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General review

Pain after stroke: A review

B. Delpont a,b, C. Blanc b, G.V. Osseby b, M. Hervieu-Bègue b, M. Giroud b,*,

Y. Béjot b
a
CHU de Dijon Bourgogne, centre anti-douleur, 21079 Dijon, France
b
Unité de soins intensifs neuro-vasculaires et réseau bourgogne-AVC, CHU de Dijon Bourgogne, 14, rue Paul-Gaffarel,
21079 Dijon cedex, France

info article abstract

Article history: Pain after stroke (PAS) is a common clinical problem that is both underdiagnosed and
Received 26 June 2017 undertreated. Yet, it induces depression and cognitive troubles, and impairs quality of life.
Received in revised form To provide tools for practitioners, this report describes the most common PAS syndromes,
23 October 2017 including central post-stroke pain, spasticity and contractures, shoulder pain and complex
Accepted 20 November 2017 regional pain syndromes, as well as headache and chondrocalcinosis, along with their risk
Available online xxx factors, their prevention and their specific treatments. In addition, to ensure that the
compulsory post-stroke clinical assessment in France is optimal, it is recommended that
Keywords: clinicians be trained in how to diagnose and treat PAS, and even to prevent it by early
Pain identification of at-risk patients, with the aim to improve patients’ motor and cognitive
Stroke functions and quality of life.
Central post-stroke pain
# 2018 Elsevier Masson SAS. All rights reserved.
Complex regional pain
Shoulder

memory impairment, while the treatment itself of pain can

1. Introduction
Pain after stroke (PAS) remains an underrecognized medical
problem. Patients may fail to describe PAS [1,2] because of
aphasia, neglect syndrome or dementia, while physicians may
find it difficult to analyze PAS and treat it [3] (due to lack of
medical experience, use of different pain scales). PAS may also
be masked by other, non-motor symptoms of stroke such as
cognitive decline [4], fatigue [5], mood disorders and depres-
sion [6]. Moreover, there are as yet no specifically dedicated
PAS scales [7–10] which, given the heterogeneity of stroke, is
understandable. Yet, PAS can induce complications such as
depression [10,11], suicide [12], fatigue [5], sleep disorders and
contribute to cognitive impairment and post-stroke headache.
However, as post-stroke clinical assessment is now compul-
sory in France and given the usefulness of therapeutic
education, it is clearly necessary to review the risk factors,
causes, mechanisms and consequences of PAS with the aim of
improving quality of life for these patients.
2. Risk factors linked to PAS
Several factors are related to the onset of PAS [5,9], and two non-
modifiable factors are well known: old age [13]; and female
gender [9]. Pre-stroke conditions [9], such as depression,

* Corresponding author.
E-mail address: maurice.giroud@chu-dijon.fr (M. Giroud).
https://doi.org/10.1016/j.neurol.2017.11.011
0035-3787/# 2018 Elsevier Masson SAS. All rights reserved.

Please cite this article in press as: Delpont B, et al. Pain after stroke: A review. Revue neurologique (2018), https://doi.org/10.1016/
j.neurol.2017.11.011
NEUROL-1946; No. of Pages 4
2 revue neurologique xxx (2018) xxx–xxx
alcohol abuse, statin use, diabetes and peripheral artery
disease, may also have an impact on PAS. In addition, the
stroke mechanism and site of lesion(s) can increase the risk of
PAS, including: large-vessel ischemic stroke [13,14]; thalamic,
parietal, brain-stem and spinal cord localizations; and clinical
features such as spasticity, sensory deficit and motor palsy of
the upper limb.
3. Causes of PAS
Among the pathophysiological mechanisms of pain, PAS
depends on both neuropathic and nociceptive mechanisms.
The usual subtypes of PAS are central post-stroke pain, pain
secondary to spasticity and contractures, headache, shoulder
pain, complex regional pain [4,15] and chondrocalcinosis.
Various pain combinations are also possible [9].
3.1. Central post-stroke pain (CPSP)
This type of neuropathic pain results from vascular injury of
the pain-conducting pathways of the face, arms and/or legs.
These pathways are located within the central nervous system
(CNS), which includes the brain, brain-stem and spinal cord.
CPSP affects 8–30% of stroke patients [3,16,17] mainly at
the subacute and chronic stages [18]. It may develop
progressively for 3 to 6 months after stroke onset [17] while,
at the same time, increasing sensory loss and the onset of
dysesthesia (‘‘pins and needles’’ sensations) [19]. Typical
characteristics of CPSP are those of neuropathic pain, with
sudden, brief, intense pain with burning sensations, or
throbbing or shooting pain. The pain is on the side of the
body affected by the stroke [20].
There are three types of CPSP: constant pain; paroxysmal
pain; and hyperalgesia/allodynia [21,22]. It can be triggered by
movement or contact with water. Risk factors include
thalamic and parietal localizations of stroke [20,21] in young
patients with previous depression or tobacco use [22–24].
Other localizations frequently associated with CPSP include
brain-stem stroke (Wallenberg syndrome), right thalamic and
parietal stroke [20–22], lacunar stroke localized to the spino-
thalamic tracts [25–27] and spinal cord infarct observed after
vertebral artery dissection and inducing neuropathic pain in
all four limbs.
3.2. Treatment
Medications improve pain in 70% of stroke survivors with
CPSP, with tricyclic antidepressants and antiepileptic drugs
such as lamotrigine, gabapentin, topiramate, pregabalin and
amitriptyline, and selective serotonin reuptake inhibitors
(SSRIs) used as first-line drugs [3,5]. On the other hand,
intravenous lidocaine [28], oral ketamine [29], methylpredni-
sone and levetiracetam have not demonstrated their effecti-
veness in CPSP.
Neurostimulation of the motor cortex is effective in 50–
77% of CPSP cases [30,31], whereas deep brain stimulation
(DBS) has been rather disappointing. However, transcranial
magnetic stimulation (TMS) of the motor cortex may be
effective [32].
Please cite this article in press as: Delpont B, et al. Pain after stroke: A review. Revue neurologique (2018), https://doi.org/10.1016/
j.neurol.2017.11.011
3.3. Spasticity and contractures
Spasticity is commonly seen after stroke with hemiplegia
because it is the main symptom of pyramidal syndrome. These
hypertonic contractions, called ‘‘spastic dystonia’’, present
with stiffness during flexion of the upper limbs and during
extension of the lower limbs. Approximately 70% of patients
with spasticity also suffer from CPSP [33]. Its impact on quality
of life is major; assessment of the upper limbs can be
performed using a robotic device [34].
Spasticity may also induce spontaneous, painful spasms
and night cramps that can damage muscles and joints. The
prevalence of spasticity-related pain tends to peak at the
chronic stage [18].
Treatments to reduce reflex activity and muscle tone [35]
include passive stretching, injections of botulinum toxin type
A into spastic muscles, and medications such as baclofen and
tizanidine to ease stiffness. Surgery to lengthen tendons is
always a treatment of last resort.
3.4. Shoulder pain
This is commonly present on the side of the body affected by
stroke [36]. Musculoskeletal shoulder pain is characterized by
two mechanisms: frozen shoulder; and shoulder subluxation.
In frozen shoulder, which is due to capsulitis, the glenohu-
meral joint is very stiff and hurts during movement, whereas
shoulder subluxation is due to weakness of the muscles
supporting this joint [37].
Shoulder pain is reported in 25–50% of stroke patients [38].
Its prevalence is higher in the subacute and chronic stages
than in the acute stage [18]. Risk factors include stroke
severity, hyperspastic hemiplegia and sensory disorders, and
the result is a severe motor and functional handicap [39].
Symptoms to help recognize post-stroke shoulder pain are
supraspinatus tenderness, biceps tendon tenderness and
shoulder pain when the arm is fully pronated in extreme
flexion [38].
Prevention is possible, but has to be taught to caregivers, as
it involves appropriate arm positions during rest and the
flaccid stage of recovery, and support for the arm during
movement with the use of a hemi-tray [40].
When shoulder pain is present, it can be reduced by
providing the patient with a shoulder sling or strapping.
Analgesics and non-steroidal, anti-inflammatory, anti-spas-
modic drugs may be helpful [9] and may be used before
transcutaneous neuromuscular electrical stimulation.
3.5. Complex regional pain syndrome
This syndrome includes several symptoms, such as pain and
edema of the hand, and sudomotor and vasomotor changes
mainly in the affected hand, associated with bone demi-
neralization. Also known as ‘‘reflex sympathetic dystrophy’’,
‘‘causalgia’’ and ‘‘post-stroke shoulder – hand syndrome’’, it is
not easy to determine its frequency due to the lack of
consensus on its diagnostic criteria.
Usually, there is no identifiable neural lesion, whereas the
roles of sympathetic tracts, CNS, peripheral nerves, muscle
hypoxia, shoulder trauma and local inflammation have been
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revue neurologique xxx (2018) xxx–xxx
discussed elsewhere [41]. Magnetic resonance imaging (MRI)
may show soft tissue edema, skin thickening and bone
demineralization associated with changes affecting the nails.
In accordance with the pathophysiological hypothesis,
sympathetic nerve blocks in the stellate ganglia [42] may
reduce the pain, and mirror therapy can improve motor
recovery [43]. Although the classic medications for neuropa-
thic pain, such as analgesic drugs, can be used, they have not
shown much success. Bisphosphonates, however, are effica-
cious in reducing this pain [44].
3.6. Post-stroke headache
While the literature is somewhat lacking, some major points
are nevertheless well known: headache at stroke onset is
significantly predictive of headache at 6 months, affecting
around 10% of patients [5,15] in the acute post-stroke stage
[18]. Headache at stroke onset is also predictive of mortality at
30 days [45].
In general, post-stroke headache resembles tension heada-
che [6,9]. However, the cause of the stroke may lead to a
specific type of post-stroke headache. Strokes associated with
giant cell arteritis are followed by chronic headache, as
observed in four stroke patients in a cohort of 57 with giant cell
arteritis [46], whereas intermittent headaches were reported
in 10 patients experiencing stroke in moyamoya disease [47].
After cerebral artery dissection, headache may either continue
after stroke onset or the pre-stroke headache may disappear
[48]. This same variability is observed with migraine [49].
3.7. Chondrocalcinosis
Even though this disorder is not clearly reported as such in
literature, it is included here because of its frequent associa-
tion with stroke. The condition is due to deposits of
microcrystals of calcium pyrophosphate within joint cartilage.
Acute pain crises are reported within the first few days after
stroke onset, with inflammatory reactions in all joints, but
mostly in the knee and hand on the side of the hemiplegia.
Treatment with anti-inflammatory drugs is efficacious,
although pain due to chondrocalcinosis can become chronic
in elderly patients.
4. Conclusion
Pain is a frequent problem after stroke and has multiple
mechanisms and causes, which explains why it is difficult to
characterize every PAS syndrome and to treat every patient
with the same degree of efficacy. Nevertheless and despite
the different time courses of PAS, systematic follow-ups
every 6 months post-stroke at outpatient clinics appear to be
justified. Unfortunately, however, very few studies have
been specifically dedicated to treatment efficacy in cases of
PAS [18].
Disclosure of interest
The authors declare that they have no competing interest.
Please cite this article in press as: Delpont B, et al. Pain after stroke: A review. Revue neurologique (2018), https://doi.org/10.1016/
j.neurol.2017.11.011
3
Acknowledgments
We would like to thank Philip Bastable for reviewing the
English used in this manuscript.
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