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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 low back pain and tension-type and migraine headache. Biofeedback training may allow clients to reduce medication consumption and emergency room visits. Medication-overuse headache (MOH) complicates migraine treatment.

Tension-type headaches are produced by an interaction of peripheral and central processes. Peripheral processes may be most important in episodic and central processes in chronic headaches. Trigeminal nerve involvement is found in chronic tension-type headache.

Vascular headaches may be triggered by a hypothesized hypothalamic headache generator. Classic migraines, which involve prodromal symptoms, are preceding by spreading cortical depression. Breakthrough headaches precede and are worsened by the dilation of cranial blood vessels. The trigeminal nerve is a final common path for headache pain. The mechanisms responsible for cluster and migraine headaches appear to differ.

The mechanism by which temperature biofeedback impacts migraine has been questioned, 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 and that temperature biofeedback may not reduce sympathetic activation. 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.

Since the release of Evidence-Based Practice in Biofeedback and Neurofeedback (3rd ed.), there has been stronger evidence of biofeedback efficacy for low back pain, pediatric headache, and repetitive strain injury.

BCIA Blueprint Coverage

This unit addresses 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).

 

This unit covers Tension-Type Headache, Vascular Headache, Raynaud's Disease and Phenomenon, Low Back Pain, Myofascial Pain, Temporomandibular Disorders (TMD), Cervical Injury, Workplace Ergonomic Applications, and Complex Regional Pain Syndrome (CRPS).

Please click on the podcast icon below to hear a full-length lecture.

EVIDENCE-BASED PRACTICE (4TH ED.)

We have updated the efficacy ratings for clinical applications covered in AAPB's Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.).

Tension-Type Headache

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


Listen to a mini-lecture on Tension-Type Headache Overview © BioSource Software LLC. Graphic © sirtravelalot/Shutterstock.com.

Demographics

TTH is the most common primary headache, and estimates of its lifetime prevalence range from 30-78%. TTH onset frequently occurs in the teenage years. There is a 3:2 female-to-male ratio (Blanda, 2015).





Graphic © Africa Studio/Shutterstock.com.

Tension-Type Headaches

TTH is divided into episodic and chronic headache. Episodic TTH 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 TTH is diagnosed when there is an average headache frequency of more than 15 days per month for more than 6 months (Martin & Elkind, 2005).

Physiology of Tension-Type Headache

The consensus view is that tension-type headaches are produced by an interaction of peripheral and central processes (Ashina, Bendtsen, & Ashina, 2005; Chen, 2009). Central sensitization appears to play a crucial role, particularly in chronic TTH cases.

This process involves increased excitability of the central nervous system, triggered by repetitive and sustained pericranial myofascial input. These changes may produce sympathetic nervous system activation that increases muscle contraction by shortening muscle spindles and constricting their blood supply (Ashina et al., 2002; Khazan, 2013). The sensitization occurs at both the spinal/trigeminal level and supraspinal level (e.g., periaqueductal grey, thalamus, somatosensory cortex, anterior cingulate cortex, and insula), potentially leading to impaired modulation of incoming stimuli in chronic TTH.

Peripheral mechanisms are thought to be more prominent in episodic TTH. These include myofascial pain and tenderness in pericranial muscles, as well as increased muscle hardness in pericranial areas. In chronic TTH, these muscular changes may become more permanent (Bhoi, Jha, & Chowdhury, 2021). However, it's important to note that the exact relationship between muscle tension and TTH remains controversial, as electromyogram (EMG) studies often fail to detect increased resting muscle tension in TTH patients (Millea & Brody, 2002).

Neurotransmitters such as nitric oxide (NO), calcitonin gene-related peptide (CGRP), substance P (SP), neuropeptide Y (NPY), and vasoactive intestinal polypeptide (VIP) are involved in pain processing and may contribute to the pathophysiology of chronic head pain, including TTH (Ashina, 2004).

Abnormalities in the metabolism of tyrosine and tryptophan, which are precursors to neurotransmitters, have been observed in chronic tension-type headache patients. Specifically, low plasma levels of tryptamine, a derivative of tryptophan, suggest insufficient serotoninergic control of the pain threshold, which may contribute to the chronicity of TTH (D'andrea et al., 2015).

While stress is a known contributor to TTH, the precise mechanisms by which it influences headache development are not fully understood. Stress may affect central pain processing, myofascial tenderness, and pain modulation and inhibition systems (Ashina, Bendtsen, & Ashina, 2005; Bhoi, Jha, & Chowdhury, 2021).

In conclusion, TTH is likely a multifactorial disorder involving both peripheral and central mechanisms. The relative importance of each factor may differ between episodic and chronic forms of the condition. Ongoing research continues to refine our understanding of TTH pathophysiology, which may lead to more targeted and effective treatments in the future.

While not linearly related to headache pain, almost two-thirds of these patients exhibit elevated SEMG activity in the cervical paraspinal, upper trapezius, frontalis, and temporalis muscles at baseline and during stressful tasks (Hatch et al., 1992).

These patients frequently show pericranial muscle tenderness and contraction, leading to central sensitization and chronic pain. The trapezius animation below is courtesy of Wikipedia.

Forehead and Pericranial Muscle SEMG Assessment

Recent studies have shown that tension-type headache patients have 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.


Listen to a mini-lecture on SEMG Findings for Tension-Type Headache © BioSource Software LLC. A frontalis or bifrontal placement is illustrated below.







A cervical paraspinal placement is indicated below.





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 could simultaneously monitor two FpN channels: left frontalis-left cervical paraspinal and right frontalis-right cervical paraspinal.

Biofeedback Treatment of Tension-Type Headache

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.


Listen to a mini-lecture on Tension-Type Headache Treatment Components © BioSource Software LLC.


Several treatment components should be considered:

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

Click on the Read More button to review complementary treatment components.

Pediatric Headache

Herman and Blanchard's (2002) review of studies involving biofeedback treatment of pediatric headache supported the efficacy of thermal biofeedback. A majority of studies found an average 50% reduction in headache symptoms.

A meta-analysis by Trautmann, Lackschewitz, and Kroner-Herwig (2006) revealed that relaxation training produced greater symptom reduction than a wait-list control for pediatric migraine and tension-type headache patients.

A meta-analysis by Verhagen et al. (2005) found no evidence of biofeedback's effectiveness in treating pediatric headaches.

Clinical Efficacy

Based on at least two independent RCTs and several quasi-experimental studie, Ethan Benore (2023) rated biofeedback for pediatric headache as efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.)

ADULT HEADACHE

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

1. good maintenance was shown in tension-type headache for biofeedback, relaxation, and cognitive interventions
   
2. long-term improvement was best for patients who practiced “some” or “as needed”
3. limited contact (3 sessions) provided comparable headache relief to intensive contact (16 sessions)
4. adding a brief cognitive stress management component to Progressive Relaxation training increased headache relief

Hudzinski (1993) recommended that clinicians use both frontal and neck placements.





Down-training neck muscles may be necessary in treating tension-type and migraine headaches for two reasons. First, contraction of these muscles may help trigger a headache episode. Second, neck muscles often contract following a breakthrough headache to reduce head movement and the pain that it might cause. Graphic © Ohyperblaster/Shutterstock.com.




A combination of frontal and neck placements may provide clients with more information. Clinicians should be aware that neither the frontal or neck placements represent other muscle sites and that reductions at either of these sites may not generalize to other muscle groups.

Vascular Headache

Migraine Classification

A migraine with aura (classic migraine) features a prodrome or neurological symptoms that precede a breakthrough headache, hours to days before headache onset. Migraine with aura 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).


Listen to a mini-lecture on Migraine Diagnostic Criteria © BioSource Software LLC.





About 64% of all migraine patients experience migraine without aura, which is also called common migraine (Launer et al., 1999; Elkind, 2005).

 

Complicated Migraines

Click on the Read More button to review complicated migraines.



Baskin (2014) observed that a migraine patient's brain is more vulnerable to psychiatric disorders. They are 5.8 times more likely to develop depression. Depression complicates treatment because depressed migraine patients are 3 times less likely to adhere to treatment and show a reduced response to both medication and behavioral interventions. Anxiety generally precedes the onset of episodic migraine and may complicate migraine treatment more than depression. Episodic migraine can transform into a chronic headache with sleep disorder and anxiety.

Overuse of rescue medication can result in medication-overuse headache (MOH). Withdrawal from caffeine and immediate relief medication can produce more severe headaches. Analgesics hamper headache treatment. Chronic daily headache (CDH) is 19.4 times more likely when patients overuse medication.

Demographics

More than 30 million Americans report at least one migraine headache each year. Migraine affects 18% of women and 6% of men. One in six women experiences migraines (Chawla, 2014).

Cluster Headache

Cluster headache (CH) 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 months of remission (Diamond & Dalessio, 1986; Martin & Elkind, 2005).




Listen to a mini-lecture on Cluster Headache Overview © BioSource Software LLC.

Demographics

The prevalence of CH in the United States is uncertain with a rate that is 2-9% of migraines. The male-to-female ratio is about 2:1, compared to a 6:1 ratio reported in the 1960s. Women are more likely to experience cluster headache onset earlier than men and a second increase in frequency after age 50 (Blanda, 2015).

Hypothalamic Headache Generator

Emerging evidence implicates the hypothalamus as a central generator in primary headache disorders, notably migraines and cluster headaches. Functional neuroimaging studies have consistently demonstrated activation of the hypothalamus during headache episodes, suggesting its pivotal role in both the initiation and modulation of these conditions (Burstein et al., 2019; Schulte & May, 2016). Hypothalamus graphic © Alila Medical Media/Shutterstock.com.



In migraines, the hypothalamus is believed to contribute to the prodromal phase, characterized by symptoms such as altered mood, fatigue, and food cravings. These premonitory symptoms, occurring hours to days before the headache onset, are thought to result from hypothalamic dysfunction affecting homeostatic processes (Giffin et al., 2003). The subsequent activation of the trigeminovascular system leads to the headache phase, with the hypothalamus modulating pain sensitivity and autonomic responses (Schulte & May, 2016).

Cluster headaches exhibit a striking circadian rhythmicity, with attacks often occurring at the same time each day. This pattern points to the involvement of the hypothalamic suprachiasmatic nucleus, the body's primary circadian pacemaker. Positron emission tomography scans have revealed activation of the posterior hypothalamus during cluster headache attacks, further supporting its role in their pathogenesis (May et al., 1998).

The hypothetical mechanism underlying hypothalamic involvement in primary headaches involves its regulatory influence over autonomic and endocrine functions. Dysregulation within the hypothalamus may lead to abnormal activation of the trigeminovascular system, resulting in the release of vasoactive neuropeptides and subsequent neurogenic inflammation. This cascade culminates in the sensitization of central pain pathways and the manifestation of headache symptoms (Burstein et al., 2019).

In summary, the hypothalamus plays a critical role in the pathophysiology of primary headaches, acting as a generator that influences the onset and characteristics of migraine and cluster headache attacks. Ongoing research into hypothalamic function and its interactions with pain pathways holds promise for developing targeted therapies for these debilitating conditions.

Key Differences Between Migraine and Cluster Headache Pathomechanics

The key differences in the pathomechanics of migraine and cluster headache are significant and multifaceted. One of the most striking distinctions is the periodicity of attacks. Cluster headaches exhibit a unique circadian and circannual rhythm, often occurring at the same time each day or during specific seasons, which is not typically observed in migraines. This pattern suggests a stronger involvement of the hypothalamus in cluster headaches.

Autonomic symptoms also differentiate these conditions. While both may present with some autonomic features, they are far more prominent and consistent in cluster headaches, manifesting as ipsilateral conjunctival injection, lacrimation, nasal congestion, or ptosis. In contrast, migraine-associated autonomic symptoms tend to be less severe and more variable.

The quality of pain differs markedly between the two. Migraine pain is characteristically throbbing or pulsating, often described as a deep ache that worsens with physical activity. Cluster headache pain, on the other hand, is typically non-throbbing, extremely severe, and often described as burning, piercing, or stabbing.

Duration is another key differentiator. Migraine attacks are generally longer-lasting, typically persisting for 4 to 72 hours if untreated. Cluster headache attacks, while intensely painful, are usually shorter, lasting between 15 minutes to 3 hours.

Finally, the behavioral response to attacks varies significantly. During a migraine, sufferers typically seek a quiet, dark environment and prefer to lie still. In stark contrast, individuals experiencing a cluster headache often become restless and agitated, frequently pacing or rocking back and forth in an attempt to alleviate the pain.

These distinct clinical features reflect the underlying differences in the pathomechanisms of migraine and cluster headache, highlighting the involvement of different neural pathways and brain regions in their respective pathogeneses.

Physiology of a Vascular Headache

The trigeminal nerve shown in yellow may be activated in all primary headaches--cluster, migraine, and tension-type. A neurovascular theory of migraine based on imaging studies has replaced the poorly supported vascular theory of the 1940s that proposed that migraines are due to blood vessel dilation.


Listen to a mini-lecture on the Neurovascular Theory of Headache © BioSource Software LLC.
Graphic © S K Chavan/Shutterstock.com.





The neurovascular theory hypothesizes that migraine sufferers are vulnerable to cortical hyperexcitability, especially in the occipital cortex. A wave of cortical spreading depression (CSD) originates in the occipital lobe at the back of the head and moves toward the frontal lobe.



Listen to a mini-lecture on the Physiology of Migraine Pain © BioSource Software LLC. Graphic © S K Chavan/Shutterstock.com.

Diet

Medina and Diamond (1978) reported that diet plays a relatively minor role in migraine pain for most patients. Khazan (2014) observed that specific foods trigger roughly 5% of migraines. For this small segment of migraine patients, the systematic elimination of alcohol, chocolate, aged cheeses, processed meats, MSG, nitrates, and nitrites may help to identify their unique triggers. Unstable blood sugar levels due to prolonged gaps between meals or poor nutrition are a more common migraine trigger than specific foods.

Designing Biofeedback Protocols

Treatment protocol design should follow medical assessment and 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 client’s unique response stereotypy.


Listen to a mini-lecture on Migraine Treatments © BioSource Software LLC. Graphic © Derya Draws/Shutterstock.com.


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

• frontal SEMG biofeedback
• trapezius SEMG biofeedback
• temperature biofeedback
  
• blood volume pulse biofeedback
• passive infrared hemoencephalography
• slow cortical potential (SCP) neurofeedback
  
• qEEG neurofeedback
• cognitive behavior therapy
• relaxation training (e.g., autogenic training)

Biofeedback Studies

Click on the Read More button to review biofeedback and neurofeedback studies that treated vascular headaches.

Clinical Efficacy

Based on eight RCTs, Tracy Brown and Patrick Steffen (2023) rated biofeedback for adult headache as level 4 - efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.).

The biofeedback modalities included EMG, HRV, neck pressure, TEMP, and vasoconstriction/ vasodilation biofeedback. Biofeedback outcomes included reduced headache frequency and severity, medication, and performance loss.

Raynaud's Phenomenon

Description

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 a color change in the digits of the hands or feet. Pallor (white color) and numbness are produced by the 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 the 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).


Listen to a mini-lecture on Raynaud's Overview © BioSource Software LLC.

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. RP graphic Pepermpron/Shutterstock.com.





Physicians divide Raynaud’s phenomenon (RP) into primary and secondary RP (Wigley & Flavahan, 2016). Primary RP is not due to an identifiable disorder. Secondary RP is caused by observable processes like trauma (carpal tunnel syndrome and shoulder girdle compression syndrome), arterial disorders (atherosclerosis), and rheumatic disorders (lupus erythematosus; Spittell, 1972).

Demographics

The prevalence of RP ranges between 3-5%, and Raynaud's is more frequently diagnosed in women and younger patients. Primary RP accounts for more than 80% of Raynaud's cases. Between 15-20% of primary RP patients later develop a significant systemic disease (Hallett, 2014).

Diagnosis

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

Pathophysiology

The pathogenesis of RP is a complex interplay of mechanisms, transcending the simplistic division between sympathetic nervous system overactivity and intrinsic vascular dysfunction (Herrick, 2012; Wigley & Flavahan, 2016).

The dual defect model posits that cold both increases sympathetic outflow and primes local a2-ARs, creating a permissive environment for vasospasm (Kahalek & Matucci-Cerinic, 2020). In primary RP, the local fault hypothesis is most prominent. This form of the condition is largely driven by hypersensitivity of a2C-adrenergic receptors, which become activated during cold exposure. Cooling triggers the movement (translocation) of these receptors to the vascular smooth muscle cell membrane, amplifying vasoconstriction even under mild conditions. This receptor-level dysfunction explains why vasospastic episodes can occur independently of systemic sympathetic input.

In contrast, secondary RP incorporates both local vascular abnormalities and heightened sympathetic activity. Structural vascular damage, such as intimal fibrosis or endothelial dysfunction, reduces arterial compliance and predisposes blood vessels to collapse during vasoconstrictive stimuli. Autoimmune conditions, such as scleroderma, further exacerbate this by impairing nitric oxide-mediated vasodilation and promoting a pro-constrictive environment. In this context, sympathetic hyperactivity plays a more significant role, as stress-induced surges in norepinephrine can easily overwhelm already compromised vasculature.

Click on the Read More button to learn more about RP pathophysiology.

RP Treatment Protocols

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

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 more significant 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 RP 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 1-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.

RP patients who received temperature biofeedback under cold challenge produced superior 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 a 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 secondary RP patients is due to a beta-adrenergic vasodilating mechanism instead of reducing the firing of sympathetic digital nerves. Temperature elevations in RP patients are not associated with changes in norepinephrine or epinephrine. Slight elevations in heart rate, skin conductance level, and systolic and diastolic blood pressures were found. Vasoconstriction in normals is mediated by efferent, sympathetic fibers.

Implications for Temperature Biofeedback

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

First, patients should be trained to vasodilate and vasoconstrict since they 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. It did not produce relaxation on heart rate, respiration rate, frontalis SEMG, or skin conductance measures in normals.

Third, the best length of a temperature biofeedback training session warrants further study. While Taub found that sessions longer than 16 minutes produced diminishing returns for RP clients, this may depend on the population trained, biofeedback protocol used, therapist skill, and individual differences in the ability to learn to self-regulate.

Sedlacek and Taub (1996) concluded in their literature review that 80-90% of Raynaud’s disease patients could 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 (reducing 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 more signficiant 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 these treatments:

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% healthy participants 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 two 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 criterion (i.e., voluntarily raising temperature to 93° F (33.9° C) for at least 15 minutes [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).

Sporbeck et al. (2012) conducted a randomized controlled trial on Raynaud's phenomenon (RP) due to systemic sclerosis that compared deep oscillation, biofeedback, and a wait-list control group. Biofeedback significantly reduced visual analog pain scores.

Clinical Efficacy

Based on eight RCTs, Fred Shaffer and Zachary Meehan (2023) rated biofeedback for RP as level 4 - efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.). TBF will not reduce the frequency of Raynaud's attacks unless patients learn to increase hand temperature (Yucha, 2016),

Low Back Pain

Clinicians classify low back pain as chronic after 3 months since connective tissue usually heals within 6-12 weeks (Wheeler, 2014). 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 a restricted range of motion.


Listen to a mini-lecture on Low Back Pain Overview © BioSource Software LLC. Graphic © Olly y/Shutterstock.com.





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

Demographics

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, 2014).

Spinal Nerves

The spinal cord is divided into 31 pairs of spinal nerves that arise at regular intervals.

The Anatomy of Thoracic, Lumbar, and Sacral Spine-Associated Muscles

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 lower back's erector spinae.

SEMG Assessment

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.

Complementary Medical Procedures

Click on the Read More button to see complementary medical procedures.

Biofeedback Treatment Protocols

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.


Listen to a mini-lecture on Low Back Pain Treatment © BioSource Software LLC.

Neblett (2002) 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. Finally, they 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 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.
   

Clinical Efficacy

Based on four RCTs, Saul Rosenthal rated biofeedback for low back pain as level 4 - efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.).

Clinicians trained clients to reduce SEMG and stabilize the trunk and relax (BART). Participants improved on depression, distress, pain intensity, disability, pain cognitions, and muscle activation.

Myofascial Pain

Chronic myofascial pain syndrome is a regional pain disorder 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. Graphic © Alila Medical MediaShutterstock.com.





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). Graphic © saap585/Shutterstock.com.





Increased sympathetic efferent signals to muscle spindles and overexertion can produce a spasm in the muscle spindle's intrafusal fibers, increasing muscle spindle capsule pressure and causing myofascial pain.

Demographics

About 14.4% of the United States population experiences chronic musculoskeletal pain. Almost everyone develops a trigger point during their lives. About 21-93% of patients diagnosed with regional pain complaints present with myofascial pain. This syndrome is equally distributed between men and women. Trigger points can be found in patients of all ages, including infants. Sedentary individuals have a higher risk of developing trigger points than individuals who daily engage in vigorous activity (Finley, 2013).

Anatomy and Physiology

Hubbard and Gevirtz have proposed that sympathetically-mediated muscle spindle spasm may be the essential local mechanism in myofascial pain.


 

Sympathetic innervation of human muscle spindles has been demonstrated through the presence of neuropeptide Y (NPY), NPY receptors, and tyrosine hydroxylase (TH) on intrafusal fibers and associated blood vessels, indicating direct sympathetic input beyond just the vascular supply (Radovanovic et al., 2015).

This sympathetic influence on muscle spindles has significant implications for understanding trigger points, muscle spasticity, and pain. Trigger points, defined as hyperirritable spots within taut bands of skeletal muscle, often exhibit increased muscle spindle sensitivity and spontaneous electrical activity (Gerwin et al., 1997). The heightened sympathetic drive—whether from stress, chronic pain, or systemic dysfunction—could exacerbate this sensitivity, contributing to sustained muscle contraction and local ischemia. This ischemia can further sensitize nociceptors, perpetuating a cycle of pain and increased muscle tone.

In muscle spasticity, typically observed in conditions like stroke or spinal cord injury, altered proprioceptive feedback through hyperactive spindles may contribute to exaggerated stretch reflexes. Sympathetic overactivity could worsen this by increasing spindle excitability, thereby enhancing muscle stiffness and reducing motor control (Dietz, 2002). Additionally, chronic sympathetic activation in conditions such as complex regional pain syndrome (CRPS) is associated with muscle hyperalgesia, potentially mediated by exaggerated spindle activity and increased afferent input to the central nervous system (Wasner et al., 2003).

Gevirtz's (2003) mediational model of muscle pain proposes that lack of assertiveness and resultant worry each trigger sympathetic activation. Graphic © Photographee.eu/Shutterstock.com.

Gevirtz (2013) hypothesizes that HRVB improvement in autonomic balance may interfere with SNS innervation of trigger points through the mechanism of accentuated antagonism (Olshansky, Sabbah, Hauptman, & Colucci, 2008).

Clinical Efficacy

Sherman, Tan, and Wei (2016) rated biofeedback for myofascial pain syndrome as level 2 - possibly efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (3rd ed.).

Fibromyalgia (FM)

Fibromyalgia (FM) is a chronic benign pain disorder that involves pain, tenderness, and stiffness in the connective tissue of muscles, tendons, ligaments, and adjacent soft tissue. Graphic © medicalstocks/Shutterstock.com.

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 the 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 muscle and joint pain (Donaldson & Sella, 2003; Tortora & Derrickson, 2021).

McGrady and Moss (2013) conceptualize FM as a “pain amplification disorder” produced by the twin mechanisms of allodynia and hyperalgesia (p. 187).

Allodynia means that patients experience previously benign stimuli as painful. Hyperalgesia means patients experience mildly painful stimuli as severely painful. While an initial injury that damages tissue may sensitize the body through peripheral and central sensitization, in other cases, there may be no identifiable precipitating event. Sequelae of negative emotion and sleep deprivation increase pain and impair cognitive performance. The graphic below depicts back pain in fibromyalgia.

Demographics

The 2010 ACR fibromyalgia adult criteria are probably met by 7.7% of women and 4.9% of men. The female-to-male ratio is probably 4:1 due to the underestimation of its prevalence in men. While fibromyalgia is mainly seen in women 20-50 years, with average onset at 47.8 years, it is also diagnosed in adolescents and the elderly. The peak prevalence in women occurs between 60-70 years. Fibromyalgia pain typically persists 78.7 months (Donaldson & Sella, 2003; Boomershine, 2015).

Anatomy and Physiology

The etiology of fibromyalgia appears to involve a central hypersensitivity to heat, cold, and electrical stimulation (Desmeules et al., 2003).

Clinical Efficacy

Based on one RCT using SEMG biofeedback and two RCTs using theta/SMR neurofeedback, Christopher Gilbert (2023) rated biofeedback for fibromyalgia at level 3 - probably efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.).

Temporomandibular Disorders (TMD)

Temporomandibular disorders (TMD) are the second most common cause of orofacial pain after toothache. Whereas 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.

Listen to a mini-lecture on TMD Overview and Treatment © BioSource Software LLC.

TMD pain is located in the preauricular area, muscles used for chewing (masseter, temporalis, and pterygoids), or the temporomandibular joint. Graphic © Alex Mit/Shutterstock.com shows the masseter and the temporomandibular joint.



TMD pain is triggered by parafunctional jaw clenching, which may be unilateral or bilateral in MPD. It is reported along with headache, other facial pain, neck pain, and pain in the shoulder and back. Check out the Alila Medical Media YouTube video TMJ and Myofascial Pain Syndrome, Animation.

Demographics

While 5%-10% of Americans may satisfy the criteria for TMD, up to 75% of Americans will present with several of its symptoms. The male-to-female ratio is 1:4. Young adults are the highest risk group, particularly women from 20-40 years (Guardia, 2014).

Joint and Muscle Anatomy of TMD

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).

Biofeedback Treatment of TMD

Click on the Read More button to review biofeedback TMD studies.

Dental and Physical Therapy Approaches

Click on the Read More botton to review dental and physical therapy approaches.

Clinical Efficacy

Based on three RCTs, Alan Glaros and Richard Ohrbach (2023) rated SEMG biofeedback for TMD pain as level 4 - efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.).

Cervical Injury

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. Graphic © design36/Shutterstock.com.

SEMG Assessment

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.

Biofeedback Treatment Protocols

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 excessive EKG artifact cannot be controlled through narrow electrode spacing. Depending upon the initial SEMG assessment results, 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

Complementary medical procedures to reduce muscle spasticity and strengthen weak muscles include:

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

Clinical Efficacy

Based on four RCTs, Saul Rosenthal (2023) rated biofeedback for cervical pain as level 4 - efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.).

Worksite Ergonomic Applications

Peper and Gibney (2006) argue 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 bodily 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

Listen to a mini-lecture on Workplace Ergonomic Applications © BioSource Software LLC.



Peper and Gibney (2006) provided the content for this Real Genius episode. Artist: Dani S@ unclebelang on Fiverr.




Incorrect and Correct Posture

Graphics © Sebastian Kaulitzki/Shutterstock.com.




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. The three standard electrode placements below are from Peper and Gibney (2005).




                                 
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. The graphic below is courtesy of Peper and Gibney (2005).


                                             


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

Healthy Computing

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

1. Work style: adopting healthy work habits. These practices include 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 the 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, alleviates stress, and increases performance

A micro-break is a 1 to 2-second 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 may involve stretching in place or leaving the computer and moving around. This exercise should be performed every 20 minutes. Graphics © ESB Professional/Shutterstock.com.





When individuals frequently alternate between muscle contraction and relaxation, this increases blood and lymph circulation and helps prevent repetitive motion injury (RMI) (Peper & Gibney, 2005).

Demographics

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).

Biofeedback Protocols

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

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, implicated in intrafusal muscle fiber spasm and chronic pain (Gevirtz, 2003).

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

Clinical Efficacy

Based on multiple RCTs with no-treatment control, Zachary Meehan and Fred Shaffer (2023) rated biofeedback for worksite-related pain as level 3 - probably efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.).

Complex Regional Pain Syndromes (CRPS)

Complex Regional Pain Syndromes (CRPS) is the current term for Reflex Sympathetic Dystrophy Syndrome (RSDS). The main symptom of CRPS is severe, often burning pain.

CRPS is divided into Types I and II based on the initiating event. CRPS Type I, which is more common, is caused by a crushing injury, soft tissue injury, or immobilization. CRPS Type II is precipitated by nerve injury (Wheeler, 2014).

The disorder may progress to dystrophy (weakness or wasting) of the area. CRPS can be divided into three progressive stages, which every patient may not experience. 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.

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

Demographics

The incidence of CRPS following a myocardial infarction is 5%, and after brain injury is 12%. The incidence of CRPS Type I is 1-2% after fractures, and the occurrence of CRPS Type II is 1-5% following peripheral nerve injury. The male-to-female ratio for CRPS ranges from 1:2 to 1:4 (Wheeler, 2014).

Biofeedback Treatment Protocols

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 years.

Blanchard (1979) reported successful treatment of a patient with chronic pain resulting from CRPS in his hand and arm following months of conservative medical care failure. Eighteen sessions of temperature biofeedback taught the patient to increase hand temperature 1-1.5° 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 in the knee area with temperature biofeedback. Biofeedback training started with hand-warming and then transferred vasodilation to the affected knee. The temperature increased in the affected knee, local vasospasms and cold intolerance ended in 10 sessions, and the patient resumed regular 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.

Clinical Efficacy

Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.) did not evaluate biofeedback for CRPS.

Glossary

α2C-adrenergic receptors (α2C-AR): These are a subtype of alpha-2 adrenergic receptors, which are part of the G protein-coupled receptor (GPCR) family. They play a key role in regulating neurotransmitter release and vascular function. In the central nervous system, a2C-ARs modulate neurotransmission, particularly during low levels of norepinephrine activity, and are involved in processes like mood and cognition. Peripherally, they are expressed on vascular smooth muscle cells in small blood vessels and contribute to cold-induced vasoconstriction by increasing the sensitivity of these vessels to norepinephrine. This makes them particularly important in conditions like Raynaud’s phenomenon, where excessive vasoconstriction occurs in response to cold exposure.

active SEMG training: Neblett’s approach that combines neuromuscular rehabilitation with general relaxation. This strategy involves a collaborative process in which the clinician and client 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. 

allodynia: the perception of benign stimuli as painful.    
                                         
asymmetry: an imbalance between the SEMG measurements of homologous left and right muscle groups. A difference of at least a 20% difference is considered pathological and may contribute to pain.

aura (prodrome): neurological symptoms that precede a breakthrough headache, hours to days before headache onset observed in migraine with aura (classic migraine). An aura is caused by cortical spreading depression (hyperpolarization).

basilar artery migraine: headache with prodromal symptoms lasting from 2-45 minutes with symptoms of total blindness, altered consciousness, vertigo, and ataxia (involving the brainstem). Clients experience severe pulsating occipital headaches with vomiting that persists for hours or until sleep.

calcitonin gene-related peptide (CGRP): a neuropeptide, that along with substance P, stimulates pain receptors and increases blood vessel dilation in migraine headaches.

Carpal Tunnel Syndrome (CTS): painful and disabling example of repetitive stress injury (RSI) due to peripheral nerve injury involving inflammation of the tendons that travel through the wrist’s carpal tunnel. These clients 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.

central sensitization: increased responsiveness of nociceptive neurons in the central nervous system to normal or subthreshold afferent input.

cervical paraspinal placement: active electrodes are placed around C2 and C5 lateral or medial to the spine over the cervical paraspinal muscles.

chronic tension-type headache: steady, nonthrobbing pain that may involve the frontotemporal vertex or occipito-cervical areas with a lateral or bilateral distribution with an average headache frequency of more than 15 days per month for more than 6 months.

classic Raynaud’s: triphasic disorder during which a patient exhibits a color change (pallor, cyanosis, and rubor) in the digits of the hands or feet. All three color changes are observed in only a minority of patients.

cluster headache: episodes that start abruptly without prodromes, 2 to 3 hours after falling asleep, and 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 (the headaches cluster in time) followed by 12 months of remission. Biofeedback is not efficacious for this type of headache.

cold pressor test: immersion of the hand in ice water container for 1 minute to measure the effect on blood pressure and heart rate. This procedire does not increase sympathetic activity in the digital nerves of Raynaud’s patients, which challenges Raynaud’s sympathetic overactivity hypothesis of this disorder.

Complex Regional Pain Syndromes (CRPS): a chronic progressive disease that involves severe (often burning) pain, swelling, and skin lesions. The International Association for the Study of Pain divides CRPS into Type I, including Reflex Sympathetic Dystrophy (RSD) when nerve damage is absent, and Type II, causalgia, when nerve damage is present. This disorder may progress to dystrophy (weakness or wasting) of the area.

computer-related disorder (CRD): Peper and Gibney’s term for pain experienced when working with a computer. Repetitive motion interacts with many other factors to produce injury and pain.

cortical spreading depression (CSD): a wave of hyperpolarization that moves across the cortex at approximately 3.6 mm/minute. CSD may be responsible for auras in migraine with aura instead of a hypothesized vasoconstrictive process.

cyanosis: in Raynaud’s, a blue skin color is caused by pooled deoxygenated blood due to minimal arteriole inflow and constricted venous outflow.

dual defect model of Raynaud's phenomenon: the explanation that vasospastic episodes arise from the combined effects of sympathetic overactivation and local vascular abnormalities. Heightened sympathetic responses to cold or stress increase norepinephrine release, while hypersensitive a2-adrenergic receptors and endothelial dysfunction in the blood vessels amplify the vasoconstrictive effects. This model unifies systemic triggers and localized vascular defects to explain the condition's pathophysiology.

dura mater: the outermost layer of the three meninges that protect the brain and spinal cord. Trigeminal nerve endings in this layer release proteins that dilate blood vessels and increase the nerves' sensitivity.

erector spinae (sacrospinalis): a muscle that maintains erect position of the spine and extends the vertebral column.

fascia: fibrous connective tissue that divides muscles into functional groups.

fibromyalgia: 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 the neck, shoulder, chest, back, arm, hip, and knee sites.

FpN placement: an active electrode is placed over a frontalis muscle and another over a cervical paraspinal muscle on the same side below the hairline.

frontalis or bifrontal placement: an active electrode is centered above each pupil, midway between the eyebrow and hairline.

Gevirtz's mediational model of muscle pain: 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 muscle spindle's intrafusal fibers, increasing muscle spindle capsule pressure and causing myofascial pain.

healthy computing: a systems approach to treating computer-related disorder (CRD) that includes work style, ergonomics, somatic awareness, stress management, regeneration, vision care, and fitness.

hyperalgesia: mildly painful stimuli are perceived as severely painful.

hypothalamus: A region of the brain responsible for regulating autonomic and endocrine functions, including circadian rhythms, appetite, and pain perception.

insertion: the more movable bone at a joint.

large movement break: leaving the computer and moving around every 20 minutes.

Lewis' local fault hypothesis: explanation that resistance vessels that precede the capillaries overreact to local cooling. This hypothesis is better supported than Raynaud’s sympathetic overactivity hypothesis.

longissimus capitis: a muscle that helps extend and rotate the head to the same side as the contracting muscle and that is retrained following cervical injury.

masseter: muscle that elevates and protracts the mandible. The masseter is down-trained in temporomandibular disorders (TMD).

median nerve: nerve within the carpal tunnel that is compressed in Carpal Tunnel Syndrome (CTS).

medication-overuse headhache: chronic headache, occurring on =15 days/month, caused by the regular overuse (for >3 months) of acute headache medications, often resolving after discontinuation of the offending medication. It typically develops in those with pre-existing primary headache disorders.

micro-break: 1 to 2-second interruption of muscle activation (like the release of forearm muscle activity when a typist reaches the end of a paragraph) about every minute.

migraine equivalent: prodromes without headaches.

migraine generator: a hypothesized circuit 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.

migraine with aura (classic migraine): a vascular headache that features a prodrome or neurological symptoms that precede a breakthrough headache, hours to days before headache onset. Migraine with arua accounts for up to 31% of all migraine patients.

migraine without aura (common migraine): a vascular headache that is not preceded by a prodrome that accounts for about 64% of all migraine patients and lasts 4-72 hours.

migrainous infarction (complicated migraine): a vascular headache with neurologic symptoms that often follow a definite sequence. This headache involves less than 1-2% of migraineurs and includes hemiplegic, ophthalmoplegic, and basilar migraines.

muscle co-contraction: SEMG levels in one muscle increase from baseline during the contraction of another muscle, for example, when head rotation increases vastus medialis SEMG activity.

muscle spindles: stretch receptors that lie in parallel with skeletal muscle fibers and trigger the monosynaptic stretch reflex.

myelogram: x-ray of nerves using an injected contrast medium to assess nerve damage.

myofascial: Relating to the fascia surrounding and separating muscle tissue.

Myofascial Pain Syndrome (MPS): regional pain disorder characterized by trigger points, which are hyperirritable regions of taut bands of skeletal muscle in the muscle belly or associated fascia (connective tissue).

nifedipine (generic): a drug that inhibits calcium ion influx into vascular smooth muscle. Nifedipine is used to control Raynaud’s disease pharmacologically.

nociceptive: related to the perception of pain.

ophthalmoplegic migraine: a vascular headache with nonpulsating, moderate pain (often with vomiting), and paralysis of one or more extraocular muscles that move the eyes. This disrupts coordinated eye movement and results in double vision.

pallor: in Raynaud’s, white skin color is produced by constriction of arterioles and venules.

palpation: examination by feeling or pressing with the hand.

paraspinal muscle placement: the erector spinae maintains the erect position of the spine and extends the vertebral column. Active pairs are located lateral to the spine, above the iliac crest (rounded upper margins of the ilium bone above the buttocks) about L4 and below the bottom of the ribs at about L2.

passive infrared hemoencephalography (HEG): detection of infrared light that theoretically corresponds to heat generated by local brain metabolism and blood oxygenation.

periaqueductal gray (PAG): midbrain region whose axons form excitatory synapses on neurons located in the nucleus raphe magnus (NRM) and the nucleus reticularis paragigantocellularis (NRPG) in the medulla. The PAG plays a role in the descending modulation of pain and control of defensive behavior. Its ability to suppress pain may be compromised by successive migraines.

pericranial: surrounding or enclosing the skull.

prazosin (Minipress): antagonist at α1-adrenergic receptors that is used to control Raynaud’s disease pharmacologically.

primary RP: The most common form of Raynaud’s, occurring without any underlying medical condition. It is usually less severe and often affects younger individuals, particularly women under 30. Its exact cause is unknown, and it is considered idiopathic (of unknown origin).

protective guarding: SEMG elevation on the side opposite an injury.

Raynaud’s phenomenon: a condition characterized by episodic narrowing (vasospasm) of blood vessels, typically in the fingers and toes, triggered by cold or stress. This leads to reduced blood flow, causing the affected areas to turn white or blue, become cold and numb, and sometimes painful. The condition can be primary (without an underlying cause) or secondary (associated with another disease)

reactive hyperemia: excessive inflow of oxygenated blood into the upper epidermis during the rubor stage of Raynaud’s.

referred pain: pain perceived at a distance from the injury site, for example, angina pectoris.

repetitive stress injury (RSI): syndrome that includes diffuse pain in the arm that worsens with activity and features weakness and lack of endurance. These symptoms do not follow nerve and tendon distributions.

rubor: in Raynaud’s, red skin color and burning sensations result from excessive inflow of oxygenated blood into the upper epidermis.

scapular winging: protrusion of the shoulder blade following a shoulder injury.

secondary RP: A more severe form of Raynaud’s linked to underlying diseases, such as autoimmune disorders (e.g., lupus or scleroderma), vascular diseases, or certain medications. Secondary RP typically develops later in life and may lead to complications like ulcers or tissue damage due to prolonged lack of blood flow.

semispinalis capitis: a muscle that helps extend the head and rotates the head to the side opposite the contracting muscle.

Sherman’s five percent rule: severe acute pain can develop and progress to chronic pain when limbs deviate five degrees from a healthy position, muscles are five percent tenser than required, and muscles remain minimally tense five percent longer than needed.

splenius capitis: a muscle that helps extend the head and rotate the head to the same side as the contracting muscle.

splinting: SEMG elevation on the injured side of the body.

sternocleidomastoid (SCM): a muscle that flexes the vertebral column and rotates the head to the opposite side (contract left SCM and head twists to the right).

substance P: peptide pain transmitter.

supraspinal: Above or superior to the spinal cord, typically referring to brain structures. The key supraspinal structures implicated in TTH central sensitization are the periaqueductal grey, rostral ventromedial medulla, thalamus, somatosensory cortex, anterior cingulate cortex, and insula.

sympathectomy: sympathetic nerve lesion that may be performed in severe cases of Raynaud’s. Symptom improvement is limited to 1-2 years.

sympathetic overactivity hypothesis: explanation that Raynaud’s symptoms are due to increased sympathetic activity in digital nerves. This position is not supported by experimental evidence.

temperature biofeedback under cold challenge: a procedure in which temperature biofeedback teaches the client to maintain peripheral temperature while the affected limb is cooled. This is the most effective biofeedback protocol for treating Raynaud’s.

temporalis: a muscle that elevates and retracts the mandible (jaw).

temporomandibular disorders (TMD): a heterogeneous group of diseases that are 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. Pain is triggered by parafunctional jaw clenching and is reported along with headache, other facial pain, neck pain, and pain in the shoulder and back.

tender points: sites of local tenderness located at a muscle's insertion that are distinct from trigger points. Compression produces local pain, but not the referred pain associated with trigger points, and may increase overall pain sensitivity.

tension-type headache: a steady, nonthrobbing pain that may involve the frontotemporal vertex or occipito-cervical areas with a lateral or bilateral distribution.

trapezius: the most superficial back muscle is a triangular muscle sheet covering the posterior neck and superior trunk. The upper trapezius elevates the scapula and helps extend the head, and maybe retrained in tension-type headache.

trigeminal autonomic cephalgias (TACs): A group of primary headache disorders, including cluster headaches, characterized by severe unilateral pain and associated autonomic symptoms.

trigeminal nerve: 5th cranial nerve that receives sensory information about the region from the jaw to the scalp and controls eight muscles. The trigeminal nerve may be activated in all primary headaches by cortical hyperexcitability, producing a breakthrough headache.

trigeminovascular system: a neural pathway involving the trigeminal nerve and associated blood vessels, playing a key role in the transmission of headache pain.

trigger points: hyperirritable regions of taut bands of skeletal muscle in the muscle belly or associated fascia characterize Myofascial Pain Syndrome (MPS). Pressure on these areas is painful, and they can produce referred pain and tenderness, motor dysfunction, and autonomic changes.

triphasic disorder: classic Raynaud’s patients experience skin color changes of pallor, cyanosis, and rubor.

vasoconstriction: narrowing of blood vessels due to the contraction of the smooth muscle in their walls. Increased firing of sympathetic efferent fibers and circulating alpha-adrenergic hormones constrict blood vessels.

vasodilation: widening of blood vessels due to the relaxation of the smooth muscle in their walls, riggered by a beta-adrenergic cascade that culminates in nitric oxide release.

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Assignment

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?

References

Al-Haggar, M. S., Al-Naggar, Z. A., & Abdel-Salam, M. A. (2006). Biofeedback and cognitive behavioral therapy for Egyptian adolescents suffering from chronic fatigue syndrome. Journal of Pediatric Neurology, 4(3), 161-169. https://doi.org/10.1055/s-0035-1557320

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