Extracellular Nucleosome Levels in the Etiopathogenesis of Sepsis Associated Coagulopathy

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 564-564 ◽  
Author(s):  
Amanda Walborn ◽  
Priya Patel ◽  
Debra Hoppensteadt ◽  
Michael Mosier ◽  
Matthew T. Rondina ◽  
...  
Keyword(s):  
Host Defense ◽  
Conflicts Of Interest ◽  
Fibrin Clot ◽  
Endothelial Damage ◽  
Coagulation Cascade ◽  
Healthy Individuals ◽  
Commercial Laboratory ◽  
Normal Individuals ◽  
Inflammatory Processes ◽  
D Dimer

Abstract Introduction: Neutrophil extracellular traps (NETs) are structures composed of DNA, histones, and bactericidal factors that are expelled by neutrophils in order to trap and neutralize bacteria. NETs play a role in host defense by trapping and killing infecting bacteria and inactivating bacterial virulence factors. Activation of the coagulation cascade by these components can lead to "immunothrombosis" and facilitate the containment and destruction of bacteria within a fibrin clot. Although extracellular nucleosomes (structures consisting of DNA wound around a histone protein core) within NETs can contribute to host defense, they can also play a role in disease pathology by leading to inflammation, endothelial damage, and pathological thrombosis. Disseminated intravascular coagulation (DIC) is a condition characterized by systemic activation of the coagulation and fibrinolytic systems that can occur in conjunction with several underlying conditions, including sepsis. Links between infection, host response, and systemic coagulation, extracellular nucleosomes may play a significant role in the pathophysiology of sepsis-associated DIC. The purpose of this study was to quantify extracellular nucleosomes in the plasma of patients with sepsis-associated DIC. Materials and Methods: Citrated, de-identified plasma samples were collected from patients with sepsis and suspected DIC at ICU admission and on ICU days 4 and 8 under an IRB approved protocol. DIC score was evaluated in each sample using the ISTH scoring algorithm incorporating platelet count, PT/INR, fibrinogen (Recombiplastin, Instrumentation Laboratory, Bedford, MA), and D-Dimer (HyphenBioMed,Neuville-Sur-Oise, France). Plasma from healthy individuals was purchased from a commercial laboratory (George King Biomedical, Overland,KS). Nucleosomes in plasma were measured using the Cell Death Detection ELISA (Roche Diagnostics, Indianapolis, IN). The correlation of variation for both intra-assay and inter-assay variation was <15%. Results: Nucleosomes were significantly elevated in patients with sepsis and suspected DIC compared to healthy individuals on ICU days 0 (p = 0.028), 4 (p < 0.0001), and 8 (p = 0.013). Results are shown in Table 1. When patients were categorized according to ISTH DIC score, a non-significant trend towards increasing nucleosomes with increasing DIC score was observed. Nucleosomes were significantly elevated in patients with overt DIC compared to normal individuals on ICU day 0 (p = 0.02). On ICU day 4, nucleosomes were significantly elevated in patients with both overt and non-overt DIC compared to healthy individuals (p < 0.01). Results are shown in Table 2. Furthermore, nucleosome levels correlated significantly (r >0.2, p<0.05) with factors involved in inflammation and coagulation. Nucleosomes correlated significantly with D-Dimer, prothrombin fragment F1.2, IL-8, and IL-10. No significant correlation was observed between nucleosomes and IL-2, IL-4, IL-6, VEGF,IFNγ, TNFα, IL-1α, IL-1β, MCP1, and EGF. Conclusion: Plasma nucleosome levels were elevated in patients hospitalized with sepsis and suspected DIC, and a trend towards increasing circulating nucleosome levels with increasing DIC score was observed. This supports the hypothesis that nucleosomes contribute to the pathophysiology of sepsis-associated DIC. The correlation of nucleosomes with the infection markers and a subset of inflammatory markers suggests that the presence of nucleosomes in the plasma of patients with sepsis-associated DIC may be due to specific, infection-related processes and not to general inflammatory processes. Additionally, the correlation of circulating nucleosome levels with markers of thrombin generation and fibrinolysis suggests that nucleosomes may play a role in the activation of coagulation observed in patients with sepsis-associated DIC. Disclosures No relevant conflicts of interest to declare.

scholarly journals Biomarkers of Hemostatic Dysregulation, Inflammation, and Infection in Patients Diagnosed with Sepsis Associated Coagulopathy

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2281-2281
Author(s):  
Amanda Walborn ◽  
Daniel Kahn ◽  
Debra Hoppensteadt ◽  
Jawed Fareed
Keyword(s):  
Conflicts Of Interest ◽  
Coagulation Factors ◽  
Endothelial Damage ◽  
Factor Ix ◽  
Response To Treatment ◽  
Coagulation Cascade ◽  
Factor Vii ◽  
Molecular Profile ◽  
Healthy Individuals ◽  
Normal Individuals

Abstract Introduction: Sepsis associated coagulopathy (SAC) is one of the major pathophysiological mechanisms of sepsis and has been shown to greatly increase mortality in septic patients. SAC is characterized by the inappropriate activation of the coagulation cascade, leading to the formation of microthrombi and the potential for multiple organ failure. Additionally, the excessive consumption of platelets and coagulation factors can create a risk of excessive bleeding. SAC is a complex syndrome, involving coagulation factors, inflammatory cytokines, and several other notable factors of varied origin. In this study, our aim was to evaluate the levels of endocan, pentraxin, and procalcitonin in individuals with SAC diagnosed according to the ISTH criteria in comparison to healthy individuals. Endocan is a soluble, circulating proteoglycan that normally binds to LFA-1 and inhibits leukocyte diapedesis. It is produced by vascular endothelial cells as well as the lung and kidney and has been proposed as a marker of endothelial dysfunction and disease severity in patients with sepsis. Endocan may be useful in the evaluation and tracking of SAC as a marker of endothelial damage caused by excessive inflammation and coagulation. Pentraxin (PTX3) is a protein structurally similar to CRP that is produced by several cell types in response to inflammatory signals and is known to be a marker of inflammation in a number of disease processes. In addition to being the precursor of the hormone calcitonin, procalcitonin is produced by a variety of tissues and may correlate with degree of infection and response to treatment in individuals with sepsis. Taken together, endocan, pentraxin, and procalcitonin may be useful in the evaluation and monitoring of SAC as they are representative of endothelial damage, inflammation, and systemic infection, respectively. Materials and Methods: Blood from 50 patients with SAC and 33 normal individuals obtained from a commercial source (George King Biomedical, Overland Park, KS) were evaluated. Levels of pentraxin, procalcitonin, endocan, and coagulation factors VII, IX, and X were measured using commercially available ELISA kits from Stago (Parsippany, NJ), Lunginnov (Lillie, France) and R&D Systems (Minneapolis, MN). All results are compiled as group mean and expressed as average mean + SD. These values are compared with normal and results were computed as percent increase or decrease. Results: The levels of coagulation factors VII and X were found to be reduced in patients with SAC compared to normal individuals (p < 0.05); the level of factor IX was statistically unchanged. The reduction in factor X was relatively modest, less than a 20% reduction compared to normal, while the reduction in factor VII was more marked, with a greater than 40% reduction compared to normal. The levels of pentraxin, proxalcitonin, and endocan were all found to be significantly elevated in blood from SAC patients compared to blood from normal healthy individuals (p < 0.05). All three markers exhibited a greater than 100% average increase when compared to normal. Discussion: These results indicate that endocan, pentraxin, procalcitonin, and factor VII are all candidates for further investigation in the identification of a more comprehensive molecular profile of SAC and in the development of diagnostic or prognostic tests. The significant degree of change observed in each marker from normal provides a baseline for future studies of these markers in SAC patients. Although these factors individually are not specific markers of SAC, each is a marker for a specific system that is dysregulated in SAC; endocan for endothelial damage, pentraxin for inflammation, procalcitonin for infection, and factor VII for coagulation. Taken together, these biomarkers may be useful in the diagnosis and monitoring of SAC. Disclosures No relevant conflicts of interest to declare.

Ruxolitinib Treatment Induces a Transition of Classical to Non-Classical Monocytes in Patients with Myelofibrosis

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2838-2838 ◽  
Author(s):  
Sanja Prijic ◽  
Taghi Manshouri ◽  
Ying Zhang ◽  
Ivo Veletic ◽  
Xiaorui Zhang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
De Novo ◽  
Conflicts Of Interest ◽  
Myeloproliferative Neoplasm ◽  
Size Reduction ◽  
Spleen Size ◽  
Healthy Individuals ◽  
Normal Individuals ◽  
Monocyte Subpopulations ◽  
Classical Monocytes

Abstract Introduction: Myelofibrosis (MF) is a clonal myeloproliferative neoplasm that develops de novo (primary myelofibrosis) or transforms from polycythemia vera or essential thrombocytosis. MF is characterized by stem cell-derived clonal myeloproliferation, abnormal cytokine expression, bone marrow fibrosis, anemia, splenomegaly, extramedullary hematopoiesis, constitutional symptoms, cachexia, leukemic progression, and shortened survival. Several studies suggested that clonal monocytes play a role in the pathobiology of MF. However whether a specific monocyte subpopulation is predominantly present in MF is largely unknown. Traditionally, three subpopulations of CD14+ monocytes have been identified: classical (CD14++/CD16-), intermediate (CD14++/CD16+), and non-classical (CD14dim+/CD16++). Whether MF patients' monocyte subpopulations are different from those of normal individuals and how ruxolitinib treatment affects them has not been elucidated. Methods: Using flow cytometry we first assessed the distribution of the three monocyte subpopulations in the bone marrow (BM) of healthy individuals and MF and then assessed their distribution in BM samples from phase I/II clinical trial of ruxolitinib in patients with primary or secondary MF (Verstovsek S. etal. N Engl J Med 12:1117, 2010). Results: Using BM samples from 7 healthy individuals and 12 untreated MF patients we found a significant decrease in the percentage of monocytes (p =0.0061) in the mononuclear gate of untreated MF patients compared to normal individuals. However, the distribution of classical vs. non-classical monocyte subpopulations in MF was similar to that of normal BM (p =0.3, p =0.3, respectively). Remarkably, ruxolitinib treatment significantly altered the distribution of classical vs. non-classical monocyte subpopulations. During treatment (years 0-3, 3-6, 6-8) we identified a progressive increase in the percentage of monocytes in the mononuclear gate (p =0.1; p =0.04, and p =0.03, respectively) with a substantial increase in the non-classical monocyte subpopulation in years 0-3 and 3-6 of treatment (p= 0.04, p= 0.005, respectively) and a decrease in the classical monocytes (p =0.07, p =0.008, respectively). This trend reversed after 6-8 years of therapy (p =0.3, p =0.2, respectively). Importantly, in ruxolitinib-treated patients with a ≥50% spleen size reduction highest percentage of non-classical monocytes was observed during the first 3 years and years 3-6 of treatment (p =0.01, p =0.01, respectively). However during years 6-8 this difference was no longer detected and the percentage of non-classical monocytes was similar to the percentage detected in the pre-treatment BM samples (p =0.4). These changes correlated with response to ruxolitinib treatment. In patients with a <50% spleen size reduction the percentage of non-classical monocytes in years 0-3 of ruxolitinib treatment was significantly lower compared to patients with ≥50% spleen reduction (p =0.005), and patients with ≥50% spleen reduction show correlation between post-treatment spleen size and percentage of non-classical monocytes (p <0.0001, r=−0.4). Conclusions: Taken together, our results suggest that ruxolitinib induces a transition of classical to non-classical monocyte subpopulation during the first years of ruxolitinib treatment and that this effect correlates with the patients' clinical response. Further studies aimed at exploring the role of monocytes and their subpopulations in the pathobiology of MF are warranted. Disclosures No relevant conflicts of interest to declare.

scholarly journals Assessment of Macrophage Inflammatory Biomarkers and Neutrophil Extracellular Traps Associated Proteins in COVID-19 Patients

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 4193-4193
Author(s):  
Laura Lopez de Frutos ◽  
Irene Serrano-Gonzalo ◽  
Barbara Menendez-Jandula ◽  
Esther Franco-Garcia ◽  
Carlos Lahoz ◽  
...  
Keyword(s):  
Health System ◽  
Macrophage Activation ◽  
Conflicts Of Interest ◽  
Clinical Manifestations ◽  
Neutrophil Extracellular Traps ◽  
Endothelial Damage ◽  
Control Group ◽  
P Value ◽  
Extracellular Traps ◽  
D Dimer

Abstract Background : The SARS-CoV-2 infection activates both innate and adaptive immune responses and induces an exaggerated cytokine storm leading to causes septic shock, acute respiratory distress syndrome, and/or multiple organ failure in critically ill patients. The knowledge of this dysregulated immune response is not well explained. One hypothesis is that the response of macrophages and neutrophils to infection is disproportionate, resulting in overproduction of cytokines and activation of neutrophils leading to the most severe complications of infection, including the production of multiple microthrombi and endothelial damage. Aim of the study: To evaluate the activation levels of macrophage biomarkers as well as indicators of the development of neutrophil extracellular traps (NET) in the first phase of infection in hospitalized patients with COVID19. Patients and Methods: We selected dry blood spot from a total of 60 previously identified SARS-CoV-2 infected subjects. Plasma samples were provided by the Aragon Health System Biobank's collection and were extracted within 5 days of symptom onset. Plasma from 60 healthy controls were used to stablish the control range for NETosis determination. The study was authorized by the Ethics Committee of the Aragon Health System and complies with the European General Data Protection Regulation (GDPR 2016/679) and LO 3/2018. Demographic characteristics, clinical manifestations, follow-up during hospitalization, associated comorbidities, and thrombotic complications were obtained from the database. Chitotriosidase activity (ChT), YKL40 chitinase and CCL18/PARC cytokine were measured as markers of macrophage activation. Myeloperoxidase (MPO), Neutrophil Elastase (NE), and S100A8/S100A9 Heterodimer (MPR) were immuno-quantified, levels of circulating free DNA (cfDNA) were measured as well as the presence of DNAsases by fluorimetry as indicators of Netosis. For the comparative analysis, we stratified patients by age groups and disease severity and used the Mann-Whitney U test for statistical comparison, considering a p-value &lt; 0.05 as statistically significant. Results : A statistically significant increase in ChT (p=0.032) and CCL18/PARC (p=0.0001) was observed in the patients´ group. A comparative study with clinical variables and other inflammation markers as ferritin, D-dimer will be shown upon acceptance. Concerning NET markers, we found a statistically significant increase in MPO, NE, and MRP in COVID-19 patients (p=0.0001; p=0.0290; p=0.0001 respectively), as well as a statistically significant decrease in DNAsa (p=0.0001). No differences in cfDNA levels were observed. The table shows the median (quartile1-quartile3) for each marker in the control group and in the patient group. Conclusions : In this study, biomarkers of macrophage activation do not appear to be more sensitive than the indicators of inflammation in routine clinical practice (ferritin, D-dimer). Clinical cases of severe COVID-19 disease show an excessive NET formation, which contributes to vascular damage and the development of thrombosis. This work was supported by a research grant from FEETEG Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

Altered fibrin clot structure/function in patients with antiphospholipid syndrome: association with thrombotic manifestation

2014 ◽  
Vol 112 (08) ◽  
pp. 287-296 ◽  
Author(s):  
Magdalena Celińska-Löwenhoff ◽  
Teresa Iwaniec ◽  
Agnieszka Padjas ◽  
Jacek Musiał ◽  
Anetta Undas
Keyword(s):  
Structure Function ◽  
Antiphospholipid Syndrome ◽  
Thrombotic Event ◽  
Fibrin Clot ◽  
Clot Lysis ◽  
Lag Phase ◽  
Lysis Time ◽  
Clot Structure ◽  
Clot Lysis Time ◽  
D Dimer

SummaryWe tested the hypothesis that plasma fibrin clot structure/function is unfavourably altered in patients with antiphospholipid syndrome (APS). Ex vivo plasma clot permeability, turbidity and susceptibility to lysis were determined in 126 consecutive patients with APS enrolled five months or more since thrombotic event vs 105 controls. Patients with both primary and secondary APS were characterised by 11% lower clot permeability (p<0.001), 4.8% shorter lag phase (p<0.001), 10% longer clot lysis time (p<0.001), and 4.7% higher maximum level of D-dimer released from clots (p=0.02) as compared to the controls. Scanning electron microscopy images confirmed denser fibrin networks composed of thinner fibres in APS. Clots from patients with “triple-antibody positivity” were formed after shorter lag phase (p=0.019) and were lysed at a slower rate (p=0.004) than in the remainder. Clots from APS patients who experienced stroke and/or myocardial infarction were 8% less permeable (p=0.01) and susceptible to lysis (10.4% longer clot lysis time [p=0.006] and 4.5% slower release of D-dimer from clots [p=0.01]) compared with those following venous thromboembolism alone. Multivariate analysis adjusted for potential confounders showed that in APS patients, lupus anticoagulant and “triple-positivity” were the independent predictors of clot permeability, while “triple-positivity” predicted lysis time. We conclude that APS is associated with prothrombotic plasma fibrin clot phenotype, with more pronounced abnormalities in arterial thrombosis. Molecular background for this novel prothrombotic mechanism in APS remains to be established.

COVID-19 AND STROKE: POSSIBLE CAUSES AND PATHOGENESIS (REVIEW)

Vestnik ◽  
2021 ◽  
pp. 103-106
Author(s):  
А.Е. Кожашева ◽  
С.О. Белесбек ◽  
Д.Ж. Абдимитова ◽  
Б.М. Сакен ◽  
А.П. Бориходжаева ◽  
...  
Keyword(s):  
Preventive Measures ◽  
Cerebrovascular Disorders ◽  
Endothelial Damage ◽  
Cytokine Release ◽  
Contributing Factors ◽  
Acute Cerebrovascular Accident ◽  
Von Willebrand ◽  
The Relationship ◽  
Willebrand Factor ◽  
D Dimer

Появляются доказательства того, что COVID-19 может вызывать выброс цитокинов, состояние гиперкоагуляции и повреждение эндотелия, которое может привести к острому нарушению мозгового кровообращения (ОНМК). В данной статье авторы обсуждают взаимосвязь между COVID-19 и ОНМК, и о возможных факторах, способствующих возникновению инсульта. Как свидетельствует увеличение D-димера, фибриногена, фактора VIII и фактора фон Виллебранда, инфекция SARS-CoV-2 вызывает коагулопатию, нарушает функцию эндотелия и способствует состоянию гиперкоагуляции. В совокупности это предрасполагает пациентов к цереброваскулярным нарушениям. Механизм, лежащий в основе COVID-19 и инсульта, требует дальнейшего изучения, равно как и разработка эффективных терапевтических или профилактических мер. Evidence is emerging that COVID-19 can cause cytokine release, hypercoagulable states, and endothelial damage that can lead to acute cerebrovascular accident (ACVI). In this article, the authors discuss the relationship between COVID-19 and stroke and the possible contributing factors to stroke. As evidenced by an increase in D-dimer, fibrinogen, factor VIII and von Willebrand factor, SARS-CoV-2 infection causes coagulopathy, disrupts endothelial function and hypercoagulability. Collectively, this predisposes patients to cerebrovascular disorders. The mechanism underlying COVID-19 and stroke requires further study, as does the development of effective therapeutic or preventive measures.

Abstract 315: Efficacy and Safety of Rivaroxaban in in vitro Experiments With the Endothelial Cells

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Kaname Seki ◽  
Yosuke Mizuno ◽  
Toku Sakashita ◽  
Jun Tanno ◽  
Shintaro Nakano ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Time Course ◽  
Umbilical Vein ◽  
Endothelial Damage ◽  
Coagulation Cascade ◽  
Elisa Assay ◽  
Mrna Levels ◽  
Factor X ◽  
Clotting Factors ◽  
Inflammatory Phase

Aim: Activated factor X (FXa) plays important roles in the thrombin generation and in inflammation, which is evoked during the endothelial damage. Although rivaroxaban is a selective FXa antagonist, it is one of the key therapies in ischemic heart disease, and yet its function in the state of inactivated coagulation cascade is uncertain. Rivaroxaban blocks FXa in the blood but not the tissue, while factor X is converted to FXa only when glutamic acid is changed to γ-carboxyglutamic acid by vitamin K following the intrinsic clotting factors and/or cellular injury activation. To uncover this aspect, we performed the following experiments. Methods and results: Human umbilical vein endothelial cells (HUVECs) were obtained from Lonza Co., Ltd. The cells were grown to 80% confluence and were treated with rivaroxaban (100nM, 500nM, 1000nM, 2000nM respectively) without FXa stimulation for 4 h, 10 h or 24 h. Cells and medium were collected and then their RNA was extracted from the cells. The qPCR of MCP-1, PAR1-4 and the DNA micro arrays (The GeneChip Human Gene 2.0 ST Array, Affymetrix) were performed. There was neither increased nor decreased gene expression significantly in either experimental time course of the qPCRs or the the DNA micro arrays. The ELISA assay of MCP-1 with medium showed non-activated MCP-1. As a next step, cells were treated with 100nM FXa and with/without rivaroxaban in same time course, and cells and medium were collected for further experiments. FXa evoked induction of mRNA levels for several pro-inflammatory cytokines including MCP-1 maximally at 4h, whereas MCP-1 was maximally evoked at 24 h in ELISA assay. Interestingly rivaroxaban inhibited both in all time course, at 4 hour inflammatory phase and at 24 hour inflammatory phase. Conclusion: Collectively, these results suggest that rivaroxaban may be safe in the inactivated coagulation state, and has the efficacy to attenuate the endothelial damage evoked by FXa and by pro-inflammatory cytokine genes.

PS01.103: THE UNUSUAL CAUSES OF ODYNOPHAGIA

2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 78-78 ◽  
Author(s):  
Kheng Tian Lim
Keyword(s):  
Complete Resolution ◽  
Conflicts Of Interest ◽  
Fish Bone ◽  
Esophageal Injury ◽  
Mediastinal Infection ◽  
Inflammatory Processes ◽  
History Of ◽  
Fish Ingestion ◽  
The Right ◽  
Esophageal Ulcers

Abstract Background Odynophagia can be caused by infective and non-infective inflammatory processes, benign and malignant esophageal disorders such as achalasia, gastro-esophageal reflux disease and carcinoma. Methods We described two unusual cases of odynophagia and their individual management. Results Case 1 is a 21 year-old Indian man presented with 2 days history of odynophagia after taking doxycycline capsules indicated for acne. An esophagogastroduodenoscopy (OGD) was performed and showed multiple mid esophageal ulcers. Esophageal biopsy taken showed inflammatory ulcer slough with no fungal infection, dysplasia or malignancy. Doxycycline was stopped and patient recovered with complete resolution of odynophagia. Case 2 is a 55 year-old Chinese man presented with 1 day history of odynophagia and severe chest pain after eating a bowl of hot fish soup. A CT Thorax was performed which showed a localised perforation of the right wall of the esophagus with extraluminal gas posterior to the trachea. An urgent OGD was performed and an L-shaped fish bone was removed successfully and an endoclip was applied to close the puncture hole of esophagus. Patient made a full recovery without any mediastinal infection. Conclusion Odynophagia from mid esophageal ulcers secondary to doxycycline intake should be recognized and can be easily managed by stopping the antibiotics with complete resolution of the symptom. Fish ingestion leading to sharp bone induced penetrating esophageal injury can be safely managed by endoscopic removal and endoclip application. Disclosure All authors have declared no conflicts of interest.

scholarly journals The surface electromyography analysis of the non-plegic upper limb of hemiplegic subjects

2010 ◽  
Vol 68 (4) ◽  
pp. 562-566 ◽  
Author(s):  
Heloyse U Kuriki ◽  
Raquel N. de Azevedo ◽  
Augusto C. de Carvalho ◽  
Fábio Mícolis de Azevedo ◽  
Rúben F Negrão-Filho ◽  
...  
Keyword(s):  
Control Group ◽  
Electromyographic Activity ◽  
Healthy Individuals ◽  
Wrist Flexion ◽  
Functional Changes ◽  
Normal Individuals ◽  
Flexor Muscles ◽  
Stroke Group ◽  
Dominant Member ◽  
Flexion And Extension

Many authors have studied physical and functional changes in individuals post-stroke, but there are few studies that assess changes in the non-plegic side of hemiplegic subjects. This study aimed to compare the electromyographic activity in the forearm muscles of spastic patients and clinically healthy individuals, to determine if there is difference between the non-plegic side of hemiplegics and the dominant member of normal individuals. 22 hemiplegic subjects and 15 clinically healthy subjects were submitted to electromyography of the flexor and extensor carpi ulnaris muscles during wrist flexion and extension. The flexor muscles activation of stroke group (average 464.6 u.n) was significantly higher than the same muscles in control group (mean: 106.3 u.n.) during the wrist flexion, what shows that the non affected side does not present activation in the standart of normality found in the control group.

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