Biofeedback and Self-Regulation, VoL 2, No. 3, 1977
Case Reports and Training Techniques
The Use of E M G Feedback in the Treatment of a Severe Case of Blepharospasm David F. Peck1 University of Edinburgh
In this case report, a 50-year-old female with a chronic blepharospasm (spasmodic winking) around both eyes was treated with 17 sessions of electromyographic (EMG) feedback. EMG level and spasm frequency were monitored during baseline, placebo, and feedback treatment sessions. There was a marked decrease in both EMG level and spasm frequency, which generalized to her everyday life. Improvement was maintained at a 4-month follow-up.
INTRODUCTION A blepharospasm may be defined as spasmodic, frequent winking, involving primarily the orbicularis oculi and frontalis muscle groups. It is a disorder that has proved resistant to opthalmological and neurological intervention, and few reports have appeared describing alternative, psychological approaches to the problem. Reckless (1972) described two cases that improved after receiving a combination of supportive psychotherapy, group therapy, and psychotropic medication. Sharpe (1974) reported a case treated by a combination of relaxation, graded practice in controlling eyelid movements, and increasing participation in reinforcing activities incompatible with the spasm. Unfortunately, these studies did not provide a detailed assessment of the spasm (in particular, no data were provided concerning the frequency of the spasm); furthermore, it is not possible to determine the crucial ingredients of the complex therapeutic "packages" reported in these studies. 'Address all correspondence to David F. Peck, University Department of Psychiatry, Royal Edinburgh Hospital, Edinburgh EHI0 5HF, Scotland. 273 This j o u r n a l is copyrighted by Plenum. Each article isavailaDle for $7.50 f r o m Plenum Pubfishing Corporation, 227 West 17th Street, N e w Y o r k , N.Y. 10011.
274
Peck
Electromyographic (EMG) feedback would appear to be particularly applicable to problems involving muscle activity such as spasms. This report describes a systematic single-case study, using EMG feedback to treat a severe case of blepharospasm.
CASE HISTORY The patient was a 50-year-old married female. The blepharospasm began in 1970, while she was working in a plant-breeding station. The pollen encountered at work may have precipitated a general allergic reaction, and subsequently there was a history of extensive but minor pathology of both eyes, in particular a marked lack of tear secretion. Frequent consultations with opthalmologists, neurologists, and psychiatrists had produced a great deal of benefit with these and other problems, but without significant effect on the spasms. Her social, professional, and domestic life had been severely disrupted by the spasm, which was very conspicuous and had produced deep facial furrows.
TREATMENT
Design An ideal design for a controlled single-case study is the A-B-A-B design. However, this type of design is appropriate only in those cases where the target behavior is reversible, and therefore it may not be appropriate with problems involving muscular control. An alternative, used in this study, is the systematic case study, in which there is systematic measurement of the problem before treatment and during treatment. This design is particularly appropriate in long-standing cases, and can provide interpretable results if a change in the problem behavior coincides with the treatment intervention (Barlow & Hersen, 1973). Data relating to EMG level and spasm frequency were collected in three phases: 1. Two baseline sessions were held during which EMG level and spasm frequency were monitored. 2. Two " p l a c e b o " sessions were then held, similar to the baseline sessions but with the addition that white noise was played over headphones to the patient. It was suggested to her that this was a distracting stimulus that would divert attention from the spasms and
EMG Feedback and Blepharospasm
275
thereby influence their intensity and frequency. These sessions were intended to control for placebo effects, possibly resulting from attending a clinic, being wired up to electronic gadgetry, discussing the spasm, and so on. (Ideally, more than two sessions of baseline and of placebo treatment would be required, but the patient's frequent contact with the health services with no consequent change in the spasm had produced a "credibility gap," which further nonspecific sessions may only have served to widen). . In this, the feedback or treatment phase, EMG level and spasm frequency were monitored, and EMG activity was fed back to the patient over headphones (see below for details). There were 17 sessions in this phase. Method Dracard disposable electrodes were placed on the patient's left frontalis and lower orbicularis oculi muscles, with a reference electrode on the temple, and connected to a Biofeedback Systems EMG 90. The EMG 90, which had a bandpass of 100 Hz to 1 kHz, amplified the electromyographic activity and converted the signal into a series of clicks with a frequency proportional to the degree of muscle tension. During the feedback sessions the patient was instructed to reduce the click frequency, and thereby to reduce muscle tension. The sessions lasted for 20 minutes, preceded by about 5 minutes during which the patient became accustomed to wearing the electrodes. Sessions were held two or three times per week. Throughout the recording the patient kept her eyes open and fixed them on a point at approximately eye level. EMG level was measured in microvolts OV) peak-to-peak and noted every 20 seconds from the meter on the EMG 90; the mean for each session was then calculated. A hand counter was used to count the number of spasms. Table I. Mean EMG Level and Spasm Frequency for the First Three and the Last Three Treatment Sessions Sessions 1 Mean EMG (~V) peak-to-peak Spasm/blinking frequency
18.88 1348
2
3
15
16
17
13.55 13.37 7°72 7.05 6.77 888
950
12
17
13
2"16
Peck
0 1500
•
0
I000 Mean
~V peak -to-[~ak
+
0
I
\
0--0
Spasms per
20 mLn.
0~0
\
•
\ / \ \ / \ o/
10"
500
250
A---.4,,~ 0
Base
IAne
Placebo
•
•
i
i
i
i
i
i
l
i
i
i
i
i
i
i
i
i
i
t
2
3
4
5
S
7
8
+
10
It
t2
t3
14
15
16
17
18
Sessions
Fig. 1. Reduction in EMG level and spasm frequency for baseline, placebo, and feedback sessions.
RESULTS The data for all sessions are presented graphically in Figure 1 and for the first three and last three treatment sessions in Table I.
DISCUSSION Inspection of Figure 1 and of the data presented in Table I supports the conclusion that the treatment intervention was highly effective in reducing the spasm. Spasm frequency reduced from approximately 1,600 per 20-minute session during the baseline and placebo sessions to approximately 15 blinks during the last three treatment sessions. Similarly, the mean pretreatment EMG level of approximately 25/aV was reduced to approximately 7/aV after seven sessions and remained at that level throughout the rest of the sessions. Not shown in the data presented are the parallel changes in the topography of the spasm. Before treatment, the spasm consisted of a massive contraction of the muscles around the eyes. However, by session 7 (inciden-
EMG Feedback and Biepharospasm
277
tally the session during which the EMG reached an asymptotic level), this had been reduced to a rather pronounced wink, and during the last three sessions it was nothing more than an ordinary blink. All control gained over the muscles around the left eye generalized immediately to the right eye. Progress within sessions was accompanied by increasing control of the spasm at home. By session 9 she was able to control the spasm for about 1 hour per day, and the degree of control gradually increased until by session 17, the spasm had been absent for a week. It returned briefly when her eye became painful because of the associated opthalmological problems, but she was soon able to restore control. The improvement was confirmed by telephone contacts with her husband. Despite these clear-cut changes, however, it is felt that no firm conclusions can be drawn concerning the etiology, or precise mechanism of change, of the spasm. The patient was followed up regularly for 4 months and the improvements were maintained.
REFERENCES Barlow, D. H., & Hersen, M. Single case experimental designs. Archives of General Psychiatry, 1973, 29, 319-327. Reckless, J. B. Hysterical blepharospasm treated by psychotherapy and conditioning procedures in a group setting. Psychosomatics, 1972, 13, 263-264. Sharpe, R. Behaviour therapy in a case of blepharospasm. British Journal of Psychiatry, 1974,
124, 603-604. (Revision received March 9, 1977)
Case Reports and Training Techniques
The Use of E M G Feedback in the Treatment of a Severe Case of Blepharospasm David F. Peck1 University of Edinburgh
In this case report, a 50-year-old female with a chronic blepharospasm (spasmodic winking) around both eyes was treated with 17 sessions of electromyographic (EMG) feedback. EMG level and spasm frequency were monitored during baseline, placebo, and feedback treatment sessions. There was a marked decrease in both EMG level and spasm frequency, which generalized to her everyday life. Improvement was maintained at a 4-month follow-up.
INTRODUCTION A blepharospasm may be defined as spasmodic, frequent winking, involving primarily the orbicularis oculi and frontalis muscle groups. It is a disorder that has proved resistant to opthalmological and neurological intervention, and few reports have appeared describing alternative, psychological approaches to the problem. Reckless (1972) described two cases that improved after receiving a combination of supportive psychotherapy, group therapy, and psychotropic medication. Sharpe (1974) reported a case treated by a combination of relaxation, graded practice in controlling eyelid movements, and increasing participation in reinforcing activities incompatible with the spasm. Unfortunately, these studies did not provide a detailed assessment of the spasm (in particular, no data were provided concerning the frequency of the spasm); furthermore, it is not possible to determine the crucial ingredients of the complex therapeutic "packages" reported in these studies. 'Address all correspondence to David F. Peck, University Department of Psychiatry, Royal Edinburgh Hospital, Edinburgh EHI0 5HF, Scotland. 273 This j o u r n a l is copyrighted by Plenum. Each article isavailaDle for $7.50 f r o m Plenum Pubfishing Corporation, 227 West 17th Street, N e w Y o r k , N.Y. 10011.
274
Peck
Electromyographic (EMG) feedback would appear to be particularly applicable to problems involving muscle activity such as spasms. This report describes a systematic single-case study, using EMG feedback to treat a severe case of blepharospasm.
CASE HISTORY The patient was a 50-year-old married female. The blepharospasm began in 1970, while she was working in a plant-breeding station. The pollen encountered at work may have precipitated a general allergic reaction, and subsequently there was a history of extensive but minor pathology of both eyes, in particular a marked lack of tear secretion. Frequent consultations with opthalmologists, neurologists, and psychiatrists had produced a great deal of benefit with these and other problems, but without significant effect on the spasms. Her social, professional, and domestic life had been severely disrupted by the spasm, which was very conspicuous and had produced deep facial furrows.
TREATMENT
Design An ideal design for a controlled single-case study is the A-B-A-B design. However, this type of design is appropriate only in those cases where the target behavior is reversible, and therefore it may not be appropriate with problems involving muscular control. An alternative, used in this study, is the systematic case study, in which there is systematic measurement of the problem before treatment and during treatment. This design is particularly appropriate in long-standing cases, and can provide interpretable results if a change in the problem behavior coincides with the treatment intervention (Barlow & Hersen, 1973). Data relating to EMG level and spasm frequency were collected in three phases: 1. Two baseline sessions were held during which EMG level and spasm frequency were monitored. 2. Two " p l a c e b o " sessions were then held, similar to the baseline sessions but with the addition that white noise was played over headphones to the patient. It was suggested to her that this was a distracting stimulus that would divert attention from the spasms and
EMG Feedback and Blepharospasm
275
thereby influence their intensity and frequency. These sessions were intended to control for placebo effects, possibly resulting from attending a clinic, being wired up to electronic gadgetry, discussing the spasm, and so on. (Ideally, more than two sessions of baseline and of placebo treatment would be required, but the patient's frequent contact with the health services with no consequent change in the spasm had produced a "credibility gap," which further nonspecific sessions may only have served to widen). . In this, the feedback or treatment phase, EMG level and spasm frequency were monitored, and EMG activity was fed back to the patient over headphones (see below for details). There were 17 sessions in this phase. Method Dracard disposable electrodes were placed on the patient's left frontalis and lower orbicularis oculi muscles, with a reference electrode on the temple, and connected to a Biofeedback Systems EMG 90. The EMG 90, which had a bandpass of 100 Hz to 1 kHz, amplified the electromyographic activity and converted the signal into a series of clicks with a frequency proportional to the degree of muscle tension. During the feedback sessions the patient was instructed to reduce the click frequency, and thereby to reduce muscle tension. The sessions lasted for 20 minutes, preceded by about 5 minutes during which the patient became accustomed to wearing the electrodes. Sessions were held two or three times per week. Throughout the recording the patient kept her eyes open and fixed them on a point at approximately eye level. EMG level was measured in microvolts OV) peak-to-peak and noted every 20 seconds from the meter on the EMG 90; the mean for each session was then calculated. A hand counter was used to count the number of spasms. Table I. Mean EMG Level and Spasm Frequency for the First Three and the Last Three Treatment Sessions Sessions 1 Mean EMG (~V) peak-to-peak Spasm/blinking frequency
18.88 1348
2
3
15
16
17
13.55 13.37 7°72 7.05 6.77 888
950
12
17
13
2"16
Peck
0 1500
•
0
I000 Mean
~V peak -to-[~ak
+
0
I
\
0--0
Spasms per
20 mLn.
0~0
\
•
\ / \ \ / \ o/
10"
500
250
A---.4,,~ 0
Base
IAne
Placebo
•
•
i
i
i
i
i
i
l
i
i
i
i
i
i
i
i
i
i
t
2
3
4
5
S
7
8
+
10
It
t2
t3
14
15
16
17
18
Sessions
Fig. 1. Reduction in EMG level and spasm frequency for baseline, placebo, and feedback sessions.
RESULTS The data for all sessions are presented graphically in Figure 1 and for the first three and last three treatment sessions in Table I.
DISCUSSION Inspection of Figure 1 and of the data presented in Table I supports the conclusion that the treatment intervention was highly effective in reducing the spasm. Spasm frequency reduced from approximately 1,600 per 20-minute session during the baseline and placebo sessions to approximately 15 blinks during the last three treatment sessions. Similarly, the mean pretreatment EMG level of approximately 25/aV was reduced to approximately 7/aV after seven sessions and remained at that level throughout the rest of the sessions. Not shown in the data presented are the parallel changes in the topography of the spasm. Before treatment, the spasm consisted of a massive contraction of the muscles around the eyes. However, by session 7 (inciden-
EMG Feedback and Biepharospasm
277
tally the session during which the EMG reached an asymptotic level), this had been reduced to a rather pronounced wink, and during the last three sessions it was nothing more than an ordinary blink. All control gained over the muscles around the left eye generalized immediately to the right eye. Progress within sessions was accompanied by increasing control of the spasm at home. By session 9 she was able to control the spasm for about 1 hour per day, and the degree of control gradually increased until by session 17, the spasm had been absent for a week. It returned briefly when her eye became painful because of the associated opthalmological problems, but she was soon able to restore control. The improvement was confirmed by telephone contacts with her husband. Despite these clear-cut changes, however, it is felt that no firm conclusions can be drawn concerning the etiology, or precise mechanism of change, of the spasm. The patient was followed up regularly for 4 months and the improvements were maintained.
REFERENCES Barlow, D. H., & Hersen, M. Single case experimental designs. Archives of General Psychiatry, 1973, 29, 319-327. Reckless, J. B. Hysterical blepharospasm treated by psychotherapy and conditioning procedures in a group setting. Psychosomatics, 1972, 13, 263-264. Sharpe, R. Behaviour therapy in a case of blepharospasm. British Journal of Psychiatry, 1974,
124, 603-604. (Revision received March 9, 1977)
