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Central error-correcting behavior in schizophrenia and depression
BIOL PSYCHIATRY 1986:21:263-213
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Central Error-Correcting Behavior in Schizophrenia and Depression Robert C. Malenka, Ronald W. Angel, Sue Thiemann, Charles J. Weitz, and Philip A. Berger
A previous study suggested that schizophrenic subjects exhibit an impaired ability to correct their own errors of movement without using exteroceptive signals. However, the performance of schizophrenic subjects was compared to that of only one other psychiatric group (alcoholic subjects), and a relatively small number of subjects was studied. To investigate the specificity of the postulated impairment, 9 schizophrenic, I I depressed, and 8 normal subjects performed a tracking task designed to prevent the use of exteroceptive cues in correcting errors of movement. The depressed and normal groups did not differ signi$cantly on any performance measure, but the schizophrenic subjects again demonstrated a gross impairment in correcting errors, yet no impairment in initiating correct responses. These findings suggest that the impaired ability to monitor ongoing motor behavior on the basis of internal, self-generated cues may be specific to schizophrenia among major psychiatric disorders.
Introduction Normal subjects can recognize and correct errors of movement under experimental conditions that preclude the use of exteroceptive signals (Rabbitt 1966a, 1968; Angel and Higgins 1969; Angel et al. 197 1; Angel 1976). In such experiments, error-correcting behavior must be presumed to depend on internal, self-generated cues. Hence, the ability to monitor movements and correct errors appears to involve central feedback pathways. In a previous study (Malenka et al. 1982), we examined the error-correcting ability of a group of schizophrenic subjects in comparison with age-matched normal and alcoholic subjects. Using a simple visual tracking task, in which feedback about the accuracy of tracking was blocked, we found that schizophrenic subjects exhibited a grossly impaired ability to correct errors of movement. We suggested that this impairment could not be
From the Department of Psychiatry and Behavioral Sciences. Stanford University School of Medicine, Stanford, CA and Palo Alto Veterans Administration Medical Center. Palo Alto, CA (R.C.M., S.T., P.A.B.); the Department of Neurology, Palo Alto Veterans Administration Medical Center and Stanford University School of Medicine (R.W.A.); and the Division uf Neurosurgery. Stanford University School of Medicine (C.J.W.). Supported in pail by NIMH Grant MH-30854 to the Norris Mental Health Clinical Research Center at Stanford University and a grant from the Research Service of the Veterans Administration to the Schizophrenia Biologic Research Center at Palo Alto VA Medical Center. Address reprint requests to Dr. Philip A. Berger, Department of Psychiatry and Behavioral Sciences, Stanford University. Stanford, CA 94305. Received July 1, 1985; revised September 14, 1985.
0 1986 Society of Bmlogical Psychiatry
0006.3223/86/$03.50
explained by nonspecific factors, such as amotivation or gross inattention. and therefort might refiect aspects of the pathophysioi~)gy underlying the schizophrenic syndrome. However. schizophrenic subjects differ from normal subjects on an eno~(~us variety of psychological and phys;oi~~gicai variables. ranging from reaction time (King 1965) and attentional tasks (Kornetsky and Orzack 197Xa) to cerebral blood flow (Ingvar and FranLen. 1974) and brain electrical activity (BEAM) (Morihisa et al. 1983). Moreover, there IS usually a signiticant overlap between the performance of schizophrenic subjects and that of normal sub,jects. making it difficult to state whether or not an observed abnormality is “specific” for schizophreni;r An experimental design that begins to address this problem is one that makes ;: conlparis~)n between the ~rf~~rmance of schizophrenic subjects and that of subjects carrying other psychiatric diagnoses. Signiticant differences between these groups cannl>t bc attributed to general features of‘ psychiatric tllness and, therefore, might have impli cations for understanding schizophrenia. In order to begin to address the question cri specificity. we compared the performances of patients carrying the diagnosis of majo) depressive disorder with thorc of schizophrenic and normal control subjects. By including the schizophrenic subjects from our previous study. we were also able to examine how eager-correcting behavior W;I~ affected by nellr~)~eptic ~nedicati(~n and severity of symp toniatolopy
Methods Our study compared three groups performing a single task. All sub_jects were right-hand dominant by verbal report. The primary experimental group comprised nine schizophrenic subjects (all men) at the Palo Alto Veterans Administratit~n Medical Center. Ages ranged from 2X to 55 years (mean 33.-3). and the average aIllount of schooling was 13.5 years. Diagnostic categories consisted of chronic schizophrenia (paranoid, 3 patients: undifferentiated. 3 patients: residual. 1 patient) and subchronic schizophrenia (undifferentiated. I patient; disorganized. I patient). Three of these patients were considered to be drug free, having taken no psychotropic medications for a minimum of 2 weeks prior to the date of the test. Six schizophrenic patients were on neuroleptic medications, speciticallv thiothixene ( 10-80 mglday) or piquindone. which is a neuroleptic presentfy under clinical investigati~~n. All diagnoses were determined by Research diagnostic Criteria (RIX’: Spitzcr et al. 1978) and were based on two focused interviews conducted by two trained personnel. a physician and a research nurse or assistant. R&ability studies demonstrdtc high interrater reliability for this system of diagnosis. with kappa values ranging from 0.77 to 0.87, depending on the diagnosticians sampled. Eight normal control subjects were tested (six men, two women). ‘Their ages ranged from 20 to 3 I years (mean 76.5). and the average educational level was 13 years. These subjects were either staff members or undergraduate students. None had any history 01 psychiatric or neurological illness. A second control group was made up of I I subjects (all men) diagnosed as major depressive disorder. Diagnoses were made by the procedure described above for the schizophrenic patients. Patients’ ages ranged from 23 to 60 (mean 35.1 ). and average educational level was 13.5 years. None of these patients was taking any psychotropic medication or had taken any for a minimum of 2. weeks prior to the test date. Written informed consent was obtained from all subjects after the purpose and possible risks of the study were explained.
Error-Correcting Behavior
Apparatus
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and Procedure
Details of the apparatus and experimental procedure have been published previously (Malenka et al. 1982). The subject was seated facing an oscilloscope screen on which two vertical lines, the target and cursor, were displayed. The location of the target line was controlled by a frequency-modulation tape recorder. At each instant, the target occupied one of three positions: the center of the screen, 3 cm to the left, or 3 cm to the right. A sequence of 100 random target jumps was presented to each subject. The target remained in the left or right lateral position for 1 set and then returned to the center position for a variable period ranging from 2 to 6 sec. The subject was instructed to track the target by moving the cursor appropriately. The subject controlled cursor position by moving a joystick with the right hand. The directional relation between movement of the joystick and movement of the cursor was controlled by a polarity switch. When in the “normal” position, the cursor moved in the same direction as the joystick. When in the “reversed” position, the cursor and joystick moved in opposite directions (i.e., movement of the joystick to the left caused the cursor to move to the right). Following a demonstration, the subject was given a brief practice session consisting of 5-10 jumps. After this session, an opaque, 6-cm wide screen was placed over the center of the oscilloscope leaving 1 cm visible at each edge. With the opaque screen in place, the target and cursor were invisible except when displaced at least 3 cm to the right or left of center. The subject therefore had no visual feedback from the cursor until his movement was nearly complete, although the target was clearly visible in the lateral positions. The subject then was given another short practice session in which the polarity switch was first in the normal position (for five jumps) and then in the reversed position (for five jumps). At this time, the subject was informed that after each block of 10 jumps, the polarity control switch would be reversed and that he would be verbally warned prior to each polarity reversal. Immediately before the start of the experiment, the polarity control was put in the normal position and the subject was requested to move the cursor so that it was barely visible, first on the left side of the opaque screen then on the right side. These positions were recorded so that the experimenter would have a record to determine whether or not the cursor had been visible at any given time during the experiment. Scoring The movements of the target and cursor were recorded on a strip-chart recorder at a paper speed of 25 mmsec or on digital tape using a Nicolet 1129 signal averager. Each response was classified as one of the following: (1) correct move, not reversed (C&-the subject moved his cursor initially in the correct direction and continued in this direction until the cursor became visible; (2) correct move, reversed (CR)--the subject began moving the cursor in the correct direction but reversed direction _while the cursor was still hidden by the opaque screen; (3) false move, not reversed (FR)--the subject started moving the cursor in the wrong direction and did not reverse direction until the cursor became visible; (4) false move, reversed (FRethe subject moved the cursor initially in the wrong direction but reversed direction while the cursor was still screened from view; and (5) reject-a given response was rejected whenever (A) the cursor was visible at the time of the target jump, (B) the cursor was moving at the time of the target jump, and/or (C)
K.C.
Malcnka
et ;li
the cursor‘s movement wa\ reversed more than once before it was visible. The numbetot rejected responses did not differ significantly between the experimental groups. Not including the rejected responses, each subject completed a total of 100 moves (TM\ Responses were analyzed without knowledge of the subject’s diagnosis. All of the schizophrenic subjects were scored weekly on the Brief Psychiatric Rating Scale (BPRS: Overall and Gorham 1962). providing an opportunity to compare severit:, of symptomatology with impaired performance on our experimental task. Scores from the week of the test were averaged with scores from the week preceding and the wech following the test to provide a more accurate description of clinical state. Three scorch were calculated for each subject: ( I) total BPRS score, (2) total score on “positivi, symptoms” t&
Nonparametric statistical techniques were used to test for differences between groups III order to avoid making any assumptions about the distribution of error-correcting abiiitb in the populations sampled. All data were entered into an IBM Model 3081 computer and were analyzed using the Statistical Analysis System software package. Groups were first compared with the Kruskal-Wallis one-way analysis of variance. If this test showed significant differences. pairwise comparisons were made using the Mann-Whitney LJ-test. To investigate associations among the variables, Spearman correlation coefticients were calculated.
Results This investigation examined the ability of schizophrenics to monitor their movements and correct errors using self-generated cues. Our experimental design provided two scores that reflect this ability: ( I) the probability that an initially false move would be reversed while the cursor wa4 still invisible [FR/(FR + FE11 and (2) the probability that an initiali] correct move would be reversed [CR/(CR + CR)]. If the subject was always able to recognize and correct error4 without using cxteroceptive signals. his score on the first
Error-Correcting Behavior
267
BIOL PSYCHIATRY 1986;21:263-273
Table 2. Diagnoses and Test Scores of Depressed Subjects Subject 1 2 3 4 5 6 7 8 9 10 11
Age/sex 42/M 57/M 23/M 54/M 43/M 55/M 35/M 60/M 44/M 53/M 52/M
Psychiatric Major Major Major Major Major Major Major Major Major Major Major
diagnosis”
depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder
CR + CR ~
FR + CR ~
TM
TM
0.82 0.92 0.78 0.84 0.97 0.90 0.92 0.91 0.82 0.67 0.85
0.14 0.03 0.22 0.11 0.03 0.07 0.06 0.06 0.14 0.30 0.12
FR FR
CR CR
0.78 0.75 1.00 0.73 1.00 0.70 0.75 0.75 0.72 0.89 0.91
0.00 0.00
0.00 0.00 0.00
0.00 0.00
0.00 0.01 0.01 0.01
“Diagnoses were made according to Research Diagnostic Criteria.
measure would be 1.O. If he was also always able to recognize a correct move as correct and therefore never reverse it, his score on the second measure would be 0. In the normal group (Table 1), the probability of reversing a false move was 0.8 1, with scores ranging from 0.60 to 1.O. Six of eight subjects (75%) had scores greater than 0.70. In the depressed group (Table 2), the probability of reversing a false move was 0.82, with scores ranging from 0.70 to 1.O. Eleven of 12 depressed subjects (92%) had a score greater than 0.70. Both normal and depressed subjects were also able to recognize correct moves. Only 2 of 8 normal subjects (25%) and 3 of 11 depressed subjects (27%) reversed any correct move (the probability of reversing a correct move was less than 0.01 for either group). There were no significant differences between normal and depressed subjects in either the probability of reversing a false move or the probability of reversing a correct move. These findings suggest that depression, per se, does not interfere with the ability to monitor movement or correct errors without exteroceptive feedback. As previously reported, the scores of the schizophrenic subjects (Table 3) are in sharp contrast to those of the control subjects. Their probability of reversing a false move was 0.53, with scores ranging from 0.25 to 1.0. Only 2 of 9 schizophrenic subjects (22%) had a score greater than 0.70. Schizophrenic subjects were also deficient in their ability to recognize correct moves. Seven of the nine schizophrenic subjects (78%) reversed at least one correct move. The schizophrenic subjects’ probability of reversing a false move was significantly different from that of either the normal 0, = 0.03) or depressed @ = 0.01) subjects (Figure 1). Their probability of reversing a correct move was also significantly different from that of depressed (p = 0.02) subjects and barely missed significance when compared with the normal group (p = 0.06). The large differences between the schizophrenic and normal or depressed subjects on these measures of error-correcting ability lend strong support to our hypothesis that schizophrenic subjects have an impaired ability to recognize and correct movement errors without using exteroceptive feedback. In our previous study, we reported no difference between groups in the ability to initiate correct responses. This ability was measured by dividing the total number of correct moves by the total number of moves [(CR + CR)/TM]. This investigation also revealed no significant difference between the schizophrenic subjects’ scores and those of the two control groups. The normal group’s probability of initiating a correct move
h 7 8 9
5
1 2 3 3
Schizophrenia. Schizophrenia, Schizophrenta. Schizophrema. Schizophrenia, Schizophrenia. Schizophrenia. Schizophrenia,
39/M 29/M 26/M 55/M 27/M 30/M 30/M 31/M
Subject5
..~
hvdrochlorldr
~20,
0.88 0.90 0.85 0.80 (I.72 0.96 0.88 0.62 0.80
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____
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.__
I201
hydrochloride
-...(80) c 10)
hydrochloride hydrochloride
MtXiGiUo~~s’
Thiothixene Thiothixene chronic. undifferentiated Piquindone chronic. paranoid Thiothiwene chronic. undifferentiated Yone chrome. residual Thiothtrene wbchromc. disorganized subchronic. undifferentlared None None chronic. paranoid Piqumdontl chronic. paranoid ._---.-
Schizophrenia. chronic. undifferentiated
P\>I tuatrlc dlagno\th’,
32/M
.-\geiscr
Diagnosis and ‘l‘eat Scores tar Schizophremc
“Dragnoses were made ~ccordmg 10 Raearch Dwgo~tic Cntsn.~ The number\ !!I parentheses are lhe ddil~ dnwge~ in nllll~grar~l~
Subject --.-
Table i C‘R
(1.08 0.06 0.04 0.15 (1.14 11.05 0. 10 0.14 0. 10
TM
_.._ ..-
FK + CR
! .fXl Cl.83 0.25 0 35
0.01 0.08 0.01 0 00 0.07 0 01
0.01 0.00
O.I!5 0.6X !).;IY
0.01 0 50
(‘R
0.5x
FR
Error-Correcting
BIOL PSYCHIATRY 1986;21:263-273
Behavior
A.
Correct Move
([CR*@]
TM)
C.Reversal,
B. Reversal
F&e
([FR+CR]:TM)
269
D. Reversal, Given
Given
Move
Correct Move
(FR,[FR*~*])
(cR,[cR~])
1.oo .80 s. I= li5 x l;z
.60
*
.40 .20 0
i
N
D
S
N
D
S
n
f
D
S
NDS
) ~obabilit: Y( )f initiating a correct Figure I. Probabilities calculated for each subject g ro up. move. (b) ProbabiIity of reversing a move. (cf ~obability of reversing a move, given that it was initially false. (d) Probability of reversing a move, given that it was initially correct. N indicates normal subjects; D indicates depressed subjects; S indicates schizophrenic subjects. Formulas in parentheses were used to calculate various probabilities. Asterisk (*) indicates statistically significant (p < 0.05) difference between the schizophrenic group and either the normal or depressed groups (c) or between the schizophrenic and depressed groups (d).
was 0.89, with scores ranging from 0.80 to 0.97. The depressed group’s scores ranged from 0.67 to 0.97, with a mean of 0.84. The schizophrenic subjects’ scores ranged from 0.62 to 0.96, with a mean of 0.82. These scores were not signilicantly different. Thus, the schizophrenic subjects exhibited a normal ability to initiate correct responses, but had a gross impairment in the ability to amend false moves. As the schizophrenic subjects were less likely to reverse a false move, we examined the probability of reversing a move without regard to its initial correctness [(CR + FR)/TM]. There was no significant difference among groups on this measure. This indicates that schizophrenic subjects’ impai~ent in reversing false moves cannot be explained by simply ~stulating that they had a decreased tendency or ability to reverse moves. Before discussing our findings, it is important to mention a number of “nonspecific” variabIes that were analyzed in order to insure that they were not affecting our results. The first is age. The depressed subjects, as a group, were significantly older than the other two groups. However, as previously noted, there were no differences between the normal and depressed groups on any performance measure. Furthermore, age did not covary with any of the scores. Both of these findings suggest that age differences between subjects cannot account for our results. A second important variable is sex differences. As our normal group contained two women, whereas the depressed and schizophrenic subjects were all men, we reanalyzed our data, deleting the women. No differences from
270
BIOL PSYCHIATK’I 198h.ll 263 273
ICC‘. Malenka et ;11
the results reported above were found. There were no differences among groups m educational level. and as the two patient groups both consisted of inpatients at the Palo Alto Veterans Administration Medical Center. it seems doubtful that environmental factors can account for the reported differences between groups.
Discussion The goals of this study were: ( I) to retest the hypothesis that schizophrenic subjects arc deficient in the ability to monitor their motor behavior without use of exteroceptive cues, and (2) to compare their performance with that of patients with major depressive disorder. In our previous study (Malenka et al. 1982). schizophrenic subjects differed from normal and alcoholic subjects both in the ability to recognize and reverse false moves and in the tendency to reverse correct moves. Both of these measurements reflect an impaired ability to monitor ongoing behavior by means of internal, self-generated cues. No significant differences were found between the normal and alcoholic groups on any test variable. We now report a significant difference between schizophrenic and depressed subjects and between schizophrenic and normal subjects in error-correcting performance. No significant differences were found between normal and depressed subjects. These results make it unlikely that nonspecilic features of psychiatric illness or ho>pitalization for its treatment can account for poor performance on our experimental task The deficit in error-correcting displayed by the schizophrenic subjects may therefore refect a central nervous system dysfunction that is unique to the schizophrenic syndrome. This conclusion must be tempered by the knowledge that a relatively small and heterogeneous group of schizophrenic subjects was studied. Furthermore. the majority of dcpressed subjects did not exhibit clinically significant thought disorder. which may affect error-correcting perfomrance independently of the diagnosis of schizophrenia. Several variables that we did not or were unable to examine directly in the schizophrenic subjects, such as IQ. motivational level, or degree of organicity. might be expected to significantly affect performance on our task. However, the schizophrenic group did not exhibit an impairment in the ability to initiate correct responses. This strongly suggests that they were able to learn and to perform the task as well as either the depressed otnormal sub.jects. Thus, as discussed previously (Malenka et al. 1982), nonspecific factors. such as inconstant motivation, are unlikely to account for the impaired performance ol schizophrenic subjects. Instead, we propose that schizophrenic subjects suffer from :I distinct defect in error-correcting processes. An analysis of when during the experiment the schizophrenic subjects made their error\ might be expected to contribute to the understanding of the defect underlying their impaired performance. Such an examination of the data revealed no significant pattern. The errors in error-correcting performance (CR and FR) seemed to be randomly distributed. The inability to tind a significant trend may be a reflection of the small number of error’ available for analysis. It is clearly important to continue this analysis as more subject4 are studied. Because of the relatively small number of subjects in this study, it was not possible to determine the effects of medication on schizophrenic subject performance. However. as this is a critical issue in all studies of schizophrenic patients, we expanded our sample size in order to make a valid comparison between medicated and nonmedicated subjects This was accomplished by including 12 subjects carrying the diagnosis of schizophrema trom our previous study (diagnostic categories included chronic paranoid, 2 subject&
Error-Correcting Behavior
BIOLPSYCHIATRY 1986:21:263-273
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chronic undifferentiated, 6 subjects; chronic residual, 1 subject; subchronic paranoid, 2 subjects; and acute undifferentiated, 1 subject), thus yielding a total of 21 subjects for comparison-10 on neuroleptic medication and 11 who had been drug free for a minimum of 2 weeks. The only significant difference between the two groups was in the probability of rerversing a move, without regard to its initial correctness [(CR + FR)/TM]. Medicated schizophrenic subjects exhibited a tendency to reverse fewer moves than nonmedicated schizophrenic subjects. Considering the well-documented Parkinson-like side effects of neuroleptic medication, this is not a surprising result. Medication status did not contribute significantly to our results, as statistical reanalysis with the medicated schizophrenic subjects deleted had no effect on the reported differences between groups. By again including the scores of the 12 schizophrenic subjects from our previous study in the data analysis, we were also able to address the effect of severity of symptomatology on error-correcting ability. Spearman correlation coefficients were calculated between all test variables and (1) total BPRS score, (2) score on “positive symptoms” subscale (see Scoring section for details), and (3) score on “negative symptoms” subscale. There was no significant correlation between the total BPRS score or the severity of positive symptoms and any test variable. Surprisingly, there was a significant correlation between the probability of reversing a false move, that is, error-correcting ability, and the severity of negative symptoms (r, = 0.64, p = 0.01). An interesting hypothesis that might account for this observation has been described by Kometsky (Kometsky and Mirsky 1966; Kometsky and Orzack 1978b). In his hyperarousal model, Kometsky has suggested that schizophrenic subjects’ impaired performance on a number of tasks (e.g., the Continuous Performance Test) reflects a deficit in attention due to a central (nervous system) state of hyperarousal. From both animal and human studies, he has further suggested an inverted U model, with performance on the ordinate and “arousal level” on the abcissa. If we accept this model and assume that a level of central hyperarousal can, at least in part, account for the schizophrenic subjects’ impaired performances on our task, then, following the inverted U model, a decrease in arousal should improve performance. A possible clinical reflection of decreased arousal could be an increase in negative symptoms, thus accounting for the initially puzzling correlation. An argument against the hyperarousal model is that patients on neuroleptics, which presumably decrease basal arousal, were no better on our task than unmedicated patients. However, our study design involved between-subject comparisons, and to evaluate fully the effect of medication on task performance, intrasubject comparisons should be made. The hypothesis that subjects utilize internal, self-generated cues to monitor and correct their moves has been presented and analyzed previously (Angel 1976; Malenka et al. 1982). We proposed either a faulty “monitor” or faulty internal feedback (possibly in the form of a corollary discharge) to account for the poor error-correcting performance of schizophrenic subjects (Malenka et al. 1982). Several lines of inquiry provide a context for understanding the possible pathophysiological and psychopathological implications of a discrete error-correcting deficit in schizophrenic subjects. The frontal lobes have long been implicated in the feedback modulation of ongoing behavior (Luria 1980). Patients with frontal lobe damage and animals that have undergone frontal lobe lesioning demonstrate marked deficits in goal-directed behavior, on tasks that require monitoring external conditions, and in organizing sequential motor behavior (Teuber 1966; Luria 1980; Levin 1984b). Recent studies of regional cerebral blood flow and metabolism have demonstrated decreased activity in the frontal lobes of schizophrenics
K.C’. Mslenka et al
when compared with control subJects (lngvar and Franzen 1974; Buchsbaum et al. 1982. Wolkin et al. 1985) (although this relative hypofrontality may not be limited only tcr schizophrenic subjects; see Buchsbaum et al. 1984). It has been suggested that onebehavioral reflection of frontal lobe dysfunction may be the well-documented abnormalit) of smooth-pursuit eye movements found in most schizophrenic subjects (Levin 1984a,b) Both smooth-pursuit eye movements and error-correcting involve extensive feedback control of ongoing behavior, and both appear to utilize corollary discharge (efferencc copy) (Angel 1976; Jeannerod et al. 1979; Malenka et al. 1982). the use of which ma> be impaired in patients with frontal lobe lesions (Teuber 1966; Levin 1984b). It is tempting to speculate that frontal lobe dysfunction may account for both error-correcting and eye tracking abnormalities in schizophrenia. Error-correcting deficits may also be related to the peculiarities of communication common to schizophrenics. Cohen ( 1978). who has studied schizophrenic language. suggests that the deficits exhibited by schizophrenics in communication accuracy are due to faulty self-editing. a construct analogous at the motor level to our proposed fault! monitor. He goes on to suggest that “the same basic perservative tendency--the inability to reject a sampled response effectively-underlies the speaker deficits in both early- and long-term schizophrenia,” (Cohen 1978). It thus appears that the same informationprocessing mechanisms (self-editing or monitoring) may be utilized at both motor and linguistic levels. A theory of the development of psychosis that implicates defective self-monitorinp has been put forth by Klein and colleagues ( IWO). They propose that we continually and spontaneously generate internal propositional templates based on experience and validate these against external data. Psychosis develops when a “match-mismatch. self-critical mechanism” becomes deranged. The only significant difference between their proposal and our central monitor is that in performing our task, the subject is given externally (hk the experimenter) an internal reference to maintain, whereas the concept of psychosi\ described above depends on spontaneously self-generated propositions. Again, an inpairment in monitoring is implicated. In summary. we have presented further evidence in support of the hypothesis that schizophrenic subjects exhibit an impaired ability to monitor ongoing motor behavior on the basis of internal. self-generated cues. This deficit is not apparent in normal or depressed subjects, suggesting it may be specific for schizophrenics. Longitudinal data, comparing the same subject’s performance during different clinical states, are needed to determine whether this is a state or trait variable
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Central Error-Correcting Behavior in Schizophrenia and Depression Robert C. Malenka, Ronald W. Angel, Sue Thiemann, Charles J. Weitz, and Philip A. Berger
A previous study suggested that schizophrenic subjects exhibit an impaired ability to correct their own errors of movement without using exteroceptive signals. However, the performance of schizophrenic subjects was compared to that of only one other psychiatric group (alcoholic subjects), and a relatively small number of subjects was studied. To investigate the specificity of the postulated impairment, 9 schizophrenic, I I depressed, and 8 normal subjects performed a tracking task designed to prevent the use of exteroceptive cues in correcting errors of movement. The depressed and normal groups did not differ signi$cantly on any performance measure, but the schizophrenic subjects again demonstrated a gross impairment in correcting errors, yet no impairment in initiating correct responses. These findings suggest that the impaired ability to monitor ongoing motor behavior on the basis of internal, self-generated cues may be specific to schizophrenia among major psychiatric disorders.
Introduction Normal subjects can recognize and correct errors of movement under experimental conditions that preclude the use of exteroceptive signals (Rabbitt 1966a, 1968; Angel and Higgins 1969; Angel et al. 197 1; Angel 1976). In such experiments, error-correcting behavior must be presumed to depend on internal, self-generated cues. Hence, the ability to monitor movements and correct errors appears to involve central feedback pathways. In a previous study (Malenka et al. 1982), we examined the error-correcting ability of a group of schizophrenic subjects in comparison with age-matched normal and alcoholic subjects. Using a simple visual tracking task, in which feedback about the accuracy of tracking was blocked, we found that schizophrenic subjects exhibited a grossly impaired ability to correct errors of movement. We suggested that this impairment could not be
From the Department of Psychiatry and Behavioral Sciences. Stanford University School of Medicine, Stanford, CA and Palo Alto Veterans Administration Medical Center. Palo Alto, CA (R.C.M., S.T., P.A.B.); the Department of Neurology, Palo Alto Veterans Administration Medical Center and Stanford University School of Medicine (R.W.A.); and the Division uf Neurosurgery. Stanford University School of Medicine (C.J.W.). Supported in pail by NIMH Grant MH-30854 to the Norris Mental Health Clinical Research Center at Stanford University and a grant from the Research Service of the Veterans Administration to the Schizophrenia Biologic Research Center at Palo Alto VA Medical Center. Address reprint requests to Dr. Philip A. Berger, Department of Psychiatry and Behavioral Sciences, Stanford University. Stanford, CA 94305. Received July 1, 1985; revised September 14, 1985.
0 1986 Society of Bmlogical Psychiatry
0006.3223/86/$03.50
explained by nonspecific factors, such as amotivation or gross inattention. and therefort might refiect aspects of the pathophysioi~)gy underlying the schizophrenic syndrome. However. schizophrenic subjects differ from normal subjects on an eno~(~us variety of psychological and phys;oi~~gicai variables. ranging from reaction time (King 1965) and attentional tasks (Kornetsky and Orzack 197Xa) to cerebral blood flow (Ingvar and FranLen. 1974) and brain electrical activity (BEAM) (Morihisa et al. 1983). Moreover, there IS usually a signiticant overlap between the performance of schizophrenic subjects and that of normal sub,jects. making it difficult to state whether or not an observed abnormality is “specific” for schizophreni;r An experimental design that begins to address this problem is one that makes ;: conlparis~)n between the ~rf~~rmance of schizophrenic subjects and that of subjects carrying other psychiatric diagnoses. Signiticant differences between these groups cannl>t bc attributed to general features of‘ psychiatric tllness and, therefore, might have impli cations for understanding schizophrenia. In order to begin to address the question cri specificity. we compared the performances of patients carrying the diagnosis of majo) depressive disorder with thorc of schizophrenic and normal control subjects. By including the schizophrenic subjects from our previous study. we were also able to examine how eager-correcting behavior W;I~ affected by nellr~)~eptic ~nedicati(~n and severity of symp toniatolopy
Methods Our study compared three groups performing a single task. All sub_jects were right-hand dominant by verbal report. The primary experimental group comprised nine schizophrenic subjects (all men) at the Palo Alto Veterans Administratit~n Medical Center. Ages ranged from 2X to 55 years (mean 33.-3). and the average aIllount of schooling was 13.5 years. Diagnostic categories consisted of chronic schizophrenia (paranoid, 3 patients: undifferentiated. 3 patients: residual. 1 patient) and subchronic schizophrenia (undifferentiated. I patient; disorganized. I patient). Three of these patients were considered to be drug free, having taken no psychotropic medications for a minimum of 2 weeks prior to the date of the test. Six schizophrenic patients were on neuroleptic medications, speciticallv thiothixene ( 10-80 mglday) or piquindone. which is a neuroleptic presentfy under clinical investigati~~n. All diagnoses were determined by Research diagnostic Criteria (RIX’: Spitzcr et al. 1978) and were based on two focused interviews conducted by two trained personnel. a physician and a research nurse or assistant. R&ability studies demonstrdtc high interrater reliability for this system of diagnosis. with kappa values ranging from 0.77 to 0.87, depending on the diagnosticians sampled. Eight normal control subjects were tested (six men, two women). ‘Their ages ranged from 20 to 3 I years (mean 76.5). and the average educational level was 13 years. These subjects were either staff members or undergraduate students. None had any history 01 psychiatric or neurological illness. A second control group was made up of I I subjects (all men) diagnosed as major depressive disorder. Diagnoses were made by the procedure described above for the schizophrenic patients. Patients’ ages ranged from 23 to 60 (mean 35.1 ). and average educational level was 13.5 years. None of these patients was taking any psychotropic medication or had taken any for a minimum of 2. weeks prior to the test date. Written informed consent was obtained from all subjects after the purpose and possible risks of the study were explained.
Error-Correcting Behavior
Apparatus
BIOL PSYCHIATRY 1986;21:263-273
265
and Procedure
Details of the apparatus and experimental procedure have been published previously (Malenka et al. 1982). The subject was seated facing an oscilloscope screen on which two vertical lines, the target and cursor, were displayed. The location of the target line was controlled by a frequency-modulation tape recorder. At each instant, the target occupied one of three positions: the center of the screen, 3 cm to the left, or 3 cm to the right. A sequence of 100 random target jumps was presented to each subject. The target remained in the left or right lateral position for 1 set and then returned to the center position for a variable period ranging from 2 to 6 sec. The subject was instructed to track the target by moving the cursor appropriately. The subject controlled cursor position by moving a joystick with the right hand. The directional relation between movement of the joystick and movement of the cursor was controlled by a polarity switch. When in the “normal” position, the cursor moved in the same direction as the joystick. When in the “reversed” position, the cursor and joystick moved in opposite directions (i.e., movement of the joystick to the left caused the cursor to move to the right). Following a demonstration, the subject was given a brief practice session consisting of 5-10 jumps. After this session, an opaque, 6-cm wide screen was placed over the center of the oscilloscope leaving 1 cm visible at each edge. With the opaque screen in place, the target and cursor were invisible except when displaced at least 3 cm to the right or left of center. The subject therefore had no visual feedback from the cursor until his movement was nearly complete, although the target was clearly visible in the lateral positions. The subject then was given another short practice session in which the polarity switch was first in the normal position (for five jumps) and then in the reversed position (for five jumps). At this time, the subject was informed that after each block of 10 jumps, the polarity control switch would be reversed and that he would be verbally warned prior to each polarity reversal. Immediately before the start of the experiment, the polarity control was put in the normal position and the subject was requested to move the cursor so that it was barely visible, first on the left side of the opaque screen then on the right side. These positions were recorded so that the experimenter would have a record to determine whether or not the cursor had been visible at any given time during the experiment. Scoring The movements of the target and cursor were recorded on a strip-chart recorder at a paper speed of 25 mmsec or on digital tape using a Nicolet 1129 signal averager. Each response was classified as one of the following: (1) correct move, not reversed (C&-the subject moved his cursor initially in the correct direction and continued in this direction until the cursor became visible; (2) correct move, reversed (CR)--the subject began moving the cursor in the correct direction but reversed direction _while the cursor was still hidden by the opaque screen; (3) false move, not reversed (FR)--the subject started moving the cursor in the wrong direction and did not reverse direction until the cursor became visible; (4) false move, reversed (FRethe subject moved the cursor initially in the wrong direction but reversed direction while the cursor was still screened from view; and (5) reject-a given response was rejected whenever (A) the cursor was visible at the time of the target jump, (B) the cursor was moving at the time of the target jump, and/or (C)
K.C.
Malcnka
et ;li
the cursor‘s movement wa\ reversed more than once before it was visible. The numbetot rejected responses did not differ significantly between the experimental groups. Not including the rejected responses, each subject completed a total of 100 moves (TM\ Responses were analyzed without knowledge of the subject’s diagnosis. All of the schizophrenic subjects were scored weekly on the Brief Psychiatric Rating Scale (BPRS: Overall and Gorham 1962). providing an opportunity to compare severit:, of symptomatology with impaired performance on our experimental task. Scores from the week of the test were averaged with scores from the week preceding and the wech following the test to provide a more accurate description of clinical state. Three scorch were calculated for each subject: ( I) total BPRS score, (2) total score on “positivi, symptoms” t&
Nonparametric statistical techniques were used to test for differences between groups III order to avoid making any assumptions about the distribution of error-correcting abiiitb in the populations sampled. All data were entered into an IBM Model 3081 computer and were analyzed using the Statistical Analysis System software package. Groups were first compared with the Kruskal-Wallis one-way analysis of variance. If this test showed significant differences. pairwise comparisons were made using the Mann-Whitney LJ-test. To investigate associations among the variables, Spearman correlation coefticients were calculated.
Results This investigation examined the ability of schizophrenics to monitor their movements and correct errors using self-generated cues. Our experimental design provided two scores that reflect this ability: ( I) the probability that an initially false move would be reversed while the cursor wa4 still invisible [FR/(FR + FE11 and (2) the probability that an initiali] correct move would be reversed [CR/(CR + CR)]. If the subject was always able to recognize and correct error4 without using cxteroceptive signals. his score on the first
Error-Correcting Behavior
267
BIOL PSYCHIATRY 1986;21:263-273
Table 2. Diagnoses and Test Scores of Depressed Subjects Subject 1 2 3 4 5 6 7 8 9 10 11
Age/sex 42/M 57/M 23/M 54/M 43/M 55/M 35/M 60/M 44/M 53/M 52/M
Psychiatric Major Major Major Major Major Major Major Major Major Major Major
diagnosis”
depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder depressive disorder
CR + CR ~
FR + CR ~
TM
TM
0.82 0.92 0.78 0.84 0.97 0.90 0.92 0.91 0.82 0.67 0.85
0.14 0.03 0.22 0.11 0.03 0.07 0.06 0.06 0.14 0.30 0.12
FR FR
CR CR
0.78 0.75 1.00 0.73 1.00 0.70 0.75 0.75 0.72 0.89 0.91
0.00 0.00
0.00 0.00 0.00
0.00 0.00
0.00 0.01 0.01 0.01
“Diagnoses were made according to Research Diagnostic Criteria.
measure would be 1.O. If he was also always able to recognize a correct move as correct and therefore never reverse it, his score on the second measure would be 0. In the normal group (Table 1), the probability of reversing a false move was 0.8 1, with scores ranging from 0.60 to 1.O. Six of eight subjects (75%) had scores greater than 0.70. In the depressed group (Table 2), the probability of reversing a false move was 0.82, with scores ranging from 0.70 to 1.O. Eleven of 12 depressed subjects (92%) had a score greater than 0.70. Both normal and depressed subjects were also able to recognize correct moves. Only 2 of 8 normal subjects (25%) and 3 of 11 depressed subjects (27%) reversed any correct move (the probability of reversing a correct move was less than 0.01 for either group). There were no significant differences between normal and depressed subjects in either the probability of reversing a false move or the probability of reversing a correct move. These findings suggest that depression, per se, does not interfere with the ability to monitor movement or correct errors without exteroceptive feedback. As previously reported, the scores of the schizophrenic subjects (Table 3) are in sharp contrast to those of the control subjects. Their probability of reversing a false move was 0.53, with scores ranging from 0.25 to 1.0. Only 2 of 9 schizophrenic subjects (22%) had a score greater than 0.70. Schizophrenic subjects were also deficient in their ability to recognize correct moves. Seven of the nine schizophrenic subjects (78%) reversed at least one correct move. The schizophrenic subjects’ probability of reversing a false move was significantly different from that of either the normal 0, = 0.03) or depressed @ = 0.01) subjects (Figure 1). Their probability of reversing a correct move was also significantly different from that of depressed (p = 0.02) subjects and barely missed significance when compared with the normal group (p = 0.06). The large differences between the schizophrenic and normal or depressed subjects on these measures of error-correcting ability lend strong support to our hypothesis that schizophrenic subjects have an impaired ability to recognize and correct movement errors without using exteroceptive feedback. In our previous study, we reported no difference between groups in the ability to initiate correct responses. This ability was measured by dividing the total number of correct moves by the total number of moves [(CR + CR)/TM]. This investigation also revealed no significant difference between the schizophrenic subjects’ scores and those of the two control groups. The normal group’s probability of initiating a correct move
h 7 8 9
5
1 2 3 3
Schizophrenia. Schizophrenia, Schizophrenta. Schizophrema. Schizophrenia, Schizophrenia. Schizophrenia. Schizophrenia,
39/M 29/M 26/M 55/M 27/M 30/M 30/M 31/M
Subject5
..~
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~20,
0.88 0.90 0.85 0.80 (I.72 0.96 0.88 0.62 0.80
Thf
____
r;R
.__
I201
hydrochloride
-...(80) c 10)
hydrochloride hydrochloride
MtXiGiUo~~s’
Thiothixene Thiothixene chronic. undifferentiated Piquindone chronic. paranoid Thiothiwene chronic. undifferentiated Yone chrome. residual Thiothtrene wbchromc. disorganized subchronic. undifferentlared None None chronic. paranoid Piqumdontl chronic. paranoid ._---.-
Schizophrenia. chronic. undifferentiated
P\>I tuatrlc dlagno\th’,
32/M
.-\geiscr
Diagnosis and ‘l‘eat Scores tar Schizophremc
“Dragnoses were made ~ccordmg 10 Raearch Dwgo~tic Cntsn.~ The number\ !!I parentheses are lhe ddil~ dnwge~ in nllll~grar~l~
Subject --.-
Table i C‘R
(1.08 0.06 0.04 0.15 (1.14 11.05 0. 10 0.14 0. 10
TM
_.._ ..-
FK + CR
! .fXl Cl.83 0.25 0 35
0.01 0.08 0.01 0 00 0.07 0 01
0.01 0.00
O.I!5 0.6X !).;IY
0.01 0 50
(‘R
0.5x
FR
Error-Correcting
BIOL PSYCHIATRY 1986;21:263-273
Behavior
A.
Correct Move
([CR*@]
TM)
C.Reversal,
B. Reversal
F&e
([FR+CR]:TM)
269
D. Reversal, Given
Given
Move
Correct Move
(FR,[FR*~*])
(cR,[cR~])
1.oo .80 s. I= li5 x l;z
.60
*
.40 .20 0
i
N
D
S
N
D
S
n
f
D
S
NDS
) ~obabilit: Y( )f initiating a correct Figure I. Probabilities calculated for each subject g ro up. move. (b) ProbabiIity of reversing a move. (cf ~obability of reversing a move, given that it was initially false. (d) Probability of reversing a move, given that it was initially correct. N indicates normal subjects; D indicates depressed subjects; S indicates schizophrenic subjects. Formulas in parentheses were used to calculate various probabilities. Asterisk (*) indicates statistically significant (p < 0.05) difference between the schizophrenic group and either the normal or depressed groups (c) or between the schizophrenic and depressed groups (d).
was 0.89, with scores ranging from 0.80 to 0.97. The depressed group’s scores ranged from 0.67 to 0.97, with a mean of 0.84. The schizophrenic subjects’ scores ranged from 0.62 to 0.96, with a mean of 0.82. These scores were not signilicantly different. Thus, the schizophrenic subjects exhibited a normal ability to initiate correct responses, but had a gross impairment in the ability to amend false moves. As the schizophrenic subjects were less likely to reverse a false move, we examined the probability of reversing a move without regard to its initial correctness [(CR + FR)/TM]. There was no significant difference among groups on this measure. This indicates that schizophrenic subjects’ impai~ent in reversing false moves cannot be explained by simply ~stulating that they had a decreased tendency or ability to reverse moves. Before discussing our findings, it is important to mention a number of “nonspecific” variabIes that were analyzed in order to insure that they were not affecting our results. The first is age. The depressed subjects, as a group, were significantly older than the other two groups. However, as previously noted, there were no differences between the normal and depressed groups on any performance measure. Furthermore, age did not covary with any of the scores. Both of these findings suggest that age differences between subjects cannot account for our results. A second important variable is sex differences. As our normal group contained two women, whereas the depressed and schizophrenic subjects were all men, we reanalyzed our data, deleting the women. No differences from
270
BIOL PSYCHIATK’I 198h.ll 263 273
ICC‘. Malenka et ;11
the results reported above were found. There were no differences among groups m educational level. and as the two patient groups both consisted of inpatients at the Palo Alto Veterans Administration Medical Center. it seems doubtful that environmental factors can account for the reported differences between groups.
Discussion The goals of this study were: ( I) to retest the hypothesis that schizophrenic subjects arc deficient in the ability to monitor their motor behavior without use of exteroceptive cues, and (2) to compare their performance with that of patients with major depressive disorder. In our previous study (Malenka et al. 1982). schizophrenic subjects differed from normal and alcoholic subjects both in the ability to recognize and reverse false moves and in the tendency to reverse correct moves. Both of these measurements reflect an impaired ability to monitor ongoing behavior by means of internal, self-generated cues. No significant differences were found between the normal and alcoholic groups on any test variable. We now report a significant difference between schizophrenic and depressed subjects and between schizophrenic and normal subjects in error-correcting performance. No significant differences were found between normal and depressed subjects. These results make it unlikely that nonspecilic features of psychiatric illness or ho>pitalization for its treatment can account for poor performance on our experimental task The deficit in error-correcting displayed by the schizophrenic subjects may therefore refect a central nervous system dysfunction that is unique to the schizophrenic syndrome. This conclusion must be tempered by the knowledge that a relatively small and heterogeneous group of schizophrenic subjects was studied. Furthermore. the majority of dcpressed subjects did not exhibit clinically significant thought disorder. which may affect error-correcting perfomrance independently of the diagnosis of schizophrenia. Several variables that we did not or were unable to examine directly in the schizophrenic subjects, such as IQ. motivational level, or degree of organicity. might be expected to significantly affect performance on our task. However, the schizophrenic group did not exhibit an impairment in the ability to initiate correct responses. This strongly suggests that they were able to learn and to perform the task as well as either the depressed otnormal sub.jects. Thus, as discussed previously (Malenka et al. 1982), nonspecific factors. such as inconstant motivation, are unlikely to account for the impaired performance ol schizophrenic subjects. Instead, we propose that schizophrenic subjects suffer from :I distinct defect in error-correcting processes. An analysis of when during the experiment the schizophrenic subjects made their error\ might be expected to contribute to the understanding of the defect underlying their impaired performance. Such an examination of the data revealed no significant pattern. The errors in error-correcting performance (CR and FR) seemed to be randomly distributed. The inability to tind a significant trend may be a reflection of the small number of error’ available for analysis. It is clearly important to continue this analysis as more subject4 are studied. Because of the relatively small number of subjects in this study, it was not possible to determine the effects of medication on schizophrenic subject performance. However. as this is a critical issue in all studies of schizophrenic patients, we expanded our sample size in order to make a valid comparison between medicated and nonmedicated subjects This was accomplished by including 12 subjects carrying the diagnosis of schizophrema trom our previous study (diagnostic categories included chronic paranoid, 2 subject&
Error-Correcting Behavior
BIOLPSYCHIATRY 1986:21:263-273
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chronic undifferentiated, 6 subjects; chronic residual, 1 subject; subchronic paranoid, 2 subjects; and acute undifferentiated, 1 subject), thus yielding a total of 21 subjects for comparison-10 on neuroleptic medication and 11 who had been drug free for a minimum of 2 weeks. The only significant difference between the two groups was in the probability of rerversing a move, without regard to its initial correctness [(CR + FR)/TM]. Medicated schizophrenic subjects exhibited a tendency to reverse fewer moves than nonmedicated schizophrenic subjects. Considering the well-documented Parkinson-like side effects of neuroleptic medication, this is not a surprising result. Medication status did not contribute significantly to our results, as statistical reanalysis with the medicated schizophrenic subjects deleted had no effect on the reported differences between groups. By again including the scores of the 12 schizophrenic subjects from our previous study in the data analysis, we were also able to address the effect of severity of symptomatology on error-correcting ability. Spearman correlation coefficients were calculated between all test variables and (1) total BPRS score, (2) score on “positive symptoms” subscale (see Scoring section for details), and (3) score on “negative symptoms” subscale. There was no significant correlation between the total BPRS score or the severity of positive symptoms and any test variable. Surprisingly, there was a significant correlation between the probability of reversing a false move, that is, error-correcting ability, and the severity of negative symptoms (r, = 0.64, p = 0.01). An interesting hypothesis that might account for this observation has been described by Kometsky (Kometsky and Mirsky 1966; Kometsky and Orzack 1978b). In his hyperarousal model, Kometsky has suggested that schizophrenic subjects’ impaired performance on a number of tasks (e.g., the Continuous Performance Test) reflects a deficit in attention due to a central (nervous system) state of hyperarousal. From both animal and human studies, he has further suggested an inverted U model, with performance on the ordinate and “arousal level” on the abcissa. If we accept this model and assume that a level of central hyperarousal can, at least in part, account for the schizophrenic subjects’ impaired performances on our task, then, following the inverted U model, a decrease in arousal should improve performance. A possible clinical reflection of decreased arousal could be an increase in negative symptoms, thus accounting for the initially puzzling correlation. An argument against the hyperarousal model is that patients on neuroleptics, which presumably decrease basal arousal, were no better on our task than unmedicated patients. However, our study design involved between-subject comparisons, and to evaluate fully the effect of medication on task performance, intrasubject comparisons should be made. The hypothesis that subjects utilize internal, self-generated cues to monitor and correct their moves has been presented and analyzed previously (Angel 1976; Malenka et al. 1982). We proposed either a faulty “monitor” or faulty internal feedback (possibly in the form of a corollary discharge) to account for the poor error-correcting performance of schizophrenic subjects (Malenka et al. 1982). Several lines of inquiry provide a context for understanding the possible pathophysiological and psychopathological implications of a discrete error-correcting deficit in schizophrenic subjects. The frontal lobes have long been implicated in the feedback modulation of ongoing behavior (Luria 1980). Patients with frontal lobe damage and animals that have undergone frontal lobe lesioning demonstrate marked deficits in goal-directed behavior, on tasks that require monitoring external conditions, and in organizing sequential motor behavior (Teuber 1966; Luria 1980; Levin 1984b). Recent studies of regional cerebral blood flow and metabolism have demonstrated decreased activity in the frontal lobes of schizophrenics
K.C’. Mslenka et al
when compared with control subJects (lngvar and Franzen 1974; Buchsbaum et al. 1982. Wolkin et al. 1985) (although this relative hypofrontality may not be limited only tcr schizophrenic subjects; see Buchsbaum et al. 1984). It has been suggested that onebehavioral reflection of frontal lobe dysfunction may be the well-documented abnormalit) of smooth-pursuit eye movements found in most schizophrenic subjects (Levin 1984a,b) Both smooth-pursuit eye movements and error-correcting involve extensive feedback control of ongoing behavior, and both appear to utilize corollary discharge (efferencc copy) (Angel 1976; Jeannerod et al. 1979; Malenka et al. 1982). the use of which ma> be impaired in patients with frontal lobe lesions (Teuber 1966; Levin 1984b). It is tempting to speculate that frontal lobe dysfunction may account for both error-correcting and eye tracking abnormalities in schizophrenia. Error-correcting deficits may also be related to the peculiarities of communication common to schizophrenics. Cohen ( 1978). who has studied schizophrenic language. suggests that the deficits exhibited by schizophrenics in communication accuracy are due to faulty self-editing. a construct analogous at the motor level to our proposed fault! monitor. He goes on to suggest that “the same basic perservative tendency--the inability to reject a sampled response effectively-underlies the speaker deficits in both early- and long-term schizophrenia,” (Cohen 1978). It thus appears that the same informationprocessing mechanisms (self-editing or monitoring) may be utilized at both motor and linguistic levels. A theory of the development of psychosis that implicates defective self-monitorinp has been put forth by Klein and colleagues ( IWO). They propose that we continually and spontaneously generate internal propositional templates based on experience and validate these against external data. Psychosis develops when a “match-mismatch. self-critical mechanism” becomes deranged. The only significant difference between their proposal and our central monitor is that in performing our task, the subject is given externally (hk the experimenter) an internal reference to maintain, whereas the concept of psychosi\ described above depends on spontaneously self-generated propositions. Again, an inpairment in monitoring is implicated. In summary. we have presented further evidence in support of the hypothesis that schizophrenic subjects exhibit an impaired ability to monitor ongoing motor behavior on the basis of internal. self-generated cues. This deficit is not apparent in normal or depressed subjects, suggesting it may be specific for schizophrenics. Longitudinal data, comparing the same subject’s performance during different clinical states, are needed to determine whether this is a state or trait variable
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