Central Post-Stroke Pain: Frequency, Clinical Characteristics, and Associated Factors

Objective: The aim of this study was to investigate the incidence of central post-stroke pain in stroke patients and the effect of central post-stroke pain on quality of life. Material and Methods: One hundred stroke patients (47 women, 53 men), admiting to the inpatient rehabilitation clinic or stroke outpatient followup clinic were included in this cross-sectional study. Patients with aphasia, intermediate and advanced levels of cognitive disorder, subarachnoid hemorrhage, arteriovenous malformation, tumor, traumatic brain injury and multiple sclerosis causing hemiplegia, having neuropathic pain and complex regional pain syndrome in the history were excluded. central pain was evaluated with Leeds assessent of neuropathic symptoms and signs pain scale (LANSS), quality of life was assessed with the Nottingham Health Profile. Results: The mean age of the patients were 60.27±11.59 years, stroke duration was 14.65 months (range 2-124). Hemiplegia was on the right side in 35 cases, left side in 65 cases. 77 patients had ischemic, 23 patients had hemorrhagic etiology. Twelve patients had central post-stroke thalamic pain. Central pain was related with a significant difference in the pain parameter of Nottingham Health Profile (NHP)(p=0.001). Conclusion: The central post-stroke pain is a complication that should not be ignored because it is not rare and has negative impact on the quality of life of patients with stroke.

Central post-stroke pain affects up to 12% of stroke survivors and is notoriously refractory to treatment. However, stroke patients often suffer from other types of pain of non-neuropathic nature (musculoskeletal, inflammatory, complex regional) and no head-to-head comparison of their respective clinical and somatosensory profiles has been performed so far. We compared 39 patients with definite central neuropathic post-stroke pain with two matched control groups: 32 patients with exclusively non-neuropathic pain developed after stroke and 31 stroke patients not complaining of pain. Patients underwent deep phenotyping via a comprehensive assessment including clinical exam, questionnaires and quantitative sensory testing to dissect central post-stroke pain from chronic pain in general and stroke. While central post-stroke pain was mostly located in the face and limbs, non-neuropathic pain was predominantly axial and located in neck, shoulders and knees (P < 0.05). Neuropathic Pain Symptom Inventory clusters burning (82.1%, n = 32, P < 0.001), tingling (66.7%, n = 26, P < 0.001) and evoked by cold (64.1%, n = 25, P < 0.001) occurred more frequently in central post-stroke pain. Hyperpathia, thermal and mechanical allodynia also occurred more commonly in this group (P < 0.001), which also presented higher levels of deafferentation (P < 0.012) with more asymmetric cold and warm detection thresholds compared with controls. In particular, cold hypoesthesia (considered when the threshold of the affected side was <41% of the contralateral threshold) odds ratio (OR) was 12 (95% CI: 3.8–41.6) for neuropathic pain. Additionally, cold detection threshold/warm detection threshold ratio correlated with the presence of neuropathic pain (ρ = −0.4, P < 0.001). Correlations were found between specific neuropathic pain symptom clusters and quantitative sensory testing: paroxysmal pain with cold (ρ = −0.4; P = 0.008) and heat pain thresholds (ρ = 0.5; P = 0.003), burning pain with mechanical detection (ρ = −0.4; P = 0.015) and mechanical pain thresholds (ρ = −0.4, P < 0.013), evoked pain with mechanical pain threshold (ρ = −0.3; P = 0.047). Logistic regression showed that the combination of cold hypoesthesia on quantitative sensory testing, the Neuropathic Pain Symptom Inventory, and the allodynia intensity on bedside examination explained 77% of the occurrence of neuropathic pain. These findings provide insights into the clinical-psychophysics relationships in central post-stroke pain and may assist more precise distinction of neuropathic from non-neuropathic post-stroke pain in clinical practice and in future trials.

Central post-stroke pain (CPSP) is a poorly diagnosed chronic pain. It is under-treated and usually mismanaged. To establish the prevalence of CPSP and its management in stroke clinics at a tertiary hospital. This was a cross-sectional design with stroke patients and health professionals from the stroke clinic at the tertiary hospital in Zimbabwe. Out of 166 stroke survivors, 8% had CPSP. Younger age (<60 years) was significantly associated with CPSP (P<0.003). Pain characteristics of CPSP were hyperaesthesia (10, 71%), electric shocks (9, 64%), temperature allodynia (9, 64%) and allodynia (12, 86%). Ten health professionals participated in the study: one (10%) reported using Douleur Neuropathique 4 (to diagnose neuropathic pain) and two (20%) reported using sensory tests. Four patients (44%) were on paracetamol (acetaminophen) and on weak opiates such as codeine. None of the patients were on anticonvulsants or antidepressants. Two medical doctors (50%) used weak opiates as second-line management. Five patients (36%) reported receiving a combination of massage, stretching, general exercise and moist heat or cryotherapy. The prevalence of CPSP in the study group is within international range. There is a need for appropriate management and use of tests and outcome measures for diagnosis of CPSP.

Neuropathy, neuropathic pain, and sickle cell disease

The International Association for the Study of Pain (IASP) defines central pain as “pain initiated or caused by a primary lesion or dysfunction of the central nervous system (CNS)” [1], at levels of spinal cord, brainstem or cerebral hemispheres. Central pain is less common in stroke than in other neurological diseases [2-4]. Central pain following stroke is a neuropathic chronic pain syndrome due to a post-stroke damage of CNS, resulting in anatomical, neurochemical, toxic, and inflammatory changes, causing an increase in neuronal excitability. Its frequency vary widely (8%–55%), reflecting small sample sizes, heterogeneous populations as well as differences in both study design, and chronic pain definition [3,5,6]. Central post-stroke pain can develops after both haemorrhagic and ischemic lesions occurring at any level of somato-sensory pathway of the brain, including medulla, thalamus, and cerebral cortex. Data from several studies indicate that the prevalence of central post-stroke pain is dependent on the location of the lesion, and occurrence is particularly high after lateral medullary infarction (or Wallenberg’s syndrome) or lesions in the ventroposterior thalamus [5]. Many of these patients will fulfil the diagnostic criteria for neuropathic pain, despite the pain being of nociceptive origin. In these cases, might be difficult to identify a central neuropathic element to the hemiplegic shoulder pain, spasticity, or other musculoskeletal pain and, in some cases, several pain types might be present in the same area of the body. The clinical manifestations of central post-stroke pain resemble those of other central and peripheral neuropathic pain syndromes [3,5]. There are no pathognomonic features or uniform signs with regard to onset, presentation, and intensity [5], and the characteristics and descriptions of central post-stroke pain vary substantially between patients. The presence of allodynia, hyperalgesia, or dysesthesia in response to the sensory examination is a predictor of central post-stroke pain [7]. The pathophysiology of central post-stroke pain is not well understood even if lack of central inhibition, imbalance of stimuli and central sensitization has been suggested. Moreover, a decrease of GABAergic inhibition has been observed at cortical, thalamic and spinal levels. Incomplete understanding of mechanisms underlying central post-stroke pain makes the development of targeted treatment demanding [3,5]. Moreover, the lack of published data from large and/or well-designed clinical trials involving patients with central post-stroke pain has created a situation where treatment guidelines are based upon “uncontrolled studies, clinical experience and expert opinion” [3].

Central post-stroke pain (CPSP) is a syndrome characterized by sensory disturbances and neuropathic pain. In 40%-60% of CPSP patients, the onset of central pain following a stroke occurs more than 1 month after the stroke, creating a source of diagnostic uncertainty or significant delay in treatment since healthcare providers familiar with CPSP may no longer be caring for the patient when the symptoms occur. In addition to chronic pain, the presence of somatosensory abnormalities is the most important diagnostic corollary of CPSP. Neuropathic or central pain has been estimated to occur in up to 8% of patients after a stroke, and about 18% of stroke patients with a somatosensory disturbance will develop CPSP. Although largely a matter of conjecture, it is generally agreed that damage to spinothalamic sensory pathways plays a significant role in the pathogenesis of CPSP. A comprehensive examination of the patient for sensory deficits is essential before treatment can be initiated. Functional disturbances such as depression, anxiety and sleep disturbances are significant comorbid conditions associated with CPSP; the physician should incorporate an assessment of these potential comorbidities into the examination. Treatment options for CPSP are limited; at present, amitriptyline is the drug of first choice. Other drugs including antidepressants, anticonvulsants, antiarrhythmics, opioids and N-methyl-d-aspartate antagonists may provide relief for some patients who do not respond to amitriptyline. Included in this review is a case study outlining the challenges of managing the patient with CPSP.

Introduction Culture has been defined as: “a tradition of knowledge and practice that is shared, albeit imperfectly, across the members of a society and across its generations” [Zou et al 2009]. It shapes people's experiences and their emotional reactions [Gard et al 2005], including their understandings of what it means to be healthy, the meanings of symptoms, attitudes towards disability and treatment, and coping strategies [Dean et al 2006; Gallaher et al 2001]. The study suggested here may offer new insights by exploring how culture shapes the experience of stroke care through the perceptions of Physical therapists working in the state of Qatar. Qatar is one of the wealthiest countries in the world. The culture reveals the modernising influences associated with oil exploration and technological advances whilst preserving collective traditions. The state provides extensive financial support for its own citizens including generous pensions and access to health care. However, in common with other Gulf st...

In the United States, the incidence rate of new or recurrent stroke is approximately 795 000 per year, and stroke prevalence for individuals over the age of 20 years is estimated at 6.5 million.1 Mortality rates in the first 30 days after stroke have decreased because of advances in emergency medicine and acute stroke care. In addition, there is strong evidence that organized postacute, inpatient stroke care delivered within the first 4 weeks by an interdisciplinary healthcare team results in an absolute reduction in the number of deaths.2,3 Despite these positive achievements, stroke continues to represent the leading cause of long-term disability in Americans: An estimated 50 million stroke survivors worldwide currently cope with significant physical, cognitive, and emotional deficits, and 25% to 74% of these survivors require some assistance or are fully dependent on caregivers for activities of daily living (ADLs).4,5 Notwithstanding the substantial progress in acute stroke care over the past 15 years, the focus of stroke medical advances and healthcare resources has been on acute and subacute recovery phases, which has resulted in substantial health disparities in later phases of stroke care. Additionally, healthcare providers (HCPs) are often unaware of not only patients’ potential for improvement during more chronic recovery phases but also common issues that stroke survivors and their caregivers experience. Furthermore, even with evidence that documents neuroplasticity potential regardless of age and time after stroke,6 the mean lifetime cost of ischemic stroke (which accounts for 87% of all strokes) in the United States is an estimated $140 000 (for inpatient, rehabilitation, and follow-up costs), with 70% of first-year stroke costs attributed to acute inpatient hospital care1; therefore, fewer financial resources appear to be dedicated to providing optimal care during the later phases of stroke recovery. Because there remains a …

Objectives: In addition to other complications in stroke patients, central post-stroke pain (CPSP) is sometimes overlooked. Considering the morbidities it causes in patients, it turns out to be a very important problem. The aim of this study is to investigate the frequency of CPSP, the factors causing CPSP, and the relationship between the CPSP and the quality of life and ambulation of individuals. Methods: A cross-sectional study was conducted on a group of patients with stroke. One hundred forty stroke patients were included in the study. Pain (The Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale), health-related quality of life (Short Form 36 Questionnaire) and ambulation (Functional Ambulation Classification) were evaluated. In addition, a special evaluation form was created for this study. With this form, demographic characteristics of the patients, stroke type, cerebral location and hemisphere affected in stroke were recorded. These data were collected for the period between May 2016 and January 2018. Patients were divided into two groups. Group 1 included patients with CPSP and Group 2 patients without neuropathic symptoms. Results: CPSP was detected in 23 of 140 patients. In terms of demographic data, only gender differences were found between group 1 and group 2. CPSP was statistically significantly higher in female patients. There was no significant difference between the two groups in terms of the affected cerebral region and stroke type, but CPSP was significantly more common in patients with left hemispheric involvement. Emotional role restriction, body pain, social funtion, general health and mental health subcategories of the SF-36 were found to be significantly lower in group 1 compared to group 2. Also ambulation was worse in patients with CPSP. Conclusions: It was concluded that CPSP is a common problem and negatively affects the quality of life of the patients. Therefore, CPSP should be recognized in the early period after stroke and treatments should be arranged accordingly.

Central poststroke pain (CPSP) is a severe type of neuropathic pain that can develop after stroke and is difficult to treat. Research into its underlying mechanisms and treatment options could benefit from a valid CPSP animal model. Nine different CPSP animal models have been published, but there are relatively few reports on successful reproductions of these models and so far only little advances in the understanding or the management of CPSP have been made relying on these models. In general, the construct validity (similarity in underlying mechanisms) of these CPSP animal models is relatively high, although this cannot be evaluated into depth because of lack of understanding the mechanisms through which thalamic stroke can lead to CPSP. The face validity (symptom similarity) is relatively low, mainly because pain in these models is tested almost exclusively through evoked mechanical/thermal hypersensitivity assessed by reflexive measures and given the conflicting results with similar tests in patients with CPSP. The predictive validity (similarity in treatment efficacy) has not been evaluated in most models and incorporates difficulties that are specific to CPSP. We compare the different models regarding these types of validity and discuss the robustness, reproducibility, and problems regarding the design and reporting of the articles establishing these models. We conclude with various proposals on how to improve the validity and reproducibility of CPSP animal models. Until further improvements are achieved, prudence is called for in interpreting results obtained through these models.

Central poststroke pain is a chronic neuropathic disorder that follows a stroke. Current research on its management is limited, and no review has evaluated all therapies for central poststroke pain. We conducted a systematic review of randomized controlled trials to evaluate therapies for central poststroke pain. We identified eligible trials, in any language, by systematic searches of AMED, CENTRAL, CINAHL, DARE, EMBASE, HealthSTAR, MEDLINE, and PsychINFO. Eligible trials (1) enrolled ≥10 patients with central poststroke pain; (2) randomly assigned them to an active therapy or a control arm; and (3) collected outcome data≥14 days after treatment. Pairs of reviewers, independently and in duplicate, screened titles and abstracts of identified citations, reviewed full texts of potentially eligible trials, and extracted information from eligible studies. We used a modified Cochrane tool to evaluate risk of bias of eligible studies, and collected patient-important outcomes according to recommendations by the Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials. We conducted, when possible, random effects meta-analyses, and evaluated our certainty in treatment effects using the Grading of Recommendations Assessment, Development, and Evaluation System. Eight eligible English language randomized controlled trials (459 patients) tested anticonvulsants, an antidepressant, an opioid antagonist, repetitive transcranial magnetic stimulation, and acupuncture. Results suggested that all therapies had little to no effect on pain and other patient-important outcomes. Our certainty in the treatment estimates ranged from very low to low. Our findings are inconsistent with major clinical practice guidelines; the available evidence suggests no beneficial effects of any therapies that researchers have evaluated in randomized controlled trials.

Central poststroke pain (CPSP) is a chronic neurological condition that results from damage to the brain's pain-processing pathways and causes hypersensitivity to pain. Despite its clinical importance, yet remains underrecognized, its estimated prevalence ranges from 8% to 35%. OBJECTIVE: This study examines the prevalence of CPSP and explores demographic and comorbidity differences among stroke survivors. METHODS: This retrospective, cross-sectional study used de-identified data from electronic health records from a large academic health center in the North Central Florida region (2014-2024). International Classification of Diseases-9 and International Classification of Diseases-10 codes were used to identify ischemic stroke, hemorrhagic stroke, and CPSP. Descriptive statistics, χ 2 , t test, and multivariable logistic regression were used for statistical analyses. RESULTS: Of 32,155 adult patients, only 99 (0.31%) were diagnosed with CPSP. The odds of being diagnosed with CPSP were higher in patients with ischemic stroke than hemorrhagic [adjusted odds ratio (AOR) = 2.00, 95% CI: 1.19-3.37, P = .009]. The mean age of CPSP patients was 59 years (SD = 13.1), significantly younger than those without CPSP (M = 64, P = .001), with no difference in sex distribution. Black patients (AOR = 0.47, 95% CI: 0.30-0.74, P = .001) and Hispanic patients (AOR = 3.31, 95% CI: 1.49-7.31, P = .003) both had significantly higher odds of a documented CPSP diagnosis compared with white and non-Hispanic patients. Hypertension (74.8%) was the most common comorbidity among patients with CPSP, while only atrial fibrillation was significantly less prevalent ( P = .006) in the CPSP group. CONCLUSION: Our findings indicate a low prevalence of CPSP in patients who have experienced stroke. The prevalence of documented poststroke pain was substantially lower than published estimates suggest. Further investigation is needed to understand the experience of CPSP in younger, black, Hispanic, and multimorbidity populations.

Safety and efficacy of pregabalin in patients with central post-stroke pain

Thalamic pain syndrome, a type of central post-stroke pain (CPSP), may develops after a hemorrhagic or ischemic stroke and results in impairment of the thalamus. There is limited experience about gabapentin in treatment of central pains like CPSP. In a prospective observational study, the intensity of pain was recorded using the Numeric Rating Scale (NRS) at the entrance to the study. Patients eligible for treating with gabapentin, received gabapentin 300 mg twice-daily. The pain intensity was measured at entrance to the study and after one month using NRS. Decrease of 3 points from the initial NRS considered being clinically significant. From a total of 180 primarily screened patients, 84 (44 men and 40 women) were recruited. There was a significant difference between pre-treatment and post-treatment NRS (5.9 ± 2.51 vs. 4.7 ± 3.01; 95% CI: 0.442-1.962, p = 0.002). Fisher's exact test showed no statistically significant effect of clinical and demographic characteristics of patients on their therapeutic response to gabapentin.Given the safety, efficacy, well tolerability and lack of interaction with other drugs we suggest gabapentin to be more considered as a first line therapy or as add-on therapy for reducing the pain severity in patients with thalamic syndrome.

Central poststroke pain (CPSP) is one of the primary sequelae following stroke, yet its underlying mechanisms are poorly understood. By lesioning the lateral thalamic nuclei, we first established a CPSP model that exhibits mechanical and thermal hypersensitivity. Innocuous mechanical stimuli following the thalamic lesion evoked robust neural activation in somatosensory corticospinal neurons (CSNs), as well as in the deep dorsal horn, where low threshold mechanosensory afferents terminate. In this study, we used viral-based mapping and intersectional functional manipulations to decipher the role of somatosensory CSNs and their spinal targets in the CPSP pathophysiology. We first mapped the post-synaptic spinal targets of lumbar innervating CSNs using an anterograde trans-synaptic AAV1-based strategy and showed these spinal interneurons were activated by innocuous tactile stimuli post-thalamic lesion. Functionally, tetanus toxin-based chronic inactivation of spinal neurons targeted by CSNs prevented the development of CPSP. Consistently, transient chemogenetic silencing of these neurons alleviated established mechanical pain hypersensitivity and innocuous tactile stimuli evoked aversion linked to the CPSP. In contrast, chemogenetic activation of these neurons was insufficient to induce robust mechanical allodynia typically observed in the CPSP. The CSNs and their spinal targets are required but insufficient for the establishment of CPSP hypersensitivity. Our study provided novel insights into the neural mechanisms underlying CPSP and potential therapeutic interventions to treat refractory central neuropathic pain conditions.