scholarly journals Microstructural plasticity in nociceptive pathways after spinal cord injury

2021 ◽  
pp. jnnp-2020-325580
Author(s):  
Sreenath P Kyathanahally ◽  
Michela Azzarito ◽  
Jan Rosner ◽  
Vince D Calhoun ◽  
Claudia Blaiotta ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Primary Motor Cortex ◽  
Statistical Parametric Mapping ◽  
Anterior Cingulate ◽  
Cervical Cord ◽  
Transverse Relaxation Rate ◽  
Microstructural Changes ◽  
Nociceptive Pathways ◽  
Cord Injury

ObjectiveTo track the interplay between (micro-) structural changes along the trajectories of nociceptive pathways and its relation to the presence and intensity of neuropathic pain (NP) after spinal cord injury (SCI).MethodsA quantitative neuroimaging approach employing a multiparametric mapping protocol was used, providing indirect measures of myelination (via contrasts such as magnetisation transfer (MT) saturation, longitudinal relaxation (R1)) and iron content (via effective transverse relaxation rate (R2*)) was used to track microstructural changes within nociceptive pathways. In order to characterise concurrent changes along the entire neuroaxis, a combined brain and spinal cord template embedded in the statistical parametric mapping framework was used. Multivariate source-based morphometry was performed to identify naturally grouped patterns of structural variation between individuals with and without NP after SCI.ResultsIn individuals with NP, lower R1 and MT values are evident in the primary motor cortex and dorsolateral prefrontal cortex, while increases in R2* are evident in the cervical cord, periaqueductal grey (PAG), thalamus and anterior cingulate cortex when compared with pain-free individuals. Lower R1 values in the PAG and greater R2* values in the cervical cord are associated with NP intensity.ConclusionsThe degree of microstructural changes across ascending and descending nociceptive pathways is critically implicated in the maintenance of NP. Tracking maladaptive plasticity unravels the intimate relationships between neurodegenerative and compensatory processes in NP states and may facilitate patient monitoring during therapeutic trials related to pain and neuroregeneration.

Cervical Cord-Canal Mismatch: A New Method for Identifying Predisposition to Spinal Cord Injury

2017 ◽  
Vol 108 ◽  
pp. 112-117 ◽  
Author(s):  
Aria Nouri ◽  
Julio Montejo ◽  
Xin Sun ◽  
Justin Virojanapa ◽  
Luis E. Kolb ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
New Method ◽  
Cervical Cord ◽  
Cord Injury

Central Nervous System Reorganization and Pain After Spinal Cord Injury: Possible Targets for Physical Therapy—A Systematic Review of Neuroimaging Studies

2020 ◽  
Vol 100 (6) ◽  
pp. 946-962
Author(s):  
Thomas Osinski ◽  
Sessi Acapo ◽  
Djamel Bensmail ◽  
Didier Bouhassira ◽  
Valéria Martinez
Keyword(s):  
Systematic Review ◽  
Spinal Cord ◽  
Central Nervous System ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Physical Therapist ◽  
Anterior Cingulate ◽  
Current Evidence ◽  
Functional Changes ◽  
Cord Injury

Abstract Background Pain is one of the main symptoms associated with spinal cord injury (SCI) and can be associated with changes to the central nervous system (CNS). Purpose This article provides an overview of the evidence relating to CNS changes (structural and functional) associated with pain in SCIs. Data Sources A systematic review was performed, according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) recommendations, on PubMed, Embase, and Web of Science in March 2018. Study Selection Studies were selected if they concerned changes in the CNS of patients with SCI, regardless of the type of imagery. Data Extraction Data were extracted by 2 blinded reviewers. Data Synthesis There is moderate evidence for impaired electroencephalographic function and metabolic abnormalities in the anterior cingulate in patients experiencing pain. There is preliminary evidence that patients with pain have morphological and functional changes to the somatosensory cortex and alterations to thalamic metabolism. There are conflicting data regarding the relationships between lesion characteristics and pain. In contrast, patients without pain can display protective neuroplasticity. Limitations and Conclusion Further studies are required to elucidate fully the relationships between pain and neuroplasticity in patients with SCIs. However, current evidence might support the use of physical therapist treatments targeting CNS plasticity in patients with SCI pain.

Deterioration following spinal cord injury

1987 ◽  
Vol 66 (3) ◽  
pp. 400-404 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Sharen Knowlton ◽  
Steven R. Garfin ◽  
Melville R. Klauber ◽  
Howard M. Eisenberg ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cervical Cord ◽  
Skeletal Traction ◽  
Systemic Complications ◽  
Content Type ◽  
Management Procedures ◽  
Cord Injury ◽  
Specific Management ◽  
Fine Print

✓ The results are presented of a prospective study of the course of 283 spinal cord-injured patients who were consecutively admitted to five trauma centers participating in the Comprehensive Central Nervous System Injury Centers' program of the National Institutes of Health. Of the 283 patients, 14 deteriorated neurologically during acute hospital management. In 12 of the 14, the decline in neurological function could be associated with a specific management event, and in nine of these 12 the injury involved the cervical cord. Nine of the 14 patients who deteriorated had cervical injuries, three had thoracic cord injuries, and two had thoracolumbar junction injuries. Management intervention was identified as the cause of deterioration in four of 134 patients undergoing operative intervention, in three of 60 with skeletal traction application, in two of 68 with halo vest application, in two of 56 undergoing Stryker frame rotation, and in one of 57 undergoing rotobed rotation. Early surgery on the cervical spine when cord injury is present appears hazardous, since each of the three patients with a cervical cord injury who deteriorated was operated on within the first 5 days. No such deterioration was observed following surgery performed from the 6th day on. In two other patients, deterioration did not appear to be related to management but was a direct product of the underlying disease or of systemic complications. Deterioration following hospitalization for spinal cord injury is relatively uncommon — 4.9% in this large series. In most instances, decline in function could be attributed to specific management procedures. These changes must not be interpreted as representing failure to provide optimal care but rather should be seen as the inevitable product of an attempt to manage patients with spinal cord and column injuries, many of which are clearly unstable.

Pediatric spinal injury: review of 174 hospital admissions

1992 ◽  
Vol 77 (5) ◽  
pp. 700-704 ◽  
Author(s):  
Mark G. Hamilton ◽  
S. Terence Mylks
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Hospital Admissions ◽  
Spinal Injury ◽  
Neurological Injury ◽  
Cervical Cord ◽  
Mature Adult ◽  
Younger Patients ◽  
Cord Injury ◽  
Radiological Abnormality

✓ Injury to the spinal column and spinal cord occurs relatively infrequently in the pediatric population. A review of 174 pediatric patients is presented, representing 5.4% of all patients admitted with spinal injury, Spinal cord injury was present in 45% of patients. A distinct injury profile, explained by anatomical and biomechanical features, distinguishes the young patient with an immature spine from older adolescents with a more mature, adult-like spine. The younger patients, while less likely to have spinal injury, had a higher incidence of neurological injury, in addition to a higher frequency of both spinal cord injury without radiological abnormality and upper cervical cord injury. In addition, younger patients with spinal cord injury and no radiological abnormality were more likely to have complete or severe cord injury. Prognosis was determined by the severity of spinal cord injury. Patients with complete cord injuries showed little improvement, while patients with incomplete injuries generally fared much better, with 74% showing significant improvement and 59% experiencing a complete recovery of neurological functions. There were six deaths, but none was attributed solely to spinal injury. The authors conclude that outcome is quite good after pediatric spinal cord injury that does not produce a physiologically complete cord deficit.

Toxic Substances in Spinal Cord Injury

Neurosurgery ◽  
1979 ◽  
Vol 4 (3) ◽  
pp. 239-243 ◽  
Author(s):  
Sherman C. Stein ◽  
Roger Q. Cracco ◽  
Peter Farmer ◽  
Curtis A. Kiest
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Evoked Potentials ◽  
Autologous Blood ◽  
Cervical Cord ◽  
Base Line ◽  
Toxic Substances ◽  
Cord Injury ◽  
Sciatic Nerve Stimulation ◽  
Clinical Changes

Abstract Several investigators have implicated norepinephrine and other toxic substances released in the region of a spinal cord injury in the genesis of the progressive pathological and clinical changes that follow spinal trauma. To test this hypothesis. we subjected cats to T-10 to T-12 laminectomy and monitored epidural spinal evoked potentials from sciatic nerve stimulation. The spinal subarachnoid space was perfused with normal saline, with norepinephrine solution, or with heparinized autologous blood or the pial surface of the spinal cord was exposed to macerated gray matter taken from the upper cervical cord. During 1- to 2-hour exposure periods, we noted no significant changes in the base line spinal evoked potentials. In another series of cats, we have shown that norepinephrine perfused over the spinal cord in this manner diffuses rapidly into the subpial white matter. Therefore, its failure to affect spinal evoked potentials does not represent a failure to penetrate the spinal cord. Putative toxins must originate either in extravasated blood or damaged neural tissue in the region of the spinal cord injury. The failure of ascending spinal tracts to react to blood or cord tissue in our experiment suggests that toxins are not involved in the spinal cord dysfunction that occurs soon after injury.

The role of the ipsilateral primary motor cortex in movement control after spinal cord injury: A TMS study

2013 ◽  
Vol 552 ◽  
pp. 21-24 ◽  
Author(s):  
Raffaele Nardone ◽  
Yvonne Höller ◽  
Peter Höller ◽  
Natasha Thon ◽  
Aljoscha Thomschewski ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Movement Control ◽  
Cord Injury

Dynamic Reorganization of Motor Networks During Recovery from Partial Spinal Cord Injury in Monkeys

2018 ◽  
Vol 29 (7) ◽  
pp. 3059-3073 ◽  
Author(s):  
Zenas C Chao ◽  
Masahiro Sawada ◽  
Tadashi Isa ◽  
Yukio Nishimura
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Time Course ◽  
Primary Motor Cortex ◽  
Premotor Cortex ◽  
Motor Preparation ◽  
Compensatory Mechanism ◽  
Primate Model ◽  
Cord Injury

Abstract After spinal cord injury (SCI), the motor-related cortical areas can be a potential substrate for functional recovery in addition to the spinal cord. However, a dynamic description of how motor cortical circuits reorganize after SCI is lacking. Here, we captured the comprehensive dynamics of motor networks across SCI in a nonhuman primate model. Using electrocorticography over the sensorimotor areas in monkeys, we collected broadband neuronal signals during a reaching-and-grasping task at different stages of recovery of dexterous finger movements after a partial SCI at the cervical levels. We identified two distinct network dynamics: grasping-related intrahemispheric interactions from the contralesional premotor cortex (PM) to the contralesional primary motor cortex (M1) in the high-γ band (>70 Hz), and motor-preparation-related interhemispheric interactions from the contralesional to ipsilesional PM in the α and low-β bands (10–15 Hz). The strengths of these networks correlated to the time course of behavioral recovery. The grasping-related network showed enhanced activation immediately after the injury, but gradually returned to normal while the strength of the motor-preparation-related network gradually increased. Our findings suggest a cortical compensatory mechanism after SCI, where two interdependent motor networks redirect activity from the contralesional hemisphere to the other hemisphere to facilitate functional recovery.

scholarly journals Neurophysiological and Spinal Cord Perfusion Changes at Dynamic Neck Positions in a Compressive Spinal Cord Injury Rat Model

2021 ◽  
Author(s):  
Zhengran Yu ◽  
Xing Cheng ◽  
Jiacheng Chen ◽  
Sixiong Lin ◽  
Hao Hu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Rat Model ◽  
Dynamic Compression ◽  
Dynamic Change ◽  
Cervical Cord ◽  
Post Injury ◽  
Doppler Flowmetry ◽  
Cord Injury ◽  
Behavioural Tests

Abstract Background: Cervical spondylotic myelopathy (CSM) is a degenerative condition of the spine that caused by static and dynamic compression of the spinal cord. However, the pathophysiological changes at dynamic neck positions remain poor. This study investigated the interplay between neurophysiological and haemodynamic responses at dynamic neck positions in a chronic compressive spinal cord injury (CCSCI) rat model. Methods: Behavioural tests including Basso, Beattie, and Bresnahan scores and an inclined plane test were used to evaluate the motor function recovery. Combined examination of dynamic motor and somatosensory evoked potentials (DMEPs and DSSEPs, respectively) was performed regularly to evaluate the dynamic motor and sensory conduction of the cervical cord. At 4 weeks post-injury (wpi), dynamic magnetic resonance imaging (MRI) and dynamic laser Doppler flowmetry (LDF) were used to demonstrate the interstructure and spinal cord blood flow (SCBF) at the compression site at dynamic neck positions. Hematoxylin and eosin (HE) staining was performed to assess the cords' pathological changes.Results: Behavioural tests and combined DMEPs and DSSEPs examination showed that spinal cord neurological function and dynamic neural conduction deteriorated gradually within a 4-week compression period. The DMEPs were mainly deteriorated upon flexion, while DSSEPs were upon all neck positions after the compression. At 4 wpi, dynamic MRI showed increased T2-weighted image (T2WI) signal intensities. Also, dynamic LDF demonstrated decreased SCBF at the spinal cord compression site. Both of them altered especially upon cervical flexion. The dynamic change in SCBF was significantly correlated with the change in DMEP amplitude upon flexion. Conclusions: This exploratory study revealed that changes in axonal conduction in the motor and somatosensory tracts of the spinal cord were significantly related to chronic compression time and neck position. Furthermore, spinal cord ischaemia may be intimately related to motor conduction dysfunction upon flexion in CCSCI models. These results indicated the potential for therapies targeting dynamic spinal cord perfusion to prevent progression and functional loss in CSM.

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