VOL
VOL XXI NO 13JUNE
Diagnosis, Prevalence, Characteristics,
Vol.XXI,Issue1
and Treatment
Editorial Board of Central Poststroke Pain
P
Editor-in-Chief
ain is a common complaint
JaneC.Ballantyne,MD,FRCA
following stroke,
Anesthesiology,PainMedicine reported
USA
in 1155% of stroke sur-
AdvisoryBoard
vivors.5,24,31,47 Poststroke
painMichaelJ.Cousins,MD,DSC
can arise from muscles, joints,
PainMedicine,PalliativeMedicine
or viscera,
Australia or from the peripheral
or central nervous system.39,63 The
most common types of poststroke
pain include hemiplegic shoulder
pain, pain due to painful spasms or
spasticity, poststroke headache, and
central poststroke pain. Patients may
have several types of poststroke pain
concomitantly. 24,39,63
Risk factors for poststroke pain
include young age, female sex, stroke
severity, spasticity, diabetes, sensory
disturbance, depression, and pain
before stroke onset. Up to 40% of
stroke patients who develop post-
stroke pain have other pre-existing
pain conditions.31 Poststroke pain
can reduce quality of life, increase
fatigue, complicate rehabilitation,
disturb sleep, affect mood and social
functioning, and increase long-term
Henriette M. Klit, MD
Henriette M. Klit, MD
Danish Pain Research Center
Aarhus, Denmark
Email: henriette.klit@clin.au.dk
Nanna Brix Finnerup, MD
Danish Pain Research Center
Aarhus, Denmark
Email: finnerup@clin.au.dk
Troels Staehelin Jensen, MD, DMSc
Danish Pain Research Center
Aarhus, Denmark
Email: tsjensen@clin.au.dk
PAIN: CLINICAL UPDATES APRIL 2015
XXIII 2013
APRIL 2015
June2013
PsychosocialAspectsofChronicPelvicPain
mortality.49,62,63 Since the incidence severe pain attributed to a vascular
of stroke increases with age and life lesion in the thalamus. This pain syn-
expectancy is rising, the prevalence drome became known as the Dejerine-
Pain is unwanted, is unfortunately common, and remains essential for survival (i.e.,
of poststroke pain,and
including central Roussy syndrome or thalamic pain of
evading danger) facilitating medical diagnoses. This complex amalgamation
poststroke pain (CPSP), is also likely syndrome. Experts later demonstrated
sensation, emotions, and thoughts manifests itself as pain behavior. Pain is a moti-
-
vating factor
to increase forfuture.
in the physician
It isconsultations
impor- 1
and extrathalamic
that for emergency vascular
department visitscan
lesions and is
tant to assess the presence
of pain in stroke survivors
because of its negative
impact on quality of life and
rehabilitation.
Central Poststroke Pain
CPSP is a central neuropathic
pain condition in which pain
arises as a direct result of
a cerebrovascular lesion in
the central somatosensory
nervous system. Other com-
also cause pain, and so the term cen-
mon causes of central neuropathic pain
tral poststroke pain is preferable.27,28,54
include multiple sclerosis, spinal cord
In this issue of Pain: Clinical Updates we
injury, syringomyelia and syringobul-
will review the diagnosis, prevalence,
bia, tumors and abscesses in the central
clinical characteristics, and evidence-
nervous system (CNS), and other
based treatment of CPSP.
inflammatory CNS diseases (e.g., my-
elitis). Like poststroke pain in general,
Diagnosing CPSP
CPSP has a negative effect on quality of
life in stroke survivors.12 It is important to distinguish between
Central poststroke pain was first nociceptive and neuropathic pain in
described by the French neurolo- stroke patients, as the choice of treat-
gist Djerine and the Swiss-French ment often differs in these conditions.
neuropathologist Roussy in 1906 in However, there are no particular
their famous paper Le syndrome features in the history or the clinical
thalamique.13 The authors reported a findings that can separate neuropathic
small series of patients with a constel- and musculoskeletal pain with cer-
lation of neurological symptoms and tainty, and making such a distinction
1
can sometimes be difficult.53 A further
complication is the fact that stroke pa-
tients often have other pain conditions.
Also, some poststroke pain conditions
may be mixed pain types, as in the case
of shoulder pain. In 2008, a new grading
system emerged for neuropathic pain
with different inclusion criteria for
neuropathic pain, but these criteria
did not include the exclusion of other
causes of pain. Therefore, in 2009 we
published a proposal for diagnostic
criteria for CPSP based on the grad-
ing system,37 including mandatory and
supportive criteria. The mandatory cri-
teria for the diagnosis of CPSP include
the following: pain within an area of
the body corresponding to the CNS
lesion, a history suggestive of a stroke
and onset of pain at or after stroke
onset, confirmation of a CNS lesion by
imaging and/or negative or positive
sensory signs confined to the area of
the body corresponding to the CNS
lesion, and, if possible, exclusion of
other causes of pain such as nocicep-
tive or peripheral neuropathic pain.
The supportive criteria include: no
primary association with movement,
inflammation, or other local tissue
damage; certain descriptors such as
Poststroke pain can reduce quality of life, increase fatigue,
complicate rehabilitation, disturb sleep, affect mood and
social functioning, and increase long-term mortality.
burning, painful cold, electric shocks,
aching, pressing, stinging, and pins
and needles; and allodynia or dyses-
thesia to touch. In the same paper, we
published a grading system, based on
the diagnostic criteria, enabling re-
searchers to classify CPSP as possible,
probable, or definite (Table 1).
As implied by the proposed
diagnostic criteria, the diagnosis of
CPSP is based on the stroke and pain
history and the clinical examination
with a focus on the sensory find-
ings. If possible, the vascular lesion
should be visualized by imaging,
either computed tomography (CT) or
magnetic resonance imaging (MRI).
Other useful tools include pain draw-
ings and standardized pain question-
naires, including neuropathic pain
scales such as the DN4 (Douleur
Neuropathique en 4 Questions) and
the Leeds Assessment of Neuropathic
Symptoms and Signs (LANSS) scale.
Sometimes it is necessary to perform
supplementary investigations, such as
quantitative sensory testing (QST),23
additional imaging, or neurophysio-
logical examinations, to rule out other
causes of pain.
Prevalence
The reported prevalence of central
poststroke pain varies between 1% and
12%.2,9,25,31,36,39,42,47,52,61,64 In a population-
based study from Denmark, based on
a questionnaire of 608 stroke patients
and a clinical examination of 51 pa-
tients with possible CPSP, the minimum
prevalence of definite or probable CPSP
was 7.3% (N = 35) and 8.6% (N = 41) if
CPSP-like dysesthesia was included.36
The median time of follow-up was 4.4
years.
In a Finnish study of CPSP in
young patients with ischemic stroke
with a median follow-up time of 8.5
years, a total of 49 out of 824 patients
had CPSP, corresponding to a preva-
23
lence of 5.9%. Out of the remaining
775 patients, 246 had sensory abnor-
malities and 529 had neither sensory

Table 1
Grading system for central poststroke pain (CPSP)*
Criteria to Be Evaluated for Each Patient Comments
1. Exclusion of other likely causes of pain No other obvious cause of pain
No primary relation to movement, inflammation, or other local tissue damage
Descriptors such as burning, painful cold, electric shocks

2. Pain with a distinct neuroanatomically plausible Pain localized unilaterally or crossed face/body in a body area corresponding to
distribution a cerebrovascular lesion

3. A history suggestive of a stroke Sudden onset of neurological symptoms with pain starting at or after stroke
onset

4. Demonstration of the distinct neuroanatomically Findings of positive and/or negative sensory signs in an anatomically plausible
plausible distribution by a clinical neurological distribution and pain localized within a territory of sensory abnormality
examination
5. Demonstration of the relevant vascular lesion Visualization of a lesion that can explain the distribution of sensory findings,
by imaging either CT or MRI
* Possible CPSP: Criteria 1 + 2 + 3 fulfilled. Probable CPSP: Criteria 1 + 2 + 3 fulfilled plus either 4 or 5. Definite CPSP: Criteria
15 fulfilled.

2 PAIN: CLINICAL UPDATES APRIL 2015

abnormalities nor CPSP. The investiga-
tors found that patients with CPSP had
a lower quality of life compared with
patients without CPSP, both with and
without sensory abnormalities. Forty
(82%) of the CPSP patients had other
concomitant pain complaints.25 In this
study, as in other studies on CPSP,
the presence of CPSP was associated
with stroke severity, but not with age
at stroke onset, sex, or stroke subtype
based on stroke etiology.
In a populationbased study from
Rimini, Italy, published in 2013, CPSP
was diagnosed in 66 out of 601 pa-
tients, corresponding to an incidence
of 11%.52 CPSP was equally prevalent in
males and females. In the majority of
patients, pain developed immediately
(58%) or within the first month after a
stroke (20%).
CPSP can develop after both isch-
emic and hemorrhagic vascular lesions
anywhere in the somatosensory part of
the CNS,41 but there are some indica-
tions that the incidence of CPSP may
be higher following lesions in certain
areas of the brain, including the thala-
mus, the opercular-insular region, and
the brainstem. 6,17,18,35,40,43,48
Given that
all patients with CPSP have sensory
abnormalities, it is not surprising that
patients with sensory abnormalities
have an increased risk of developing
CPSP. Findings of early evoked dyses-
thesia or evoked pain at stroke onset
are also associated with an increased
risk of developing CPSP. 38
Pain Characteristics
The time reported from stroke to
pain onset varies. In the majority of
patients, pain onset is either immedi-
ate or within the first 13 months
after a stroke. 2,25,36,52
The onset of pain
is often insidious.
The symptoms range from bother-
some dysesthesia to severe pain. The
PAIN: CLINICAL UPDATES APRIL 2015
majority of patients report moderate
pain.2,44,52,64 In a population-based study,
the reported median pain intensity
was 5 on a numeric rating scale (range
010).36 The pain can be spontaneous,
evoked, or both. Pain-evoking factors
can be internal stimuli, such as stress
and emotions, or external stimuli,
such as touch and cold.9,44 Pain usually
seems to be chronic, often life-long and
constant, but in a few patients, the pain
reduces over time. 38
Sensory descriptors used in
patients with CPSP include burning,
aching, pricking, lacerating, shooting,
squeezing, throbbing, sharp, stabbing,
painful pins and needles, dull, and
cramping. 2,7,22,44,55,64
Clinical Findings
Sensory function can be examined
using simple bedside testing, such
as cotton wool for touch, a sharp or
pointed stimulus for pain, a metal
thermal roller (or any metal object) for
cold sensation, and a soft brush for dy-
namic allodynia.23 The area of pain in
patients with CPSP varies in size and
distribution.2,9,36,38,44 In some patients
only small areas are involved, such as
parts of the face or one foot. In other
patients, the pain affects larger areas
such as one side of the body, an arm
or a leg, or one entire half of the body
(always contralateral to a hemispheric
vascular lesion). The pain is always
located within an area of sensory
abnormalities.2,9,44 As in other neuro-
pathic pain conditions, there is often a
combination of positive and nega-
tive sensory findings on the sensory
examination. Thus, there may be loss
of sensitivity to one sensory modality
combined with hypersensitivity to an-
other sensory modality, such as loss of
sensitivity to heat and hypersensitiv-
ity to touch. Hyperalgesia, dysesthesia,
and allodynia are common findings in
Sensory descriptors used
in patients with CPSP
include burning, aching,
pricking, lacerating, shooting,
squeezing, throbbing, sharp,
stabbing, painful pins and
needles, dull, and cramping.
patients with CPSP. For a definition of
these terms, see the pain taxonomy
published by IASP.1 In one study,36
pinprick hyperalgesia was present in
57%, cold allodynia in 40%, and brush-
evoked dysesthesia in 51% of patients
with CPSP.
Abnormal pain and tempera-
ture sensation is found in almost
all patients with CPSP. The sensory
processing of temperature and pain
occurs via the spinothalamic tract and
the spinotrigeminothalamic projecting
system. Abnormal pain and tempera-
ture sensation is quite common in
stroke patients without CPSP.2,8,58 For
this reason, some experts suggest that
a lesion of the spinothalamic tracks is
necessary, but not sufficient, to cause
CPSP. There are further indications
that patients with a partial lesion of
the spinothalamic-thalamocortical
pathways may be more prone to de-
velop CPSP compared to patients with
complete lesions in these pathways.30
Other Findings
There are no universal non-sensory
neurological findings in CPSP.44 The
clinical non-sensory findings in pa-
tients with CPSP reflect the location
and size of the vascular lesion and are
not correlated to the pain. Choreoath-
etoid movements, which were part of
the original description of thalamic
pain as described by Dejerine and
Roussy,13 only rarely occur in patients
with CPSP.6,10
3

Editorial Board
Editor-in-Chief
Jane C. Ballantyne, MD, FRCA
Anesthesiology, Pain Medicine
USA
Advisory Board
Michael J. Cousins, MD, DSC
Pain Medicine, Palliative Medicine
Australia
Maria Adele Giamberardino, MD
Internal Medicine, Physiology
Italy
Robert N. Jamison, PhD
Psychology, Pain Assessment
USA
Patricia A. McGrath, PhD
Psychology, Pediatric Pain
Canada
M.R. Rajagopal, MD
Pain Medicine, Palliative Medicine
India
Maree T. Smith, PhD
Pharmacology
Australia
Claudia Sommer, MD
Neurology
Germany
Harrit M. Wittink, PhD, PT
Physical Therapy
The Netherlands
Publishing
Daniel J. Levin, Publications Director
Elizabeth Endres, Consulting Editor
Timely topics in pain research and treatment
have been selected for publication, but the
information provided and opinions expressed
have not involved any verification of the find-
ings, conclusions, and opinions by IASP. Thus,
opinions expressed in Pain: Clinical Updates do
not necessarily reflect those of IASP or of the
Officers or Councilors. No responsibility is as-
sumed by IASP for any injury and/or damage
to persons or property as a matter of product
liability, negligence, or from any use of any
methods, products, instruction, or ideas con-
tained in the material herein.
Because of the rapid advances in the
medical sciences, the publisher recommends
independent verification of diagnoses and
drug dosages.
Copyright 2014 International Association
for the Study of Pain. All rights reserved.
For permission to reprint or translate
this article, contact:
International Association
for the Study of Pain
1510 H Street NW, Suite 600,
Washington, D.C. 20005-1020, USA
Tel: +1-202-524-5300
Fax: +1-202-524-5301
Email: iaspdesk@iasp-pain.org
www.iasp-pain.org
4 PAIN: CLINICAL UPDATES APRIL 2015
Imaging studies have illustrated
that a lesion anywhere in the somato-
sensory pathways, including the
thalamus and the thalamocortical
projections (especially to the oper-
cular-insular region) 20,30
can cause
CPSP.2,11 PET studies have document-
ed flow changes in the thalamus in
patients with CPSP, both at rest and
with evoked pain. 19,51
Neurophysiolog-
ical recordings with microelectrodes
have measured abnormal spontane-
ous and evoked activity in the thala-
mus of patients with CPSP. 29,45
More
recently, MRI with diffusion tensor
tractography has illustrated changes
in the spinothalamic tracts.30
It is still puzzling why,
in patients with almost
identical stroke lesions
and clinical findings, some
patients develop CPSP and
others do not.
Pathophysiology
The underlying pathophysiology of
CPSP is not well understood. It is still
puzzling why, in patients with almost
identical stroke lesions and clinical
findings, some patients develop CPSP
and others do not. As already men-
tioned, lesions of the spinothalamic
tracts have been implicated in the
development of CPSP. A structural MRI
study of stroke patients with thalamic
lesions, with and without pain, found
a high odds ratio for developing CPSP
in patients with lesions involving the
ventral posterior nucleus/pulvinar bor-
der zone of the thalamus, an area pre-
viously linked to signaling of pain and
temperature. Given that all patients
56
have pain within an area of sensory
abnormalities, deafferentation is also
thought to play an important role. The
fact that findings of hypersensitivity is
common and can precede the develop-
ment of CPSP in stroke patients implies
that mechanisms involving neuronal
hyperexcitability, such as central
sensitization or disinhibition, may be
involved.38 Alterations in activity seen
on functional imaging and changes in
electric activity as illustrated by neu-
rophysiological findings suggest that
neuroplasticity may also play a role.
Treatment
Treatment of CPSP is difficult owing
to the limited efficacy of the available
drugs and their dose-limiting side
effects. Treating CPSP is therefore
a continuous challenge. Only a few
double-blinded, placebo-controlled tri-
als have been published on CPSP. These
trials are summarized in Table 2.32
In line with other neuropathic
pain conditions, CPSP may respond
to pregabalin and amitriptyline,15
although one negative study has been
published.34 Lamotrigine may be effec-
tive against ongoing pain and cold-
evoked pain in CPSP,57 but its effect
in other neuropathic pain conditions
is inconsistent. Duloxetine relieved
dynamic mechanical and cold allodynia
in patients with CPSP or spinal cord
injury,60 but the effect on ongoing pain
did not reach statistical significance (P
= 0.056). Given the limited evidence for
treatment of CPSP, it seems reasonable
to try treatments that have efficacy in
other central pain conditions or periph-
eral neuropathic pain conditions, and
the results of trials in CPSP do not con-
tradict general treatment recommen-
dations for neuropathic pain. Tricyclic
antidepressants (TCAs), serotonin-
norepinephrine reuptake inhibitors
(SNRIs), pregabalin, and gabapentin
are proposed as first-line treatment,
while tramadol is recommended as
second-line and strong opioids as third
 Table 2
Oral double-blinded placebo-controlled trials on CPSP
Dosage Drop-
Drug (mg/day) Outcome No. Patients outs NNT Reference Design
Pregabalin 125600 Positive 40 mixed CP (19 7 4.0 Vranken et al. Parallel, flexible-dose
CPSP, 21 SCI) 200859
Lamotrigine 200 Positive 30 CPSP 10 NA Vestergaard et Crossover
al. 200157
Amitriptyline 75 Positive 15 CPSP 0 1.7 Leijon et al. Crossover, 3-phase
198944
Carbamazepine 800 Negative 14 CPSP 0 - Leijon et al. Crossover, 3-phase
198944
Levetiracetam 10003000 Negative 42 CPSP 9 - Jungehulsing Crossover
et al. 201332
Pregabalin 150600 Negative 219 CPSP 36 - Kim et al. Parallel, flexible-dose
201134
Duloxetine 60120 Negative 48 mixed CP (13 4 - Vranken et al. Parallel, flexible-dose
CPSP, 34 SCI, 1 201160
other)
Abbreviations: CP, central pain; CPSP, central poststroke pain; NNT, number needed to treat; SCI, spinal cord injury.

line-treatment.15 At present there is no
evidence for combination therapy in
CPSP and only limited evidence for its
use in other neuropathic pain condi-
tions. It may, however, be indicated in
patients with partial relief from taking
two drugs.21 When deciding on treat-
ment, the clinician should keep in mind
potential side effects and contraindica-
tions, but also concomitant symptoms,
such as depression or sleep disorders,
that may respond well to certain treat-
ments. Other concomitant nociceptive
pain conditions should be identified
and managed as well.
Nonpharmacological treatment
including repetitive transcranial mag-
netic stimulation (rTMS), deep brain
stimulation (DBS) and motor cortex
stimulation (MCS)has been reported
in case series and brief reports, but
there are no controlled trials in this
field. In a recent review of interven-
tional treatment of neuropathic pain,
the authors conclude that owing to
low-quality evidence, recommenda-
tions for MCS and DBS are inconclu-
sive in the treatment of CPSP. In this
14
review, the authors recommend that
spinal cord stimulation (SCS) should
generally not be used for CPSP, on
the basis of a single unfavorable case
series. Single sessions of rTMS can give
short-lasting pain relief in patients
with CPSP and other pain conditions.
There are some indications that re-
peated application of rTMS may offer
longer-lasting pain relief.26,32,50 Some
patients may benefit from other treat-
ment possibilities including psycho-
logical or behavioral therapy, physio-
therapy, or educational programs.46
In our clinic, we use a person-
alized pharmacological treatment
strategy, taking into account concom-
itant medication and other diseases
and symptoms, such as depression
or sleep problems, and continuously
weighing benefits and side effects.
We usually start with an antidepres-
sant (TCA or SNRI), gabapentin, or
pregabalin. The typical starting dose
of the TCA is 25 mg at night, increas-
ing slowly (especially in the elderly)
by 10 mg per week. If the TCA is not
tolerated or is contraindicated, an
SNRI can be used at night instead.
The starting dose of gabapentin is
usually 300 mg, increasing by 300 mg
every 37 days up to a maximum dose
of 2400 mg/day. If gabapentin is not
tolerated, pregabalin can be tried with
a starting dose of 25 mg/day. If pain
3,4
relief is not sufficient, a combination
of antidepressants and antiepileptics
can be tried. Tramadol can be used as
an add-on medication.15,16 The most
common side effects of gabapentin and
pregabalin include sedation, dizziness,
and edema. TCA side effects include
cardiac, anticholinergic, and sedation
issues. If necessary, we refer patients
to the pain clinics physiotherapist or
psychologist for individual treatment.
Future Perspectives
There is a great need to identify better
treatment regimes. Unfortunately,
at present, only a few high-quality
double-blinded randomized trials have
focused on the treatment of CPSP.
In recent years, several animal
models mimicking CPSP have been
developed. We hope they will offer
new insight into the pathophysiology
of CPSP, enabling the development of
mechanism-based treatment trials.

PAIN: CLINICAL UPDATES APRIL 2015 5

Combination therapy is often used in
clinical practice. Future trials in this
field should guide us to the best combi-
nations and dosages.
Looking at several combined pre-
dictors of CPSP such as localization in
certain thalamic regions and findings
of early evoked pain and dysesthesia
could perhaps identify patients at
higher risk for the development of
CPSP. In these patients, preventive
trials could be feasible. Also it could
be of interest to study the natural his-
tory of CPSP in long-term follow-up
studies. Such studies could hopefully
contribute to our understanding of
the prognosis and mechanisms be-
hind CPSP.

References
1. International Association for the Study of Pain. IASP pain taxonomy.
Available at: http://iasp-pain.org/taxonomy.
2. Andersen G, Vestergaard K, Ingeman-Nielsen M, Jensen TS. Incidence of
central post-stroke pain. Pain 1995;61:18793.
3. Andre-Obadia N, Mertens P, Gueguen A, Peyron R, Garcia-Larrea L. Pain
relief by rTMS: differential effect of current flow but no specific action on pain
subtypes. Neurology 2008;71:83340.
4. Andre-Obadia N, Peyron R, Mertens P, Mauguiere F, Laurent B, Garcia-
Larrea L. Transcranial magnetic stimulation for pain control. Double-blind
study of different frequencies against placebo, and correlation with motor
cortex stimulation efficacy. Clin Neurophysiol 2006;117:153644.
5. Appelros P. Prevalence and predictors of pain and fatigue after stroke: a
population-based study. Int J Rehabil Res 2006;29:32933.
6. Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: clinical syndromes,
etiology, and prognosis. Neurology 1988;38:83748.
7. Boivie J. Central post-stroke pain. In: Cervero F, Jensen TS, editors. Hand-
book of clinical neurology, Vol. 81 (3rd series). Elsevier; 2006. p. 71530.
8. Boivie J, Leijon G, Johansson I. Central post-stroke pain: a study of
the mechanisms through analyses of the sensory abnormalities. Pain
1989;37:17385.
21. Gilron I, Dickenson AH. Emerging drugs for neuropathic pain. Expert Opin
Emerg Drugs 2014;19:32941.
22. Greenspan JD, Ohara S, Sarlani E, Lenz FA. Allodynia in patients with
post-stroke central pain (CPSP) studied by statistical quantitative sensory test-
ing within individuals. Pain 2004;109:35766.
23. Haanp M, Attal N, Backonja M, Baron R, Bennett M, Bouhassira D,
Cruccu G, Hansson P, Haythornthwaite JA, Iannetti GD, Jensen TS, Kauppila
T, Nurmikko TJ, Rice AS, Rowbotham M, Serra J, Sommer C, Smith BH, Treede
RD. NeuPSIG guidelines on neuropathic pain assessment. Pain 2011;152:1427.
24. Hansen AP, Marcussen NS, Klit H, Andersen G, Finnerup NB, Jensen TS.
Pain following stroke: a prospective study. Eur J Pain 2012;16:112836.
25. Harno H, Haapaniemi E, Putaala J, Haanp M, Makela JP, Kalso E, Tatlisu-
mak T. Central poststroke pain in young ischemic stroke survivors in the
Helsinki Young Stroke Registry. Neurology 2014;83:114754.
26. Hasan M, Whiteley J, Bresnahan R, MacIver K, Sacco P, Das K, Nurmikko
T. Somatosensory change and pain relief induced by repetitive transcranial
magnetic stimulation in patients with central poststroke pain. Neuromodula-
tion 2014;17:7316.
27. Head H, Holmes G. Sensory Disturbances from cerebral lesions. Brain
1911;34:102254.

9. Bowsher D. Central pain: clinical and physiological characteristics. J Neurol
Neurosurg Psychiatry 1996;61:629.
10. Bowsher D, Lahuerta J, Brock L. Twelve cases of central pain, only three
with thalamic lesions. Pain 1984;18:S83.
11. Bowsher D, Leijon G, Thuomas KA. Central poststroke pain: correlation of
MRI with clinical pain characteristics and sensory abnormalities. Neurology
1998;51:13528.
12. Choi-Kwon S, Choi JM, Kwon SU, Kang DW, Kim JS. Factors that affect the
quality of life at 3 years post-stroke. J Clin Neurol 2006;2:3441.
13. Dejerine J, Roussy G. La syndrome thalamique. Rev Neurol (Paris)
1906;14:52132.
14. Dworkin RH, OConnor AB, Kent J, Mackey SC, Raja SN, Stacey BR, Levy
RM, Backonja M, Baron R, Harke H, Loeser JD, Treede RD, Turk DC, Wells CD.
Interventional management of neuropathic pain: NeuPSIG recommendations.
Pain 2013;154:224961.
15. Finnerup NB, Attal N, Haroutounian S, McNicol E, Baron R, Dworkin RH,
Gilron I, Haanp M, Hansson P, Jensen TS, Kamerman PR, Lund K, Moore
A, Raja SN, Rice AS, Rowbotham M, Sena E, Siddall P, Smith BH, Wallace M.
Pharmacotherapy for neuropathic pain in adults: a systematic review and
meta-analysis. Lancet Neurol 2015;14:16273.
16. Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for
neuropathic pain treatment: an evidence based proposal. Pain 2005;118:289
305.
17. Fitzek S, Baumgartner U, Fitzek C, Magerl W, Urban P, Thomke F, Marx J,
Treede RD, Stoeter P, Hopf HC. Mechanisms and predictors of chronic facial
pain in lateral medullary infarction. Ann Neurol 2001;49:493500.
18. Garcia-Larrea L. Insights gained into pain processing from patients with
focal brain lesions. Neurosci Lett 2012;520:18891.
19. Garcia-Larrea L, Maarrawi J, Peyron R, Costes N, Mertens P, Magnin M,
Laurent B. On the relation between sensory deafferentation, pain and tha-
lamic activity in Wallenbergs syndrome: a PET-scan study before and after
motor cortex stimulation. Eur J Pain 2006;10:67788.
20. Garcia-Larrea L, Perchet C, Creach C, Convers P, Peyron R, Laurent B,
Mauguiere F, Magnin M. Operculo-insular pain (parasylvian pain): a distinct
central pain syndrome. Brain 2010;133:252839.
28. Henry JL, Yashpal K, Lalloo C. Central poststroke pain: a persective. In:
Henry JL, Panju A, Yashpal K, editors. Central neuropathic pain: focus on
poststroke pain. Seattle: IASP Press; 2007. p. 35.
29. Hirayama T, Dostrovsky JO, Gorecki J, Tasker RR, Lenz FA. Recordings of
abnormal activity in patients with deafferentation and central pain. Stereotact
Funct Neurosurg 1989;52:1206.
30. Hong JH, Choi BY, Chang CH, Kim SH, Jung YJ, Lee DG, Kwon YH, Jang
SH. The prevalence of central poststroke pain according to the integrity of the
spino-thalamo-cortical pathway. Eur Neurol 2012;67:127.
31. Jonsson AC, Lindgren I, Hallstrom B, Norrving B, Lindgren A. Prevalence
and intensity of pain after stroke: a population based study focusing on pa-
tients perspectives. J Neurol Neurosurg Psychiatry 2006;77:5905.
32. Jungehulsing GJ, Israel H, Safar N, Taskin B, Nolte CH, Brunecker P, Wer-
necke KD, Villringer A. Levetiracetam in patients with central neuropathic
post-stroke pain: a randomized, double-blind, placebo-controlled trial. Eur J
Neurol 2013;20:3317.
33. Khedr EM, Kotb H, Kamel NF, Ahmed MA, Sadek R, Rothwell JC. Longlast-
ing antalgic effects of daily sessions of repetitive transcranial magnetic
stimulation in central and peripheral neuropathic pain. J Neurol Neurosurg
Psychiatry 2005;76:8338.
34. Kim JS, Bashford G, Murphy TK, Martin A, Dror V, Cheung R. Safety
and efficacy of pregabalin in patients with central post-stroke pain. Pain
2011;152:101823.
35. Kim JS, Choi-Kwon S. Sensory sequelae of medullary infarction: differenc-
es between lateral and medial medullary syndrome. Stroke 1999;30:2697703.
36. Klit H, Finnerup NB, Andersen G, Jensen TS. Central poststroke pain: a
population-based study. Pain 2011;152:81824.
37. Klit H, Finnerup NB, Jensen TS. Central post-stroke pain: clinical charac-
teristics, pathophysiology, and management. Lancet Neurol 2009;8:85768.
38. Klit H, Hansen AP, Marcussen NS, Finnerup NB, Jensen TS. Early
evoked pain or dysesthesia is a predictor of central poststroke pain. Pain
2014;155:2699706.
39. Kong KH, Woon VC, Yang SY. Prevalence of chronic pain and its impact
on health-related quality of life in stroke survivors. Arch Phys Med Rehabil
2004;85:3540.

6 PAIN: CLINICAL UPDATES APRIL 2015

40. Krause T, Brunecker P, Pittl S, Taskin B, Laubisch D, Winter B, Lentza ME, 52. Raffaeli W, Minella CE, Magnani F, Sarti D. Population-based study of
Malzahn U, Villringer K, Villringer A, Jungehulsing GJ. Thalamic sensory central post-stroke pain in Rimini district, Italy. J Pain Res 2013;6:70511.
strokes with and without pain: differences in lesion patterns in the ventral
53. Rasmussen PV, Sindrup SH, Jensen TS, Bach FW. Symptoms and signs in
posterior thalamus. J Neurol Neurosurg Psychiatry 2012;83:77684.
patients with suspected neuropathic pain. Pain 2004;110:4619.
41. Kumar B, Kalita J, Kumar G, Misra UK. Central poststroke pain: a review of
54. Riddoch G. The clinical features of central pain. I. Lancet 1938;231:10938.
pathophysiology and treatment. Anesth Analg 2009;108:164557.
55. Sposato LA, Sharma HA, Khan AR, Bartha R, Hachinski V. Thalamic cram-
42. Kuptniratsaikul V, Kovindha A, Suethanapornkul S, Manimmanakorn
plike pain. J Neurol Sci 2014;336:26972.
N, Archongka Y. Complications during the rehabilitation period in Thai
patients with stroke: a multicenter prospective study. Am J Phys Med Rehabil 56. Sprenger T, Seifert CL, Valet M, Andreou AP, Foerschler A, Zimmer C, Col-
2009;88:929. lins DL, Goadsby PJ, Tolle TR, Chakravarty MM. Assessing the risk of central
post-stroke pain of thalamic origin by lesion mapping. Brain 2012;135:253645.
43. Lampl C, Yazdi K, Roper C. Amitriptyline in the prophylaxis of central
poststroke pain. Preliminary results of 39 patients in a placebo-controlled, 57. Vestergaard K, Andersen G, Gottrup H, Kristensen BT, Jensen TS.
long-term study. Stroke 2002;33:30302. Lamotrigine for central poststroke pain: a randomized controlled trial. Neurol-
ogy 2001;56:18490.
44. Leijon G, Boivie J, Johansson I. Central post-stroke pain: neurological
symptoms and pain characteristics. Pain 1989;36:1325. 58. Vestergaard K, Nielsen J, Andersen G, Ingeman-Nielsen M, Arendt-Niel-
sen L, Jensen TS. Sensory abnormalities in consecutive, unselected patients
45. Lenz FA, Tasker RR, Dostrovsky JO, Kwan HC, Gorecki J, Hirayama T,
with central post-stroke pain. Pain 1995;61:17786.
Murphy JT. Abnormal single-unit activity recorded in the somatosensory
thalamus of a quadriplegic patient with central pain. Pain 1987;31:22536. 59. Vranken JH, Dijkgraaf MG, Kruis MR, van der Vegt MH, Hollmann MW,
Heesen M. Pregabalin in patients with central neuropathic pain: a random-
46. Lofgren M, Norrbrink C. But I know what workspatients experi-
ized, double-blind, placebo-controlled trial of a flexible-dose regimen. Pain
ence of spinal cord injury neuropathic pain management. Disabil Rehabil
2008;136:1507.
2012;34:213947.
60. Vranken JH, Hollmann MW, van der Vegt MH, Kruis MR, Heesen M, Vos
47. Lundstrom E, Smits A, Terent A, Borg J. Risk factors for stroke-related pain
K, Pijl AJ, Dijkgraaf MGW. Duloxetine in patients with central neuropathic
1 year after first-ever stroke. Eur J Neurol 2009;16:18893.
pain caused by spinal cord injury or stroke: a randomized, double-blind,
48. MacGowan DJ, Janal MN, Clark WC, Wharton RN, Lazar RM, Sacco placebo-controlled trial. Pain 2011;152:26773.
RL, Mohr JP. Central poststroke pain and Wallenbergs lateral medullary
61. Weimar C, Kloke M, Schlott M, Katsarava Z, Diener HC. Central post-
infarction: frequency, character, and determinants in 63 patients. Neurology
stroke pain in a consecutive cohort of stroke patients. Cerebrovasc Dis
1997;49:1205.
2002;14:2613.
49. Naess H, Lunde L, Brogger J, Waje-Andreassen U. Post-stroke pain on
62. Widar M, Ahlstrom G, Ek AC. Health-related quality of life in persons with
long-term follow-up: the Bergen stroke study. J Neurol 2010;257:144652.
long-term pain after a stroke. J Clin Nurs 2004;13:497505.
50. Ohn SH, Chang WH, Park CH, Kim ST, Lee JI, Pascual-Leone A, Kim YH.
63. Widar M, Ek AC, Ahlstrom G. Coping with long-term pain after a stroke. J
Neural correlates of the antinociceptive effects of repetitive transcranial
Pain Symptom Manage 2004;27:21525.
magnetic stimulation on central pain after stroke. Neurorehabil Neural Repair
2012;26:34452. 64. Widar M, Samuelsson L, Karlsson-Tivenius S, Ahlstrom G. Long-term pain
conditions after a stroke. J Rehabil Med 2002;34:16570.
51. Peyron R, Garcia-Larrea L, Gregoire MC, Convers P, Richard A, Lavenne
F, Barral FG, Mauguiere F, Michel D, Laurent B. Parietal and cingulate pro-
cesses in central pain. A combined positron emission tomography (PET) and
functional magnetic resonance imaging (fMRI) study of an unusual case. Pain
2000;84:7787.

Do you still want to receive Pain: Clinical Updates by mail?

To save printing and postage costs, IASP hopes to reduce the number of copies we mail. Every issue appears on
our website, and we will alert you to new editions through the Pain: E-Monthly e-newsletter. If you would no
longer like to receive these printed copies, please send an email to iaspdesk@iasp-pain.org.

PAIN: CLINICAL UPDATES APRIL 2015 7