The biopsychosocial model is a compelling approach to conceptualizing and treating chronic pain disorders. Practitioners who utilize this model understand the importance of the medical, psychological, and psychophysiological assessment of pain patients. Biofeedback is often efficacious and cost effective in treating common pain disorders like tension-type and migraine headache. Biofeedback training may allow clients to reduce medication consumption and emergency room visits. The client's adoption of a sick role and dependence on analgesic and muscle relaxant medication are major challenges to effective therapy.

Migraine research has supported a model in which the trigeminal nerve plays a central role in all forms of primary headache. Activation of a trigeminal headache generator appears to precede blood vessel swelling and pain, in contrast to the traditional model which identified these events as the proximal causes of migraine. The efficacy of temperature biofeedback for treating migraine has been challenged, especially by research showing that the direction of temperature training does not affect treatment outcome.

Research in Raynaud's disease has yielded unexpected benefits for the field of biofeedback. We have learned that hand-warming and hand-cooling involve separate mechanisms, temperature biofeedback is not intrinsically relaxing, and procedures like frontal SEMG biofeedback and autogenic exercises do not reliably produce hand-warming. Raynaud's research has also supported the local fault model of Raynaud's disease and challenged the traditional model that effective treatment reduces sympathetic arousal.



This unit covers the Chronic neuromuscular pain (IV-C), General treatment considerations (IV-D), Target muscles, typical electrode placements, and SEMG treatment protocols (IV-E), and Pathophysiology, biofeedback modalities, and treatment protocols for specific ANS biofeedback applications (V-D).
 
Students completing this unit will be able to discuss:

  1. SEMG differences between chronic pain subjects and normal pain subjects
  2. General treatment considerations
    A. Standard physical rehabilitation techniques and procedures
    B. SEMG assessment strategies
    C. SEMG down training strategies
    D. SEMG up training strategies
  3. Target muscles, typical electrode placements, and SEMG treatment protocols
    A. Tension-type headache
    B. Temporomandibular disorders
    C. Posterior neck and upper back pain
    D. Low back pain
    E. Worksite ergonomic applications
  4. Pathophysiology, biofeedback modalities, and treatment protocols for specific ANS biofeedback
    applications
    A. Migraine headache
    B. Raynaud’s disease

 


Tension-type headache is characterized by a steady, nonthrobbing pain that may involve the fronto-temporal vertex and/or occipito-cervical areas with a lateral or bilateral distribution. This headache has a duration of 30 minutes to 7 days.



Tension-type headache is the most common primary headache and estimates of its prevalence range from 30-80%.








Tension-type headache is divided into episodic and chronic headache. Episodic tension-type headache is diagnosed when the patient has at least 10 previous headaches, fewer than 15 days per month, and no evidence of a secondary headache disorder.



Chronic tension-type headache is diagnosed when there is an average headache frequency of more than 15 days per month for more than 6 months (Martin & Elkind, 2005).



Recent studies have shown that tension-type headache patients showed higher SEMG levels than healthy controls. Researchers have monitored frontalis, occipitalis, temporalis, and trapezius muscles to study the role of muscle activity in tension-type headache. A frontalis or bifrontal placement is shown below.







A cervical paraspinal placement is shown below.








Hudzinski and Lawrence (1988) reported that both right- and left-sided FpN (frontalis and posterior neck) placements significantly discriminated between chronic tension-type headache patients when they had a headache and when they were headache-free.

An FpN placement involves an active electrode over a frontalis muscle and another over a cervical paraspinal muscle on the same side below the hairline (Schwartz & Andrasik, 2003). A clinician might simultaneously monitor two FpN channels, left frontalis-left cervical paraspinal and right frontalis-right cervical paraspinal.

Schoenen et al. (1991) reported higher left frontalis, temporalis, and trapezius muscles during reclining, standing, and math stressor conditions (62.5% of patients exceeded 2 SD). Studies of tension-type headache patients do not consistently show elevated SEMG activity during headache episodes, compared with when they are headache free. One study actually found that frontal SEMG levels were significantly lower during a tension-type headache (Hatch et al., 1992).

The inconsistency among studies may be due to differences in recording sites, positions, tasks, and patient characteristics.



The design of a treatment protocol should be based on the clinical outcome literature for the population you are treating (e.g., children, adults, elderly) and the findings of a psychophysiological profile that examines multiple response systems during resting, stress, and recovery conditions. Tailor treatment to your patient’s unique response stereotypy.

Several treatment components should be considered based on the tension-type headache literature:

  1. frontal SEMG biofeedback
  2. masseter SEMG biofeedback
  3. temporalis SEMG biofeedback
  4. trapezius SEMG biofeedback
  5. temperature biofeedback
  6. relaxation training
  7. cognitive behavior therapy

Complementary treatment components include:

  1. heat packs and diathermy
  2. ice packs
  3. massage
  4. muscle relaxants like Vanaflex
  5. physical therapy exercises to increase range of motion




Evidence-Based Practice in Biofeedback and Neurofeedback (2004) rates SEMG biofeedback for adult headache at level 4 efficacy, efficacious. The criteria for level 4 efficacy include:"

  1. In a comparison with a no-treatment control group, alternative treatment group, or sham (placebo) control utilizing randomized assignment, the investigational treatment is shown to be statistically significantly superior to the control condition or the investigational treatment is equivalent to a treatment of established efficacy in a study with sufficient power to detect moderate differences, and
  2. The studies have been conducted with a population treated for a specific problem, for whom inclusion criteria are delineated in a reliable, operationally defined manner, and
  3. The study used valid and clearly specified outcome measures related to the problem being treated, and
  4. The data are subjected to appropriate data analysis, and
  5. The diagnostic and treatment variables and procedures are clearly defined in a manner that permits replication of the study by independent researchers, and
  6. The superiority or equivalence of the investigational treatment has been shown in at least two independent research settings" (pp.23-24).
     


Blanchard (1992) summarized the findings of his headache studies since 1980:



Hudzinski (1993) recommended that clinicians use both frontal and neck placements. The neck may be more useful for SEMG reduction and the two placements provide patient with more information. Clinicians should be aware that neither the frontal or neck placements represent other muscle sites and reductions at either site should not be expected to generalize.
 


Arena, Bruno, Hannah, and Meader (1995) compared forehead and trapezius SEMG biofeedback with a Progressive Muscle Relaxation control condition for treatment of tension headache. Trapezius SEMG biofeedback produced the best clinical outcomes.



The National Institutes of Health Technology Assessment Panel (1996) concluded that SEMG biofeedback was superior to psychological placebo and comparable to relaxation therapies in treating tension headache.



The National Headache Foundation's Standards of care for headache diagnosis and treatment (1999) found that "biofeedback has been shown to be an excellent treatment in the long term management of migraine and tension-type headache disorders" (p. 17).



A meta-analysis by McCrory, Penzien, Rains, et al. (1996) showed that SEMG biofeedback, relaxation therapy, and cognitive-behavioral therapy were moderately effective treatments for tension-type headache.



A review of more than 100 studies by McGrady, Andrasik, Davies, et al. (1999) found that biofeedback, relaxation training, and stress management training produced an average 50% reduction of headache pain.


Barton and Blanchard (2001) reported treatment failure with 10 of 12 patients (83%) suffering from moderate-to-high intensity chronic daily headaches who completed training. The treatment program consisted of 20 sessions of training in progressive muscle relaxation, thermal biofeedback, and cognitive stress coping therapy. The authors warned that these patients are relatively refractory to self-regulatory training.



Moss, Andrasik, McGrady, Perry, and Baskin (2001) argue: "Biofeedback also has particular advantages over most medical treatments for headaches. Not only can it produce long-term remission of symptoms, but it does so without side effects. On the contrary, common side effects of medical treatments of headache include weight gain, sedation, and impaired concentration, and headache medications frequently lose their effectiveness over time. There is even preliminary evidence to suggest that successful treatment with biofeedback and relaxation can result in substantial cost savings."



Several studies have shown that tension-type headache patients with elevations on measures of depression, like the (Beck depression inventory and MMPI scale 2, respond more poorly to biofeedback and relaxation training (Jacob et al., 1983; Blanchard, Andrasik, Evans, et al., 1985; Neff et al., 1985).

Antidepressants have been shown to be effective in chronic tension-type headache. Fluoxetine (Prozac) was shown helpful in a double-blind placebo-controlled trial conducted by Saper et al. (1994). Amitryptiline (Elavil) was more effective for prophylactic treatment than citalopram (Celexa) and placebo in a double-blind study by Bendtsen et al. (1996).




A migraine with aura (classic migraine) features a prodrome or neurological symptoms that precede a breakthrough headache, hours to days before headache onset, and accounts for up to 31% of all migraine patients (Launer et al., 1999). The headache is preceded (10-20 minutes) by painless neurological symptoms that are mainly visual (scintillating scotomata and visual field defects) and last from 20-60 minutes. Headache onset may occur at any time and lasts 4-72 hours (Martin & Elkind, 2005).






A migraine without aura (common migraine) accounts for about 64% of all migraine patients (Launer et al., 1999). This headache lasts 4-72 hours (Martin & Elkind, 2005).
 




Prodromes without headaches are called migraine equivalents.

Migrainous infarction (complicated migraine) involves less than 1-2% of migraineurs and includes hemiplegic, ophthalmoplegic, and basilar migraine. Complicated migraine is a vascular headache with neurologic symptoms that often follow a definite sequence. In severe cases, permanent neurologic deficits may follow the attack (Diamond & Dalessio, 1986).

Ophthalmoplegic migraine involves nonpulsating, moderate pain (often with vomiting) and paralysis of one or more extraocular muscles that move the eyes. This disrupts alignment of eye movement and results in double vision. Following the headache, these symptoms may persist from 45 minutes to 2 months (Cruciger & Mazow, 1978).

Basilar artery migraine has prodromal symptoms that last from 2-45 minutes. Symptoms include total blindness, altered consciousness, and vertigo and ataxia (involving the brainstem). Patients experience severe pulsating occipital headache with vomiting that persists for hours or until sleep. This headache is seen in adolescent girls.



The one-year prevalence of migraine in the United States and Western Europe is estimated at 11%, affecting 6% of men and 15-18% of women. The lifetime prevalence in North America is 18%. The median migraine frequency in North America is 1.5 per month with a median duration of 24 hours (Launer et al., 1999).



Cluster headache episodes start abruptly without prodromes, 2 to 3 hours after falling asleep. They feature intense, throbbing, unilateral pain involving the eye, temple, neck, and face for 15 to 90 minutes. A typical pattern is one headache every 24 hours for 6-12 weeks followed by a 12-month period of remission (Diamond & Dalessio, 1986; Martin & Elkind, 2005).



While estimates of cluster headache prevalence vary considerably, one survey reported a rate of .24% (Martin & Elkind, 2005).







The trigeminal nerve may be activated in all primary headaches--cluster, migraine and tension-type. Cortical hyperexcitability may activate the trigeminal nerve producing a breakthrough headache. The trigeminal nerve receives sensory information about the region from the jaw to the scalp and controls eight muscles. These muscles include the masseter, temporalis, lateral and medial pterygoids, tensor veli palatini, mylohyoid, digastric (anterior), and tensor tympani.

Migraine patients may be hypersensitive to headache triggers and have an abnormally low threshold for activating the trigeminal nerve, compared with occasional tension-type headache patients. Repeated migraine episodes may reduce migraineurs' ability to block pain.



Caption: This image illustrates the lateral view of the female torso, with the nerves of the head and neck represented in relation to a lateral view of the right side of the skull, vertebral column, and thorax. The trigeminal nerve is shown in yellow with its three main branches: ophthalmic nerve (sensory), maxillary nerve (sensory), and mandibular nerve (motor and sensory).



Diverse internal triggers (hormonal fluctuations, stress, sleep deprivation) and external triggers (allergens, diet, and weather changes) increase the firing of neurons in the brainstem, and hypothalamus and cortex, which send signals to the migraine generator that produce nausea and vomiting.

A hypothesized migraine generator in the dorsal raphe nucleus in the upper brainstem activates the trigeminal nerve, whose extensive branches cover the brain "like a helmet" and initiate the migraine. Trigeminal nerve endings in the brain's dura mater release proteins that dilate blood vessels and increase the nerves' sensitivity. Thus, blood vessel swelling is the effect, instead of the cause, of a migraine.


Caption: This image illustrates the lateral view of the male head and neck, with arterial blood supply to the brain in relation and vertebral column represented. The following arteries are represented: arteria carotis interna, arteria carotis communis, arteria vertebralis, arteria cerebri media, arteria cerebri anterior, arteria basilaris, and arteria cerebri posterior.



Siniatchkin and colleagues (2000) reported that young migraine patients without aura showed greater slow cortical potential (SCP) amplitudes and less ability to reduce cortical negativity than healthy controls. SCP biofeedback training reduced cortical excitability and headache symptoms.

Kropp, Siniatchkin, and Gerber (2002) found that SCP amplitude and the delay of habituation were greatest in the few days before the next migraine attack. They concluded that these findings support the model that migraine results from "cortical hypersensitivity, hyperactivity, and a lack of habituation" (p. 203).

Lang and colleagues (2004) used magnetoencephalography to identify a population of hyperexcitable primary somatosensory cortical neurons that may play a role in migraine. They found that neuron hyperexcitability in the interictal state (between headache episodes) is correlated with migraine frequency and proposed that it underlies the brain's vulnerability to migraine episodes.

MRI studies have shown that migraine pain is not primarily due to vasodilation. Increased blood flow occurs hours after an aura has ended and a breakthrough headache has started. Cutrer (1999) demonstrated that the auras that precede classic migraines are due to cortical spreading depression instead of vasoconstriction.

Throbbing headache pain is produced by dilation of blood vessels in the dura mater of the brain, which contains sensory neurons. Activation of these nerve fibers releases neuropeptides like calcitonin gene-related peptide (CGRP) and substance P that stimulate pain receptors and increase blood vessel dilation (Mathew & Buchholz, 2002). Pain signals travel to the trigeminal nucleus caudalis in the brainstem and to the thalamus and cortex in the forebrain for processing (Baskin & Weeks, 2003).

These neuropeptides may further irritate trigeminal pain sensors to lower the pain threshold and prolong a migraine for up to 72 hours (Cutrer, 1999). Successive migraine episodes may impair the periaqueductal gray matter's ability to suppress pain, due to increased deposition of iron in this region (Welch, 2002).

Several researchers have reported elevated pericranial muscle contraction in migraine (Bakal & Kaganov, 1977; Gannon et al., 1987; Lichstein et al., 1991).



Etminan's (2004) meta-analysis of 14 studies revealed that male and female migraine patients, with and without aura, had twice the risk of stroke compared with those without migraine. A more controversial finding was that female migraine patients who also used birth control pills had about eight times the risk of stroke compared with women without migraine not using this medication. Migraine, birth control pills, and smoking may additively increase stroke risk by promoting clot formation.



Medina and Diamond (1978) reported that diet plays a relatively minor role in migraine pain. Radnitz (1990) proposed that vasoactive substances like tyramine affect about 5% of migraine patients. The main triggers are alcohol, chocolate, and red wine. There is little evidence that MSG, nitrates, or nitrites trigger headache.



Evidence-Based Practice in Biofeedback and Neurofeedback (2004) rates biofeedback for adult headache at level 4 efficacy, efficacious. The criteria for level 4 efficacy include:"

  1. In a comparison with a no-treatment control group, alternative treatment group, or sham (placebo) control utilizing randomized assignment, the investigational treatment is shown to be statistically significantly superior to the control condition or the investigational treatment is equivalent to a treatment of established efficacy in a study with sufficient power to detect moderate differences, and
  2. The studies have been conducted with a population treated for a specific problem, for whom inclusion criteria are delineated in a reliable, operationally defined manner, and
  3. The study used valid and clearly specified outcome measures related to the problem being treated, and
  4. The data are subjected to appropriate data analysis, and
  5. The diagnostic and treatment variables and procedures are clearly defined in a manner that permits replication of the study by independent researchers, and
  6. The superiority or equivalence of the investigational treatment has been shown in at least two independent research settings" (pp. 23-24).
     


Diamond et al. (1979) reported that 75% of 556 migraine patients treated with biofeedback and relaxation training experienced pain reduction. Pain reductions were relatively permanent in 37% of these patients.



Diamond and Montrose (1984) reported that 51% of 693 migraine patients treated with biofeedback and relaxation training experienced excellent or moderate improvement.



Sargent, Solbach, Coyne, Spohn, and Segerson (1986) found that 136 patients who received thermal biofeedback with autogenic training, autogenic training, or frontal SEMG biofeedback experienced greater reductions in headache activity than the no-contact control group. The three treatment groups did not differ in their reduction of headache activity.



There is little demonstrated efficacy of biofeedback and relaxation for cluster headache. Blanchard, Andrasik, Jurish, and Teders (1982) found modest improvement in 2 of 11 (19%) patients at 22-30 month follow-up. Blanchard (1992) concluded that the efficacy of behavioral treatments for cluster headache has not been demonstrated.




      


Blanchard et al. (1985) reported that relaxation alone resulted in improvement in 23.8% of vascular headache patients and 41% of tension headache patients. Relaxation with temperature biofeedback resulted in improvement in 52% of combined tension headache and vascular headache patients, and 52% of vascular headache patients. The strongest treatment outcome predictors were patient age, trait anxiety, and MMPI scales 1 (Hyponchondriasis) and 3 (Hysteria). Symptom reduction was maintained for 1 year following treatment.

Blanchard, Appelbaum, Radnitz, Morrill, et al. (1990) reported in a study of 148 patients with migraine or combined headache that the effectiveness of thermal biofeedback with relaxation was not increased by adding cognitive therapy. The two biofeedback conditions were not superior to the pseudomedication placebo condition.

Blanchard and Diamond (1996) cautioned that there has never been a demonstration of the superiority of temperature biofeedback or temperature biofeedback combined with relaxation to a credible placebo. Blanchard (1992) concluded in his summary of his headache research since 1980 that both hand-warming and hand-cooling provided comparable headache relief.

Blanchard and colleagues (1997) randomly assigned 70 patients with chronic vascular headache to one of four treatments that consisted of 12 treatment sessions, scheduled twice a week:

Based on comparisons of headache diary data four weeks prior to treatment and four weeks post-treatment, the researchers concluded that there were significant reductions in both the headache index and medication index, and all treatment groups achieved comparable reductions on both indices. All treatment groups achieved comparable global self-reports of improvement at post- treatment. The direction of TFB was irrelevant to improvement in vascular headache activity.



Holroyd and Penzien's (1990) meta-analytic review revealed that both propranolol and relaxation/ biofeedback reduced migraine headache activity an average 43% based on daily recordings and 63% based on other outcome measures (physician/therapist ratings). They also reported that propranolol and relaxation/ biofeedback did not differ in effectiveness.



Cott et al. (1992) compared eight weeks of autogenic training alone, autogenic training combined with SEMG (frontalis) biofeedback, and autogenic training combined with temperature biofeedback over a 12-month follow-up period. Autogenic training combined with SEMG biofeedback produced superior headache activity reduction than autogenic training alone or autogenic training combined with temperature biofeedback.



McGrady, Wauquier, McNeil, and Gerard (1994) reported that biofeedback-assisted relaxation produced greater improvement in transcranial  Doppler measurements of cerebral blood flow than self-guided relaxation.



An Agency for Health Care Policy and Research meta-analysis concluded that temperature biofeedback, relaxation, and cognitive-behavioral interventions were at least moderately effective for treating migraine, when compared to a wait-list control (Goslin, Gray, McCrory, et al., 1999).



Silberstein's (2000) review of migraine treatment for the American Academy of Neurology-U.S. Consortium recommended SEMG and temperature biofeedback as effective treatments when delivered in the context of relaxation training.



Siniatchkin and colleagues (2000) studied the efficacy of SCP neurofeedback in treating 10 children with migraine without aura. The neurofeedback group was compared with 10 healthy children and 10 children with migraine placed on a waiting list. Following 10 training sessions, the children who received SCP training increased their regulation of cortical negativity during transfer trials (where no feedback was provided), reduced cortical excitability, and reported fewer days with migraine and improvement in other headache symptoms. The authors speculated that SCP training may have helped these patients by normalizing their regulation of cortical excitability.



Moss, Andrasik, McGrady, Perry, and Baskin (2001) argue: "Biofeedback also has particular advantages over most medical treatments for headaches. Not only can it produce long-term remission of symptoms, but it does so without side effects. On the contrary, common side effects of medical treatments of headache include weight gain, sedation, and impaired concentration, and headache medications frequently lose their effectiveness over time. There is even preliminary evidence to suggest that successful treatment with biofeedback and relaxation can result in substantial cost savings."



            



Design of a treatment protocol should follow medical assessment and should be based on the clinical outcome literature for the population you are treating (e.g., children, adults, elderly) and the findings of a psychophysiological profile that examines multiple response systems during resting, stress, and recovery conditions. Tailor treatment to your patient’s unique response stereotypy.

A broad spectrum of treatment components should be considered based on the migraine headache outcome literature:






Maurice Raynaud described a syndrome involving painful vasospasms located in peripheral vessels in 1862. Classic Raynaud’s is a triphasic disorder during which a patient exhibits color change in the digits of the hands or feet. Pallor (white color) and numbness are produced by constriction of arterioles and venules. Dilation of the anastomoses removes blood from the digits. Cyanosis (blue color) reflects pooled deoxygenated blood due to minimal arteriole inflow and constricted venous outflow. Rubor (red color) and burning sensations result from excessive inflow of oxygenated blood into the upper epidermis (called reactive hyperemia). This stage continues until the skin resumes a pink color (Surwit & Jordan, 1987).

Clinicians see the complete triphasic syndrome in only a fraction of Raynaud’s patients. The majority of patients exhibit only cyanosis or pallor (Porter et al., 1981). Patients typically report coldness at the tips of the digits which progresses downward.

A Mayo Clinic sample of 474 patients reported symptoms in the fingers in 55% of the cases, fingers and toes in 44%, and toes in 2% (Gifford & Hines, 1957). The cheeks, earlobes, and nose are sometimes affected (Hoffman, 1980).

Why do Raynaud’s symptoms mainly involve the fingers and toes? The extremities are vulnerable since our digits are nourished by superficial, peripheral vessels and are exposed to cold and trauma.

Raynaud’s episodes last from minutes to hours. Patients report coldness, impaired manual dexterity, and disruptive pain. In extreme cases, chronic vasoconstriction or frequent cyanosis can produce gangrene (tissue death) or lesions at the tips of digits (Surwit & Jordan, 1987). Amputation is necessary in about 0.5% of cases (Harrison, 1977).





Raynaud's disease is mainly controlled pharmacologically by drugs like prazosin and nifedipine. A sympathectomy (sympathetic nerve lesion) may be performed in severe cases. Unfortunately, symptom improvement is limited to 1-2 years.

Physicians divide Raynaud’s syndrome into Raynaud’s disease and Raynaud’s phenomenon. Raynaud’s disease is the primary form which is not due to an identifiable disorder. Raynaud’s phenomenon is the secondary form due to observable processes like trauma (carpal tunnel syndrome and shoulder girdle compression syndrome), arterial disorders (atherosclerosis), and rheumatic disorders (lupus erythematosis) (Spittell, 1972).



The prevalence of Raynaud's disease and phenomenon ranges between 3-5%, and Raynaud's is more frequently diagnosed in women and younger patients. Primary Raynaud's accounts for more than 80% of Raynaud's cases. Between 15-20% of primary Raynaud's patients later develop a major systemic disease (The Merck manual of diagnosis and therapy, 2006).



Physicians usually diagnose Raynaud’s disease using Allen and Brown’s (1932) criteria of bilateral color change due to cold or emotion, absence of severe gangrene and primary systemic diseases that could produce Raynaud’s symptoms, and a symptom history of over two years.



While Raynaud proposed that Raynaud's disease is due to sympathetic overactivity, Lewis's (1949) local fault hypothesis contended that resistance vessels that precede the capillaries overreact to local cooling.

 



              


The sympathetic overactivity hypothesis would be supported if Raynaud's disease patients showed elevated stress hormone levels or increased sympathetic firing in the digital nerves. Neither has been observed. Raynaud's disease patients have not consistently shown predicted elevations in epinephrine and norepinephrine levels when compared to normals (Surwit & Allen, 1983).

Raynaud's disease patients have neither shown increased sympathetic activity in digital nerves. Microelectrode studies reveal that cold pressor tests and other sympathetic stimuli do not increase sympathetic activity in skin nerves (Fagius & Blumberg, 1985). Raynaud's disease patients and normals responded comparably to diverse sympathetic stimuli (reflex cooling, indirect heating, and intra-arterial tyramine infusions) (Freedman, Mayes, & Sabharwal, 1989). Experimentally-induced vasospastic attacks in Raynaud's disease patients were not halted by lidocaine nerve blocks of sympathetic efferent digital nerves (Freedman, Mayes, & Sabharwal, 1989). Finally, finger-temperature biofeedback with Raynaud's disease patients, with and without cold challenge, increases temperature without reducing sympathetic arousal (Freedman, Ianni, & Wenig, 1983).

While sympathetic activation does not appear to be the primary mechanism in Raynaud's disease, it may contribute to this disorder by progressively increasing vascular tone, constricting resistance vessels (Turton, Kent, & Kester, 1998).

Several studies have supported the local fault hypothesis by demonstrating abnormalities in α1- and α -adrenergic receptors. Raynaud's disease patients have more responsive α2-adrenergic receptors than normals (Freedman, Moten, Migaly, & Mayes, 1993; Freedman, Sabharwal, Desai, Wenig, & Mayes, 1989). This finding is consistent with studies showing increased platelet α2-adrenergic receptor density in Raynaud's disease patients compared with normals (Graafsma et al., 1991). Finger cooling increased α2-adrenergic vasoconstriction in Raynaud's patients, but not in normals (Freedman, Sabharwal, Moten, Migaly, & Mayes, 1993). Antagonists of α2-adrenergic receptors, but not α1-adrenergic receptors, blockaded vasospastic attacks in Raynaud's disease patients (Freedman, Baer, & Mayes, 1995). While the activation of α1-adrenoceptors is not necessary for vasospastic attacks, they are hypersensitive in Raynaud's disease patients during baseline conditions (Edwards, Phinney, Taylor, Keenan, & Porter, 1987; Graafsma et al., 1991).

Collectively, these studies suggest that there is a local fault in peripheral microcirculation in Raynaud's disease. Hypersensitive α2-adrenergic receptors appear to trigger Raynaud's attacks due to cooling, and both α1- and α2- adrenoceptors may initiate attacks due to ordinary catecholamine increases that accompany reflex cooling or stress (Karavidas, Tsai, Yucha, McGrady, & Lehrer, 2006). The association of Raynaud's attacks with migraine headache, pulmonary hypertension, and variant angina (chest pain caused by coronary artery spasms) may imply shared vasomotor pathology (The Merck manual of diagnosis and therapy, 2006).

Successful Raynaud's disease training protocols may modify patients’ resistance vessel response to cold and cold-related stimuli resulting in increased capillary blood flow.



Evidence-Based Practice in Biofeedback and Neurofeedback (2004) rates biofeedback for Raynaud's disease 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" (p. 30). A level 2 rating was awarded due to mixed results.



Guglielmi, Roberts, and Patterson (1982) reported that temperature biofeedback, SEMG biofeedback, and a control condition produced comparable symptom reductions in their double-blind study.



Freedman and Ianni (1983) compared temperature biofeedback with autogenic training, SEMG biofeedback, and instructions to raise temperature. Only subjects receiving temperature biofeedback achieved significant temperature increases during the first 12 minutes. These increases did not involve relaxation on heart rate, respiration rate, frontalis SEMG, or skin conductance measures.

Consistent finger temperature increases during training were necessary for response generalization to the environment. Their results suggested that training sessions should be limited to 16 minutes and that 10 sessions produced no greater finger temperature increase than 6 sessions.



Freedman, Ianni, and Wenig (1983) compared the efficacy of finger temperature biofeedback, finger temperature biofeedback under cold stress, frontalis SEMG biofeedback, and autogenic training with Raynaud's disease patients.

Both temperature groups increased finger temperature without evidence of relaxation. The frontalis SEMG biofeedback and autogenic training groups did not increase finger temperature, but reduced muscle tension and self-reported stress.

At one-year follow-up, the finger temperature biofeedback under cold stress group showed higher voluntary finger temperatures during voluntary control and cold stress than the finger-temperature biofeedback only group. While 24-hour measurements of tonic blood flow showed no change, both temperature groups required lower temperatures to trigger vasospastic attacks.

Raynaud's patients who received temperature biofeedback under cold challenge produced greater symptom reduction (92.5%) than temperature (66.8%), autogenic training (32.6%), or frontal SEMG (17%) patients. Cognitive stress management training, which was provided to half of the subjects in each condition, had no significant effect. Reductions in attack frequency were maintained at 3-year follow-up (Freedman, lanni, & Wenig, 1985).



Freedman (1991) demonstrated that different mechanisms are responsible for vasodilation and vasoconstriction produced by temperature biofeedback.

Vasodilation in normals and Raynaud's disease patients is due to a beta-adrenergic vasodilating mechanism instead of a reduction in the firing of sympathetic digital nerves. Temperature elevations in Raynaud's patients is not associated with changes in norepinephrine or epinephrine. Small elevations in heart rate, skin conductance level, and systolic and diastolic blood pressures were found. Vasoconstriction in normals is mediated by efferent, sympathetic fibers.



Freedman and colleagues' research has profound implications for temperature biofeedback.

First, patients should be trained to both vasodilate and vasoconstrict since these are different skills involving separate mechanisms. Training in both skills may teach more effective thermoregulation.

Second, temperature biofeedback should not be used alone as a general relaxation procedure since it did not produce relaxation on heart rate, respiration rate, frontalis SEMG, or skin conductance measures in normals.

Third, temperature training sessions should be no longer than 16 minutes since lengthier sessions may produce diminished returns.

Fourth, procedures like autogenic exercises and frontal SEMG biofeedback did not reliably produce hand-warming and should not be used for this purpose.



Sedlacek and Taub (1996) concluded in their literature review that 80-90% of Raynaud’s disease patients can achieve significant improvement with 10-20 biofeedback treatments over 3-6 months, with several follow-up sessions over the next few years. Failure to provide the most effective office treatment and assign home temperature training may produce results no better than verbal relaxation training, autogenic training, or medication (a reduction of vasospastic attacks in 10-40% of Raynaud’s patients).
 


The Raynaud's Treatment Study Investigators (2000) examined 313 primary Raynaud's patients and reported that nifedipine, a calcium-channel blocker, produced greater symptom reduction than thermal biofeedback, SEMG biofeedback, and placebo.

Middaugh and colleagues (2001) reported the results of the multicenter Raynaud’s Treatment Study that compared the efficacy of the following treatments in primary Raynaud’s:

  1. digital skin temperature biofeedback
  2. frontal SEMG biofeedback
  3. nifedipine-XL
  4. medication placebo

The authors reported that only 34.6% of the temperature biofeedback group and 55.4% of the SEMG biofeedback group learned the desired physiological response. In comparison, 67.4% of a normal temperature biofeedback group learned hand warming. Coping strategies, anxiety, gender, and clinic site predicted hand-warming success, while the severity of primary Raynaud’s did not. Vasoconstriction was observed at the onset of biofeedback training. Performance in initial biofeedback sessions was critical to training success.



Karavidas, Tsai, Yucha, McGrady, and Lehrer (2006) reviewed 8 randomized controlled trials (RCTs) and 2 follow-up studies of temperature biofeedback (TBF) for primary Raynaud's disease. They rated temperature biofeedback for primary Raynaud's disease as "efficacious" because three small independently conducted RCTs provided evidence for the “superiority or equivalence” of treatments that incorporated TBF. A large study that achieved negative outcomes did not successfully train subjects to warm their hands.

The authors proposed the following treatment guidelines for primary Raynaud's disease:
"1. Subjects should be trained to a predetermined criteria (i.e., voluntarily raising temperature to 93◦F for at least 15 min [Sedlacek, 1979]) to ensure the acquisition of the specific vasodilation response.
2. Include cold stress conditions in the training.
3. Include a no feedback session to facilitate the transfer of skills outside the laboratory.
4. Include home practice and applied practice in the natural environment.
5. Consider a multiple treatment approach.
6. Address anxiety and comorbid emotional disorders that may complicate treatment." (pp. 214-215).




While more than 95% of low back pain cases are acute and improve within 1 to 3 months of therapy, under 5% of cases are chronic and do not resolve within 6 months (Sella, 2003). Chronic low back pain may involve paravertebral muscle misuse causing ligament strain, muscle tear, spinal facet injury, disk prolapse (protrusion), and psychological processes. Clinicians often observe a cycle of injury, protective bracing, and chronic contraction that produces muscle asymmetry and restricted range of motion.

Apkariana and colleagues (2004) reported that chronic low back pain can produce atrophy of the prefrontal cortex and impair judgment on the Iowa Gambling Test.



About 80% of Americans suffer low back pain during their lifetime. Low back pain temporarily disables 3-4% and permanently disables 1% of working-age Americans. The annual prevalence of low back pain in the United States is 15-20%. Low back pain ranks behind colds as a cause of lost work hours and accounts for 19% of workers compensation claims. While men and women report comparable rates of low back pain, women report this disorder more frequently than men after age 60 (Wheeler & Stubbart, 2004).



The spinal cord is divided into 31 pairs of spinal nerves that arise at regular intervals:
cervical nerves (C1-C8) in the neck region
thoracic nerves (T1-T12) in the chest region
lumbar nerves (L1-L5) in the lower back region
sacral nerves (S1-S5) at the sacrum
coccygeal nerves (1 pair) near the coccyx



The muscles that move the vertebral column (backbone) have diverse origins and insertions, extend in different directions, and are layered on top of each other. The muscles of primary interest include the trapezius in the upper back and the erector spinae of the lower back.

The trapezius, the most superficial back muscle, is a triangular muscle sheet that covers the posterior neck and superior trunk. The two trapezius muscles form a trapezoid. The upper trapezius elevates the scapula (shoulder blade) and helps extend the head.

The erector spinae, the largest back muscle, is located on both sides of the spine and consists of three muscle groups: iliocostalis group (iliocostalis cervicis, iliocostalis thoracic, and iliocostalis lumborum), longissimus group (longissimus capitis, longissimus cervicis, and longissimus thoracis), and spinalis group (spinalis capitis, spinalis cervicis, and spinalis thoracis.

The erector spinae is the primary muscle that extends the vertebral column, and plays an important role in its flexion, lateral flexion, and rotation. Place SEMG electrodes vertically just above the iliac crest (top of the pelvic girdle) 3 cm out on both sides of the spine for a erector spinae (L3 paraspinal) placement.



Geisser et al. (2005) conducted a meta-analysis of 44 articles that compared patients diagnosed with low back pain (LBP) and healthy controls. For static assessment, standing produced the largest effect size. LBP subjects had higher paraspinal SEMG amplitudes.

For dynamic assessment, flexion-relaxation discriminated best between subjects with LBP and normals. Flexion-relaxation produced a very large effect size and LBP subjects demonstrated deficient paraspinal SEMG relaxation during terminal flexion. Re-extension after full flexion produced a large effect size. Trunk rotation produced a moderate-to-large effect size. SEMG assessment during isometric exercise and recovery after exercise yielded inconsistent results.

A paraspinal muscle active electrode placement is shown below.






Assessing patients across diverse positions increases the chance of detecting elevated and asymmetrical patterns of muscle use. The scan may be more revealing if the patient experiences low back pain on the day of the scan. Pay special attention to asymmetries, which may be more closely associated with pain than overall SEMG levels.

A BioGraph ® Infiniti two-channel SEMG assessment of a client diagnosed with chronic low back is shown below. The yellow and blue traces represented left and right paraspinal activity, respectively. He was monitored during sitting, standing (neutral), turning left, turning right, and standing (neutral).

Paraspinal SEMG measurements are profoundly influenced by posture. An anatomically neutral position should produce symmetrical SEMG patterns within a relaxed range. In contrast, rotation to one side should produce asymmetrical SEMG patterns. A consistent rule is that symmetrical movements produce symmetrical SEMG patterns, and asymmetrical movements produce asymmetrical SEMG patterns. The side opposite to the rotation usually has higher readings. A 20% difference between left and right paraspinal SEMG values during static postures and symmetrical movements is considered clinically significant (Donaldson & Donaldson, 1990).

There was slight left paraspinal asymmetry during standing when the client turned to the left and right, and returned to a neutral posture. The elevated SEMG values show muscle bracing during standing and co-contraction during left and right rotation (Neblett, 2006).



Standing Left






 Standing Right






 Standing (neutral)






Complementary medical procedures to reduce muscle spasticity include:

  1. heat packs and diathermy
  2. ice packs
  3. massage
  4. muscle relaxants like Vanaflex
  5. physical therapy exercises to increase strength and range of motion
  6. Transcutaneous Electrical Nerve Stimulation (TENS)



A clinician may modify patient body mechanics like posture, teach muscle discrimination (since this is often deficient in chronic pain patients), incorporate strengthening and stretching exercises (paravertebral muscles, hamstrings, and hip flexors), recommend appropriate weight-lifting, and provide left and right side paraspinal SEMG biofeedback during standing and movement.

Neblett (2002a) advocates combining active SEMG training in which a clinician combines neuromuscular re-education with general relaxation. Active SEMG training is a collaborative process that involves continuous dialog between the clinician and client. They share SEMG biofeedback and the client's self-reports to identify patterns of muscle bracing associated with pain and restricted range of motion, and evaluate strategies to correct these problems.




Several assumptions underlie active SEMG training:

  1. Poor posture can create muscle tension in all spinal muscles from the neck to the low back. 
  2. Muscles should relax after they perform work.
  3. Continuous muscle bracing can become an unconscious habit that generates or worsens pain.
  4. Chronic pain patients often have limited awareness of their own muscle tension and require muscle tension discrimination training.
  5. Chronic pain patients often show poor recovery to baseline SEMG levels following muscle contraction, and require contraction/recovery training.
  6. Muscle training in several postural positions may be required since muscle relaxation skills often do not automatically generalize from one position (sitting) to another (standing).
  7. SEMG training should be bilateral to correct SEMG asymmetry.

A clinician usually conducts active SEMG training with the client's eyes open, in routine postures (like sitting upright in a straight-backed chair), during a client's typical activities (like typing on a computer keyboard), across a range of movements (including standing, bending, and walking).

A client's treatment plan is based on multi-channel SEMG assessment during activities like sitting, standing, bending, and turning to one side, and walking. A clinician examines client performance for elevated SEMG values, speed and completeness of recovery following contraction (like bending forward and returning to an upright position), co-contraction, and asymmetry.

Muscle co-contraction occurs when SEMG levels in one muscle increase from baseline during the contraction of another muscle. For example, when head rotation increases vastus medialis SEMG activity (Donaldson et al., 2002).

Steven Wolf has proposed two rules regarding symmetry and asymmetry in non-pain and pain subjects (Cram, 1988). A typical symmetrical movement is flexion/extension of the waist (Donaldson & Donaldson, 1990).

Rule 1: "In non-pain subjects symmetrical movement produces symmetrical patterns."
Rule 2: "In pain patients, symmetrical movement produces asymmetrical patterns."

An imbalance of 5-10% during movement is typically observed in non-pain subjects. Donaldson measures imbalance at maximum contraction by subtracting SEMG values from two opposite sides. These measurements strongly correlate (r = .61) with pain reports (Donaldson, 1989).

Pathological asymmetry is present when there is at least a 20% difference between left and right muscle groups (Donaldson & Donaldson, 1990). Two patterns of SEMG asymmetry are splinting and protective guarding. Splinting involves SEMG elevation on the injured side of the body. Protective guarding is an SEMG elevation on the side opposite an injury.

When the body is properly aligned with balanced weight bearing, it can maintain an upright posture while allowing antigravity muscles to relax. Chronic pain can result in asymmetrical postural adjustments, and asymmetrical posture can, in turn, overload joints and muscles, and worsen pain (Middaugh, Kee, & Nicholson, 1994; Neblett, 2002b).

Sherman (2004) has proposed a five percent rule that severe acute pain can develop and progress to chronic pain when:

  1. limbs deviate five degrees from a healthy position
  2. muscles are five percent more tense than required
  3. muscles remain minimally tense five percent longer than required

A clinician should visually inspect client posture and use the SEMG to evaluate the muscle bracing patterns produced by abnormal posture and to help correct body alignment, weight distribution, and muscle activation. Elevating the chest, releasing the shoulders, and/or tilting the pelvis forward can reduce standing SEMG activity in the neck, shoulders, chest, and lower back. Sitting against a backrest that supports the lower back, lowering the shoulders, and "floating" the head can reduce sitting SEMG activity in the neck, shoulder, and upper back (Neblett, 2000b).

A clinician often integrates postural and recovery training during musculoskeletal interventions. When a client sits or stands, restoring postural balance allows the antigravity muscles to relax. After performing a movement, the restoration of postural balance makes muscle recovery possible (Neblett, 2000b).

Two-channel SEMG training should reduce muscle spasticity and co-contraction, increase awareness of muscle tension, and restore muscle symmetry (during neutral posture) and flexion-relaxation. Since chronic pain patients are often unable to quickly return to baseline SEMG levels after muscle contraction, recovery training may be crucial to their improvement.

Active SEMG training requires a detailed understanding of muscle action. For example, following shoulder injury, a client may present with scapular winging (protrusion of the shoulder blade) and pain during flexion. Treatment may require up training the lower trapezius, which depresses the scapula, and down training the upper trapezius, which elevates the scapula (Neblett, 2006).



Evidence-Based Practice in Biofeedback and Neurofeedback (2004) rates SEMG biofeedback for chronic back pain at level 3 efficacy, probably efficacious. The criteria for level 3 efficacy include "Multiple observational studies, clinical studies, wait list controlled studies, and within subject and intrasubject replication studies that demonstrate efficacy" (pp. 14-15).

SEMG biofeedback-assisted therapy appears to be comparable to cognitive therapy and superior to a wait-list control (Newton-John, Spence, & Schotte, 1995; Vlaeyan and colleagues, 1995).

Newton-John, Spence, and Schotte (1995) compared SEMG biofeedback and cognitive therapy against a wait-list control. Both treatments produced comparable improvement that was maintained at 6-months follow-up, and these treatments were superior to the wait-list control.

Vlaeyan and colleagues (1995) compared SEMG biofeedback and cognitive training against a wait-list control and operant conditioning for 71 chronic back pain patients. SEMG biofeedback and cognitive training produced equivalent outcomes, which were superior to a wait-list control and operant conditioning.

Sella (2003) argues that the combination of SEMG biofeedback with traditional medical and physical therapy is a pragmatic and cost-effective approach because it shortens therapy (usually to three months), teaches muscle self-regulation, and reduces dysfunctional muscle use and resulting pain.




Myofascial Pain Syndrome (MPS) is a regional pain disorder that is characterized by trigger points, which are hyperirritable regions of taut bands of skeletal muscle in the muscle belly or associated fascia (connective tissue). Pressure on trigger points is painful. Trigger points can produce referred (remote) pain and tenderness, motor dysfunction, and autonomic changes. Trigger points cannot be detected using SEMG electrodes, but can be identified using needle EMG electrodes and palpation (examination by feeling or pressing with the hand).



About 14.4% of the United States population experiences chronic musculoskeletal pain. Almost everyone develops a trigger point during their lives. Men and women share comparable rates of MPS. Trigger points are found in individuals at all ages, including infants. Sedentary individuals are more likely to develop active trigger points than those who vigorously exercise daily (Finley, 2005).



Hubbard and Gevirtz have proposed that sympathetically-mediated muscle spindle spasm may be the major local mechanism in myofascial pain. An important implication of this theory is that muscle spindles may be activated by stress and anxiety.

Muscle spindles detect muscle length, tension, and pressure. They are activated by the sympathetic branch of the autonomic nervous system when epinephrine binds to α-1 adrenergic receptors. Inserted EMG electrodes reveal muscle spasm in the affected muscle fiber, shown by elevated inserted EMG amplitudes, while nearby fibers in the same muscle are electrically silent. Consistent with this model, intrafusal muscle spasm is terminated by α-1 adrenergic antagonists like phentolamine and phenoxybenzamine, but not curare. Gevirtz (2003) contends that intrafusal muscle spasm accounts for most of the variance in chronic pain, whereas neurological factors that influence afferent pain pathways account for a minority of the variance in chronic pain.
 


Gevirtz's (2003) mediational model of muscle pain proposes that lack of assertiveness and resultant worry each trigger sympathetic activation. Increased sympathetic efferent signals to muscle spindles and overexertion can produce a spasm in the intrafusal fibers of the muscle spindle, increasing muscle spindle capsule pressure and causing myofascial pain.
 



            




Fibromyalgia is a chronic benign pain disorder that involves pain, tenderness, and stiffness in the connective tissue of muscles, tendons, ligaments, and adjacent soft tissue. The American College of Rheumatology (ACR) adult criteria include widespread pain for at least 3 months on both sides of the body and pain during gentle palpation on 11 of 18 tender points on neck, shoulder, chest, back, arm, hip, and knee sites. Patients also present with attentional deficits, depression, severe fatigue, headaches, impaired multitasking, irritable bowel syndrome, memory deficits, sleep disturbance, and temporomandibular joint pain (Donaldson & Sella, 2003; Tortora & Derrickson, 2006).



The ACR fibromyalgia adult criteria are met by 3-5% females and 0.5-1.6% males. The female-to-male ratio is 9:1. While fibromyalgia is mainly seen in women 40-64 years, with average onset at 47.8 years, it is also diagnosed in adolescents and the elderly. Fibromyalgia pain typically persists 78.7 months (Donaldson & Sella, 2003; Winfield, 2002).



The etiology of fibromyalgia appears to involve a central hypersensitivity to heat, cold, and electrical stimulation (Desmeules et al., 2003). Fibromyalgia patients may have low levels of serotonin, amino acids like tryptophan, and insulin-like growth factor (IGF-1), and high levels of substance P and ACTH.

Patients present with multiple tender points, which are distinct from trigger points. Tender points are located at a muscle's insertion (the tendonous attachment to a movable bone) instead of the muscle belly or associated fascia. Tender points are associated with local tenderness. When compressed, they produce local pain, but not the referred pain associated with trigger points. Pressure on tender points may increase overall pain sensitivity.




                                        


Fibromyalgia is sometimes confused with Myofascial Pain Syndrome (MPS) because both syndromes involve muscle tenderness and local pain during palpation. Also, patients may present with both fibromyalgia and MPS, and have both tender points and trigger points. Accurate diagnosis requires careful examination by an experienced clinician (Alvarez & Rockwell, 2002).

Evidence-Based Practice in Biofeedback and Neurofeedback (2004) rates biofeedback for fibromyalgia 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" (p. 21-22). A level 2 rating was awarded due to negative results in some studies.

At this point, there is no evidence that biofeedback is superior to other mind-body therapies. No randomized controlled trials have shown that biofeedback significantly reduces fibromyalgia symptoms when administered by itself or that it potentiates the effectiveness of treatments like massage therapy, physical exercise, and physical therapy.

SEMG and neurofeedback have been administered with cognitive behavior therapy, hypnosis, and physical exercise. Reviews by Hadhazy, Ezzo, Creamer, and Berman (1990) and Sim and Adams (1999) found no evidence that either form of biofeedback was superior to the other mind-body therapies. Instead, a combination of mind-body therapies and exercise appeared to produce the greatest clinical gains.

A retrospective study by Donaldson, Sella, and Mueller (1998) treated subjects with a multidisciplinary program, including SEMG biofeedback, massage therapy, physiotherapy, and neurofeedback. At one-year follow-up of 44 program graduates, 4 reported increased symptoms, 10 reported a 100% decrease in symptoms, and 30 reported some improvement.

Mur et al. (1999) and Sarnoch, Adler, and Scholz (1997) reported on uncontrolled trials where SEMG biofeedback produced improvement by itself.

Mueller et al. (2001) reported on another uncontrolled trial where EEG-driven stimulation resulted in symptomatic improvement.




Temporomandibular disorders (TMD) are the second most common cause of orofacial pain after toothache. While TMD is a heterogeneous group of disorders, orofacial pain and/or masticatory problems may be classified as TMD secondary to myofascial pain and dysfunction (MPD), TMD secondary to articular disease, or both. TMD is characterized by dull pain around the ear, tenderness of jaw muscles, a clicking or popping noise when opening or closing the mouth, limited or abnormal opening of the mouth, headache, tooth sensitivity, and abnormal wearing of the teeth.

TMD pain is located in the preauricular area, muscles used for chewing (masseter, temporalis, and pterygoids), or the temporomandibular joint (TMJ).




                    

TMD pain is triggered by parafunctional jaw clenching, which may be unilateral or bilateral in MPD, and is reported along with headache, other facial pain, neck pain, and pain in the shoulder and back.

Glaros and Burton (2004) demonstrated that subjects without TMD, who were trained during 20-minute SEMG biofeedback sessions over 5 consecutive days to increase left and right masseter and temporalis SEMG levels, experienced increased pain at posttreatment. Pain severity was highly correlated with masseter activity. After completion of training, an examiner who was blind to their clinical status diagnosed 2 SEMG-increase subjects and no SEMG-decrease subjects with TMD pain, although they were actually pain-free when they started the experiment.



More than 10 million Americans are estimated to suffer from TMD. The highest incidence is found among young adults. Women, particularly those 20-40, are most often diagnosed with TMD. The male-to-female ratio is 1 to 4 (Chaudhary & Appelbaum, 2004).



The temporomandibular joint uses a “ball and socket” mechanism as it first opens. The condyle rotates within the articular fossa. As it opens wider, the condyle translates over the articular eminence (or dislocates over a protrusion in the upper jaw).

The primary muscles that move the jaw include the:

  1. masseter muscles (elevate and retract the mandible)
  2. temporalis muscles (elevate and retract the mandible)
  3. lateral (external) pterygoid muscle (protracts and depresses the mandible, and moves it laterally)
  4. medial (internal) pterygoid muscle (elevates and protracts the mandible, and moves it laterally)

The masseter and temporalis muscles are shown below. The sternocleidomastoid muscle is pictured, but not labeled, ascending from the bottom left.


                                                   

               



TMD patients may also have problems with the sternocleidomastoid muscles, hyoid muscles, and digastric muscles.

A patient should ideally be diagnosed by dental professional who specializes in TMD. If a dental examination reveals that excessive activity in facial and/or masticatory muscles contributes to TMD, a bilateral SEMG profile should be completed to determine which muscles should be trained. Training should be conducted bilaterally, with gradual reduction of SEMG activity in the more active and then the less active of left and right muscle sites (left and right masseter).



Evidence-Based Practice in Biofeedback and Neurofeedback (2004) rates SEMG biofeedback for TMD pain at level 4 efficacy, efficacious. The criteria for level 4 efficacy include:"

  1. In a comparison with a no-treatment control group, alternative treatment group, or sham (placebo) control utilizing randomized assignment, the investigational treatment is shown to be statistically significantly superior to the control condition or the investigational treatment is equivalent to a treatment of established efficacy in a study with sufficient power to detect moderate differences, and
  2. The studies have been conducted with a population treated for a specific problem, for whom inclusion criteria are delineated in a reliable, operationally defined manner, and
  3. The study used valid and clearly specified outcome measures related to the problem being treated, and
  4. The data are subjected to appropriate data analysis, and
  5. The diagnostic and treatment variables and procedures are clearly defined in a manner that permits replication of the study by independent researchers, and
  6. The superiority or equivalence of the investigational treatment has been shown in at least two independent research settings" (p. 33).



Dohrmann and Laskin (1978) compared SEMG masseter biofeedback with a sham control over twelve 30-minute sessions provided over a six-week period. Blind evaluation following nine sessions showed that 94% of the biofeedback group and 28% of the control did not need further treatment. After one year, 75% of the biofeedback group and 28% of the control group still did not need further treatment.



Crockett, Foreman, Alden, and Blasberg (1986) randomly assigned 28 patients to SEMG biofeedback training combined with relaxation training, intraoral splinting combined with physical therapy, or transcutaneous electrical nerve stimulation (TENS). Each group received eight weekly 1-hour sessions and was asked to perform 30 minutes of homework each day. The SEMG biofeedback with relaxation training group was superior to the TENS group on palpation pain and daily self-reported pain severity and frequency. The SEMG biofeedback with relaxation training group was not superior to the intraoral splinting combined with physical therapy group.



Turk, Zaki, and Rudy (1993) randomly assigned 80 patients to SEMG biofeedback with cognitive-behavioral therapy, intraoral splint, or a wait-list control. The SEMG biofeedback with cognitive-behavioral therapy group received six weekly 1-hour training sessions. The intraoral splint group was instructed to constantly wear their appliance for the first six weeks.

The SEMG biofeedback with cognitive-behavioral therapy group was superior to the wait-list control group on pain reduction and depression from pre-treatment to post-treatment. At 6-month follow-up, the SEMG biofeedback group showed increased pain reduction. The SEMG group was equivalent to the intraoral splint group on reduction in pain severity and depression from pretreatment to post-treatment. At 6-month follow-up, the SEMG group reported greater reduction in depression than the intraoral splint group, which relapsed to pretreatment values.



Crider and Glaros (1999) conducted a meta-analysis of 13 studies of SEMG biofeedback and stress management treatments of TMD. The SEMG sites were the masseter and/or frontalis muscles. Their main findings were:









Gardea, Gatchel, and Mishra (2001) randomly assigned 108 TMD patients to biofeedback-assisted relaxation training (BART), cognitive-behavioral therapy (CBT), combined BART and CBT, or a no-treatment control group. The treatments were administered over twelve 1-2 hour sessions over eight weeks. The BART condition combined relaxation training with 15 minutes of temperature and frontal SEMG biofeedback during each session.

The BART and combined BART and CBT groups achieved greater pain reduction than the control group. The combined BART and CBT, and CBT groups achieved greater mandibular function than the control group.



Crider, Glaros, and Gevirtz (2005) reported that five of six randomized controlled trials of biofeedback-based treatments provided evidence of efficacy when compared with controls. They concluded that SEMG training combined with cognitive-behavioral therapy is efficacious and that SEMG biofeedback for the masticatory muscles and biofeedback-assisted relaxation for global relaxation are each probably efficacious.
 


Dental therapy approaches include:

Physical therapy approaches include:



Several cervical muscles are responsible for balance and head movement. The sternocleidomastoid (SCM) muscles originate at the sternum and clavicle (collarbone), and insert at the mastoid process of the temporal bone.

Bilateral contraction of the two sternocleidomastoid muscles flexes the cervical spine and flexes the head. Unilateral contraction of a single sternocleidomastoid muscle laterally extends and rotates the head to the opposite side. A sternocleidomastoid placement is shown below.






The semispinalis capitis originates in cervical and thoracic vertebrae and inserts at the occipital bone. The splenius capitis originates in cervical and thoracic vertebrae and inserts at the occipital bone and mastoid process of the temporal bone. The longissimus capitis originates in the thoracic and cervical vertebrae and inserts at the mastoid process of the temporal bone.

Bilateral contraction of the semispinalis capitis, splenius capitis, and longissimus capitis extends the head. Unilateral contraction of the semispinalis capitis rotates the head to the side opposite to the contracting muscle. Unilateral contraction of the splenius capitis and longissimus capitis rotates the head to the same side as the contracting muscle.

The trapezius, the most superficial back muscle, is a triangular muscle sheet that covers the posterior neck and superior trunk. The two trapezius muscles form a trapezoid. The upper trapezius elevates the scapula (shoulder blade) and helps extend the head. The neck contains the cervical segment of the spinal cord. When the vertebrae that protect the spinal cord are damaged, this can produce pain due to pressure on spinal nerves and can trigger reflex spasm in adjacent muscles that can increase the patient’s pain.



About 85% of reported neck pain may be caused by acute or repeated neck injuries, or chronic misuse. In a single year, the prevalence of neck and shoulder pain is estimated at 16-18% (Dreyer, 1998). Chronic neck pain is diagnosed in 9.5% of men and 13.5% of women (Hunter, 2005).



Medical assessment should always precede biofeedback treatment to ensure an accurate diagnosis and appropriate training. When SEMG biofeedback is medically appropriate, a clinician should begin with a two-channel SEMG assessment that includes bilateral monitoring of the cervical paraspinal and upper trapezius muscles during sitting, neutral standing, standing rotation, recovery after contraction, and walking.

Four-channel SEMG assessment is definitely needed if the client reports restriction and/or pain during head rotation. In this case, the clinician needs to monitor the left/right SCM and left/right cervical paraspinal. There is a very stereotyped muscle pattern that is visible during left and right head rotation. When rotating to the left, you should see strong activation of the right SCM and moderate activation of the left cervical paraspinal. The left SCM and right paraspinal will show very little activation. The opposite is true for rotation to the right.

One can very easily determine whether co-contraction and inhibition are problems with cervical pain patients. If an abnormal pattern is identified, the treatment goal is to normalize it. This is usually done by encouraging increased activation (up training) of the correct muscles. After patients are able to perform head rotation and demonstrate a more normal pattern of muscle use, they will often show an increased range of motion and report decreased pain during this movement (Neblett, 2006).



A clinician should monitor four SEMG channels during dynamic training and two SEMG channels for static relaxation, postural training, and recovery training. A wide bandpass should be used unless there is excessive EKG artifact that cannot be controlled through narrow electrode spacing. Depending upon the results of the initial SEMG assessment, a clinician may train the client during sitting, neutral standing, standing rotation, and walking. As with low back pain training, treatment should reduce muscle spasticity, restore muscle symmetry (during neutral posture), improve recovery to baseline SEMG levels after muscle contraction, and increase discrimination of muscle tension.



Complementary medical procedures to reduce muscle spasticity include:

  1. heat packs and diathermy
  2. ice packs
  3. massage
  4. muscle relaxants like Vanaflex
  5. physical therapy exercises to increase range of motion
  6. training to strengthen weak antigravity muscles
  7. Transcutaneous Electrical Nerve Stimulation (TENS)




Peper and Gibney (2006) contend that it is misleading to primarily attribute pain experienced when working with a computer to repetitive movement. They propose adoption of the term computer-related disorder (CRD) because repetitive motion interacts with many other factors to produce injury and pain, including:

  1. limited breaks and movement
  2. lack of somatic awareness
  3. poor ergonomics
  4. misaligned posture
  5. stress experienced at home and in the workplace
  6. excessive physiological reactivity
  7. muscle overactivation in regions like the neck and shoulders

Consistent with findings in other chronic pain populations, untrained individuals lack awareness of their muscle tension and breathing pattern. They overuse their muscles and breathe thoracically.

Shumay and Peper (1995) monitored trapezius, deltoid, and forearm muscle SEMG while participants worked at varying distances from the keyboard.




                                 

They obtained shoulder tension ratings at each keyboard position and found that shoulder tension ratings were not correlated with trapezius and deltoid SEMG. They concluded that since their subjects lacked awareness of small increases and decreases in muscle tension, they could not voluntarily reduce muscle tension, even with an optimal ergonomic setup.




                                             

A representative recording of a person working at the computer is shown above. Note how trapezius-deltoid and forearm extensor muscle tension increase without micro-breaks. Also, observe the increase in respiration rate. Yet, the person is totally unaware of these major physiological changes.




Healthy computing represents a systems approach to treating CRD. The eight components of healthy computing include:

  1. Work style: adopting healthy work habits like micro-breaks, large movement breaks, and pacing workflow.
  2. Ergonomics: adjusting the workspace and hardware to facilitate healthy posture and movement.
  3. Somatic awareness: developing awareness of muscle tension and physiological reactivity, and learning how to physically, cognitively, and emotionally let go.
  4. Stress management: learning skills to effectively cope with unavoidable stressors at home and at work in ways that promote health.
  5. Regeneration: learning skills like meditation to recover from stress to prevent burnout and illness.
  6. Vision care: preventing eye strain and dryness through use of appropriate prescription glasses, ergonomic monitor position, vision breaks, and glare reduction.
  7. Fitness: regular stretching, muscle strengthening, and movement practice to avoid injury while working at the computer.
  8. Positive workstyle: Social support reduces arousal, ameliorates stress, and increases performance.

A micro-break is a 1 to 2-s interruption of muscle activation (like the release of forearm muscle activity when a typist reaches the end of a paragraph) about every minute. A large movement break involves leaving the computer and moving around. This should be performed every 20 minutes. When individuals frequently alternate between muscle contraction and relaxation, this increases the circulation of blood and lymph, and helps prevent repetitive motion injury (RMI) (Peper & Gibney, 2005).



Peper and Gibney (1999) reported that 97.8% of surveyed individuals experienced some discomfort during an average 2.7 hours a day working with a computer. From 20-30% of employees who use a computer at work experience repetitive strain injury (Chauhan, 2003). More than 50% of employees who use a computer more than 15 hours per week complained of musculoskeletal pain during their first year of employment (Gerr et al., 2002).



SEMG biofeedback plays a critical role in healthy computing by improving client awareness of muscle tension and physiological reactivity, helping to adjust the workspace, posture, and movement to minimize muscle tension, and teaching them to rapidly release unnecessary muscle tension and dampen excessive reactivity.

Stress management is crucial since the repetition of the fight-or-flight response many times a day can unconsciously increase muscle bracing, particularly in shoulder and neck muscles. Linton and Kamwendo (1989) observed that an "approximately 3-fold increased risk for neck and shoulder pain was found for those experiencing a 'poor' as compared with those experiencing a 'good' psychological work environment."

Stress management may also reduce sympathetic nervous system activation of muscle spindles, which has been implicated in intrafusal muscle fiber spasm and chronic pain (Gevirtz, 2003).



Peripheral nerves consist of individual neurons that innervate body tissue. Peripheral nerves can be damaged by inflammation of surrounding tissue, reduced blood supply, friction against muscle fibers or tendons, and compression by ruptured spinal discs.



Carpal Tunnel Syndrome (CTS) is a painful and disabling example of repetitive stress injury (RSI) due to peripheral nerve injury. These patients experience inflammation of the tendons that travel through the wrist’s carpal tunnel. These patients experience tingling, numbness, pain in the lower thumb and the first three fingers, muscle weakness in the thenar eminence of the hand, and reduced skin electrical activity and skin temperature.

A medical explanation of CTS emphasizes factors like the compression of the median nerve within the carpal tunnel, repetitive motion, excessive muscle contraction in the neck, shoulders, and arms, and co-contraction of multiple muscle groups during head movements. However, from a system's perspective, these factors interact with many others to produce injury and pain. The same factors implicated in computer-related disorder (CRD) may be equally important in CTS (Neblett, 2006; Peper & Gibney, 2002).

A neurologist can assess nerve damage through nerve conduction studies and myelograms (x-ray of nerves using an injected contrast medium).



CTS is the most common peripheral compressive neuropathy. In the United States, the lifetime risk of developing CTS is 10%. The incidence of CTS among adults is 0.1% and its prevalence is 2.7%. CTS is diagnosed more often in women and middle-aged individuals (Steele, 2004).



Temperature biofeedback is indicated if the patient complains of cold hands. Surface EMG biofeedback can be combined with ergonomic training to reduce repetitive strain injury. Treatment should also incorporate the eight components of healthy computing (Peper & Gibney, 2002).



Evidence-Based Practice in Biofeedback and Neurofeedback (2004) rates biofeedback for repetitive strain injury 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" (p. 31). A level 2 rating was awarded due to insufficient investigation.

Moore and Wiesner (1996) reported that temperature biofeedback and autogenic training resulted in greater pain reductions than a wait-list control in a randomized controlled experiment involving 30 upper extremity RSI patients.



Complex Regional Pain Syndrome (CRPS) is the current term for Reflex Sympathetic Dystrophy Syndrome (RSDS). The main symptom of CRPS is severe, often burning pain. The disorder may progress to dystrophy (weakness or wasting) of the area. CRPS can be divided into three progressive stages, which may not be experienced by every patient. These three stages include (1) burning pain, most often in the hand and foot, (2) spreading of pain to the center of the body, often producing muscle spasms, and (3) wasting and contraction of muscles and other tissues, causing impaired joint movement.

CRPS occurs in approximately 1-15% of patients with peripheral nerve injury and often follows fractures, sprains, and damage to soft tissue. Many cases are not associated with an identifiable nerve injury.

There is no agreement on the cause of CRPS. Current hypotheses include injury to central or peripheral neural tissue, tonic activity in myelinated mechanoreceptor afferents, and peripheral nervous system pathology.



The incidence of causalgia following peripheral nerve injury is 1-5%. The incidence of RSDS is 1-2% following fractures and 2-5% following peripheral nerve injury (Singh & Patel, 2005). In a prospective study by Veldman and colleagues (1993), 76% of women and 24% of men were diagnosed with RSDS. The median age of RSDS diagnosis in this study was 42.



Biofeedback can reduce the musculoskeletal and ischemic (decreased supply of oxygenated blood) causes of CRPS. A combination of SEMG and temperature biofeedback can reduce subjective pain ratings for a period of years.

Blanchard (1979) reported successful treatment of a patient with chronic pain resulting from CRPS in his hand and arm following the failure of months of conservative medical care. Eighteen sessions of temperature biofeedback taught the patient to increase hand temperature 1-1.5 degrees C. Hand and arm pain significantly decreased during training and was absent at 1-year follow-up.

Barowsky, Zweig, and Moskowitz (1987) treated a 12-year-old male with CRPS pain of the knee area with temperature biofeedback. Biofeedback training started with hand-warming and then transferred vasodilation to the affected knee. Temperature increased in the affected knee, local vasospasms and cold intolerance ended in 10 sessions, and the patient resumed normal activity.

Grunert and colleagues (1990) trained 20 patients with CRPS, who failed to respond to traditional medical treatment, with thermal biofeedback, relaxing training, and supportive psychotherapy. Patients significantly increased initial and post-relaxation hand temperatures. They reduced subjective pain ratings, maintained at 1-year follow-up. Fourteen of 20 patients returned to work within 1 year.









Now that you have completed this unit, think about how you would explain the medical causes of migraine and tension-type headache to your clients and how biofeedback training produces improvement. Why do practitioners sometimes confuse fibromyalgia with Myofascial Pain Syndrome (MPS). How are they different?




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