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OBM Neurobiology

(ISSN 2573-4407)

OBM Neurobiology is an international peer-reviewed Open Access journal published quarterly online by LIDSEN Publishing Inc. By design, the scope of OBM Neurobiology is broad, so as to reflect the multidisciplinary nature of the field of Neurobiology that interfaces biology with the fundamental and clinical neurosciences. As such, OBM Neurobiology embraces rigorous multidisciplinary investigations into the form and function of neurons and glia that make up the nervous system, either individually or in ensemble, in health or disease. OBM Neurobiology welcomes original contributions that employ a combination of molecular, cellular, systems and behavioral approaches to report novel neuroanatomical, neuropharmacological, neurophysiological and neurobehavioral findings related to the following aspects of the nervous system: Signal Transduction and Neurotransmission; Neural Circuits and Systems Neurobiology; Nervous System Development and Aging; Neurobiology of Nervous System Diseases (e.g., Developmental Brain Disorders; Neurodegenerative Disorders).

OBM Neurobiology publishes a variety of article types (Original Research, Review, Communication, Opinion, Comment, Conference Report, Technical Note, Book Review, etc.). Although the OBM Neurobiology Editorial Board encourages authors to be succinct, there is no restriction on the length of the papers. Authors should present their results in as much detail as possible, as reviewers are encouraged to emphasize scientific rigor and reproducibility.

Publication Speed (median values for papers published in 2024): Submission to First Decision: 7.6 weeks; Submission to Acceptance: 13.6 weeks; Acceptance to Publication: 6 days (1-2 days of FREE language polishing included)

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Open Access Research Article

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

Riki Sukiandra 1,2,* ORCID logo, Dini Hanania 3, M. Zacky Haikal 3, Muhammad Faaiz Adlii 3

  1. Department of Neurology, Faculty of Medicine Riau University, Pekanbaru, Indonesia

  2. Department of Neurology, Arifin Achmad General Hospital, Pekanbaru, Indonesia

  3. Faculty of Medicine Riau University, Pekanbaru, Indonesia

* Correspondence: Riki Sukiandra ORCID logo

Academic Editor: Nicola Montemurro

Received: December 09, 2025 | Accepted: March 24, 2026 | Published: March 27, 2026

OBM Neurobiology 2026, Volume 10, Issue 1, doi:10.21926/obm.neurobiol.2601329

Recommended citation: Sukiandra R, Hanania D, Haikal MZ, Adlii MF. Central Post-Stroke Pain: Frequency, Clinical Characteristics, and Associated Factors. OBM Neurobiology 2026; 10(1): 329; doi:10.21926/obm.neurobiol.2601329.

© 2026 by the authors. This is an open access article distributed under the conditions of the Creative Commons by Attribution License, which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is correctly cited.

Abstract

Central post-stroke pain (CPSP) is a frequently underrecognized complication that contributes to long-term disability among stroke survivors. This study aimed to determine the frequency of CPSP and to describe its clinical characteristics and associated factors among stroke patients treated at Arifin Achmad General Hospital. A cross-sectional design was employed and included adult stroke patients with diagnoses confirmed by neuroimaging. CPSP was diagnosed based on the clinical criteria proposed by Klit et al., and neuropathic pain was assessed using the Indonesian version of the Douleur Neuropathique 4 questionnaire. Pain intensity was evaluated using the Numeric Rating Scale. Among 270 patients, 44 were identified with CPSP. Age and lesion site were significantly associated with CPSP. The median onset of pain was three months after stroke, with most patients reporting continuous, moderate pain affecting the face, trunk, and limbs. Burning pain and paresthesias were the most frequently reported, and hypoesthesia to pinprick was the most common sensory finding. Greater clinical awareness and systematic assessment are essential to improve recognition and management of CPSP in stroke survivors.

Keywords

Central post-stroke pain; frequency; clinical features; associated factors

1. Introduction

Stroke is one of the leading causes of long-term disability [1]. This disability results from various complications that develop after the stroke event [2]. One of the relatively common yet frequently underreported complications is pain. Post-stroke pain can arise through two mechanisms: peripheral mechanisms related to immobilization, spasticity, or other factors, and central mechanisms caused by lesions within the central nervous system. Post-stroke pain caused by central mechanisms is referred to as central post-stroke pain (CPSP) [3]. The prevalence of central post-stroke pain among stroke survivors ranges from 5% to 35% [4,5,6]. Symptoms typically appear within weeks to several months after a stroke and manifest as neuropathic pain on the side of the body that was affected [7,8]. Because of its delayed onset and wide range of symptoms, CPSP is frequently missed or not given enough attention [9]. Therefore, this study aimed to determine the frequency of CPSP and to describe its clinical characteristics using standardized diagnostic criteria comprehensively. In contrast to earlier studies that primarily focused on prevalence or limited clinical variables, this study integrates frequency, detailed standardized neuropathic pain profiling, lesion site analysis, and associated demographic and clinical factors. In addition, data from Indonesia remain limited, and no prior study has described CPSP characteristics. By addressing these gaps, this study seeks to contribute specific evidence to improve recognition and clinical evaluation of CPSP among stroke survivors.

2. Materials and Methods

2.1 Participants

This study employed a cross-sectional design. The study population consisted of patients diagnosed with stroke at Arifin Achmad General Hospital between July 2023 and June 2025. Patients were recruited from those attending follow-up visits at the neurology outpatient clinic during the study, August−October 2025. Consecutive sampling was applied. A total of 327 patients were assessed for eligibility. Of these, 57 were excluded for not meeting or for fulfilling exclusion criteria.

Inclusion criteria comprised stroke patients aged over 18 years whose diagnosis had been confirmed by a CT scan or MRI and who agreed to participate in the study. A one-month threshold was applied to avoid inclusion of patients in the acute phase. Patients with a history of neuropathic pain, cognitive impairment, or aphasia were excluded from the study. The final study sample consisted of 270 participants.

2.2 Ethics Statement

This study was approved by the Ethics Committee of Arifin Achmad General Hospital and the Faculty of Medicine, Riau University. Written informed consent was obtained from all patients who participated in this study.

2.3 Procedure

Clinical characteristics were obtained from the patient’s medical records. The diagnostic criteria applied in this study were those developed by Klit et al. The Indonesian version of the Douleur Neuropathique 4 (DN4) questionnaire was used to distinguish neuropathic from nociceptive pain and to describe the pain characteristics experienced by patients. Additional instruments included a data collection sheet used to record information on pain onset, localization, and frequency. Pain intensity was assessed using the Numeric Rating Scale (NRS). Clinical profile data were analyzed using descriptive frequency statistics. The Chi-square test was used to determine the differences in CPSP status and clinical characteristics. DN4 pain features were presented as frequency distributions and analyzed using multiple-response analysis.

3. Results

Out of 270 stroke patients included in the sample in this study, 44 patients (16.4%) were identified with CPSP. A statistically significant difference was observed in the age distribution between the CPSP and non-CPSP groups (p < 0.001). Clinical characteristics of stroke patients with CPSP and without CPSP are presented in Table 1. Furthermore, a significant difference in lesion location was observed between the CPSP and non-CPSP groups. The distribution of lesion sites among patients with CPSP is summarized in Table 2.

Table 1 Clinical characteristics of stroke patients with CPSP and without CPSP.

Table 2 Lesion Site of Stroke Patients with CPSP.

The onset of CPSP occurred at a median of 3 months post-stroke. The majority of CPSP patients reported symptoms simultaneously in the face, trunk, and limbs occurring continuously with moderate intensity. The most frequently reported pain quality was a burning sensation. Pins and needles were the most common abnormal sensation reported among patients with CPSP. The most common abnormal sensory finding on examination was hypoesthesia to pinprick. Pain characteristics of stroke patients with CPSP are shown in Table 3.

Table 3 Pain characteristics of stroke patients with CPSP.

4. Discussion

The frequency of CPSP in this study was found in 16.4% stroke survivors. This result aligns with the reported prevalence range of 5-35% [4,5,6]. Variability in this result may be attributed to differences in follow-up duration, diagnostic criteria, and sample size across studies [9,10].

This study demonstrated a significant association between CPSP and age. Younger stroke patients generally have higher survival rates compared to older individuals, allowing sufficient time for CPSP to develop, as its onset typically requires a gradual progression [11,12,13]. Younger stroke survivors tend to exhibit greater neuroplastic potential than older survivors, who are more prone to degenerative changes. Neuroplasticity may proceed in a maladaptive manner, and this process plays a major role in the development of CPSP [14,15].

Males were more frequently affected. Some studies support this finding, whereas others report contradictory results [4,5,7,16]. Vascular risk factors such as alcohol consumption, smoking, and higher rates of dyslipidemia are more prevalent among men [17]. Conversely, estrogen in women may enhance pain sensitivity [18,19,20]. However, current evidence remains insufficient to establish a definitive association between gender and CPSP.

CPSP occurred more often following ischemic stroke in this study. Ischemic stroke itself is the most frequently encountered type of stroke [1]. Unlike hemorrhagic stroke, which more prominently leads to elevated intracranial pressure and neuroinflammation due to hemoglobin breakdown, neuronal damage in ischemic stroke tends to be more localized. It develops progressively through mechanisms dominated by ischemia and hypoxia [21,22,23].

A statistically significant association was found between lesion site and CPSP. The thalamus serves as a central structure for integrating sensory signals. Extrathalamic regions encompass a broader range of structures beyond the thalamus and play distinct roles within the somatosensory system. When these regions are affected by stroke, alterations in somatosensory pathways can occur, and this may lead to the development of CPSP [24].

No significant difference was found between the lesion side and CPSP frequency. Previous studies have reported conflicting results, with some suggesting dominance on the right side while others suggest dominance on the left [6]. Currently, no definitive research has established a clear association between the side of the lesion and CPSP.

The median onset of CPSP in the present study was 3 months post-stroke. This finding is consistent with several studies reporting a temporal range for CPSP, including 1 week and 1 year post-stroke [25,26]. The variability in the initial manifestation of CPSP may be related to the differences in the rate of neuroplastic changes. Furthermore, the process of central sensitization, considered the principal pathophysiological theory underlying CPSP, can take weeks to months to become fully established [15,23].

In this study, CPSP patients reported experiencing pain simultaneously in the face, trunk, and extremities. This observation is consistent with several studies indicating a multifocal origin of pain [25,26]. The somatotopic map becomes more complex at higher levels of the nervous system [27]. The Ventral Posterior Lateral (VPL) nucleus is responsible for sensory input from the trunk and extremities, whereas the Ventral Posterior Medial (VPM) nucleus mediates sensation from the face. Lesions at the thalamic level can impair the integration of incoming sensory information. The internal capsule forms a major part of the thalamocortical pathway, and lesions in this region may impair signal transmission between these structures. Cortical lesions can interfere with the interpretation of sensory information and may be exacerbated by the sensory homunculus that tends to reorganize and potentially invade the damaged area [15,24].

Most patients with CPSP experienced pain continuously. This observation is in line with previous studies [4,26]. The pathophysiological theory of central sensitization in CPSP leads to neuronal hyperexcitability that persists even in the absence of external stimuli and cannot be adequately suppressed by existing inhibitory mechanisms within the central nervous system [3,15].

Pain intensity reported by patients with CPSP was generally moderate. Partial sensory impairment may reduce the integrity of sensory information processing [24]. However, current evidence remains insufficient to clarify the relationship between these factors.

The DN4 scores in this study indicate the involvement of neuropathic mechanisms in CPSP. Burning sensation was the most frequently reported pain quality. Lesions affecting the spinothalamic tract, which conveys pain and temperature information, may account for this finding. Pin and needle sensations were the most commonly reported abnormal sensations. Central sensitization can lead to ectopic neuronal activity in the central nervous system. Pinprick hypoesthesia was the most prevalent sensory abnormality observed. Superficial pain assessed through this examination is transmitted via the spinothalamic pathway. Stroke-related lesions at this level can disrupt the integration of conveyed sensory information. Lesions in extrathalamic structures, such as the cortex and internal capsule, may interfere with the transmission and interpretation of sensory inputs [3,15,24].

This study has several limitations. Although a minimum post-stroke duration of one month was required, not all patients had exceeded three months after stroke onset at the time of assessment. Since CPSP may develop weeks to months after stroke onset, at the time of assessment. Since CPSP may develop weeks to months following stroke, some patients might not yet have manifested neuropathic pain, potentially leading to underestimation. Also, patients with aphasia or significant cognitive impairment were not included, which may limit generalizability to more severe stroke populations.

5. Conclusions

In this outpatient-based study, the frequency of central post-stroke pain is 16.4% among stroke survivors evaluated more than one month after stroke. Younger age and lesion location are significantly associated with CPSP. The median onset occurs at three months post-stroke, and the condition is predominantly characterized by continuous moderate pain with burning and pins-and-needles sensations, frequently accompanied by hypoesthesia to pinprick

These findings underscore the importance of systematic pain assessment during post-stroke follow-up, particularly in younger patients and those with specific lesion locations. Early recognition of neuropathic pain features facilitates timely management and potentially reduces long-term functional burden.

Future studies with larger sample sizes, longitudinal follow-up, and broader inclusion of patients with varying neurological severity are warranted to estimate the true burden of CPSP better.

Author Contributions

Riki Sukiandra: contribute to research design and critical revision of the manuscript. Dini Hanania: manuscript drafting and data analysis M. Zacky Haikal: manuscript drafting and data collection M. Faaiz Adlii: data collection.

Funding

This research received no external funding.

Competing Interests

The authors have declared that no competing interests exist.

Data Availability Statement

The datasets produced and/or examined in this study can be obtained from the corresponding author upon reasonable request.

AI-Assisted Technologies Statement

The authors used ChatGPT and Gemini solely to assist with grammar review and refinement of writing style during manuscript preparation. All contents, research activities, ideas, and intellectual contributions are entirely the responsibility of the authors.

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