Neuropsychologia, Vol. 25, No. lB, pp. 21 l-220. 1987 Prmted m Great Britain.

W28-3932/87 S3.00+000 f;# 1987 Pergamon Journals Ltd.

AMNESIC SENSITIVITY TO PROACTIVE INTERFERENCE: ITS RELATIONSHIP TO PRIMING AND THE CAUSES OF AMNESIA

ANDREW R. MAYES,*$ ALAN PICKERING* and ANDREW FAIRBAIRN?

*Department of Psychology, University of Manchester, Manchester Ml3 9PL, U.K tSt. Nicholas Hospital, Gosforth, Newcastle-upon-Tyne, U.K.

(Accepted 26 April 1986)

Abstract-A group of alcoholic amnesics was compared with a group of controls on an A-B, AC word pairs interference paradigm. With memory instructions the amnesics needed 5 presentation trials to their controls’ single trials to match the groups on A-B cued recall. Under these conditions they still showed more proactive interference on the A-C list. When both groups were given five presentation trials for each list and ‘free association’ instructions, then they both showed this level of interference. This suggested that the amnesic interference effect only occurs because priming is not modulated by conscious memory, i.e. it is an effect ofpoor conscious memory. This interpretation was further supported by the tinding that amnesics forgot the A--B list faster over 2 hr than their controls, when memory instructions were given.

INTRODUCTION

AMNESICS have been reported to be more susceptible than control subjects to both proactive interference [S, 12, 13, 161 and retroactive interference [16]. The studies, in which these

findings were reported, used the A-B, A-C interference paradigm and two kinds of learning task. In the first task, subjects learned lists of words and memory was tested by providing the first three letters of each word as a cue. For each word in the A-B list there was a corresponding word in the A-C list, beginning with the same three letters, e.g. if ‘stamp’ was a word in the A-B list, ‘station’ might be the corresponding word in the A-C list (see [6, 12, 133). In the second task, subjects learned lists of semantically related word pairs and memory was tested by giving the first word of the pair as a cue. For each pair in the A-B list there was a corresponding pair in the second list, which had the same first word, e.g. if

‘soldier-rifle’ was a pair in the A-B list, ‘soldier-army’ might be the corresponding pair in the A-C list (see [ 161). For both kinds of learning task, it was reported that amnesics learned the A--B list as well as controls whether subjects received one or four trials. Amnesics did not learn the A-C list as well as controls, however, showing a greater tendency to make intrusion errors from the first list. This deficit was apparent on the first A-C trial when the task involved learning related word pairs, but only became significant after the first trial when the task involved learning words.

These results suggest that abnormal sensitivity to interference may cause, or contribute to, the memory deficits shown by amnesics. If this is so, there is still a need to explain why amnesics are abnormally sensitive to interference. It has been suggested that the sensitivity arises because of inadequate encoding [4], because of a deficit in processing background

IAddress correspondence to: Dr. Andrew Mayes, Department of Psychology, University of Manchester, Manchester, M 13 9PL, U.K.

21 I

212 ANDREW R. MAYES, ALAN PICKERING and ANDREW FAIRBAIRN

contextual information so that patients cannot determine whether a response comes from an A-B or A-C list [15, 161, or because ofthe slower extinction or long-term forgetting ofearlier learnt material [13]. The first explanation lacks direct support. The contextual information processing deficit account has difficulty in explaining why amnesics only show more interference after the first A-C trial with cued words. The second explanation that amnesics show slower extinction and/or forgetting is implausible and has difficulty explaining why amnesics show more interference from the first A-C trial with related word pairs.

There is, however, another possible explanation of the sensitivity to interference, shown by amnesics in the A--B, A-C paradigm. This is that the sensitivity is an effect of poor memory rather than related to its cause. At first sight it might seem that this possibility has been excluded because, in the studies just described, amnesics and their controls were matched on their tested memory for the A-B list. If they are truly matched, then greater amnesic sensitivity to interference on the A-C list could not be an effect of their initially worse memory. This conclusion is, however, unwarranted. There is growing evidence that although amnesics are very impaired on tests of conscious memory, such as recall and recognition, for recently presented material, another indication of memory for that material, known as priming, may be unimpaired (see [ 11, 161 for reviews). Priming can be defined as a change in the efficiency of processing material, which results from having recently perceived it. Like conscious memory, it is item-specific. Amnesics often show normal priming to recently presented items that they fail to recognize [4, 6, 141. It is therefore possible that in the A--B, A-C paradigm, with cued words or related word pairs, amnesics are matched to controls on the A-B list because both groups are relying largely on priming-the amnesics do so because they have little conscious memory and the controls do so as, for some reason, they have opted not to use their available conscious memory. If so, the greater interference shown with the A-C list could arise because amnesics’ inferior conscious memory prevents them from monitoring their A-C responses, whereas their controls, under these circumstance opt to use their superior conscious memory.

It was originally suggested that good amnesic cued recall for words and the response term

of related word pairs was possible because the cues reduced the number of competing responses down to a very small number [12]. This suggestion implies that the cues are assisting conscious memory in the amnesics. Recently, however, WARRINGTON and WEISKRANTZ [ 13, 141 have rejected this view partly because cues that constrain competing responses to a very narrow range do not give amnesics a differential benefit relative to less constrictive cues [ 131. Perhaps more importantly, it is also found that amnesics show little conscious memory for correctly cued words [6, 141. The implication is that conscious memory depends on some process(es), not required for priming, which are disrupted in

amnesia. Although amnesic cued words and paired associate memory may depend largely on

priming, this seems unlikely to apply to normal subjects, who have available conscious memory for the words and word pairs. One might therefore expect control subjects to perform better than amnesics unless differences are concealed by ceiling effects or, for some reason, the control subjects do not make use of their conscious memory. In some studies, control subjects have been found to outperform amnesics, both on cued word recall [6] and cued word pair recall [lo]. In WIN~CUR and WEISKRANTZ’S study [21] of word pair learning, although there were no significant group differences, controls were numerically better on A-B recall in each experiment, so a real difference may have been concealed by a ceiling effect. The explanation of these anomalies may also be found in the way subjects interpret their

AMNESIC SENSITIVITY TO PROACTIVE INTERFERENCE 213

instructions. When subjects are told clearly that they are required to remember a list of words or related word pairs and to use cues as aids to recall, then amnesics are outperformed by their controls both on cued word recall [7] and paired word recall [ 111. If instead of receiving these memory instructions, subjects are not encouraged to treat the task as one of memory and are asked to give the first response that comes to mind when the cues are presented, then amnesic performance is hardly affected but control performance drops to amnesic levels on the A-B words and word pairs [2, 111. It is plausible that such ‘word completion’ or ‘free association’ instructions prevent subjects using conscious memory even when it is available, and instead, make them rely on the processes that underlie priming. If these explicit non-

memory instructions are not given the behaviour of controls may be unpredictable so that they may use little conscious memory to mediate A-B recall, but use it to a much greater extent when faced with the trickier task of A-C recall.

The possibility that amnesic sensitivity of proactive interference is an effect of their very poor conscious memory has been considered. If true, when applied to the learning of related paired words, three predictions follow. First, it would be predicted that controls should behave like amnesics with the A-C as well as the A-B list provided they are given free association instruction, i.e. they should show poor recall of the A-C list and make intrusion errors. On the other hand, if clear memory instructions are given the control subjects will recall more response terms from the A-B list unless amnesics are given more exposure trials. The extra trials will strengthen amnesic priming but should have little effect on their impaired conscious memory. Even if amnesics and controls are matched in this way on A-B recall, the performance of controls will depend mainly on conscious memory whereas that of amnesics will depend mainly on priming. The second and third predictions follow from this claim. The second is that even when procedures used with the A-B list, are repeated with the A-C list, amnesics will show worse recall of A-C and more intrusions as has been reported before [ 163. The third prediction is that if recall of A-B with memory instructions is delayed for 2 hr, then amnesic performance will be worse than that of their controls. This prediction follows because there is some evidence suggesting that priming or ‘free association’ memory for related word pairs largely dissipates over 2 hr [l l] in both amnesics and their controls, whereas with memory instructions, performance remains good for much longer in normal subjects [9]. It has also been found that alcoholic amnesics show a normal forgetting rate when matched to their controls on conscious memory, tested a few minutes after presentation [3]. If such amnesics forget the A-B list faster over 2 hr than their controls when both groups are given memory instructions, it therefore follows that their performance does not depend on conscious memory unlike that of their controls.

The experiment, reported here, is designed to test these three predictions with the learning of related word pairs in a group of alcoholic amnesics and normal controls. The results support the view that amnesic sensitivity to interference is a result of their poor conscious memory in a task where performance can be based on priming, which is a form of non- conscious memory. If this is correct, then previous studies using the A-B, A-C interference paradigm have not directly illuminated the causes of the poor conscious memory found in amnesics. These studies and subsequent ones have, however, made clear that amnesics show normal priming with words and related word pairs.

METHODS In this experiment a group of alcoholic amnesics and their normal controls learned four separate A-B, A-C lists of

214 ANDREW R. MAYES, ALAN PICKEKING and ANDREW FAIRBAIKK

related paired words under four instructional conditions. The first condition was designed to show that, wtth memory instructions, when subjects are matched for A-B memory at a short delay then amncsics show worse memory for A C and more A--B intrusions than their normal controls. The second condition was designed to determine whether, with ‘free association’ instructions, controls performed like amnesics on both A B and A C lists and showed considerable proactive intereference on the A-C list, when both groups received the same number of trials. The third condition was designed to determine whether, with conditions otherwise like those ofcondition one. the amnesics showed more forgetting of the A-B list after a 2 hr delay. It was also used to see whether amnesic memory for the AC list, after a short delay, was relatively improved because the A-B list had been largely forgotten. The fourth condition was identical to the third except that A-B recall was not required after the 2 hr delay, but A C learning took place as before with recall after the same brief delay. This condition was included to see whether amnesics would show better A C recall because, unlike in the previous condition, they had not recently produced their own largely incorrect responses to the A B list. It was postulated that these self-generated responses might interfere with learning of and/or memory for the A-C list.

Subjects

Eight amnesics, with an aetiology of chronic alcoholism, formed the experimental group. Three of the amnesics were Manchester patients who had appeared in previous studies. One of these patients (J. W.) died after completing conditions one and three. The other five amnesics were in-patients at St. Nicholas and St Mary’s Hospital in Newcastle. One of these patients (A. F.) died shortly after completing the last condition, before completing the performance tests of the WAIS. The details of the patients’ ages, WAIS scores, with age-scaled scores on the vocabulary, similarities and picture completion subtests, and WMS MQs are shown in Table I, All patients scored zero on the logical memory test of the WMS at 10 min delay, except S. T.. who scored 0.5.

Table 1.

WAIS WAIS WAIS Age Scaled Age Scaled Age Scaled Age Full Scale Verbal Performance Vocabulary Similarities Picture Completion WMS

1. K.H. 48 104* 108* 100* 10 13 I2 77 2. J.W. 64 101 104 96 11 12 12 62 3. S.M. 59 96 98 95 10 x 10 81 4. H.K. 45 100 98 103 11 10 I3 79 5. A.F. 68 101 II 8 11 80 6. A.D. 65 100 92 97 10 12 II 63 7. S.T. 64 98 102 102 IO II 12 77 8. R.S. 49 103* 104 101* 11 II I 0 Xl Mean 58 100 101 99 10.6 10.4 Il.4 75

* Pro-rated score

Seven Manchester University porters and technicians acted as control subjects for the patients. They were matched on socio-economic background and had a mean age of 59 yr. Their mean age scaled score on the WAIS vocabulary test was 10.1, on the WAIS similarities test Il.4 and on the WAIS picture completion test was 12.3. Although closely matched to the amnesics on these intelligence test scores, the controls’memory was far superior as their mean score on the WMS logical memory test at 10 min delay was 7.3 (six subjects were tested).

Forty-eight triads of words were selected to comprise four separate A B, A-~C lists of 12 related word pairs, so that, for example, in one list ‘Bee-Wasp’ was an A-B pair. and ‘Bee Honey’ was its matching pair from A C. Initially, 64 common concrete nouns were given on sheets to 30 control subjects, who were instructed to look at each target work and generate the first word that came to mind that was strongly associated with that target word. Forty- eight words were then selected for which two response words had been generated by not less than 10% ofthe subjects and not more than 30%. These 48 word triads were then divided into four A-B, A C lists so that, for each list (within less than I %) 20% of the subjects had generated B responses and 20% had generated C responses. This was done to ensure that the associative strength of the A-B and A C was matched and to give a guessing rate for the responses of around 20%. The word pairs of the four A B, AC lists were written individually in capitals on file cards and for each of the four sets a test list was written with each stimulus word followed by a dash on separate file cards.

Procedurr

List order and instructional condition were balanced. as far as possible, using a Grecko-Latin Square. The four

AMNESIC SENSITIVITY TO PROACTIVE INTERFERENCE 215

conditions were given on separate days to be subjects and when a condition involved a 2 hr delay other non-verbal tests were given in part of the interval. In condition one, subjects were told that they would be required to learn a list

of related word pairs. The A-B list was then shown to the subjects with the pairs in different random orders at a rate of 2 set per pair and they were asked to read them aloud to ensure concentration. Whereas the control subjects received only one trial, the amnesics were given five with a few seconds between each trial using presentation orders that differed randomly from trial to trial. This difference in number of trials was designed to match amnesic and control memory, and was based on previous experience with the patients. There was then a 2 min delay, filled with conversation, after which the subjects were shown the first word ofeach pair from the A-B list and asked to recall the word they had just been shown, which went with it. They were reminded that words should be related. Order of test presentation differed randomly from that used for learning trials and from subject to subject. A few seconds after the completion of recall, the whole procedure was repeated exactly for the A-C list. This condition was run first for all subjects because it was essential to match amnesics and controls on A-B recall after the 2 min delay.

In the second condition everything was the same as in the first condition, except in three respects. First, both groups ofsubjects received five trials on the A-B and, later, the A--C lists. Second, subjects were not told that the task involved memory specifically at any stage, but were asked to rate the strength of association for each pair on a IO point scale. They were told to make the assessment as independently as possible on each of the five trials. Third, after the 2 min delay, subjects were shown the first word ofeach pair and asked to produce the first response that came to mind that was related to it. They were encouraged to respond quickly and told there was no right or wrong answer. In the third condition memory instructions were once again used and the procedure was the same as in condition one, except that after the A-B trial or trials had been given, there was a 2 hr delay before recall was tested. A-C list learning followed immediately and A-C recall was tested 2 min later, as in condition one. The fourth condition was exactly like the third, except that after the 2 hr delay which followed A-B learning, A-B recall was not tested, but instead subjects learned A-C, recall for which was tested after a 2 min delay. A record was kept of the number of responses subjects got right on the A-B and A-C lists and the number of A-B intrusions they made when being tested on an A-C list.

RESULTS

The results are shown in Table 2. In the first condition, after a 2 min delay the amnesics’ cued recall of A-B was closely matched to that of their controls (t =0.02, df= 13, N.S.). The first aim of the study was therefore achieved by giving the amnesics five trials to their controls’ one. Informal observations strongly suggested that the controls’ cued recall would have been at ceiling if they had been given five learning trials. Amnesic recall of A-C was, however, significantly worse than that of their controls (t = 4.2, df= 13, P-c 0.001) despite the fact that, just as with A-B they received five learning trials to their controls’ one. A second analysis confirmed that the drop in amnesics’ scores between A-B and A-C was significantly greater than that of the controls (t = 3.83, df= 13, Pz 0.001). The amnesics therefore showed more proactive interference than the controls, who on the basis of their A-B and A-C scores, seemed to show none at all. They did, however, make some prior list intrusions when attempting to recall A-C although the amnesics made significantly more (t = 5.25, df= 13, P<O.OOl). As has previously been reported [21, 221, amnesics also made a significantly greater number of intrusions as a percentage of their total number of errors (t = 1.88, df= 13, PcO.05, one-tailed test). Whereas on average, 56% of amnesic errors were intrusions, the figure was 3 1% for controls. Subjects were encouraged to respond and made no omission errors. The remaining errors were semantic intrusions as would be expected. For example, if the A-B pair was ‘Wound-Blood’ and the matching A-C pair was ‘Wound-Hurt’, then a semantic intrusion might by ‘Stab’ to the cue ‘Wound’. Sometimes a subject made the same semantic intrusion with both A-B and A-C lists although such errors were not systematically recorded for all subjects. In this first condition then, the amnesics showed more interference than their controls on the second list as indicated by worse memory for this list relative to the first list, and both more total intrusions and more intrusions as a percentage of overall errors on the second list.

In the second condition, where both groups received five trials on the A-B and A-C lists

Tab

le

2.

Con

ditio

n O

ne

Con

ditio

n T

wo

Con

ditio

n T

hree

C

ondi

tion

Four

N

o.

of

No.

of

N

o.

of

No.

of

Su

bjec

ts

A-B

A

-C

Intr

usio

ns

Subj

ects

A

-B

A-C

In

trus

ions

Su

bjec

ts

A-B

A

-C

Intr

usio

ns

Subj

ects

A

B

A

-C

Intr

usio

ns

Am

nesi

cs

8 1.

9 3.

5 4.

8 7

6.9

4.0

4.3

8 3.

4 5.

4 2.

5 7

6.9

2.0

Con

trol

s 7

7.6

1.6

1.9

7 7.

4 4.

6 3.

6 7

5.7

5.9

2.0

7 6.

0 1.

6

Mea

n sc

ores

of

am

nesi

cs

and

cont

rols

un

der

cond

ition

on

e (c

ued

reca

ll at

2 m

in

dela

y),

cond

ition

tw

o (f

ree

asso

ciat

ion

at 2

min

de

lay)

, co

nditi

on

thre

e (c

ued

reca

ll at

2

hr

dela

y fo

r A

B

, 2

min

de

lay

for

A-C

). an

d co

nditi

on

four

(t

he

sam

e as

thr

ee,

exce

pt

cued

re

call

of A

-B

was

no

t te

sted

).

AMNESIC SENSITIVITY TO PROACTIVE INTERFERENCE 217

and free association instructions, there were no differences between the groups. A 2 x 2 split-

plot analysis of variance showed there was no significant effect of group [F (1, 12) < 1, N.S.] and that the interaction between groups and the first and second lists was also insignificant [F (1, 12) < 1, N.S.]. Free association scores on the A-C list were, however, significantly worse than those on the A-B list [F (1, 12) = 13.0, P<O.Ol] indicating the operation of proactive interference in both amnesics and controls. Further comparison of the scores of the amnesics between condition one and condition two, for the seven patients who were subjects in both, indicated no differences. A 2 x 2 repeated measures analysis of variance revealed no main effect of condition [F (1,6)= 1.8, N.S.] and an insignificant interaction between conditions and score on the A-B and A-C lists [F (1, 6) < 1, N.S.], although A-C scores were much worse than A-B ones [F (1,6)=27.2, P<O.Ol]. Comparison of the number of intrusions made by amnesics and controls with the A-C list in the free association condition also showed there to be no difference (t< 1, df= 12, N.S.). The number of intrusion errors made in condition one and condition two by the seven amnesics, who were subjects in both conditions, was also found not to differ (t < 1, df= 6, N.S.). These results indicate that with free association instructions amnesics and controls do not differ on A-B memory and intrusions, and that both groups show proactive interference. They also show that free association and memory instructions are associated with no differences in amnesic performance.

Condition three was identical to condition one except that A-B was tested after a 2 hr delay. After this delay the amnesics. cued recall of A-B was worse than that of their controls (t=2.88, df= 13, PcO.02). In a second analysis the drop in amnesics’ cued recall of A-B between conditions one and three (2 min vs 2 hr delay) was compared with that of the controls (t = 1.86, df= < 13, P-c 0.10). The failure of this analysis to yield a conventionally significant result was due to the anomalous behaviour of patient A. F., whose 2 hr cued recall was almost as good as her 2 min recall in marked contrast to the other amnesics. Without her inclusion the amnesics showed a greater drop in A-B cued recall between 2 min and 2 hr (t = 3.10, df= 12, PC 0.01). Patient A. F. unfortunately died before her cognitive and memory functions could be adequately assessed. On some tests she certainly appeared to be severely amnesic. She was however, possibly more variable in her memory performance than the other patients. Her memory may then have been working better, for unknown reasons, during conditions three and four. Her performance on A-C in conditions three and four was also very bad, unlike that of all the other patients, and in these conditions she made twice as many intrusions as any of the other patients. This pattern is consistent with her having more conscious memory that was lost more slowly than priming over the 2 hr delay. It is therefore probably the case that amnesics forget A-B faster over 2 hr than do the controls. In contrast, condition three cued recall of A-C does not differ between the groups (t < 1, df = 13, N.S.) and neither does the number of intrusions they make (t< 1, df= 13, N.S.). Between conditions one and three the amnesics show a significantly greater drop in the number of intrusions made (t=2.44, df= 13, PcO.05) even with the inclusion of patient A. F. As the A-B cued recall performance of condition one is a baseline condition in which little or no proactive interference should be operating, it is of interest to compare A-B cued recall in this condition with A-C cued recall in condition three in order to see whether A-C cued recall is back to baseline levels when there has been a 2 hr delay from A-B learning. When A-C cued recall in condition three is compared with A-B cued recall in condition one for the controls, there is a trend for A-C recall to be worse (t = 2.03, df = 6, P < 0.10). The same comparison for the amnesics shows that A-C cued recall is just significantly worse (t=2.88, df= 7, P-cO.05).

218 ANDREW R. MAYES, ALAN PICKERING and ANDREW FAIRBAIRN

There is therefore, some evidence of proactive interference affecting amnesic cued recall of A-C, the origins of which need to be explained.

In the fourth condition everything was the same as in condition three except that A-B cued recall was not tested after the 2 hr delay. The main reason for the inclusion of this condition was to see whether having to recall the A-B list just before learning A-C might cause A-C recall to be worse than the baseline cued recall of A-B in condition one. As in the previous condition there was no group difference on A-C cued recall or intrusions (in both cases t < 1, df= 13, N.S.). More importantly, comparison of A-C cued recall in condition four with A-B cued recall in the baseline condition one revealed no difference for the amnesics, who took part in both conditions (t < 1, df= 6, N.S.) or for the controls (t = 1.72, df= 6, N.S.). But there was no improvement in the cued recall of the A-C list between conditions three and four [F (1, 6) = 2.2, N.S.], nor was the insignificant improvement shown by the amnesics greater than the minute change seen in the controls (t= 1.01, df= 12, N.S.). Thus, although cued recall of A-C in condition four is not different from the performance one would expect to see with baseline levels of proactive interference, there is no convincing evidence that not having to recall A-B just before learning A-C improves A-C recall in either group. It is impossible to predict whether larger numbers of subjects would have revealed a trend as exactly half the subjects improved-three controls and four amnesics.

DISCUSSION

The results of this experiment are clearcut. When memory instructions are given, with the learning of related word pairs, amnesics are more sensitive to proactive interference as shown by their worse A-C cued recall and their greater number of intrusions, both absolutely and as a proportion of total errors. When free association instructions are given, however, amnesic performance does not change, but the performance of their controls does change so as to become identical with that of the amnesics in showing poor A-C cued recall and many

intrusions. Furthermore, whereas, under memory instructions, amnesics need five trials on A-B learning to the controls’ one, if the groups are to be matched at cued recall after a 2 min delay, with ‘free association’ or priming instructions the groups are matched with the same number of trials, as has been previously reported [l 11.

These results are most naturally interpreted by the proposal that, with memory instructions, amnesic performance depends mainly on priming whereas control performance rests mainly on the more ‘powerful’ conscious memory. Under ‘free association’ instructions, performance depends for both groups on priming, but whereas this constitutes no change for the amnesics, for the controls, it means that performance depends on a less effective memory system. This system does not sustain performance at the same high level as when conscious memory is also involved, and with memory for related pairs at least, is associated with greater sensitivity to interference. Support for this proposal can be drawn from evidence that priming memory for related pairs largely dissipates after 2 hr [ll]. If, with memory instructions, amnesic performance rests mainly on priming then they should forget faster than controls over a 2 hr retention interval. This effect was observed although confirmatory support would be desirable as in a previous experiment, where controls and amnesics were not matched on immediate test, the amnesics only showing an insignificant trend towards faster forgetting

over 2 hr [l 11. In that study, faster amnesic fogetting may have been masked by a floor effect with the patients. If, as has been reported [l 11, amnesic priming memory (and ufortiori their conscious memory) has largely dissipated after 2 hr then proactive interference from the A-B

AMNESIC SENSITIVITY TO PROACTIVE INTERFERENCE 219

list should not affect cued recall of the A-C list. Evidence on this point was not completely unequivocal as in condition three amnesic cued recall of A-C had not returned to baseline levels. Although A-C cued recall did return to baseline levels in condition four the improvement was not significant, so it was not possible to conclude that obviating the need to recall A-B responses just before learning the A-C list was reducing the proactive interference acting on A-C. If such interference had operated in condition three, it would have come largely from the incorrect responses amnesics gave to the stimuli words of the A-B list. It can be concluded that in condition four minimal intereference was acting on the A-C list in the amnesics.

The proposal, considered above, is therefore supported by the results. It would seem then that related work pair priming is very sensitive to proactive interference provided performance is uninfluenced by the modulatory effects of conscious memory. We would expect the same pattern of results with word completion priming in the A-B, A-C interference paradigm provided both amnesics and controls were given around five trials on both lists. If only one trial had been given high levels of proactive interference may well not have been found because WARRINGTON and WEISKRANTZ [12, 131 have reported that amnesic sensitivity to such interference takes more than one A-C trial to develop. If this difference should be found it is our view that it reveals a subtle distinction between two kinds of priming rather than anything about the causes of amnesia.

In summary, amnesic sensitivity to proactive interference in cued recall tasks, as demonstrated in the literature, is a result of the patients’ very poor conscious memory. The evidence indicates that such sensitivity to proactive interference is the natural consequence when conscious memory is not or cannot be used. This conclusion leaves unanswered two, possibly related, questions. First, what functional deficit(s) causes conscious memory to be so poor amnesics? Second, do amnesics also show more sensitivity to proactive interference than their controls, in interference tasks that are mediated solely by conscious memory? The questions may be related because one popular answer to the first question is that a selective deficit in the ability to remember background spatiotemporal contextual features, associated with target events, is the cause of amnesics’ poor memory (see [S] for a review). If this hypothesis is correct, one might predict that amnesics will be more sensitive to proactive and retroactive interference, even when memory does not depend upon priming, because the ability to identify whether an item comes from an A-B or an A-C list probably involves accessing salient contextual information. This heightened amnesic sensitivity to proactive interference should occur even when amnesics and their controls are matched on A-B memory by allowing the amnesics additional learning trials (which they also would receive with A-C) because the context memory deficit is hypothesized to be selective. Without such a matching control evidence of heightened sensitivity to interference is open to the usual criticism that the effect is merely a result of poor amnesic conscious memory.

There is one recent study that seems to show greater sensitivity to interference in amnesics, which employs a kind of task, performance on which cannot be mediated by priming Cl]. In this study, subjects were read four brief stories, comprising 23 ideas each, one at a time. Halfa minute after being read a story, subjects were required to recall as much of it as they could. Although alcoholic amnesics, Alzheimer patients and Huntington choreics were equally impaired at recalling the stories, only the first two groups showed an abnormally great number of intrusions from stories read earlier-an indirect indication of sensitivity to interference. Despite the fact that this study does not include the essential control of matching normal and amnesic conscious memory of the first list by some appropriate

220 ANDREW R. MAYES, ALAN PICKERING and ANDREW FAIRBAIRN

manipulation, the performance of the three patient groups is approximately matched on this measure and two of the groups still show more intrusion errors than the third group. Greater sensitivity to proactive interference should, however, be evinced not only by the occurrence ofmore intrusion errors, but also, by worse memory for the later stories. As this second effect was not found, the production oflarge numbers of intrusion errors may not have been caused by the kind of interference effect so often observed in normal subjects. It therefore remains to be shown that the limbic or diencephalic lesions, critical in organic amnesia, cause an increase in interference sensitivity, that is not a result of concomitantly impaired conscious memory. At present, it remains true to say that amnesics’ memory performance is only excessively disrupted by proactive interference in tasks where memory can be mediated by both priming and conscious memory. This effect arises because priming is not modulated by conscious memory, which is poor in amnesics, and does not in itself reveal why amnesics have poor conscious memory.

Ackno~~ledgements-The authors would like to thank Simon Metcalf and Jon Bradshawe for their assistance in testing the control subjects, and Fran Morris who typed this paper.

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