Biofeedback and Self-Regulation, Vol. 16, No. 2, 1991
The Effects of Electromyographic Feedback Training on Suppression of the Oral-Lingual Movements Associated with Tardive Dyskinesia I Ronald C. Fudge 2 and Sheryl A. Thailer Franklin Delano Roosevelt Veterans Hospital
Murray Alpert New York University Medical Center
Joanne Intrator and Cecile E. Sison Franklin Delano Roosevelt Veterans Hospital
The efficacy of electromyographic feedback training in reducing the magnitude and frequency of the oral-lingual movements associated with tardive dyskinesia (TD) was investigated in a groups design. Twenty adult male inpatients diagnosed as having TD using the Abnormal Involuntary Movements Scale (AIMS) were randomly assigned to one of two treatment conditions. Following identification, all participants were initially reduced to the lowest effective dosage of neuroleptics, and then discontinued from anticholinergics. Following one month on this regimen, they were given a course of feedback training consisting of ten 14-minute sessions. Group one participants were provided with a tone contingent upon oral-lingual movements above a yoked threshold. Group two participants were given noncontingent feedback tones generated randomly. Weekly AIMS were administered as well as an initial baseline during each session to determine current level of oral-lingual activity. An analysis of session effects indicated significantly more suppression of oral-lingual activity in the contingent group versus the noncontingent feedback group. Jaw and forehead IThis work was sponsored in part by a Research Advisory Grant from the Department of Veterans Affairs awarded to Joanne Intrator. We gratefully acknowledge the valuable contributions of K. Duvvi, S. Kemble, and L. Kolman. 2Address all correspondence to Dr. Ronald C. Fudge, FDR Hospital, Psychology Service (116B), Montrose, New York 10548. 117 o363-3586t91/o6oo-o1175o6.5o/o© 1991 PlenumPublishingCorporation
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activity also measured showed reductions of similar magnitudes for both groups. KEY WORDS: electromyographicbiofeedback;tardive dyskinesia;neuroleptics; movementdisorders.
Tardive dyskinesia (TD), an involuntary movement disorder occurring subsequent to chronic neuroleptic administration, has most often b e e n a s s o c i a t e d with o r a l - b u c c o - l i n g u a l m o v e m e n t s ( T a r s y & Baldessarini, 1984; Barnes, 1987; Yagi & Itoh, 1987; Barnes, 1988). Such movements often involve tongue protrusion, grimacing, and masticatory movements. Typically, these abnormal involuntary movements have been characterized as being out of the awareness of the patient (Alexopoulos, 1979). Such movements are likely to increase when the patient is involved in simple motor tasks, although engaging the patient's attention while relaxed may also be associated with large amplitude, regular movements. While the etiology of TD is thought to be related to the physiological concomitants of pharmacological interventions, motor awareness, and attentional factors have also been reported to be involved in movement f r e q u e n c y and amplitude (Jeste & Wyatt, 1982; Kane, W o e r n e r , Lieberman, & Kinon, 1984). Biofeedback and other behavioral techniques have often been thought to be effective by enhancing the awareness of a particular behavior, and thereby enabling increasing control over that behavior (Brener, 1974; Fudge & Adams, 1985; Bayles & Cleary, 1986). Our investigation of the phenomena of TD led us to conclude that increasing a subject's awareness of certain TD movements may lead to a reduction in the frequency and severity of movements (Taylor, Zlutnick, & Hoehle, 1979). Since the oralbucco-lingual movements of TD necessarily involve somatic muscle activity, electromyographic feedback of the oral area seemed logical. A search of the biofeedback literature led us to four reports in which electromyographic (EMG) biofeedback was used to suppress the involuntary movements of TD (Albanese & Gaarder, 1977; Farrar, 1976; Sherman, 1979; Jackson, Schonfeld, & Griffith, 1983) with some evidence of positive benefit. However, all four studies lacked systematic controls, were extremely small in their numbers of participants, and in general produced results that were difficult to interpret. While these four studies provided limited support for using biofeedback with TD, there is a more substantial literature on the usefulness of biofeedback for other motor disorders, including torticollis (e.g., Roxanas, Thomas, & Rapp, 1978), stroke paralysis (e.g., Bodenhamer, Coleman, & Achterberg, 1986; Fields, 1987), hemifacial spasm (e.g., Rubow, Rosenbek, Collins, & Celesia, 1984), and sphincter
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control (e.g., MacLeod, 1983), with some evidence for efficacy. These motor disorders, while phenomenologically different from TD, provided a basis for investigating the efficacy of biofeedback with TD. The present study was designed to examine issues in utilizing an E M G biofeedback training procedure with chronic psychiatric inpatients. Such patients are typically maintained on the same psychotropic medications implicated in the pathogenesis of the disorder. Our initial focus was on the signal value of a mildly noxious tone made contiguous with tongue activity. We included a group of participants presented with a randomized noncontingent tone. We also examined jaw and brow motor activity, two areas also frequently affected in TD, for insight into the specificity of the tongue activity feedback. Additionally, we examined within session and progressive cross-session changes, as well as generalization from the feedback laboratory to the clinic situation and to the ward.
METHODS
Participants Twenty males, inpatients at the F D R VA Hospital, Montrose, New York, volunteered and provided written informed consent for the study. Patients were rated weekly on an assessment battery that included the Abnormal Involuntary Movement Scale (AIMS; Guy, 1976). Those patients with a score indicating at least mild T D (rated as 2) in 2 of the first 4 AIMS areas (areas involving facial movements), or a single score of 3 (moderate) in one of these areas were considered for the study. Mean pretreatment total AIMS scores were 19.2, with a range of 13-28. Three AIMS raters were calibrated with each other at baseline, achieving an interrater reliability of r = .71. All volunteers had at least a 9-month history of TD, and a minimum of 2 years of neuroleptic medication. Ten participants were randomly assigned to one of two groups (true feedback or false feedback). Participants were excluded if they had a concurrent neurological disorder or severe, u n c o r r e c t e d d e n t a l p a t h o l o g y which might mask or p o t e n t i a t e T D symptoms. The Mini-Mental Examination (Folstein, Folstein, & McHugh, 1975) was administered at baseline to identify patients who were too severely d e m e n t e d to c o o p e r a t e . Participants with a score g r e a t e r than 20 qualified for the study. The mean Mini-Ment score was 26.3, with a range of 22-30. In addition, the Brief Psychiatric Rating Scale (BPRS, Overall & Gorham, 1962) was administered weekly to monitor psychopathology during the course of
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the study. BPRS scores averaged 14.6, with a range of 4-32. DSM-III-R (APA, 1987) diagnoses were determined by experienced clinicians using the Schedule for Affective Disorders and Schizophrenia (SADS; Endicott & Spitzer, 1978). T e n participants were diagnosed as Schizophrenia, Chronic Undifferentiated type; 3 as Schizoaffective, Mainly Depressed; 6 as Bipolar Disorder; and 1 as Major Depressive Disorder. Participants ranged in age from 45 to 72 years, with an average of 61 years.
PROCEDURES
Apparatus E M G signals were recorded using Grass model 7P511 amplifiers with a .3-second time constant. Amplified E M G signals were integrated via Coulbourn integrators, interfaced with an IBM AT/PC computer through a Coulbourn 8-bit A/D converter. Physiological data were recorded on line using an IBM/AT PC computer with a sampling rate of 1 ms/sample. Feedback and data transformations, and storage were all processed by computer. E M G activity was detected using 1-cm silver-silver chloride prejelled disposable electrodes (Ver Med Associates). Participants were seated in a reclining chair, adjusted to their needs, in an air conditioned sound attenuating room. To reduce extraneous noise, participants received their instructions and feedback tones through headphones. Both groups were given the same instructions: "Occasionally you will hear a tone when you are making mouth movements. Try to relax your mouth and turn off the tone."
Dose Adjustment Prior to initiation of the feedback phase of the study neuroleptic and anticholinergic medications were reduced in an attempt to find the "lowest effective dose" for each patient according to the following rules: 1. 2.
Patients on more than one neuroleptic were shifted to a single drug. The dose of the neuroleptic was reduced in weekly 20% decrements. Reductions were titrated against BPRS scores and ceased when a zero dose was achieved, or BPRS scores (raters were blind as to dose adjustment) increased by 20%. Under these conditions all patients failed to achieve a zero dose.
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Table I. Psychotropic Medications in Mean Dosage per Day
Neuroleptics
Number
Chlorpromazine Thioridazine Haloperidol Fluphenazine Thiothixene Perphenazine Mesoridazine
4 2 3 2 3 1 1
Other medications Lithium Clonazepam Lorazepam Imipramine
3.
CPZ Equiv. mg/day 480 415 650 600 160 100
Number
Mean Dose mg/day
2 2 1 1
900 1 1 100
After establishing the lowest functional neuroleptic dosage, anticholinergics were lowered in a similar fashion with placebos substituted for anticholinergics so that the n u m b e r of pills administered per day was constant. Extrapyramidal side effects were monitored on a blind basis. With the exception of one patient in the true f e e d b a c k group, who r e q u i r e d 6 rag/day of trihexphenidyl, it was possible to eliminate anticholinergic medications.
All patients were stabilized for at least one month on their lowest dose of neuroleptic before feedback training was started. Psychotropic medications taken by the study patients are described in Table I.
Training Sessions Each session began with a 4-minute baseline period, during which E M G lingual activity was determined and a threshold set. During this period no feedback was provided. Ten minutes of feedback training followed. D a t a were recorded continuously and integrated into 15-second epochs. E M G activity was recorded using bipolar electrodes from three sites; lingual, masseter, and frontalis. Lingual activity was detected from leads 1.5 cm apart on the ventral surface of the genioglossus muscle, midway between the neck and chin. Masseter activity was recorded with leads 1.5 cm apart on the dominant side at the temporo-mandibular junction. Frontalis activity was recorded from placements 1 cm above the nasion and 1 cm apart.
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Feedback The feedback signal was 440 Hz tone at 75 dB, contingent on lingual lead activity exceeding threshold levels. A moving window was used to determine and maintain threshold levels. This window permitted a degree of automated shaping. The window was established by averaging the initial three 15-second epochs of lingual activity. Starting with the fourth epoch, and continuing until the end of each training session, the threshold was recalculated by averaging the current epoch value with the mean of the two preceding epochs. The tone was enabled when the current E M G reading exceeded the threshold. Participants given noncontingent feedback received the same instructions as the true feedback group. The rate of false feedback was computergenerated at random intervals and calculated to match that of the true feedback group, so that the probability of a response occurring simultaneously with a real tongue movement remained at chance. Treatment was under double blind conditions, with feedback contingencies unknown to either the research technician or the participants.
Sessions All participants received daily sessions on ten consecutive weekdays. Each session consisted of an initial adaptation period of 4 minutes duration followed by 10 minutes of biofeedback training. AIMS ratings were done weekly.
Transformations of the EMG Data To facilitate between participant comparisons, and to ensure that each participant contributed equally to their treatment group, raw E M G levels were transformed as follows. Means were calculated separately for the tongue, jaw, and forehead E M G levels for all 15-second epochs of each session. For each participant, on each measure, the range (maximal minus minimal) for all epochs was calculated for each lead. The mean score for each participant was subtracted from each observed score and divided by the full range of the measure, thus yielding a range corrected score for E M G levels. These values were then used to determine a score reflecting the average E M G level during the initial 2 minutes of each session, for each measure (termed "First") and, similarly, for the last 2 minutes of each session (termed "Last"). These were the measures subm i t t e d to the statistical analyses described below. F o r simplicity of
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20 10 0 -10 -20 -30 -40 -50
;
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;
i
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lO
SESSIONS GROUPS CON-FEEDBACK
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Fig. l. TongueEMGscores. Last-Firstscoresoverallsessionsbygroups.
presentation, we also calculated a change score by subtracting the Last score f r o m the First score. While the graphic presentation is based on c h a n g e s c o r e s , t h e s t a t i s t i c a l analysis was b a s e d on A N O V A and A N C O V A of the First and Last scores.
RESULTS To examine the effects of biofeedback training on oral-buccal movements, the following analyses w e r e c o n d u c t e d : F o r e a c h group, a 3 (measures) x 10 (sessions) repeated measures A N C O V A procedure was done using the Last measure with First as covariate, to determine session training effects. A significant main effect was obtained for the true feedback group F(1, 12) -- 5.75, p < .05, indicating that scores tended to be lower by the end of each session. Effects for the false feedback group were not significant. In addition, there was a main effect of m e a s u r e F(2, 12) = 41.99, p < .001. T o n g u e E M G scores showed larger amounts of within session change than did those for jaw or forehead. T h e r e was also a main effect of sessions F(9, 12) = 2.64, p < .01. As will be seen below, this was
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30 20 10 0 -10 -20
-30
I
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i
L
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10
SESSIONS GROUPS CON-FEEDBACK
i
NONCON-FEEDBACK
~g. 2. Jaw EMGscores. Last-Firstscoresoverallsessionsbygroups.
not a reflection of a tendency for progressive improvement from day to day. Use of change scores (Last minus First) for each session is the easiest way to portray these effects, and these scores are presented in Figures 1, 2, and 3. T o examine the hypothesis that contingent feedback would produce a greater effect on oral-lingual movement than false feedback, the FirstLast intervals were examined over sessions for each measure. A two factor A N C O V A procedure, Last covaried with First, was employed to examine group differences. Significant group differences were found for the Tongue measure F (1, 10) = 4.89,p < .01. The true feedback group did significantly better than did the noncontingent feedback group on sessions 4 F (1, 17) = 6.39, p < .05, and 8 F ( 1 , 16) = 5.99, p < .05. No main effects for group were found on either the Jaw measure of the Forehead measure, indicating that training was specific to contingent feedback. The weekly AIMS scores (Sum of items 1-4, and Total Score) were examined in an A N C O V A comparing the true and false feedback groups with baseline as the covariate. No significant differences emerged. In fact, the scores for the two groups remained close throughout the rating period (see Figure 4).
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4O 30 2O 10 0 -10 -20 -30 -40
1
r
I
i
~
2
3
4
5
J___
6
I
L
q
7
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10
SESSIONS GROUPS ~< C O N - F E E D B A C K
I
NONCON
- FEEDBACK
Fig. 3. Forehead EMG scores. Last-First scores over all sessions by groups.
DISCUSSION Our results indicate that for within sessions, contingent feedback training produced a modest suppressive effect on lingual activity. This effect was specific to the target channel (tongue), with neither jaw nor brow activity showing a similar suppression of EMG levels. Our first goal was to replicate previous reports using double-blind procedures, randomized assignments to treatment groups, and a sufficient number of participants to support statistical analysis. While these results are somewhat more circumscribed than earlier reports, E M G feedback did produce a suppressive effect on the oral-buccal movements of TD. Since our design required a tightly controlled double blind with placebo control, we feel that these results are due to specific training effects rather than nonspecific placebo effects. Traditionally, biofeedback training is made contingent on a specific measure, providing an "if-then" signal for feedback. Since other muscle groups are known to be affected by TD (mainly jaw and forehead), the "if-then" (if tongue is > criterion, t h e n . . . ) contingency may not be the most productive m e t h o d o l o g y . C o n t i n g e n c i e s utilizing " a n d / o r " for
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25 20 15 10 5 0
FEEDBACK NO FEEDBACK
I
FEEDBACK
~
NO FEEDBACK
Fig. 4. Abnormal Involuntary Movements Scale. Total scores by groups during training.
activity of individual or groups of muscles in several facial areas would provide feedback for patterns of movement. We are examining our data base to identify such patterns across muscles and across patients in anticipation of follow-up studies. Utilization of " a n d / o r " contingencies would individualize f e e d b a c k training, and a c c o m m o d a t e idiosyncratic patterns of movement. Our training sessions were designed to be relatively brief to accommodate our participant population. All participants were psychiatric inpatients, with the most common diagnosis being schizophrenia. Although we had first reduced their neuroleptic medications to the minimally effective dosages, we noted attentional deficits. Each of the feedback sessions required 4 minutes to set thresholds and 10 minutes of training. For many of our participants it was difficult to remain alert throughout the session. Some became drowsy, while others became restless. It is our impression that our participants showed attentional as well as the m o t o r disturbances typically seen in T D patients. The use of a m o r e intact population would have allowed longer, and conversely, m o r e intensive training sessions. Since T D is not a c o m m o n occurrence in such a population, it was felt that our present course of training was more appropriate for our psychiatric population. Similarly, limiting
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our training sessions to ten was also compensation for our population. The total time for this study from initial identification until the last day of feedback training was 2-4 months, depending upon a participant's response to medication change. As many of our patients are discharged in from 2 to 6 months on average, we faced some constraints on our time. In our hands the AIMS suffers as a measure of TD. The severity of movements during the examination are noted to be different from the amplitude of movement seen in the patient's everyday activities (Barnes & Kidger, 1979; Gardos & Cole, 1980). Additionally, the sensitivity of the AIMS to extremely low-amplitude movement, or those movements with a long period, is poor. We are presently evaluating the correlation between AIMS ratings and E M G activity to determine sensitivity and specificity (for muscle group). The use of behavioral approaches makes it important to use measures of T D severity that are ecologically valid (e.g., Jeste & Wyatt, 1982; Firth & Ardern, 1985; Klawans, 1985); we question the reliability of the AIMS as such a measure. E M G m e a s u r e s m a y c o n t r i b u t e to o u r u n d e r s t a n d i n g o f the pathophysiological mechanisms underlying the dyskinetic movements. Examination of the pathology data from the BPRS and subsequent performance during feedback training indicates a nonsignificant trend In general, those participants with high BPRS scores on several of the affect-related items did slightly better than those with lower scores. While this observation proved to be less than statistically significant, this trend may point at a relationship between affect and T D in schizophrenia. It is not clear why the tongue and hands are so vulnerable to the development of dyskinetic movements. It may be that the large representation of the mouth and hand areas on the cortical motor strip is the basis for the disorder. The pathophysiologic process may be one of disinhibition, and larger areas may be more susceptible to release from inhibition. Given this, we might expect that different muscles involved in dyskinesia, e.g., tongue and jaw or fingers, would be excited simultaneously or, at least, with a constant time delay. E M G approaches would make study of the temporal patterning of abnormal involuntary movements accessible.
REFERENCES Albanese, H., & Gaarder, K. (1977). Biofeedback treatment of tardive dyskinesia: Two case reports. American Journal of Psychiatry, 134, 1149-1150. Alexopoulos, G. S. (1979). Lack of complaints in schizophrenics with tardive dyskinesia. Journal of Nervous and Mental Disease, 167, 125-127.
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American Psychiatric Association (1987). Diagnostic and statistical manual of mental disorders - Revised (DSM-111-R) (3rd ed. revised). Washington, DC:APA. Barnes, T. R. E. (1987). The present status of tardive dyskinesia and akathisia in the treatment of schizophrenia. Psychiatric Developments, 4, 301-319. Barnes, T. R. E. (1988). Tardive dyskinesia. British Medical Journal, 296, 150-151. Barnes, T. R. E., & Kidger, T. (1979). The concept of tardive dyskinesia. Trends in Neuroscience, 2, 135-136. Bayles, G. H., & Cleary, P. J. (1986). The role of awareness in the control of frontalis muscle activity. Biological Psychology, 22, 23-35. Bodenhamer, E., Coleman, C., & Achterberg, J. (1986). Self-directed EMG training for the control of pain and spasticity in paraplegia: A case study. Biofeedback and Self-Regulation, 11, 199-205. Brener, J. (19xx). A general model of voluntary control applied to the phenomena of learned cardiovascular change. In P. A. Obrist, A. H. Black, J. Brener, & L. V. DiCara (Eds.),
Cardiovascular psychophysiology: Current issues in response mechanisms, biofeedback, and methodology, Chicago: Aldine-Atherton. Endicott, J., & Spitzer, R. I. 91978). A diagnostic interview: The Schedule for Affective Disorders and Schizophrenia. Archives of General Psychiatry, 35, 836-844. Farrar, W. B. (1976). Using electromyographic biofeedback in treating orofacial dyskinesia. Journal of Prosthetic Dentistry, 35, 384-387. Fields, R. W. (1987). Electromyographically triggered electric muscle stimulation for chronic hemiplegia. Archives of Physical and Medical Rehabilitation, 68, 407-414. Firth, W. R., & Ardern, M. H. (1985). Measuring abnormal movement in tardive dyskinesia: A pilot study. British Journal of Psychiaoy, 147, 723-726. Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975). Mini-mental state: A practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research, 12, 189-198. Fudge, R., & Adams, H. E. (1985). The effects of discrimination training on voluntary control of cephalic vasomotor activity. Psychophysiology, 22, 300-306. Gardos, G., & Cole, J. D. (1980). Problems in the assessment of tardive dyskinesia. In R. C. Smith, W. E. Fann, & J. M. Davis (Eds.), Tardive dyskinesia: Research and treatment. New York: Spectrum Books. Guy, W. (1976). ECDEU Assessment Manual for psychopharmacology: U.S. Department of Health Education and Welfare Publication 76-338. Washington, DC, DHEW, Psychopharmacology Research Branch, pp. 534-537. Jackson, G. M., Schonfeld, L. I., & Griffith, K. (1983). A comparison of two behavioral treatments in decreasing the orofacial movement of tardive dyskinesia. Biofeedback and Self-Regulation, 8, 547-553. Jeste, D. V., & Wyatt, R. J. (1980). Understanding and treating tardive dyskinesia. New York: Guilford Press. Kane, J. M., Woerner, M., Lieberman, J., & Kinon, B. (1984). Tardive dyskinesia. In D. V. Jeste & R. J. Wyatt (Eds.), Neuropsychiatric movement disorders. Washington, DC: American Psychiatric Press. Klawans, H. L. (1985). Recognition and diagnosis of tardive dyskinesia. Journal of Clinical Psychiatry, 46, 3-7. MacLeod, J. H. (1983). Biofeedback in the management of partial anal incontinence. Diseases of the Colon and Rectum, 26, 244-246. Overall, J. E., & Gorham, D. R. (1962). The Brief Psychiatric Rating Scale. Psychological Reports, 10, 799-812. Roxanas, M. R., Thomas, M. R., & Rapp, M. S. (1978). Biofeedback treatment of blepharospasm with spasmodic torticollis. Canadian Medical Association Journal, 119, 48-49. Rubow, R. T., Rosenbek, J. C. Collins, M. J., & Celesia, G. G. (1984). Reduction of hemifacial spasm and dysarthria following EMG biofeedback. Journal of Speech and Hearing Disorders, 49, 26-33.
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Sherman, R. A. (1979). Successful treatment of one case of tardive dyskinesia with electromyographic feedback from the masscter muscle. Biofeedback and Self-Regulation, 4, 367-370. Tarsy, D., & Baldessarini, R. J. (1984). Tardive dyskinesia. Annual Review of Medich~e, 35, 605-623. Taylor, C. B., Zlutnick, S. I., & Hoehle, W. (1979). The effects of behavioral procedures on tardive dyskinesia. Behavior Therapy, 10, 37-45. Yagi, G., & Itoh, H. (1987). Follow-up study of 11 patients with potentially reversible tardive dyskinesia, American Journal of Psychiatry, 144, 1496-1498.
The Effects of Electromyographic Feedback Training on Suppression of the Oral-Lingual Movements Associated with Tardive Dyskinesia I Ronald C. Fudge 2 and Sheryl A. Thailer Franklin Delano Roosevelt Veterans Hospital
Murray Alpert New York University Medical Center
Joanne Intrator and Cecile E. Sison Franklin Delano Roosevelt Veterans Hospital
The efficacy of electromyographic feedback training in reducing the magnitude and frequency of the oral-lingual movements associated with tardive dyskinesia (TD) was investigated in a groups design. Twenty adult male inpatients diagnosed as having TD using the Abnormal Involuntary Movements Scale (AIMS) were randomly assigned to one of two treatment conditions. Following identification, all participants were initially reduced to the lowest effective dosage of neuroleptics, and then discontinued from anticholinergics. Following one month on this regimen, they were given a course of feedback training consisting of ten 14-minute sessions. Group one participants were provided with a tone contingent upon oral-lingual movements above a yoked threshold. Group two participants were given noncontingent feedback tones generated randomly. Weekly AIMS were administered as well as an initial baseline during each session to determine current level of oral-lingual activity. An analysis of session effects indicated significantly more suppression of oral-lingual activity in the contingent group versus the noncontingent feedback group. Jaw and forehead IThis work was sponsored in part by a Research Advisory Grant from the Department of Veterans Affairs awarded to Joanne Intrator. We gratefully acknowledge the valuable contributions of K. Duvvi, S. Kemble, and L. Kolman. 2Address all correspondence to Dr. Ronald C. Fudge, FDR Hospital, Psychology Service (116B), Montrose, New York 10548. 117 o363-3586t91/o6oo-o1175o6.5o/o© 1991 PlenumPublishingCorporation
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activity also measured showed reductions of similar magnitudes for both groups. KEY WORDS: electromyographicbiofeedback;tardive dyskinesia;neuroleptics; movementdisorders.
Tardive dyskinesia (TD), an involuntary movement disorder occurring subsequent to chronic neuroleptic administration, has most often b e e n a s s o c i a t e d with o r a l - b u c c o - l i n g u a l m o v e m e n t s ( T a r s y & Baldessarini, 1984; Barnes, 1987; Yagi & Itoh, 1987; Barnes, 1988). Such movements often involve tongue protrusion, grimacing, and masticatory movements. Typically, these abnormal involuntary movements have been characterized as being out of the awareness of the patient (Alexopoulos, 1979). Such movements are likely to increase when the patient is involved in simple motor tasks, although engaging the patient's attention while relaxed may also be associated with large amplitude, regular movements. While the etiology of TD is thought to be related to the physiological concomitants of pharmacological interventions, motor awareness, and attentional factors have also been reported to be involved in movement f r e q u e n c y and amplitude (Jeste & Wyatt, 1982; Kane, W o e r n e r , Lieberman, & Kinon, 1984). Biofeedback and other behavioral techniques have often been thought to be effective by enhancing the awareness of a particular behavior, and thereby enabling increasing control over that behavior (Brener, 1974; Fudge & Adams, 1985; Bayles & Cleary, 1986). Our investigation of the phenomena of TD led us to conclude that increasing a subject's awareness of certain TD movements may lead to a reduction in the frequency and severity of movements (Taylor, Zlutnick, & Hoehle, 1979). Since the oralbucco-lingual movements of TD necessarily involve somatic muscle activity, electromyographic feedback of the oral area seemed logical. A search of the biofeedback literature led us to four reports in which electromyographic (EMG) biofeedback was used to suppress the involuntary movements of TD (Albanese & Gaarder, 1977; Farrar, 1976; Sherman, 1979; Jackson, Schonfeld, & Griffith, 1983) with some evidence of positive benefit. However, all four studies lacked systematic controls, were extremely small in their numbers of participants, and in general produced results that were difficult to interpret. While these four studies provided limited support for using biofeedback with TD, there is a more substantial literature on the usefulness of biofeedback for other motor disorders, including torticollis (e.g., Roxanas, Thomas, & Rapp, 1978), stroke paralysis (e.g., Bodenhamer, Coleman, & Achterberg, 1986; Fields, 1987), hemifacial spasm (e.g., Rubow, Rosenbek, Collins, & Celesia, 1984), and sphincter
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control (e.g., MacLeod, 1983), with some evidence for efficacy. These motor disorders, while phenomenologically different from TD, provided a basis for investigating the efficacy of biofeedback with TD. The present study was designed to examine issues in utilizing an E M G biofeedback training procedure with chronic psychiatric inpatients. Such patients are typically maintained on the same psychotropic medications implicated in the pathogenesis of the disorder. Our initial focus was on the signal value of a mildly noxious tone made contiguous with tongue activity. We included a group of participants presented with a randomized noncontingent tone. We also examined jaw and brow motor activity, two areas also frequently affected in TD, for insight into the specificity of the tongue activity feedback. Additionally, we examined within session and progressive cross-session changes, as well as generalization from the feedback laboratory to the clinic situation and to the ward.
METHODS
Participants Twenty males, inpatients at the F D R VA Hospital, Montrose, New York, volunteered and provided written informed consent for the study. Patients were rated weekly on an assessment battery that included the Abnormal Involuntary Movement Scale (AIMS; Guy, 1976). Those patients with a score indicating at least mild T D (rated as 2) in 2 of the first 4 AIMS areas (areas involving facial movements), or a single score of 3 (moderate) in one of these areas were considered for the study. Mean pretreatment total AIMS scores were 19.2, with a range of 13-28. Three AIMS raters were calibrated with each other at baseline, achieving an interrater reliability of r = .71. All volunteers had at least a 9-month history of TD, and a minimum of 2 years of neuroleptic medication. Ten participants were randomly assigned to one of two groups (true feedback or false feedback). Participants were excluded if they had a concurrent neurological disorder or severe, u n c o r r e c t e d d e n t a l p a t h o l o g y which might mask or p o t e n t i a t e T D symptoms. The Mini-Mental Examination (Folstein, Folstein, & McHugh, 1975) was administered at baseline to identify patients who were too severely d e m e n t e d to c o o p e r a t e . Participants with a score g r e a t e r than 20 qualified for the study. The mean Mini-Ment score was 26.3, with a range of 22-30. In addition, the Brief Psychiatric Rating Scale (BPRS, Overall & Gorham, 1962) was administered weekly to monitor psychopathology during the course of
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the study. BPRS scores averaged 14.6, with a range of 4-32. DSM-III-R (APA, 1987) diagnoses were determined by experienced clinicians using the Schedule for Affective Disorders and Schizophrenia (SADS; Endicott & Spitzer, 1978). T e n participants were diagnosed as Schizophrenia, Chronic Undifferentiated type; 3 as Schizoaffective, Mainly Depressed; 6 as Bipolar Disorder; and 1 as Major Depressive Disorder. Participants ranged in age from 45 to 72 years, with an average of 61 years.
PROCEDURES
Apparatus E M G signals were recorded using Grass model 7P511 amplifiers with a .3-second time constant. Amplified E M G signals were integrated via Coulbourn integrators, interfaced with an IBM AT/PC computer through a Coulbourn 8-bit A/D converter. Physiological data were recorded on line using an IBM/AT PC computer with a sampling rate of 1 ms/sample. Feedback and data transformations, and storage were all processed by computer. E M G activity was detected using 1-cm silver-silver chloride prejelled disposable electrodes (Ver Med Associates). Participants were seated in a reclining chair, adjusted to their needs, in an air conditioned sound attenuating room. To reduce extraneous noise, participants received their instructions and feedback tones through headphones. Both groups were given the same instructions: "Occasionally you will hear a tone when you are making mouth movements. Try to relax your mouth and turn off the tone."
Dose Adjustment Prior to initiation of the feedback phase of the study neuroleptic and anticholinergic medications were reduced in an attempt to find the "lowest effective dose" for each patient according to the following rules: 1. 2.
Patients on more than one neuroleptic were shifted to a single drug. The dose of the neuroleptic was reduced in weekly 20% decrements. Reductions were titrated against BPRS scores and ceased when a zero dose was achieved, or BPRS scores (raters were blind as to dose adjustment) increased by 20%. Under these conditions all patients failed to achieve a zero dose.
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Table I. Psychotropic Medications in Mean Dosage per Day
Neuroleptics
Number
Chlorpromazine Thioridazine Haloperidol Fluphenazine Thiothixene Perphenazine Mesoridazine
4 2 3 2 3 1 1
Other medications Lithium Clonazepam Lorazepam Imipramine
3.
CPZ Equiv. mg/day 480 415 650 600 160 100
Number
Mean Dose mg/day
2 2 1 1
900 1 1 100
After establishing the lowest functional neuroleptic dosage, anticholinergics were lowered in a similar fashion with placebos substituted for anticholinergics so that the n u m b e r of pills administered per day was constant. Extrapyramidal side effects were monitored on a blind basis. With the exception of one patient in the true f e e d b a c k group, who r e q u i r e d 6 rag/day of trihexphenidyl, it was possible to eliminate anticholinergic medications.
All patients were stabilized for at least one month on their lowest dose of neuroleptic before feedback training was started. Psychotropic medications taken by the study patients are described in Table I.
Training Sessions Each session began with a 4-minute baseline period, during which E M G lingual activity was determined and a threshold set. During this period no feedback was provided. Ten minutes of feedback training followed. D a t a were recorded continuously and integrated into 15-second epochs. E M G activity was recorded using bipolar electrodes from three sites; lingual, masseter, and frontalis. Lingual activity was detected from leads 1.5 cm apart on the ventral surface of the genioglossus muscle, midway between the neck and chin. Masseter activity was recorded with leads 1.5 cm apart on the dominant side at the temporo-mandibular junction. Frontalis activity was recorded from placements 1 cm above the nasion and 1 cm apart.
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Feedback The feedback signal was 440 Hz tone at 75 dB, contingent on lingual lead activity exceeding threshold levels. A moving window was used to determine and maintain threshold levels. This window permitted a degree of automated shaping. The window was established by averaging the initial three 15-second epochs of lingual activity. Starting with the fourth epoch, and continuing until the end of each training session, the threshold was recalculated by averaging the current epoch value with the mean of the two preceding epochs. The tone was enabled when the current E M G reading exceeded the threshold. Participants given noncontingent feedback received the same instructions as the true feedback group. The rate of false feedback was computergenerated at random intervals and calculated to match that of the true feedback group, so that the probability of a response occurring simultaneously with a real tongue movement remained at chance. Treatment was under double blind conditions, with feedback contingencies unknown to either the research technician or the participants.
Sessions All participants received daily sessions on ten consecutive weekdays. Each session consisted of an initial adaptation period of 4 minutes duration followed by 10 minutes of biofeedback training. AIMS ratings were done weekly.
Transformations of the EMG Data To facilitate between participant comparisons, and to ensure that each participant contributed equally to their treatment group, raw E M G levels were transformed as follows. Means were calculated separately for the tongue, jaw, and forehead E M G levels for all 15-second epochs of each session. For each participant, on each measure, the range (maximal minus minimal) for all epochs was calculated for each lead. The mean score for each participant was subtracted from each observed score and divided by the full range of the measure, thus yielding a range corrected score for E M G levels. These values were then used to determine a score reflecting the average E M G level during the initial 2 minutes of each session, for each measure (termed "First") and, similarly, for the last 2 minutes of each session (termed "Last"). These were the measures subm i t t e d to the statistical analyses described below. F o r simplicity of
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Fig. l. TongueEMGscores. Last-Firstscoresoverallsessionsbygroups.
presentation, we also calculated a change score by subtracting the Last score f r o m the First score. While the graphic presentation is based on c h a n g e s c o r e s , t h e s t a t i s t i c a l analysis was b a s e d on A N O V A and A N C O V A of the First and Last scores.
RESULTS To examine the effects of biofeedback training on oral-buccal movements, the following analyses w e r e c o n d u c t e d : F o r e a c h group, a 3 (measures) x 10 (sessions) repeated measures A N C O V A procedure was done using the Last measure with First as covariate, to determine session training effects. A significant main effect was obtained for the true feedback group F(1, 12) -- 5.75, p < .05, indicating that scores tended to be lower by the end of each session. Effects for the false feedback group were not significant. In addition, there was a main effect of m e a s u r e F(2, 12) = 41.99, p < .001. T o n g u e E M G scores showed larger amounts of within session change than did those for jaw or forehead. T h e r e was also a main effect of sessions F(9, 12) = 2.64, p < .01. As will be seen below, this was
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~g. 2. Jaw EMGscores. Last-Firstscoresoverallsessionsbygroups.
not a reflection of a tendency for progressive improvement from day to day. Use of change scores (Last minus First) for each session is the easiest way to portray these effects, and these scores are presented in Figures 1, 2, and 3. T o examine the hypothesis that contingent feedback would produce a greater effect on oral-lingual movement than false feedback, the FirstLast intervals were examined over sessions for each measure. A two factor A N C O V A procedure, Last covaried with First, was employed to examine group differences. Significant group differences were found for the Tongue measure F (1, 10) = 4.89,p < .01. The true feedback group did significantly better than did the noncontingent feedback group on sessions 4 F (1, 17) = 6.39, p < .05, and 8 F ( 1 , 16) = 5.99, p < .05. No main effects for group were found on either the Jaw measure of the Forehead measure, indicating that training was specific to contingent feedback. The weekly AIMS scores (Sum of items 1-4, and Total Score) were examined in an A N C O V A comparing the true and false feedback groups with baseline as the covariate. No significant differences emerged. In fact, the scores for the two groups remained close throughout the rating period (see Figure 4).
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4O 30 2O 10 0 -10 -20 -30 -40
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Fig. 3. Forehead EMG scores. Last-First scores over all sessions by groups.
DISCUSSION Our results indicate that for within sessions, contingent feedback training produced a modest suppressive effect on lingual activity. This effect was specific to the target channel (tongue), with neither jaw nor brow activity showing a similar suppression of EMG levels. Our first goal was to replicate previous reports using double-blind procedures, randomized assignments to treatment groups, and a sufficient number of participants to support statistical analysis. While these results are somewhat more circumscribed than earlier reports, E M G feedback did produce a suppressive effect on the oral-buccal movements of TD. Since our design required a tightly controlled double blind with placebo control, we feel that these results are due to specific training effects rather than nonspecific placebo effects. Traditionally, biofeedback training is made contingent on a specific measure, providing an "if-then" signal for feedback. Since other muscle groups are known to be affected by TD (mainly jaw and forehead), the "if-then" (if tongue is > criterion, t h e n . . . ) contingency may not be the most productive m e t h o d o l o g y . C o n t i n g e n c i e s utilizing " a n d / o r " for
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25 20 15 10 5 0
FEEDBACK NO FEEDBACK
I
FEEDBACK
~
NO FEEDBACK
Fig. 4. Abnormal Involuntary Movements Scale. Total scores by groups during training.
activity of individual or groups of muscles in several facial areas would provide feedback for patterns of movement. We are examining our data base to identify such patterns across muscles and across patients in anticipation of follow-up studies. Utilization of " a n d / o r " contingencies would individualize f e e d b a c k training, and a c c o m m o d a t e idiosyncratic patterns of movement. Our training sessions were designed to be relatively brief to accommodate our participant population. All participants were psychiatric inpatients, with the most common diagnosis being schizophrenia. Although we had first reduced their neuroleptic medications to the minimally effective dosages, we noted attentional deficits. Each of the feedback sessions required 4 minutes to set thresholds and 10 minutes of training. For many of our participants it was difficult to remain alert throughout the session. Some became drowsy, while others became restless. It is our impression that our participants showed attentional as well as the m o t o r disturbances typically seen in T D patients. The use of a m o r e intact population would have allowed longer, and conversely, m o r e intensive training sessions. Since T D is not a c o m m o n occurrence in such a population, it was felt that our present course of training was more appropriate for our psychiatric population. Similarly, limiting
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our training sessions to ten was also compensation for our population. The total time for this study from initial identification until the last day of feedback training was 2-4 months, depending upon a participant's response to medication change. As many of our patients are discharged in from 2 to 6 months on average, we faced some constraints on our time. In our hands the AIMS suffers as a measure of TD. The severity of movements during the examination are noted to be different from the amplitude of movement seen in the patient's everyday activities (Barnes & Kidger, 1979; Gardos & Cole, 1980). Additionally, the sensitivity of the AIMS to extremely low-amplitude movement, or those movements with a long period, is poor. We are presently evaluating the correlation between AIMS ratings and E M G activity to determine sensitivity and specificity (for muscle group). The use of behavioral approaches makes it important to use measures of T D severity that are ecologically valid (e.g., Jeste & Wyatt, 1982; Firth & Ardern, 1985; Klawans, 1985); we question the reliability of the AIMS as such a measure. E M G m e a s u r e s m a y c o n t r i b u t e to o u r u n d e r s t a n d i n g o f the pathophysiological mechanisms underlying the dyskinetic movements. Examination of the pathology data from the BPRS and subsequent performance during feedback training indicates a nonsignificant trend In general, those participants with high BPRS scores on several of the affect-related items did slightly better than those with lower scores. While this observation proved to be less than statistically significant, this trend may point at a relationship between affect and T D in schizophrenia. It is not clear why the tongue and hands are so vulnerable to the development of dyskinetic movements. It may be that the large representation of the mouth and hand areas on the cortical motor strip is the basis for the disorder. The pathophysiologic process may be one of disinhibition, and larger areas may be more susceptible to release from inhibition. Given this, we might expect that different muscles involved in dyskinesia, e.g., tongue and jaw or fingers, would be excited simultaneously or, at least, with a constant time delay. E M G approaches would make study of the temporal patterning of abnormal involuntary movements accessible.
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