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Central poststroke pain (CPSP) is a central neuropathic pain syndrome that can occur after stroke in the part of the body corresponding to the cerebrovascular lesion. CPSP is characterized by pain and sensory abnormalities localized to the affected area; and, a diagnosis can be made only after having ruled out other potential causes of nociceptive, psychogenic, or peripheral neuropathic pain.1


See Definition and Pathoanatomy/Pathophysiology sections.

Epidemiology including risk factors and primary prevention

  1. CPSP has a prevalence of 8 to 55% in stroke patients.  The wide range is indicative of the difficulty in diagnosing this disease.2,11
  2. Most cases present within the first 6 months after stroke, with the majority of cases developing within the first three months. Though rare, it is possible for CPSP to develop immediately after stroke; or, more than 6 months after stroke. 2,4,16
  3. Female sex predominance has been demonstrated in studies.12
  4. Younger patients are more susceptible.15,16
  5. Higher NIHSS score has also been associated with increased occurrence of CPSP.15
  6. Early evoked pain or dysesthesia at onset of stroke have been identified as a risk factor for future development of CPSP.18
  7. No intervention can prevent the development of CPSP.


CPSP is believed to occur after a lesion at any level of the somatosensory pathway of the brain (cerebral cortex, thalamus, medulla, spinothalamic pathways, thalamocortical pathways) with resultant maladaptive neuroplastic changes within the central nervous system causing aberrant sensory perception.1,3 It is a common misperception that only strokes in the thalamic region can precipitate CPSP.  While some studies have shown that CPSP is more likely to occur after a thalamic stroke, others have contradicted these findings.11  Nevertheless, potential causes of CPSP include:1

  1. Central sensitization resulting from increased neuronal excitability of central nociceptive neurons.
  2. Disinhibition of pain-signaling structures resulting from damage to inhibitory structures.
  3. Thalamic dysfunction resulting from direct thalamic injury or thalamic deafferentation.  More typically, these strokes involve the posterolateral region of the thalamus.  Specifically, a lesion involving the border of the ventral posterior nucleus and pulvinar region has particular significance.12,17
  4. Derangement of an oscillatory pattern inside a sensory corticothalamocortical reverbatory loop causing the experience of pain (dynamic reverberation theory).

CPSP likely has multiple potential pathophysiological causes.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

No prospective, longitudinal studies have documented the clinical course of CPSP; however, it is considered a potentially life-long complication that is burdensome to the patient and leads to decreased quality of life and interference with rehabilitation.1

Specific secondary or associated conditions and complications

While no specific conditions and complications secondary to CPSP have been identified, it may restrict a patient’s ability to participate in rehabilitation programs, thus leading to worsening of spasticity, development of contracture, and functional limitations.



CPSP is a diagnosis of exclusion, thus, careful elimination of other potential causes of pain after stroke must occur prior to diagnosing CPSP. These potential causes include (but are not limited to) complex regional pain syndrome, radiculopathy, plexopathy, peripheral mononeuropathy, hemiparetic shoulder pain (impingement syndrome, rotator cuff injury, adhesive capsulitis, bursitis, painful spasticity, shoulder subluxation), and deep venous thrombosis. Keys to CPSP symptomatology include:1-5,12

  1. Pain is localized to the area affected by the lesion. Larger body areas are affected more commonly than smaller body areas.  The upper extremity is more frequently involved.
  2. Pain is characterized most often as burning or aching; however, pricking, lacerating, shooting, squeezing, throbbing, heaviness are all possible qualitative descriptors.
  3. Gradual onset is more common.
  4. Pain can be spontaneous or evoked (with spontaneous symptoms occurring continuously and/or paroxysmally and evoked symptoms resulting from nociceptive and/or nonnociceptive stimuli).
  5. Symptoms may be aggravated by movement, touch, temperature (cold > warm), emotional stress; and, may be palliated by movement, temperature (warm), rest, distraction. Note that movement and warmth (for example) may aggravate or palliate symptoms.
  6. It is generally accepted that there are no pain features pathognomonic for or universally present in CPSP.

Physical examination

There are no uniform signs associated with CPSP. Negative and positive sensory events are characteristic of CPSP.1,3,11,16

  1. Negative sensory events including decreased sensation to thermal (particularly cold) and pain (pinprick) stimuli within the painful area are common in CPSP. Less common negative sensory events include decreased sensation to light touch and changes in joint position.
  2. Positive sensory events including hyperalgesia to pinprick, allodynia to light touch and thermal stimuli (particularly cold), and hyperaesthesia (increased response to stimulus) are common in CPSP. One systematic review found that allodynia and hyperaesthesia occurred in 85% of patients with CPSP.  The same review found thermal allodynia to appear in 33% of patients.  Less common positive sensory events include aftersensations, radiation of pain, and summation.

Laboratory studies

No laboratory studies are currently used for the assessment of CPSP.


Identification of a central lesion with MRI or CT that corresponds to the painful body area is an important and appropriate component in the diagnosis of CPSP.  Strokes are more typically seen in the cortex, thalamus, or brainstem.  It is rare to develop CPSP after a basal ganglia stroke.15

Supplemental assessment tools

Pain drawings, pain scales, and other pain assessment tools are appropriate for the initial assessment of CPSP and also are useful to monitor the efficacy of interventions.


Available or current treatment guidelines

The treatment of CPSP is challenging and must incorporate pharmacologic and non-pharmacologic interventions in order to maximize potential for success. Generally speaking, treatment benefits only a fraction of patients diagnosed with CPSP; and, response to treatment is incomplete for those whose symptoms do improve. Goals of treatment, then, should be focused on reduction, not elimination, of symptoms and return to functional activity. Treatment algorithms typically follow a trial-and-error approach and the concomitant use of various treatments in one patient is common.

Pharmacologic Management:1,3,5,6,11,12 Various antidepressants, anticonvulsants, opioids, N-methyl-D-aspartate (NMDA) antagonists, antiarrythmics, and gamma-aminobutyric acid (GABA) agonists have been assessed for efficacy in the treatment of CPSP. An attempt at organizing the various pharmacologic options with regard to efficacy has been made to help the provider.

  1. Antidepressants: Amitriptyline (1st line) and fluvoxamine (3rdline) are considered to be beneficial in the treatment of CPSP, whereas citalopram and reboxetine are considered ineffective. Fluvoxamine may be particularly useful in the CPSP patient with concomitant depression.
  2. Anticonvulsants: Carbamazepine has proven useful in the treatment of CPSP, whereas gabapentin (2nd line) may be effective in the treatment of CPSP.  Phenytoin and zonisamide may possess some efficacy while topiramate and levetiracetam are likely ineffective.  Lamotrigine and pregabalin were initially thought to be significantly effective, however, further studies have shown that point to be debatable.  Still, pregabalin is considered a first-line treatment agent.
  3. Opioids: Tramadol, morphine, and levorphanol (all 3rd line) may be useful in the treatment of CPSP. If opioids are selected as a treatment option, the aforementioned opiods medications in addition to tapentadol, methadone, buprenorphine, and oxycodone should be used preferentially. Naloxone (opioid antagonist) is considered ineffective in the treatment of CPSP.
  4. NMDA antagonists: Ketamine may possess some efficacy, however, side effects and administration route limit its utility. Dextromethorphan is considered ineffective in the treatment of CPSP.
  5. Antiarrythmics: Mexiletine and lidocaine (both 3rd line) may be useful in the treatment of CPSP. Their utility is limited, however, given poor patient tolerance and need for intravenous administration, respectively.
  6. GABA agonists: Intrathecal baclofen possibly has a role in the treatment of CPSP with oral baclofen likely not being useful. Propofol and thiamylal/thiopental also possibly have roles in the treatment of CPSP, however, only in the short-term relief of intractable pain.

Nonpharmacologic Management:1,3,5,6,7,11,12 A number of nonpharmacologic interventions have been assessed for efficacy in the treatment of CPSP. Psychological treatment (for example, relaxation techniques and biofeedback), exercise therapy, and desensitization techniques may be beneficial in CPSP. Transcutaneous electrical nerve stimulation (TENS) is likely not effective and may actually increase pain symptoms in some patients.  Acupuncture was found in one randomized control trial to significantly reduce pain in CPSP.  Repetitive transcranial magnetic stimulation (rTMS), transcranial direct current stimulation (tDCS), and vestibular caloric stimulation have demonstrated efficacy in the treatment of CPSP. Deep brain stimulation (DBS) and motor cortex stimulation via implanted stimulators show variable efficacy and should be reserved for patients with significant symptomatology who have exhausted pharmacological and less invasive nonpharmacologic treatment strategies.  Spinal cord stimulation has preliminarily been utilized in patients with intractable pain with some finding significant pain relief, however, studies are thus far limited.  It has been more successful in patients under 60 years old with non-thalamic strokes.  Mirror therapy and virtual reality have also shown promise in CPSP.

Patient & family education

The patient and family should be educated on the unclear etiology of CPSP, its likely chronic duration, the trial-and-error algorithm typically used for treatment, and the goals of treatment (reduction, not elimination, of symptoms and return to functional activity). Family training/involvement in nonpharmacologic interventions (for example, psychological treatments, desensitization techniques) may be beneficial.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Interdisciplinary management of CPSP is most appropriate, with goals focused on reducing symptoms and improving function. Initial management includes medication management (amitriptyline with tramadol as needed for breakthrough symptoms) coupled with desensitization technique training and relaxation and/or biofeedback training. Frequent reassessment with adjustment of pharmacological and nonpharmacological interventions affords patients the best opportunity to reduce symptoms and improve function.


Cutting edge concepts and practice

Complex regional pain syndrome (CRPS) is another poorly understood painful condition that presents with allodynia and hyperalgesia. CRPS, however, also possesses additional signs and symptoms including motor, sudomotor, vasomotor, and trophic abnormalities. CRPS after stroke and CPSP are considered distinct entities; however, the possibility of these two diagnoses existing on a continuum is not unreasonable. Pharmacologically, CRPS is treated similarly to CPSP, suggesting the possibility of similar pathophysiology. Demonstratively, one study reported resolution of symptoms in 91.2% patients with CRPS after stroke using an oral methylprednisolone taper,8 while another demonstrated significant improvements in patients with CPSP also receiving an oral methylprednisolone taper.9

The serotonin-norepinephrine reuptake inhibitors (SNRIs) and methadone have proven efficacy in other instances of neuropathic pain10 and may be reasonable options for the treatment of CPSP. Additionally, given its overlap in mechanism of action with tramadol, tapentadol may also be a reasonable option for as needed pain relief in patients with CPSP. Finally, as alluded to above, exploring oral corticosteroid administration as an abortive treatment in CPSP might be a worthwhile endeavor as well.


The establishment of a universally accepted definition of and diagnostic criteria for CPSP is of paramount importance both clinically and for research purposes. Consensus on these items as well as consensus on treatment algorithms should be the focus of national committees. Proposals for diagnostic criteria exist by Klit et al.1 and Pellicane et al.6; however, neither have been studied or validated.

Because most evidence for the treatment of CPSP is based on studies with a small number of subjects, large clinical trials are needed to further assess existing and novel approaches to the treatment of CPSP.  A large study evaluating a multi-drug program is of particular importance, as more than one medication is usually required to have pain relief.  These could also include evaluation of spinal cord stimulators, motor cortex stimulation, and acupuncture as treatment options.11,12


  1. Klit H, Finerup NB, Jensen TS. Central post-stroke pain: clinical characteristics, pathophysiology, and management. Lancet Neurol. 2009;8:857-868.
  2. Andersen G, Vestergaard K, Ingeman-Nielsen M, Jensen TS. Incidence of central post-stroke pain. Pain. 1995;61(2):187 – 193.
  3. Harvey RL. Central poststroke pain syndrome. Top Stroke Rehabil. 2010;17(3):163-172.
  4. Leijon G, Boivie J, Johansson I. Central post-stroke pain – neurological symptoms and pain characteristics. Pain. 1989;36:13-25.
  5. Kumar B, Kalita J, Kumar G, Misra UK. Central poststoke pain: a review of pathophysiology and treatment. Anesth Analg. 2009;108(5):1645-1657.
  6. Pellicane AJ, Harvey RL (2015). Central Poststroke Pain. In Stroke Recovery and Rehabilitation, Second Edition (pp. 249-266). New York. NY: Demos Medical Publishing, LLC.
  7. Bae SH, Kim GD, Kim KY. Analgesic effect of transcranial direct current stimulation on central post-stroke pain. Tohoku J Exp Med. 2014; 234(3): 189-95.
  8. Braus DF, Krauss JK, Strobel J. The shoulder-hand syndrome after stroke: a prospective clinical trial. Ann Neurol. 1994;36(5):728-733.
  9. Pellicane AJ, Millis SR. Efficacy of methylprednisolone versus other pharmacologic interventions for the treatment of central-post stroke pain: a retrospective analysis. J Pain Res. 2013; 6: 557-563.
  10. Baron R, Binder A, Wasner G. Neuropathic pain: diagnosis, pathophysiological mechanisms, and treatment. Lancet Neurol. 2010;9:807-819.
  11. Singer J, Conigliaro S, Spina E, Law S W, Levine S R.  (2017).  Central poststroke pain: a systematic review.  International Journal of Stroke, 12(4), 343-355.
  12. Akyuz G, Kuru P.  (2016).  Systematic review of central post stroke pain: what is happening in the central nervous system?.  American Journal of Physical Medicine & Rehabilitation, 95(8), 618-627.
  13. Aly M M, Saitoh Y, Hosomi K, Oshino S, Kishima H, Yoshimine T (2010).  Spinal cord stimulation for central poststroke pain.  Operative Neurosurgery, 67(3), 206-212.
  14. Tanei T, Kajita Y, Takebayashi S, Aoki K, Nakahara N, Wakabayashi T.  (2019).  Predictive Factors Associated with Pain Relief of Spinal Cord Stimulation for Central Post-stroke Pain.  Neurologia medico-chirurgica, 59(6), 213.
  15. Vukojevic Z, Kovacevic A D, Peric S, Grgic S, Bjelica B, Basta I, Lavrnic D.  (2018).  Frequency and features of the central poststroke pain.  Journal of the neurological sciences, 391, 100-103.
  16. Klit H, Finnerup N B, Andersen G, Jensen T S.  (2011).  Central poststroke pain: a population-based study.  PAIN, 152(4), 818-824.
  17. Sprenger T, Seifert C L, Valet M, Andreou A P, Foerschler A, Zimmber C, Chakravarty M M.  (2012).  Assessing the risk of central post-stroke pain of thalamic origin by lesion mapping.  Brain, 135(8), 2536-2545.
  18. Klit H, Hansen A P, Marcussen N S, Finnerup N B, Jensen T S.  (2014).  Early evoked pain or dysesthesia is a predictor of central poststroke pain.  PAIN, 155(12), 2699-2706.

Original Version of Topic

Anthony Pellicane, MD. Central Poststroke Pain. 11/10/2011.

Previous Revision(s) of the Topic

Anthony Pellicane, MD. Central Poststroke Pain. 9/17/2015

Author Disclosure

Tomas Salazar MD
Nothing to disclose

Eric Liu DO
Nothing to disclose

Christine Greiss DO
Nothing to disclose