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Fibromiyalji Sendromunda “Nöro-geribildirim Tedavisi” Kitap Bölümümüz Amerika Birleşik Devletleri’nde Yayınlandı

Kronik ağrı (fibromiyalji sendromu) ile ilgili ABD yazarları ile birlikte yazdığımız “Clinical Neurotherapy” kitabı yayınlandı. Bu kitapta, beyin dalgalarının çeşitli hastalıklarda tedavi programları doğrultusunda değiştirilebilmesini konu alan Nöro-feedback (Nöro-geribildirim) konusu tüm detayları ile incelendi. Bu kitapta, Prof. Dr. Erbil Dursun ve Prof. Dr. Nigar Dursun ise nöro-geribildirim tedavisinin kronik ağrıda (fibromiyalji sendromu) kullanımını yazdı. Aşağıda bu kitapta yazılmış bölümü sizlere sunuyoruz.

 

Fibromiyalji Sendromu

 

 

 

 

 

 

 

 

 

Erbil Dursun and Nigar Dursun

CHAPTER TEN: Treating Chronic Pain Disorders

Chronic pain is a common problem and expensive to treat. The success

rate of all the available treatments for this condition is limited, because it

rarely responds to the therapeutic measures that are successful in treating

acute pain.1 For the majority of patients, the currently used treatments can

not eliminate pain adequately.2 Besides, most of the pharmacological treatments

used for chronic pain often have adverse effects, especially dependence

on pain medications. For these reasons, as the mechanisms of pain

become better understood, new interventions that may affect pain at the

cortical level are being developed.3–5

For many years, biofeedback and relaxation therapies have been used

in addition to medical approaches to treat acute and chronic pain syndromes.

The term biofeedback covers a group of therapeutic procedures

that use electronic or electromechanical instruments to properly measure,

process and feed back to patients in the form of auditory and/or visual

signals using information about their normal and/or abnormal neuromuscular

and autonomic activity.6 Biofeedback is used to help patients

develop a greater awareness of and an increase in voluntary control over

their physiological processes, which are otherwise involuntary and unfelt.

In psychiatry, biofeedback has been used in a wide range of clinical conditions,

such as motor weakness,7,8 balance and gait disturbances,9,10 spasticity,

11 neurogenic bladder12 and bowel dysfunction,13,14 and speech15 and

swallowing problems.16 It has also been used in the management of various

acute and chronic painful conditions, such as temporomandibular joint

dysfunction,17 headaches,18 lower back pain19 and patellofemoral pain

syndrome.20,21 In addition, biofeedback treatment is also suggested to be

helpful in the management of fibromyalgia syndrome (FMS).22

Electroencephalographic (EEG) biofeedback is an operant conditioning

procedure that can alter the amplitude, frequency or coherence of the

neurophysiological dynamics of the brain. Therapeutic application of EEG

biofeedback is often referred to as neurofeedback, and it has various clinical

applications, such as migraine,23,24 epilepsy,25 attention deficit hyperactivity

disorder (ADHD),26–28 alcohol abuse,29 sleep disorders30 and chronic

fatigue.31 Sensorimotor rhythm (SMR) training is a commonly applied

neurofeedback protocol that is normally associated with a quiet body

and an active mind, and appears to facilitate thalamic inhibitory mechanisms.

32 On the other hand, studies in epileptic patients with SMR training

showed significantly increased EEG spindle densities during sleep and

prolonged sleep episodes, and a related decrease in state conversions.33,34

In this way, SMR treatment suppresses some of the pathological consequences

of epilepsy and potentially reduces vulnerability to a convulsion.

 

As described by the International Association for the Study of Pain

(IASP), pain is an unpleasant sensory and emotional experience associated

with actual or potential tissue damage, or is described in terms of such damage.

According to IASP, pain is unquestionably a sensation in a part or parts

of the body, but it is also always unpleasant, and therefore also an emotional

experience. The IASP website continues: “Many people report pain in the

absence of tissue damage or any likely pathophysiological cause; usually this

happens for psychological reasons. There is usually no way to distinguish

their experience from that due to tissue damage if we take the subjective

report. If they regard their experience as pain, and if they report it in the

same ways as pain caused by tissue damage, it should be accepted as pain.”

 

If pain is considered only as a symptom associated with physical damage,

and is understood as a simple response to physical damage, then nociception

must be transmitted via a simple channel directly to a “pain perception area”

in the brain. If we consider it like this, pain must be thought of as being

related only to physical damage that occurs in the periphery. In this regard

the brain is seen as a passive perceiver of sensory information. Melzak and

Wall35 integrated the physiological and psychological aspects of pain according

to the gate control theory of pain. This theory declares that the dorsal

horn of the spinal cord acts like a gate, regulating the flow of impulses from

the peripheral nerve fibers to the brain. The gate is influenced by peripheral

fiber activity and by descending influences from the central nervous system.

Thus, this system explains how pain stimuli are adjusted in the spinal

cord before moving to the brain. At present, as we better understand the

mechanisms of pain in relation to the brain itself, our perceptions regarding

pain are changing from the periphery and spinal cord to the brain itself.

Supraspinal mechanisms are increasingly accepted as playing a major role in

the representation and modulation of pain.36

 

Nociceptive stimuli are influenced on many levels in the brain, such as

the cortex, insula, anterior cingulate and thalamus. Hyperalgesia is related

to changes at the site of injury as well as to hyperexcitability in the central

nervous system, which results in long-term changes to the nervous

system, known as plasticity.37 This hyperexcitability is also known as central

sensitization and leads to increased activity at higher brain centers. It

is likely perceived as more intense and prolonged pain.38 A number of

pathophysiological processes are suggested as responsible for the diffuse

pain of FMS, including central pain processing systems, the hypothalamopituitary–

adrenal axis and the autonomic nervous system, in which central

pain syndromes are the most productive area of research.39 There is

increased tenderness to pressure in FMS, and augmentation of pain caused

by central mechanisms. Augmentation of pain, such as windup,40 or weakened

effects of descending antinociceptive pathways, are examples of

central mechanisms.41 FMS patients have not only sensitivity to pressure

stimuli but also decreased nociceptive thresholds with regard to heat, cold,

electrical stimuli and even sound. The review by Williams and Clauw39

focuses on their current understanding of FMS as a prototypical central

pain syndrome. They stress that the terms central augmentation or central

pain threshold are different from central sensitization, and because the

tenderness or hyperalgesia occurs far away from the area of pain, central

augmentation or central pain are likely to be more suitable terms for what

is seen in FMS.

 

Deactivation of inhibitory processes in the central nervous system

arouses interest.38,42–44 Because the caudate nucleus and thalamus are both

involved in signaling the occurrence of noxious events, low regional cerebral

blood flow, which indicates decreased functional activity, is a marker

for impaired inhibition of nociceptive transmission by these brain structures.

38 In chronic pain states, thalamic blood flow is reduced, whereas

acute pain increases thalamic blood flow.45,46 In a controlled study47

the total Fibromyalgia Impact Questionnaire (FIQ) score in patients

was positively correlated with blood flow in the parietal lobe, including

the postcentral cortex. This correlation was seen in the areas of significant

hyperfusion. Also the total FIQ score was negatively correlated with

blood flow in a left anterior temporal cluster, one of the areas of significant

hypoperfusion. The authors concluded that brain perfusion abnormalities

in patients with FMS are correlated with the clinical severity of

the disease. Mountz et al.46 measured resting-state regional cerebral blood

flow in the hemithalami and left and right heads of the caudate nucleus in

 

10 untreated women with FMS and seven normal control women using

single-photon emission CT (SPECT). They also evaluated pain thresholds

at tender and control points. Regional cerebral blood flow in the left and

right hemithalami and the left and right heads of the caudate nucleus was

found to be significantly lower in women with FMS, as were lower pain

threshold levels. The authors concluded that abnormal pain perception in

women with FMS might result from a functional abnormality within the

central nervous system. Kwiatek et al.45 measured regional cerebral blood

flow using improved SPECT and advanced complementary analytic techniques

in resting female FMS patients and in age-, gender-, and education-

matched healthy controls. They confirmed that thalamic regional

cerebral blood flow is reduced in FMS, but to a statistically significant

extent only on the right. Low thalamic regional cerebral blood flow has

been observed not only in patients with FMS, but also in patients with

other chronic pain disorders, such as chronic neuropathic pain, metastatic

cancer and mononeuropathy.38 It may be that low thalamic regional cerebral

blood flow, which indicates decreased functional activity, is a marker

for impaired inhibition of nociceptive transmission by brain structures

such as the caudate nucleus and thalamus.

 

Several studies suggest that P300 indicates the activation of inhibitory

processes in the central nervous system, and a reduced P300 amplitude

may demonstrate a deficit in these inhibitory mechanisms.48 It was

reported that P300 amplitudes were reduced in clinical conditions such as

alcoholism, ADHD and Alzheimer’s disease.49–51 Hada et al.52 declared that

the lower P3a amplitude and weaker sources in alcoholics suggests disorganized

inefficient brain functioning, and this global electrophysiological

pattern suggests cortical disinhibition perhaps reflecting underlying central

nervous system hyperexcitability in alcoholics.52 Reduced P300 amplitudes

are seen in patients with FMS, and sertraline was shown to increase

the amplitude of P300 within 8 weeks.53,54 SMR training increases P300

amplitudes, which supports the observation that SMR training facilitates

thalamocortical inhibitory mechanisms.55

 

These findings have important implications regarding treatment, because

the pain of tissue or nerve damage can be attacked at the site of the injury

where it is initiated, as well as at central nervous system sites where it is maintained.

38 Interventions that reprogram or interrupt central sensitization could

provide significant relief for some individuals with chronic pain, and the

understanding that pain experience is modulated at many levels of the central

nervous system opens the door to interventions that might affect pain at

the cortical level, including treatments such as neurofeedback.56 On the other

hand, with regard to P300, we can assume that neurofeedback treatment may

play an inhibitory role on the central nervous system, and this may alter central

augmentation in FMS. In this way, we can hypothesize that neurofeedback

treatment will be effective in alleviating the symptoms and signs of FMS.

 

Ibric and Dragomirescu57 discusses 147 chronic pain patients, 10

of whom were presented as case studies. All of the 147 patients had little

resolution of pain with other treatment modalities. The 10 case study

patients had diagnoses including reflex sympathetic dystrophy, headache,

neuropathy, myofascial pain, left inguinal pain, chronic lower back and leg

pain, and FMS. In all cases the neurofeedback treatment involved SMR

enhancement as well as theta and high beta discouragement. The patients

had positive improvements after the neurofeedback treatment. The authors

noted that the results of neurofeedback were highly dependent on the

number of sessions: when sessions numbered 19 or fewer, the rate of success

was very reduced, but when the patients had completed more than 19

sessions of neurofeedback training, the success rate was evident.

 

In our rater-blinded controlled study5 involving 40 patients with FMS

randomized into either a neurofeedback (enhanced SMR activity and

decreased theta activity) or a control (escitalopram treatment) group, each

neurofeedback session was 30 minutes long and the patients had five sessions

per week. Each patient was trained at the same time of day for 4

weeks. The symptoms of FMS and the clinical grading scales were noted

at baseline, and at the second, fourth, eighth, 16th and 24th weeks for both

groups. The Visual Analogue Scale (VAS) for pain, VAS for fatigue, FIQ

and Short Form-36 (SF-36), Hamilton Depression Scale (HDS), Beck

Depression Scale (BDS), Hamilton Anxiety Scale (HAS) and Beck Anxiety

Scale (BAS) were applied. Also, the mean amplitudes of alpha, beta 1, beta

2, theta, delta, SMR and theta/SMR ratios were recorded at baseline and

at the second, fourth, eighth, 16th and 24th weeks in the neurofeedback

group.VAS pain and VAS fatigue scores were significantly decreased by the

end of the study period in the two groups. However, the values of the

neurofeedback group were significantly lower than in the control group

at all posttreatment assessments, even at the end of the 24th week. These

findings emphasize the positive effects of neurofeedback on pain and

fatigue, with the reorganization of the brain structures perhaps owing to

facilitation of the thalamocortical inhibitory mechanisms.

 

Besides pain, patients with FMS have many other diagnostic symptoms,

such as fatigue, sleep difficulties, a swollen feeling in tissues, paresthesias,

cognitive dysfunction, dizziness, increased tenderness in multiple points,

morning stiffness, psychological disorders, abdominal pain, dysmenorrhea,

irritable bowel syndrome, headaches and restless legs syndrome. There is evidence

for central sensitization in these conditions.58 A neurogenic form has

also developed, suggesting that functional dysregulation of central pain pathways

could account for many of the clinical manifestations of FMS.45 The frequent

joining of chronic pain with several other chronic disabilities may not

be coincidental. A meta-analysis shows that the brain network for acute pain

perception in normal subjects is at least partially distinct from that seen in

chronic clinical pain conditions, and that chronic pain engages brain regions

critical for cognitive/emotional assessments, implying that this component

of pain may be a distinguishing feature between chronic and acute pain.36

There are brain regions that reduce their activity during task performance,

and these regions are the component members of the default-mode network.

Raichle et al.59 used quantitative metabolic and circulatory measurements

from positron-emission tomography to obtain the oxygen extraction fraction

regionally throughout the brain. Areas of activation were prominent by their

absence, and increases indicated deactivations. Baliki et al.60 proposed that

long-term pain alters the functional connectivity of cortical regions known

to be active at rest. They demonstrated that chronic pain has a widespread

impact on overall brain function, where the default-mode network shown

by functional magnetic resonance imaging is imbalanced and disrupted, and

disorders of the default-mode network may account for the development of

accompanying cognitive and behavioral impairments. Therefore, neurofeedback’s

effect in positively altering the brain functions may be founded on its

supporting effect in the correction of this cortical disruption.

 

As neurofeedback improves attention deficits, Caro and Winter61 reasoned

that FMS patients with cognitive and attention complaints might

benefit from an EEG-based modality. In their experience many FMS

symptoms correlate with one another. Because of this, they speculated

that if neurofeedback positively improved cognitive symptoms in FMS, it

might also improve somatic complaints. They included 15 FMS patients

with attention problems who completed 40 or more neurofeedback sessions

where the SMR protocol was used, which augmented 12–15 Hz

brain waves while simultaneously inhibiting 4–7 Hz brain waves (theta)

and 22–30 Hz brain waves (high beta). Sixty-three FMS patients who

received standard medical treatment but who did not receive EEG biofeedback

were included as controls. The neurofeedback group showed

significant improvements in visual attention, tenderness, pain and fatigue.

 

Albeit not statistically significant, there was also a trend toward improvement

in psychological distress and morning stiffness.

 

In an uncontrolled clinical trial, Mueller et al.62 prospectively followed

30 FMS patients through a brainwave-based intervention known as EEGdriven

stimulation. Besides this, patients had also other treatments, including

massage therapy, physical therapy and surface electromyographic neuromuscular

retraining. Before and after treatment and during an extended followup,

comparison of the number of positive tender points and pain thresholds,

psychological and physical functioning indices, and specific FMS symptom

ratings revealed statistically significant improvements. In our study,5 posttreatment

assessments revealed that neurofeedback and control treatments

caused significant improvements in depressive symptoms and anxiety; i.e.,

all the depression and anxiety scores (HDS, BDS, HAS and BAS) showed

significant improvements in both the neurofeedback and the SF control

groups, but the neurofeedback group displayed greater benefits than controls.

In addition, FIQ and SF-36 revealed significant improvements in both

of the groups, but the values of the neurofeedback group were significantly

better than those of the escitalopram treatment group during the whole

study period. These findings underline the positive effects of the neurofeedback

treatment on psychosocial aspects, quality of life and physical functioning,

in addition to other symptomatology of FMS. On the other hand,

the therapeutic efficacy of neurofeedback was found to begin in the second

week and reached its maximum effect in the fourth week, whereas the

improvements in escitalopram treatment were also detected to begin in the

second week but reached its maximum effect at the eighth week. This early

effect of neurofeedback may be related to a faster brain plasticity process and

certainly can be considered one of the advantages of this treatment.

 

Pain may be associated with relatively lower amplitudes of slower wave

(delta, theta and alpha) activity and relatively higher amplitudes of faster

wave (beta) activity.56 Morphine treatment alters brain waves in the lowfrequency

range (2–4 Hz) during the first 300 ms after stimulus, whereas

active brain waves remain unchanged after placebo treatment.63 The results

show significant slowing of the EEG in spinal cord-injured patients with

neuropathic pain, consistent with the presence of thalamocortical dysrhythmia.

64 Intense painful stimulation causes an increase in beta wave

activity and tends to reduce mostly alpha (slower) wave activity.56 Mueller

et al.62 obtained statistically significant reductions in delta, theta and alpha

waves after treatment. The relative predominance of low-frequency (delta,

theta and low alpha) activity detected at the beginning of treatment had

normalized by the end of treatment. In our study,5 no statistically significant

changes were noted regarding mean amplitudes of EEG rhythms.

However, the theta/SMR ratio showed a significant decrease by the fourth

week compared to baseline in the neurofeedback group. The detected

decrease in theta/SMR ratio is important and may show a concrete finding

concerning neurofeedback treatment. Thus, SMR neurofeedback

treatment may have a facilitator effect on thalamic inhibitory mechanisms

by arranging brain activity via increasing the slower waves and decreasing

the faster waves of the brain. Further well-organized controlled studies

with higher patient numbers are needed to verify this finding.

 

Pain is regulated by interactions between ascending and descending

pathways, and brain mechanisms are increasingly being accepted as having

a major role in the modulation of pain. Understanding these mechanisms

is crucial if fully effective treatments for clinical pain conditions are to be

developed.36

 

The etiologic factors of chronic pain syndromes and the relationship

between chronic pain and central nervous system mechanisms need to

be clarified in future investigations. Because the EEG is an important

physiological tool, studies that use more quantitative EEG evaluations

with respect to pain would be very helpful. On the other hand, it is obvious

that scientific data are insufficient for neurofeedback interventions

regarding pain modulation. Many well-designed controlled prospective

studies with larger patient populations must be carried out in order to be

certain about the role of neurofeedback interventions on pain management

and its therapeutic mechanisms.

 

REFERENCES

 

1.

Bennett RM. Emerging concepts in the neurobiology of chronic pain: evidence of

abnormal sensory processing in fibromyalgia. Mayo Clin Proc. 1999;74(4):385–398.

2.

Turk DC. Clinical effectiveness and cost-effectiveness of treatments for patients with

chronic pain. Clin J Pain. 2002;18(6):355–365.

3.

Fregni F, Freedman S, Pascual-Leone A. Recent advances in the treatment of chronic

pain with non-invasive brain stimulation techniques. Lancet Neurol. 2007;6:188–191.

4.

Green AL, Wang S, Bittar RG, et al. Deep brain stimulation for pain relief: a metaanalysis.

J Clin Neurosci. 2005;12:515–519.

5.

Kayiran S, Dursun E, Dursun N, Ermutlu N, Karamürsel S. Neurofeedback intervention

in fibromyalgia syndrome; a randomized, controlled, rater blind clinical trial. Appl

Psychophysiol Biofeedback. 2010;35(4):293–302.

6.

Dursun E. Biofeedback. In: Stone JH, Blouin M, eds. International Encyclopedia of

Rehabilitation. Available online: <http://cirrie.buffalo.edu/encyclopedia/article.php?

id=23&language=en>.

7.

Intiso D, Santilli V, Grasso MG, Rossi R, Caruso I. Rehabilitation of walking

with electromyographic biofeedback in foot-drop after stroke. Stroke.

1994;25(6):1189–1192.

8.

Wissel J, Ebersbach G, Gutjahr L, Dahlke F. Treating chronic hemiparesis with modified

biofeedback. Arch Phys Med Rehabil. 1989;70(8):612–617.

9.

Dursun E, Dursun N, Alican D. Effects of biofeedback treatment on gait in children

with cerebral palsy. Disabil Rehabil. 2004;26(2):116–120.

10.

Petrofsky JS. The use of electromyogram biofeedback to reduce Trendelenburg gait.

Eur J Appl Physiol. 2001;85(5):491–495.

11.

Nash J, Neilson PD, O’Dwyer NJ. Reducing spasticity to control muscle contracture

of children with cerebral palsy. Dev Med Child Neurol. 1989;31(4):471–480.

12.

Middaugh SJ, Whitehead WE, Burgio KL, Engel BT. Biofeedback in treatment of urinary

incontinence in stroke patients. Biofeedback Self Regul. 1989;14(1):3–19.

13.

Chiarioni G, Salandini L, Whitehead WE. Biofeedback benefits only patients with

outlet dysfunction, not patients with isolated slow transit constipation. Gastroenterology.

2005;129(1):86–97.

14.

Ho YH, Tan M. Biofeedback therapy for bowel dysfunction following low anterior

resection. Ann Acad Med Singapore. 1997;26(3):299–302.

15.

Draizar A. Clinical EMG feedback in motor speech disorders. Arch Phys Med Rehabil.

1984;65(8):481–484.

16.

Denk DM, Kaider A.Videoendoscopic biofeedback: a simple method to improve the

efficacy of swallowing rehabilitation of patients after head and neck surgery. ORL J

Otorhinolaryngol Relat Spec. 1997;59(2):100–105.

17.

Crider A, Glaros AG, Gevirtz RN. Efficacy of biofeedback-based treatments for temporomandibular

disorders. Appl Psychophysiol Biofeedback. 2005;30(4):333–345.

18.

Stokes DA, Lappin MS. Neurofeedback and biofeedback with 37 migraineurs: a clinical

outcome study. Behav Brain Funct. 2010;6:9.

19.

Neblett R, Mayer TG, Brede E, Gatchel RJ. Correcting abnormal flexion-relaxation

in chronic lumbar pain: responsiveness to a new biofeedback training protocol. Clin J

Pain. 2010;26(5):403–409.

20.

Dursun N, Dursun E, Kili Z. Electromyographic biofeedback-controlled exercise

versus conservative care for patellofemoral pain syndrome. Arch Phys Med Rehabil.

2001;82(12):1692–1695.

21.

Yip SL, Ng GY. Biofeedback supplementation to physiotherapy exercise programme

for rehabilitation of patellofemoral pain syndrome: a randomized controlled pilot

study. Clin Rehabil. 2006;20(12):1050–1057.

22.

Babu AS, Mathew E, Danda D, Prakash H. Management of patients with fibromyalgia

using biofeedback: a randomized control trial. Indian J Med Sci. 2007;61(8):455–461.

23.

Kropp P, Siniatchkin M, Gerber WD. On the pathophysiology of migraine–links

for ‘empirically based treatment’ with neurofeedback. Appl Psychophysiol Biofeedback.

2002;27(3):203–213.

24.

Siniatchkin M, Hierundar A, Kropp P, Kuhnert R, Gerber WD, Stephani U.

Selfregulation of slow cortical potentials in children with migraine: an exploratory

study. Appl Psychophysiol Biofeedback. 2000;25(1):13–32.

25.

Saxena VS, Nadkarni VV. Nonpharmacological treatment of epilepsy. Ann Indian Acad

Neurol. 2011;14(3):148–152.

26.

Lofthouse N, Arnold LE, Hurt E. Current status of neurofeedback for attention-deficit/

hyperactivity disorder. Curr Psychiatry Rep. 2012;14(5):536–542.

27.

Monastra VJ. Quantitative electroencephalography and attention-deficit/hyperactivity

disorder: Implications for clinical practice. Curr Psychiatr Rep. 2008;10:432–438.

28.

Monastra VJ, Monastra DM, George S. The effects of stimulant therapy, EEG biofeedback,

and parenting style on the primary symptoms of attention-deficit/hyperactivity

disorder. Appl Psychophysiol Biofeedback. 2002;27(4):231–249.

29.

Sokhadze TM, Cannon RL, Trudeau DL. EEG biofeedback as a treatment for substance

use disorders: review, rating of efficacy, and recommendations for further

research. Appl Psychophysiol Biofeedback. 2008;33(1):1–28.

30.

Hammer BU, Colbert AP, Brown KA, Ilioi EC. Neurofeedback for insomnia: a pilot

study of Z-score SMR and individualized protocols. Appl Psychophysiol Biofeedback.

2011;36(4):251–264.

31.

Hammond DC. Treatment of chronic fatigue with neurofeedback and self-hypnosis.

NeuroRehabilitation. 2001;16(4):295–300.

32.

Sterman MB. Physiological origins and functional correlates of EEG rhythmic activities:

implications for self-regulation. Biofeedback Self Regul. 1996;21:3–33.

33.

Sterman MB, Howe RD, MacDonald LR. Facilitation of spindle-burst sleep

by conditioning of electroencephalographic activity while awake. Science.

1970;167:1146–1148.

34.

Sterman MB, Shouse MN. Quantitative analysis of training, sleep EEG, and clinical

response to EEG operant conditioning in epileptics. Electroencephalogr Clin

Neurophysiol. 1980;49:558–576.

35.

Melzack R,Wall PD. Pain mechanisms: a new theory. Science. 2005;50:971–979.

36.

Apkarian AV, Bushnell MC, Treede RD, Zubieta JK. Human brain mechanisms of

pain perception and regulation in health and disease. Eur J Pain. 2005;9(4):463–484.

37.

Dubner R, Ruda MA. Activity-dependent neuronal plasticity following tissue injury

and inflammation. Trends Neurosci. 1992;15(3):96–103.

38.

Pillemer SR, Bradley LA, Crofford LJ, Moldofsky H, Chrousos GP. The neuroscience

and endocrinology of fibromyalgia. Arthritis Rheum. 1997;40(11):1928–1939.

39.

Williams DA, Clauw DJ. Understanding fibromyalgia: lessons from the broader pain

research community. J Pain. 2009;10(8):777–791.

40.

Staud R, Price DD, Robinson ME, Mauderli AP, Vierck CJ. Maintenance of windup

of second pain requires less frequent stimulation in fibromyalgia patients compared to

normal controls. Pain. 2004;110:689–696.

41.

Leffler AS, Hansson P, Kosek E. Somatosensory perception in a remote pain-free area

and function of diffuse noxious inhibitory controls (DNIC) in patients suffering from

long-term trapezius myalgia. Eur J Pain. 2002;6:149–159.

42.

Howe RC, Sterman MB. Cortical-subcortical EEG correlates of suppressed motor

behavior during sleep and waking in the cat. Electroencephalogr Clin Neurophysiol.

1972;32(6):681–695.

43.

Lautenbacher S, Rollman GB. Possible deficiencies of pain modulation in fibromyalgia.

Clin J Pain. 1997;13(3):189–196.

44.

Staud R,Vierck CJ, Cannon RL, Mauderli AP, Price DD. Abnormal sensitization and

temporal summation of second pain (wind-up) in patients with fibromyalgia syndrome.

Pain. 2001;91(1–2):165–175.

45.

Kwiatek R, Barnden L, Tedman R, et al. Regional cerebral blood flow in fibromyalgia:

single-photon-emission computed tomography evidence of reduction in the

pontine tegmentum and thalami. Arthritis Rheum. 2000;43(12):2823–2833.

46.

Mountz JM, Bradley LA, Modell JG, et al. Fibromyalgia in women. Abnormalities of

regional cerebral blood flow in the thalamus and the caudate nucleus are associated

with low pain threshold levels. Arthritis Rheum. 1995;38(7):926–938.

47.

Guedj E, Cammilleri S, Niboyet J, et al. Clinical correlate of brain SPECT perfusion

abnormalities in fibromyalgia. J Nucl Med. 2008;49(11):1798–1803.

48.

Zhang XL, Cohen HL, Porjesz B, Begleiter H. Mismatch negativity in subjects at

high risk for alcoholism. Alcohol Clin Exp Res. 2001;25(3):330–337.

49.

Ozdag MF, Yorbik O, Ulas UH, Hamamcioglu K, Vural O. Effect of methylphenidate

on auditory event related potential in boys with attention deficit hyperactivity disorder.

Int J Pediatr Otorhinolaryngol. 2004;68(10):1267–1272.

50.

Pokryszko-Dragan A, Slotwin´ski K, Podemski R. Modality-specific changes in

P300 parameters in patients with dementia of the Alzheimer type. Med Sci Monit.

2003;9(4):130–134.

51.

Van der Stelt O, Geesken R, Gunning WB, Snel J, Kok A. P3 scalp topography to target

and novel visual stimuli in children of alcoholics. Alcohol. 1998;15(2):119–136.

52.

Hada M, Porjesz B, Begleiter H, Polich J. Auditory P3a assessment of male alcoholics.

Biol Psychiatry. 2000;48(4):276–286.

53.

Alanog^ lu E, Ulas¸ UH, Ozdag^ F, Odabas¸i Z, Cakçi A, Vural O. Auditory event-related

brain potentials in fibromyalgia syndrome. Rheumatol Int. 2005;25(5):345–349.

54.

Ozgocmen S, Yoldas T, Kamanli A, Yildizhan H, Yigiter R, Ardicoglu O. Auditory

P300 event related potentials and serotonin reuptake inhibitor treatment in patients

with fibromyalgia. Ann Rheum Dis. 2003;62(6):551–555.

55.

Egner T, Gruzelier JH. Learned self-regulation of EEG frequency components

affects attention and event-related brain potentials in humans. Neuroreport.

2001;12(18):4155–4159.

56.

Jensen MP, Hakimian S, Sherlin LH, Fregni F. New insights into neuromodulatory

approaches for the treatment of pain. J Pain. 2008;9(3):193–199.

57.

Ibric VL, Dragomirescu LG. Neurofeedback in pain management. In: Budzynski

T, Budzynski H, Evans J, Abarbanel A, eds. Introduction to Quantitative EEG and

Neurofeedback–Advanced Theory and Applications. New York, NY: Elsevier; 2008:417–451.

58.

Yunus MB. Role of central sensitization in symptoms beyond muscle pain, and

the evaluation of a patient with widespread pain. Best Pract Res Clin Rheumatol.

2007;21(3):481–497.

59.

Raichle ME, MacLeod AM, Snyder AZ, Powers WJ, Gusnard DA, Shulman GL. A

default mode of brain function. Proc Natl Acad Sci USA. 2001;98(2):676–682.

60.

Baliki MN, Geha PY, Apkarian AV, Chialvo DR. Beyond feeling: chronic pain

hurts the brain, disrupting the default-mode network dynamics. J Neurosci.

2008;28(6):1398–1403.

61.

Caro XJ, Winter EF. EEG biofeedback treatment improves certain attention and

somatic symptoms in fibromyalgia: a pilot study. Appl Psychophysiol Biofeedback.

2011;36:193–200.

62.

Mueller HH, Donaldson CC, Nelson DV, Layman M. Treatment of fibromyalgia

incorporating EEG-driven stimulation: a clinical outcomes study. J Clin Psychol.

2001;57(7):933–952.

63.

Lelic D, Olesen AE, Brock C, Staahl C, Drewes AM. Advanced pharmaco-EEG

reveals morphine induced changes in the brain’s pain network. J Clin Neurophysiol.

2012;29(3):219–225.

64.

Boord P, Siddall PJ, Tran Y, Herbert D, Middleton J, Craig A. Electroencephalographic

slowing and reduced reactivity in neuropathic pain following spinal cord injury. Spinal

Cord. 2008;46(2):118–123.

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