ArticlePDF AvailableLiterature Review

Neuromodulation of Cancer Pain

Abstract and Figures

Managing cancer-related chronic pain is challenging to health care professionals as well as cancer patients and survivors. The management of cancer-related pain has largely consisted of pharmacological treatments, which has caused researchers to focus on neurotransmitter activity as a mediator of patients' perception of pain rather than the electrical activity during neurobiological processes of cancer-related pain. Consequently, brain-based pain treatment has focused mainly on neurotransmitters and not electrical neuromodulation. Neuroimaging research has revealed that brain activity is associated with patients' perceptions of symptoms across various diagnoses. The brain modulates internally generated neural activity and adjusts perceptions according to sensory input from the peripheral nervous system. Cancer-related pain may result not only from changes in the peripheral nervous system but also from changes in cortical activity over time. Thus, cortical reorganization by way of the brain's natural, plastic ability (neuroplasticity) may be used to manage pain symptoms. Physical and psychological distress could be modulated by giving patients tools to regulate neural activity in symptom-specific regions of interest. Initial research in nononcology populations suggests that encouraging neuroplasticity through a learning paradigm can be a useful technique to help treat chronic pain. Here we review evidence that indicates a measurable link between brain activity and patient-reported psychological and physical distress. We also summarize findings regarding both the neuroelectrical and neuroanatomical experience of symptoms, review research examining the mechanisms of the brain's ability to modify its own activity, and propose a brain-computer interface as a learning paradigm to augment neuroplasticity for pain management.
Content may be subject to copyright.
Integrative Cancer Therapies
2014, Vol. 13(1) 30 –37
© The Author(s) 2013
Reprints and permission:
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DOI: 10.1177/1534735413477193
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Technological advances have yielded insight into the
mechanisms of brain function and consequently provide
new ways of understanding treatment options for patients.
In this review, we offer the reader an understanding of the
possible relationship between brain activity and pain in
cancer patients that may alter current treatment paradigms
as well as provide background for further research.
Cancer Pain
Cancer pain, which can enable the progression of meta-
static disease, may be an important predictor of survival;
consequently, adequate pain relief may not only improve
quality of life but also extend life itself.1 The management
of cancer-related chronic pain is an ongoing challenge to
health care professionals and patients. Cancer pain man-
agement has emotional, social, and physical implications
and may be complicated by the multiple factors associated
with the disease process. In cancer patients, pain may be
caused by tumor progression, tumor invasion, surgeries,
systemic treatments, cancer-related infections, inactivity,
and generalized fatigue2 and may involve inflammatory,
neuropathic, ischemic, and compression mechanisms at
multiple sites. Pharmacological treatments for cancer-
related pain often cause myriad side effects, including
altered awareness and emotional states, and may contrib-
ute to a patient’s sense of loss of control over their body
and illness. Patients may also develop tolerance of, and
become addicted to, such treatments.
People often experience pain as a threat to their present
bodily state, future well-being, and life in general.3 Acute
pain is adaptive and may orient attentional resources toward
the stimuli necessary to elicit an appropriate behavioral and/
477193ICTXXX10.1177/153473541347719
3Integrative Cancer TherapiesPrinsloo et al
2013© The Author(s) 2010
Reprints and permission: http://www.
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1The University of Texas MD Anderson Cancer Center, Houston, TX,
USA
2Mount Mercy University, Cedar Rapids, IA, USA
Corresponding Author:
Sarah Prinsloo, Department of General Oncology, The University of
Texas MD Anderson Cancer Center, Unit 410, PO Box 301439, Houston,
TX 77230, USA.
Email: SPrinsloo@MDAnderson.org
Neuromodulation of Cancer Pain
Sarah Prinsloo, PhD1, Stephanie Gabel, MA1, Randall Lyle, PhD2,
and Lorenzo Cohen, PhD1
Abstract
Managing cancer-related chronic pain is challenging to health care professionals as well as cancer patients and survivors.
The management of cancer-related pain has largely consisted of pharmacological treatments, which has caused researchers
to focus on neurotransmitter activity as a mediator of patients’ perception of pain rather than the electrical activity
during neurobiological processes of cancer-related pain. Consequently, brain-based pain treatment has focused mainly on
neurotransmitters and not electrical neuromodulation. Neuroimaging research has revealed that brain activity is associated
with patients’ perceptions of symptoms across various diagnoses. The brain modulates internally generated neural activity
and adjusts perceptions according to sensory input from the peripheral nervous system. Cancer-related pain may result
not only from changes in the peripheral nervous system but also from changes in cortical activity over time. Thus, cortical
reorganization by way of the brain’s natural, plastic ability (neuroplasticity) may be used to manage pain symptoms. Physical
and psychological distress could be modulated by giving patients tools to regulate neural activity in symptom-specific
regions of interest. Initial research in nononcology populations suggests that encouraging neuroplasticity through a learning
paradigm can be a useful technique to help treat chronic pain. Here we review evidence that indicates a measurable link
between brain activity and patient-reported psychological and physical distress. We also summarize findings regarding both
the neuroelectrical and neuroanatomical experience of symptoms, review research examining the mechanisms of the brain’s
ability to modify its own activity, and propose a brain-computer interface as a learning paradigm to augment neuroplasticity
for pain management.
Keywords
cancer pain, brain-computer interface, cancer survivorship, EEG, neurofeedback, neuromodulation
Article
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Prinsloo et al 31
or physiological response4 and produce temporary analge-
sia.5 Chronic pain may have catastrophic consequences: at a
minimum, it can diminish quality of life; in the worst case, it
can lead to suicide. In patients in whom pain cannot be elim-
inated, treatment success depends largely on the patient’s
ability to adapt to symptoms and self-manage the pain.
Consequently, some researchers have focused their efforts
on identifying the factors that promote well-being and func-
tioning despite the presence of chronic pain.6,7 The experi-
ence of pain is not only emotional and physical but the two
are also neurally linked8,9; thus, treating the physical aspect
of pain may improve the emotional, and treating the emo-
tional aspects of pain may improve the physical.
Biopsychosocial Model of Cancer Pain
Biopsychosocial models of chronic pain predict pain and
subsequent behavioral responses better than solely biologi-
cal models do.10 For example, the high levels of depression
and anxiety related to a cancer diagnosis, cancer pain, or
treatment side effects can not only increase emotional suf-
fering but also contribute to physiological changes such as
heightened central nervous system activity, vasoconstric-
tion, and muscle spasm. Conversely, the physical pain from
cancer and its treatments can cause feelings of anxiety,
depression, fear, anger, helplessness, and hopelessness.10
Cancer, from its diagnosis and treatment through the sur-
vivorship phase, is described as a chronic stressor because
it poses a ubiquitous threat to life. Even before a cancer
diagnosis is made, cancer testing and screening can pro-
mote fear, anxiety, and other psychological distress.11 In a
review of 19 studies of cancer pain and psychosocial fac-
tors, Zaza and Baine12 found that 14 studies reported a sig-
nificant association between psychological distress and
pain. Several other studies have emphasized the role fear
plays in the cancer experience. Ashing-Giwa et al,13 in a
study of 1377 cancer survivors of various ethnic back-
grounds, found that “fear of finding cancer” was the most
frequently cited explanation for delays in diagnostic testing.
Klikovac and Djurdjevic14 found that 85% of participants
reported fear, 65% reported anger and anxiety, and 90%
reported nervousness and irritability as psychological
aspects of a cancer diagnosis. Lemay et al,15 after control-
ling for depression and physical symptoms, found that fear
of pain predicted limitations in function in cancer patients
but not patients with chronic pain who did not have can-
cer.15 Although a conventional model of pain causation pre-
dicts that pain precedes distress, studies in humans and
animals have revealed that stress can increase nociception,
and experiencing distress prior to pain exposure predicts
worse pain outcomes.16-18 This is consistent with the notion
that similar neural structures are involved in perceiving
emotional and nociceptive pain, and one type of pain sensi-
tizes the other within similar neural networks.
Brain Activity and Pain
Many factors influence the way in which pain at the periph-
ery is perceived in the central nervous system. Contrary to
the predictions of traditional cause-and-effect models, pain
perception often is not linearly related to the activity of the
brain.19-21 From a neurobiological perspective, pain per-
ceived in regions of the body has direct spinal inputs to the
lower brainstem and limbic (emotional processing) struc-
tures. Spinothalamic pathways are involved in the regions
of the brain that process body state (insular cortex), atten-
tion, and response priorities (anterior cingulate cortex
[ACC]). The ACC receives a major serial input from a
somatosensory-limbic pathway that contributes to varying
degrees of cognitive evaluation of pain affect.3 Because of
its integrated network connections, the ACC is involved in
various sensory, emotional, and cognitive functions, includ-
ing pain. Neurons in the ACC interconnect with neurons in
the amygdala, a structure critical to experiencing fear and
anxiety, emotional states that increase the synaptic strength
in the lateral amygdala.22 In addition to its association with
changes in synaptic strength, increased amygdala activity
has been associated with decreased insular and ACC activ-
ity, signifying a decreased ability of the amygdala to regu-
late pain perception owing to an interruption in a common
network of regulation. In pain paradigms, brain activation
occurs along the somatosensory cortex, insula, amygdala,
and finally ACC, where increased insular and ACC activity
may indicate an early stage in the transition from acute to
chronic pain.23,24
Chronic pain is a persistent stressor that indirectly affects
the feedback loop of the hypothalamic-pituitary-adrenal
(HPA) axis by involving brain regions in the limbic sys-
tem.25 The hippocampus inhibits, whereas the amygdala
excites, the neurons in the HPA axis, thereby controlling the
activity of the axis. Prolonged exposure to a chronic stressor
such as pain may damage hippocampal neurons and inhibit
neurogenesis.26 The HPA axis also activates in response to
psychological stressors such as depression and anxiety.25
To summarize, attentional networks and networks under-
lying pain processing, emotional processing, learning, and
memory have overlapping areas of cerebral activity; there-
fore, brain activity across many symptoms and behaviors
relies on a network model of operation. This suggests that a
network approach to the evaluation and treatment of chronic
pain will elicit the best outcomes.
Electrophysiological Measurement
of Brain Activity
Electroencephalography (EEG) is a measurement of elec-
trophysiological activity in the cortex, which comprises the
upper 6 neuronal layers of the brain. The summation of
synchronous neural activity oscillates at many frequencies
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32 Integrative Cancer Therapies 13(1)
and is classified according to the range of the frequencies.
These frequency ranges are referred to as delta (1-3 Hz),
theta (4-7 Hz), alpha (8-11 Hz), beta (12-32 Hz), and
gamma (32 Hz and above) bandwidths. Brainwave frequen-
cies change with brain states. For example, delta may be
predominant during certain stages of sleep; theta is corre-
lated with drowsy states, whereas alpha activity is associ-
ated with a relaxed state. Beta activity is associated with an
engaged state as reflected during attention tasks and cogni-
tive processing, and gamma is associated with cognitive
processing, working memory, and intelligence.27-29 This
measured electrical activity normally fluctuates according
to stimuli from the environment, though the overall EEG is
stable over time.30
EEG activity correlates with neuronal activity in patients
who experience acute or chronic pain; it has been hypothe-
sized that the activity measured in various EEG bandwidths
is representative of the underlying mechanisms that trigger
the emotional experience and physical perception of pain.
Therefore, pain may be thought of as a mental perception
that physiologically changes the brain’s resting state or orga-
nized baseline activity by modifying the functional frequen-
cies of groups of pyramidal cells throughout various regions
of the cortex. In a chronic pain state, cortical restructuring
may occur, making sensory input neither sufficient nor nec-
essary for the experience of pain, suggesting that the brain
plays a complex role in the experience of chronic pain.31
Pain without a known sensory input includes tinnitus,
phantom limb pain, and neuropathy. Therefore, quantifying
EEG findings to explore the potential signatures the brain
exhibits when symptomatic is an important step to under-
standing how the brain works under pathological condi-
tions. Researchers could use brain-mapping techniques
such as quantitative EEG to delineate regions of interest and
site-specific electrical activity to determine an individual-
ized, mechanistic approach to treating cancer pain that tar-
gets both psychological and physical distress. Such an
approach has already been used in nononcology popula-
tions. For example, in a summary of 8 EEG studies, Jensen
et al32 found that although intense and painful stimulation
(ie, acute pain) increases all EEG frequencies, the relative
increase of power within beta frequencies is greater than
that of other bandwidths, whereas the relative power of
alpha frequencies (8-12 Hz) is lower than that of other
bandwidths. Therefore, relief from acute pain may increase
relative alpha activity and decrease relative beta activity.33
Conversely, Sarnthein et al34 found that theta band (7-9
Hz) EEG activity in all electrodes in patients with chronic
neurogenic pain was higher than that in a healthy control
group, suggesting that chronic pain is associated with
heightened activity in lower-frequency bands. This effect
was seen in patients who were taking centrally acting medi-
cations as well as in those who were not. Like patients with
acute pain, patients with chronic pain may demonstrate
excessive amplitudes of beta activity32; however, additional
research is needed to determine what, if any, differences
exist between patients who show increases in fast-wave
EEG activity and those who show increases in slow-wave
EEG activity.
To summarize, EEG studies of pain report varied fre-
quency band activity across brain regions. The reason for
varying outcomes often depends on the chronicity of symp-
toms; however, influences such as genetics, environment,
and experience also contribute to individual brain activity.
Additionally, in the oncology population, patients may have
specific neurophysiological changes as a result of chemo-
therapy and other cancer treatments.
Neuroplasticity, Brain-Computer
Interface, and Learned Control of
Cortical Activity
The nervous system’s fundamental feature is its neuroplas-
ticity, that is, its ability to adapt to changing environmental
conditions.35 As neuronal activity reflects environmental
stimuli, the activity-dependent neuronal plasticity gradually
tunes neural networks to optimally code for environmental
information. Each time a person accesses the state-depen-
dent memory, learning, and behavior processes that encode
a problem, he or she has an opportunity to reassociate and
reorganize that problem in a manner that resolves the prob-
lem.36 Control over the endogenous pain modulatory sys-
tem could enable a unique mechanism for control over
pain.37 Because the brain experiences pain based in part on
cortical restructuring, pain may also be alleviated by simi-
lar cortical reorganization via a mechanism utilizing repeti-
tion, learning, and memory.
One technique that can help in cortical reorganization is
neurofeedback. Neurofeedback enables patterns of neuro-
nal activity to change via a brain-computer interface in
which a patient studies a visual representation of his or her
own brain activity. Auditory and visual modalities are used
to reward the patient when the presence of the desired
brainwave is detected by the EEG in specific brain regions.
Over time and after a number of sessions, the brain becomes
flexible enough to call on alternative pathways that may
make pain and its concomitant emotional complexities
more manageable. At a neuronal level, this reorganization
strengthens or changes existing pathways to accommodate
new learning and may facilitate coherent neuronal oscilla-
tions that correlate with perception and affect systemic syn-
aptic plasticity. Brain-computer interface learning
modalities such as neurofeedback can be used to modify
patterns of cortical activation in the EEG and are under vol-
untary control as demonstrated in human and animal
research.38-40 In neurofeedback, electrical physiology is
paired with knowledge of neuroanatomy to design
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Prinsloo et al 33
treatment protocols. Neurofeedback facilitates endogenous
change in which plastic changes in the brain can be shown
after 1 session,41 although there is a temporal correlation
with training and long-term change. In terms of neurofeed-
back, neuroplasticity may equal persistent change in neuro-
transmission. To illustrate changes in a nonpain patient,
Figures 1 and 2 show brain maps before training and then
after 50 sessions of EEG-based neurofeedback.
Neurofeedback to elicit electroencephalographic changes
dates back to the 1960s when Sterman’s original research
showed that animals could be taught to modify brainwave
activity.42 Interest grew in the use of neurofeedback as a
Figure 1. A. Baseline cortical activity: neurofeedback protocols may be designed from quantitative EEG maps. For this patient, alpha
(7.5-12 Hz) in the posterior portion of the head was inhibited, whereas beta (13-21 Hz) was also inhibited in the frontal lobes. B.
Cortical activity after neurofeedback showing a change in alpha and beta activity. The remapping was done after approximately 12
weeks of training.
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34 Integrative Cancer Therapies 13(1)
treatment modality after, for example, it was demonstrated
that operant training the sensory motor rhythm over the
motor cortex served as a protective mechanism against epi-
leptic seizures in animals.43 Neurofeedback has since been
used to address a variety of psychological and physical con-
ditions, including pain, addiction, attention-deficit hyperac-
tivity disorder, and traumatic brain injuries.44-47 It has also
been used to enhance academic and athletic performance.48-50
Although neurofeedback has been used in many other set-
tings, it is a novel approach to treating cancer-related pain.
Few studies have investigated the use of neurofeedback
to alter the perception of pain. However, as early as the
1970s, Gannon and Sternbach51 found that increasing alpha
activity (8-12 Hz) in a headache patient decreased the inten-
sity and duration of the headaches.51 Studies examining the
effects of neurofeedback on chronic pain conditions such as
fibromyalgia, trigeminal neuralgia, and complex regional
pain syndrome type 1 reported reductions in pain intensity,
fatigue, depression, and anxiety.52-55 Ibric et al56 found that
of 74 patients who had been unsuccessfully treated for pain
from chronic disease, injury, surgery, or other sources, 68
(92%) reported a clinically significant improvement in their
pain following at least 19 sessions of neurofeedback. One
patient in the study who had been diagnosed with leukemia
and colon cancer reported a 50% reduction in pain, better
control of anxiety and depression, better sleep, and
decreased use of medications for 2.5 years following her
last neurofeedback session. Other studies report neurofeed-
back eliciting similar decreases in pain symptoms. Caro and
Winter52 found that neurofeedback treatment significantly
decreased physician-assessed tenderness, pain, attention,
and fatigue in 15 fibromyalgia patients. In a randomized
controlled trial of neurofeedback versus escitalopram for
the treatment of fibromyalgia symptoms, both groups
showed improvement in all outcome measures; however,
therapeutic efficacy for those receiving neurofeedback
Figure 2. A. Low-resolution brain electromagnetic tomography (LORETA) imaging at baseline for the patient in Figure 1. B. LORETA
imaging after neurofeedback showing a change in activity of targeted frequency bands.
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Prinsloo et al 35
reached a maximum effect at week 4 of treatment compared
with the control group, for whom it did not reach maximum
effect until week 8.53 A retrospective analysis of 18 patients
who had complex regional pain syndrome 1 and underwent
neurofeedback training as a part of a multidisciplinary pain
treatment program revealed a statistically and clinically sig-
nificant decrease in pain intensity at the primary pain site
posttraining, statistically significant improvements in pain
intensity at 2 additional sites, and improvements in muscle
spasm, muscle tension, perceived deep ache, and overall
well-being.57 Although previous research has demonstrated
that neurofeedback improves various types of pain in vary-
ing patient populations, most of these studies were case
reports or small, single-arm trials.53
Cortical reorganization is a potential treatment for psy-
chological pain, specifically depression. Rosenfeld58 inves-
tigated whether the EEG patterns of patients who were
treated twice weekly with both neurofeedback and psycho-
therapy (50% time dedicated to each modality) could be
modified and, if so, whether those patterns could cause a
change in mood. The results of the study indicated that
asymmetry between left and right hemispheres was indeed
modifiable in 9 of the 13 “normal” participants, and because
they were subject to the influence of phasic psychological
states under a participant’s self-control, sources of variance
in frontal cortical activation asymmetry were also associ-
ated with state and trait characteristics. Prior to this study,
EEG patterns in patients with depression were thought to be
“trait” patterns and thus potentially less apt to be modified
using neurofeedback. In terms of pain management, parietal
and sensory motor areas integrate somatosensory input with
learning and memory and are at the origin of a pathway that
converges on the same cortical and subcortical limbic struc-
tures (the ACC, insular cortex, and amygdala) that receive
direct input from spinal pain pathways.59 This example of
overlapping physical and emotional neural routes may ana-
tomically model the networks responsible for pain reduc-
tion via neurofeedback.
The field of neurofeedback is expanding, with novel
methods to facilitate and augment neuroplasticity as a
mechanism of brain change. One such technique is
EEG low-resolution brain electromagnetic tomography
(LORETA). LORETA enables researchers to localize the
electrical activity in the brain based on scalp potentials from
a multiple-channel EEG and determine the relative activity
of regions in the brain using surface electrodes.57 LORETA
neurofeedback utilizes this localization in real-time training
of specific regions of interest. Although few studies have
investigated the use of LORETA neurofeedback, it has been
shown to be an effective means of modifying the brain
activity implicated in pain processing and perception.
Cannon et al60 found that healthy participants could use
LORETA neurofeedback to increase low beta activity (spe-
cifically 14-18 Hz) in the cognitive division of the anterior
cingulate gyrus. The researchers also found that LORETA
neurofeedback of the anterior cingulate gyrus and right and
left dorsolateral prefrontal cortices, which are implicated in
the processing of both emotional and physical pain, could
be used to enhance functioning as measured by the Working
Memory Index and Processing Speed Index of the Wechsler
Adult Intelligence Scale in a network of related brain
regions. These findings suggest that LORETA feedback is a
neural-specific form of neurofeedback. Exploring the dif-
ferences between LORETA and conventional neurofeed-
back is an area of current investigation; early studies suggest
that one advantage LORETA has over conventional neuro-
feedback is that it requires less training time before differ-
ences in patient-reported measures are noted. Because
LORETA has demonstrated efficacy in training brain
regions identical to those implicated in pain processing, the
modality’s utility in treating pain is encouraging.
In addition to EEG biofeedback approaches, real-time
functional MRI (rtfMRI) training of neuronal structures
may be effective in modulating pain perception. In one
study, investigators used rtfMRI to guide the training of the
ACC; participants were able not only to change the percep-
tion of pain when a noxious stimulus was applied (ie, acute
pain) but also reported decreases in the level of chronic pain
after training. These studies of LORETA and rtfMRI,
though preliminary, provide examples of self-regulation of
pain through direct neuromodulation.37
The next step toward utilization of neuromodulatory
approaches for symptom management is the identification
of brain regions specific to types of cancer pain. For exam-
ple, neuropathic pain may have neurophysiological markers
different from postsurgical pain. If characteristic EEG pat-
terns are found in cancer pain, these patterns may be cor-
rected by common neurofeedback protocols. For example,
it is possible that the central nervous system is somehow
“changed” as a result of cancer treatments such as chemo-
therapy and that these changes may be predictable. However,
because of the dynamic properties of the brain and unique
responses to treatment, it is likely that different personal-
ized protocols resulting from quantitative EEG analysis will
be the most helpful. Because pain is a unique perceptive
experience for each cancer patient, even though similarities
across patients may exist in regional brain activity, the chal-
lenge will be to quantify these unique perceptive experi-
ences, so that replicability of study results is possible.
Summary
Pain is an intricate interaction of psychophysiological com-
ponents that involve the peripheral and central nervous
systems. Neurophysiological studies of the cerebral effects
of biopsychosocial factors such as fear and stress have
revealed similarities in the neural networks involved in the
emotional and physical experiences of pain. In patients
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36 Integrative Cancer Therapies 13(1)
with cancer pain, these factors may be present throughout
diagnosis, treatment, recovery, and survivorship. Neur ofee dbac k
is a potentially effective and economical tool with which
to manage cancer pain through modulating neural path-
ways. By harnessing quantified electrical neurophysiologi-
cal patterns and the brain’s neuroplastic ability to learn and
change, researchers could use neurofeedback to affect
many factors—especially those related to mental and
physical pain—that are particularly problematic for oncol-
ogy patients.
Declaration of Conflicting Interests
The authors declared no potential conflicts of interest with respect
to the research, authorship, and/or publication of this article.
Funding
The authors disclosed receipt of the following financial support
for the research, authorship, and/or publication of this article: This
work was supported in part by the National Institutes of Health
through MD Anderson’s Cancer Center Support Grant CA016672,
the American Cancer Society (PF-11-169-01-PCSM), and The
Hille Foundation.
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... The disruption in thalamocortical rhythms (thalamocortical dysrhythmia) can be detected by surface electroencephalography (EEG) [15,16]. EEG signals can be assessed as different frequency bands, such as theta (4-7 Hz), alpha (8)(9)(10)(11)(12), and beta (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). Thalamocortical dysrhythmia is characterized by a common resting-state EEG pattern of increased theta and low-frequency alpha rhythms [17,18]. ...
... Three single-arm trials have demonstrated that BCI-N interventions can reduce SCI neuropathic pain [22][23][24]. These studies used a BCI-N protocol, which consisted of suppressing theta and low-frequency alpha rhythms (4)(5)(6)(7)(8), and high-frequency beta rhythms (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), along with enhancing high-frequency alpha rhythms (9)(10)(11)(12). Although these preliminary studies suggested that BCI-N can be effective in reducing SCI neuropathic pain, further studies are needed to provide more definitive evidence regarding the effectiveness of BCI-N interventions for people with neuropathic pain following SCI. ...
... Current BCI-N interventions for both SCI neuropathic pain [20,22,24] and chronic pain [25][26][27] have mostly relied on a single mode of virtual interaction, such as increasing or decreasing the height of a bar presented on a computer screen. However, preliminary evidence suggests that greater pain relief may be achieved from interactive, goal-directed engagement with a gaming environment, in comparison with a single virtual interaction format [28][29][30][31]. ...
... The disruption in thalamocortical rhythms (thalamocortical dysrhythmia) can be detected by surface electroencephalography (EEG) [15,16]. EEG signals can be assessed as different frequency bands, such as theta (4-7 Hz), alpha (8)(9)(10)(11)(12), and beta (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). Thalamocortical dysrhythmia is characterized by a common resting-state EEG pattern of increased theta and low-frequency alpha rhythms [17,18]. ...
... Three single-arm trials have demonstrated that BCI-N interventions can reduce SCI neuropathic pain [22][23][24]. These studies used a BCI-N protocol, which consisted of suppressing theta and low-frequency alpha rhythms (4)(5)(6)(7)(8), and high-frequency beta rhythms (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), along with enhancing high-frequency alpha rhythms (9)(10)(11)(12). Although these preliminary studies suggested that BCI-N can be effective in reducing SCI neuropathic pain, further studies are needed to provide more definitive evidence regarding the effectiveness of BCI-N interventions for people with neuropathic pain following SCI. ...
... Current BCI-N interventions for both SCI neuropathic pain [20,22,24] and chronic pain [25][26][27] have mostly relied on a single mode of virtual interaction, such as increasing or decreasing the height of a bar presented on a computer screen. However, preliminary evidence suggests that greater pain relief may be achieved from interactive, goal-directed engagement with a gaming environment, in comparison with a single virtual interaction format [28][29][30][31]. ...
Article
Full-text available
Background: Neuropathic pain is a debilitating secondary condition for many individuals with spinal cord injury (SCI). SCI neuropathic pain often remains poorly responsive to existing pharmacological and non-pharmacological treatments. A growing body of evidence supports the potential for brain-computer interface (BCI) systems to reduce SCI neuropathic pain via electroencephalography (EEG) neurofeedback. However, further studies are needed to provide more definitive evidence regarding the effectiveness of this intervention. Objective: The primary objective of this study is to evaluate the effectiveness of a multi-day course of BCI-N intervention in a gaming environment to provide pain relief for individuals with neuropathic pain following SCI. Methods: We have developed a novel BCI-based neuromodulative (BCI-N) intervention for SCI neuropathic pain. Our BCI-N treatment includes an interactive gaming interface, and a neuromodulation protocol targeted to suppress theta (4-8 Hz) and high beta (20-30 Hz) frequency powers, and enhance alpha (9-12 Hz) power. A single-case experimental design (SCED) with multiple baselines will be used to examine the effectiveness of our self-developed BCI-N intervention for the treatment of SCI neuropathic pain. Three participants with SCI neuropathic pain will be recruited. Each participant will be randomly allocated to a different baseline phase (i.e., 7, 10 or 14 days), which will then be followed by 20 sessions of 30-min BCI-N intervention over a 4-week period. The visual analogue scale assessing average pain intensity will serve as the primary outcome measure. Pain interference will also be assessed as a secondary outcome domain. Generalisation measures will assess quality of life, sleep quality, anxiety and depressive symptoms as well as resting-state EEG and thalamic γ-aminobutyric acid concentration (GABA). Results: This study was approved by the Human Research Committees of the University of New South Wales (HC190411) in July 2019 and the University of Technology Sydney (ETH19-4090) in January 2020. The trial has been planned to commence in October 2020, and the results are expected to be published by the end of 2021. Conclusions: This clinical trial using SCED methodology has been designed to evaluate the effectiveness of a novel BCI-N treatment for people with neuropathic pain after SCI. SCEDs are considered a viable alternative approach to randomised clinical trials to identify evidence-based practices in the field of technology-based health interventions when recruitment of large samples is not feasible.
... The disruption in thalamocortical rhythms (thalamocortical dysrhythmia) can be detected by surface electroencephalography (EEG) [15,16]. EEG signals can be assessed as different frequency bands, such as theta (4-7 Hz), alpha (8)(9)(10)(11)(12), and beta (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). Thalamocortical dysrhythmia is characterized by a common resting-state EEG pattern of increased theta and low-frequency alpha rhythms [17,18]. ...
... Three single-arm trials have demonstrated that BCI-N interventions can reduce SCI neuropathic pain [22][23][24]. These studies used a BCI-N protocol, which consisted of suppressing theta and low-frequency alpha rhythms (4)(5)(6)(7)(8), and high-frequency beta rhythms (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), along with enhancing high-frequency alpha rhythms (9)(10)(11)(12). Although these preliminary studies suggested that BCI-N can be effective in reducing SCI neuropathic pain, further studies are needed to provide more definitive evidence regarding the effectiveness of BCI-N interventions for people with neuropathic pain following SCI. ...
... Current BCI-N interventions for both SCI neuropathic pain [20,22,24] and chronic pain [25][26][27] have mostly relied on a single mode of virtual interaction, such as increasing or decreasing the height of a bar presented on a computer screen. However, preliminary evidence suggests that greater pain relief may be achieved from interactive, goal-directed engagement with a gaming environment, in comparison with a single virtual interaction format [28][29][30][31]. ...
Preprint
Background: Neuropathic pain is a debilitating secondary condition for many individuals with spinal cord injury (SCI). SCI neuropathic pain often remains poorly responsive to existing pharmacological and non-pharmacological treatments. A growing body of evidence supports the potential for brain-computer interface (BCI) systems to reduce SCI neuropathic pain via electroencephalography (EEG) neurofeedback. However, further studies are needed to provide more definitive evidence regarding the effectiveness of this intervention. Objective: The primary objective of this study is to evaluate the effectiveness of a multi-day course of BCI-N intervention in a gaming environment to provide pain relief for individuals with neuropathic pain following SCI. Methods: We have developed a novel BCI-based neuromodulative (BCI-N) intervention for SCI neuropathic pain. Our BCI-N treatment includes an interactive gaming interface, and a neuromodulation protocol targeted to suppress theta (4-8 Hz) and high beta (20-30 Hz) frequency powers, and enhance alpha (9-12 Hz) power. A single-case experimental design (SCED) with multiple baselines will be used to examine the effectiveness of our self-developed BCI-N intervention for the treatment of SCI neuropathic pain. Three participants with SCI neuropathic pain will be recruited. Each participant will be randomly allocated to a different baseline phase (i.e., 7, 10 or 14 days), which will then be followed by 20 sessions of 30-min BCI-N intervention over a 4-week period. The visual analogue scale assessing average pain intensity will serve as the primary outcome measure. Pain interference will also be assessed as a secondary outcome domain. Generalisation measures will assess quality of life, sleep quality, anxiety and depressive symptoms as well as resting-state EEG and thalamic γ-aminobutyric acid concentration (GABA). SCEDs are considered a viable alternative approach to randomised clinical trials to identify evidence-based practices in the field of technology-based health interventions when recruitment of large samples is not feasible. Ethics approval: This trial was approved by the University of New South Wales (HC190411) and University of Technology Sydney (ETH19-4090) Human Ethics Committees. Trial registration: Australian New Zealand Clinical Trials Registry (ANZCTR) ACTRN12620000556943
... In chronic pain stimulation, numerous microstructural and functional changes occur in the brain, such as synaptic plasticity, blood perfusion, and connectivity properties of the functional and structural networks (Kuner and Flor, 2017;Iwabuchi et al., 2020;Barroso et al., 2021). These changes are closely related to the onset of pain, which may not only be adaptive changes in response to peripheral pain stimulation but also a key intermediate link to pain perception (Prinsloo et al., 2014). Han et al. found using tracer-based MRI that peripheral pain stimulation induces changes in ISF drainage and the spatial structure of ECS in the deep brain (Li et al., 2020). ...
Article
Full-text available
Cancer pain (CP) is one of the most common symptoms affecting life quality, and there is considerable variation in pain experience among patients with malignant tumors. Previously, it has been found that the fluid drainage function in the brain can be regulated by peripheral pain stimulation. However, the relationship between cancer pain and functional changes of the glymphatic system (an important pathway for fluid drainage in the brain) remains unclear. In this study, 97 participants were enrolled, which included 40 participants in the cancer pain (CP) group, 27 participants in the painless cancer (PLC) group and 30 participants in the control (NC) group. Differences in glymphatic system function among the three groups and between before and after pain pharmacological intervention were analyzed by measuring diffusivity and the index along the perivascular space (ALPS index) using diffusion tensor imaging. We found that diffusivity and the ALPS index were significantly lower in the CP group than in the PLC and NC group and increased following intervention with pain relief. Moreover, the ALPS index was negatively correlated with the degree of pain in the CP group. The present study verified that alterations in glymphatic function are closely related to cancer pain, and the quantification of functional changes reflects pain severity. Our findings support the use of neuroimaging biomarkers for cancer pain assessment and indicate that pain can be alleviated by regulating brain function status.
... The understanding of the critical role of maladaptive functional brain changes in the development and maintenance of chronic pain has led researchers to focus on pain treatments that aim to modulate brain activity [9,10]. Previously, neurosurgical methods, such as cordotomy and thalamotomy, were considered to be effective in the control of abnormal brain activity, such as increased theta frequency power, resulting in a significant pain reduction [11,12]. ...
Article
Full-text available
Background Electroencephalographic (EEG) neurofeedback has been utilized to regulate abnormal brain activity associated with chronic pain. Methods In this systematic review, we synthesized the evidence from randomized controlled trials (RCTs) to evaluate the effect of EEG neurofeedback on chronic pain using random effects meta-analyses. Additionally, we performed a narrative review to explore the results of non-randomized studies. The quality of included studies was assessed using Cochrane risk of bias tools, and the GRADE system was used to rate the certainty of evidence. Results Ten RCTs and 13 non-randomized studies were included. The primary meta-analysis on nine eligible RCTs indicated that although there is low confidence, EEG neurofeedback may have a clinically meaningful effect on pain intensity in short-term. Removing the studies with high risk of bias from the primary meta-analysis resulted in moderate confidence that there remained a clinically meaningful effect on pain intensity. We could not draw any conclusion from the findings of non-randomized studies, as they were mostly non-comparative trials or explorative case series. However, the extracted data indicated that the neurofeedback protocols in both RCTs and non-randomized studies mainly involved the conventional EEG neurofeedback approach, which targeted reinforcing either alpha or sensorimotor rhythms and suppressing theta and/or beta bands on one brain region at a time. A posthoc analysis of RCTs utilizing the conventional approach resulted in a clinically meaningful effect estimate for pain intensity. Conclusion Although there is promising evidence on the analgesic effect of EEG neurofeedback, further studies with larger sample sizes and higher quality of evidence are required.
... They conclude that NF is a potentially effective, noninvasive, and economical tool in order to manage cancer impairments through modulating neural pathways. 35 The purpose of this review will be to explore the effect of NF on various impairments and long-term symptoms commonly experienced by cancer survivors. So far, there is no such review that deals with various cancer impairments. ...
Article
Full-text available
Introduction: Neurofeedback (NF) or electroencephalogram (EEG)-Biofeedback is a drug-free form of brain training to directly alter the underlying neural mechanisms of cognition and behavior. It is a technique that measures a subject's EEG signal, processes it in real time, with the goal to enable a behavioral modification by modulating brain activity. The most common application of the NF technology is in epilepsies, migraine, attention-deficit/hyperactivity disorder, autism spectrum disorder, affective disorders, and psychotic disorders. Few studies have investigated the use of NF in context of psychosomatic illnesses. Little is known about the use in cancer patients or postcancer survivors despite the high number of this patient group. Objectives: We here provide a systematic review of the use and effect of NF on symptoms and burden in cancer patients and long-term cancer survivors. Methods: In conducting this systematic review, we followed the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) Statement. Results: Our search resulted in only 3 experimental studies, 1 observational study, and 2 case reports. Given the heterogeneity of the intervention systems and protocols, no meta-analysis was conducted. Conclusion: Altogether, there is initial evidence that NF is a complementary, drug-free, and noninvasive therapy that has the potential to ameliorate symptoms in this patient group, such as pain, fatigue, depression, and sleep. Further studies are highly needed.
... Results of an integrative review suggest neurofeedback for management of cancer pain. [16] A systematic review provides preliminary evidence of use neurofeedback to manage fatigue and cognitive impairment. [14] One study in this review demonstrated the feasibility of neurofeedback in a sample of breast cancer survivors who showed significant improvements in cognition, fatigue, psychological symptoms, and sleep. ...
Article
Objective: Cancer survivors may experience persistent physical and psychological symptoms following completion of cancer treatment. Neurofeedback is a noninvasive form of brain training reported to help with symptoms including pain, fatigue, depression, anxiety, insomnia, and cognitive decline; however, there is a lack of research exploring its use with cancer survivors. The objective of this study was to describe the experiences of neurofeedback and its impact on the lives of posttreatment cancer survivors as perceived by neurofeedback providers and cancer survivor clients. Methods: This qualitative descriptive study employed semi-structured interviews and thematic analysis of interview transcripts. A convenience sample of twelve neurofeedback providers and five cancer survivor clients participated in this study. Results: Thematic analysis revealed seven overarching themes as follows: (1) paying it forward; (2) transforming lives; (3) regaining control; (4) brain healing itself; (5) comforting experience, (6) accessibility, and (7) failure to respond. The first five themes related to benefits of neurofeedback, and the final two related to challenges of using neurofeedback with cancer survivors. Conclusions: Results support the use of neurofeedback to improve quality of life for cancer survivors; however, more research is needed to determine which neurofeedback systems and protocols are most effective for this population with persistent symptoms.
... Results of an integrative review suggest neurofeedback for management of cancer pain. [16] A systematic review provides preliminary evidence of use neurofeedback to manage fatigue and cognitive impairment. [14] One study in this review demonstrated the feasibility of neurofeedback in a sample of breast cancer survivors who showed significant improvements in cognition, fatigue, psychological symptoms, and sleep. ...
Article
Full-text available
Objective Cancer survivors may experience persistent physical and psychological symptoms following completion of cancer treatment. Neurofeedback is a noninvasive form of brain training reported to help with symptoms including pain, fatigue, depression, anxiety, insomnia, and cognitive decline; however, there is a lack of research exploring its use with cancer survivors. The objective of this study was to describe the experiences of neurofeedback and its impact on the lives of posttreatment cancer survivors as perceived by neurofeedback providers and cancer survivor clients. Methods This qualitative descriptive study employed semi-structured interviews and thematic analysis of interview transcripts. A convenience sample of twelve neurofeedback providers and five cancer survivor clients participated in this study. Results Thematic analysis revealed seven overarching themes as follows: (1) paying it forward; (2) transforming lives; (3) regaining control; (4) brain healing itself; (5) comforting experience, (6) accessibility, and (7) failure to respond. The first five themes related to benefits of neurofeedback, and the final two related to challenges of using neurofeedback with cancer survivors. Conclusions Results support the use of neurofeedback to improve quality of life for cancer survivors; however, more research is needed to determine which neurofeedback systems and protocols are most effective for this population with persistent symptoms.
... Tumours often trigger pain via a combination of inflammatory, neuropathic, ischaemic and tissue compression mechanisms and also by chemical mediators released by cancer cells (Prinsloo et al., 2013). Systemic administration of flupirtine displayed analgesic efficacy in a rat model of prostate bone metastasis (Kolosov et al., 2012), suggesting that a general dampening of excitability within the pain pathways via M channel potentiation might have potential as a treatment for cancer pain. ...
Article
Full-text available
Pathological pain is a hyperexcitability disorder. Since the excitability of a neuron is set and controlled by a complement of ion channels it expresses, in order to understand and treat pain, we need to develop a mechanistic insight into the key ion channels controlling excitability within the mammalian pain pathways and how these ion channels are regulated and modulated in various physiological and pathophysiological settings. In this review, we will discuss the emerging data on the expression in pain pathways, functional role and modulation of a family of voltage‐gated K⁺ channels called ‘M channels’ (KCNQ, Kv7). M channels are increasingly recognized as important players in controlling pain signalling, especially within the peripheral somatosensory system. We will also discuss the therapeutic potential of M channels as analgesic drug targets. Linked Articles This article is part of a themed section on Recent Advances in Targeting Ion Channels to Treat Chronic Pain. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.12/issuetoc/
Article
Background: Evidence suggests the usefulness of complementary and alternative medicine approaches, like neurofeedback and virtual reality, for the management of cancer-related pain and mood. It is not well-understood whether neurofeedback delivered through virtual reality is feasible and acceptable to patients actively undergoing cancer treatment. Objective: The purpose of this study was to explore the feasibility and acceptability of a nature-based virtual reality combined with neurofeedback as a non-pharmacologic strategy for managing cancer-related pain and anxiety. Methods: This study utilized a mixed-methods approach. Participants included 15 cancer patients undergoing treatment. Patients engaged in a 22-minute nature-based virtual reality experience, wearing a virtual reality headset with a Brainlink headband measuring EEG activity. Participants were asked to complete the Edmonton Symptom Assessment System revised version (ESAS-r) before (T1) and after (T3) the experience to measure pain and anxiety. They were asked their level of pain midway through the experience (T2) and completed a follow-up interview afterward. Results: This study revealed feasible delivery of a virtual reality intervention combined with neurofeedback for patients seeking cancer treatment. All participants (100%) completed the intervention experience. Patients report this is an acceptable approach to managing cancer-related pain and anxiety. Comparisons between patients’ pain scores at T1, T2, and T3 reveal statistically significant reductions in pain (p .001). Patients also report decreased depression and anxiety. Conclusion: This is the first study examining virtual reality combined with neurofeedback as a non-pharmacologic intervention for managing cancer symptoms during treatment. The study reveals it is a promising for managing cancer-symptoms.
Chapter
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Abstract Chapter 16 “Neurofeedback in Pain Management”, in the book Introduction to Quantitative EEG and Neurofeedback” eds. Budzynski, Budzynski, and Abarbanel, presents the latest theories on chronic pain and a study of the amelioration/ minimization of chronic pain. 147 subjects with chronic pain syndromes have been evaluated and treated in the office of the first author and statistically analyzed by the second author. Chronic pain syndromes were of various etiologies, and they varied from migraine headaches to complex regional sympathetic dystrophy (CRPS). Many patients suffered from various co-morbidities and they have been previously treated with other modalities that had little resolution of pain. Each subject has been evaluated prior, post and periodically during the Neurofeedback treatment. The evaluations were complex from medical to psychophysiological, cognitive and EEG measures. QEEG, quantitative EEG were performed in cases that suffered traumatic head injuries, TBI and some had been monitored for blood perfusion using HEG, hemoencephalography measurements. Pain was analyzed as a “disease” but mostly as a “symptom” and each case was individually treated with a specific BF/NF procedure. From the 147 cases (95 women, 52 men) analyzed for the efficacy of the BF/ NF, 10 cases were presented in detail. A direct correlation, between the number of sessions and the positive results has been reported. In the case of the patients who completed more than 19 sessions of NF, the success rate was evident: 92% with clinical significant improvement (CSI), and up to 95% total success if we consider all CSI plus ameliorated cases. Lack of success in some cases of those who have completed over 20 sessions BF / NF (total approx. 5%) may be linked to too many co-morbidities and the excessive length of time of these pain syndromes. NF, with its emphasis on volitional control, has been found useful in the reduction of pain. Abbreviations: BF, Biofeedback; NF, Neurofeedback; EEG, electroencephalography; QEEG, quantitative EEG; HEG, hemoencephalography; TBI, traumatic brain injury; CSI, Clinical Significant Improvement; CRPS, complex regional sympathetic dystrophy Rezumat In Capitolul 16 “Neurofeedback in Pain Management” din cartea “Introduction in Quantitative EEG and Neurofeedback”, eds. Budzynski, Budzynski and Abarbanel se prezinta date generale de ultima ora despre durerea cronica si un studiu privind ameliorarea / minimalizarea durerii cronice prin BF si NF. In cadrul cabinetului primului autor – trainer si mentor de BF si NF in Pasadena, USA au fost tratati 147 de subiect cu cu dureri cronice. Datele au fost analizate si interpretate statistic de al doilea autor, professor si PhD in biostatistica in Bucharest, Romania. Durerile cronice au fost de cele mai diverse etiologii (variind de la migrene, la sindroame complexe de dureri cronice regionale) si multi subiecti au avut diverse co-morbiditati. Acesti pacienti au fost tratati inainte de BF/NF prin alte modalitati diferite de tratament si au avut o reducere nesemnificativa a durerii. Fiecare subiect a fost evaluat inainte, dupa antrenamente dar si periodic in cele mai multe cazuri. Evaluarile a fost de o mare complexitate: de tip medical, psihofiziologic, teste cognitive obiective, psihologice si profil EEG. QEEG (Quantitative EEG) au fost utilizate in cazuri de dureri asociate cu injurii ale creierului (TBI, traumatic brain injury) si in unele cazuri perfuzia sanguina a fost monitorizata prin HEG (hemoencepalography).Durerea a fost abordata atat ca boala (definita medical) dar mai ales ca afectiune (definite prin suferintele subiective ale subiectului) si fiecare caz a primit o procedura de BF/NF individualizata. Eficacitatea antrenarii prin BF si NF a celor 147 de subiecti (95 femei, 52 barbati) este analizata si 10 cazuri sunt prezentate detaliat. S-a evidentiat o corelatie directa intre numarul de sesiuni si rezultatele positive. In cazul subiectilor care au efectuat maimult de 19 sesiuni de NF training, rata de success a fost evidenta: 92% au avut o Imbunatatire ClinicaSemnificativa (ICS) si peste 95% au fost cazuri de succes, daca luam in considerare toti cu ICS=CSI (in English) plus cazurile doar ameliorate. Lipsa de success in unele cazuri dintre cei care au urmat peste 20 de sesiuni de BF/NF (total cca. 5%) poate fi legata de un numar prea mare de co-morbiditati associate cat si de durata excesiva a acestor sindroame dureroase. NF cu accent pe controlul volitiv a fost gasit util in reducerea durerii cronice. Abrevieri: BF, Biofeedback; NF, Neurofeedback; EEG, electroencephalography; QEEG, quantitative EEG; HEG, hemoencephalography; TBI, traumatic brain injury; CSI, Clinical Significant Improvement (English); ICS, ImbunatatireClinicaSemnificativa
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Introduction. This study examines the EEG spectral power and coherence changes that occur as a result of LORETA neurofeedback (LNFB) training, which is a recently developed spatial-specific neurofeedback protocol in which it has been demonstrated that human beings can learn to change activity in their own anterior cingulate gyrus. We trained individuals to increase low-beta (14–18 Hz) activity in the cognitive division of the anterior cingulate gyrus (ACcd).Methods. This study was conducted with eight non-clinical students with a mean age of 22. The participants completed over 30 sessions of LNFB training. We utilized the WAIS-III for pre- and post-psychometric measures to assess the influence of this training protocol.Results. We selected training Sessions 5, 10, 15, 20, 25, and 30 for comparison to Session 1. There are significant increases in absolute power and coherence over sessions. There is significant increase in the working memory and processing speed subtest scores.Discussion. The anterior regions of the cortex increase in the low-beta frequency relative to the ACcd at significant levels. The superior prefrontal cortex and occipital regions increase in the higher beta frequencies, but not in the trained frequency. The improvements in the working memory and processing speed scores suggest that LNFB had an overall positive effect in attentional processes, working memory, and processing speed.
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Introduction. Complex Regional Pain Syndrome Type I (CRPS-I) is a devastating pain condition that is refractory to standard care. Preliminary evidence suggests the possibility that neurofeedback training might benefit patients with chronic pain, including patients with CRPS-I. The current study sought to address the need for more information about the effects of neurofeedback on pain in persons with chronic pain by (1) determining the average decrease in pain in patients with CRPS-I following neurofeedback training, (2) identifying the percent of patients reporting pain decreases that are clinically meaningful, and (3) documenting other benefits of neurofeedback training.Method. Eighteen individuals with CRPS-I participating in a multidisciplinary treatment program were administered 0–10 numerical rating scale measures of pain intensity at their primary pain site, as well as pain at other sites and other symptoms, before and after a 30 minute neurofeedback training session. A series of t-tests were performed to determine the significance of any changes in symptoms observed. We also computed the effect sizes and percent change associated with the observed changes in order to help interpret the magnitude of observed improvements in symptoms.Results. There was a substantial and statistically significant pre- to post-session decrease in pain intensity at the primary pain site on average, with half of the study participants reporting changes in pain intensity that were clinically meaningful. Five of seven secondary outcome measures also showed statistically significant improvements following neurofeedback treatment.Conclusions. The findings suggest that many patients who receive neurofeedback training report significant and substantial short-term reductions in their experience of pain, as well as improvements in a number of other pain- and nonpain-specific symptoms. The findings support the need for additional research to further examine the long-term effects and mechanisms of neurofeedback training for patients with chronic pain.
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Background. This study reports on a new method for golf performance enhancement employing personalized real-life neurofeedback during golf putting.Method. Participants (n = 6) received an assessment and three real-life neurofeedback training sessions. In the assessment, a personal event-locked electroencephalographic (EEG) profile at FPz was determined for successful versus unsuccessful putts. Target frequency bands and amplitudes marking optimal prefrontal brain state were derived from the profile by two raters. The training sessions consisted of four series of 80 putts in an ABAB design. The feedback in the second and fourth series was administered in the form of a continuous NoGo tone, whereas in the first and third series no feedback was provided. This tone was terminated only when the participants EEG met the assessment-defined criteria. In the feedback series, participants were instructed to perform the putt only after the NoGo tone had ceased.Results. From the personalized event-locked EEG profiles, individual training protocols were established. The interrater reliability was 91%. The overall percentage of successful putts was significantly larger in the second and fourth series (feedback) of training compared to the first and third series (no feedback). Furthermore, most participants improved their performance with feedback on their personalized EEG profile, with 25% on average.Conclusions. This study demonstrates that the “zone” or the optimal mental state for golf putting shows clear recognizable personalized patterns. The learning effects suggest that this real-life approach to neurofeedback improves learning speed, probably by tapping into learning associated with contextual conditioning rather than operant conditioning, indicating perspectives for clinical applications.
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Poor pain assessment is cited as one barrier to the adequate treatment of cancer pain. The identification of relevant psychosocial factors may improve the assessment of chronic cancer pain. This article presents: 1) a critical review of the evidence for an association between chronic cancer pain and psychological distress, social support, and coping; 2) clinical implications of the findings; and 3) recommendations for future research. Fourteen of the 19 reviewed studies on psychological distress found a significant association between increased pain and increased distress. Seven of the eight studies on social support found significant association between higher levels of pain and decreased levels of social activities and social support. Three of the four studies that examined coping strategies found that increased catastrophizing was significantly associated with more intense pain. Based on several criteria, the evidence is considered Strong for psychological distress, Moderate for social support, and Inconclusive for coping. This review suggests that comprehensive chronic pain assessment should include routine screening for psychological distress.
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