This article was downloaded by: [UQ Library] On: 11 November 2014, At: 08:25 Publisher: Routledge Informa Ltd Registered in England and Wales Registered Number: 1072954 Registered office: Mortimer House, 37-41 Mortimer Street, London W1T 3JH, UK
Journal of Clinical and Experimental Neuropsychology Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/ncen19
Cognition in eating disorders a
a
Barbara Pendleton Jones , Connie C. Duncan , Pim a
Brouwers & Allan F. Mirsky
a
a
Laboratory of Psychology and Psychopathology, National Institute of Mental Health , Published online: 04 Jan 2008.
To cite this article: Barbara Pendleton Jones , Connie C. Duncan , Pim Brouwers & Allan F. Mirsky (1991) Cognition in eating disorders, Journal of Clinical and Experimental Neuropsychology, 13:5, 711-728, DOI: 10.1080/01688639108401085 To link to this article: http://dx.doi.org/10.1080/01688639108401085
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sublicensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
Journal of Clinical and Experimental Neuropsychology 1991, VOI. 13. NO. 5, pp. 71 1-728
0 168-8634D 1/1305-07 11$3.00 Q Swets & Zeitlinger
Cognition in Eating Disorders* Barbara Pendleton Jones, Connie C. Duncan, P i m Brouwers, and Allan F. Mirsky Laboratory of Psychology and Psychopathology, National Institute of Mental Health
Downloaded by [UQ Library] at 08:25 11 November 2014
ABSTRACT Cognitive functions were investigated in four groups of women: 30 underweight anorexics, 38 normal-weight bulimics, 20 long-term weight-restored anorexics, and 39 normal controls. A MANOVA was used to examine performance on five neuropsychological domains derived from prior principal components analyses of a comprehensive neuropsychological battery. Underweight anorexics performed more poorly than normal controls in four of five neuropsychological domains (focusing/execution, verbal, memory, and visuospatial), while normal-weight bulimics showed poorer performances only in focusing/execution. The absolute differences in scores between eating disorder groups and normal controls were for the most part small, suggesting subtle rather than frank cognitive difficulties. Poorer neuropsychological test performance was associated with anxiety but not depression as measured by the Tryon, Stein, and Chu Tension scale and scale 2 of the MMPI respectively. The findings support previous reports of attentional difficulties in eating disorders but do not support the hypothesis of differential right-hemisphere dysfunction in eating disorders.
Until relatively recently, etiological discussions of the eating disorders, anorexia
nervosa and bulimia, have centered on family interaction patterns and intrapsychic phenomena (e.g., Bruch, 1970; Minuchin, Rosman, & Baker, 1978). S i n c e the late 1970s, however, reports h a v e appeared suggesting central nervous system dysfunction in association with eating disorders. Goldberg, Halmi, and their colleagues (Goldberg, Halmi, Casper, Eckert, & Davis, 1977; Halmi, Goldberg, Eckert, Casper, & Davis, 1977) have reported an increased incidence of compli-
* The authors wish to thank Drs. David Jimerson, Walter Kaye, Arlene Hegg, and Timothy Brewerton for their cooperation in referring subjects and Mrs. Marie Elliott, Ms. Kathleen Squillace, Mr. Gene Tassone, and Mrs. Audrey Weinberg for assistance in data collection and analysis. We also wish to extend special thanks to Dr. John Bartko for assistance with issues of statistical analysis. Address reprint requests to Dr. B.P. Jones, Laboratory of Psychology and Psychopathology, National Tnstitute of Mental Health, 9000 Rockville Pike, Building 10, Room 4C110, Bethesda, MD 20892, USA. Dr. Brouwers is currently with the National Cancer Institute, Bethesda, MD. Accepted for publication: December 17, 1990.
Downloaded by [UQ Library] at 08:25 11 November 2014
712
BARBARA PENDLETON JONES ET AL.
cations in pregnancy and delivery (Le., historical evidence suggestive of perinatal brain injury) in subjects who later developed anorexia nervosa and a positive correlation between the number of such complications and severity of prognosis in these patients. In a series of 94 cases, Halmi (1974) found a significantly greater maternal and paternal age at time of the anorexic patient’s birth and a greater incidence of both low and high birth weights compared with the general population. In addition, there is evidence for a genetic factor in anorexia nervosa: Hsu (1990) has recently reviewed the available twin studies and found that in the studies with established zygosity and explicit diagnostic criteria, of 28 monozygotic twin pairs with at least one anorexic twin, 50% were concordant for anorexia nervosa, while for 14 dizygotic twin pairs, the concordance rate was 7%. In addition, investigators have reported abnormal findings in eating disorder patients in computerized tomographic (CT) brain scan (Enzmann & Lane, 1977; Heidrich & Schmidt-Matthias, 1961; Heinz, Martinez, & Haenggeli, 1977), brain event-related potential (Duncan, Kaye, Perlstein, Jimerson, & Mirsky, 1985), neurotransmitter (Halmi, Dekirmenjian, Davis, Casper, & Goldberg. 1978; Kaye, Ebert, Raleigh, & Lake, 1984), and neuropeptide (Gold, Kaye, Robertson, & Ebert, 1983) studies. While the cerebral atrophy seen in underweight anorexics may be related to protein loss and/or fluid retention and has been found to be reversible in at least some cases (Heinz et al., 1977; Sein, Searson, Nicol, & Hall, 1981), the abnormalities in norepinephrine (NE) metabolism appear to be stateindependent (Kaye, Jimerson, Lake, & Ebert, 1985) and may contribute to the characteristic changes in mood, behavior, and neuroendocrine function in eating disorders. Prior neuropsychological studies of patients with eating disorders have for the most part been interpreted as showing right-hemisphere dysfunction and/or attentional deficits, but a number of these studies have contained serious methodological flaws. Fox (1981) found relative impairment in 15 anorexic patients (compared to a mixed group of psychiatric controls) on WAIS-R Information and Wide Range Achievement test arithmetic scores; on the basis of the anorexics’ impaired performance on arithmetic and the Benton Visual Retention Test, she speculated about right-hemisphere dysfunction in anorexia. However, her mixed psychiatric control group included subjects with a variety of diagnoses, including conduct disorder, hyperkinesis, and schizophrenia; and its gender distribution (8 females, 7 males) differed markedly from the anorexic group (14 females, 1 male). In the light of what is known about sex differences in arithmetic and visuospatial skills (Buffery & Gray, 1972; Lezak, 1983; Maccoby & Jacklin, 1974), the latter problem alone raises questions about her conclusions. Maxwell, Tucker, and Townes (1984) reported relative deficiencies in spatial cognition in three anorexic patients; however, given the inadequate n, the fact that one subject was not at a low weight at the time of testing, and the fact that the other two were atypical in age of onset (30 and 69), it would seem impossible to draw any conclusions about anorexia nervosa from this study. McKay, Humphries, Allen, and Clawson (1986) compared 30 bulimic patients to 30 normal controls on the
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
713
Luria Nebraska Neuropsychological Battery and reported that the bulimics were impaired on tasks vulnerable to right frontal lobe dysfunction, primarily speed of drawing geometric figures. While all of these groups of researchers concluded that there may be righthemisphere dysfunction in eating disorders, Hamsher, Halmi, and Benton (1981) emphasized attentional deficits in their group of 20 anorexic patients. Studies have shown an association between scores on reaction-time tasks (Hamsher et al., 1981) or other attentional tasks (WAIS Arithmetic and Digit Span; Small, Madero, Teagno, & Ebert, 1983) and subsequent weight gain and/or maintenance. Witt, Ryan, and Hsu (1985) emphasized learning deficits on the Symbol-Digit Learning Test in their anorexic patients; but as their assessment of attention was limited to the WAIS-R (or WISC-R) Digit Span, it is possible that the learning impairment was secondary to an attentional deficit not revealed by Digit Span performance. Based on the foregoing observations, the present study was designed to address the following questions: (1) Do patients with eating disorders show deficits in attention, concentration, and vigilance? (2) Are patients with eating disorders impaired in other cognitive functions, particularly in functions implicating the right hemisphere? (3) What are the relationships between cognitive performance and depression and anxiety in patients with eating disorders?
METHODS Subjects
There were four groups of women: underweight anorexics, normal-weight bulimics, longterm weight-restored anorexics (hereafter referred to as weight-restored anorexics), and normal controls. Groups were matched overall for age, education, and handedness; all of the subjects were white. All eating disorder patients were inpatients or outpatients of clinical research units of the National Institutes of Health Clinical Center, National Institute of Mental Health, and all met (or, in the case of the weight-restored anorexics, had previously met) established criteria (Diagnostic and Statistical Manual of Mental Disorders, [3rd ed., DSM-1111)for anorexia nervosa or for normal-weight bulimia (American Psychiatric Association, 1980). Prior to admission, each hospitalized underweight anorexic patient had maintained a body weight of less than 75% of her ideal body weight (according to the Metropolitan Life Insurance Company tables) for a periodof at least 6 months (M = 27.8 mo, SD = 9.4). Patients who had medical problems or were underweight to a degree requiring immediate medical intervention were not admitted to the study. Patients who had electrolyte abnormalities secondary to vomiting or laxative abuse were first rehydrated so that electrolyte values were within normal limits. Underweight anorexics were then maintained at a stable weight (k 1.O kg) on a nutritionally balanced diet for at least one month before neuropsychological testing. The weight-restored anorexics were a separate group of anorexic patients who had been weight-restored for at least 6 months prior to the study ( M = 47.1 mo, SD = 3 1.6). Potential eating disorder subjects were excluded if they had a history of learning disabilities. Two of 30 underweight anorexics and 2 of 38 normal-weight bulimics had histories of substance abuse; with the exception of solvents and sedative-hypnotics (which were not abused by these four patients), drug abuse has not been shown to be linked with substan-
714
BARBARA PENDLETON JONES ET AL.
Table 1. Characteristics of Subject Groups.
N
Age
Education
Underweight anorexics
30
Normal-weight bulimics
38
Weight-restored anorexics
20
Normal controls
39
24.4 5.3 24.1 4.0 26.0 6.2 24.9 4.4
14.0 2.2 14.6 1.6 15.1 2.3 15.0 1.6
Subject group
Downloaded by [UQ Library] at 08:25 11 November 2014
a
Weight (kg) 33.8 4.4 55.2 5.6 51.3 6.1 57.8 6.3
%IBW~ 59.4 6.6 94.0 7.3 87.8 11.2 98.2 7.5
Means above, standard deviations below. 8 Ideal body weight, according to the Metropolitan Life Insurance Company tables.
tial neuropsychological dysfunction (for a review, see Carlin, 1986). The normal controls were subjects recruited by newspaper advertisements or from among National Institutes of Health employees and were screened with the use of the Schedule for Affective Disorders and Schizophrenia-Lifetime Version (SADS-L; Spitzer, Endicott, & Robins, 1978) and sections of the Diagnostic Survey for Eating Disorders (DSED; Johnson, 1985); potential controls who received any diagnosis on the SADS-L or who had any symptoms of an eating disorder on the DSED were excluded. All subjects had given informed consent for the study. Normal controls had no physical illness, no personal or family history (fmtdegree relatives) of psychiatric disorder, and no history of learning disabilities. All subjects had been free of medication for at least 4 weeks prior to testing. We did not follow the common practice of using psychiatric patients as controls because it has been firmly established that there is cognitive dysfunction associated with a number of psychiatric syndromes (e.g., Grant & Adams, 1986; Heaton & Crowley, 1981). In order to determine whether our eating disorder patients were cognitively impaired, we considered it essential to compare them with a group of normal women. The question of how patients with eating disorders might differ in their patterns of cognitive dysfunction from patients with other neuropsychiatric syndromes is a separate question, one that we hope to address in future studies. The notion that changes in the neuropsychological functioning of eating disorder patients might be “due to depression,” that one can partial out the amount of change “due to depression” by using a depressed control group, and that can one can conclude that the remaining variance is “due to the eating disorder” reflects a fundamental misconception about eating disorders.’ Depressive symptoms are a part of the eating disorder itself (Goodwin & Andersen, 1984; Halmi et al., 1977; Heaog, 1984; Hudson, Pope, Jonas, & Yurgelen-Todd. 1983; Piran. Kennedy, Garfiiel. & Owens, 1985); regression analysis provides a logical means of examining the correspondence between depressive symptomatology and cognitive dysfunction in eating disorders. Table 1 presents summary data for the subjects in this study. There were no significant differences in age or level of education among the four groups.
-By analogy, one might reason that in studies of patients with Alzheimer’s disease, since many of these patients have frontal lobe atrophy, and since frontal lobe atrophy affects neuropsychological functioning, a neuropsychological study of Alzheimer’s disease must include a control group of patients with frontal lobe lesions.
715
COGNITION IN EATING DISORDERS
Table 2. Other Lifetime Psychiatric Diagnoses in Eating Disorder Patients’
Major depression Bipolar disorder Hypomanic episodes Dysthymia, minor depression, atypical depression, secondary depression Substance abuse None ~
Downloaded by [UQ Library] at 08:25 11 November 2014
a
UA
NB
WA
47 3 0
26 3 0
50 10 5
7 7 13
39
20
5 11
20
5
~
Percentages. UA = underweight anorexics (n = 30); NB = normal-weight bulimics ( n = 38); WA = weight-restored anorexics (n = 20).
Table 2 presents data about other psychiatric diagnoses (present or past) received by the eating disorder patients; these were diagnoses noted either in the SADS-L report or in the patient’s medical record.
Neuropsychological Measures Table 3 presents a listing of the neuropsychological measures employed in the study. The battery was selected to address the particular questions concerning attention and righthemisphere functioning in this study, but in addition to assess a broad range of cognitive functions. The majority of the tests are described in Lezak (1983). Tests not included in Lezak are described as follows: Eioptor Vision Test. This is a standardized test of visual acuity.
Buschke Selective Reminding Test (Buschke & Fuld, 1974). The subject recalls as many words as he/she can from a 12-noun list immediately after it has been read to him/her; after each trial, the examiner repeats any list words omitted by the subject. Trials, followed by selective reminding, continue until the subject recalls the whole list twice consecutively or until 8 trials have been completed. Continuous Performance Test (Rosvold, Mirsky, Sarason, Bransome, & Beck, 1956). This is a visual vigilance task in which the subject is required to press a response key only to certain target letters; X is the target letter in the “X” task, and X following A is the target letter in the “AX” task. Letters appear on a display screen at 1-s intervals with a stimulus duration of 0.2 s; targets are 25% of the stimuli in the X taqk and 20% of the stimuli in the A X task. Talland Letter Cancellation Test-Revised. This is identical to the test described by Talland and Schwab (1964), except that in Test B, subjects cross out all letters preceding or following double spaces. Semantic Aphasia Test. In this test devised by Goldberg (personal communication) along the lines of Luria’s investigation of semantic aphasia, the subject has first to draw a series of pairs of items (e.g., “Draw a triangle below a square”) and then to answer a series of questions in the following categories: quasi-spatial, temporal, height, and kinship (e.g., “Mike was hit by Steve. Who got hurt?”). Tirmus SKereO Tesrs. These are simple tests of stereoscopic vision.
716
BARBARA PENDLETON JONES ET AL.
Table 3. Eating Disorders Study Neuropsychological Test Battery. Function
Test
Executive Sequencing, Attention Attention (Focus, Execute)
Trail Making Test Stroop Color-Word Interference Test Talland Letter Cancellation Test-Revised Concept Formation (Capacity to Shift) Wisconsin Card Sorting Test Abstraction Category Test (Halstead)
Downloaded by [UQ Library] at 08:25 11 November 2014
General Intelligence Language Initiation Written Comprehension
Wechsler Adult Intelligence Scale-Revised (WAIS-R) Controlled Oral Word Association Test Boston Diagnostic Aphasia Examination - Narrative Writing Token Test (Spreen & Benton version, 1969)
Semantic Aphasia Test (Goldberg) Memory Global Recent Verbal Recent and Remote Verbal Recent Visuospatial Recent and Remote Visuospatial
Wechsler Memory Scale (WMS) Buschke Selective Reminding Test Rey Auditory Verbal Learning Test Babcock Story Recall Test Recurring Figures Test (Kimura) Complex Figure Test (Rey-Osterrieth; Taylor)
Motor Functions
Purdue Pegboard Test Boston Diagnostic Aphasia ExaminationApraxia Test
Personality
Minnesota Multiphasic Personality Inventory (MMPI)
Sensory and Perceptual
Bioptor Vision Test Dvorine Pseudo-isochromatic Plates Titmus Stereo Test Harris Test of Hand Dominance Eye Dominance Test
Vigilance (Sustained Attention)
Continuous Performance Test
Visuospatial
Butters’ Embedded Figures Test Embedded Figures Test (Witkin) Hooper Visual Organization Test Raven Standard Progressive Matrices
COGNITION IN EATING DISORDERS
717
Table 4. Domains of Neuropsychological Functioning. Domain
Measures
Vigilance
CPT mean % hits, X and AX tasks' CPT mean % commission errors, X and AX tasksb CPT mean reaction time, X and AX tasks WAIS-R Digit Symbol, scaled score Trail Making Test, A time + B time correct I Talland Letter Cancellation Test-Revised, mean # WAIS-R Similarities, scaled score WAIS-R Comprehension, scaled score WAIS-R Vocabulary, scaled score Babcock Story Recall Test, immediate recall score Wechsler Memory Scale, Logical Memory score Buschke Selective Reminding Test, recall score Rey-Osterrieth Complex Figure, delayed recall score Embedded Figures Test, time WAIS-R Block Design, scaled score
Focus/execute Verbal
Downloaded by [UQ Library] at 08:25 11 November 2014
Memory Visuospatial
a
Hits are defined as responses to target stimuli occurring within 700 ms. Commission errors are responses to nontarget stimuli.
Statistical Analyses In order to reduce the number of variables from the rather large neuropsychological battery employed in this study, we relied upon prior principal components analyses of neuropsychological measures in use in the Laboratory of Psychology and Psychopathology (LPP; Jones, Duncan, Mirsky, & Brouwers, 1988; Mirsky, 1989). These analyses have yielded five readily identifiable components or factors: two attention factors (vigilance and focusing/execution), a verbal factor, a mixed memory/comprehension factor, and a visuospatial factor. The two attention factors (vigilance and focusing/execution) appear to be in essence the same as the vigilance and focusing/execution factors which have been found in a number of factor analyses of attentional measures in this laboratory (Mirsky, 1989); attention factors are likely to be more prominent in our battery than in most others because of our inclusion of more attentional measures than in other batteries. Verbal and nonverbal (here termed visuospatial) factors have consistently emerged in factor analytic studies of neuropsychological batteries (e.g., Shelly & Goldstein, 1982) and of the WAIS subtests (for a review, see Lezak, 1983; see also Siegert, Patten, Taylor, & McCormick, 1988). From 29 variables submitted to the principal components analysis, we chose the 15 variables which had the highest loadings for the five factors (i.e,, the three highestloading measures for each of the five factors).2 Table 4 presents the five neuropsychological domains and their component measures. A subsequent principal components analysis using these 15 measures for the present study population yielded the same five factors and accounted for 73% of the variance: vigilance (17.1%). focusinglexecution (14.6%), verbal (14.5%). memory (13.7%), and visuospatial(13.1%). The one exception was the choice of the fifth-highest measure (Buschke Selective Reminding Test, loading 0.52) for the memory/comprehension factor rather than the third- (WAIS-R Picture Arrangement, loading 0.58) or fourth-highest measure (Token Test, loading 0.56); this yielded a composite score of more conceptual unity for the present study. This factor is hereafter referred to as a memory factor.
718
BARBARA PENDLETON JONES ET AL.
Downloaded by [UQ Library] at 08:25 11 November 2014
Rather than analyzing factor scores based on the five factors, each of which contains loadings from all 15 measures, we chose to look at composite scores for each of the five neuropsychological domains which had been identified (Table 3). Scores for each subject on all 15 measures were transformed into z scores; for each neuropsychological domain, the three z scores were averaged to yield a domain score. A multivariate analysis of variance (MANOVA) was then carried out on the domain scores. Posthoc testing was accomplished with the use of Newman-Keuls tests. Finally, in order to assess the Idationship between cognitive performance in eating disorders and symptoms of depression and anxiety, we performed two multivariate analyses of covariance (MANCOVAs) using Minnesota Multiphasic Personality Inventory (MMPI) scores on scale 2 (Depression) and on the Tryon, Stein, and Chu Tension scale (TSC/T; Stein, 1968; Tryon, 1966) as covariates. The TSC/T is thought to be the best available MMPI scale for the measurement of anxiety (Levitt, 1989).
RESULTS The MANOVA yielded a significant F(15, 328.91) = 2.43, p < 0.0023 (Wilks’ criterion [see Rao, 1973, p. 5551). There were significant group differences in four of the five neuropsychological domains. The vigilance domain yielded no group differences [F(3, 123) = 1.45, p < 0.23; Figure 11. In the focusing/execu-
0.2
2
0.0
sf
-cm g
-0.2
n
-0.6
UA
0
P a
WA .
Nc
4
Groupr
Fig. 1. Vigilance domain scores. UA = underweight anorexics; NB = normal-weight bulimics; WA = weight-restored anorexics; NC = normal controls.
~
719
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
-"."
. UA
NB
WA
Nc
Groups
Fig. 2. Focusing/execution domain scores. UA = underweight anorexics; NB = normalweight bulimics; WA = weight-restoredanorexics; NC = normal controls.
?!
0
0 u)
.-Cm
E
0
-"."
. UA
NB
WA
rn
Groups
Fig. 3. Verbal domain scores. UA =underweight anorexics;NB = normal-weightbulimics; WA = weight-restored anorexics; NC = normal controls.
720
BARBARA PENDLETON JONES ET AL. 0.4 I
0.2
0.0
Downloaded by [UQ Library] at 08:25 11 November 2014
-0.2
-0 -0.6
UA
WA
N3
Nc
Groups
Fig. 4. Memory domain scores. UA =underweightanorexics; NB = normal-weight b u l i c s ; WA = weight-restoredanorexics; NC = normal controls.
tion domain [F(3, 123) = 5.84, p c .0009], the two acute eating disorders groups (i.e., underweight anorexics and normal-weight bulimics) performed more poorly than normal controls (Figure 2). In the verbal domain [F(3,123) = 5 . 0 9 , c ~ .0024], the underweight anorexics scored lower than all other groups (Figure 3); in the memory domain [F(3, 123) = 4.40, p < .006] and in the visuospatial domain [F(3, 123) = 3.18, p < .03], underweight anorexics performed worse than normal controls (Figures 4 and 5 ) . Table 5 presents the mean scores for each group on the measures comprising the five neuropsychological domains, and Table 6 presents group means on the WAIS-R IQ scores, It is apparent that overall, the women in this study are above average in their level of cognitive functioning. Reviewing seven epidemiological studies of anorexia performed between 1970 and 1988, Hsu (1990) noted a preponderance of patients from the higher socioeconomic classes was found in all but two studies. These findings suggest that eating disorders may affect women from higher socioeconomic or IQ groups preferentially. The MANCOVA using MMPI scale 2 (Depression) scores as a covariate yielded an F score which was still highly significant, F(15,326.15)= 1 . 9 7 , < ~ .02. However, the MANCOVA using the TSCD scores as a covariate produced a
721
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
V."
. UA
WA
Fs
t c
Groups
Fig. 5. Visuospatial domain scores. UA = underweight anorexics; NB = normal-weight bulimics; WA = weight-restored anorexics; NC = normal controls.
result which was not significant, F (15,326.15) = 1.48, p < .11. These results suggest that symptoms of anxiety, but not depression, are associated with neuropsychological changes in eating disorders, in that when the variance associated with symptoms of anxiety is statistically removed, the F score for overall group effects falls short of significance.
DISCUSSION In the present study, differences were seen between one or more of the groups of patients with eating disorders and normal controls in four of five domains of neuropsychological functioning (the focusing/execution aspect of attention, verbal functioning, memory, and visuospatial functioning). The absolute differences in test scores between the eating disorder groups and normal controls were small. For the most part, the eating disorder groups' mean scores differed little from published norms, suggesting subtle rather than frank neuropsychological dysfunction in the eating disorder groups.
722
BARBARA PENDLETON JONES ET AL.
Table 5. Group Mean Raw Scores on Neuropsychological Measures' Measure
NB
UA
Downloaded by [UQ Library] at 08:25 11 November 2014
Vigilance CPT Ihits CPT % CEb CPT mean RTC
WA
96.5 (4.8) 0.8 (0.9) 451.2 (57.3)
Focustexecute Digit Symbol Trail Making Part A Part B Talland Letter
NC
97.2 (3.3) 94.1 (8.7) 0.7 (0.6) 1.3 (1.8) 451.7 (81.0) 442.4 (54.2)
LL2w
12.4
urn 2uiIM.l m u
25.4 (8.0) 52.8 (29.0) 78.9 (12.3)
Verbal Similarities Comprehension Vocabulary
12.5 13.2 12.1
(1.9) (2.4) (2.3)
12.2 13.0 12.7
(2.4) (3.1) (2.4)
12.4 12.7 13.1
(2.2) (2.8) (2.8)
Memory Babcock Logical Memory Buschke Recall
13.2 9.4 10.1
(3.6) (3.0)
13.0 8.2 10.2
(3.9) (3.2) (1.2)
15.6 11.1 10.2
(3.7) (3.3) (1.1)
Visuospatial Rey -0sterrieth Emb. Figures Block Design a
(1.1)
20.8 (7.2) 596.9 (304.8) 10.8 (2.5)
(2.1)
12.9
(2.2)
24.7 (6.7) 48.8 (12.9) 84.8 (10.2)
21.6 (5.6) 22.0 (5.1) 698.7 (362.1) 467.3 (246.1) 11.4 (3.1) 12.4 (2.3)
Means (standard deviations). Underlined scores differed significantly from those of normal controls. UA = underweight anorexics; NB = normal-weight bulimics; WA = weight-restored anorexics; NC = nonnal controls. CE = commission errors. RT = reaction time.
Table 6. Group WAIS-R IQ Scores' Group
N
Underweight anorexics Normal-weight bulimics Weight-restored anorexics Normal controls
30 38 20 39
a
Means (standard deviations).
Verbal IQ
103.0 (10.7) (9.8) 108.9 111.3 (13.9) 114.6 (13.8)
Performance IQ
104.4 106.5 109.3 111.9
(12.6) (12.6) (15.5) (13.1)
Full Scale IQ
103.9 109.0 111.4 113.5
(11.2) (10.9) (15.9) (11.8)
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
723
There are several possible explanations for this pattern of findings. First, it could be that the statistically significant differences between the eating disorder patients and normal controls in this study were due to a sampling bias, and that in fact, the normal controls were drawn from a “brighter” population. This seems unlikely in that all groups came from a largely middle-to-upper-middle class population and were matched overall for educational level. While we could have matched subject groups in advance on a measure such as vocabulary score in an attempt to control for premorbid ability levels, vocabulary knowledge is known to be significantly related to many of the measures which were under examination in the current study. Moreover, Goldberg, Halmi and their colleagues have found an increased incidence of complications in pregnancy and delivery (i.e., historical evidence suggestive of perinatal brain injury) in subjects who later developed anorexia nervosa and a positive correlation between the number of such complications and severity of prognosis in these patients (Goldberg et al., 1977; Halmi et al., 1977). This finding argues for very early differences between subjects with eating disorders and normal controls; therefore, in matching groups on vocabulary score, we would have been biasing the outcome in the direction of nonsignificant findings by selecting a nonrepresentative (i.e., unusually high functioning) group of eating disorder patients. The underweight anorexics showed more cognitive difficulties than the normal-weight bulimics; they scored lower than the normal controls in four of five neuropsychological domains. Their lower verbal scores (Figure 3) suggests that this is a more compromised group, from a neuropsychological standpoint. Fox (1981) reported a similar finding: anorexic patients scored significantly lower on WAIS Information than a mixed group of psychiatric control patients. The longterm weight-restored anorexics may be somewhat atypical of anorexics in that they were able to restore their weight and maintain it over a long period of time (M= 47.1 mo). Recent outcome studies have found that in the intermediate term (4-12 years after evaluation), between one-half and two-thirds of treated anorexics have regained normal weight, but the crude mortality rate at 20-year follow-up may be as high as 15 to 20% (Hsu, 1990). An important question concerns whether starvation itself leads to neuropsychological impairment. For a number of reasons, some more obvious than others, there is relatively little relevant literature. Many would regard the experimental imposition of starvation on research subjects as ethically unacceptable, while study of the neuropsychological consequences of starvation in countries where famine is endemic raises, in addition to ethical questions, questions about the generalizability of the results because of cross-cultural differences and confounding factors such as war, dislocation, and other concomitant and profound stressors. Studying subjects on diets is unsatisfactory in that if the weight loss is not commensurate with that in anorexia, one has no adequate control group; on the other hand, if the weight loss is commensurate, the dieting subjects may in fact be anorexic. However, the literature contains one landmark study which is germane to the
Downloaded by [UQ Library] at 08:25 11 November 2014
724
BARBARA PENDLETON JONES ET AL.
effects of starvation on cognitive functioning. In 1944, in response to the need to evaluate and treat millions of starvation victims in the aftermath of World War 11, an experimental study of starvation was carried out at the University of Minnesota (Keys, Brozek, Henschel, Mickelsen, & Taylor, 1950) in which 32 conscientious objectors and other volunteers underwent 24 weeks of semi-starvation in order to increase scientific knowledge concerning the effects of starvation and methods of refeeding. Among the measures employed to study the psychological effects of starvation were the following: the MMPI (these findings will be reviewed in a separate paper); six timed tests assessing perception of spatial relations, word fluency, memory, number facility, inductive reasoning, and perceptual speed; and four untimed tests assessing sentence completion, arithmetic, vocabulary, and directions. This study differed from our study in a number of ways apart from the issue of anorexia versus experimental starvation: these subjects were all men; subjects with any signs or symptoms of psychiatric abnormality were excluded; and subjects were used as their own controls. The subjects in the starvation study were above average in intellectual ability; all premorbid Army Classification Test scores were at or above the 85th percentile, whereas in the present study, the mean Full Scale IQ scores of the groups ranged from about the 60th percentile for underweight anorexics to the 85th percentile for normal controls. No significant changes were found on any of the timed tests after 24 weeks of semi-starvation; small but significant decrements were seen on arithmetic and directions, and a small but significant improvement was seen on the vocabulary measure. The experimenters concluded that “the measured intellective performances did not change importantly in either starvation or rehabilitation” (p. 863). Our eating disorder subjects arguably showed more in the way of subtle cognitive dysfunction than the starvation subjects in that one or more groups differed from the normal controls in four of five neuropsychological domains. The question arises as to whether the decline on measures of arithmetic and directions in the starvation subjects was due to impaired attention; reduced attentional capacities were reflected in our two acute eating disorder groups but not in the weight-restored anorexics3. Thus, attention may be adversely affected by the transitory metabolic and other changes accompanying severe weight loss and/or repeated bingeing, vomiting, and laxative abuse. The two MANCOVAs performed in order to reveal the relationships between depressive symptoms, anxiety, and cognitive performance indicated that there is a significant correspondence between anxiety as measured by the T S W scale of the MMPI and performance on the neuropsychological measures, but not between depression and neuropsychological performance. This pattern of findings __
In the present study underweight anorexics and normal-weight bulimics scored lower on WAIS-R Arithmetic than did normal controls (F[3, 1231= 6.07,p c 0.0007). In our laboratory’s more detailed studies of the elements of attention, WAIS-R Arithmetic has been found to load on the encode factor of attention (Mirsky, 1989).
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
725
is in precise agreement with those of Halmi et al. (1977). Other studies have also found a high incidence of symptoms of anxiety in patients with eating disorders (e.g., Smart, Beumont, & George, 1976; Theander, 1970). It could be argued that the observed decrements in test performance are not subtle neuropsychological deficits but rather reflect simply the effects of anxiety. However, an equally valid interpretation is that both anxiety and subtle neuropsychological deficits are features of eating disorders. With regard to the hypothesis of differential right-hemisphere dysfunction in eating disorders, we note that the underweight anorexics scored lower than normal controls in the verbal and memory domains as well as in the visuospatial domain. Further, the normal-weight bulimics did not differ from the normal controls in the visuospatial domain. Although we have as yet to demonstrate the lateralizing capability of the verbal and visuospatial domain scores used in the current study, the greater sensitivity of the WAIS-R Vocabulary, Similarities, and Comprehension scores to left- as opposed to right-hemisphere dysfunction is well known (Lezak, 1983; McFie, 1975; Parsons, Vega, & Burn, 1969). While the three measures in the visuospatial domain are generally sensitive to large lesions in either hemisphere, the greater disruption of Rey-Osterrieth (Bachtler, Roth, Smith, & Weber, 1990; Binder, 1982) and Block Design (Lezak, 1983; McFie, 1975) performances with right- as opposed to left-hemisphere dysfunction has been demonstrated. As for the third component of the visuospatial domain score, the Embedded Figures Test, Russo and Vignolo (1967) showed that right-hemisphere lesion patients were inferior to left-hemisphere lesion patients without aphasia on the Gottschaldt figures (later published as the Embedded Figures). Thus, the present findings do not appear to lend support to the hypothesis of differential right-hemisphere dysfunction in eating disorders. As in previous studies (Hamsher et al., 1981; Small et al., 1983), we saw some (subtle) diminution of attentional capacities in underweight anorexics. It should be noted that in terms of Mirsky’s (1989) conceptualization of the elements of attention, this diminution was seen on the focusing/execution measures of attention and not on the vigilance (CPT) measures. In addition, since lower scores in the focusing/ execution domain were seen also in the normal-weight bulimics but not in the weight-restored anorexics, it seems likely that impaired attention is related to metabolic and other changes accompanying severe weight loss and/or bingeing, vomiting, and laxative abuse. Alternatively, the diminished attentional capacities of the underweight anorexics and normal-weight bulimics are consistent with the hypothesis that at least some of these patients have a central nervous system disorder which can compromise their capacity for recovery; Small et al. (1981) found that anorexics’ scores on WAIS Arithmetic and Digit Span accounted for half of the variance in multiple regression analyses for subsequent weight gain, and Hamsher et al. (1986) found that evidence of cognitive impairment, particularly longer reaction times, was associated with inadequate weight gain or maintenance on one-year follow-up.
726
BARBARA PENDLETON JONES ET AL.
Downloaded by [UQ Library] at 08:25 11 November 2014
REFERENCES American Psychiatric Association. (1 980). Diagnostic and statistical manual of mental disorders (3rd ed.). Washington, DC: Author. Bachtler, S.D..Roth. D.L., Smith, G.E.. & Weber, A.M. (1990).Qualitative performance of the Rey-Osterrieth Complex Figure in patients with complex partial seizures. Journal of Clinical and Experimental Neuropsychology, 12.75 (Abstract). Binder, L.M. (1982).Constructional strategies on complex figure drawings after unilateral brain damage. Journal of Clinical Neuropsychology, 4.5 1-58. Bruch. H. (1970).Psychotherapy in primary anorexia nervosa. Journal of Nervous and Mental Disease, 150.51-67. Buffery, A.W.H., & Gray, J.A. (1972).Sex differences in the development of spatial and linguistic skills. In C. Ounsted & D.C. Taylor (Eds.), Gender diflerences: Their ontology and significance (pp. 123-157).Baltimore: Williams & Wilkins. Buschke, H., & Fuld, P. A. (1974).Evaluating storage, retention, and retrieval in disordered memory and learning. Neurology, 24,1019-1025. Carlin, A.S. (1986).Neuropsychological consequences of drug abuse. In I. Grant & K.M. Adams (Eds.), Neuropsychological assessment of neuropsychiatric disorders (pp. 478497). New York: Oxford University Press. Duncan, C.C., Kaye, W.H., Perlstein, W.M., Jimerson, D.C.. & Mirsky. A.F. (1985). Cognitive processing in eating disorders: An ERP analysis. Psychophysiology, 22,588. Enzmann. D.R.. & Lane, B.L. (1977).Cranial computed tomography findings in anorexia nervosa. Journal of Computer Assisted Tomography, I , 410-414. Fox, C.F. (1 981). Neuropsychologicalcorrelates of anorexia nervosa. International Journal of Psychiatry in Medicine, 11,285-290. Gold, P.W., Kaye, W., Robertson, G.L.,& Ebert, M. (1983).Abnormalities in plasma and cerebrospinal-fluid arginine vasopressin in patients with anorexia nervosa. New England Journal of Medicine, 308, 1 117-1123. Goldberg, E.(Unpublished). Semantic aphasia test. Goldberg, S.C.. Halmi, K.A., Casper, R.. Eckert. E., &,Davis, J.M. (1977). Pretreatment predictors of weight change in anorexia nervosa. In R.A. Vigersky (Ed.), Anorexia nervosa (pp. 31-41).New York Raven Press. Goodwin, R.. & Andersen, A.E. (1984). The MMPI in three groups of patients with significant weight loss. Hillside Hospital Journal of Clinical Psychiatry, 6. 188-203. Grant, I., & Adams, K.M. (Eds.) (1986).Neuropsychological assessment of neuropsychiatric disorders. New York: Oxford University Press. Halmi, K.A. (1974). Anorexia nervosa: Demographic and clinical features in 94 cases. Psychosomatic Medicine. 36,18-26. Halmi, K.A. Dekirmenjian, H., Davis, J.N., Casper, R., & Goldberg, S.C. (1978). Catecholaminemetabolism in anorexia nervosa. Archivesof General Psychiatry, 35,458460. Halmi, K.A.. Goldberg, S.C., Eckert, E., Casper,R., & Davis. J. M.(1977).Pretreatment evaluation in anorexia nervosa. In R.A. Vigersky (Ed.), Anorexia nervosa (pp. 43-54). New York: Raven Press. Hamsher, K. de S., Halmi, K.A., & Benton, A.L. (1981).Prediction of outcome in anorexia nervosa from neuropsychological status. Psychiatry Research. 4.79-88. Heaton, R.K., & Crowley, T.J.(1981).Effects of psychiatric disordexs and their somatic treatments on neuropsychological test results. In S.B. Filskov & T.J. Boll (Eds.), Handbook of clinical neuropsychology (pp. 481-525).New York: Wiley Interscience. Heidrich, R., & Schmidt-Matthias, H. (1961).Encephalographische Befunde bei Anorexia nervosa. Archiv fur Psychiatrie und Nervenkrankheiten, 202,183-201. Heinz. E.R., Martinez, J., & Haenggeli, A. (1977).Reversibility of cerebral atrophy in
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
727
anorexia nervosa and Cushing's syndrome. Journal of Computer Assisted Tomography, I, 415- 418. Heaog, D.B. (1984). Are anorexic and bulimic patients depressed? American Journal of Psychiatry, 141,1594-1597. Hsu, L.K.G. (1990). The eating disorders. New York: Guilford. Hudson, J.I., Pope, H.G., Jr., Jonas, J.M., & Yurgelen-Todd, D. (1983). Phenomenologic relationship of eating disorders to major affective disorder. Psychiatry Research, 9,345354. Johnson, C. (1985). The initial consultation for patients with bulimia and anorexia nervosa. In D.M. Gamer & P.E. Garfinkel (Eds.), Handbook of psychotherapy for anorexia nervosa and bulimia (pp. 19-51). New York: Guilford Press. Jones, B.P., Duncan, C.C., Mirsky, A.F., & Brouwers, P. (1988). Unpublished data. Kaye, W.H., Ebert, M.H., Raleigh, M., & Lake, C.R. (1984). Abnormalities in CNS monoamine metabolism in anorexia nervosa. Archives of General Psychiatry, 41,350355. Kaye, W.H., Jimerson. D.C., Lake, C.R., & Ebert, M.H. (1985). Altered norepinephrine metabolism following long-term weight recovery in patients with anorexia nervosa. Psychiatry Research, 14,333-342. Keys, A., Brozek, J., Henschel, A., Mickelsen, O., & Taylor, H.L. (1950). The biology of human starvation. Minneapolis: University of Minnesota Press. Levitt, E.E. (1989). The clinical application of MMPI special scales. Hillsdale, NJ: Erlbaum. Lezak, M.D. (1983). Neuropsychological assessment (2nd ed.). New York: Oxford. Maccoby, E.E.. & Jacklin, C.N. (1974). The psychology of sex differences. Stanford, CA: Stanford University Press. Maxwell, J.K., Tucker, D.M.. & Townes, B.D. (1984). Asymmetric cognitive function in anorexia nervosa. International Journal of Neuroscience, 24, 37-44. McFie, J. (1975). Assemnent of organic impairment. London: Academic Press. McKay, S.E.,Humphries, L.L.. Allen, M.E., & Clawson, D.R. (1986). Neuropsychological test performance of bulimic patients. International Journal of Neuroscience, 30,7380. Minuchin, S., Rosman, B.L., & Baker, L. (1978). Psychosomatic families: Anorexia nervosa in context. Boston: Harvard University Press. Mirsky, A.F. (1989). The neuropsychology of attention: Elements of a complex behavior. In E. Perecman (Ed.), Integrating theory andpractice in clinical neuropsychology (pp. 75-91). Hillsdale, NJ: Erlbaum. Parsons, O.A., Vega, A. Jr., & Bum, J. (1969). Differential psychological effects of lateralized brain damage. Journal of Consulting and Clinical Psychology, 33,551-557. Piran, N., Kennedy, W., Garfinkel, P.E., & Owens, M. (1985). Affective disturbance in eating disorders. Journal of Nervous and Mental Disease, 173,395-400. Rao, C.R. (1973). Linear statistical inference and its applications (2nd ed.). New York: Wiley. Rosvold,H.E.,Mirsky,A.F.,Sarason,I., Bransome,E.D.,& Beck,L.H. (1956). Acontinuous performance test of brain damage. Journal of Consulting Psychology, 20,343-350. Russo, M., & Vignolo, L.A. (1967). Visual figure-ground discrimination in patients with unilateral cerebral disease. Cortex, 3, 118-127. Sein, P., Searson, S . , Nicol, A.R., & Hall, K. (1981). Anorexia nervosa and pseudoatrophy of the brain. British Journal of Psychiatry, 139, 257-258. Shelly, C., & Goldstein, G. (1982). Psychometric relations between the LurkNebraska and Halstead-Reitan Neuropsychological Test Batteries in a neuropsychiatric setting. Clinical Neuropsychologist, IV (3), 128-133. Siegert, R.J., Patten, M.D., Taylor, A.J.W., & McCormick, LA. (1988). Factor analysis of the WAIS-R using the factor replication procedure, FACTOREP. Multivariate Behavioral Research, 23,481-489.
728
BARBARA PENDLETON JONES ET AL.
Small, A.. Madero. J.. Teagno, L.. & Eben. M.(1983). Intellect, perceptual characteristics, and weight gain in anorexia nervosa. Journal of Clinical Psychology, 39,780-782. Smart, D.E., Beumont, P.J.V.. &George, G.C.W. (1976). Some personality characteristics of patients with anorexia nervosa. British Journal of Psychiatry, 128. 57-60. Spitzer, R.L., Endicott. J., & Robins. E.(1978). Research Diagnostic Criteria: Rationale and reliability. Archives of General Psychiatry, 35,773-782. Stein, K.B.(1968). The TSC Scales: The outcome of a cluster analysis of the 550 MMPI items. In P. McReynolds (Ed.), Advances in psychological assessment (Vol. I ) (pp. 80104). Palo Alto, CA: Science and Behavior Books. Talland, G.A.. & Schwab. R.S. (1964). Performance with multiple sets in Parkinson’s disease. Newopsychologia, 2.45-53. Theander, S . (1970). Anorexia nervosa. Acta Psychiatrica Scandinavica, 214, (Suppl.): 1-
Downloaded by [UQ Library] at 08:25 11 November 2014
194.
Tryon, R.C. (1966). Unrestricted cluster and factor analysis, with applications to the MMPI and Holzinger-Harman problems. Multivariate Behavioral Research, 1,229-244. Witt, E.D., Ryan, C., & Hsu. L.K.G.(1985). Learning deficits in adolescents with anorexia nervosa. Journal of Nervous and Mental Disease, 173. 182-184.
Journal of Clinical and Experimental Neuropsychology Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/ncen19
Cognition in eating disorders a
a
Barbara Pendleton Jones , Connie C. Duncan , Pim a
Brouwers & Allan F. Mirsky
a
a
Laboratory of Psychology and Psychopathology, National Institute of Mental Health , Published online: 04 Jan 2008.
To cite this article: Barbara Pendleton Jones , Connie C. Duncan , Pim Brouwers & Allan F. Mirsky (1991) Cognition in eating disorders, Journal of Clinical and Experimental Neuropsychology, 13:5, 711-728, DOI: 10.1080/01688639108401085 To link to this article: http://dx.doi.org/10.1080/01688639108401085
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sublicensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
Journal of Clinical and Experimental Neuropsychology 1991, VOI. 13. NO. 5, pp. 71 1-728
0 168-8634D 1/1305-07 11$3.00 Q Swets & Zeitlinger
Cognition in Eating Disorders* Barbara Pendleton Jones, Connie C. Duncan, P i m Brouwers, and Allan F. Mirsky Laboratory of Psychology and Psychopathology, National Institute of Mental Health
Downloaded by [UQ Library] at 08:25 11 November 2014
ABSTRACT Cognitive functions were investigated in four groups of women: 30 underweight anorexics, 38 normal-weight bulimics, 20 long-term weight-restored anorexics, and 39 normal controls. A MANOVA was used to examine performance on five neuropsychological domains derived from prior principal components analyses of a comprehensive neuropsychological battery. Underweight anorexics performed more poorly than normal controls in four of five neuropsychological domains (focusing/execution, verbal, memory, and visuospatial), while normal-weight bulimics showed poorer performances only in focusing/execution. The absolute differences in scores between eating disorder groups and normal controls were for the most part small, suggesting subtle rather than frank cognitive difficulties. Poorer neuropsychological test performance was associated with anxiety but not depression as measured by the Tryon, Stein, and Chu Tension scale and scale 2 of the MMPI respectively. The findings support previous reports of attentional difficulties in eating disorders but do not support the hypothesis of differential right-hemisphere dysfunction in eating disorders.
Until relatively recently, etiological discussions of the eating disorders, anorexia
nervosa and bulimia, have centered on family interaction patterns and intrapsychic phenomena (e.g., Bruch, 1970; Minuchin, Rosman, & Baker, 1978). S i n c e the late 1970s, however, reports h a v e appeared suggesting central nervous system dysfunction in association with eating disorders. Goldberg, Halmi, and their colleagues (Goldberg, Halmi, Casper, Eckert, & Davis, 1977; Halmi, Goldberg, Eckert, Casper, & Davis, 1977) have reported an increased incidence of compli-
* The authors wish to thank Drs. David Jimerson, Walter Kaye, Arlene Hegg, and Timothy Brewerton for their cooperation in referring subjects and Mrs. Marie Elliott, Ms. Kathleen Squillace, Mr. Gene Tassone, and Mrs. Audrey Weinberg for assistance in data collection and analysis. We also wish to extend special thanks to Dr. John Bartko for assistance with issues of statistical analysis. Address reprint requests to Dr. B.P. Jones, Laboratory of Psychology and Psychopathology, National Tnstitute of Mental Health, 9000 Rockville Pike, Building 10, Room 4C110, Bethesda, MD 20892, USA. Dr. Brouwers is currently with the National Cancer Institute, Bethesda, MD. Accepted for publication: December 17, 1990.
Downloaded by [UQ Library] at 08:25 11 November 2014
712
BARBARA PENDLETON JONES ET AL.
cations in pregnancy and delivery (Le., historical evidence suggestive of perinatal brain injury) in subjects who later developed anorexia nervosa and a positive correlation between the number of such complications and severity of prognosis in these patients. In a series of 94 cases, Halmi (1974) found a significantly greater maternal and paternal age at time of the anorexic patient’s birth and a greater incidence of both low and high birth weights compared with the general population. In addition, there is evidence for a genetic factor in anorexia nervosa: Hsu (1990) has recently reviewed the available twin studies and found that in the studies with established zygosity and explicit diagnostic criteria, of 28 monozygotic twin pairs with at least one anorexic twin, 50% were concordant for anorexia nervosa, while for 14 dizygotic twin pairs, the concordance rate was 7%. In addition, investigators have reported abnormal findings in eating disorder patients in computerized tomographic (CT) brain scan (Enzmann & Lane, 1977; Heidrich & Schmidt-Matthias, 1961; Heinz, Martinez, & Haenggeli, 1977), brain event-related potential (Duncan, Kaye, Perlstein, Jimerson, & Mirsky, 1985), neurotransmitter (Halmi, Dekirmenjian, Davis, Casper, & Goldberg. 1978; Kaye, Ebert, Raleigh, & Lake, 1984), and neuropeptide (Gold, Kaye, Robertson, & Ebert, 1983) studies. While the cerebral atrophy seen in underweight anorexics may be related to protein loss and/or fluid retention and has been found to be reversible in at least some cases (Heinz et al., 1977; Sein, Searson, Nicol, & Hall, 1981), the abnormalities in norepinephrine (NE) metabolism appear to be stateindependent (Kaye, Jimerson, Lake, & Ebert, 1985) and may contribute to the characteristic changes in mood, behavior, and neuroendocrine function in eating disorders. Prior neuropsychological studies of patients with eating disorders have for the most part been interpreted as showing right-hemisphere dysfunction and/or attentional deficits, but a number of these studies have contained serious methodological flaws. Fox (1981) found relative impairment in 15 anorexic patients (compared to a mixed group of psychiatric controls) on WAIS-R Information and Wide Range Achievement test arithmetic scores; on the basis of the anorexics’ impaired performance on arithmetic and the Benton Visual Retention Test, she speculated about right-hemisphere dysfunction in anorexia. However, her mixed psychiatric control group included subjects with a variety of diagnoses, including conduct disorder, hyperkinesis, and schizophrenia; and its gender distribution (8 females, 7 males) differed markedly from the anorexic group (14 females, 1 male). In the light of what is known about sex differences in arithmetic and visuospatial skills (Buffery & Gray, 1972; Lezak, 1983; Maccoby & Jacklin, 1974), the latter problem alone raises questions about her conclusions. Maxwell, Tucker, and Townes (1984) reported relative deficiencies in spatial cognition in three anorexic patients; however, given the inadequate n, the fact that one subject was not at a low weight at the time of testing, and the fact that the other two were atypical in age of onset (30 and 69), it would seem impossible to draw any conclusions about anorexia nervosa from this study. McKay, Humphries, Allen, and Clawson (1986) compared 30 bulimic patients to 30 normal controls on the
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
713
Luria Nebraska Neuropsychological Battery and reported that the bulimics were impaired on tasks vulnerable to right frontal lobe dysfunction, primarily speed of drawing geometric figures. While all of these groups of researchers concluded that there may be righthemisphere dysfunction in eating disorders, Hamsher, Halmi, and Benton (1981) emphasized attentional deficits in their group of 20 anorexic patients. Studies have shown an association between scores on reaction-time tasks (Hamsher et al., 1981) or other attentional tasks (WAIS Arithmetic and Digit Span; Small, Madero, Teagno, & Ebert, 1983) and subsequent weight gain and/or maintenance. Witt, Ryan, and Hsu (1985) emphasized learning deficits on the Symbol-Digit Learning Test in their anorexic patients; but as their assessment of attention was limited to the WAIS-R (or WISC-R) Digit Span, it is possible that the learning impairment was secondary to an attentional deficit not revealed by Digit Span performance. Based on the foregoing observations, the present study was designed to address the following questions: (1) Do patients with eating disorders show deficits in attention, concentration, and vigilance? (2) Are patients with eating disorders impaired in other cognitive functions, particularly in functions implicating the right hemisphere? (3) What are the relationships between cognitive performance and depression and anxiety in patients with eating disorders?
METHODS Subjects
There were four groups of women: underweight anorexics, normal-weight bulimics, longterm weight-restored anorexics (hereafter referred to as weight-restored anorexics), and normal controls. Groups were matched overall for age, education, and handedness; all of the subjects were white. All eating disorder patients were inpatients or outpatients of clinical research units of the National Institutes of Health Clinical Center, National Institute of Mental Health, and all met (or, in the case of the weight-restored anorexics, had previously met) established criteria (Diagnostic and Statistical Manual of Mental Disorders, [3rd ed., DSM-1111)for anorexia nervosa or for normal-weight bulimia (American Psychiatric Association, 1980). Prior to admission, each hospitalized underweight anorexic patient had maintained a body weight of less than 75% of her ideal body weight (according to the Metropolitan Life Insurance Company tables) for a periodof at least 6 months (M = 27.8 mo, SD = 9.4). Patients who had medical problems or were underweight to a degree requiring immediate medical intervention were not admitted to the study. Patients who had electrolyte abnormalities secondary to vomiting or laxative abuse were first rehydrated so that electrolyte values were within normal limits. Underweight anorexics were then maintained at a stable weight (k 1.O kg) on a nutritionally balanced diet for at least one month before neuropsychological testing. The weight-restored anorexics were a separate group of anorexic patients who had been weight-restored for at least 6 months prior to the study ( M = 47.1 mo, SD = 3 1.6). Potential eating disorder subjects were excluded if they had a history of learning disabilities. Two of 30 underweight anorexics and 2 of 38 normal-weight bulimics had histories of substance abuse; with the exception of solvents and sedative-hypnotics (which were not abused by these four patients), drug abuse has not been shown to be linked with substan-
714
BARBARA PENDLETON JONES ET AL.
Table 1. Characteristics of Subject Groups.
N
Age
Education
Underweight anorexics
30
Normal-weight bulimics
38
Weight-restored anorexics
20
Normal controls
39
24.4 5.3 24.1 4.0 26.0 6.2 24.9 4.4
14.0 2.2 14.6 1.6 15.1 2.3 15.0 1.6
Subject group
Downloaded by [UQ Library] at 08:25 11 November 2014
a
Weight (kg) 33.8 4.4 55.2 5.6 51.3 6.1 57.8 6.3
%IBW~ 59.4 6.6 94.0 7.3 87.8 11.2 98.2 7.5
Means above, standard deviations below. 8 Ideal body weight, according to the Metropolitan Life Insurance Company tables.
tial neuropsychological dysfunction (for a review, see Carlin, 1986). The normal controls were subjects recruited by newspaper advertisements or from among National Institutes of Health employees and were screened with the use of the Schedule for Affective Disorders and Schizophrenia-Lifetime Version (SADS-L; Spitzer, Endicott, & Robins, 1978) and sections of the Diagnostic Survey for Eating Disorders (DSED; Johnson, 1985); potential controls who received any diagnosis on the SADS-L or who had any symptoms of an eating disorder on the DSED were excluded. All subjects had given informed consent for the study. Normal controls had no physical illness, no personal or family history (fmtdegree relatives) of psychiatric disorder, and no history of learning disabilities. All subjects had been free of medication for at least 4 weeks prior to testing. We did not follow the common practice of using psychiatric patients as controls because it has been firmly established that there is cognitive dysfunction associated with a number of psychiatric syndromes (e.g., Grant & Adams, 1986; Heaton & Crowley, 1981). In order to determine whether our eating disorder patients were cognitively impaired, we considered it essential to compare them with a group of normal women. The question of how patients with eating disorders might differ in their patterns of cognitive dysfunction from patients with other neuropsychiatric syndromes is a separate question, one that we hope to address in future studies. The notion that changes in the neuropsychological functioning of eating disorder patients might be “due to depression,” that one can partial out the amount of change “due to depression” by using a depressed control group, and that can one can conclude that the remaining variance is “due to the eating disorder” reflects a fundamental misconception about eating disorders.’ Depressive symptoms are a part of the eating disorder itself (Goodwin & Andersen, 1984; Halmi et al., 1977; Heaog, 1984; Hudson, Pope, Jonas, & Yurgelen-Todd. 1983; Piran. Kennedy, Garfiiel. & Owens, 1985); regression analysis provides a logical means of examining the correspondence between depressive symptomatology and cognitive dysfunction in eating disorders. Table 1 presents summary data for the subjects in this study. There were no significant differences in age or level of education among the four groups.
-By analogy, one might reason that in studies of patients with Alzheimer’s disease, since many of these patients have frontal lobe atrophy, and since frontal lobe atrophy affects neuropsychological functioning, a neuropsychological study of Alzheimer’s disease must include a control group of patients with frontal lobe lesions.
715
COGNITION IN EATING DISORDERS
Table 2. Other Lifetime Psychiatric Diagnoses in Eating Disorder Patients’
Major depression Bipolar disorder Hypomanic episodes Dysthymia, minor depression, atypical depression, secondary depression Substance abuse None ~
Downloaded by [UQ Library] at 08:25 11 November 2014
a
UA
NB
WA
47 3 0
26 3 0
50 10 5
7 7 13
39
20
5 11
20
5
~
Percentages. UA = underweight anorexics (n = 30); NB = normal-weight bulimics ( n = 38); WA = weight-restored anorexics (n = 20).
Table 2 presents data about other psychiatric diagnoses (present or past) received by the eating disorder patients; these were diagnoses noted either in the SADS-L report or in the patient’s medical record.
Neuropsychological Measures Table 3 presents a listing of the neuropsychological measures employed in the study. The battery was selected to address the particular questions concerning attention and righthemisphere functioning in this study, but in addition to assess a broad range of cognitive functions. The majority of the tests are described in Lezak (1983). Tests not included in Lezak are described as follows: Eioptor Vision Test. This is a standardized test of visual acuity.
Buschke Selective Reminding Test (Buschke & Fuld, 1974). The subject recalls as many words as he/she can from a 12-noun list immediately after it has been read to him/her; after each trial, the examiner repeats any list words omitted by the subject. Trials, followed by selective reminding, continue until the subject recalls the whole list twice consecutively or until 8 trials have been completed. Continuous Performance Test (Rosvold, Mirsky, Sarason, Bransome, & Beck, 1956). This is a visual vigilance task in which the subject is required to press a response key only to certain target letters; X is the target letter in the “X” task, and X following A is the target letter in the “AX” task. Letters appear on a display screen at 1-s intervals with a stimulus duration of 0.2 s; targets are 25% of the stimuli in the X taqk and 20% of the stimuli in the A X task. Talland Letter Cancellation Test-Revised. This is identical to the test described by Talland and Schwab (1964), except that in Test B, subjects cross out all letters preceding or following double spaces. Semantic Aphasia Test. In this test devised by Goldberg (personal communication) along the lines of Luria’s investigation of semantic aphasia, the subject has first to draw a series of pairs of items (e.g., “Draw a triangle below a square”) and then to answer a series of questions in the following categories: quasi-spatial, temporal, height, and kinship (e.g., “Mike was hit by Steve. Who got hurt?”). Tirmus SKereO Tesrs. These are simple tests of stereoscopic vision.
716
BARBARA PENDLETON JONES ET AL.
Table 3. Eating Disorders Study Neuropsychological Test Battery. Function
Test
Executive Sequencing, Attention Attention (Focus, Execute)
Trail Making Test Stroop Color-Word Interference Test Talland Letter Cancellation Test-Revised Concept Formation (Capacity to Shift) Wisconsin Card Sorting Test Abstraction Category Test (Halstead)
Downloaded by [UQ Library] at 08:25 11 November 2014
General Intelligence Language Initiation Written Comprehension
Wechsler Adult Intelligence Scale-Revised (WAIS-R) Controlled Oral Word Association Test Boston Diagnostic Aphasia Examination - Narrative Writing Token Test (Spreen & Benton version, 1969)
Semantic Aphasia Test (Goldberg) Memory Global Recent Verbal Recent and Remote Verbal Recent Visuospatial Recent and Remote Visuospatial
Wechsler Memory Scale (WMS) Buschke Selective Reminding Test Rey Auditory Verbal Learning Test Babcock Story Recall Test Recurring Figures Test (Kimura) Complex Figure Test (Rey-Osterrieth; Taylor)
Motor Functions
Purdue Pegboard Test Boston Diagnostic Aphasia ExaminationApraxia Test
Personality
Minnesota Multiphasic Personality Inventory (MMPI)
Sensory and Perceptual
Bioptor Vision Test Dvorine Pseudo-isochromatic Plates Titmus Stereo Test Harris Test of Hand Dominance Eye Dominance Test
Vigilance (Sustained Attention)
Continuous Performance Test
Visuospatial
Butters’ Embedded Figures Test Embedded Figures Test (Witkin) Hooper Visual Organization Test Raven Standard Progressive Matrices
COGNITION IN EATING DISORDERS
717
Table 4. Domains of Neuropsychological Functioning. Domain
Measures
Vigilance
CPT mean % hits, X and AX tasks' CPT mean % commission errors, X and AX tasksb CPT mean reaction time, X and AX tasks WAIS-R Digit Symbol, scaled score Trail Making Test, A time + B time correct I Talland Letter Cancellation Test-Revised, mean # WAIS-R Similarities, scaled score WAIS-R Comprehension, scaled score WAIS-R Vocabulary, scaled score Babcock Story Recall Test, immediate recall score Wechsler Memory Scale, Logical Memory score Buschke Selective Reminding Test, recall score Rey-Osterrieth Complex Figure, delayed recall score Embedded Figures Test, time WAIS-R Block Design, scaled score
Focus/execute Verbal
Downloaded by [UQ Library] at 08:25 11 November 2014
Memory Visuospatial
a
Hits are defined as responses to target stimuli occurring within 700 ms. Commission errors are responses to nontarget stimuli.
Statistical Analyses In order to reduce the number of variables from the rather large neuropsychological battery employed in this study, we relied upon prior principal components analyses of neuropsychological measures in use in the Laboratory of Psychology and Psychopathology (LPP; Jones, Duncan, Mirsky, & Brouwers, 1988; Mirsky, 1989). These analyses have yielded five readily identifiable components or factors: two attention factors (vigilance and focusing/execution), a verbal factor, a mixed memory/comprehension factor, and a visuospatial factor. The two attention factors (vigilance and focusing/execution) appear to be in essence the same as the vigilance and focusing/execution factors which have been found in a number of factor analyses of attentional measures in this laboratory (Mirsky, 1989); attention factors are likely to be more prominent in our battery than in most others because of our inclusion of more attentional measures than in other batteries. Verbal and nonverbal (here termed visuospatial) factors have consistently emerged in factor analytic studies of neuropsychological batteries (e.g., Shelly & Goldstein, 1982) and of the WAIS subtests (for a review, see Lezak, 1983; see also Siegert, Patten, Taylor, & McCormick, 1988). From 29 variables submitted to the principal components analysis, we chose the 15 variables which had the highest loadings for the five factors (i.e,, the three highestloading measures for each of the five factors).2 Table 4 presents the five neuropsychological domains and their component measures. A subsequent principal components analysis using these 15 measures for the present study population yielded the same five factors and accounted for 73% of the variance: vigilance (17.1%). focusinglexecution (14.6%), verbal (14.5%). memory (13.7%), and visuospatial(13.1%). The one exception was the choice of the fifth-highest measure (Buschke Selective Reminding Test, loading 0.52) for the memory/comprehension factor rather than the third- (WAIS-R Picture Arrangement, loading 0.58) or fourth-highest measure (Token Test, loading 0.56); this yielded a composite score of more conceptual unity for the present study. This factor is hereafter referred to as a memory factor.
718
BARBARA PENDLETON JONES ET AL.
Downloaded by [UQ Library] at 08:25 11 November 2014
Rather than analyzing factor scores based on the five factors, each of which contains loadings from all 15 measures, we chose to look at composite scores for each of the five neuropsychological domains which had been identified (Table 3). Scores for each subject on all 15 measures were transformed into z scores; for each neuropsychological domain, the three z scores were averaged to yield a domain score. A multivariate analysis of variance (MANOVA) was then carried out on the domain scores. Posthoc testing was accomplished with the use of Newman-Keuls tests. Finally, in order to assess the Idationship between cognitive performance in eating disorders and symptoms of depression and anxiety, we performed two multivariate analyses of covariance (MANCOVAs) using Minnesota Multiphasic Personality Inventory (MMPI) scores on scale 2 (Depression) and on the Tryon, Stein, and Chu Tension scale (TSC/T; Stein, 1968; Tryon, 1966) as covariates. The TSC/T is thought to be the best available MMPI scale for the measurement of anxiety (Levitt, 1989).
RESULTS The MANOVA yielded a significant F(15, 328.91) = 2.43, p < 0.0023 (Wilks’ criterion [see Rao, 1973, p. 5551). There were significant group differences in four of the five neuropsychological domains. The vigilance domain yielded no group differences [F(3, 123) = 1.45, p < 0.23; Figure 11. In the focusing/execu-
0.2
2
0.0
sf
-cm g
-0.2
n
-0.6
UA
0
P a
WA .
Nc
4
Groupr
Fig. 1. Vigilance domain scores. UA = underweight anorexics; NB = normal-weight bulimics; WA = weight-restored anorexics; NC = normal controls.
~
719
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
-"."
. UA
NB
WA
Nc
Groups
Fig. 2. Focusing/execution domain scores. UA = underweight anorexics; NB = normalweight bulimics; WA = weight-restoredanorexics; NC = normal controls.
?!
0
0 u)
.-Cm
E
0
-"."
. UA
NB
WA
rn
Groups
Fig. 3. Verbal domain scores. UA =underweight anorexics;NB = normal-weightbulimics; WA = weight-restored anorexics; NC = normal controls.
720
BARBARA PENDLETON JONES ET AL. 0.4 I
0.2
0.0
Downloaded by [UQ Library] at 08:25 11 November 2014
-0.2
-0 -0.6
UA
WA
N3
Nc
Groups
Fig. 4. Memory domain scores. UA =underweightanorexics; NB = normal-weight b u l i c s ; WA = weight-restoredanorexics; NC = normal controls.
tion domain [F(3, 123) = 5.84, p c .0009], the two acute eating disorders groups (i.e., underweight anorexics and normal-weight bulimics) performed more poorly than normal controls (Figure 2). In the verbal domain [F(3,123) = 5 . 0 9 , c ~ .0024], the underweight anorexics scored lower than all other groups (Figure 3); in the memory domain [F(3, 123) = 4.40, p < .006] and in the visuospatial domain [F(3, 123) = 3.18, p < .03], underweight anorexics performed worse than normal controls (Figures 4 and 5 ) . Table 5 presents the mean scores for each group on the measures comprising the five neuropsychological domains, and Table 6 presents group means on the WAIS-R IQ scores, It is apparent that overall, the women in this study are above average in their level of cognitive functioning. Reviewing seven epidemiological studies of anorexia performed between 1970 and 1988, Hsu (1990) noted a preponderance of patients from the higher socioeconomic classes was found in all but two studies. These findings suggest that eating disorders may affect women from higher socioeconomic or IQ groups preferentially. The MANCOVA using MMPI scale 2 (Depression) scores as a covariate yielded an F score which was still highly significant, F(15,326.15)= 1 . 9 7 , < ~ .02. However, the MANCOVA using the TSCD scores as a covariate produced a
721
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
V."
. UA
WA
Fs
t c
Groups
Fig. 5. Visuospatial domain scores. UA = underweight anorexics; NB = normal-weight bulimics; WA = weight-restored anorexics; NC = normal controls.
result which was not significant, F (15,326.15) = 1.48, p < .11. These results suggest that symptoms of anxiety, but not depression, are associated with neuropsychological changes in eating disorders, in that when the variance associated with symptoms of anxiety is statistically removed, the F score for overall group effects falls short of significance.
DISCUSSION In the present study, differences were seen between one or more of the groups of patients with eating disorders and normal controls in four of five domains of neuropsychological functioning (the focusing/execution aspect of attention, verbal functioning, memory, and visuospatial functioning). The absolute differences in test scores between the eating disorder groups and normal controls were small. For the most part, the eating disorder groups' mean scores differed little from published norms, suggesting subtle rather than frank neuropsychological dysfunction in the eating disorder groups.
722
BARBARA PENDLETON JONES ET AL.
Table 5. Group Mean Raw Scores on Neuropsychological Measures' Measure
NB
UA
Downloaded by [UQ Library] at 08:25 11 November 2014
Vigilance CPT Ihits CPT % CEb CPT mean RTC
WA
96.5 (4.8) 0.8 (0.9) 451.2 (57.3)
Focustexecute Digit Symbol Trail Making Part A Part B Talland Letter
NC
97.2 (3.3) 94.1 (8.7) 0.7 (0.6) 1.3 (1.8) 451.7 (81.0) 442.4 (54.2)
LL2w
12.4
urn 2uiIM.l m u
25.4 (8.0) 52.8 (29.0) 78.9 (12.3)
Verbal Similarities Comprehension Vocabulary
12.5 13.2 12.1
(1.9) (2.4) (2.3)
12.2 13.0 12.7
(2.4) (3.1) (2.4)
12.4 12.7 13.1
(2.2) (2.8) (2.8)
Memory Babcock Logical Memory Buschke Recall
13.2 9.4 10.1
(3.6) (3.0)
13.0 8.2 10.2
(3.9) (3.2) (1.2)
15.6 11.1 10.2
(3.7) (3.3) (1.1)
Visuospatial Rey -0sterrieth Emb. Figures Block Design a
(1.1)
20.8 (7.2) 596.9 (304.8) 10.8 (2.5)
(2.1)
12.9
(2.2)
24.7 (6.7) 48.8 (12.9) 84.8 (10.2)
21.6 (5.6) 22.0 (5.1) 698.7 (362.1) 467.3 (246.1) 11.4 (3.1) 12.4 (2.3)
Means (standard deviations). Underlined scores differed significantly from those of normal controls. UA = underweight anorexics; NB = normal-weight bulimics; WA = weight-restored anorexics; NC = nonnal controls. CE = commission errors. RT = reaction time.
Table 6. Group WAIS-R IQ Scores' Group
N
Underweight anorexics Normal-weight bulimics Weight-restored anorexics Normal controls
30 38 20 39
a
Means (standard deviations).
Verbal IQ
103.0 (10.7) (9.8) 108.9 111.3 (13.9) 114.6 (13.8)
Performance IQ
104.4 106.5 109.3 111.9
(12.6) (12.6) (15.5) (13.1)
Full Scale IQ
103.9 109.0 111.4 113.5
(11.2) (10.9) (15.9) (11.8)
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
723
There are several possible explanations for this pattern of findings. First, it could be that the statistically significant differences between the eating disorder patients and normal controls in this study were due to a sampling bias, and that in fact, the normal controls were drawn from a “brighter” population. This seems unlikely in that all groups came from a largely middle-to-upper-middle class population and were matched overall for educational level. While we could have matched subject groups in advance on a measure such as vocabulary score in an attempt to control for premorbid ability levels, vocabulary knowledge is known to be significantly related to many of the measures which were under examination in the current study. Moreover, Goldberg, Halmi and their colleagues have found an increased incidence of complications in pregnancy and delivery (i.e., historical evidence suggestive of perinatal brain injury) in subjects who later developed anorexia nervosa and a positive correlation between the number of such complications and severity of prognosis in these patients (Goldberg et al., 1977; Halmi et al., 1977). This finding argues for very early differences between subjects with eating disorders and normal controls; therefore, in matching groups on vocabulary score, we would have been biasing the outcome in the direction of nonsignificant findings by selecting a nonrepresentative (i.e., unusually high functioning) group of eating disorder patients. The underweight anorexics showed more cognitive difficulties than the normal-weight bulimics; they scored lower than the normal controls in four of five neuropsychological domains. Their lower verbal scores (Figure 3) suggests that this is a more compromised group, from a neuropsychological standpoint. Fox (1981) reported a similar finding: anorexic patients scored significantly lower on WAIS Information than a mixed group of psychiatric control patients. The longterm weight-restored anorexics may be somewhat atypical of anorexics in that they were able to restore their weight and maintain it over a long period of time (M= 47.1 mo). Recent outcome studies have found that in the intermediate term (4-12 years after evaluation), between one-half and two-thirds of treated anorexics have regained normal weight, but the crude mortality rate at 20-year follow-up may be as high as 15 to 20% (Hsu, 1990). An important question concerns whether starvation itself leads to neuropsychological impairment. For a number of reasons, some more obvious than others, there is relatively little relevant literature. Many would regard the experimental imposition of starvation on research subjects as ethically unacceptable, while study of the neuropsychological consequences of starvation in countries where famine is endemic raises, in addition to ethical questions, questions about the generalizability of the results because of cross-cultural differences and confounding factors such as war, dislocation, and other concomitant and profound stressors. Studying subjects on diets is unsatisfactory in that if the weight loss is not commensurate with that in anorexia, one has no adequate control group; on the other hand, if the weight loss is commensurate, the dieting subjects may in fact be anorexic. However, the literature contains one landmark study which is germane to the
Downloaded by [UQ Library] at 08:25 11 November 2014
724
BARBARA PENDLETON JONES ET AL.
effects of starvation on cognitive functioning. In 1944, in response to the need to evaluate and treat millions of starvation victims in the aftermath of World War 11, an experimental study of starvation was carried out at the University of Minnesota (Keys, Brozek, Henschel, Mickelsen, & Taylor, 1950) in which 32 conscientious objectors and other volunteers underwent 24 weeks of semi-starvation in order to increase scientific knowledge concerning the effects of starvation and methods of refeeding. Among the measures employed to study the psychological effects of starvation were the following: the MMPI (these findings will be reviewed in a separate paper); six timed tests assessing perception of spatial relations, word fluency, memory, number facility, inductive reasoning, and perceptual speed; and four untimed tests assessing sentence completion, arithmetic, vocabulary, and directions. This study differed from our study in a number of ways apart from the issue of anorexia versus experimental starvation: these subjects were all men; subjects with any signs or symptoms of psychiatric abnormality were excluded; and subjects were used as their own controls. The subjects in the starvation study were above average in intellectual ability; all premorbid Army Classification Test scores were at or above the 85th percentile, whereas in the present study, the mean Full Scale IQ scores of the groups ranged from about the 60th percentile for underweight anorexics to the 85th percentile for normal controls. No significant changes were found on any of the timed tests after 24 weeks of semi-starvation; small but significant decrements were seen on arithmetic and directions, and a small but significant improvement was seen on the vocabulary measure. The experimenters concluded that “the measured intellective performances did not change importantly in either starvation or rehabilitation” (p. 863). Our eating disorder subjects arguably showed more in the way of subtle cognitive dysfunction than the starvation subjects in that one or more groups differed from the normal controls in four of five neuropsychological domains. The question arises as to whether the decline on measures of arithmetic and directions in the starvation subjects was due to impaired attention; reduced attentional capacities were reflected in our two acute eating disorder groups but not in the weight-restored anorexics3. Thus, attention may be adversely affected by the transitory metabolic and other changes accompanying severe weight loss and/or repeated bingeing, vomiting, and laxative abuse. The two MANCOVAs performed in order to reveal the relationships between depressive symptoms, anxiety, and cognitive performance indicated that there is a significant correspondence between anxiety as measured by the T S W scale of the MMPI and performance on the neuropsychological measures, but not between depression and neuropsychological performance. This pattern of findings __
In the present study underweight anorexics and normal-weight bulimics scored lower on WAIS-R Arithmetic than did normal controls (F[3, 1231= 6.07,p c 0.0007). In our laboratory’s more detailed studies of the elements of attention, WAIS-R Arithmetic has been found to load on the encode factor of attention (Mirsky, 1989).
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
725
is in precise agreement with those of Halmi et al. (1977). Other studies have also found a high incidence of symptoms of anxiety in patients with eating disorders (e.g., Smart, Beumont, & George, 1976; Theander, 1970). It could be argued that the observed decrements in test performance are not subtle neuropsychological deficits but rather reflect simply the effects of anxiety. However, an equally valid interpretation is that both anxiety and subtle neuropsychological deficits are features of eating disorders. With regard to the hypothesis of differential right-hemisphere dysfunction in eating disorders, we note that the underweight anorexics scored lower than normal controls in the verbal and memory domains as well as in the visuospatial domain. Further, the normal-weight bulimics did not differ from the normal controls in the visuospatial domain. Although we have as yet to demonstrate the lateralizing capability of the verbal and visuospatial domain scores used in the current study, the greater sensitivity of the WAIS-R Vocabulary, Similarities, and Comprehension scores to left- as opposed to right-hemisphere dysfunction is well known (Lezak, 1983; McFie, 1975; Parsons, Vega, & Burn, 1969). While the three measures in the visuospatial domain are generally sensitive to large lesions in either hemisphere, the greater disruption of Rey-Osterrieth (Bachtler, Roth, Smith, & Weber, 1990; Binder, 1982) and Block Design (Lezak, 1983; McFie, 1975) performances with right- as opposed to left-hemisphere dysfunction has been demonstrated. As for the third component of the visuospatial domain score, the Embedded Figures Test, Russo and Vignolo (1967) showed that right-hemisphere lesion patients were inferior to left-hemisphere lesion patients without aphasia on the Gottschaldt figures (later published as the Embedded Figures). Thus, the present findings do not appear to lend support to the hypothesis of differential right-hemisphere dysfunction in eating disorders. As in previous studies (Hamsher et al., 1981; Small et al., 1983), we saw some (subtle) diminution of attentional capacities in underweight anorexics. It should be noted that in terms of Mirsky’s (1989) conceptualization of the elements of attention, this diminution was seen on the focusing/execution measures of attention and not on the vigilance (CPT) measures. In addition, since lower scores in the focusing/ execution domain were seen also in the normal-weight bulimics but not in the weight-restored anorexics, it seems likely that impaired attention is related to metabolic and other changes accompanying severe weight loss and/or bingeing, vomiting, and laxative abuse. Alternatively, the diminished attentional capacities of the underweight anorexics and normal-weight bulimics are consistent with the hypothesis that at least some of these patients have a central nervous system disorder which can compromise their capacity for recovery; Small et al. (1981) found that anorexics’ scores on WAIS Arithmetic and Digit Span accounted for half of the variance in multiple regression analyses for subsequent weight gain, and Hamsher et al. (1986) found that evidence of cognitive impairment, particularly longer reaction times, was associated with inadequate weight gain or maintenance on one-year follow-up.
726
BARBARA PENDLETON JONES ET AL.
Downloaded by [UQ Library] at 08:25 11 November 2014
REFERENCES American Psychiatric Association. (1 980). Diagnostic and statistical manual of mental disorders (3rd ed.). Washington, DC: Author. Bachtler, S.D..Roth. D.L., Smith, G.E.. & Weber, A.M. (1990).Qualitative performance of the Rey-Osterrieth Complex Figure in patients with complex partial seizures. Journal of Clinical and Experimental Neuropsychology, 12.75 (Abstract). Binder, L.M. (1982).Constructional strategies on complex figure drawings after unilateral brain damage. Journal of Clinical Neuropsychology, 4.5 1-58. Bruch. H. (1970).Psychotherapy in primary anorexia nervosa. Journal of Nervous and Mental Disease, 150.51-67. Buffery, A.W.H., & Gray, J.A. (1972).Sex differences in the development of spatial and linguistic skills. In C. Ounsted & D.C. Taylor (Eds.), Gender diflerences: Their ontology and significance (pp. 123-157).Baltimore: Williams & Wilkins. Buschke, H., & Fuld, P. A. (1974).Evaluating storage, retention, and retrieval in disordered memory and learning. Neurology, 24,1019-1025. Carlin, A.S. (1986).Neuropsychological consequences of drug abuse. In I. Grant & K.M. Adams (Eds.), Neuropsychological assessment of neuropsychiatric disorders (pp. 478497). New York: Oxford University Press. Duncan, C.C., Kaye, W.H., Perlstein, W.M., Jimerson, D.C.. & Mirsky. A.F. (1985). Cognitive processing in eating disorders: An ERP analysis. Psychophysiology, 22,588. Enzmann. D.R.. & Lane, B.L. (1977).Cranial computed tomography findings in anorexia nervosa. Journal of Computer Assisted Tomography, I , 410-414. Fox, C.F. (1 981). Neuropsychologicalcorrelates of anorexia nervosa. International Journal of Psychiatry in Medicine, 11,285-290. Gold, P.W., Kaye, W., Robertson, G.L.,& Ebert, M. (1983).Abnormalities in plasma and cerebrospinal-fluid arginine vasopressin in patients with anorexia nervosa. New England Journal of Medicine, 308, 1 117-1123. Goldberg, E.(Unpublished). Semantic aphasia test. Goldberg, S.C.. Halmi, K.A., Casper, R.. Eckert. E., &,Davis, J.M. (1977). Pretreatment predictors of weight change in anorexia nervosa. In R.A. Vigersky (Ed.), Anorexia nervosa (pp. 31-41).New York Raven Press. Goodwin, R.. & Andersen, A.E. (1984). The MMPI in three groups of patients with significant weight loss. Hillside Hospital Journal of Clinical Psychiatry, 6. 188-203. Grant, I., & Adams, K.M. (Eds.) (1986).Neuropsychological assessment of neuropsychiatric disorders. New York: Oxford University Press. Halmi, K.A. (1974). Anorexia nervosa: Demographic and clinical features in 94 cases. Psychosomatic Medicine. 36,18-26. Halmi, K.A. Dekirmenjian, H., Davis, J.N., Casper, R., & Goldberg, S.C. (1978). Catecholaminemetabolism in anorexia nervosa. Archivesof General Psychiatry, 35,458460. Halmi, K.A.. Goldberg, S.C., Eckert, E., Casper,R., & Davis. J. M.(1977).Pretreatment evaluation in anorexia nervosa. In R.A. Vigersky (Ed.), Anorexia nervosa (pp. 43-54). New York: Raven Press. Hamsher, K. de S., Halmi, K.A., & Benton, A.L. (1981).Prediction of outcome in anorexia nervosa from neuropsychological status. Psychiatry Research. 4.79-88. Heaton, R.K., & Crowley, T.J.(1981).Effects of psychiatric disordexs and their somatic treatments on neuropsychological test results. In S.B. Filskov & T.J. Boll (Eds.), Handbook of clinical neuropsychology (pp. 481-525).New York: Wiley Interscience. Heidrich, R., & Schmidt-Matthias, H. (1961).Encephalographische Befunde bei Anorexia nervosa. Archiv fur Psychiatrie und Nervenkrankheiten, 202,183-201. Heinz. E.R., Martinez, J., & Haenggeli, A. (1977).Reversibility of cerebral atrophy in
Downloaded by [UQ Library] at 08:25 11 November 2014
COGNITION IN EATING DISORDERS
727
anorexia nervosa and Cushing's syndrome. Journal of Computer Assisted Tomography, I, 415- 418. Heaog, D.B. (1984). Are anorexic and bulimic patients depressed? American Journal of Psychiatry, 141,1594-1597. Hsu, L.K.G. (1990). The eating disorders. New York: Guilford. Hudson, J.I., Pope, H.G., Jr., Jonas, J.M., & Yurgelen-Todd, D. (1983). Phenomenologic relationship of eating disorders to major affective disorder. Psychiatry Research, 9,345354. Johnson, C. (1985). The initial consultation for patients with bulimia and anorexia nervosa. In D.M. Gamer & P.E. Garfinkel (Eds.), Handbook of psychotherapy for anorexia nervosa and bulimia (pp. 19-51). New York: Guilford Press. Jones, B.P., Duncan, C.C., Mirsky, A.F., & Brouwers, P. (1988). Unpublished data. Kaye, W.H., Ebert, M.H., Raleigh, M., & Lake, C.R. (1984). Abnormalities in CNS monoamine metabolism in anorexia nervosa. Archives of General Psychiatry, 41,350355. Kaye, W.H., Jimerson. D.C., Lake, C.R., & Ebert, M.H. (1985). Altered norepinephrine metabolism following long-term weight recovery in patients with anorexia nervosa. Psychiatry Research, 14,333-342. Keys, A., Brozek, J., Henschel, A., Mickelsen, O., & Taylor, H.L. (1950). The biology of human starvation. Minneapolis: University of Minnesota Press. Levitt, E.E. (1989). The clinical application of MMPI special scales. Hillsdale, NJ: Erlbaum. Lezak, M.D. (1983). Neuropsychological assessment (2nd ed.). New York: Oxford. Maccoby, E.E.. & Jacklin, C.N. (1974). The psychology of sex differences. Stanford, CA: Stanford University Press. Maxwell, J.K., Tucker, D.M.. & Townes, B.D. (1984). Asymmetric cognitive function in anorexia nervosa. International Journal of Neuroscience, 24, 37-44. McFie, J. (1975). Assemnent of organic impairment. London: Academic Press. McKay, S.E.,Humphries, L.L.. Allen, M.E., & Clawson, D.R. (1986). Neuropsychological test performance of bulimic patients. International Journal of Neuroscience, 30,7380. Minuchin, S., Rosman, B.L., & Baker, L. (1978). Psychosomatic families: Anorexia nervosa in context. Boston: Harvard University Press. Mirsky, A.F. (1989). The neuropsychology of attention: Elements of a complex behavior. In E. Perecman (Ed.), Integrating theory andpractice in clinical neuropsychology (pp. 75-91). Hillsdale, NJ: Erlbaum. Parsons, O.A., Vega, A. Jr., & Bum, J. (1969). Differential psychological effects of lateralized brain damage. Journal of Consulting and Clinical Psychology, 33,551-557. Piran, N., Kennedy, W., Garfinkel, P.E., & Owens, M. (1985). Affective disturbance in eating disorders. Journal of Nervous and Mental Disease, 173,395-400. Rao, C.R. (1973). Linear statistical inference and its applications (2nd ed.). New York: Wiley. Rosvold,H.E.,Mirsky,A.F.,Sarason,I., Bransome,E.D.,& Beck,L.H. (1956). Acontinuous performance test of brain damage. Journal of Consulting Psychology, 20,343-350. Russo, M., & Vignolo, L.A. (1967). Visual figure-ground discrimination in patients with unilateral cerebral disease. Cortex, 3, 118-127. Sein, P., Searson, S . , Nicol, A.R., & Hall, K. (1981). Anorexia nervosa and pseudoatrophy of the brain. British Journal of Psychiatry, 139, 257-258. Shelly, C., & Goldstein, G. (1982). Psychometric relations between the LurkNebraska and Halstead-Reitan Neuropsychological Test Batteries in a neuropsychiatric setting. Clinical Neuropsychologist, IV (3), 128-133. Siegert, R.J., Patten, M.D., Taylor, A.J.W., & McCormick, LA. (1988). Factor analysis of the WAIS-R using the factor replication procedure, FACTOREP. Multivariate Behavioral Research, 23,481-489.
728
BARBARA PENDLETON JONES ET AL.
Small, A.. Madero. J.. Teagno, L.. & Eben. M.(1983). Intellect, perceptual characteristics, and weight gain in anorexia nervosa. Journal of Clinical Psychology, 39,780-782. Smart, D.E., Beumont, P.J.V.. &George, G.C.W. (1976). Some personality characteristics of patients with anorexia nervosa. British Journal of Psychiatry, 128. 57-60. Spitzer, R.L., Endicott. J., & Robins. E.(1978). Research Diagnostic Criteria: Rationale and reliability. Archives of General Psychiatry, 35,773-782. Stein, K.B.(1968). The TSC Scales: The outcome of a cluster analysis of the 550 MMPI items. In P. McReynolds (Ed.), Advances in psychological assessment (Vol. I ) (pp. 80104). Palo Alto, CA: Science and Behavior Books. Talland, G.A.. & Schwab. R.S. (1964). Performance with multiple sets in Parkinson’s disease. Newopsychologia, 2.45-53. Theander, S . (1970). Anorexia nervosa. Acta Psychiatrica Scandinavica, 214, (Suppl.): 1-
Downloaded by [UQ Library] at 08:25 11 November 2014
194.
Tryon, R.C. (1966). Unrestricted cluster and factor analysis, with applications to the MMPI and Holzinger-Harman problems. Multivariate Behavioral Research, 1,229-244. Witt, E.D., Ryan, C., & Hsu. L.K.G.(1985). Learning deficits in adolescents with anorexia nervosa. Journal of Nervous and Mental Disease, 173. 182-184.
