Persistent Neurobehavioral Problems Following Mild Traumatic Brain Injury

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Archives of Clinical Neuropsychology 16 (2001) 561–570 Downloaded from https://academic.oup.com/acn/article/16/6/561/2043 by guest on 23 September 2021 Persistent neurobehavioral problems following mild traumatic brain injury

Lawrence C. Hartlagea,*, Denise Durant-Wilsona, Peter C. Patcha,b

aAugusta Neuropsychology Center, 4227 Evans to Locks Road, Evans, GA 30809, USA bUS Penitentiary, Atlanta, GA, USA

Accepted 9 May 2000

Abstract

Accumulating research documents typical rates in the range of 85% of mild traumatic brain injury (MTBI) showing prompt, complete resolution with 15% suffering from persistent neurobehavioral impairments. Studies of neurobehavioral symptoms of MTBI have not separated these two populations, resulting in either inconclusive or contradictory conclusions concerning the relationship of MTBI with residual behavioral problems. This project studied 70 MTBI patients with persistent neurobehavioral problems at two time intervals post-injury to determine whether there are consistent neurobehavioral patterns considered to be sequelae of MTBI. A matched group of 40 normal subjects provided control data. While most behavioral problems showed improvement, 21% tended to show significant behavioral impairment compared to controls at 12 or more months post-injury. Neurochemical bases of neuronal degeneration may account for some of the behavioral deterioration following MTBI. D 2001 National Academy of Neuropsychology. Published by Elsevier Science Ltd.

Keywords: Persistent neurobehavioral problems; Brain; MTBI

The scientific literature is replete with reports of behavioral abnormalities following traumatic brain injury. From case reports such as that of Phineas Gage (Harlow, 1868) to studies of groups of individuals with brain injury and reviews of such studies, there is fairly consistent evidence suggesting that, following at least some cases of traumatic brain injury, instances of behavior abnormality occur and may be causally related to such injury (Dikmen, Reitan, & Temkin, 1983; Levin, Eisenberg, & Benton, 1989; Lishman, 1988; Prigatano, 1992; Reitan & Wolfson, 1986; Satz et al., 1997). Although

* Corresponding author. Tel.: +1-706-860-5363; fax: +1-706-860-5363.

0887-6177/01/$ – see front matter D 2001 National Academy of Neuropsychology. PII: S0 887-6177(00)00067-6 562 L.C. Hartlage et al. / Archives of Clinical Neuropsychology 16 (2001) 561–570 such phenomena have been recognized for more than a century, they have not received the attention directed toward neurocognitive sequelae of brain trauma. Explanations of behavioral abnormalities following traumatic brain injury have been approached from a number of perspectives. A traditional explanation has related presence or extent of behavioral abnormalities to severity of brain injury, with behavioral abnormalities typically attributed to deficits in cortical (mainly frontal) processing combined with reactions to loss of neurocognitive abilities (Binder, Rohling, & Larrabee, Downloaded from https://academic.oup.com/acn/article/16/6/561/2043 by guest on 23 September 2021 1997; Crooks, 1991; Dikmen, Machamer, Winn, & Temkin, 1995; Gronwall & Wrightson, 1974; Klonoff, Costa, & Snow, 1986; Levin, 1990; Ommaya, 1982). Behavioral abnormalities associated with mild traumatic brain injury (MTBI) have represented an area of controversy, as well as special interest. Controversy has especially enveloped reports of behavioral changes caused by MTBI, since by traditional criteria, there should be few, if any, behavioral sequelae. To some extent, the proposition that severity of injury is directly related to severity of outcome has been refuted or at least attenuated by a number of reports concluding that loss of consciousness or even blows to the head are not required for the production of measurable neuropsychological sequelae (Binder, 1986; Boll & Barth, 1983; Hartlage, 1997a; Varney & Varney, 1995; Zasler, 1993). Special interest in MTBI relates to its epidemiological significance insofar as approximately 90% of brain injury is classifiable as MTBI, making this a phenomenon with millions of new cases each year in the United States (Annegers, Grabow, Kurland, & Laws, 1980; Caveness, 1977, 1979; Hartlage, 1984, 1990; Kraus & Nourjah, 1989; Sorenson & Kraus, 1991). A considerable literature has related behavioral sequelae of MTBI to neurotic (Binder, 1997; Lishman, 1988; Newcombe, Rabbitt, & Briggs, 1994; Straus & Savitsky, 1934) or post-traumatic stress factors (Bryant, 1996; Bryant & Harvey, 1998; Lishman, 1988) exacerbated by either pre-injury abnormality or increased propensity toward risky behaviors (Brown & Davidson, 1978; Fenton, McClelland, Montgomery, MacFlynn, & Rutherford, 1993; Whitlock, Stroll, & Rekhdahl, 1977; Wood, 1990). The base rate phenomenon has also been explained and offered as explanation for at least some behavioral abnormalities observed following MTBI (Cullum & Thompson, 1997; Fox, Lees-Haley, Earnest, & Dolezal-Wood, 1995; Gouvier, Uddo-Crane, & Brown, 1988; Lees-Haley & Brown, 1993; Wong, Regennitter, & Barrios, 1994). Exaggeration of symptoms or frank malingering has received considerable attention. There has been an impressive literature addressed to this factor as a possible contributor, component of, or even explanation for much of the behavioral abnormalities noted following MTBI (Binder, 1997; Gouvier, Hayes, & Smiroldo, 1998; Miller, 1996; Nies & Sweet, 1994; Parker, 1994; Reynolds, 1998; Rutherford, Merrett, & McDonald, 1979). Litigation status has also been proposed as a factor influencing reports of behavioral abnormalities following MTBI (Miller, 1961; Rutherford et al., 1979; Varney, 1990). A number of researchers have concluded that this does not appear to be salient (Binder, 1986; Bornstein, Miller, & van Schoor, 1989; Deb, Lyons, Koutzoukis, Ali, & McCarthy, 1999; Hartlage, 1997b; Rimel, Giordani, Barth, Boll, & Jane, 1981; Stuss et al., 1985). L.C. Hartlage et al. / Archives of Clinical Neuropsychology 16 (2001) 561–570 563

An important confounding factor in assessing possible behavioral sequelae of MTBI involves the finding that approximately 85% of cases apparently resolve within 1–3 months without any sequelae, while the remaining approximately 15% may have persistent symptoms of potentially disabling severity (Alexander, 1995; Barth et al., 1983; Gentilini, Nichelli, & Schoenhuber, 1985; Hartlage, 1997b; Hatcher, Johnson, & Walker, 1996; Kurtzke & Kurland, 1993; Levin et al., 1987; Rimel et al., 1981). No study has specifically addressed the pattern of neurobehavioral changes among indivi- Downloaded from https://academic.oup.com/acn/article/16/6/561/2043 by guest on 23 September 2021 duals with persistent behavioral abnormalities following MTBI; rather, data from those with persistent neurobehavioral sequelae have been commingled with data from those making good recovery. Another confounding factor involves the timing of reported behavioral abnormalities following MTBI. It has been argued that any behavioral abnormalities of purely neurologic etiology should be manifested immediately following the injury, with abnormal behaviors not manifested (or reported) until some period following injury likely of psychogenic nature (Bohnen, Twijnstra, & Jolles, 1993; Bryant, 1996; Lishman, 1988; Wrightson & Gronwall, 1981). However, emerging research has suggested mechanisms involved in progressive neuronal loss from traumatic brain injury (Andersen & Marmarou, 1992; Bergsneider, Hovda, & Shalmon, 1997; Bigler, 1992; Bigler et al., 1994; Crooks, 1991; Hovda, 1998; Levin, Williams, Eisenberg, High, & Guinto, 1992; Oder et al., 1992; Oppenheimer, 1968), raising the issue of possible neurogenic substrates of chronic behavioral problems in those patients with MTBI with persistent symptoms. Support for this position is provided by recent research demonstrating unique sensitivity to brain injury, as well as vulnerability to Alzheimer’s disease among individuals with the apolipoprotein E-epsilon4 (APOE- epsilon4) allele (Friedman et al., 1999).

1. Method

This project assessed behavioral changes from pre-injury baseline with 70 consecutive patients referred for neuropsychological examination following minor brain injury with persistent neurobehavioral problems. Behavioral changes involved post-injury presenting complaints such as absentmindedness, fearfulness, agitation, and increased anger. The patient sample was divided into two groups according to time of assessment post-injury: within 6 months and 12 or more months. All were involved in litigation at some point, with 62% in pending litigation. Mean age was 35 years, and 45% of patients were male. Mean Halstead Reitan Impairment Index was 0.6, with a range from 0.3 to 1.0. None had pre-injury history of psychiatric diseases or treatment. Behavior change data were collected as part of a comprehensive neuropsychological examination. A control group (N=40) from the standardization cross-validation sample of the Behavior Change Inventory (BCI) (Hartlage, 1989; Kixmiller, Briggs, Hartlage, & Dean, 1993) with no history of traumatic brain injury completed the BCI to indicate changes in behavior pre- and post-injury. Controls did not differ substantially from MTBI patients on age, education, or gender. 564 L.C. Hartlage et al. / Archives of Clinical Neuropsychology 16 (2001) 561–570

1.1. Procedure

Data concerning pre-injury and post-injury behavioral status were collected from both the patient and independently from another individual knowledgeable about the patient’s pre- and post-injury behavioral status (e.g., spouse, close family member). For a behavior to be considered changed, both patient and independent informant had to indicate change from pre-injury baseline on that behavior. Any behavior change noted Downloaded from https://academic.oup.com/acn/article/16/6/561/2043 by guest on 23 September 2021 by only one respondent was not counted as showing change.

1.2. Measurement

Pre- and post-injury behavior status was assessed with the BCI, a 68-item scale previously demonstrated to be sensitive to behavior change following brain injury (Hartlage, 1989, 1990; Hartlage, Williams, & Haney, 1988b; Johnson & Hartlage, 1989; Lewis & Hartlage, 1986; Roth & Hartlage, 1998; Spencer, 1992). Use of this scale was elected to help control possible contaminants or confounds related to pre- existing behavior abnormality (Spencer, 1992; Wilson & Hartlage, 1999). Behaviors included such phenomena as absentmindedness, agitation, and irrational anger.

2. Results

Chi-square analyses were conducted comparing patient responses on the 68 behaviors identified by the BCI. The first comparison was between the 35 MTBI patients whose neuropsychological examinations occurred within 6 months of injury with 40 control subjects whose responses were used in the norming of the BCI (Hartlage, 1989). Of these 68 behaviors, more patients reported changes between pre-injury and time of examination than controls on 39 behaviors, significant at the p<0.005 level. These behaviors and the direction of change are listed in Table 1. In order to assess whether the behavior changes from pre-injury persisted over time, chi- square analyses were conducted comparing the number of individuals reporting behavior change in the group whose neuropsychological examinations took place 12 months or more from the time of injury. The analyses used the same control group data as that for the analyses of the 6 months or less group. Of the 39 behaviors identified by patients and significant others as having changed between time of injury and examination in the 6 months or less group, 36 were identified by the 12 months or more group as having changed compared to pre-injury baseline, reaching significance at the p<0.005 level. Two behaviors, ‘‘more quarrelsome’’ and ‘‘less polite’’ did not show continued change. One behavior, which was identified by the 6 months or less group, ‘‘more concerned,’’ was identified by significantly fewer members of the 12 months or longer group. Lastly, chi-square analyses were conducted on the originally identified 39 behaviors in order to determine whether the number of persons reporting behavior change increased over time. Of the originally identified 39 behaviors, three were identified by more individuals in the 12 months or longer group compared to the 6 months or less group, L.C. Hartlage et al. / Archives of Clinical Neuropsychology 16 (2001) 561–570 565

Table 1 Behaviors identified by patients and significant others as changing within 6 months of injurya Behavior Behavior more absent-minded less good-natured more agitated less happy more angry more impatient less calm more irritable Downloaded from https://academic.oup.com/acn/article/16/6/561/2043 by guest on 23 September 2021 less carefree less patient less cheerful less pleasant more complaining less polite more concerned more quarrelsome more confused more sad more cross/irritable more shakey more depressed more short-tempered more distractible more slow more easily upset less strong less energetic more temperamental less enthusiastic more tense more fearful more tired more forgetful less understanding less friendly more unhappy more gloomy more worrisome

a Italics indicate direction of change. with significance at the p<0.005 level. These behaviors were ‘‘more distractible,’’ ‘‘less cheerful,’’ and ‘‘more afraid.’’ As stated above, a fourth behavior, ‘‘more concerned,’’ was identified by fewer members of the 12 months or more group than the 6 months or less group, with significance at the p<0.005 level.

3. Discussion

Differences found between MTBI patients and controls are compatible with prior studies indicating sensitivity of the BCI to behavioral sequelae of MTBI (Hartlage, 1989; Hartlage et al., 1988a, 1988b; Kixmiller et al., 1993). Findings from this study expand the database to assess temporal sequence of behavioral changes subsequent to TBI. While findings provide clear support for the concept of some long-term neurobehavioral sequelae of MTBI, two caveats are indicated. One involves the fact that litigation was involved or potentially involved in all cases. Two steps were taken to mitigate this potential source of bias. One required the patient and another individual with knowledge concerning the patient’s behavioral status both prior and subsequent to the injury to complete the BCI independently of each other, and only tabulating those behaviors that both indicated change from baseline. Given the typical insensitivity of many brain-injured patients to changes in or abnormalities of their own behaviors, combined with the independence of raters, it was anticipated that indices of behavior change requiring both respondents to indicate a change in behavior from pre-injury status would represent a 566 L.C. Hartlage et al. / Archives of Clinical Neuropsychology 16 (2001) 561–570 conservative measure of behavior change. Comparison of behavior changes reported by individuals with potential litigation pending with those with litigation concluded revealed no difference, although there was a slight improvement on anxiety for those whose cases had settled. Thus, pending litigation was not found to be a factor in reports of behavior change, a finding also reported by other investigators (Binder, 1986; Hartlage, 1997b; Miller, 1996; Parker, 1994; Varney, 1990). A second caveat involves the fact that while the study reported longitudinal behavioral Downloaded from https://academic.oup.com/acn/article/16/6/561/2043 by guest on 23 September 2021 changes, the data were collected on a cross-sectional basis. The choice was made to favor cross-sectional data in order to preserve the in vivo pattern. Since both ethical and humanitarian concerns would have mandated some form of palliative intervention to alleviate or ameliorate subjective distress in a cohort of MTBI patients followed longitudinally, such intervention could reasonably be expected to alter the pattern or sequence of neurobehavioral problems emergent from MTBI. These individuals were referred to other providers for on- going and follow-up treatment. An informal comparison of the study population with a much smaller group (N=18) of patients seen for longitudinal treatment of MTBI sequelae revealed fairly good congruence among the pattern of neurobehavioral symptoms. Neurobehavioral symptoms were consider- ably less severe among treated patients and, in fact, showed progressive lessening over time. Given these caveats, data documented both persistent neurobehavioral sequelae from MBTI and a tendency among untreated MBTI patients for some neurobehavioral sequelae to be more pronounced as a function duration since injury. There remains the unresolved issue concerning whether neurobehavioral sequelae of MTBI are of neurogenic vs. psychogenic nature. It is postulated that at least for those neurobehavioral sequelae of MTBI with fairly consistent and high incidence occurrence persisting since time of injury, neurogenic factors must be considered. A progressive worsening of sequelae of neurogenic origin is compatible with progressive alteration of brain metabolism involving receptor agonist mechanisms documented in mild brain injury (Anderson & Bigler, 1995; Bigler, 1992; Bigler et al., 1994; Binder, 1986; Boll & Barth, 1983; Faden et al., 1989; Gale, Johnson, Bigler, & Blatter, 1995; Hayes, Jenkins, & Lyeth, 1992; Hayes, Lyeth, & Jenkins, 1989; Siejo & Wielock, 1985), morphologic injury of axonal and cytoskeletal structures (Kontos, Wei, & Povlishock, 1980; Oppenheimer, 1968; Taft, Yang, Dixon, & Hayes, 1992), or some combination or permutation of such factors, including the special sensitivity to brain insult among that subset of individuals with the APOE-epsilon4 allele (Friedman et al., 1999). However, one cannot rule out psychological reactions to cumulative recognition of impaired function. Further research to clarify these issues is needed so that optimal ameliorative therapy may address realistic expectations or goals. In the meantime, neuropsychologists and other neurological or rehabilitative profes- sionals involved with providing support to patients with MTBI and their families are encouraged to recognize that although statistically, the likelihood of complete recovery from MTBI is in the range of 85%, for those remaining (approximately 15%), the neurobehavioral residue may be persistent, severe, and even disabling. Given an annual incidence in the range of 10 million TBI cases in the US each year, with the very large majority involving MTBI, residual neurobehavioral problems involving 15% make this a phenomenon deserving of recognition. L.C. Hartlage et al. / Archives of Clinical Neuropsychology 16 (2001) 561–570 567

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