Abstract TP147: Central Post Stroke Pain: A Systematic Review

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jonathan Singer ◽  
Alyssa Conigliaro ◽  
Elizabeth Spina ◽  
Susan Law ◽  
Steven Levine

Background: Central Post Stroke Pain (CPSP) is reportedly due to strokes in the thalamic region (Dishinbition Theory); however, the Central Imbalance Theory states that CPSP is due to damage to the spinothalamic pathway (STP). Aims: 1) Clarify the role of thalamic strokes and STP damage in CPSP patients. 2) Gain a current understanding of anatomic substrates, brain imaging, and treatment of CPSP. Methods: Two independent reviewers systematically reviewed PUBMED, CINAHL and Web of Science for studies including original, clinical studies and randomized controlled trials (RCTs) using PRISMA guidelines. Studies had to assess CPSP, using a single question or pain scale. Results: Search from January – July 2016, identifying 731 publications. We extracted data from 23 studies and categorized the articles’ aims into 4 sections: somatosensory deficits (5 studies), STP (3 studies), brain imaging (7 studies), and RCTs (8 studies). Somatosensory studies showed high rates of CPSP; however, the underlying causes of these deficits were unclear. Most studies did not refer to stroke location as playing a role in CPSP, but that pathways may. STP studies displayed consistent evidence that the STP plays a major role in CPSP, delineating that CPSP can occur even when the stroke is not in the thalamic region but in other regions (e.g. cerebellum, basal ganglia, medulla). Four of the brain imaging studies found CPSP not related and 3 found it was related to thalamic strokes. All 7 studies had major limitations including sample size, no control groups, and selection bias. RCTs were mostly negative, but brain stem and motor cortex stimulation studies showed the most promise. Conclusions: While CPSP has been linked to the thalamic region since the early 1900’s, the peer-reviewed literature showed equivocal results when examining location of stroke. Our systematic review suggests damage to the STP is associated with CPSP and this could provide insights into mechanisms and treatment. Moreover, historical connection of strokes in the thalamic region and CPSP should be reevaluated as many studies noted that strokes in other regions of the brain also produce CPSP.

2017 ◽  
Vol 12 (4) ◽  
pp. 343-355 ◽  
Author(s):  
Jonathan Singer ◽  
Alyssa Conigliaro ◽  
Elizabeth Spina ◽  
Susan W Law ◽  
Steven R Levine

Background Physical, psychological, and/or social impairment can result after a stroke and can be exacerbated by pain. One type of pain after stroke, central poststroke pain, is believed to be due to primary central nervous system mechanisms. Estimated prevalence of central poststroke pain ranges widely from 8% to 55% of stroke patients, suggesting a difficulty in reliably, accurately, and consistently identifying central poststroke pain. This may be due to the absence of a generally accepted definition. Aim We aimed to clarify the role of thalamic strokes and damage to the spinothalamic pathway in central poststroke pain patients. Also, we aimed to gain a current understanding of anatomic substrates, brain imaging, and treatment of central poststroke pain. Summary of review Two independent reviewers identified 10,144 publications. Based on Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines, we extracted data from 23 papers and categorized the articles’ aims into four sections: somatosensory deficits, pathway stimulation, clinical trials, and brain imaging. Conclusions Our systematic review suggests that damage to the spinothalamic pathway is associated with central poststroke pain and this link could provide insights into mechanisms and treatment. Moreover, historical connection of strokes in the thalamic region of the brain and central poststroke pain should be reevaluated as many studies noted that strokes in other regions of the brain have high occurrence of central poststroke pain as well.


2020 ◽  
Vol 21 (18) ◽  
pp. 6739
Author(s):  
Sharmeelavathi Krishnan ◽  
Yasaswi Shrestha ◽  
Dona P. W. Jayatunga ◽  
Sarah Rea ◽  
Ralph Martins ◽  
...  

Neurodegenerative diseases result in a range of conditions depending on the type of proteinopathy, genes affected or the location of the degeneration in the brain. Proteinopathies such as senile plaques and neurofibrillary tangles in the brain are prominent features of Alzheimer’s disease (AD). Autophagy is a highly regulated mechanism of eliminating dysfunctional organelles and proteins, and plays an important role in removing these pathogenic intracellular protein aggregates, not only in AD, but also in other neurodegenerative diseases. Activating autophagy is gaining interest as a potential therapeutic strategy for chronic diseases featuring protein aggregation and misfolding, including AD. Although autophagy activation is a promising intervention, over-activation of autophagy in neurodegenerative diseases that display impaired lysosomal clearance may accelerate pathology, suggesting that the success of any autophagy-based intervention is dependent on lysosomal clearance being functional. Additionally, the effects of autophagy activation may vary significantly depending on the physiological state of the cell, especially during proteotoxic stress and ageing. Growing evidence seems to favour a strategy of enhancing the efficacy of autophagy by preventing or reversing the impairments of the specific processes that are disrupted. Therefore, it is essential to understand the underlying causes of the autophagy defect in different neurodegenerative diseases to explore possible therapeutic approaches. This review will focus on the role of autophagy during stress and ageing, consequences that are linked to its activation and caveats in modulating this pathway as a treatment.


2022 ◽  
Vol 12 ◽  
Author(s):  
Zhengwu Zhang ◽  
Jennifer S. Gewandter ◽  
Paul Geha

The prevalence of chronic pain has reached epidemic levels. In addition to personal suffering chronic pain is associated with psychiatric and medical co-morbidities, notably substance misuse, and a huge a societal cost amounting to hundreds of billions of dollars annually in medical cost, lost wages, and productivity. Chronic pain does not have a cure or quantitative diagnostic or prognostic tools. In this manuscript we provide evidence that this situation is about to change. We first start by summarizing our current understanding of the role of the brain in the pathogenesis of chronic pain. We particularly focus on the concept of learning in the emergence of chronic pain, and the implication of the limbic brain circuitry and dopaminergic signaling, which underly emotional learning and decision making, in this process. Next, we summarize data from our labs and from other groups on the latest brain imaging findings in different chronic pain conditions focusing on results with significant potential for translation into clinical applications. The gaps in the study of chronic pain and brain imaging are highlighted in throughout the overview. Finally, we conclude by discussing the costs and benefits of using brain biomarkers of chronic pain and compare to other potential markers.


2016 ◽  
Vol 31 (1) ◽  
pp. 40-52 ◽  
Author(s):  
Ling-Feng Zeng ◽  
Ye Cao ◽  
Lu Wang ◽  
Yun-Kai Dai ◽  
Ling Hu ◽  
...  

2017 ◽  
Vol 33 (S1) ◽  
pp. 227-227 ◽  
Author(s):  
Setefilla Luengo-Matos ◽  
Mar Polo-Desantos ◽  
Luis Maria Sanchez-Gomez ◽  
Juan Pablo Chalco Orrego

INTRODUCTION:Alzheimer's disease (AD) is the most common type of dementia. Plasmapheresis is a procedure consisting of removing the plasma, or specific elements which are considered to be involved in pathological processes. Plasmapheresis could reduce the A beta peptides load in the brain. The objective is to study the safety and efficacy of plasmapheresis for AD.METHODS:Systematic review, with all studies published before April 2016 reviewed. Selected studies included patients with AD treated with plasmapheresis. GRADE was used to assess quality. Efficacy outcomes include: (i) Cognitive, functional and behavior status, through Mini Mental State Examination, and Alzheimer Disease Assessment Scale-Cognitive test; (ii) Plasma and cerebrospinal fluid A beta levels; (iii) Brain-imaging and functional neuroimaging studies. Safety outcomes included side effects related to the treatment.RESULTS:Two papers reporting results from three studies were selected: (i) pilot study (n = 10), (ii) its extended study (12 months more of follow-up) (n = 7), and (iii) clinical trial (n = 39). The quality of evidence was very low. About efficacy, the studies didn't report quantitative results and were inconclusive. The pilot study and its extended study reported (1): a tendency towards stabilization in cognitive status; the plasma levels of A beta peptides didn't show a clear pattern; and the brain-imaging assessment suggested a progressive volume increase in the hippocampus. The clinical trial reported in the experimental group vs control (2): a better score for the cognitive status; an increase of plasma A beta peptides; and did not find significant differences between groups for cerebrospinal fluid A beta peptides. The brain-imaging assessment showed a progressive loss of hippocampus volume in both groups. Regarding safety, the studies didn't report quantitative data. We didn't find economic evaluation studies.CONCLUSIONS:The included studies had very high risk of bias and very low quality. We found no evidence on efficacy and safety of plasmapheresis treating AD. Plasmapheresis isn't a priority line in research of AD treatment.


2020 ◽  
Vol 21 (11) ◽  
pp. 3933
Author(s):  
Nika Zharichenko ◽  
Dolores B. Njoku

Interleukin (IL)-33 is a member of the IL-1 family of proteins that have multiple roles in organ-specific inflammation. Many studies suggest diagnostic and therapeutic implications of this cytokine. Many studies have reported pro-inflammatory roles for IL-33 in innate immune responses involving the heart and lung. Recent studies also describe pro-inflammatory and regulatory roles for IL-33 in the pathogenesis of brain and liver disorders in addition to regulatory roles for this cytokine in the heart and lung. In this focused systematic review, we will review the literature regarding pro-inflammatory and regulatory effects of IL-33 in the brain and liver. We will also assess the potential risk of bias in the published literature in order to uncover gaps in the knowledge that will be useful for the scientific community. We utilized guidelines set by preferred reporting items for systemic reviews and meta-analyses. The electronic database was PubMed. Eligibility criteria included organ-specific inflammation in mice and humans, organ-specific inflammation in the central nervous and hepatic systems, and IL-33. Outcomes were pro-inflammatory or regulatory effects of IL-33. Risk of bias in individual studies and across studies was addressed by adapting the Cochrane Rob 2.0 tool. We discovered that a source of bias across the studies was a lack of randomization in human studies. Additionally, because the majority of studies were performed in mice, this could be perceived as a potential risk of bias. Regarding the central nervous system, roles for IL-33 in the development and maturation of neuronal circuits were reported; however, exact mechanisms by which this occurred were not elucidated. IL-33 was produced by astrocytes and endothelial cells while IL-33 receptors were expressed by microglia and astrocytes, demonstrating that these cells are first responders for IL-33; however, in the CNS, IL-33 seems to induce Th1 cytokines such as IL-1β and TNF-α chemokines such as RANTES, MCP-1, MIP-1α, and IP-10, as well as nitric oxide. In the liver, similar risks of bias were determined because of the lack of randomized controlled trials in humans and because the majority of studies were performed in mice. Interestingly, the strain of mouse utilized in the study seemed to affect the role of IL-33 in liver inflammation. Lastly, similar to the brain, IL-33 appeared to have ST2-independent regulatory functions in the liver. Our results reveal plausible gaps in what is known regarding IL-33 in the pathogenesis of brain and liver disorders. We highlight key studies in the lung and heart as examples of advancements that likely occurred because of countless basic and translational studies in this area. More research is needed in these areas in order to assess the diagnostic or therapeutic potential of IL-33 in these disorders.


Land ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 463
Author(s):  
Lila Juniyanti ◽  
Herry Purnomo ◽  
Hariadi Kartodihardjo ◽  
Lilik Budi Prasetyo

Indonesia has experienced one of the world’s greatest dynamic land changes due to forestry and agricultural practices. Understanding the drivers behind these land changes remains challenging, partly because landscape research is spread across many domains and disciplines. We provide a systematic review of 91 studies that identify the causes and land change actors across Sumatra and Kalimantan. Our review shows that oil palm expansion is the most prominent (65 studies) among multiple direct causes of land change. We determined that property rights are the most prominent issue (31 studies) among the multiple underlying causes of land change. Distinct combinations of mainly economic, institutional, political, and social underlying drivers determine land change, rather than single key drivers. Our review also shows that central and district governments as decision-making actors are prominent (69 studies) among multiple land change actors. Our systematic review indicates knowledge gaps that can be filled by clarifying the identification and role of actors in land change.


2020 ◽  
Vol 31 (6) ◽  
pp. 659-674
Author(s):  
Umar M. Bello ◽  
Stanley J. Winser ◽  
Chetwyn C.H. Chan

AbstractMirror-induced visual illusion obtained through mirror therapy is widely used to facilitate motor recovery after stroke. Activation of primary motor cortex (M1) ipsilateral to the moving limb has been reported during mirror-induced visual illusion. However, the mechanism through which the mirror illusion elicits motor execution processes without movements observed in the mirrored limb remains unclear. This study aims to review evidence based on brain imaging studies for testing the hypothesis that neural processes associated with kinaesthetic motor imagery are attributed to ipsilateral M1 activation. Four electronic databases were searched. Studies on functional brain imaging, investigating the instant effects of mirror-induced visual illusion among stroke survivors and healthy participants were included. Thirty-five studies engaging 78 stroke survivors and 396 healthy participants were reviewed. Results of functional brain scans (n = 20) indicated that half of the studies (n = 10, 50%) reported significant changes in the activation of ipsilateral M1, which mediates motor preparation and execution. Other common neural substrates included primary somatosensory cortex (45%, kinaesthesia), precuneus (40%, image generation and self-processing operations) and cerebellum (20%, motor control). Similar patterns of ipsilateral M1 activations were observed in the two groups. These neural substrates mediated the generation, maintenance, and manipulation of motor-related images, which were the key processes in kinaesthetic motor imagery. Relationships in terms of shared neural substrates and mental processes between mirror-induced visual illusion and kinaesthetic motor imagery generate new evidence on the role of the latter in mirror therapy. Future studies should investigate the imagery processes in illusion training for post-stroke patients.


Author(s):  
Bernadetta Germia Aridamayanti ◽  
Gevi Melliya Sari ◽  
Wimar Anugrah Romadhon

Background: Motor Imagery (MI) is an intervention to improve motor skills in post stroke hemiparesis patients by focusing on weak body parts. Objective: To describe the effectiveness of providing MI in the rehabilitation of post stroke patients. Method: The database used to identify suitable articles obtained from Scopus, ProQuest and Pubmed was limited to the last 5 years of publication from 2016 to 2020, English, and fulltext articles. The literature review used the keyword "Motor Imagery" AND "Stroke Rehabilitation". In searching articles used "AND". Only 8 articles met the inclusion criteria. This review was from these 8 articles. Results: MI has effectiveness in cognitive, sensory and motor post-stroke patients by stimulating neuroplasticity in various areas of the brain so that it accelerates the increase in O2, glucose and various metabolites that lead to increased regional metabolism through dilation of cerebral arterioles and capillaries. MI which is given routinely will help the recovery of motor function of post-stroke patients and increase patient independence. Conclusion: MI has a lot of effectiveness in the rehabilitation of post stroke patients. Suggestion: MI is considered necessary to be applied in hospitals in Indonesia. Keywords: motor imagery; stroke; rehabilitation ABSTRAK Latar belakang: Motor Imagery (MI) merupakan intervensi untuk meningkatkan keterampilan motorik pada pasien hemiparesis post stroke dengan berfokus pada bagian tubuh yang lemah. Tujuan: Untuk menjabarkan efektivitas pemberian MI pada rehabilitasi pasien post stroke. Metode: Database yang digunakan dalam penelitian ini adalah Scopus, Proquest dan Pubmed terbatas untuk publikasi 5 tahun terakhir dari 2016 hingga 2020, full text article dan berbahasa Inggris. Kata kunci yang digunakan adalah “Motor Imagery” AND “Stroke Rehabilitation”. Systematic review ini menggunakan 8 artikel yang sesuai dengan kriteria inklusi. Hasil: MI memiliki efektivitas pada kognitif, sensorik dan motorik pasien post stroke dengan merangsang neuroplastisitas pada berbagai area otak sehingga memperlancar peningkatan O2, glukosa dan berbagai metabolit yang mengarah ke peningkatan metabolisme regional melalui dilatasi arteriol serebral dan kapiler. Motor Imagery (MI) yang diberikan secara rutin akan membantu pemulihan fungsi motorik pasien post stroke dan meningkatkan kemandirian pasien. Simpulan: MI memiliki banyak efektivitas pada rehabilitasi pasien post stroke Saran: MI dipandang perlu untuk diterapkan di rumah sakit yang ada di Indonesia. Kata kunci: motor imagery; stroke; rehabilitation


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