scholarly journals Biomarkers in spinal cord compression Ethics and perspectives

2016 ◽  
Vol 30 (3) ◽  
pp. 316-320
Author(s):  
A.St. Iencean ◽  
A. Tascu ◽  
St. M. Iencean
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Compression ◽  
Biological Response ◽  
Cord Compression ◽  
Therapeutic Interventions ◽  
Post Injury ◽  
Cord Injury ◽  
Complete Spinal Cord Injury ◽  
Predictive Indicator

Abstract The phosphorylated form of the high-molecular-weight neurofilament subunit NF-H (pNF-H) in serum or in cerebro-spinal fluid (CSF) is a specific lesional biomarker for spinal cord injury. The lesional biomarkers and the reaction biomarkers are both presented after several hours post-injury. The specific predictive patterns of lesional biomarkers could be used to aid clinicians with making a diagnosis and establishing a prognosis, and evaluating therapeutic interventions. Diagnosis, prognosis, and treatment guidance based on biomarker used as a predictive indicator can determine ethical difficulties by differentiated therapies in patients with spinal cord compression. At this point based on studies until today we cannot take a decision based on biomarker limiting the treatment of neurological recovery in patients with complete spinal cord injury because we do not know the complexity of the biological response to spinal cord compression.

scholarly journals Improved rat spinal cord injury model using spinal cord compression by percutaneous method

2013 ◽  
Vol 14 (3) ◽  
pp. 329 ◽  
Author(s):  
Wook-Hun Chung ◽  
Jae-Hoon Lee ◽  
Dai-Jung Chung ◽  
Wo-Jong Yang ◽  
A-Jin Lee ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Rat Spinal Cord ◽  
Spinal Cord Injury Model ◽  
Injury Model ◽  
Cord Injury

The therapeutic window for spinal cord decompression in a rat spinal cord injury model

2005 ◽  
Vol 3 (4) ◽  
pp. 302-307 ◽  
Author(s):  
Christopher B. Shields ◽  
Y. Ping Zhang ◽  
Lisa B. E. Shields ◽  
Yingchun Han ◽  
Darlene A. Burke ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Stenosis ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Therapeutic Window ◽  
Content Type ◽  
Significant Difference ◽  
Cord Injury ◽  
Fine Print

Object. There are no clinically based guidelines to direct the spine surgeon as to the proper timing to undertake decompression after spinal cord injury (SCI) in patients with concomitant stenosis-induced cord compression. The following three factors affect the prognosis: 1) severity of SCI; 2) degree of extrinsic spinal cord compression; and 3) duration of spinal cord compression. Methods. To elucidate further the relationship between varying degrees of spinal stenosis and a mild contusion-induced SCI (6.25 g-cm), a rat SCI/stenosis model was developed in which 1.13- and 1.24-mm-thick spacers were placed at T-10 to create 38 and 43% spinal stenosis, respectively. Spinal cord damage was observed after the stenosis—SCI that was directly proportional to the duration of spinal cord compression. The therapeutic window prior to decompression was 6 and 12 hours in the 43 and 38% stenosis—SCI lesions, respectively, to maintain locomotor activity. A significant difference in total lesion volume was observed between the 2-hour and the delayed time(s) to decompression (38% stenosis—SCI, 12 and 24 hours, p < 0.05; 43% stenosis—SCI, 24 hours, p < 0.05) indicating a more favorable neurological outcome when earlier decompression is undertaken. This finding was further supported by the animal's ability to support weight when decompression was performed by 6 or 12 hours compared with 24 hours after SCI. Conclusions. Analysis of the findings in this study suggests that early decompression in the rat improves locomotor function. Prolongation of the time to decompression may result in irreversible damage that prevents locomotor recovery.

Neurological Recovery Is Impaired by Concurrent but Not by Asymptomatic Pre-existing Spinal Cord Compression After Traumatic Spinal Cord Injury

Spine ◽  
2012 ◽  
Vol 37 (17) ◽  
pp. 1448-1455 ◽  
Author(s):  
Kensuke Kubota ◽  
Hirokazu Saiwai ◽  
Hiromi Kumamaru ◽  
Kazu Kobayakawa ◽  
Takeshi Maeda ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Neurological Recovery ◽  
Traumatic Spinal Cord Injury ◽  
Cord Injury

Cerebrospinal fluid lactate and electrolyte levels following experimental spinal cord injury

1976 ◽  
Vol 44 (6) ◽  
pp. 715-722 ◽  
Author(s):  
Douglas K. Anderson ◽  
Leon D. Prockop ◽  
Eugene D. Means ◽  
Lawrence E. Hartley
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Spinal Cord Tissue ◽  
Post Injury ◽  
Content Type ◽  
Protein Levels ◽  
Cord Injury ◽  
Csf Lactate

✓ Cerebrospinal fluid (CSF) lactate, sodium (Na+), potassium (K+), calcium (Ca++), magnesium (Mg++), and chloride (Cl−) levels were determined for 17 to 21 days following experimental spinal cord compression in cats. Laminectomies were performed at L-2 under general anesthesia with aseptic techniques. Paraplegia was produced by applying a 170-gm weight transdurally for 5 minutes. Significant increases in CSF lactate levels were observed on the first through ninth days post injury with peak levels (50% above normal) occurring at Day 5. The only significant postinjury CSF electrolyte changes were elevation in Ca++ concentration on Days 3, 9, 11, 13, and 15, elevation in K+ concentration on Days 9 and 11 and decline in Cl− levels on the first day. The CSF K+ increase probably reflected cellular loss of K+ from damaged tissue whereas the Ca++ rise may have resulted from increased CSF protein levels. The prolonged elevation of CSF lactate indicates that tissue hypoxia plays a role in spinal cord compression paralysis, and that there is a continuing hypoxia of metabolically active spinal cord tissue for several days post injury.

The dura causes spinal cord compression after spinal cord injury

2016 ◽  
Vol 30 (5) ◽  
pp. 582-584 ◽  
Author(s):  
Samira Saadoun ◽  
Melissa C. Werndle ◽  
Luis Lopez de Heredia ◽  
Marios C. Papadopoulos
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Cord Injury

Effects of Tetramethylpyrazine on Microglia Activation in Spinal Cord Compression Injury of Mice

2013 ◽  
Vol 41 (06) ◽  
pp. 1361-1376 ◽  
Author(s):  
Jung-Won Shin ◽  
Ja-Young Moon ◽  
Ju-Won Seong ◽  
Sang-Hoon Song ◽  
Young-Jin Cheong ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Cytokines ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Microglia Activation ◽  
Compression Injury ◽  
Neuroprotective Effects ◽  
Cord Injury ◽  
Pro Inflammatory Cytokines

Secondary mechanisms, including inflammation and microglia activation, serve as targets for the development and application of pharmacological strategies in the management of spinal cord injury (SCI). Tetramethylpyrazine (TMP), an active ingredient of Ligusticum wallichii (chuanxiong), has shown anti-inflammatory and neuroprotective effects against SCI. However, it remains uncertain whether the inflammation-suppressive effects of TMP play a modulatory role over microglia activation in SCI. The present study investigated the effects of TMP on microglia activation and pro-inflammatory cytokines in spinal cord compression injury in mice. For a real-time PCR measurement of pro-inflammatory cytokines, SCI was induced in mice by the clip compression method (30 g force, 1 min) and TMP (15 or 30 mg/kg, i.p.) was administered once, 30 minutes before the SCI induction. For immunohistochemistry, TMP (30 mg/kg, i.p.) treatment was given three times during the first 48 hours after the SCI. 30 mg/kg of TMP treatment reduced the up-regulation of TNF-α, IL-1β and COX-2 mRNA in the spinal tissue at four hours after the SCI induction. TMP also significantly attenuated microglia activation and neutrophil infiltration at 48 hours after the SCI induction. In addition, iNOS expression in the spinal tissue was attenuated with TMP treatment. These results suggest that TMP plays a modulatory role in microglia activation and may protect the spinal cord from or potentially delay secondary spinal cord injury.

scholarly journals Intramedullary lesion expansion on magnetic resonance imaging in patients with motor complete cervical spinal cord injury

2012 ◽  
Vol 17 (3) ◽  
pp. 243-250 ◽  
Author(s):  
Bizhan Aarabi ◽  
J. Marc Simard ◽  
Joseph A. Kufera ◽  
Melvin Alexander ◽  
Katie M. Zacherl ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Therapeutic Effects ◽  
Female Ratio ◽  
Factors Associated ◽  
Cord Injury ◽  
Principal Factors ◽  
Mri Study

Object The authors performed a study to determine if lesion expansion occurs in humans during the early hours after spinal cord injury (SCI), as has been established in rodent models of SCI, and to identify factors that might predict lesion expansion. Methods The authors studied 42 patients with acute cervical SCI and admission American Spinal Injury Association Impairment Scale Grades A (35 patients) and B (7 patients) in whom 2 consecutive MRI scans were obtained 3–134 hours after trauma. They recorded demographic data, clinical information, Injury Severity Score (ISS), admission MRI-documented spinal canal and cord characteristics, and management strategies. Results The characteristics of the cohort were as follows: male/female ratio 37:5; mean age, 34.6 years; and cause of injury, motor vehicle collision, falls, and sport injuries in 40 of 42 cases. The first MRI study was performed 6.8 ±2.7 hours (mean ± SD) after injury, and the second was performed 54.5 ± 32.3 hours after injury. The rostrocaudal intramedullary length of the lesion on the first MRI scan was 59.2 ± 16.1 mm, whereas its length on the second was 88.5 ± 31.9 mm. The principal factors associated with lesion length on the first MRI study were the time between injury and imaging (p = 0.05) and the time to decompression (p = 0.03). The lesion's rate of rostrocaudal intramedullary expansion in the interval between the first and second MRI was 0.9 ± 0.8 mm/hour. The principal factors associated with the rate of expansion were the maximum spinal cord compression (p = 0.03) and the mechanism of injury (p = 0.05). Conclusions Spinal cord injury in humans is characterized by lesion expansion during the hours following trauma. Lesion expansion has a positive relationship with spinal cord compression and may be mitigated by early surgical decompression. Lesion expansion may be a novel surrogate measure by which to assess therapeutic effects in surgical or drug trials.

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