Asymmetry of recall in depression.

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Asymmetry of Recall in Depression a

b

Dennis Deptula , Alan Manevitz & Allan Yozawitz

c

a

Department of Geriatric Psychiatry, Nathan S. Kline , Institute for Psychiatric Research , Orangeburg, NY b

Department of Psychiatry , New York Hospital - Cornell Medical Center , New York c

Neuropsychology Unit , Hutchings Psychiatric Center , Syracuse, NY Published online: 04 Jan 2008.

To cite this article: Dennis Deptula , Alan Manevitz & Allan Yozawitz (1991) Asymmetry of Recall in Depression, Journal of Clinical and Experimental Neuropsychology, 13:6, 854-870, DOI: 10.1080/01688639108405103 To link to this article: http://dx.doi.org/10.1080/01688639108405103

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Journal of Clinical and Experimental Neuropsychology 1991. Vol. 13, NO.6,pp. 854-870

0168-8634/91/1306-0854$3.00 Q Swets & Zeitlinger


Asymmetry of Recall in Depression* Dennis Deptula', Alan Manevitz2, and Allan Yozawitz3 'Department of Geriatric Psychiatry, Nathan S. Kline. Institute for Psychiatric Research Orangeburg, NY 2Departmentof Psychiatry, New York Hospital - Cornell Medical Center, New York 3NeuropsychologyUnit, Hutchings Psychiatric Center, Syracuse, NY

ABSTRACT We compared the verbal (auditory/semantic)and nonverbal (visual/configurational) recall of carefully defined depressed patients with a demographically matched control group of normal volunteers. Whereas controls were split as to whether their nonverbal recall exceeded or was inferior to their verbal recall, 89% of depressed patients demonstrated an asymmetry characterized by poorer nonverbal than verbal recall. Depressive subgroups (determined by clinical and psychoendocrinecriteria) differed from controls, but not from each other, in demonstratingthis asymmetry of recall. In contrast, depressed patients did not individuallydemonstratean asymmetry between verbal and nonverbal recognition that differed from controls.

Neuropsychological studies have shown verbal memory performance to be influenced predominantly by the language-dominant hemisphere and nonverbal memory performance by the nondominant hemisphere (Kimura, 1961,1963; Milner, 1968). Whereas disordered memory has been recognized as a common clinical manifestation of depression (Stromgren, 1977), there has been n o consensus regarding the specific nature of this deficit (i.e., whether the effect of depression on cognitive processes differentially impairs verbal or nonverbal memory) (Cutting, 1979; Weingartner, Cohen, Murphy, Martello, & Gerdt, 1981). Electrophysiologic (d'Elia & Perris, 1973, 1974; Perris, 1975) and clinical studies (Robinson & Price, 1982) have demonstrated an association between depression and dysfunction of the dominant hemisphere. There also is a considerable literature demonstrating an association between depression and dysfunction of the nondominant hemisphere (Bruder, Sutton, Berger-Gross, Quitkin, & Davies, 1981; Flor-Henry, 1979; Fromm & Schopflocher, 1984; Gainotti, 1972; Gruzelier & Venables, 1974; Kronfol, Hamsher, Digre, & Waziri, 1978; Myslobodsky &

* Portions of these data were presented at the 12th annual meeting of the International Neuropsychological Society, Houston, Texas, February 4, 1984 and at the 137th annual meeting of the American Psychiatric Association, Los Angeles, California, May 8, 1984. Requests for reprints should be sent to Allan Yozawitz, Ph.D., Neuropsychology Unit, Hutchings Psychiatric Center, 620 Madison Street, Syracuse, New York 13210, USA. Accepted for publication: February 5 , 1991.


ASYMMETRY OF RECALL

855

Horesh, 1978; Silberman, Weingartner, Stillman, Chen, & Post, 1983; Tucker, 1981; Yozawitz et at., 1979). Based upon these studies, and the aforementioned predominant influence of the left and right hemispheres upon verbal and nonverbal memory, it is reasonable to conjecture that the memory dysfunction of depression may be predominantly verbal or nonverbal in character. This notion of an asymmetry of memory dysfunction in depression is contrary to the widely held clinical perception that the memory disorder of depression is pervasive and undifferentiated (Caine, 1986; Calev, Korin, Shapira, Kugelrnass, & Lerer, 1986; Chronholm & Ottosson, 1961; Cohen, Weingartner, Smallberg, Pickar, & Murphy, 1982; McAllister, 1981). If an asymmetry of predominantly verbal or nonverbal memory dysfunction could be identified in depression, detailed memory assessment may provide a useful cognitive index that could: a) suggest greater specificity for the treatment of depression; and/or b) identify individual vulnerability t o and/or remission from depressive episodes (Bruder et al., 1981; Wexler & Heninger, 1979). This study compared the verbal (auditory/semantic) and nonverbal (visual/ configurational) memory of a carefully defined group of depressed patients with a control group matched for age, IQ, educational background, and gender. Memory was studied for subgroups of depressed patients (Miller, 1975) that were determined by clinical as well as psychoendocrine criteria. It was posited that clinically determined bipolar patients and psychoendocrine determined nonsuppressors on the Dexamethasone Suppression Test (DST) (Carroll, 1982) would be more likely to show an asymmetric impairment of memory because they represent subgroups of greater neurobiologic homogeneity (Dunner, Dwyer, & Fieve, 1976; Katz, Robins, Croughan, Secunda, & Swann, 1982; Schatzberg et al., 1982, 1983).

METHODS Subjects Subjects were 28 depressed patients and 14 controls who did not demonstrate behavior pathology. All subjects were determined to have consistent right hand preference on the Annett questionnaire (Annett, 1967). Subjects were evaluated with a semistructured psychiatric interview (Yozawitz et al., 1979) and all depressed patients met consensual criteria between two raters for DSM-III diagnoses of Major Depressive Episode. Of the 28 depressed patients, 20 were identified as unipolar depressives and eight were bipolars. Alternatively, half of depressed patients were suppressors and half nonsuppressors on the DST (cortisol > 5 pg% at 4 or 11 pm.). Nonsuppression suggests failure to inhibit hypothalamic-pituitary-adrenal hyperarousal. Each patient was administered an oral dose of 1 mg of dexamethasone at 11 p.m. Blood was sampled the next day at 4 p.m. and 11 p.m. Plasma cortisol concentration > 5 pg% was considered nonsuppression (Brown, 1981). Depressives were selected from among inpatients at Payne Whitney Clinic, New York Hospital-Cornell Medical Center. They were relatively young (ranging from 25 to 45 years), acute (M = 1.0 previous hospitalization), and of average intelligence as assessed by the Satz-Mogel short form of the WAIS-R (Dinning & Kraft. 1983). They were high school graduates and predominantly female (ratio 6: 1). Controls were nonpatients who


856

DENNIS DEPTULA ET AL

were recruited to match the age. education level, and gender of our patient sample. Patients and controls were screened to have histories free of brain damage, epileptic seizures, ECT treatment, drug and alcohol abuse, and penal incarceration. Identifying data for the principal groups of depressed patients and controls are given in Table 1 along with identifying data for clinical (unipolar/bipolar) and psychoendocrine (suppressor/nonsuppressor)subdivisions of the depressed group. A series of two-tailed t tests revealed that depressed patients and controls did not differ in age, education, VIQ, or FSIQ. Nevertheless, depressives were inferior to controls in PIQ ( r (40)= 2.44. p < .02). One-way analyses of variance (ANOVAs) and Newman-Keuls multiple comparisons across subgroups revealed that bipolars were somewhat more educated (F(2,39) = 4.62, p < .02) than uNpolars (p < .01) and controls (p c .01). Also, nonsuppressors were inferior in PIQ (F(2,39) = 8.50, p c .W1) to controls (p < .01) and to suppressors (p < .01). Approximately two-thirds of the depressed patient group was treated with medication. The most common were tricyclic antidepressants (12 patients). Other medications consisted of antipsychotics (6 patients), trazodone (two patients), diazepam (one patient), and lithium carbonate (one patient). Medication was begun an average of one week and a maximum of two weeks prior to testing.

Table 1. Demographic and Psychometric Characteristics for the Control (C) and Depressed (D) Subject Groups and for the Suppressor (S). Nonsuppressor (NS), Unipolar (U), and Bipolar (B) Subgroups. Groups

N

14

28

14

14

Mean age

34.5 (5.5)'

34.2 (6.8)

34.8 (5.5)

33.7 (6.9)

35.5 (6.4)

31.1 (4.5)

Mean education

14.9 (2.3)

14.9 (2.4)

15.4 (2.4)

14.5 (2.3)

14.2 (2.3)

16.9 (1.0)

20

Mean Full Scale IQ

102.4 (10.6)

98.5 (11.8)

103.4 (13.7)

94.1 (7.3)

98.4 (10.9)

99.4 (14.6)

Mean Verbal IQ

102.5 (10.7)

102.4 (13.4)

105.9 (15.3)

98.9 ( 10.7)

101.3 (12.7)

105.1 (15.7)

Mean Performance IQ

102.4 (10.9)

93.6 (11.0)

99.6 (11.4)

88.0 (6.6)

94.8 (11.3)

91.4 (10.7)

23.1 (6.2)

20.6 (3.9)

25.6 (7.2)

23.0 (3.5)

23.4 (10.8)

Mean Hamilton scores 'Standard deviation

ASYMMETRY OF RECALL

857


Verbal Memory Test The verbal memory test was an abbreviated version of the Mattis, Kovner, and Goldmeier (1978) paradigm, which has been successful in differentiating amnesic syndromes of different neuroanatomic subtypes. The test stimuli were an auditorily presented list of 20 "target" words, all names of four-legged animals (e.g., dog, giraffe, mouse, wolf) that were repeated by the subject to ensure attention and stimulus reception. Verbal recall was assessed on each of four trials, of 2'/2 min duration, during which subjects were encouraged to spontaneously recall as many target words as possible in any sequence. After each trial, subjects were reminded of only those words that had not been recalled on any previous trial. Verbal recognition was assessed on each of two probes, administered on the second and fourth trials, after subjects had completed recall but before being reminded of target words. The subjects' task for the probe was to recognize the 20 target words that were randomly presented among 20 distractor words. The distractors also were names of fourlegged animals and were matched with the target words for the likelihood of being spontaneously recalled (e.g., camel, hippo, rat, fox). Subjects were requested to respond, yes or no, whether each of the words of the probe was from the target list. Immediate verbal feedback was provided after each response.

----I-

f t J

Fig. 1. The 10 target stimuli of the nonverbal memory test.


858

DENNIS DEETJLA ET AL.

Nonverbal Memory Test The nonverbal memory test paralleled the verbal test in design, with four recall trials and two recognition probes. However, instead of auditorily presented verbal stimuli, the stimuli were visually presented geometric designs printed in black on white file cards (see Figure 1). They were designed to be moderately complex and difficult to verbally encode. The test consisted of 10 individually presented target designs to be remembered. Subjects were instructed to examine each figure closely and to copy it to ensure adequacy of visualmotor skill, attention, and stimulus reception. Recall memory was assessed on each of four trials, of 3 ‘/zmin duration, during which subjects were encouraged to draw as many target designs as possible in any sequence. AS in the verbal procedure, subjects were “restrictively” reminded of only those designs that had not been drawn correctly on any previous trial. Predetermined scoring rules for intrusions (see Deptula. 1984) guided judgments about the correctness of each drawing. Correctness appeared to be reliably judged, evidenced by a classification agreement of 97% between independent raters. Nonverbal recognition probes were added to trials two and four, after subjects had completed recall but before being reminded of target designs. The probes consisted of a randomization of the 10 target designs with 10 distractor designs of similar complexity (see Figure 2). Subjects were requested to respond, yes or no, whether each of the designs of the probe was from the target list. Immediate verbal feedback was provided after each response.

2

e,

0

x

7-I

Fig. 2. The 10 distractor stimuli of the nonverbal memory test.

ASYMMETRY OF RECALL

859

Test Presentation


After the nature of the procedure had been fully explained, written informed consent was obtained for all subjects. Thereafter,verbal and nonverbal memory tests were presented in counterbalanced order. All testing was done at approximately the same time of day (between 3 and 5 p.m.) to minimize the effects of diurnal variability upon performance. Patients were tested from 1 to 53 days (A4= 10.2, SD = 12.2) after admission.

RESULTS

Recall Memory Since interpretations were the same for analyses based on raw and corrected recall data, this section will focus upon the presentation of corrected recall data (i.e., adjusted percent correct recall). Mattis et al. (1978) suggested this correction to partial-out the contribution of guessing to total recall. The adjustment consisted of subtracting each subject’s intrusion score (the percentage of items recalled that were not target items) from their percent correct recall. The mean adjusted percent correct recall for each trial of the verbal and nonverbal tests is presented in Figure 3 for depressed patients and controls. Inspection of Figure 3 suggested that performance differences between groups were particularly marked for nonverbal recall. Split-plot ANOVAs and NewmanKeuls multiple comparisons of recall performance confirmed that impression. Two split-plot ANOVAs (Groups x Trials for verbal and for nonverbal recall) revealed a main effect of groups for nonverbal recall (F(1,40) = 24.50, p < .W1) but not for verbal recall (F(1,40) = 2.36, p > .05). A Trial x Group interaction for verbal recall (F(3,120) = 3.54, p < .05) and Newman-Keuls multiple comparisons revealed that groups differed in verbal recall only on the last trial ( p < .OOl). The comparability of initial verbal recall performance between patients and controls indicated that depressives’ poor nonverbal recall could not simply be attributable to group differences in overall performance level. A significant trial main effect for verbal recall (F(3,120) = 29.18, p < .OOOl) suggested that depressed patients were task attentive and demonstrated verbal learning across trials. To correct for individual differences in level of recall performance, adjusted percent correct difference scores (verbal minus nonverbal) were calculated for each subject. To permit this intertest comparison, verbal and nonverbal standard (Z)scores were derived for each subject, separately from the verbal and from the nonverbal adjusted percent correct scores of the control group, for each recall trial. Difference scores were then determined for each trial by subtracting each subject’s nonverbal standard score from their verbal standard score. Summed across trials, depressives’ asymmetry of recall was 1.4 standard deviations greater than controls’ asymmetry of recall (F(1,40) = 13.81, p < .OOl>. Table 2 illustrates the distribution of asymmetry of recall for individual subjects. Whereas normal controls were split as to whether their nonverbal recall exceeded or was inferior to their verbal recall, 89% of depressed patients dem-

DENNIS DEPIULA ET AL.

860

Recall Verbal

Nonverbal

1


70

c E

30

-

Controls

0-0

x----

10

1

2

3

4

1

2

3

x

Depressed Patients

4

Trials

Fig. 3. The mean verbal and nonverbal recall by trial (adjusted percent correct) of de-

pressed patients and controls. onstrated inferior nonverbal recall relative to their verbal recall (x2 (1, N = 42) = 5.92, p c .OS) (corrected for continuity). Depressed patients continued to significantly differ from controls in asymmetry of recall after being divided into clinical (F(2,39) = 9.12, p < ,001) and psychoendocrine subgroups (F(2.39) = 6.90, p < .005). Newman-Keuls multiple comparisons revealed that unipolars and bipolars (p < .Ol), and suppressors and nonsuppressors (p < .Ol), each differed from controls. Subgroups of depressed patients, however, did not significantly differ from each other in their asymmetries of recall. Nevertheless, it was of interest to note that bipolars and nonsuppressors exhibited the poorest nonverbal recall (see Table 3).

Table 2. Chi-square Distribution of Asymmetry of Recall (Adjusted Percent Correct): Depressed Patients vs. Normal Controls. -

~~

~

~~

Asymmetry of recall Verbal > Nonverbal

Nonverbal > Verbal

Depressed

25

Controls

7

3 7

Groups

861

ASYMMETRY OF RECALL


Table 3. Mean Recall (adjusted percent correct), Z Score Asymmetry of Recall, and Mean Percent Intrusions: All Groups. Verbal Recall

Z Score Nonverbal Asymmetry of Recall Recall’

Percent Verbal Intrusions

Percent Nonverbal Intrusions

Groups

N

Controls

14

60.0 (13.1)b

51.8 (13.4)

0 (1.2)

2.2 (2.9)

5.7 (2.8)

Depressed

28

54.7 (8.9)

21.9 (20.4)

1.4 (1.6)

2.5 (2.4)

13.1 (7.4)

Unipolars

20

54.7 (9.6)

26.1 (21.0)

1.1 (1.6)

2.4 (1.9)

11.5 (7.0)

8

54.7 (7.5)

11.6 (15.2)

2.0 (1.6)

2.8 (3.5)

17.2 (7.4)

Suppressors

14

57.7 (8.9)

27.3 (22.2)

1.3 (1.6)

2.1 (1.7)

12.5 (8.0)

Nonsuppressors

14

51.7 (8.1)

16.6 (17.5)

1.5 (1.8)

2.9 (2.9)

13.8 (7.5)

Bipolars

a

Verbal minus Nonverbal Standard deviation

Depressives’ recall differed qualitatively from controls’ recall by an excess of nonverbal intrusions (i.e., nonverbal items recalled which were not target items) (F(1,40) = 12.81, p < .001). This was evident, as well, for the clinically determined subgroups (F(2,39) = 6.42, p < .005) (see Table 3). Newman-Keuls multiple comparisons revealed that bipolars exceeded unipolars ( p < .05) and controls (p < .0l) in nonverbal intrusions, although there were no subgroup differences in verbal intrusions. It should be remembered that adjusted percent correct recall scores were, by definition, lowered by intrusions. Nevertheless, correcting for intrusions could not account for the distinctive asymmetry of recall in depressed patients. Even without adjustment, depressed patients were markedly poorer than controls in nonverbal recall (F(1,40) = 16.54, p < .0005>,whereas they did not differ from controls in verbal recall (F(1,40) = 2.30, p > .05). Depressives’ asymmetry of recall summed across trials without adjustment for intrusions was significantly greater than controls’ asymmetry of recall (F(1,40) = 9.44, p < .005).

Medication Analysis It could be argued that the asymmetry of recall of the depressed patients may have been confounded by medication. Sixty-eight percent of patients were treated


862

DENNIS D E m A ET AL.

with antidepressants, antipsychotics, and in one case, a benzodiazepine. Of particular concern was the anticholinergic nature of these medications which, in high plasma concentrations, can produce cognitive impairment and has been postulated to cause intrusions on memory assessment (Fuld, Katzman, Davies, & Terry, 1982). It is important, therefore, to note that two split-plot ANOVAs (Medication x Trials for verbal and for nonverbal recall) revealed that medicated patients did not differ from unmedicated patients in adjusted percent recall on either the verbal (F(1,26) = 308,p > .05) or the nonverbal (F(1,26) = .069, p > .05) memory test. Additionally, none of the memory indices correlated significantly with antidepressant dosage level (plasma levels for antidepressants were not available). Notably, the bipolar subgroup, despite having shown the poorest nonverbal recall and the greatest number of intrusions, was composed of the lowest percentage of medicated patients (25%).

Task Matching Check Calev et al. (1986) suggested that our finding of an asymmetry between verbal and nonverbal recall in depressives might have been a methodological artifact of differential sensitivity for the verbal and nonverbal recall tasks. We explored this possibility by comparing our control group's score distributions for the verbal and nonverbal recall tests (Chapman & Chapman, 1973,1978). Although the size Table 4. Task Matching Check. Verbal recall test

Nonverbal recall test

.83

.75

24.89

23.00

22.74 18.90

28.00 21.11 -.62 -.62

Tests Alpha coefficient (reliability) Meana Variance' True score variance Skewness Kurtosis

-.12 -1.26

Item difficulty Mean Variance Skewness Kurtosis

.62 .04 -.34 -.86

.56 .06 -.65

-.39

Since the verbal test had twice as many items as the nonverbal test, a half-point was scored for a correct response on the verbal test and a full point was scored for a correct response on the nonverbal test.

863


ASYMMETRY OF RECALL

of our control group was small ( n = 14), the analysis suggested that the nonverbal and verbal recall tests were well matched in difficulty and discriminatory power. As shown in Table 4, reliabilities, means, and true score variances (test variances minus error variances) appeared well matched. Fairly comparable measures of kurtosis and skewness suggested similar shapes to the distribution. Distributions of item difficulty also looked similar. Consequently, it did not appear that our finding of an asymmetry between verbal and nonverbal recall in depressed patients was attributable to inherent differences in sensitivity or in task difficulty between our verbal and nonverbal recall measures.

Recognition Memory The forced-choice design of the recognition memory probes permitted the calculation of recognition sensitivity (d') scores (Green & Swets, 1966) (see Table 5). Two split-plot ANOVAs on these scores (Groups x Probes for verbal and for nonverbal recognition) revealed a main effect of groups for nonverbal recognition (F(1,40) = 8.01, p < . O l ) but not for verbal recognition (F(1,40) = 3.60, p > .05).

Table 5. Mean Recognition ( d ) , Z Score Asymmetry of Recognition, and Mean Percent False Positives: All Groups. Verbal Nonverbal RecogRecognition(d') nition(d')

N Groups

Z Score Percent Percent Asymmetry Verbal Nonverbal of False False Recognition' Positives Positives

~~

Controls

14

3.10 (.58)b

2.46 (55)

0 (1.49)

5.9 (5.7)

15.4 (14.6)

Depressed

28

2.67 (.74)

1.93 (.58)

.29 (1.38)

12.5 (10.2)

27.7 (13.2)

Unipolars

20

2.65 (.64)

1.99 (54)

.16 (1.38)

12.3 (9.9)

26.0 (12.0)

Bipolars

8

2.73 (.99)

1.77 (.69)

.62 (1.42)

13.1 (1 1.6)

31.9 (16.0)

Suppressors

14

2.94 (.64)

2.08 (.46)

.45 (1.45)

8.2 (6.2)

23.9 (11.6)

Nonsuppressors

14

2.39 C.74)

1.78 (.67)

.12 (1.31)

16.8 (11.7)

31.4 (14.1)

a

Verbal minus Nonverbal

'Standard deviation


864

DENNIS DEFTULA ET AL.

To correct for individual differences in level of recognition performance, d‘ difference scores (verbal minus nonverbal) were calculated for each subject. Verbal and nonverbal standard (2)scores were derived for each subject, separately from the verbal and from the nonverbal d’ scores of the control group, for each recognition probe. Difference scores were then determined for each probe by subtracting each subject’s nonverbal standard score from their verbal standard score. In marked contrast to the asymmetry of recall that was evident for individual depressives, there was little asymmetry of recognition upon individual analysis. Summed across probes, depressives’ asymmetry of recognition was only .29 standard deviation different than the control group’s asymmetry of recognition. Moreover, asymmetries of recognition were not significant for individual bipolar or nonsuppressor patients. The absence of a distinctive asymmetry of recognition for depressives upon analysis of individual performance, despite a group main effect for nonverbal recognition, suggested marked individual differences in level of recognition performance. Since recognition errors (false positives) may be responsible for lowering level of recognition performance (d) by definition, it was reasoned that exploring the nature of these errors (with error analysis) could provide insight about how subjects differed in recognition performance.

Error Analysis The recognition memory performance of the depressed patient group was characterized by a greater false positive score (the percentage of distractor items misidentified as target items) than the control group. This was evident for nonverbal (F(1,40)= 92.22, p e .Ol) and for verbal recognition performance (F(1,40) = 5.04, p < .05) (see Table 5). Of particular note was the observation that the depressed group’s verbal errors on recognition (false positives) were more numerous than their verbal errors on recall (intrusions) of the same target words. Considering this incongruence of verbal performance across recall and recognition, it appeared unlikely that depressives’ high verbal false positive rate could reflect a cognitive disturbance specific to verbal functioning. Instead, depressives’ high verbal false positive rate may have reflected a nonverbal perceptual/cognitive process. The verbal recognition task required subjects to attend to each word, compare it with memory traces of target words, and make a judgment as to the novelty or familiarity of each word. Verbal false positive responses may have been generated by a tendency for depressives to dwell on the visually imaged similarity between distractor and target words (e.g., wolf/fox, mousehat) rather than attend to the novelty of the distractor words. This process may have been similar to that governing depressives’ nonverbal recall performance. Poor nonverbal recall may have been generated by a tendency for depressives to dwell on familiar features of designs (e.g., redundantly expressing them as intrusions) rather than attend to the novelty of distinctive features to aid recall. To explore whether verbal recognition and nonverbal recall might have reflected


ASYMMETRY OF RECALL

865

the same perceptual/cognitive substrate, d’ scores were correlated with adjusted percent correct recall scores for all subjects. Consistent with the notion of perceptual/ cognitive commonality, a significant correlation was obtained between verbal recognition and nonverbal recall (r(40) = .43, p < .01). In contrast, verbal recall was not correlated with nonverbal recognition (r(40) = .19, p > .05). It should be noted that one could not interpret the correlation between verbal recognition and nonverbal recall as simply attributable to high rates of false positives and intrusions. Raw percent correct nonverbal recall, independent of intrusions, also correlated with verbal recognition (r(40) = .45, p < .Ol), whereas raw percent correct verbal recall was not correlated with nonverbal recognition (r(40) = .17, p >

.05). Symptom Correlates of Memory Performance In an effort to explore the association between depressed patients’ memory and their affective state, Pearson correlations were determined between memory measures and clinical symptoms based upon Hamilton Depression Scale ratings (Hamilton, 1960) and dexamethasone challenge. Interestingly, depressives’ nonverbal memory (recall and recognition) did not correlate significantly with any clinical measures. Only verbal memory, recall (r(26) = -.43, p < .05) and recognition (r(26) = -.40, p < .05), correlated with the Hamilton endogenous (vegetative) rating (as defined by Bruder et al., 1981). Verbal recall also correlated with 4 p.m. cortisol level ( r ( 2 6 ) = -.40, p < .05).

DISCUSSION

To our knowledge, this is the first study to have demonstrated a distinctive asymmetry between verbal and nonverbal recall in depressed patients. Our findings stand in contrast to a reported study of depressives that did not observe significant asymmetry between verbal and nonverbal recall on a similar matched-task assessment (Calev et al., 1986). Nevertheless, it may be that differences between studies along other methodological dimensions were responsible for these disparate findings. Of particular relevance may have been the Calev et al. (1986) reliance upon a single trial paradigm. In our study, depressives’ nonverbal recall deficit was smallest on the initial trial (see Figure 3). Two-tailed f tests comparing depressives and controls on the first trial did not show the significant asymmetry between verbal and nonverbal recall that was observed on latter trials (two through four). It is conceivable that multitrial tasks (i.e., which incorporate opportunities for learning through feedback and which rely upon delayed recall) may be necessary components for a methodological design that is sensitive to nonverbal recall dysfunction in depressed patients. This study differed from most previous studies of depressed patients by identifying a memory deficit that was not correlated with clinical indices of affective


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symptom severity (e.g., Cohen et al., 1982; Sternberg & Jarvik, 1976). This may have reflected the known tendency of depressed patients to deny symptoms (Ross & Rush, 1981). Alternatively, as some studies have suggested, it may be that depressives’ memory deficit truly is independent of clinical state (Coughlan & Hollows, 1984; Friedman, 1964; Kopelman, 1986). If so, asymmetry of recall might be a trait variable in depressed patients. It is suggested that future studies employ longitudinal design methodology to assess this possibility. It was posited that clinically determined bipolar patients and psychoendocrine determined nonsuppressors on the DST would be more likely to show an asymmetry of recall because they represent subgroups of greater neurobiologic homogeneity. Our finding that depressive subgroups did not differ from each other in their asymmetries of recall did not support this hypothesis. Nevertheless, further study with larger subgroups would appear necessary before conclusively rejecting the notion that bipolars and nonsuppressors may distinctively evidence asymmetries of recall. Extended study of the recall performance of depressive subgroups might be prudent considering the related observations that: a) bipolars and nonsuppressors exhibited the poorest nonverbal recall, and b) bipolars significantly exceeded unipolars in nonverbal intrusions. It is conceivable that the absence of a distinctive asymmetry of recognition in contrast to depressives’ distinctive asymmetry of recall may have reflected a difference across recall and recognition tasks in performance difficulty. Since recognition tasks are considerably easier than recall tasks for individuals without amnesic disorder, one might conjecture that depressed patients would not generate sufficient error on recognition performance (i.e., a possible “ceiling effect”) to afford this task much discriminatory power. Nevertheless, on group analysis, depressives performed significantly poorer on nonverbal recognition than controls. This evidence notwithstanding, future studies might attempt to increase the difficulty of recognition tasks by substituting a word or figure completion paradigm for simple identification or by decreasing the detectability of target or distractor stimuli with manipulations of exposure time and/or stimulus degradedness. It is possible that depressives indeed manifested only an asymmetry of recall that differed from controls, without a correspondingly distinctive asymmetry of recognition. Assuming such a relationship existed, it may serve a heuristic purpose to consider the following explanation: Depressives’ memory dysfunction may involve feature analysis more than retentive/amnesic mechanisms. It is conceivable that the nature of depressives’ processing limitation could interfere with their ability to extract and analyze stimulus features with sufficient accuracy to permit accurate recall. Nevertheless, because sufficient retention of these features would have been achieved to permit accuracy of verification against an externally presented model of the stimulus, recognition would be relatively unimpaired. Interestingly, other studies employing signal detection analyses have noted preserved recognition memory in depressives (Dunbar & Lishman, 1984; Miller & Lewis, 1977). Moreover, one study (Calev & Erwin, 1985) observed a dissociation between preserved recognition memory and disturbed recall in unipolar depressives.


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We must caution that our study did not employ left- and nght-lesioned controls to validate the specificity of our verbal and nonverbal measures to lateralized cerebral dysfunction. Consequently, we could not determine whether the obtained asymmetry of recall memory in depressives directly supported an association between depression and nondominant hemisphere dysfunction. Interestingly, a study assessing recall on a verbal task that was similar to ours found a gross verbal deficit for the performance of left but not of right hemisphere lesioned patients (Barbizet & Cany, 1969). The identification of a PIQ limitation in depressed patients strengthened our assertion, based upon the task matching analysis previously reported, that the observed asymmetry of depressives’ recall was not simply an artifact of a more difficult nonverbal recall task. The findings that depressed patients were both inferior to controls in PIQ and achieved greater asymmetry than controls between verbal and nonverbal recall suggested that these behavioral outcomes were likely mediated, in common, by a legitimate perceptual/cognitive dysfunction. Moreover, the observation that depressives produced more verbal false positives than verbal intrusions suggested that their perceptual/cognitive disturbance was not specific to verbal functioning, instead reflecting the mediation of a nonverbal cognitive process. Robertson and Taylor (1985) identified a specific dysfunction for the processing of spatial information by depressives. Although our data appeared consistent with that finding, the design of our study did not permit us to differentiate between the perceptual and/or cognitive limitations which may be shared by depressed patients. Future studies should be constructed to separate the sensoryspecific from the cognitive-specific components of the nonverbal task to independently explore these components of depressives’ recall (i.e., sensory-specific: auditory vs. visual, and cognitive-specific: semantic vs. configuration) (Ross, 1980). In addition to its heuristic value for clinical investigation, the identification of a distinctive asymmetry between verbal and nonverbal recall in depressed patients may have current utility for treatment. For example, it may be helpful to recognize that the memory disorder of depressives may be neither pervasive/ undifferentiated nor predominantly verbal when considering strategies for psychotherapeutic programming. Moreover, cognitive training interventions might be designed (Erickson & Binder, 1986; Townes et al., 1985; Yozawitz, 1986; Yozawitz & Charters, 1985), utilizing depressives’ relative strength in verbal recall, to develop adaptive strategies for academic, vocational, and social activities. Should future studies support an association between asymmetry of recall in depressed patients and lateralized dysfunction of the nondominant hemisphere, there may be additional therapeutic benefits. These might include selecting more appropriate psychopharmacological agents (Mandell, 1979; Mandell & Knapp, 1979; Oke, Keller, Mefford, & Adams, 1978), determining unilateral or bilateral ECT (Kronfol et al., 1978; Sackeim, Decina, Epstein, Bruder, & Malitz, 1983; Sackeim et al., 1983), and selecting other novel therapeutic approaches that are

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directed at enhancing nondominant frontotemporal functioning (Gur et al., 1984; Shakhnovich, Serbinenko, Razumovsby, Rodionov, & Oskolok, 1980).


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Encoding origin of the terminal asymmetry effect in recall.

Are secular trends in major depression an artifact of recall?

EEG asymmetry in borderline personality disorder and depression following rejection.

Depression and mild cognitive impairment in the general population: results of the Heinz Nixdorf recall study.

Gait asymmetry, ankle spasticity, and depression as independent predictors of falls in ambulatory stroke patients.

Kynurenine pathway metabolites are associated with hippocampal activity during autobiographical memory recall in patients with depression.

Developmental changes in electroencephalographic frontal asymmetry in young children at risk for depression.

Effect of depression on the speed of recall of pleasant and unpleasant experiences.

Comparative physiological reactivity during script-driven recall in depression and posttraumatic stress disorder.

Resting and task-elicited prefrontal EEG alpha asymmetry in depression: support for the capability model.

Design and Implementation of an Intervention Development Study: Retaining Cognition While Avoiding Late-Life Depression (ReCALL).

Functional brain asymmetry and visuospatial perception in mania, depression, and psychotropic medication.

Frontal alpha asymmetry as a pathway to behavioural withdrawal in depression: Research findings and issues.

Selective recall of positive and negative feedback, self-control behaviors, and depression.

Temporal lobe asymmetry with iofetamine (IMP) SPECT imaging in patients with major depression.

Frontal EEG Asymmetry as a Promising Marker of Depression Vulnerability: Summary and Methodological Considerations.

Frontal alpha EEG asymmetry before and after behavioral activation treatment for depression.

Perceptual asymmetry and youths' responses to stress: Understanding vulnerability to depression.

Cerebral asymmetry in infants.

Misunderstanding recall.

Gist recall in multiple sclerosis.

Semantic effects in sentence recall: the contribution of immediate vs delayed recall in language assessment.

Asymmetry in the skull.

EEG power asymmetry and functional connectivity as a marker of treatment effectiveness in DBS surgery for depression.