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Persistent Neurobehavioral Problems Following Mild Traumatic Brain Injury

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Persistent Neurobehavioral Problems Following Mild Traumatic Brain Injury 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 abnormal- ities 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
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