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Pain After Stroke: A Review: Sciencedirect
Pain After Stroke: A Review: Sciencedirect
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General review
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
* 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
alcohol abuse, statin use, diabetes and peripheral artery 3.3. Spasticity and contractures
disease, may also have an impact on PAS. In addition, the
stroke mechanism and site of lesion(s) can increase the risk of Spasticity is commonly seen after stroke with hemiplegia
PAS, including: large-vessel ischemic stroke [13,14]; thalamic, because it is the main symptom of pyramidal syndrome. These
parietal, brain-stem and spinal cord localizations; and clinical hypertonic contractions, called ‘‘spastic dystonia’’, present
features such as spasticity, sensory deficit and motor palsy of with stiffness during flexion of the upper limbs and during
the upper limb. 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
3. Causes of PAS performed using a robotic device [34].
Spasticity may also induce spontaneous, painful spasms
Among the pathophysiological mechanisms of pain, PAS and night cramps that can damage muscles and joints. The
depends on both neuropathic and nociceptive mechanisms. prevalence of spasticity-related pain tends to peak at the
The usual subtypes of PAS are central post-stroke pain, pain chronic stage [18].
secondary to spasticity and contractures, headache, shoulder Treatments to reduce reflex activity and muscle tone [35]
pain, complex regional pain [4,15] and chondrocalcinosis. include passive stretching, injections of botulinum toxin type
Various pain combinations are also possible [9]. A into spastic muscles, and medications such as baclofen and
tizanidine to ease stiffness. Surgery to lengthen tendons is
3.1. Central post-stroke pain (CPSP) always a treatment of last resort.
This type of neuropathic pain results from vascular injury of 3.4. Shoulder pain
the pain-conducting pathways of the face, arms and/or legs.
These pathways are located within the central nervous system This is commonly present on the side of the body affected by
(CNS), which includes the brain, brain-stem and spinal cord. stroke [36]. Musculoskeletal shoulder pain is characterized by
CPSP affects 8–30% of stroke patients [3,16,17] mainly at two mechanisms: frozen shoulder; and shoulder subluxation.
the subacute and chronic stages [18]. It may develop In frozen shoulder, which is due to capsulitis, the glenohu-
progressively for 3 to 6 months after stroke onset [17] while, meral joint is very stiff and hurts during movement, whereas
at the same time, increasing sensory loss and the onset of shoulder subluxation is due to weakness of the muscles
dysesthesia (‘‘pins and needles’’ sensations) [19]. Typical supporting this joint [37].
characteristics of CPSP are those of neuropathic pain, with Shoulder pain is reported in 25–50% of stroke patients [38].
sudden, brief, intense pain with burning sensations, or Its prevalence is higher in the subacute and chronic stages
throbbing or shooting pain. The pain is on the side of the than in the acute stage [18]. Risk factors include stroke
body affected by the stroke [20]. severity, hyperspastic hemiplegia and sensory disorders, and
There are three types of CPSP: constant pain; paroxysmal the result is a severe motor and functional handicap [39].
pain; and hyperalgesia/allodynia [21,22]. It can be triggered by Symptoms to help recognize post-stroke shoulder pain are
movement or contact with water. Risk factors include supraspinatus tenderness, biceps tendon tenderness and
thalamic and parietal localizations of stroke [20,21] in young shoulder pain when the arm is fully pronated in extreme
patients with previous depression or tobacco use [22–24]. flexion [38].
Other localizations frequently associated with CPSP include Prevention is possible, but has to be taught to caregivers, as
brain-stem stroke (Wallenberg syndrome), right thalamic and it involves appropriate arm positions during rest and the
parietal stroke [20–22], lacunar stroke localized to the spino- flaccid stage of recovery, and support for the arm during
thalamic tracts [25–27] and spinal cord infarct observed after movement with the use of a hemi-tray [40].
vertebral artery dissection and inducing neuropathic pain in When shoulder pain is present, it can be reduced by
all four limbs. providing the patient with a shoulder sling or strapping.
Analgesics and non-steroidal, anti-inflammatory, anti-spas-
3.2. Treatment modic drugs may be helpful [9] and may be used before
transcutaneous neuromuscular electrical stimulation.
Medications improve pain in 70% of stroke survivors with
CPSP, with tricyclic antidepressants and antiepileptic drugs 3.5. Complex regional pain syndrome
such as lamotrigine, gabapentin, topiramate, pregabalin and
amitriptyline, and selective serotonin reuptake inhibitors This syndrome includes several symptoms, such as pain and
(SSRIs) used as first-line drugs [3,5]. On the other hand, edema of the hand, and sudomotor and vasomotor changes
intravenous lidocaine [28], oral ketamine [29], methylpredni- mainly in the affected hand, associated with bone demi-
sone and levetiracetam have not demonstrated their effecti- neralization. Also known as ‘‘reflex sympathetic dystrophy’’,
veness in CPSP. ‘‘causalgia’’ and ‘‘post-stroke shoulder – hand syndrome’’, it is
Neurostimulation of the motor cortex is effective in 50– not easy to determine its frequency due to the lack of
77% of CPSP cases [30,31], whereas deep brain stimulation consensus on its diagnostic criteria.
(DBS) has been rather disappointing. However, transcranial Usually, there is no identifiable neural lesion, whereas the
magnetic stimulation (TMS) of the motor cortex may be roles of sympathetic tracts, CNS, peripheral nerves, muscle
effective [32]. hypoxia, shoulder trauma and local inflammation have been
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
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
[21] Tasker RR. Microelectrode findings in the thalamus in randomized controlled trial. Lancet Neurol 2015;14(10):992–
chronic pain and other conditions. Stereotact Funct 1001.
Neurosurg 2011;77:166–8. [36] Gamble GE, Barberan E, Bowsher D, Tyrrell PJ, Jones AK.
[22] Klit H, Finnerup NB, Jensen TS. Central post-stroke pain: Post stroke shoulder pain: more common than previously
clinical characteristics, pathophysiology, and realized. Eur J Pain 2000;4:313–5.
management. Lancet Neurol 2009;8:857–68. [37] Razaq S, Rathore FA. An overview of pathophysiology,
[23] Harno H, Haaspaniemi E, Putaala J, Haanpaa M, Makela JP, assessment and management strategies of post-stroke
Kalso E, et al. Central post-stroke pain in young ischemic shoulder subluxation. Pak J of Neurol Sci 2016;11(3):41–8.
stroke survivors in the Helsinki young stroke registry. [38] Dromerick AW, Edwards DF, Kumar A. Hemiplegic shoulder
Neurology 2014;83:1147–54. pain syndrome: frequency and characteristics during
[24] Sahin-Onat S, Ünsal-Delialioglu S, Kulakli F. The effects of inpatient stroke rehabilitation. Arch Phys Med Rehabil
central post-stroke pain on quality of life and depression in 2008;89(8):1589–93.
patients with stroke. J Phys Ther Sci 2016;28:96–101. [39] Van Ouwenaller C, Laplace PM, Chantraine A. Painful
[25] Benavente OR, Pearce LA, Bazan C, Roldan AM, Catanese L, shoulder in hemiplegia. Arch Phys Med Rehabil 1986;67:23–6.
Bhat Livezey VM, et al. Clinical-MRI correlations in a [40] Dawson AS, Knox J, McClure A, Foley N, Teasell R. Stroke
multiethnic cohort with recent lacunar stroke: the SPS3 rehabilitation. Best practices writing group: management
trial. Int J Stroke 2014;9:1057–64. of shoulder pain following stroke. In: Lindsay MP, Gubitz G,
[26] Bhattacharyya R, Goswani S, Chaudra-Ghosh K, Ghosh S, Bayley M, Phillips S, editors. Canadian best practice
Prasad-Mondal G. Clinical features and imaging of central recommendations for stroke care. Ottawa, Ontario,
post-stroke pain. Indian J Pain 2016;30:34–7. Canada: Heart and Strok Foundation and the Canadian
[27] Kumar G, Rasiklal-Soni C. Central post-stroke pain: current Stroke Network; 2013. p. 47–50.
evidence. J Neurol Sci 2009;284:10–7. [41] Koban M, Leis S. Schutze-Mosgan. Pain 2003;104:149–57.
[28] Attal N, Gaude V, Brasseur L, Dupuy M, Guirimand F, Parker [42] Wasner G, Schattschneider J, Binder A, Baron R. Complex
F, et al. Intravenous lidocaine in central pain: a double- regional pain syndrome – diagnostic, mechanisms, CNS
blind, placebo-controlled, psychophysical study. Neurology involvement and therapy. Spinal Cord 2003;41:61–75.
2000;54:564–74. [43] Altschuler EL, Wisdom SB, Stone L, Foster C, Galasko D,
[29] Vick PG, Lamer TJ. Treatment of central post-stroke pain Llewellyn DME, et al. Rehabilitation of hemiparesis after
with oral ketamine. Pain 2001;92:311–3. stroke with a mirror: early recanalisation in acute
[30] Nguyen JP, Lefaucheur JP, Decq P, Uchiyama T, Carpentier ischaemic stroke saves tissue at risk defined by MRI. Lancet
A, Fontaine D, et al. Chronic motor cortex stimulation in 1999;353:2036–7.
the treatment of central and neuropathic pain. Correlations [44] Gierthmuhlen J, Binder A, Baron R. Mechanism-based
between clinical, electrophysiological and anatomical data. treatment in complex regional pain syndromes. Nat Rev
Pain 1999;82:245–51. Neurol 2014;10:518–28.
[31] Morishita T, Inoue T. Brain stimulation therapy for central [45] Abadie V, Jacquin A, Daubail B, vialatte AL, Lainay C, Durier
post-stroke pain from a perspective of inter-hemispheric J, et al. Prevalence and prognostic value of headache on
neural network remodeling. Front Hum Neurosci 2016. early mortality in acute stroke: the Djion Stroke Registry.
http://dx.doi.org/10.3389/fnhum.2016.00166. Cephalalgia 2014;24(11):887–94.
[32] Khedr EM, Kotb H, Kamel NF, Ahmed MD, Sadek R, [46] Samson M, Jacquin A, Audia S, Daubail B, Devilliers H,
Rothwell JC. Long-lasting antalgic effects of daily sessions Petrella T, et al. Stroke associated with giant cell arteritis: a
of repetitive trans-cranial magnetic stimulation in central population-based study. J Neurol Neurosurg Psychiatry
and peripheral neuropathic pain. J Neurol Neurosurg 2015;86:216–21.
Psychiatry 2005;76:833–8. [47] Blanc C, Janoura S, Pallot C, Mettey L, Bardin F, Ricolfi F,
[33] Wissel J, Schelosky LD, Scott J, Christie W, Faiss JH, Mueller et al. Moya moya disease: diagnosis, clinical features,
J. Early development of spasticity following stroke: a evolution and treatment in 10 patients. Rev Neurol
prospective, observational trial. J Neurol 2010;257:1067–72. 2015;171:58–64.
[34] Dehem S, Gilliaux M, Lejeune T, Detrembleur C, Galinski D, [48] Debette S, Compter A, Labeyrie MA, Vyttenboogaart M,
Sapin J, et al. Assessment of upper limb spasticity in stroke Metso TM, Majersik J, et al. Epidemiology, pathophysiology,
patients using the robotic device reaplan. J Rehebil Med diagnosis, and management of intracranial artery
2017;49:567–71. dissection. Lancet Neurol 2015;14:640–54.
[35] Gracies JM, Brashear A, Jech R, Mc Allister P, Banach M, [49] Norton J, Portet F, Gabelle A, Debette S, Ritchie K, Toudron J,
Valkovic P, et al. Safety and efficacy of abobotulinumtoxin. et al. Are migraine and non-migrainous headache risk
A for hemiparesis in adults with upper limb spasticity after factors for stroke in the elderly? Findings from a 12-year
stroke or traumatic brain injury: a double-blind cohort follow-up. Eur J Neurol 2016;23:1463–70.
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