuropathology of traumatic brain injury and its neurocog-nitive consequences provides a foundation for understandingcases in which autonomy is compromised even though legalcompetency may be preserved. Respecting autonomy inthese cases is not always straightforward; it may entail bothspecial ethical obligations and consideration of tactics thatwould not be morally permissible under other circumstances.Key Words: Autonomy, axonal strain injury, executive func-tion, self-assessment, self-awareness, traumatic brain injury.

INTRODUCTION

Autonomy is a word derived from the Greek for ‘self’(autos) and ‘law’ (nomos), and central to the concept isthe idea of self-governance.1,2 Both acts, includingchoices, and persons may be referred to as autonomous;in both instances, genuine self-guidance free from exter-nal control is essential for full autonomy. Respect forautonomy, particularly as it relates to treatment choices,is one of the core principles of biomedical ethics.2

Implicit in the attitudes that underlie the way in whichthis principle is applied in many, if not most, chronicstable clinical circumstances encountered in Americanhealthcare is the assumption that legally competentadults in our society can properly be regarded as sub-stantially autonomous persons. As a consequence, suchadults are generally allowed to make treatment decisionson their own behalf, and there are ethical, as well aslegal, constraints on what others are permitted to do toinfluence those decisions or to impede or alter the be-haviors that flow from them. Physical restraint, admin-istration of drugs to modify behavior without consent,

and coercion, for example, are among the actions con-sidered ethically inappropriate in a way that transcendslegal requirements, in that such actions fail in respectingthe autonomy of the individuals who are their objects.When the threshold for legal competency is not met

and a surrogate must be appointed, actions not previouslypermitted on ethical grounds may be allowed by thesurrogate—but only if ethically justified under the “sub-stituted judgment,” “best interests,” or “reasonable treat-ment” standards.3 In the legal setting, moreover, the na-ture of these matters requires the use of a dichotomousapproach to determining competency that incorporates athreshold determination. In the bioethical domain, a par-allel and analogous approach to autonomy is critical tothe ethical justification of actions that would not other-wise be morally acceptable.However, few philosophers, if any, would seriously

defend an account of autonomy that regarded autonomyitself as an inherently dichotomous property of eitheracts or persons. Rather, observations in both normal in-dividuals and persons with neurological impairment sug-gest that the richness and complexity of human behaviorsfall along a broad continuum of more or less autonomousactions. Moreover, ascriptions of autonomy to personsvary widely not only among individuals but also withinthe same individual as time, place, and situation change.

Address correspondence and reprint requests to: Warren E. Lux,MD, U.S. Environmental Protection Agency, 1200 PennsylvaniaAvenue, NW, Mail Code 8105R, Washington, DC 20460. E-mail:lux.warren@epa.gov.

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A related observation from a more specifically clinicalperspective is that autonomous actions require an arrayof cognitive capacities that are present to varying degreesin different individuals and that are to varying degreesactivated and applied by the same individual at differenttimes and in different circumstances.Traumatic brain injury (TBI) can affect cognitive ca-

pacities critical to the effective exercise of autonomy.One of the notable features of this disorder is that TBIcan produce survivors who retain normal or near-normalintellectual abilities, such that they may be adjudged tobe competent and not in need of a guardian or othersurrogate decisionmaker, but who nonetheless have animpaired ability to assess their own behaviors and capac-ities accurately. Accurate self-assessment, however, iscritical to the maintenance and exercise of autonomy: itis a key faculty underlying self-correction and thereforegenuine self-guidance.4 Moreover, the degree to whichthe actions of persons with impaired self-assessment ac-tually stray off course as a consequence of that impair-ment may differ significantly from one environment toanother, particularly in response to changes in environ-mental structure.The picture is further complicated by the fact that

when these individuals remain self-directed, they appearto be more self-guiding than they actually are. Further-more, their impaired self-assessment causes them tothink of themselves as more self-guiding than the factsjustify. Thus, both the ascription of autonomy by othersand the assertion of autonomy by the individual may besubject to error.These changes can occur after TBI with a severity and

persistence that warrants a finding of legal incompetenceand the appointment of a guardian, but they can alsooccur at a level that does not warrant such an action. Inthe latter circumstance, the legal status of these individ-uals is decoupled from their autonomy status to a degreethat varies with the fluctuations in their genuine self-guidance. As a consequence, the ethical framework thatshould guide the actions of family, friends, caregivers,and others in their interactions with these persons is notalways straightforward and is worth examining moreclosely.In order to raise some of the ethical issues and ques-

tions in a preliminary but grounded way, this article willfirst examine the neuropathology of TBI and the clinicalneurocognitive changes that result as a basis for under-standing how and under what circumstances autonomymay be compromised in these individuals. That reviewwill be followed by the presentation of a hypotheticalcase derived from the composite clinical experience ofthe author that will highlight the practical difficulties,which will in turn lead to a presentation of some of therelevant ethical considerations.

THE NEUROPATHOLOGY OF TBI AND ITSCOGNITIVE CONSEQUENCES

Axonal strain injuriesWhen the head is accelerated and decelerated in space,

particularly when accompanied by a torsional compo-nent, strain forces are applied to axons throughout thebrain.5,6 The resulting axonal strain injuries are propor-tional in amount to injury severity and represent theprimary, fundamental neuropathological change seen inTBI due to closed mechanisms.7 Blunt-force trauma pro-duces particularly violent acceleration–deceleration phe-nomena, so the most severe injuries tend to be producedby high-speed head impacts against immoveable objectsas in falls from height and motor vehicle accidents.7

The anatomic and physiologic consequences of axonalstrain are multiple. There may be axotomy, manifestedby irreversible axonal shearing injuries, including grossinjuries that are immediately visible on neuroimagingstudies. Delayed axotomy secondary to evolving patho-logical processes set off by the initial injury has also beenwell demonstrated.8 Axons damaged at a level that doesnot cause frank axotomy may nonetheless show alter-ations in electrophysiological function.6 Other aspects ofneuronal physiology may be altered as well, includingacute and chronic levels of monoaminergic neurotrans-mitters.9–13 Moreover, these neurochemical changes canbe correlated clinically with a number of well-docu-mented post-TBI syndromes in which monoaminergicfunction has been implicated.14–17

The axonal injuries described here are called diffuse—which may be something of a misnomer, for althoughthese injuries are multifocal and widespread, they are notuniformly distributed throughout the brain. The brain-stem, particularly the upper brainstem, may be subjectedto strains greater than would otherwise be expected, be-cause of the relatively small attachment of the mesen-cephalon to the large masses of the cerebral hemispheres,and the specific biomechanics of an individual traumaticevent will also modify the exact injury distribution.6 Inaddition, as injury severity increases and supratentorialaxonal strain injuries accumulate, the injury shows ananterior–posterior gradient, at least in humans. Althoughthe differences in gross brain anatomy make animalmodels less informative here, human clinical experiencesuggests that this gradient is an important phenomenon.Supporting evidence comes particularly from the neuro-imaging literature, which has demonstrated that frontaland anterior temporal lesions are significantly more fre-quent than lesions more posterior in the cerebral hemi-spheres.18–20

The neurocognitive consequencesIn the neurocognitive realm, the pathological changes

described in the previous section translate first into im-pairment of what has been called power function (the

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concept is elaborated in the next section), due to thewidespread axonal inefficiency resulting from the axonalstrain injuries and their physiological consequences, andsecond into impairment of executive function and self-awareness, due to the anterior–posterior gradient. Notethat the more posterior perceptual–motor and intellectualfunctions may be relatively well preserved, comparedwith these other functions, and may even be spared al-together.

Power function. The most fundamental neurocogni-tive disturbance seen after closed TBI is the impairmentin power function, a term that refers to the basic mentalfunctions necessary for the brain to engage in any cog-nitive task, regardless of what that task may be. The twocritical components are arousal and channel capacity,and alteration in arousal at onset is a primary feature ofclosed TBI. Once arousal recovers, however, the clinicalpicture is dominated by the channel capacity disturbance.This disturbance is characterized clinically by difficultiesin three important domains: processing speed, multitask-ing, and cognitive endurance. Virtually all persons whoare symptomatic after TBI of any severity will demon-strate impairments in these domains, whether they haveadditional deficits or not.When the deficit is severe enough to cause symptoms,

the impairment in cognitive processing speed usuallypresents directly as slowed thinking. Even in asymptom-atic patients, however, a slowing of cognitive processingspeed can be demonstrated.21

The multitasking deficit commonly translates itselfinto difficulty performing a cognitive task efficiently in adistracting environment, where mental suppression ofdistraction and performance of the target task are re-quired simultaneously. The patient’s complaint may re-flect this type of problem directly (“I can’t think clearlywhen there’s too much going on around me”), but it mayrelate instead to the cognitive domain to which the taskitself belongs. The patient may say, for example, “I can’tconcentrate” or “I’m having problems with my mem-ory,” yet show good memory and attention if placed in astimulus-controlled environment. It is simply that thepatient cannot actually use the complex systems requiredfor memory and attention effectively when subject to amultitasking requirement, even if there is no primaryimpairment in any of the specific components of theunderlying systems.That is not to say that TBI does not affect primary

components of the attention and memory systems di-rectly, particularly in the more severe injuries in whichthere is a greater burden of structural frontal and tempo-ral damage. However, it is important to highlight howfundamental the disturbance in power function is tomany of the cognitive complaints that arise after TBI. Itmay be the sole cause of cognitive symptoms. Evenwhen it is not, and when there are primary impairments

in other cognitive domains, the power function distur-bance has the potential to exacerbate symptom severity,perhaps markedly.The impairment in processing speed shares this prop-

erty, as one would expect. So too does the impairment incognitive endurance, although in that case the clinicalpresentation, like that of slowed processing speed, isusually straightforward. Symptomatic TBI patients areoften simply unable to sustain any cognitive effort for aslong as before the injury. Related to this reduction incognitive endurance is the frequent complaint that life ingeneral, and cognitive tasks in particular, are more ef-fortful. Evidence in support of an organic basis for thiscomplaint was provided in a recent functional magneticresonance imaging study by McAllister et al.22 Perfor-mance on a cognitive task was equivalent for both theexperimental (TBI) group and the control (normal)group, but the experimental group activated more cortexin doing so.A self-evident final point about power function is that

a breakdown in otherwise uncompromised cognitive do-mains in the face of inadequate power function is mostlikely to occur in those domains that are complex andparticularly difficult or effortful to execute even underconditions of full power. Thus, if such a domain is alsoin fact compromised by the injury, the power functiondisturbance has the potential to have an even more dev-astating effect. In the types of TBI patients under dis-cussion here, executive function is precisely such adomain.

Executive function. The term executive function re-fers to that set of neurocognitive capacities that areactivated when one plans, initiates, and performs a goal-directed activity over time with appropriate self-moni-toring and self-correction as one proceeds. Among thekey components of executive function are anticipation,goal selection, planning, initiation, sequencing, monitor-ing (error detection), and self-correction (initiation ofnovel responses).23 It gives structure and coherence tohuman action in novel situations and is necessary forperforming goal-directed activities successfully in un-structured real-world settings. Executive function relieson the activity of the frontal lobes anterior to the primarymotor cortex, so it is vulnerable to the anterior–posteriorgradient of structural brain lesions in TBI, particularly asinjury severity increases.Closely related to the primary components of execu-

tive function is the capacity for self-assessment. Theimportance of this capacity to executive function derivesfrom the fact that effective task execution is possibleonly when one has the ability to accurately assesswhether one has the physical and mental skills requiredto perform an intended act. Consider, for example, thecase of a woman who wants to get from one place toanother a few feet away but has severe leg weakness and

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is unable to ambulate without assistance. If she cannotaccurately assess her ability to bear weight on her legsand as a result believes that she can walk independentlywhen she cannot, she will fall when she tries to ambulate.If, on the other hand, accurate self-assessment is pre-served, she will use crutches or a wheelchair or get helpfrom an attendant and so succeed in executing her in-tended task.Mental as well as physical capacities are subject to

self-assessment, including the components of executivefunction itself. Thus, if someone is unable to detect er-rors well, for example, and is at the same time unable toassess one’s own error-detection capacity, then multipleand even fatal errors are possible during task execution.If accurate self-assessment is preserved, however, andone knows that one has a problem with error detection, anumber of strategies are available, such as double-check-ing one’s work or seeking contemporaneous review byothers.The impaired self-awareness associated with self-

assessment disorders in frontal TBI patients has someadditional distinguishing features relevant to the capacityof these individuals to act autonomously. In particular,these individuals may in fact be able to recognize theirdeficits when the deficits are demonstrated to them, par-ticularly in a highly structured setting. In that regard,their self-awareness deficits differ from those typicallyseen in patients with parietal (particularly right parietal)disease.In the parietal cases, patients appear unable to perceive

their deficits. In the frontal cases, on the other hand,ability to perceive the deficit is preserved, but there is aloss of the capacity to incorporate the knowledge of theperceived deficit into a global sense of one’s self as anagent of action. Thus, persons with this syndrome can—and do—acknowledge deficits that are demonstrated tothem in concrete situations, but their subsequent behav-ior, verbal and otherwise, often does not reflect an aware-ness of the deficits in any meaningful way. As a conse-quence, they will say and do things in novel situations asif they did not in fact have the deficits that they wereearlier able to acknowledge.4

To express it in a slightly different way, the primarydisturbance in the TBI cases under consideration is in theability to use available data about one’s self to build anadequately accurate sense of who one is as a person. Thatis, the difficulty does not lie with the data themselves norwith the ability to acquire them in the first place. Thus,although autonomy may be compromised in both theparietal and the frontal cases, the mechanisms and clin-ical features are distinguishable, and the frontal patientsare particularly alienated from themselves as agents ofactions precisely when the opposite is required for gen-uine self-guidance.

A HYPOTHETICAL CASE

The patient under consideration in a matter of treat-ment refusal is a 24-year-old man who sustained a closedhead injury in a motor vehicle accident 3 weeks earlier.He was unconscious at the scene, and his Glasgow ComaScale score on admission to the emergency room was 9.Computed tomographic scanning of the brain on admis-sion showed a few bilateral frontal punctuate white mat-ter hemorrhages, perhaps reflective of some gross axonalshearing lesions, but no surgical lesions. No MRI scanwas done. Apart from the brain injury, there were noother significant injuries.The patient emerged from coma on the third hospital

day and went through an agitated phase lasting approx-imately a week. During this period, he was grossly con-fused and disoriented but was medically stable enough tobe transferred to the hospital’s rehabilitation unit. As hisagitation subsided, his confusion also began to clearslowly but progressively. By the end of his third week inthe hospital, the patient was alert and fully oriented. Hewas also freely ambulatory, albeit with a high-level bal-ance disorder and problems with fine motor control. Hewas attending a full schedule of therapies.Abnormalities on his cognitive examination included

findings in the area of executive function. He had diffi-culty organizing and sequencing his day, but was able tocompensate with the use of a day timer. This compen-sation would occasionally break down, however, result-ing in missed therapy appointments, either at the end ofthe day when he was fatigued or when he had been offthe rehabilitation unit and subject to the less structuredand more distracting environment of the general hospital.The patient’s depth of awareness of his own capacities

was shallow, and he had little insight into either hiscognitive changes or his mild motor disorder, althoughhe was able to acknowledge both when they were dem-onstrated to him. Memory and attention were impairedonly when he was subjected to environmental distrac-tions. Otherwise, his cognitive examination was remark-ably intact. Language expression and comprehensionwere normal, as was calculation ability. Object recogni-tion and constructional abilities were likewise normal.Geographic orientation was intact, and he was able tofind his way around the rehabilitation unit and through-out the entire hospital without difficulty. He was able tounderstand facts and to reason logically from them.Moreover, he was fully self-directed, and although hewas not cognitively normal, there was no question of hiscompetence in a legal sense. Indeed, the question ofseeking guardianship never arose after the acute phase ofhis injury was behind him.His social history revealed that he was married and

had an 18-month-old daughter. His wife, a beautician,had stopped working just prior to the birth of their child.

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At the time of his accident, the patient was employed asan auto mechanic at a local car dealership. The patient’sparents lived nearby and were supportive. Prior to hisaccident, the patient had lived an essentially normal life.He did not smoke and used alcohol in moderation. Hewas calm in temperament, well-liked by his friends, andregarded as a good husband and father.At this point, the patient decided that he wanted to stop

all therapy and return home. He argued that his remain-ing deficits were minimal, and that it was his decisionand intent to return to work “as soon as his employerwould have him back.” The treatment team recom-mended an additional one to two weeks of inpatientrehabilitation, to be followed by an outpatient work re-entry program. The latter program would be specificallydesigned to deal with both the cognitive and the motorchanges that he acknowledged and that affected his abil-ity to do his work but that he was unable to incorporateinto his greater sense of self as an agent. The programwould also work with his employer to coordinate hisreturn to work under structured, stimulus-controlled con-ditions that would maximize his chance of success. Hiswife and parents, more aware of the patient’s changesthan he was himself, also wanted to see him completethis course of treatment.

SOME ETHICAL CONSIDERATIONS

What actions are ethically justified on the part of thetreatment team and the patient’s family at this point?Should they accede to his decision, which he is legallyentitled to make, allow him to leave the hospital, and tryto develop an alternate treatment plan even though itmight offer a lesser chance of success? Or should anattempt be made to keep him in the hospital against hisexpressed wishes and contrary to his own decision on thegrounds that his decision is not fully autonomous be-cause of his compromised executive function and self-awareness? And if the latter, what tactics are ethicallypermissible to accomplish this?If a structured treatment contract presented in a stim-

ulus-controlled setting in which deficits can be demon-strated compensates for his executive dysfunction suchthat he is able to make an arguably more autonomousdecision to remain in the hospital, how far is his familypermitted to go in encouraging him to accept the con-tract? In real situations of this sort, families commonlyresort to coercive rhetorical pressure, sometimes withconsiderable force and persistence. Is this ever ethicallyjustified, and if so, under what circumstances?Raising these issues as they emerge in this kind of

case, particularly against the background of the neuro-cognitive analysis of TBI, highlights two ethically rele-vant points, as introduced at the outset of this review.The first is the distinction between autonomous acts and

autonomous persons, a distinction that has always beenapparent but that takes on notable ethical relevance in thecontext of this kind of decision-making.Individuals with TBI who possess many or most of the

capacities of autonomous persons, such that they arejustifiably adjudged to be legally competent, may none-theless have deficits that lead them to engage in individ-ual actions and make particular choices in ways that areclearly not autonomous. Moreover, it can be argued thatnormal individuals without such deficits also do the samething at times. In such cases, however, it is usually amore inconsistent occurrence, whereas individuals withTBI have a propensity for this to happen on the basis ofparticular deficits. In either case, however, application ofthe principle of respect for autonomy requires an analysisof the act in question and cannot be adequately addressedby exclusive reference to the overall autonomy of theperson. Beauchamp and Childress2 make this same point.The current example of TBI serves to highlight it.The second point is that autonomy failure is sensitive

to the situational elements that surround it. Again, this istrue of both normal individuals and persons with TBI.Using the TBI example, however, allows many of theseelements to be defined clinically and further understoodon the basis of neurocognitive analysis. Although thismay not inform all instances of autonomy failure innormal persons—or even in persons with TBI, for thatmatter—it may be helpful in at least some cases. Inaddition, it implies that autonomy failure is treatable, inthat it can respond to appropriate environmental inter-ventions directed at those situational elements that areundermining autonomy.Thus, the simple expedient of changing the decision-

making milieu from a distracting environment to a quiet,stimulus-controlled environment may suffice to convert anonautonomous decision into an autonomous one. More-over, an ethical imperative to apply interventions that canhave such results is implied by the principle of respectfor autonomy for both normal persons and those withcognitive impairments.Given the particular impairments in this case, and the

ethical considerations that derive from the case, success-ful application of treatment interventions may involvethe participants in a striking paradox. TBI and conditionslike it may produce circumstances that would lead one toconsider tactics (such as coercion, in this example) thatcompromise the autonomy of the person in the short termin order to enable autonomous choice later when it wouldotherwise be precluded.Justifying such a tactic would have to include, at a

minimum, the aim of reestablishing the relative auton-omy of the person over the longer term and to a degreethat would not otherwise occur. There should be reason-able evidence for the clinical efficacy of the proposedintervention in the particular case under consideration,

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and that evidence would need to be brought to bear withan Aristotelian sort of prudential judgment in the ethicalas well as the clinical realm.

Acknowledgments: Some of the ideas contained in thiswork were first presented at a problem case conference at theCenter for Clinical Bioethics at Georgetown University inSeptember 2002 and later at a symposium on the neuroethics ofbrain damage held at Washington University in St. Louis inDecember 2002. I have benefited from discussions with col-leagues at both institutions, and their critical feedback is grate-fully acknowledged. I would also like to acknowledge mycolleagues in the Office of the Science Advisor at the U.S.Environmental Protection Agency for their support of a workculture in which ideas matter. The views expressed in thisarticle, however, are solely those of the author and do notreflect official positions of the U.S. Environmental ProtectionAgency nor of the U.S. Government.

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