Elsevier

The Lancet Neurology

Volume 8, Issue 9, September 2009, Pages 857-868
The Lancet Neurology

Review
Central post-stroke pain: clinical characteristics, pathophysiology, and management

https://doi.org/10.1016/S1474-4422(09)70176-0Get rights and content

Summary

Central post-stroke pain (CPSP) is a neuropathic pain syndrome that can occur after a cerebrovascular accident. This syndrome is characterised by pain and sensory abnormalities in the body parts that correspond to the brain territory that has been injured by the cerebrovascular lesion. The presence of sensory loss and signs of hypersensitivity in the painful area in patients with CPSP might indicate the dual combination of deafferentation and the subsequent development of neuronal hyperexcitability. The exact prevalence of CPSP is not known, partly owing to the difficulty in distinguishing this syndrome from other pain types that can occur after stroke (such as shoulder pain, painful spasticity, persistent headache, and other musculoskeletal pain conditions). Future prospective studies with clear diagnostic criteria are essential for the proper collection and processing of epidemiological data. Although treatment of CPSP is difficult, the most effective approaches are those that target the increased neuronal hyperexcitability.

Introduction

The concept of central pain was first introduced by Edinger in 1891.1 15 years later, in their famous paper “Le syndrome thalamique”,2, 3 Déjerine and Roussy provided descriptions of central post-stroke pain (CPSP) that have since been widely cited. These researchers described a small series of patients (n=8) with several neurological symptoms and signs ascribed to a lesion in the optic thalamus. The syndrome included “…severe, persistent, paroxysmal, often intolerable, pains on the hemiplegic side, not yielding to any analgesic treatment”. Pathological studies of three of these patients revealed lesions of the thalamus and parts of the posterior limb of the internal capsule. In 1911, Head and Holmes4 described in detail the sensory deficits and pain narratives of 24 patients with stroke who had clinical symptoms of lesions of the optic thalamus and central pain. These neurologists noted that the patients often developed pain and hypersensitivity to stimuli during recovery of function. Subsequently, in 1938, Riddoch5, 6, 7 provided an extensive presentation of the clinical features of central pain of thalamic and extra-thalamic origin. As central pain also occurs after vascular lesions in parts of the CNS other than the thalamus, and as only a few patients present with the classic “Dejerine and Roussy syndrome”,8, 9 the term CPSP is now preferred to describe neuropathic pain after stroke.

CPSP belongs to a group of chronic pain disorders that are termed central neuropathic pain (Panel 1, Panel 2)10, 11, 12 because the pain is due to a lesion or dysfunction of the CNS.10 Because of the difficulty in differentiating this syndrome from other pain conditions associated with CNS disorders, an alternative definition of central neuropathic pain has recently been suggested as “pain arising as a direct consequence of a lesion or disease affecting the central somatosensory system”.11 To complicate matters further, other painful disorders such as headache, painful spasms, contractures, hemiplegic shoulder pain, and other types of musculoskeletal pain can blur the clinical picture of CPSP.

In this Review, we outline the epidemiology, clinical characteristics, mechanisms, and treatment of CPSP, and discuss diagnostic problems of this syndrome.

Section snippets

Post-stroke pain

In 2000, the incidence of stroke in Europe was about 1·1 million per year, and this rate is expected to rise to 1·5 million per year by 2025, owing to an increase in the proportion of elderly people.13 Chronic pain after stroke occurs in 11–55% of patients,14, 15, 16, 17, 18, 19, 20, 21 but the pain is not always associated with stroke16 (table 1) and pre-existing chronic pain disorders are common in patients who develop post-stroke pain.9, 16 The most common forms of chronic post-stroke pain

Definition of CPSP

The new proposed grading system for neuropathic pain11 suggests that a diagnosis of definite neuropathic pain requires the presence of pain with a distinct plausible distribution, a history suggestive of a relevant lesion, indication of negative or positive sensory signs within the area, and confirmation of the lesion by a diagnostic test.

At present, the diagnosis of CPSP is one of exclusion, as there are no pathognomonic features of this syndrome. As chronic pain is common in the elderly and

Epidemiology of CPSP

There are only a few epidemiological studies of CPSP. The prevalence of CPSP in patients with stroke is between 1% and 12% (table 1).8, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28 Development of CPSP is associated with sensory impairment, and, in one study, the prevalence of CPSP was as high as 18% in patients with sensory deficits, compared with 8% in all patients with stroke.15, 22 Therefore, CPSP does not seem to be a rare disorder and the examination of sensory symptoms

Clinical characteristics of CPSP

The clinical characteristics of CPSP resemble those of other central and peripheral neuropathic pain syndromes.40, 41, 42 There are no pathognomonic features or uniform signs with regard to onset, presentation, and intensity,9 and the characteristics and descriptions of CPSP vary substantially between patients.

CPSP is often described as long-lasting, even life-long, but there are no prospective studies that have documented this. Most studies are based on patients from pain clinics, which might

Diagnostic measures

A definite diagnosis of CPSP is difficult, mainly because of the variable clinical picture, the frequent concurrence of several pain types, and the lack of clear diagnostic criteria for CPSP. The diagnosis should be based on a combination of the history, a clinical and sensory examination, imaging of lesions (CT or MRI), and other clinical measures (panel 3). The history of stroke should be confirmed by imaging (either CT or MRI) to visualise the lesion (type, location, and size) and to exclude

Pathophysiology: possible mechanisms

The pathophysiological features of multiple sclerosis, traumatic brain injury, and stroke are obviously different, although the underlying pain mechanisms might not differ substantially. In fact, the clinical characteristics of CPSP resemble those of other central and peripheral neuropathic pain syndromes,40, 41, 42, 45 and different neuropathic pain conditions might have a common or overlapping range of mechanisms. However, even within brain lesions, the underlying pattern of

Management of CPSP

CPSP is, as is the case for other neuropathic disorders, often difficult to treat; the treatment response is mostly moderate, and the dosage is limited by side-effects, particularly in elderly patients. In clinical practice, the treatment of patients with CPSP is often based on trial and error until pain relief is found, and the result is usually a combination of several drugs. There are only a few randomised controlled studies on CPSP treatment (ie, class I studies; table 2),104, 105, 106, 107

Conclusions and future perspectives

Chronic post-stroke pain is common, but this pain is not always due to CPSP, and several types of pain can occur in the same patient concomitantly. It is important to identify the origin and type of pain to find the relevant treatment for the patient, as the efficacy of a drug varies with the underlying pain type (ie, nociceptive pain or CPSP). Recently, a new definition of neuropathic pain was proposed, which might help to differentiate between pain as a direct consequence of the lesion (ie,

Search strategy and selection criteria

References for this Review were identified through searches of PubMed and Embase with the search terms “central pain”, “pain and stroke”, “post-stroke pain”, “thalamic syndrome”, “Dejerine and Roussy”, “Wallenberg and pain”, “brainstem and pain”, and “medulla and pain” from 1966 until May, 2009. Only papers published in English were reviewed. The bibliographies of the papers, articles from our own files, and relevant book chapters were also searched. The final reference list was generated

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