discussion #9 disease

Psychological Pain Interventions and
Neurophysiology

Implications for a Mechanism-Based Approach

Herta Flor
Central Institute of Mental Health, Mannheim, Germany, and Heidelberg University

This article provides an illustrative overview of neurophys-
iological changes related to acute and chronic pain involv-
ing structural and functional brain changes, which might
be the targets of psychological interventions. A number of
psychological pain treatments have been examined with
respect to their effects on brain activity, ranging from
cognitive- and operant behavioral interventions, medita-
tion and hypnosis, to neuro- and biofeedback, discrimina-
tion training, imagery and mirror treatment, as well as
virtual reality and placebo applications. These treatments
affect both ascending and descending aspects of pain pro-
cessing and act through brain mechanisms that involve
sensorimotor areas as well as those involved in affective-
motivational and cognitive-evaluative aspects. The analy-
sis of neurophysiological changes related to effective psy-
chological pain treatment can help to identify subgroups of
patients with chronic pain who might profit from different
interventions, can aid in predicting treatment outcome, and
can assist in identifying responders and nonresponders,
thus enhancing the efficacy and efficiency of psychological
interventions. Moreover, new treatment targets can be de-
veloped and tested. Finally, the use of neurophysiological
measures can also aid in motivating patients to participate
in psychological interventions and can increase their ac-
ceptance in clinical practice.

Keywords: neurophysiological, pain, psychological treat-
ment, magnetic resonance imaging

Psychological treatments for chronic pain include alarge variety of cognitive-behavioral interventionsranging from biofeedback to pain management
training to hypnosis. In general, these interventions have
been shown to be successful, with effect sizes in the me-
dium to high range (Williams, Eccleston, & Morley, 2012).
In recent years, more information has become available
about the structural and functional brain changes that are
related to pain (for a review, see Davis & Moayedi, 2013),
and successful treatments should reverse these changes. It
will be interesting to see whether and how these assess-
ments can help in designing better treatment interventions.
Moreover, only a few studies have examined which com-
ponents of these often very broad treatment approaches are
effective and how they affect brain function and peripheral
physiological responses. In this overview I first describe
typical brain changes associated with the experience of

acute and, especially, chronic pain and then discuss how
psychological interventions might impact them. Finally, I
outline areas of future research and discuss how neurophys-
iological examinations can help provide a better under-
standing of chronic pain and aid in the development of new
and more refined psychological treatments.

Neurophysiological Characteristics of
Acute and Chronic Pain
There are numerous brain changes that have been associ-
ated with acute and chronic pain. In acute pain, functional
magnetic resonance imaging (fMRI) revealed regions such
as the anterior cingulate cortex (ACC), the amygdala, the
periaqueductal gray, the anterior insula, and the nucleus
accumbens to be associated with affective and motivational
processing; the primary (S1) and secondary (S2) somato-
sensory cortex, the posterior insula, and the thalamus with
sensory processing; and frontal areas, including the ACC,
with the cognitive modulation of pain (cf. Apkarian,
Hashmi, & Baliki, 2011). In addition, social and other
context variables such as learnt associations with pain or
social reinforcement and empathy can affect how nocice-
ptive stimulation will be processed by the brain and turned
into a pain experience. Here, not only is activation in
certain brain areas important, but multiple networks may
interact at any given point in time and contribute to several
aspects of pain. In addition, not only do these regions seem

Editor’s note. This article is one of nine in the February–March 2014
American Psychologist “Chronic Pain and Psychology” special issue.
Mark P. Jensen was the scholarly lead for the special issue.

Author’s note. This research was supported by the Award for Basic
Research of the State of Baden-Württemberg, Germany; the PHANTOMMIND
project (“Phantom Phenomena: A Window to the Mind and the Brain,”
which receives research funding from the European Community’s Sev-
enth Framework Programme, FP7/2007-2013/ERC Grant Agreement
230249); and the research Consortium LOGIN (“Localized and General-
ized Musculoskeletal Pain: Psychobiological Mechanisms and Implica-
tions for Treatment”), funded by the German Federal Ministry of Educa-
tion and Research (01EC1010D). This manuscript reflects only the
author’s views, and the European Community is not liable for any use that
may be made of the information contained therein.

Correspondence concerning this article should be addressed to Herta
Flor, Department of Cognitive and Clinical Neuroscience, Central Insti-
tute of Mental Health, Square J5, D-68159 Mannheim, Germany. E-mail:
[email protected]

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188 February–March 2014 ● American Psychologist
© 2014 American Psychological Association 0003-066X/14/$12.00

Vol. 69, No. 2, 188 –196 DOI: 10.1037/a0035254

mailto:[email protected]

http://dx.doi.org/10.1037/a0035254

to be relevant for the processing of pain, but they may
reflect a general salience detection system (Legrain, Ian-
netti, Plaghki, & Mouraux, 2011). It will be interesting to
see how ongoing research efforts to differentiate pain from
other attention-capturing and salient events will succeed in
defining the core brain processes defining pain perception. For
example, recent research using multivariate pattern analysis ar-
rived at the conclusion that there is no single brain region
subserving the experience of pain but that the most accurate
prediction of pain perception related to acute laser stimuli
was enabled by the combined activity in these regions,
commonly referred to as the “pain matrix” (Brodersen et
al., 2012). In chronic pain states, the medial prefrontal
cortex has been identified as a region that best reflects
spontaneous fluctuations of pain (Baliki et al., 2006). Many
of these areas have been found to have altered gray matter
density (cf. May, 2011), and they also show changes in the
brain’s default mode network and other resting state net-
works (Baliki, Geha, Apkarian, & Chialvo, 2008; Napadow
et al., 2010), suggesting long-lasting brain changes related
to the presence of chronic pain. In addition, white matter
changes have been examined using diffusion tensor imag-
ing. Here, specifically reduced connectivity in tracts in-
volved in descending pain modulation has been observed in
chronic pain patients, and these changes have also been
related to deficient cognitive pain control (for a review, see
Davis & Moayedi, 2013). It is a matter of debate to what
extent the brain changes seen in chronic pain are pain-
specific or may reflect comorbid states such as anxiety or
depression, may reflect medication effects, or may be in-
duced by the long-lasting states of pain themselves. Elec-
troencephalographic (EEG) and magnetoencephalographic
(MEG) recordings have also revealed a number of ab-
normal brain signatures related to chronic pain, such as

a shift or expansion of the representation of painful and
nonpainful stimuli in sensorimotor cortex (Moseley &
Flor, 2012), general hyperreactivity to pain-related stim-
ulation (e.g., Buchgreitz, Egsgaard, Jensen, Arendt-
Nielsen, & Bendtsen, 2008; Flor, Knost, & Birbaumer,
1997; Richter, Eck, Straube, Miltner, & Weiss, 2010), as
well as altered oscillatory activity (Hauck, Lorenz, & En-
gel, 2008). These central changes are accompanied by
alterations in peripheral somatosensory processing, includ-
ing deficient perception of muscle tension and tactile
stimulation (e.g., Flor, Schugens, & Birbaumer, 1992;
Maihöfner, Handwerker, & Birklein, 2006; Moseley, 2008)
as well as a distorted body image (e.g., Lewis et al., 2010;
Lotze & Moseley, 2007), that are site-specific and mirrored
in specific changes in sensorimotor representations and
limbic pain responses. A special role in this brain– body
interaction has been assigned to the anterior insula, which
is viewed as an integrative relay station for interoceptive
input from the body (Craig, 2003). Maihöfner, Seifert, and
Decol (2011) described a network involving the anterior
insula that responds to sympathetic activation, and Po-
mares, Faillenot, Barral, and Peyron (2013) suggested that
the anterior and posterior insula contribute differentially to
the experience of pain.

Changes in peripheral responses have also been ob-
served in chronic pain that range from enduring as well as
event-related changes in muscle tension, autonomic func-
tioning, or endocrinological responses (cf. Flor & Turk,
1989; Valença, Medeiros, Martins, Massaud, & Peres,
2009). Effective psychological treatments need to address
these changes and reverse them.

Cognitive-Behavioral and
Operant-Behavioral Treatments
Although cognitive-behavioral and operant-behavioral
treatments, including exposure treatment and acceptance
and commitment-based approaches, are the most com-
monly used psychological treatments for chronic pain and
among the most effective (cf. Flor, Fydrich, & Turk, 1992;
Glombiewski et al., 2010; Hoffman, Papas, Chatkoff, &
Kerns, 2007), relatively few studies have examined their
neurophysiological correlates. In a pioneering study, Lack-
ner et al. (2006) used a brief cognitive-behavioral interven-
tion that involved education, cognitive coping strategies,
and problem solving training in patients with painful irri-
table bowel syndrome and achieved significant reductions
in pain, anxiety, and gastrointestinal symptoms. These im-
provements were accompanied by reduced activations in
the parahippocampal gyrus, the amygdala, and the sub-
genual ACC including the medial frontal cortex, all regions
involved in affective and cognitive modulation of pain.
Bonifazi et al. (2006) studied endocrinological changes in
patients with fibromyalgia syndrome as a consequence of
cognitive-behavioral treatment and observed improved cor-
tisol function as well as improved glucocorticoid receptor
alpha RNA expression in peripheral mononuclear blood
cells following effective treatment.

Herta Flor

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189February–March 2014 ● American Psychologist

Several studies in healthy humans have specifically
examined cognitive processes related to psychological pain
modulation and have shed light on core brain regions
involved in effective cognitive interventions. For example,
Bantick et al. (2002) found that cognitive distraction re-
duced pain intensity ratings and increased activation in the
rostral ACC and decreased activation in the dorsal ACC.
Lawrence, Hoeft, Sheau, and Mackey (2011) compared
reappraisal and attention diversion and found specific ef-
fects of the two strategies on brain activity measures.
Whereas attention diversion involved frontal, parietal, and
occipital regions, reappraisal involved the ventral lateral
prefrontal cortex, the midcingulate cortex, the thalamus,
and the amygdala. The postcentral gyrus was active in both
conditions. Wiech et al. (2006) also found that self-control
over pain was correlated with activation in right anterolat-
eral prefrontal cortex and the dorsal anterior cingulate
cortex. Enduring cognitive changes that alter pain process-
ing have also been observed in meditators, in whom the
anticipation and experience of pain were accompanied by
altered activation of the anterior insula (Lutz, McFarlin,
Perlman, Salomons, & Davidson, 2013). Cognitive and
learning factors also play a role in placebo analgesia, which
can be viewed as a type of psychological modulation of
pain. Here a descending network involving the anterior
cingulate cortex and the periaqueductal gray has been iden-
tified (for a review, see Colloca, Klinger, Flor, & Bingel,
2013) that alters the transmission of nociceptive input
already at the level of the spinal cord (Eippert, Finster-
busch, Bingel, & Büchel, 2009). K. B. Jensen et al. (2012)
showed that cognitive-behavioral treatment specifically al-
ters activity in the prefrontal cortex in response to pain in
fibromyalgia patients. Operant-behavioral treatments have
been advocated for persons who have low activity levels,
display high pain behaviors, and have significant others
who reinforce them for the display of pain behaviors (cf.
Thieme, Flor, & Turk, 2006; Thieme, Turk, & Flor, 2007).
Diers et al. (2012) showed that patients with fibromyalgia
who underwent a pain extinction training based on operant
principles displayed a shift from more activation in the
anterior insula pretreatment to more activation in the pos-
terior insula posttreatment. Changes in pain-related inter-
ference were closely related to changes in blood-oxygen-
level-dependent activations in the posterior insula, primary
somatosensory cortex, thalamus, and striatum, suggesting
more sensory than affective processing and better pain
prediction following successful pain control. These
changes differ from those shown by K. B. Jensen et al. for
cognitive-behavioral treatment and thus suggest that differ-
ent behavioral treatments may impact different brain cir-
cuits.

Meditation
Several studies have examined structural and functional
brain changes related to meditation and pain perception.
Zeidan et al. (2011) used arterial spin labeling fMRI to
analyze the neural mechanisms underlying pain control
achieved by mindfulness meditation in healthy humans.

They found that four days of meditation training signifi-
cantly reduced pain intensity and unpleasantness ratings in
response to noxious stimulation. In line with these changes,
activity in contralateral primary somatosensory cortex was
reduced. In addition, activity in the ACC and anterior
insula was increased when pain intensity was lower, and
thalamic deactivation as well as orbitofrontal activation
were associated with unpleasantness reductions. These data
suggest that the afferent input to the brain is actively
modulated by meditation.

Brown and Jones (2010) examined how experienced
meditators anticipated and controlled experimental laser
pain using EEG recordings. More experienced meditators
perceived the pain as less unpleasant than did controls, with
meditation experience correlating inversely with unpleas-
antness ratings. Event-related potential (ERP) source data
for anticipation showed that in meditators, lower activity in
midcingulate cortex relative to controls was related to the
lower unpleasantness ratings and was predicted by lifetime
meditation experience. Meditators also reversed the normal
positive correlation between medial prefrontal cortical ac-
tivity and pain unpleasantness during anticipation. Medita-
tion was also associated with lower activity in S2 and
insula during the pain-evoked response, although the ex-
periment could not disambiguate this activity from the
preceding anticipation response. Thus, meditation seems to
have strong effects specifically on the anticipation of pain.

Grant, Courtemanche, Duerden, Duncan, and Rain-
ville (2010) examined the thickness of gray matter of the
brain in long-term Zen meditators and found that they had
lower pain sensitivity, which was associated with thicker
cortex in the dorsal ACC and secondary somatosensory
cortex. Moreover, more years of meditation training were
associated with changes in anterior cingulate, and hours of
experience were associated with more gray matter in the
primary somatosensory cortex. These data suggest that
structural brain changes and pain sensitivity are related and
that meditation may impact this relationship. In a very
interesting study that used functional imaging, Grant, Cour-
temanche, and Rainville (2011) also looked at brain acti-
vation and connectivity changes in Zen meditators and
observed that those with the most intense meditation prac-
tice reduced activation in areas related to the cognitive-
evaluative and emotional components of pain, such as the
prefrontal cortex, amygdala, and hippocampus, and in-
creased activation in thalamus, insula, and anterior cingu-
late cortex. Moreover, they showed reduced connectivity
between brain regions involved in executive function and
pain processing. This suggests that meditation, in contrast
to cognitive strategies, induces a more passive type of pain
regulation that results in a decoupling of cognitive and
sensory processing, which is in line with notions about the
role of passive attention in meditative techniques.

In line with these findings, Gard et al. (2012) exam-
ined persons who practiced mindfulness meditation and
showed they had substantial reductions in pain intensity
and unpleasantness compared to a control condition, reduc-
tions which were associated with reduced lateral prefrontal
and increased right posterior insula activation. In addition,

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190 February–March 2014 ● American Psychologist

anticipation of pain was associated with increased rostral
anterior cingulate activity. Again, decreased cognitive con-
trol and increased sensory processing were observed, sug-
gesting an alternate route to effective pain reduction than
that of the enhanced cognitive control seen in cognitive-
behavioral techniques.

Hypnosis
Seminal studies in healthy humans used hypnosis to induce
either affective or sensory components of pain and found
them associated with increased activation in either the
anterior cingulate or the primary somatosensory cortex
(Hofbauer, Rainville, Duncan, & Bushnell, 2001; Rain-
ville, Carrier, Hofbauer, Bushnell, & Duncan, 1999; Rain-
ville, Duncan, Price, Carrier, & Bushnell, 1997). Since
then, several studies have focused on the effects of hypno-
sis on pain processing in healthy humans or in patients with
chronic pain. In general, hypnotic techniques are very
effective in modulating both acute and chronic pain (cf.
M. P. Jensen, 2009, for a review). Derbyshire, Whalley,
and Oakley (2009) instructed fibromyalgia patients to ex-
perience their clinical pain as differentially intense with
and without hypnotic suggestions. These researchers found
(a) changes in pain intensity according to instructions that
were more pronounced during hypnotic induction and (b)
altered activation in a number of brain regions related to the
processing of pain such as the thalamus, somatosensory
and midcingulate cortex, the insula, and prefrontal regions.
Similar results were previously reported by these research-
ers for pain induced by hypnosis or imagery in healthy
persons (Derbyshire, Whalley, Stenger, & Oakley, 2004).

Nusbaum et al. (2011) used positron emission tomog-
raphy to examine the effects of hypnotic analgesia in
chronic low back pain, and they also observed changes in
brain networks involved in both emotional and cognitive
processing. Abrahamsen et al. (2010) used hypnosis to
induce either increased or decreased pain perception (hy-
peralgesia or hypoalgesia) in patients with temporoman-
dibular disorder pain. They found increased activity in the
right posterior insula and BA6 and left BA40 during hy-
peralgesia and increased activity in the right posterior in-
sula during hypoalgesia. In addition, S1 activity decreased
during hyperalgesia. Hypnotic hypoalgesia, compared to a
control condition, showed significant decreases in activity
in right posterior insula and BA21, as well as left BA40.
These data suggest similarities between hypnotic analgesia
and cognitive-behavioral interventions.

Sensory Discrimination Training
Phantom limb pain and other neuropathic pain states are
characterized by reorganization of the sensorimotor cortex
such that neural activity from regions adjacent to the site of
the injury expands into the vacated space (in amputees) or
changes its size (in complex regional pain syndromes). The
magnitude of these changes is correlated with the pain
these patients experience in the missing or affected limb.
Such patients also show a number of structural changes (cf.
Flor, Nikolajsen, & Jensen, 2006; see Henry, Chiodo, &

Yang, 2011, for a review). These pain states can be treated
by changing the input to the brain region that has been
altered. For example, phantom limb pain has been reduced
by improving tactile acuity in regions close to the ampu-
tation line in order to restore normal input to the brain
region affected by the amputation. Two weeks of sensory
discrimination training that involved the perception of the
frequency and the location of two out of eight possible
stimuli to the residual limb were provided. In the course of
the training, the discriminability of the stimulus-pairs (in
terms of frequency and location) was reduced in a shaping
procedure. Verbal and visual feedback was provided. The
treatment led to a significant improvement in both fre-
quency and location discrimination, which was also re-
flected in improved two-point discrimination. It resulted in
a more than 60% reduction in phantom limb pain and a
significant reversal of cortical reorganization, with a shift
of the mouth representation back to its original location
(Flor, Denke, Schäfer, & Grüsser, 2001). The alterations in
discrimination ability, pain, and cortical reorganization
were significantly positively correlated. A control group of
patients who received standard medical treatment and gen-
eral psychological counseling in this time period did not
show similar changes in cortical reorganization and phan-
tom limb pain. These findings were confirmed by a study
that used a similar protocol (Huse, Preissl, Larbig, &
Birbaumer, 2001) with asynchronous tactile stimulation of
the mouth and hand region.

Imagery, Mirrors, and Virtual Reality
Treatment
Ramachandran, Rogers-Ramachandran, and Cobb (1995)
employed a mirror to train patients with phantom limb pain
to move the phantom and reduce phantom limb pain. A
mirror was placed in a box, and the patient inserted his or
her intact arm and the arm with the phantom. The patient
was then asked to look at the mirror image of the intact
arm, which was perceived as an intact arm in the location
where the amputated arm used to be. The patients were
then asked to make symmetric movements with both the
intact and the phantom hands, thus suggesting real move-
ment from the lost arm to the brain. This procedure seemed
to re-establish control over the phantom and to reduce
phantom limb pain in some but not all patients in this
anecdotal study.

Extended mirror treatment was highly effective in
reducing phantom limb pain in a controlled study (Chan et
al., 2007), where it was compared with movement without
a mirror and imagined movement. Diers, Christmann,
Köppe, Ruf, and Flor (2010) contrasted a session of mirror
training in amputees with and without phantom pain and
healthy controls with imagery of movement and with actual
movement and found that persons with phantom limb pain
failed to activate the area in the somatosensory cortex that
represented the limb seen in the mirror, whereas patients
without pain showed a normal representation related to the
mirrored hand and movement. The magnitude of the rep-
resentation was negatively correlated with phantom limb

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191February–March 2014 ● American Psychologist

pain. This suggests that there is a failure in amputees with
pain to adequately integrate the amputated limb in their
body image and thus a failure to inhibit maladaptive plastic
changes related to pain. Compared with mirror training,
imagery had similar but weaker effects in this study. In
healthy humans, Egsgaard, Petrini, Christoffersen, and Ar-
endt-Nielsen (2011) examined EEG correlates of the mirror
illusion and found that in men more than in women short-
term plasticity of the primary somatosensory cortex as
evident in early components of the ERP was present.

It can be assumed that imagined movement activates
similar but not identical brain regions as actual movement,
which can lead to a facilitation of normal movement with
an accompanying reduction in pain (Raffin, Mattout,
Reilly, & Giraux, 2012). Giraux and Sirigu (2003) showed
that phantom limb pain was greatly reduced when patients
imagined movements of the hand that had been amputated.
The imagined movements led to a site-specific activation in
the primary motor cortex. MacIver, Lloyd, Kelly, Roberts,
and Nurmikko (2008) also found that therapeutic mental
imagery caused a significant reduction in phantom limb
pain with a concomitant normalization of brain activation
in the sensorimotor cortex. These studies suggest that mod-
ification of input into the affected brain region by visual
feedback and imagery alone may alter pain sensation and
cortical plasticity. However, it needs to be determined
whether imagined movements or executed movements of
the phantom hand (which amputees can differentiate) are
more effective (Raffin, Giraux, & Reilly, 2012). A virtual
reality treatment that uses, for example, movement of the
intact limb that is then fed back as movement from the
phantom limb in virtual reality (e.g., Murray et al., 2007)
and the use of full-body virtual feedback (e.g., Schmalzl et
al., 2011) might also be useful treatment options and could
be even more effective in altering the distorted body image
and restoring function.

Neurofeedback and Biofeedback
Neurofeedback refers to all techniques that make use of
brain activity to influence the processing of pain-related
stimuli or the experience of chronic pain. In the electroen-
cephalogram, three types of ERPs have been identified as
correlates of pain perception (they cannot be called mea-
sures of pain because they are influenced by a number of
factors such as attention and general activation): (a) brain-
stem potentials (10 to 15 ms after the application of the
stimulus); (b) potentials of short latency (15 to 20 ms after
the application of the stimulus), which are probably based
on thalamocortical sources; and (c) potentials of long la-
tency (50 to 200 ms after the stimulus), which have a
cortical basis (Flor & Meyer, 2011). Subjective pain per-
ception correlates with the amplitude of the ERP in the
150 –260 ms range, which may provide information in
addition to the pain rating.

The effects of EEG feedback on pain-related cortical
responses were studied by Miltner, Larbig, and Braun
(1988), who showed that the pain-related brain potential
can be modified by feedback and that the increased or

decreased amplitude of the N150/P260 components of the
electroencephalogram is also reflected in increased or de-
creased pain ratings. Dowman (1996) could not replicate
these reports that the operantly conditioned P260 compo-
nent of the somatosensory evoked potential is correlated
with altered pain ratings and altered nociceptive reflexes.
There is still no evidence that these potentials can be
changed by feedback in patients with chronic pain.

EEG measures have also been used to study the char-
acteristics of headache patients, especially those with mi-
graine. Siniatchkin, Gerber, Kropp, and Vein (1998) inves-
tigated slow cortical potentials of the electroencephalogram
in migraineurs and found them to be elevated, indicative of
cortical hyperexcitability. They tested the efficacy of bio-
feedback training of slow cortical potentials in young mi-
graineurs. Children with migraine are characterized by
increased cortical excitability they cannot control. During
extended training, the children acquired this skill and could
reduce cortical negativity, which was accompanied by a
significant reduction of days with migraine and other head-
ache parameters.

The EEG power spectrum provides a measure of the
relative “power” of the EEG waves within a certain fre-
quency band. Usually the bands that are discriminated are
delta (0.5–3.5 Hz; profound sleep and pathology), theta
(3.5–7.5 Hz; deep sleep, but also focused attention if lo-
calized in the frontal area), alpha (8 –12 Hz; relaxed wake-
fulness with the eyes closed), and beta (13–30 Hz; …

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  • Unlimited revisions
  • Plagiarism-free guarantee
  • Money-back guarantee
  • 24/7 support
On-demand options
  • Writer’s samples
  • Part-by-part delivery
  • Overnight delivery
  • Copies of used sources
  • Expert Proofreading
Paper format
  • 275 words per page
  • 12 pt Arial/Times New Roman
  • Double line spacing
  • Any citation style (APA, MLA, Chicago/Turabian, Harvard)

Our guarantees

We value our customers and so we ensure that what we do is 100% original..
With us you are guaranteed of quality work done by our qualified experts.Your information and everything that you do with us is kept completely confidential.

Money-back guarantee

You have to be 100% sure of the quality of your product to give a money-back guarantee. This describes us perfectly. Make sure that this guarantee is totally transparent.

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Zero-plagiarism guarantee

The Product ordered is guaranteed to be original. Orders are checked by the most advanced anti-plagiarism software in the market to assure that the Product is 100% original. The Company has a zero tolerance policy for plagiarism.

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Free-revision policy

The Free Revision policy is a courtesy service that the Company provides to help ensure Customer’s total satisfaction with the completed Order. To receive free revision the Company requires that the Customer provide the request within fourteen (14) days from the first completion date and within a period of thirty (30) days for dissertations.

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Privacy policy

The Company is committed to protect the privacy of the Customer and it will never resell or share any of Customer’s personal information, including credit card data, with any third party. All the online transactions are processed through the secure and reliable online payment systems.

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Fair-cooperation guarantee

By placing an order with us, you agree to the service we provide. We will endear to do all that it takes to deliver a comprehensive paper as per your requirements. We also count on your cooperation to ensure that we deliver on this mandate.

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Calculate the price of your order

550 words
We'll send you the first draft for approval by September 11, 2018 at 10:52 AM
Total price:
$26
The price is based on these factors:
Academic level
Number of pages
Urgency

Order your paper today and save 15% with the discount code HAPPY

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Feel free to ask questions, clarifications, or discounts available when placing an order.