Biofeedback for Treatment of Chronic Insomnia
September 1, 1998
Biofeedback for Treatment of Chronic Insomnia
September 1998; Volume 1: 103-106
By Arthur Hartz, MD, PhD
Insomnia may be the most prevalent health complaint after pain.1 Estimates of the prevalence of insomnia range from 20% to 40%,2 and 10-15% of adults complain of chronic insomnia.3,4 The general diagnostic category of insomnia includes a heterogeneous group of sleep-disturbances. The etiology of insomnia includes psychological factors (e.g., depression and other psychopathology, neurotic and personality disorders, stress), physical disorders (e.g., nocturnal myoclonus, gastroesophageal reflux, sleep apnea, chronic pain), chronic ingestion of CNS depressants or stimulants, circadian rhythm problems, poor sleep environment, or poor sleep habits. For all these causes, treatment of the insomnia is considered secondary to treatment of the cause.
Most insomnia, however, is considered primary or idiopathic. Although some research has found that patients with primary insomnia are more neurotic or anxious than those with secondary insomnia, these results are inconsistent. The psychopathology profiles are clearer if insomnia is divided into three groups: those with only long sleep latency (time to initiate sleep), those with only frequent awakenings, and those with both.5
Current Pharmacological and Behavioral Treatments of Insomnia
Pharmacologic treatments for insomnia are usually recommended for short-term therapy to deal with acute situational stress or to break up a vicious circle of sleeplessness and worry over sleep. Several consequences of pharmacologic therapy limit its desirability as sole treatment of chronic insomnia:
1. Decreasing effectiveness over time
2. Development of psychological dependence or addiction
3. Rebound insomnia that complicates the process of withdrawal
4. Impaired sleep quality
5. Deteriorating daytime functioning.6
Research suggests that the most successful individual behavioral therapy is stimulus control. This therapy involves the following behaviors: go to bed only when sleepy, avoid naps, awaken at the same time each morning, avoid the bed for activities other than sleep or sex, and leave the bed when awake for more than 10-20 minutes.
Relaxation methods include a variety of procedures, such as progressive muscle relaxation (perhaps the most commonly used), autogenic training (a form of autosuggestion in which the subject thinks repetitiously of simple, standard phrases focusing mainly on heaviness and warmth in the extremities), transcendental meditation, yoga, and hypnosis. All of these relaxation methods have been found to be about equally effective in controlled studies.7,8
Interest in relaxation therapies is based on the finding that poor sleepers have hyperaroused levels of autonomic activity just prior to and during sleep.9 Although subsequent studies have not found this hyperarousal, relaxation methods have been consistently more effective than placebo in reducing sleep latency.
Other nonpharmacologic methods, in order of effectiveness, include sleep restriction to a certain number of hours, multicomponent therapies, stimulus control, and cognitive relaxation. Chronotherapy (delaying bedtime by three hours each night), bright light therapy (to shift the phase of the sleep rhythm), and paradoxical intention, in which the subject attempts to stay awake as long as possible to reduce sleep-incompatible performance anxiety, can also be effective in some patients.
Definition
Another successful behavioral treatment for insomnia is biofeedback. Biofeedback has been defined as "the technique of using equipment (usually electronic) to reveal to human beings some of their internal physiological events, normal and abnormal, in the form of visual and auditory signals to teach them to manipulate these otherwise involuntary or unfelt events by manipulating the displayed signal."10
History
Biofeedback was made possible by the development of high quality instrumentation post World War II for measuring physiologic events accurately. Much of the experimental groundwork for biofeedback was performed in the 1960s.
Mechanism of Action
An image that illustrates the need for biofeedback is of a blindfolded basketball novice learning to shoot baskets. Just as the basketball player cannot improve without having more information on actions associated with success, a person cannot learn to regulate an autonomic state without knowing how the state is changed by an intervention.
By making the early signs of slight progress conspicuous, biofeedback can encourage and motivate patients who may otherwise lack confidence in their ability to control processes outside usual conscious awareness. Experiments with biofeedback have found that it is possible to control several autonomic responses including blood pressure, vasomotor responses, salivation, galvanic skin responses, and cardiac rates and rhythms.
Procedure-EMG
The workhorse of biofeedback is the electromyograph (EMG). The EMG uses surface electrodes contacting the skin above a particular muscle or muscle group to monitor an electrical activity associated with muscle contraction. Subjects become aware of the tension in their muscles by the pitch or frequency of an EMG-mediated sound, and they learn to control their muscle tension by developing a strategy for varying the sound. In other words, "The old college try drives up the tone. Learn to do the opposite."11
Subjects who initially have little awareness of muscle tension may use EMG biofeedback to develop strategies for decreasing muscle tension. Initially, they learn how to change tension in small increments, and eventually they learn how to make larger reductions in tension.
The goals of relaxation training with EMG are measurable and standardized. Less than 2 microvolts indicates a relaxed state. Although the relaxation process is learned with EMG biofeedback, the subject becomes able to recognize and reduce muscle tension even when not connected to the machine. This use of EMG biofeedback is a specific type of relaxation therapy.
Procedure-EEG
Much less commonly used than EMG biofeedback is EEG biofeedback, or feedback from rhythmic cerebral electrical activity. This rhythmic activity is an inherent property of cells within many thalamic nuclei. Specific thalamocortical fibers relay this rhythmic activity between subcortical nuclei and the cerebral cortex. Rhythmic firings originating in the thalamus are blocked by cerebral activity associated with attention or with sensory or motor activity.
Greek letters are used to designate the frequency of the rhythm: delta (0-3 Hz), theta (4-7 Hz), alpha (8-13 Hz), and beta (14+ Hz). Delta activity is most prevalent during Stages 3 and 4 of deep sleep. Theta activity can be recorded from many portions of the cortex or from the cerebrum in both awake and sleeping individuals. Alpha activity is linked to an alert but relaxed state. No clear behavioral states are related to beta frequencies.
Biofeedback can help people learn how to modulate the brain waves described above. Since there are often accompanying changes in electromyographic (EMG) activity and peripheral blood flow, the change in EEG activity may not be conditioned directly.
Biofeedback for Insomnia
Psychologists working in sleep disorder clinics sometimes use biofeedback for the treatment of insomnia. Most often they train patients to relax the frontalis muscle using EMG biofeedback. Once trained with biofeedback, subjects can, without equipment, apply their relaxation strategies when they are trying to go to sleep.
Studies of EMG biofeedback find that biofeedback is better than placebo.7,8 On the other hand, there is no evidence that EMG biofeedback is more effective on average than other relaxation methods.7,8
Two other forms of biofeedback have been developed that are specific for insomnia. One type conditions EEG theta waves. Theta conditioning has been used successfully for individuals whose sleep onset is inhibited by a "flood of thought" associated with tension and anxiety.12 Theta EEG waves define stage 1 (i.e., the transition phase between full wakefulness and clear sleep). Theta waves indicate a very deep stage of relaxation characteristic of advanced meditation. With the onset of theta waves, patients do not experience a blank mind, but instead report that their thought content changes from disturbing and ruminating to more pleasant themes.
A second type of EEG feedback reinforces a 12-14 Hz rhythm over the sensorimotor cortex (SMR). As with the Greek letter rhythms, this rhythm may also represent an idling of pools of subcortical neurons. The SMR rhythm is blocked by movement.
Clinical Studies
Based on findings that good sleepers had a stronger waking SMR than insomniacs and that SMR rhythm was unrelated to the frontalis tone measured by the EMG, a study was performed to compare the effectiveness of SMR biofeedback to other types of biofeedback for the treatment of insomnia.13 The three biofeedback methods were tested in a study of 48 insomniacs assigned to four groups: 1) EMG feedback; 2) EMG and theta feedback; 3) SMR; and 4) controls. Sleep was measured at baseline, after therapy, and after nine months. The investigators found that subjects who had biofeedback did not, as a group, do better than controls. When the insomniacs were divided into those with tension or long sleep latencies and those with difficulty maintaining sleep, the authors found that the relaxation therapies (EMG and theta biofeedback) improved both long-term and short-term outcome for patients who were anxious or had long sleep latencies. SMR biofeedback did not help anxious subjects, but it did improve long- and short-term outcomes for patients who had frequent awakenings. Mixing two types of biofeedback was found to be inferior to only one type of biofeedback. A replication study confirmed that tense and anxious insomniacs benefited only from theta feedback but not SMR and that non-anxious insomniacs benefited from SMR but not theta biofeedback.14
Availability
Treatment with biofeedback is easily available. It may be provided by the complete spectrum of psychological counselors and by many others with minimal training in counseling. It does not require a license. Although there is a credentialing process for biofeedback that depends on course work, apprenticeship, and an examination, these credentials do not guarantee quality, and their absence does not preclude quality. Biofeedback for the treatment of insomnia requires special expertise not available to the great majority of biofeedback practitioners. Treatment for insomnia that includes biofeedback should be provided by a psychologist trained in both sleep therapy and biofeedback.
Adverse Effects
With the exception of excessive reliance on the machine that some patients develop, there are no reported major risks to biofeedback.11
Conclusion
EMG and EEG theta wave biofeedback are relaxation therapies that have been used effectively to treat insomnia. Neither has been shown to be consistently more effective than other relaxation methods. Because the equipment for biofeedback introduces additional cost and complexities, biofeedback's primary use should be for patients who require relaxation therapy but cannot learn how to relax using other methods. The more typical solutions-pharmacological, stimulus control, sleep restriction, and other relaxation therapy-should be tried first.
Biofeedback is one component of effective behavioral intervention for insomnia. It should not be considered to be a mechanical sleeping pill substitute that can be used in isolation. As a tool for learning relaxation, it is only reliably effective in the hands of a skilled practitioner who knows how to coach subjects in the cognitive strategies of relaxation and how to use different forms of biofeedback in effective combination.
EEG SMR rhythm biofeedback is an intriguing technique that probably promotes sleep by a different mechanism of action than other biofeedback methods. This method has been shown to increase sleep efficiency for the difficult-to-treat, non-anxious patient who cannot maintain sleep. Because it requires, on average, more than 20 training sessions, it is not widely available in the United States.
The author acknowledges David Young, MA; Dedra Diehl, MLS; and Steven Anderson, PhD, for providing helpful information.
References
1. Morin CM, Kwentus JA. Behavioral and pharmacologic treatments for insomnia. Ann Behav Med 1988;10(3):91-100.
2. Kales A, Kales JD. Evaluation and Treatment of Insomnia. New York: Oxford University Press; 1984.
3. Mellinger GD, Balter MB, Uhlenhuth EH. Insomnia and its treatment: Prevalence and correlates. Arch Gen Psychiatry 1985;42:225-232.
4. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders: An opportunity for prevention? JAMA 1989;262:262.
5. Beutler LE, Thornby JI, Karacan I. Psychological variables in the diagnosis of insomnia. In: Williams RL, Karacan I (eds). Sleep Disorders: Diagnosis and Treatment. New York: Wiley; 1978.
6. Murtagh DRR, Greenwood KM. Identifying effective psychological treatments for insomnia: A meta-analysis. J Consult Clin Psychol 1995;63(1):79-89.
7. Van Oot PH, Lane TW, Borkovec TD. Sleep disturbances. In: Adams HE, Sutker PB (eds). Comprehensive Handbook of Psychopathology. New York: Plenum; 1984:683-723.
8. Morin CM, Culbert JP, Schwarta SM. Nonpharmacological interventions for insomnia: A meta-analysis of treatment efficacy. Am J Psychiatry 1994;151(8): 1172-1180.
9. Monroe L. Psychological and physiological differences between good and poor sleepers. J Abnormal Psychol 1967;72:255-264.
10. Basmajian JV. Introduction, Principles and Background. In: Basmajian JV (ed). Biofeedback Principles and Practice for Clinicians. Baltimore, MD: Williams and Wilkins; 1989:1-15.
11. Stoyva JM. Autogenic training and biofeedback combined: A reliable method for the induction of general relaxation. In: Basmajian JV (ed). Biofeedback Principles and Practice for Clinicians. Baltimore, MD: Williams and Wilkins; 1989:169-186.
12. Lubar JF. Electroencephalographic biofeedback and neurological applications. In: Basmajian JV (ed). Biofeedback Principles and Practice for Clinicians. Baltimore, MD: Williams and Wilkins; 1989:67-90.
13. Hauri P. Treating psychophysiologic insomnia with biofeedback. Arch Gen Psychiatry 1981;38:752-758.
14. Hauri PJ, Percy L, Hellekson C, et al. The treatment of psychophysiologic insomnia with biofeedback: A replication study. Biofeedback and Self-Regulation 1982;7(2):223-235.
Dr. Hartz is Associate Professor of Medicine and Staff Doctor, Department of Family Practice, The University of Iowa Hospital and Clinics, Iowa City, IA.
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