Neuropsychological function in female victims of intimate partner violence with and without posttraumatic stress disorder

Neuropsychological function in female victims of intimate partner violence with and without posttraumatic stress disorder

Neuropsychological Function in Female Victims of Intimate Partner Violence with and without Posttraumatic Stress Disorder Murray B. Stein, Colleen M. ...

90KB Sizes 0 Downloads 76 Views

Neuropsychological Function in Female Victims of Intimate Partner Violence with and without Posttraumatic Stress Disorder Murray B. Stein, Colleen M. Kennedy, and Elizabeth W. Twamley Background: Various aspects of neuropsychologic function have been reported to be abnormal in patients with posttraumatic stress disorder (PTSD); however, the majority of these data come from studies of seriously ill, treatment-seeking samples with substantial substance use comorbidity. Few studies have included similarly traumaexposed subjects without PTSD, and fewer still have focused on women. Methods: Thirty-nine female victims of intimate partner violence (IPV; 22 without lifetime PTSD and 17 with current PTSD), and 22 nonvictimized comparison (NC) subjects were administered tests of attention, working memory, visuoconstruction, language ability, learning and memory, and executive functioning. Results: The IPV and NC subjects did not demonstrate statistically significant differences on most neuropsychologic tests, with the exception of those in the realm of working memory, visuoconstruction, and executive functioning. The IPV subjects, regardless of PTSD status, had poorer performance on tasks of speeded, sustained auditory attention and working memory (Paced Auditory Serial Addition Test) and response inhibition (Stroop). The IPV subjects with PTSD performed worse than NCs on a set-shifting task (Trail Making Test, Part B). No consistent relationships were noted between neuropsychologic functioning and severity of childhood abuse or domestic violence experiences. Conclusions: Cognitive deficits in IPV subjects were confined to measures of working memory, visuoconstruction, and executive function; were subtle; and were not uniformly worse among those with current PTSD. This pattern, however, is consistent with frontal–subcortical dysfunction in traumatized women. The clinical signifi-

From the Veterans Affairs San Diego Healthcare System (MBS, CMK), San Diego, California, and Department of Psychiatry, University of California, San Diego (MBS, EWT), La Jolla, California Address reprint requests to Murray B. Stein, M.D., Department of Psychiatry (0985), 9500 Gilman Drive, La Jolla CA 92093. Received November 19, 2001; revised March 21, 2002; accepted April 8, 2002.

© 2002 Society of Biological Psychiatry

cance of these findings deserves further study. Biol Psychiatry 2002;52:1079 –1088 © 2002 Society of Biological Psychiatry Key Words: Attention, memory, domestic violence, posttraumatic stress disorder, trauma, women

Introduction

E

pidemiologic studies have shown that 25% to 40% of women are at risk for exposure to criminal victimization during their lifetimes and that many of these women will develop posttraumatic stress disorder (PTSD; Breslau et al 1998; Kessler et al 1995; Stein et al 1997). Women are at a severalfold increased risk for PTSD compared with men, but reasons for this increased susceptibility remain unclear (Breslau et al 1999; Stein et al 2000). Thus, the current literature can be enhanced with additional research on PTSD in women. The neuropsychologic functioning of persons with PTSD is emerging as an important area of inquiry, but thus far there have been few studies addressing women’s cognitive functioning in the context of trauma and PTSD.

Learning and Memory Problems in PTSD Psychologic stressors (Lupien and McEwen 1997) or exogenously administered glucocorticoids at similar levels to those achieved during stress (Newcomer et al 1999) affect hippocampal function (Bremner 1999; Kaufman et al 2000; Sapolsky 1996, 2000). These observations provide a strong theoretical basis for hypothesizing that individuals experiencing severe psychological trauma would experience problems with learning and memory. It should be noted, however, that the preclinical literature would not predict why these problems should be confined to persons with PTSD beyond the fact that increased trauma severity is a PTSD risk factor (i.e., therefore indicating that those who experience PTSD may have experienced the highest “dose” of trauma). Several studies have found evidence of learning and memory problems in combat veterans with PTSD (Brem0006-3223/02/$22.00 PII S0006-3223(02)01414-2

1080

M.B. Stein et al

BIOL PSYCHIATRY 2002;52:1079 –1088

ner et al 1993; Gilbertson et al 2001; Sachinvala et al 2000; Uddo et al 1993; Yehuda et al 1995); however, the nature and extent of memory dysfunction has varied markedly among studies, with some failing to find memory problems at all (Gurvits et al 1993). A study of Persian Gulf War veterans, which had the advantage of studying young subjects with relatively recent onset of PTSD, found a pattern of poor initial acquisition of information and increased susceptibility to retroactive interference (Vasterling et al 1998). There have been few studies of neuropsychologic function in women with PTSD, and the results have been mixed, with some finding deficiencies in learning and memory (Jenkins et al 1998) and some not (Stein et al 1999). Other investigators have warned that memory impairment in patients with PTSD may be primarily attributable to comorbid major depression (Barrett et al 1996). Although most studies have acknowledged the effects of comorbid alcohol dependence on cognitive function (Sullivan et al 2000) and have attempted to control for these possible influences, this nonetheless looms as a possible explanation for previous findings in this area. Thus, the status of memory dysfunction as a consistent and prototypical feature of PTSD, particularly in younger, otherwise healthy patients, remains unclear (Wolfe and Schlesinger 1997).

Additional Domains of Possible Neuropsychologic Dysfunction in PTSD It is important to note that despite the emphasis in the published literature on memory performance in PTSD, studies have also found abnormalities in sustained attention, selective attention, and executive functions in persons with PTSD (Beckham et al 1998; Jenkins et al 2000; Koenen et al 2001; Vasterling et al 1998). Abnormalities in attention and higher order cognitive processes such as executive functioning would be predicted based on involvement of frontal- subcortical circuitry in anxiety and stress (Arnsten 1998; Davidson and Irwin 1999; Kaufman et al 2000; Krystal et al 1995; Mizoguchi et al 2000).

Intelligence and Risk for PTSD De Bellis et al found that maltreated children had lower IQs than nonmaltreated comparison subjects (De Bellis et al 1999). Several additional studies in maltreated children have highlighted their poorer cognitive performance and academic outcomes (Carrey et al 1999; Perez and Widom 1994; Saigh et al 1997). These findings are remarkably consistent with the adult literature, in which studies have shown that lower IQ is a risk factor for the development of PTSD following combat exposure (Macklin et al 1998; McNally and Shin 1995). Furthermore, a recent study

suggests that PTSD is associated with neurologic soft signs and lower IQ, individual differences that are posited to occur early in life and may act as risk factors for PTSD (Gurvits et al 2000). These studies raise the possibility that there may be cognitive vulnerability factors for PTSD that predate the trauma, further confounding a simple cause– effect relationship. In summary, there is a growing consensus that individuals with PTSD exhibit deficits in cognitive function (Buckley et al 2000); however, the type(s) of cognitive impairment (e.g., including learning and memory, attention, and executive dysfunction) observed have varied considerably across studies. Possible reasons for this variability include differences in sample characteristics (e.g., substance abuse comorbidity; prior head injury) across studies. The literature is also inconsistent regarding whether neuropsychologic impairment is (or, hypothetically, should be) a feature of trauma exposure, PTSD, or even a preexisting risk factor for either (or both). A prospective, longitudinal design is required to address these hypotheses with impunity. Short of this, however, one approach would be to study various domains of neuropsychologic function in three subject groups: those experiencing serious psychological trauma who have not developed PTSD, those experiencing serious psychological trauma who have developed PTSD, and subjects who have not experienced serious psychological trauma. This is the strategy we employed in this study. Our study focuses exclusively on women, excluding those with established risk factors for cognitive impairment (e.g., history of brain injury, learning disability, and substance abuse), with the additional goal of clarifying the nature and extent of neuropsychologic dysfunction in traumatized women with and without PTSD. We chose for this purpose to study women who experienced intimate partner violence (IPV; domestic violence), a highly prevalent form of serious, usually chronic, trauma known to result in high rates of PTSD (Bell et al 1996; Cascardi et al 1999; Eisenstat and Bancroft 1999; Greenfeld et al 1998; Stein and Kennedy 2001; Weinbaum et al 2001).

Methods and Materials Participants Thirty-nine victims of IPV (17 with current PTSD [PTSD⫹] and 22 without lifetime PTSD [PTSD⫺]) and 22 nontraumatized comparison subjects (NC) participated in our studies. Subjects were recruited through the use of posted advertisements and ongoing personal contacts with community services in San Diego County specializing in domestic violence (e.g., YWCA, Center for Community Solutions, Women’s Resource Center). All subjects gave informed written consent to participate in this study, which was approved by the University of California School of Medicine, Human Research Protections Program.

Neuropsychological Function and Domestic Violence

The NC subjects could have no lifetime exposure to a PTSD DSM-IV Criterion A stressor (American Psychiatric Association 1994). All participants spoke English fluently and had at least an 8th-grade reading ability. The NC subjects were similar to IPV subjects in terms of age, education level, and socioeconomic status as measured by the Hollingshead scale (Hollingshead 1975). The IPV subjects were victims of physical or sexual abuse (or both) by an intimate partner, and they had all extricated themselves from their abusive relationship at least 4 weeks, but no longer than 2 years, before enrollment in the study. In response to our posted advertisements, 184 IPV victims contacted us and were screened for eligibility. Of these, 126 were deemed ineligible for one or more of the following most common reasons: English not their first language, still in the abusive relationship, extensive substance abuse history, serious head injury, or current psychotropic medication use. Of 58 eligible participants, 19 chose not to participate or did not complete the neuropsychologic assessments, leaving the current group of 39 participants with a history of recent IPV. No participant had a history of psychotic illness or neurologic disorder. Furthermore, individuals were excluded from the study if any of the following applied: use of any psychotropic medication within 6 weeks before participation; use of oral or intramuscular steroids within 4 months before participation; reported history of learning disability or attention-deficit disorder, head injury (with loss of consciousness greater than 10 min), or seizure disorder; history of schizophrenia or any other psychotic disorder. To ensure that our findings could not be attributable to drug or alcohol abuse, we took precautions to exclude subjects with these problems. Drug and alcohol use was assessed using the Addiction Severity Index (ASI; McLellan et al 1992). During the past year, none of the subjects had used alcohol to intoxication more than five times or any drugs, with the exception of one IPV subject without PTSD who used marijuana twice. Overall, fewer than 9% of subjects had ever abused any drug or had used alcohol to intoxication for more than 2 years in the past. Given these rigorous selection criteria, we are confident that our findings do not reflect the effects of substance abuse or of serious preexisting head injury, attentiondeficit disorder, or learning disability. By excluding people with histories of attention-deficit disorder or learning disability, one might argue that we are excluding some of the very people who are prone to developing PTSD (Gurvits et al 2000), but this was unavoidable at this stage of research to test our primary hypotheses.

Procedures DIAGNOSTIC AND SYMPTOM SEVERITY MEASURES. To assess the presence and severity of PTSD, participants were administered the Clinician Administered PTSD Scale for DSM-IV (CAPS; Blake et al 1995), with questions directed specifically to experiences of domestic violence. Participants were also administered the PTSD module of the Structured Clinical Interview for the DSM-IV (SCID-P; First et al 1997) to assess presence or absence of lifetime PTSD for any trauma other than domestic violence. Based on these assessments, participants

BIOL PSYCHIATRY 2002;52:1079 –1088

1081

were classified as having either current (i.e., past 30 days) PTSD, past but not current PTSD, and no lifetime PTSD. Only one subject had past but not current PTSD; she was excluded from the analyses to permit the comparison of the mutually exclusive current PTSD (PTSD⫹; n ⫽ 17) and no lifetime PTSD (PTSD⫺; n ⫽ 22) IPV groups. The major depression disorder (MDD), panic disorder, and generalized anxiety disorder modules of the SCID-P were also administered to assess for the presence of these diagnoses. None of the NC subjects had any of these diagnoses, and of the IPV victims, the rate of lifetime MDD was similar in the PTSD⫹ (13 of 17) and PTSD⫺ (15 of 22) subjects (␹2 ⫽ 0.045, df ⫽ 1, p ⫽ .832). Comorbidity in this sample is described in greater detail in a previous report (Stein and Kennedy 2001). The Impact of Event Scale—Revised (IES-R; Weiss and Marmar 1997), a 22-item self-report measure, was administered to examine severity of PTSD symptoms over the week before testing. Severity of intimate partner violence was measured using the revised version of the Conflict Tactics Scale (CTS⫺2; Straus et al 1996), a 39-item self-report measure with five subscales (Negotiation, Psychological Aggression, Physical Assault, Sexual Coercion, and Injury) assessing various aspects of the domestic abuse experience. Level of depression was assessed in all subjects, using the Center for Epidemiologic Studies— Depression Scale (CES-D; Radloff 1977), a 20-item self-report measure examining depressive symptoms within the previous week. Pathologic dissociation was measured using the eight items from the Dissociative Experiences Scale (DES-T; Bernstein and Putnam 1986) that have been reported to index this construct (Waller et al 1996).

Neuropsychologic Tests Neuropsychologic tests assessing several cognitive domains were administered to all subjects by a neuropsychologist (CMK). Scoring followed standardized procedures. Language was assessed with the Controlled Oral Word Association Test (“FAS,” and “animals, fruits, vegetables”; Spreen and Strauss 1998) and the Vocabulary subtest of the Wechsler Adult Intelligence Scale—III (WAIS-III; Wechsler 1997a). Verbal learning and memory were assessed with the California Verbal Learning Test (CVLT; Delis et al 1987) and the Verbal Paired Associates (Reitan and Wolfson 1993) and Logical Memory subtest (one story only was administered, and thus there is a maximum score of 25 points) of the Wechsler Memory Scale—III (WMS-III; Wechsler 1997b). Visuoconstruction and visual memory were assessed with the Continuous Visual Memory Test (CVMT; Trahan and Larabee 1988) and the copy, 30-min delay, and savings (i.e., 30-min delay divided by copy ⴱ 100%) scores of the Rey–Osterrieth Complex Figure Test (Rey–Osterrieth CFT; Spreen and Strauss 1998); we used the Denman itemized scoring criteria (Mitrushina et al 1999). Auditory attention and working memory were assessed with the WAIS-III Digit Span subtest and Auditory Consonant Trigrams (Lezak 1995). Speeded sustained attention was assessed with the Digit Vigilance Test (Lewis and Rennick 1979) and the Paced Auditory Serial Addition Task (PASAT; Levin et al 1987). Psychomotor speed was assessed with Part A of the Trail Making Test (Hays 1995; Reitan 1992).

1082

M.B. Stein et al

BIOL PSYCHIATRY 2002;52:1079 –1088

Table 1. Sociodemographic and Clinical Characteristics NC

IPV PTSD⫺

IPV PTSD⫹

Measure

n

M (SD)

n

M (SD)

n

M (SD)

Tukeya

Age, years Education, years Hollingshead score IES-R CAPS total DES-T CES-D CTS-2 Physical Assault Injury Psychological Aggression Sexual Coercion Negotiation

22 22 22 22 22 22 22

29.4 (10.7) 13.9 (1.5) 37.7 (10.9) — — 1.0 (1.3) 4.3 (3.4)

22 22 22 22 19 22 22

34.5 (9.0) 13.3 (2.3) 33.4 (12.8) 21.6 (16.1) 24.3 (13.8) 4.8 (7.1) 13.8 (9.6)

17 17 17 17 16 17 17

33.8 (9.8) 12.6 (1.7) 30.6 (12.5) 46.0 (18.7) 63.3 (22.8) 12.9 (14.7) 31.4 (12.2)

2–3 2–3 1,2–3 1–2–3

22 22 22 22 22

0.1 (0.2) 0.1 (0.4) 5.6 (13.2) 0.3 (0.9) 83.9 (53.4)

21 21 21 21 21

55.9 (72.7) 13.2 (18.4) 69.1 (57.7) 20.6 (42.3) 41.0 (36.5)

16 16 16 16 16

86.9 (91.1) 29.2 (37.7) 85.3 (68.4) 34.9 (47.9) 37.5 (31.9)

1–2,3 1–3 1–2,3 1–3 1–2,3

NC, nonvictimized comparison subjects; IPV, intimate partner violence; PTSD⫺, IPV subjects without lifetime posttraumatic stress disorder; PTSD⫹, IPV subjects with current posttraumatic stress disorder; CES-D, Center for Epidemiologic Studies—Depression Scale; DES-T, Dissociative Experiences Scale—Traumatic; IES-R, Impact of Event Scale—Revised; CAPS, Clinician Administered PTSD Scale; CTS-2: Revised Conflict Tactics Scale (Higher scores indicate more severe abuse, with the exception of the negotiation subscale, where higher scores indicate healthier response to conflict resolution). a 1, NC; 2, PTSD⫺; and 3, PTSD⫹; groups separated by a dash differ significantly (p ⬍ .05).

Executive functioning was assessed with Part B of the Trail Making Test, the Category Test (Reitan and Wolfson 1993), and the Stroop Color–Word Interference Test (Golden 1978). We also calculated an organizational score (ranging from 0 to 6, with higher scores indicating better peformance) for the Rey–Osterrieth CFT as an additional measure of executive functioning (Deckersbach et al 2000).

Statistical Analyses Analysis of variance (ANOVA) with post hoc testing using the Tukey test was used to compare means of symptom and sociodemographic parameters between groups. To limit the number of statistical tests performed, we conducted multivariate analysis of variance (MANOVA) for all pertinent subtests of a single test (or family of tests, where indicated). Only when the overall MANOVA was statistically significant did we proceed with ANOVA and post hoc Tukey testing to localize the effects. Associations of neuropsychologic performance and symptom or abuse severity were examined using the Spearman correlation coefficient. All statistical tests were two-tailed, and p values ⬍ .05 were considered statistically significant.

Results Characteristics of Study Participants Characteristics of the study participants are detailed in Table 1. The three groups were similar in terms of age, education level, and socioeconomic status. As would be expected, PTSD⫹ subjects had higher scores on the measures of PTSD and dissociative and depressive symptoms. They also had been exposed to more severe intimate partner violence.

Learning, Memory, and Language Subjects’ performance on tests of learning, memory, visuoconstruction, and language are shown in Table 2. There were no statistically significant differences between groups on any of the measures of verbal learning and memory; however, the NC subjects performed better than the IPV subjects on measures of visuoconstruction and visual memory (i.e., Rey–Osterrieth CFT copy, recall, and savings). Importantly, the visuoconstructional differences did not appear to be due to differences in visuospatial organization (i.e., the executive function component of the task; see Table 3 and results below). The three groups were similar in language ability, with the exception of the WAIS-III Vocabulary raw score, which was marginally lower in PTSD⫹ subjects compared with either NC or PTSD⫺ subjects.

Attention, Working Memory, and Executive Function Subjects’ performance on tests of attention, working memory, and executive function are shown in Table 3. On a challenging measure of sustained attention and auditory working memory, the PASAT, IPV subjects performed less well than NC subjects; there were no significant differences, however, between PTSD⫹ and PTSD⫺ subjects. The groups did not differ in performance on Part A of the Trail Making Test, a simple test of psychomotor speed; however, on Part B, a test of executive function involving shifting of cognitive set, PTSD⫹ subjects took significantly and markedly longer to complete the task than NC

Neuropsychological Function and Domestic Violence

BIOL PSYCHIATRY 2002;52:1079 –1088

1083

Table 2. Performance on Tests of Learning, Memory, Visuoconstruction, and Language NC Test Verbal Learning and Memory WMS-III Logical Memoryc Immediate Recall Delayed Recall % Retained California Verbal Learning Test Sum Trials 1–5 Short Delay Free Recall Long Delay Free Recall Verbal Paired Associates List A–D total score Delayed Recall % Retained Total Recognition Score Visuoconstruction and Visual Memory Continuous Visual Memory Test Total Score Rey–Osterrieth CFT Copy score 30-Min Delay score Savings Score (%) Language Controlled Oral Word Association “FAS” Total score Animals, fruits, vegetables Total score WAIS-III Vocabulary

IPV PTSD⫺

IPV PTSD⫹

n

M (SD)

n

M (SD)

n

M (SD)

22 22 22

13.9 (4.1) 12.4 (4.2) 87.3 (15.6)

21 21 21

12.7 (4.5) 11.6 (4.8) 89.2 (16.5)

17 17 17

13.6 (3.7) 12.2 (3.8) 88.3 (11.6)

22 22 22

61.1 (7.9) 13.2 (2.5) 13.3 (2.4)

22 22 22

56.4 (10.4) 12.4 (2.1) 12.2 (3.5)

17 17 17

57.3 (8.6) 12.5 (2.4) 13.1 (2.4)

20 20 20 20

24.1 (6.0) 7.1 (1.8) 93.0 (14.8) 24.0 (0.2)

17 17 17 17

20.7 (6.7) 7.0 (1.7) 96.0 (9.9) 23.9 (0.2)

13 13 13 13

17.8 (7.5) 6.2 (2.2) 94.6 (10.3) 23.9 (0.2)

19

77.0 (7.7)

15

73.6 (6.8)

13

74.5 (8.5)

20 20 20

68.2 (4.1) 41.6 (11.0) 60.6 (14.3)

19 19 19

63.1 (6.2) 28.2 (9.6) 44.6 (14.2)

13 13 13

62.1 (9.2) 33.5 (15.7) 53.3 (22.1)

20 20

40.5 (10.2) 51.9 (6.9)

16 16

42.4 (11.9) 53.9 (12.2)

13 13

40.4 (14.4) 52.5 (9.2)

19

45.9 (7.4)

18

40.1 (11.1)

13

37.1 (11.1)

pa

Tukeyb

ns

ns

ns

ns .05 1–2,3 1–2 1–2 ns

.05

1,2–3

All scores are raw scores unless otherwise indicated. Sample sizes differ for various measures because some tests were added later in the course of the study. NC, nonvictimized comparison subjects; IPV, intimate partner violence; PTSD⫺, IPV subjects without lifetime posttraumatic stress disorder; PTSD⫹, IPV subjects with current posttraumatic stress disorder; CFT, Complex Figure Test. a Measures for each test included in a single multivariate analysis of variance (MANOVA; or analysis of variance if only one measure for that test); p value shown is for main effect of diagnostic group. Post hoc testing (Tukey) for individual measures conducted only if p ⬍ .05 for MANOVA (Wilks’s lambda). ns, not significant at probability level of 0.05. b 1, NC; 2, PTSD⫺; and 3, PTSD⫹; groups separated by a dash differ significantly (p ⬍ .05). c One trial; maximum score ⫽ 25 points.

subjects; the performance of the PTSD⫺ subjects was intermediate between these two groups. This same pattern of effects was detected when time to complete Part A was subtracted from time to complete Part B (i.e., correcting for the component of this task that indexes psychomotor speed). The IPV subjects made more errors than the NC subjects on the Category Test (a task requiring rule learning in response to verbal feedback), but only the difference between PTSD⫺ and NC subjects reached statistical significance. PTSD⫹ and PTSD⫺ subjects performed significantly worse than NC subjects on the Stroop Test Color (speeded identification of colors) and Interference (speeded identification of colors requiring inhibition of a natural word-reading response) trials. The groups did not differ significantly in performance on WAIS-III Digit Span, Auditory Consonant Trigrams, the Digit Vigilance Test, or organization of the Rey– Osterrieth CFT.

Relationships between Symptom and Abuse Severity and Executive Function To limit the number of statistical tests performed, we examined correlations only for those tasks for which differences between groups were detected. We further limited correlations to the IPV subjects, with the goal of accounting for variance in performance among individuals in this group. With these constraints, we failed to find any significant correlations between PTSD severity (IES-R), depressive severity (CES-D), severity of dissociative symptoms (DES-T), or IPV severity (CTS-2 subscales) and any of the neuropsychologic measures.

Discussion Most studies of neuropsychologic function in subjects with PTSD have found some type of cognitive deficit(s), although their specificity for particular functional do-

1084

M.B. Stein et al

BIOL PSYCHIATRY 2002;52:1079 –1088

Table 3. Performance on Tests of Sustained and Selective Attention, Working Memory, and Executive Function NC Test Attention and working memory WAIS-III Digit Span Forward Backward Total Auditory Consonant Trigrams 0-sec delay 3-sec delay 9-sec delay 18-sec delay Digit Vigilance Test Total time PASAT Total score Psychomotor speed Trail Making Test Part A (sec) Executive functioning Trail Making Test Part B (sec) Part B - Part A (sec) Category Test Total errors Stroop Color–Word Interference Test Color Word Interference Rey–Osterrieth CFT Organization score (0 – 6)

IPV PTSD⫺

IPV PTSD⫹ pa

Tukeyb

n

M (SD)

n

M (SD)

n

M (SD)

22 22 22

9.1 (1.8) 7.4 (1.9) 16.5 (3.3)

22 22 22

8.5 (2.2) 6.7 (2.8) 15.2 (4.2)

17 17 17

8.7 (2.2) 7.2 (3.6) 15.2 (4.1)

20 20 20 20

14.9 (0.4) 11.7 (3.0) 9.3 (3.3) 9.0 (2.8)

15 15 15 15

14.9 (0.4) 12.5 (2.5) 10.3 (2.6) 7.5 (3.3)

13 13 13 13

15.0 (0.0) 11.9 (2.3) 9.2 (3.4) 7.2 (2.7)

22

350.4 (80.2)

22

344.3 (75.8)

17

368.5 (73.8)

ns

20

124.4 (29.8)

18

95.4 (35.1)

13

94.5 (38.4)

.02

22

23.9 (8.6)

22

30.1 (13.7)

17

31.2 (13.0)

ns

22 22

55.0 (18.3) 31.1 (14.9)

22 22

76.9 (33.8) 46.8 (24.7)

17 17

95.1 (61.9) 63.9 (60.9)

.01 .03

1–3 1–3

20

30.4 (11.7)

19

42.6 (15.4)

13

38.3 (15.6)

.03 .005

1–2

22 22 22

85.2 (12.1) 106.5 (16.7) 50.9 (9.3)

22 22 22

73.9 (14.3) 102.5 (17.1) 42.7 (10.8)

17 17 17

73.9 (12.9) 94.1 (15.2) 41.8 (8.6)

20

3.8 (1.6)

18

2.8 (1.3)

11

3.8 (1.5)

ns

ns

1–2,3

1–2,3 1–2,3 ns

NC, nonvictimized comparison subjects; IPV, intimate partner violence; PTSD⫺, IPV subjects without lifetime posttraumatic stress disorder; PTSD⫹, IPV subjects with current posttraumatic stress disorder; WAIS-III, Wechsler Adult Intelligence Scale—Third Edition; PASAT, Paced Auditory Serial Addition Test; CFT, Complex Figure Test. a Measures for each test included in a single multivariate analysis of variance (MANOVA; analysis of variance if only one measure for that test); p value shown is for effect of diagnostic group. Post hoc testing (Tukey) for individual measures conducted only if p ⬍ .05 for MANOVA (Wilks’s lambda); ns, not significant at probability level of .05. b 1, NC; 2, PTSD⫺; 3, PTSD⫹; groups separated by a dash differ significantly (p ⬍ .05).

mains, and their severity, has varied markedly across studies. As such, it should probably not be surprising that our findings in women with histories of IPV are consistent with some studies and not others. We found no evidence of deficits in verbal learning or memory in our subjects— irrespective of their PTSD status—although such deficits have been evident in other studies (e.g., Bremner et al 1993). In our study, effect sizes (Cohen’s d) for differences between nontraumatized subjects and those with PTSD on verbal learning and memory (on the WMS-III) were very small (d ⬍ 0.10), whereas in some other studies in combat veterans (Bremner et al 1993) and patients with histories of early trauma (Bremner et al 1995), the effect sizes were much larger (d ⬎ 1.0). In contrast, for Trail Making B time (an index of executive function involving set shifting), the effect size in our study for the difference between nontraumatized and PTSD subjects (d ⫽ 0.36) is similar to previous studies (d ⫽ 0.73 in Beckham et al 1998 and d ⫽ 1.17 in Gilbertson et al 2001). It is unclear why these disparities across studies exists, although it is

reasonable to suspect that sample selection and inclusion– exclusion criteria weigh heavily in this regard. Furthermore, it must be strongly considered that not all forms of trauma or PTSD are identical in the kinds of neuropsychologic abnormalities they evince. Many different types of trauma can result in PTSD, and they do so with different attributable risks (Breslau et al 1998; Bromet et al 1998). Even within uniform trauma types, traumatic exposure can vary in severity, intensity, and duration. Moreover, individual differences in pretrauma characteristics, including but not limited to IQ (Gurvits et al 2000; McNally and Shin 1995), interact with differences in trauma exposure to determine PTSD susceptibility. Given this tremendous variation in factors leading to the development of PTSD, it would indeed be remarkable if all forms of PTSD were associated with a uniform pattern of cognitive abnormalities. Although certain cognitive characteristics (e.g., executive function problems) may eventually be shown to be common across different types of PTSD, differences are to be expected. Studying the

Neuropsychological Function and Domestic Violence

mechanisms that lead to the expression of these cognitive differences will undoubtedly enhance our understanding of the pathways that lead to (and protect from) psychiatric consequences of traumatic stress. Our findings emphasizing visuoconstruction, visual memory, and executive function difficulties can be broadly considered to reflect probable frontal-subcortical dysfunction in female victims of IPV (Cummings 1993; Malloy et al 1998). Similar patterns of deficits have been found by other investigators in their studies of traumatized subjects (e.g., Vasterling et al 1998). Of interest, this pattern of deficits is generally consistent with our main morphometric finding of reduced frontal gray matter volumes in IPV subjects compared with nonvictimized controls (Fennema-Notestine et al 2002). The findings, including in particular the differences in Stroop performance (Grachev et al 2001), are also in accord with findings of reduced N-acetylaspartate (a marker of neuronal density) in anterior cingulate of children and adolescents with PTSD (De Bellis et al 2000) and with functional neuroimaging studies that support alterations in frontal– subcortical circuits in PTSD (Bremner et al 1999; Bremner et al 2000; Lanius et al 2001; Liberzon et al 1999; Shin et al 1999). Within the IPV subjects as a group, we found little consistent evidence of relationships between severity of PTSD symptoms and neuropsychologic performance. Although small sample sizes cannot be excluded as an explanation for our failure to see differences between subjects with and without PTSD, the global pattern of results suggests that if such differences exist, they are likely to be small and of questionable clinical significance. Thus, we are left to conclude tentatively that many of the neuropsychologic differences observed here—and by inference, in at least some other studies of PTSD—are better explained by the effects of trauma or by preexisting (i.e., before the trauma) differences in cognitive function that are more common in persons at risk for IPV exposure. Nonetheless, replication in larger samples is definitely warranted. Recent research in Vietnam combat veterans continues to point to cognitive impairment among those with PTSD (Vasterling et al 2002). Our largely discrepant findings with regard to PTSD may reflect differences in the makeup of the studied samples (e.g. men vs. women; combat vs. interpersonal violence); this is a question for further research. In our sample, the magnitude of differences in cognitive performance between subjects with and without IPV experiences was fairly small. Furthermore, differences in performance between IPV subjects with and without PTSD were even smaller, only rarely reaching statistical significance, and even then not consistently showing poorer performance for those subjects with PTSD. Thus,

BIOL PSYCHIATRY 2002;52:1079 –1088

1085

we identified a pattern of subtle impairments in the IPV group. Although the clinical significance of some of these impairments remains uncertain, others are very likely to be clinically significant. For example, the average score of the PTSD⫹ subjects on Part B of the Trail Making Test would be equivalent to a t score of 33, almost two standard deviations below normal, and would be considered mildly to moderately impaired (Heaton et al 1991). Even mild or subtle impairments on neuropsychologic tests in the laboratory can translate into clinically significant difficulties in the real world, however, because real-world situations involve more complex processing demands in the context of increased distraction in the environment. Consequently, what appears in the laboratory to be subtle impairment in executive functioning, for example, can translate into meaningful impairment in activities of daily living, particularly under stress. Consideration should be given to studying the functional implications of these kinds of neuropsychologic deficits in IPV victims with and without PTSD. It is conceivable that difficulties with executive functioning, for example, may render certain individuals prone to encounter violence, or less able to successfully leave a violent situation or partner. Therapeutic techniques, directed at helping these individuals learn suitable strategies for coping with and circumventing their cognitive deficits, may prove useful as an adjunct to more traditional psychosocial and legal approaches to preventing and treating the sequelae of IPV.

This study was supported by a VA Merit Review Grant to Dr. Stein. The authors thank the staff and clients of the San Diego YWCA, the San Diego Center for Community Solutions, and the San Diego Women’s Resource Center for their assistance with this project. We also thank Dr. Cary Savage for sharing with us his expertise on the use and interpretation of the organizational scoring method for the Rey-Osterrieth Complex Figure Test.

References American Psychiatric Association (1994): Diagnostic and Statistical Manual for Mental Disorders, 4th ed. Washington, DC: American Psychiatric Press. Arnsten AFT (1998): The biology of being frazzled. Science 280:1711–1712. Barrett DH, Green ML, Morris R, Giles WH, Croft JB (1996): Cognitive functioning and posttraumatic stress disorder. Am J Psychiatry 153:1492–1494. Beckham JC, Crawford AL, Feldman ME (1998): Trail Making Test performance in Vietnam combat veterans with and without posttraumatic stress disorder. J Traum Stress 11:811– 819. Bell R, Duncan M, Eilenberg J, Fullilove M, Hein D, Innes L, et al (1996): Violence Against Women in the United States: A Comprehensive Background Paper, 2nd ed. New York: Co-

1086

BIOL PSYCHIATRY 2002;52:1079 –1088

lumbia University, the Commonwealth Fund commission on Women’s Health.

M.B. Stein et al

Delis DC, Kramer JH, Kaplan E, Ober BA (1987): The California Verbal Learning Test: Test and Manual. New York: Psychological Corporation.

Bernstein EM, Putnam FW (1986): Development, reliability and validity of a dissociation scale. J Nerv Ment Dis 174:725– 737.

Eisenstat SA, Bancroft L (1999): Domestic violence. N Engl J Med 341:886 –892.

Blake DD, Weathers FW, Nagy LM, Kaloupek DG, Gusman FD, Charney DS, Keane TM (1995): The development of a clinician-administered PTSD scale. J Traum Stress 8:75–90.

Fennema-Notestine C, Stein MB, Kennedy CM, Archibald SL, Jernigan TL (2002): Brain morphometry in female victims of intimate partner violence with and without posttraumatic stress disorder. Biological Psychiatry 52:1089 –1101.

Bremner JD (1999): Does stress damage the brain? Biol Psychiatry 45:797–805. Bremner JD, Narayan M, Staib LH, Southwick SM, McGlashan T, Charney DS (2000): Neural correlates of memories of childhood sexual abuse in women with and without posttraumatic stress disorder. Am J Psychiatry 156:1787–1795. Bremner JD, Scott TM, Delaney RC, Southwick SM, Mason JW, Johnson DR, et al (1993): Deficits in short-term memory in posttraumatic stress disorder. Am J Psychiatry 150:1015– 1019. Bremner JD, Staib LH, Kaloupek DG, Southwick SM, Soufer R, Charney DS (1999): Neural correlates of exposure to traumatic pictures and sound in Vietnam combat veterans with and without posttraumatic stress disorder: A positron emission tomography study. Biol Psychiatry 45:806 –816. Breslau N, Chilcoat HD, Kessler RC, Peterson EL, Lucia VC (1999): Vulnerability to assaultive violence: Further specification of the sex difference in post-traumatic stress disorder. Psychol Med 29:813–821. Breslau N, Kessler RC, Chilcoat HD, Schultz LR, Davis GC, Andreski P (1998): Trauma and posttraumatic stress disorder in the community. Arch Gen Psychiatry 55:626 –632. Bromet E, Sonnega A, Kessler RC (1998): Risk factors for DSM-III-R posttraumatic stress disorder: Findings from the National Comorbidity Survey. Am J Epidemiol 147:353–361. Buckley TC, Blanchard EB, Neill WT (2000): Information processing and PTSD: A review of the empirical literature. Clin Psychol Rev 28:1041–1065. Carrey NJ, Butter HJ, Persinger MA, Bialik RJ (1999): Physiological and cognitive correlates of child abuse. J Am Acad Child Adolesc Psychiatry 34:1067–1075. Cascardi M, O’Leary KD, Schlee KA (1999): Co-occurrence and correlates of posttraumatic stress disorder and major depression in physically abused women. J Fam Viol 14:227–249. Cummings JL (1993): Frontal-subcortical circuits and human behavior. Arch Neurol 50:873–880.

First MB, Spitzer RL, Gibbon M, Williams JBW (1997): Structured Clinical Interview for DSM-IV Axis I Disorders— Clinician Version (SCID-1). Washington, D.C.: American Psychiatric Press. Gilbertson MW, Gurvits TV, Lasko NB, Orr SP, Pitman RK (2001): Multivariate assessment of explicit memory function in combat veterans with posttraumatic stress disorder. J Traum Stress 14:413–432. Golden CJ (1978): Stroop Color and Word Test. Chicago, IL: Stoelting. Grachev ID, Kumar R, Ramachandran TS, Szevereny NM (2001): Cognitive interference is associated with neuronal marker N-acetyl aspartate in the anterior cingulate cortex: An in vivo 1H-MRS study of Stroop Color–Word task. Mol Psychiatry 6:529 –539. Greenfeld LA, Rand MR, Craven D, Klaus PA, Perkins CA, Ringel C, et al (1998): Violence by Intimates: Analysis of Data on Crimes by Current or Former Spouses, Boyfriends, and Girlfriends. Washington, DC: U.S Department of Justice. Gurvits TV, Gilbertson MW, Lasko NB, Tarhan AS, Dimeon DS, Macklin ML, et al (2000): Neurologic soft signs in chronic posttraumatic stress disorder. Arch Gen Psychiatry 57:181–186. Gurvits TV, Lasko NB, Schachter SC, Kuhne AA, Orr SP, Pitman RK (1993): Neurological status of Vietnam veterans with chronic post-traumatic stress disorder. J Neuropsychiatry Clin Neurosci 5:183–188. Hays JR (1995): Trail Making tests norms for psychiatric patients. Percept Motor Skills 80:187–191. Heaton RK, Grant I, Matthews CG (1991): Comprehensive Norms for an Expanded Halstead–Reitan Battery: Demographic Corrections, Research Findings, and Clinical Applications. Odessa, FL: Psychological Assessment Resources. Hollingshead AB (1975): Four factor index of social status (unpublished manuscript). New Haven, CT: Yale University.

Davidson RJ, Irwin W (1999): The functional neuroanatomy of emotion and affective style. Trends Cogn Sci 3:11–21.

Jenkins MA, Langlais PJ, Delis D, Cohen R (1998): Learning and memory in rape victims with posttraumatic stress disorder. Am J Psychiatry 155:278 –279.

De Bellis MD, Keshavan MS, Clark DB, Casey BJ, Giedd JN, Boring AM, et al (1999): Developmental traumatology part II: Brain development. Biol Psychiatry 45:1271–1284.

Jenkins MA, Langlais PJ, Delis D, Cohen RA (2000): Attentional dysfunction associated with posttraumatic stress disorder among rape survivors. Clin Neuropsychol 14:7–12.

De Bellis MD, Keshavan MS, Spencer S, Hall J (2000): N-Acetylaspartate concentration in the anterior cingulate of maltreated children and adolescents with PTSD. Am J Psychiatry 157:1175–1177.

Kaufman J, Plotsky PM, Nemeroff CB, Charney DS (2000): Effects of early adverse experiences on brain structure and function: clinical implications. Biol Psychiatry 48:778 –790.

Deckersbach T, Savage CR, Henin A, Mataix-Cols D, Otto MW, Wilhelm S, et al (2000): Reliability and validity of a scoring system for measuring organizational approach in the Complex Figure Test. J Clin Exp Neuropsych 22:640 –648.

Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB (1995): Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 52:1048 –1060. Koenen KC, Driver KL, Oscar-Berman M, Wolfe J, Folsom S, Huang MT, et al (2001): Measures of prefrontal system

Neuropsychological Function and Domestic Violence

dysfunction in posttraumatic stress disorder. Brain Cogn 45:64 –78. Krystal JH, Bennett A, Bremner JD, Southwick SM, Charney DS (1995): Toward a cognitive neuroscience of dissociation and altered memory functions in post-traumatic stress disorder. In: Friedman MJ, Charney DS, Deutch AY, editors. Neurobiological and Clinical Consequences of Stress. Philadelphia: Lippincott-Raven, pp 239 –270. Lanius RA, Williamson PC, Densmore M, Boksman K, Gupta MA, Neufeld RWJ, et al (2001): Neural bases of emotion dysregulation in posttraumatic stress disorder: A functional MRI investigation. Am J Psychiatry 158:1920 –1922. Levin HS, Mattis S, Ruff RM, Eisenberg HM, Marshall LF, Tabaddor K, et al (1987): Neurobehavioral outcome following minor head injury: A three-center study. J Neurosurg 66:234 –243. Lewis RF, Rennick PM (1979): Manual for the Repeatable Cognitive Perceptual Motor Battery. Grosse Pointe Park, MI: Axon Publishing Company. Lezak MD (1995): Neuropsychological Assessment, 3rd ed. New York: Oxford University Press. Liberzon I, Taylor SF, Amdur R, Jung TD, Chamberlain KR, Minoshima S, et al (1999): Brain activation in PTSD in response to trauma-related stimuli. Biol Psychiatry 45:817– 826. Lupien SJ, McEwen BS (1997): The acute effects of corticosteroids on cognition: Integration of animal and human model studies. Brain Res Rev 24:1–27. Macklin ML, Metzger LJ, Litz BT, McNally RJ, Lasko NB, Orr SP, et al (1998): Lower precombat intelligence is a risk factor for posttraumatic stress disorder. J Consult Clin Psychol 66:323–326. Malloy RF, Cohen RA, Jenkins MA (1998): Frontal lobe function and dysfunction. In: Snyder PJ, Nussbaum PD, editors. Clinical Neuropsychology. Washington, DC: American Psychological Association, pp 573–590. McLellan AT, Kushner H, Metzger D, Peters R, Smith I, Grissom G, et al (1992): The fifth edition of the Addiction Severity Index. J Subst Abuse Treatment 9:199 –213. McNally RJ, Shin LM (1995): Association of intelligence with severity of posttraumatic stress disorder symptoms in Vietnam combat veterans. Am J Psychiatry 152:936 –938. Mitrushina MN, Boone KB, D’Elia LF (1999): Rey–Osterrieth Complex Figure Handbook of Normative Data for Neuropsychological Assessment. New York: Oxford University Press, pp 157–185. Mizoguchi K, Yuzurihara M, Ishige A, Sasaki H, Chui D-H, Tabira T (2000): Chronic stress induces impairment of spatial working memory because of prefrontal dopaminergic dysfunction. J Neurosci 20:1568 –1574. Newcomer JW, Selke G, Melson AK, Hershey T, Craft S, Richards K, et al (1999): Decreased memory performance in healthy humans induced by stress-level cortisol treatment. Arch Gen Psychiatry 56:527–533. Perez C, Widom CS (1994): Childhood victimization and longterm intellectual and academic outcomes. Child Abuse Neglect 18:617–633. Radloff LS (1977): The CES-D scale: A self-report depression scale for research in the general population. Psychol Meas 1:385–401.

BIOL PSYCHIATRY 2002;52:1079 –1088

1087

Reitan RM (1992): Trail Making Test. Manual for Administration and Scoring. Tucson, AZ: Reitan Neuropsychological Laboratory. Reitan RM, Wolfson D (1993): The Halstead-Reitan Neuropsychological Test Battery: Theory and Clinical Interpretation, 2nd ed. Tucson, AZ: Neuropsychology Press. Sachinvala N, von Scotti H, McGuire M, Fairbanks L, Bakst K, McGuire M, et al (2000): Memory, attention, function and mood among patients with chronic posttraumatic stress disorder. J Nerv Ment Dis 188:818 –823. Saigh PA, Mroweh M, Bremner JD (1997): Scholastic impairment among traumatized adolescents. Behav Res Ther 35:429 –436. Sapolsky RM (1996): Why stress is bad for your brain. Science 273:749 –750. Sapolsky RM (2000): Glucocorticoids and hippocampal atrophy in neuropsychiatric disorders. Arch Gen Psychiatry 57:925– 935. Shin LM, McNally RJ, Kosslyn SM, Thompson WL, Rauch SL, Alpert NM, et al (1999): Regional cerebral blood flow during script-driven imagery in childhood sexual abuse-related PTSD: A PET investigation. Am J Psychiatry 156:575–584. Spreen O, Strauss E (1998): A Compendium of Neuropsychological Tests: Administration, Norms and Commentary, 2nd ed. New York: Oxford University Press. Stein MB, Hanna C, Vaerum V, Koverola C (1999): Memory functioning in adult women traumatized by sexual abuse. J Traum Stress 12:527–534. Stein MB, Kennedy CM (2001): Major depressive and posttraumatic stress disorder comorbidity in female victims of intimate partner violence. J Affect Disord 66:133–138. Stein MB, Walker JR, Forde DR (2000): Gender differences in susceptibility to posttraumatic stress disorder. Behav Res Ther 38:619 –628. Stein MB, Walker JR, Hazen AL, Forde DR (1997): Full and partial posttraumatic stress disorder: Findings from a community survey. Am J Psychiatry 154:1114 –1119. Straus M, Hamby SL, Boney-McCoy SB, Sugarman DB (1996): The Revised Conflict Tactics Scales (CTS2): Development and preliminary psychometric data. J Fam Issues 17:283– 316. Sullivan EV, Rosenbloom MJ, Lim KO, Pfefferbaum A (2000): Longitudinal changes in cognition, gait, and balance in abstinent and relapsed alcoholic men: Relationship to changes in brain structure. Neuropsychology 14:178 –188. Trahan DE, Larabee GJ (1988): Continuous Visual Memory Test. Odessa, FL: Psychological Assessment Resources. Uddo MM, Vasterling JJ, Brailey K, Sutker PB (1993): Memory and attention in posttraumatic stress disorder. J Psychopathol Behav Assess 15:43–52. Vasterling JJ, Brailey K, Constans JI, Sutker PB (1998): Attention and memory dysfunction in posttraumatic stress disorder. Neuropsychology 12:125–133. Vasterling JJ, Duke LM, Brailey K, Constans JI, Allain AN, Sutker PB (2002): Attention, learning, and memory performance and intellectual resources in Vietnam veterans: PTSD and no disorder comparisons. Neuropsychology 16:5–14.

1088

BIOL PSYCHIATRY 2002;52:1079 –1088

Waller NG, Putnam FW, Carlson EB (1996): Types of dissociation and dissociative types: A taxometric analysis of dissociative experiences. Psychol Meth 1:300 –321. Wechsler D (1997a): Wechsler Adult Intelligence Scale—Third Edition (WAIS-III). San Antonio, TX: Psychological Corporation. Wechsler D (1997b): Wechsler Memory Scale—Third Edition (WMS-III). San Antonio, TX: Psychological Corporation. Weinbaum Z, Stratton TL, Chavez G, Motylewski-Link C, Barrera N, Courtney JG (2001): Female victims of intimate partner physical domestic violence (IPP-DV), California 1998. Am J Prev Med 21:313–319.

M.B. Stein et al

Weiss DS, Marmar CR (1997): The Impact of Events Scale— Revised. In: Wilson JP, Keane TM, editors. Assessing Psychological Trauma and PTSD. New York: Guilford Press, pp 577–591. Wolfe J, Schlesinger LK (1997): Performance of PTSD patients on standard tests of memory. Proc N Y Acad Sci 821:208 – 218. Yehuda R, Keefe RS, Harvey PD, Levengood RA, Gerber DK, Geni J, et al (1995): Learning and memory in combat veterans with posttraumatic stress disorder. Am J Psychiatry 152:137– 139.