This unit covers the Pathophysiology, biofeedback modalities, and treatment protocols for specific ANS biofeedback applications (IV-D).
Students completing this unit will be able to discuss:
Below is a BioTrace+ / NeXus-10 screen that displays several of the modalities that could be used to treat autonomic disorders like arthritis.
Arthritis is a subtype of rheumatism
in which inflammation produces painful joint swelling and stiffness. In
rheumatoid arthritis, the immune
system bilaterally attacks cartilage and joint linings, resulting in a
thickened synovial membrane and swollen joint. In
osteoarthritis, aging, irritation, and "wear-and-tear"
progressively destroy cartilage in the synovial joints, especially those
that bear weight (Tortora & Derrickson, 2006).
The prevalence of rheumatoid arthritis (RA) in the United States is about 1% and the male-to-female ratio is 1 to 3. While RA can occur at any age, the age of onset is usually between 25 and 50, and prevalence peaks in the 40s and 50s. Juvenile rheumatoid arthritis (JRA) appears before the 16 years (King & Worthington, 2005).
About 80-90% of patients over 65 present with primary osteoarthritis. In those over 55, osteoarthritis is more prevalent among women and targets the distal interphalangeal joints of the fingers and knee joints. However, men disproportionately experience osteoarthritis of the hip. Under 45, osteoarthritis is more prevalent among men than women. The prevalence of osteoarthritis increases nonlinearly with age and accelerates after age 50 (Stacy & Basu, 2005).
Temperature biofeedback may increase clearance of inflammatory cytokines
(IL6, IL8 and GM-CSF), prostaglandins, and protease enzymes, reducing
arthritis pain.
Flor, Haag, Turk, and Koehler (1983)
compared SEMG biofeedback, a credible pseudotherapy, and conventional
medical treatment for 24 patients diagnosed with chronic rheumatic back
pain. Patients were treated for 4 weeks as inpatients and then evaluated
at 4-month follow-up. Only the SEMG biofeedback group showed significant
SEMG reduction and improvement in back pain duration, intensity, and
quality.
Lavigne and colleagues (1992)
evaluated the efficacy of a six-session treatment protocol that included
relaxation training, SEMG biofeedback, and thermal biofeedback for
children diagnosed with juvenile rheumatoid arthritis, and training to
help mothers manage physical therapy and school attendance.
Visual inspection of the multiple baseline data for four children who
received immediate treatment showed modest evidence of reduction in child
and parent ratings of pain intensity, and in parent ratings of the
frequency of pain behaviors at the end of treatment and at 6-month
follow-up. There was no reduction in the physical therapist’s rating of
pain during evaluation.
Edema is swelling due to the abnormal
accumulation of interstitial fluid produced by excessive capillary
filtration or inadequate fluid reabsorption. In cases of inflammation and
allergic reactions, temperature biofeedback may help remove accumulated
fluid from the edematose region by dilating peripheral arteries.
Preeclampsia or pregnancy-induced hypertension (PIH) affects about 5% of pregnancies in the United States. Preeclampsia is a major cause of perinatal morbidity and mortality, and is responsible for about 35-300 deaths per 1000 births. While the risk of preeclampsia is highest for pregnant women in the youngest and oldest age ranges, women under 20 are at greatest risk (Brooks, 2005).
Somers, Gevirtz, Jasin, and Chin (1989)
examined the efficacy of a biobehavioral intervention to help treat mild
pregnancy-induced hypertension (PIH),
which is characterized by the development of hypertension, proteinuria,
and edema late in pregnancy. The researchers randomly assigned 45 women
with symptoms of PIH to one of three treatment conditions: bed rest
alone, bed rest with individualized compliance enhancement training, or a
four-session biobehavioral treatment consisting of bed rest, compliance
enhancement training, and individualized thermal biofeedback- assisted
relaxation training.
Subjects in the biobehavioral group achieved significantly lower blood
pressures than those in the bed rest or compliance enhancement
conditions, whose pressures increased and risked both maternal and infant
Patients with
irritable bowel syndrome (IBS)
respond to stressors with alternating diarrhea and constipation,
associated with abdominal pain, cramping, excessive mucus in the feces,
flatulence, loss of appetite, and nausea.
IBS has an estimated prevalence of 10-20% and an incidence of 1-2% in the United States. About 10-20% of persons with IBS receive medical treatment for this disorder. In Western nations, women develop IBS three times more often than men. About 50% of IBS patients report onset of symptoms before age 35 (Lehrer & Lichtenstein, 2005).
Evidence-Based Practice in
Biofeedback and Neurofeedback (2004) rates biofeedback
for IBS at level 2 efficacy, possibly efficacious. The criteria
for level 2 efficacy include "At least one study of sufficient
statistical power with well identified outcome measures, but lacking
randomized assignment to a control condition internal to the study" (pp.
26-27). A level 2 rating was awarded due to mixed findings.
While
Schwartz, Taylor, Scharff, and Blanchard
(1990) reported that biofeedback reduced IBS symptoms up to 4
years posttreatment, two controlled studies reported by
Blanchard et al. (1992) found no
advantage for an established multimodal program (cognitive therapy,
relaxation, and temperature biofeedback) over attention-placebo or
symptom monitoring control groups.
More recently, Leahy, Clayman, Mason, Lloyd, and
Epstein (1998) reported that training with a computer-based
biofeedback game that monitored electrodermal activity successfully
reduced IBS symptoms.
An International Consensus Meeting for the Outpatient Management of Neuropathy described diabetic neuropathy as "the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after exclusion of other causes." Patients with diabetic neuropathy present with diverse sensory (numbness), motor (impaired fine coordination), and autonomic (sensitivity to bright light) symptoms (Soliman & Gellido, 2005).
Prevalence estimates of diabetic neuropathy vary widely due to discrepant diagnostic criteria, sampling, and evaluation
procedures. From 10-65% of diabetics are diagnosed with peripheral neuropathy. There is a higher incidence of diabetic neuropathy in men than women. While diabetic neuropathy can occur at any age, its symptoms are most often detected in patients over 50 (Soliman & Gellido, 2005).
Fiero,
Galper, Cox, Phillips, and Fryburg (2003) studied the effect
of neuropathy on the acquisition of thermal biofeedback-trained foot-warming by 24 diabetics (5 type I and 19 type II). Training consisted of
two hand-warming and four foot-warming sessions. Despite
mild-to-moderate neuropathy, participants increased foot temperature an
average 2.2o F across six thermal biofeedback sessions.
However, lower extremity sympathetic-autonomic and sensory neuropathies
accounted for 41% of the variance in foot-warming and limited skill
acquisition. This study's findings were weakened by the lack of a
no-treatment control group.
The authors did not find a similar relationship between upper extremity
neuropathy and hand-warming. They speculated that a ceiling effect--most
patients approached the criterion temperature during their first
session--prevented detection of any relationship between neuropathy and
hand-warming success.
Diabetics risk foot ulcers due to neurologic and microvascular causes.
Progressive damage to peripheral sensory nerves, called peripheral
neuropathy, can reduce or eliminate sensation from the foot and/or leg
so that patients are unaware of traumatic injuries for days or weeks. In
Charcot foot deformity, loss of pressure information causes patients to
place excessive stress on their feet, resulting in reduced tissue blood
flow (ischemia), localized tissue death (necrosis), and microfractures
in the bones of the feet (Fishman, 2004).
About 3-4% of diabetics have foot ulcers or deep infections and 15% will suffer foot ulcers. Foot ulcer raises the risk of amputation by a factor of 8. Two years after transtibial amputation, 36% will have died (Pinzur, 2004).
Rice, Kalker, Schindler, and Dixon (2001)
reported that temperature biofeedback increased healing of chronic
nonhealing foot ulcers in a randomized controlled study of 32 patients.
Healing occurred in 87.5% of the temperature biofeedback group and 43.8%
of the control group.
Evidence-Based Practice in Biofeedback and
Neurofeedback (2004)
rates biofeedback for foot ulcers at level 2 efficacy, possibly efficacious
(p. 22).
Hyperhidrosis involves excessive sweating. While it is normal to perspire when excited or following
physical exertion, these individuals constantly perspire, often without
obvious triggers, from their palms and soles, and less frequently from
their armpits, chest, and back.
Generalized hyperhidrosis may be caused by autonomic
dysregulation or it may be due to a metabolic disease, fever-inducing
illness, or cancer. Localized hyperhidrosis
may be due to abnormal regrowth of damaged sympathetic axons, an
abnormal number or arrangement of eccrine sweat glands, or other
vascular abnormalities. Where generalized hyperhidrosis often starts in
adulthood, localized hyperhidrosis is often first seen in childhood or
adolescence. Both forms of hyperhidrosis can severely embarrass these
individuals and produce occupational disability (Altman, 2004).
Conventional therapies for this disorder include antiperspirants, Botox
injections, lotions, oral medications, and in extreme cases, endoscopic
transthoracic sympathectomy (ETS).
Hyperhidrosis affects more
than 200,000 Americans. Internationally, palmoplantar hyperhidrosis (excessive sweating from the hands
and feet) affects the Japanese 20 times more often than other ethnic
groups (Altman, 2004). The incidence of hyperhidrosis in adolescents and young adults in the United States is estimated at 0.6-1.0%. This condition affects both men and women, and all age groups (Schwartz & Altman, 2005).
The rationale for using electrodermal biofeedback to treat hyperhidrosis
is that sympathetic activation can increase sweating, which raises skin
conductivity, and that decreasing skin conductivity can both reduce
sympathetic arousal and resultant perspiration. Also, in cases where
hyperhidrosis is triggered or exacerbated by stressors, a
biofeedback-assisted intervention could improve patient symptoms through
better stress management. The evidence of biofeedback efficacy in
hyperhidrosis is weak, based on small pretest-posttest studies without
control groups.
Gentry (1980) reported successful
visual water vapor biofeedback treatment of 11 of 14 adults who reduced their
excessive sweating 6 weeks following the end of treatment. The author
hypothesized that the relaxation component of treatment may have been
responsible for their improvement.
Singh and Singh (1993) reported that
a program of electrodermal biofeedback-assisted relaxation helped 6 of
10 male patients significantly reduce their sweating. The authors found
that clinical improvement was strongly correlated with reductions in
skin conductivity.
Now that you have completed this module, compare the evidence supporting
the diverse autonomic applications. For which disorders is the evidence
of efficacy strongest and weakest?
Altman, R. (2004). Hyperhidrosis. eMedicine.
Blanchard, E. B., Schwartz, S. P., Suls, J. M., Gerardi, M. A., Scharff,
L., Greene, B., et al. (1992). Two controlled evaluations of
multicomponent psychological treatment of irritable bowel syndrome.
Behavioral Research and Therapy, 30(2), 175-189.
Brooks, M. B. (2005). Pregnancy, preeclampsia. eMedicine.
Duller, P. G. (1980). Use of biofeedback in treating chronic
hyperhidrosis: A preliminary report. Br J Dermatol, 103(2),
143-146.
Fiero, P. L., Galper, D. I., Cox, D. J., Phillips, L. H., & Fryburg, D.
A. (2003). Thermal biofeedback and lower extremity blood flow in adults
with diabetes: Is neuropathy a limiting factor? Applied
Psychophysiology and Biofeedback, 28(3), 193-203.
Fishman, T. D. (2004). Wound care information network.
Flor, H, Haag, G, Turk, D. C., & Koehler, H. (1983). Efficacy of EMG
biofeedback, pseudotherapy, and conventional medical treatment for
chronic rheumatic back pain. Pain, 1(17), 21-31.
Guyton, A. C., & Hall, J. E. (1997). Human physiology and mechanisms of
disease. Philadelphia: W. B. Saunders Company.
King, R. W., & Worthington, R. (2005). Arthritis, rheumatoid. eMedicine.
Lavigne, J. V., Ross, C. K., Berry, S. L., Hayford, J. R., & Pachman, L.
M. (1992). Evaluation of a psychological treatment package for treating
pain in juvenile rheumatoid arthritis. Arthritis Care and Research, 5(2),
101-110.
Leahy, A., Clayman, C., Mason, I., Lloyd, G., & Epstein, O. (1998).
Computerised biofeedback games; A new method for teaching stress
management and its use in irritable bowel syndrome. Journal of the
Royal College of Physicians of London, 32(6), 552-556.
Lehrer, J. K., & Lichtenstein, G. R. (2005). Irritable bowel syndrome. eMedicine.
McGrady, A., Kern-Buell, C., Bush, E., Devonshire, R., Claggett, A. L.,
& Grubb, B. P.(2003). Biofeedback-assisted relaxation therapy in
neurocardiogenic syncope: A pilot study. Applied Psychophysiology and
Biofeedback, 28(3), 183-192.
Palumbo, P. J., & Melton, L. J. (1985). Diabetes in America: Diabetes
data compiled in 1984. (NIH publication No, 851468). Washington, DC:
U.S. Government Printing Office.
Pinzur, M. S. (2004). Diabetic foot. eMedicine.
Rice, B., Kalker, A. J., Schindler, J. V., & Dixon, R. M. (2001). Effect
of biofeedback-assisted relaxation training on foot ulcer healing.
Journal of the American Podiatric Medical Association, 91(3)
132-141.
M. S.
Schwartz, & F. Andrasik (Eds.). (2003). Biofeedback: A practitioner's guide
(3rd ed.).
New
York: The Guilford Press.
Schwartz, R. A., & Altman, R. (2005). Hyperhidrosis. eMedicine.
Schwartz, S. P., Taylor, A. C., Scharff, L., & Blanchard, E. B. (1990).
Behaviorally treated irritable bowel syndrome patients: A four-year
follow-up. Behavioral Research and Therapy, 28(4), 331-335.
Singh, G., & Singh, G. (1993). Biofeedback assisted relaxation (BAR) in
management of hyperhidrosis: A preliminary study. Indian Journal of
Dermatology, Venereology, and Leprology, 59(4), 187-189.
Soliman, E., & Gellido, C. (2005). Diabetic neuropathy. eMedicine.
Stacy, G., & Basu, A. P. (2005). Osteoarthritis, primary. eMedicine.
Tortora, G. J., & Derrickson, B. H. (2006). Principles of anatomy and
physiology (11th ed.). New York: John Wiley & Sons, Inc.
Yucha, C. B., & Gilbert, C. D. (2004). Evidence-based practice in
biofeedback and neurofeedback. Wheat Ridge: AAPB.