scholarly journals Hyperextension cervical spine injuries and traumatic central cord syndrome

2008 ◽  
Vol 25 (5) ◽  
pp. E9 ◽  
Author(s):  
Bizhan Aarabi ◽  
Michael Koltz ◽  
David Ibrahimi
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Spinal Cord Compression ◽  
Bladder Dysfunction ◽  
Cord Compression ◽  
Sensory Loss ◽  
Future Research ◽  
Lesion Length ◽  
Cord Injury ◽  
Central Cord Syndrome

Traumatic central cord syndrome (TCCS), regardless of its biomechanics, is the most frequently encountered incomplete spinal cord injury. Patients with TCCS present with disproportionate weakness of the upper extremities, and variable sensory loss and bladder dysfunction. Fractures and/or subluxations, forced hyperextension, and herniated nucleus pulposus are the main pathogenetic mechanisms of TCCS. Nearly 50% of patients with TCCS suffer from congenital or degenerative spinal stenosis and sustained their injuries during hyperextension as originally described by Schneider in 1954. Immunohistochemical and imaging studies indicate mild to moderate insult to axons and their ensheathing myelin in the lateral funiculi culminating in cytoskeletal injury and impaired conduction. More than one-half of these patients enjoy spontaneous recovery of motor weakness; however, as time goes on, lack of manual dexterity, neuropathic pain, spasticity, bladder dysfunction, and imbalance of gait render their activities of daily living nearly impossible. Based on the current level of evidence, there is no clear indication of the timing of decompression for relief of sustained spinal cord compression in hyperextension injuries. Future research, taking advantage of validated digital imaging data such as maximum canal compromise, maximum spinal cord compression, and lesion length on the CT and MR images, as well as more sensitive measures of bladder and hand function, spasticity, and neuropathic pain may help tailor surgery for a specific group of these patients.

scholarly journals Management and outcome of spontaneous cervical epidural hematoma: Case report and review of the literature

2021 ◽  
Vol 12 (3) ◽  
pp. 094-097
Author(s):  
Yao Christian Hugues DOKPONOU ◽  
Adil BELHACHMI ◽  
Fernand Nathan IMOUMBY ◽  
Alngar DJIMRABEYE ◽  
Brahim El MOSTARCHID ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Cervical Spinal Cord ◽  
Acute Attack ◽  
Cord Compression ◽  
Neurological Deficits ◽  
Sensory Loss ◽  
Neurologic Outcomes ◽  
Cord Injury ◽  
Spinal Cord Compression Syndrome

Spontaneous spinal epidural hematomas are rare and potentially disabling neurological emergencies. Its lead to devastating neurologic outcomes and most patient does not recover completely. The clinical presentation is diverse and includes a severe acute attack, radiating pain at the back, interscapular, or neurological deficits. We report a case of a young woman, 24-year-old, that was admitted to our department for sudden non-traumatic cervical spinal cord compression syndrome (Type A of the American Spinal Cord Injury Association “ASIA A”) including intense cervical back pain, sensory loss, and tetraplegia. Her past medical history was unremarkable. The MRI confirmed a cervical mass responsible for the spinal cord compression and the emergent surgical intervention allow us to evacuate acute C3-C7 hematoma. The patient never recovers from the neurologic deficit despite the emergent management of her case followed by functional musculoskeletal rehabilitation for two years.

scholarly journals Role of macrophages and activated microglia in neuropathic pain associated with chronic progressive spinal cord compression

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Naoto Takeura ◽  
Hideaki Nakajima ◽  
Shuji Watanabe ◽  
Kazuya Honjoh ◽  
Ai Takahashi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Suitable Model ◽  
Chronic Neuropathic Pain ◽  
Activated Microglia ◽  
Cord Injury ◽  
Blood Spinal Cord Barrier ◽  
Compressive Myelopathy

Abstract Neuropathic pain (NeP) is commonly encountered in patients with diseases associated with spinal cord damage (e.g., spinal cord injury (SCI) and compressive myelopathy). Recent studies described persistent glial activation and neuronal hyperactivity in SCI, but the pathomechanisms of NeP in chronic compression of the spinal cord remains elusive. The purpose of the present study was to determine the roles of microglia and infiltrating macrophages in NeP. The study was conducted in chimeric spinal hyperostotic mice (ttw/ttw), characterized by chronic progressive compression of the spinal cord as a suitable model of human compressive myelopathy. The severity of spinal cord compression correlated with proportion of activated microglia and hematogenous macrophages. Spinal cord compression was associated with overexpression of mitogen-activated protein kinases (MAPKs) in infiltrating macrophages and reversible blood-spinal cord barrier (BSCB) disruption in the dorsal horns. Our results suggested that chronic neuropathic pain in long-term spinal cord compression correlates with infiltrating macrophages, activated microglial cells and the associated damage of BSCB, together with overexpression of p-38 MAPK and p-ERK1/2 in these cells. Our findings are potentially useful for the design of new therapies to alleviate chronic neuropathic pain associated with compressive myelopathy.

scholarly journals FTY720 Attenuates Neuropathic Pain after Spinal Cord Injury by Decreasing Systemic and Local Inflammation in a Rat Spinal Cord Compression Model

2020 ◽  
Vol 37 (15) ◽  
pp. 1720-1728 ◽  
Author(s):  
Kazuyoshi Yamazaki ◽  
Masahito Kawabori ◽  
Toshitaka Seki ◽  
Soichiro Takamiya ◽  
Takahiro Tateno ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropathic Pain ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Local Inflammation ◽  
Rat Spinal Cord ◽  
Compression Model ◽  
Cord Injury

scholarly journals Transplanted Human Stem Cell-Derived Interneuron Precursors Mitigate Mouse Bladder Dysfunction and Central Neuropathic Pain after Spinal Cord Injury

2016 ◽  
Vol 19 (4) ◽  
pp. 544-557 ◽  
Author(s):  
Thomas M. Fandel ◽  
Alpa Trivedi ◽  
Cory R. Nicholas ◽  
Haoqian Zhang ◽  
Jiadong Chen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropathic Pain ◽  
Stem Cell ◽  
Bladder Dysfunction ◽  
Human Stem Cell ◽  
Central Neuropathic Pain ◽  
Cord Injury

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.

scholarly journals Walking with Neuropathic Pain: Paradoxical Shift from Burden to Support?

2015 ◽  
Vol 2015 ◽  
pp. 1-3 ◽  
Author(s):  
David J. Kopsky ◽  
Jan M. Keppel Hesselink ◽  
Roberto Casale
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropathic Pain ◽  
Unusual Case ◽  
Body Schema ◽  
The Body ◽  
Sensory Loss ◽  
Pain Patient ◽  
Rehabilitation Programs ◽  
Cord Injury

Baclofen 5% cream can be used for the treatment of neuropathic pain. We describe an unusual case of a neuropathic pain patient with spinal cord injury. A 71-year-old woman with a partial spinal cord injury lesion at L4 complained of tingling, pins and needles, and burning in her legs. She scored her pain as 6 before adding baclofen 5% cream to her pain medication (pregabalin 450 mg, acetaminophen 3000 mg, and diclofenac 150 mg daily). One month later she experienced complete pain relief, though experienced increased difficulties in walking, leading to frequent falls. Her steadier walking without stumbling and falling was more important to her than pain reduction. Thus she decided to stop using baclofen. This unusual case report discusses two important issues that relate to pain medicine and rehabilitation in patients with painful spinal cord lesions: (1) the presence of wide areas of sensory loss “covered” by the presence of painful sensations and (2) pathological sensations that can be used and integrated in the body schema to create an improved spatiovisual orientation and thus mobility. Both these aspects have to be taken into account when treating pain and design rehabilitation programs.

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