Transplant-derived astrocytes migrate into host lumbar and cervical spinal cord after implantation of El4 fetal cerebral cortex into adult thoracic spinal cord

1987 ◽  
Vol 17 (4) ◽  
pp. 391-403 ◽  
Author(s):  
W. J. Goldberg ◽  
J. J. Bernstein
Keyword(s):  
Spinal Cord ◽  
Cerebral Cortex ◽  
Cervical Spinal Cord ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

scholarly journals Combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management

1999 ◽  
Vol 6 (1) ◽  
pp. E6 ◽  
Author(s):  
Fernando L. Vale ◽  
Jennifer Burns ◽  
Amie B. Jackson ◽  
Mark N. Hadley
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injuries ◽  
Cervical Spinal Cord ◽  
Bladder Function ◽  
Thoracic Spinal Cord ◽  
Arterial Blood ◽  
Thoracic Spinal ◽  
Cord Injury

The optimal management of acute spinal cord injuries remains to be defined. The authors prospectively applied resuscitation principles of volume expansion and blood pressure maintenance to 77 patients who presented with acute neurological deficits as a result of spinal cord injuries occurring from C-1 through T-12 in an effort to maintain spinal cord blood flow and prevent secondary injury. According to the Intensive Care Unit protocol, all patients were managed by Swan-Ganz and arterial blood pressure catheters and were treated with immobilization and fracture reduction as indicated. Intravenous fluids, colloid, and vasopressors were administered as necessary to maintain mean arterial blood pressure above 85 mm Hg. Surgery was performed for decompression and stabilization, and fusion in selected cases. Sixty-four patients have been followed at least 12 months postinjury by means of detailed neurological assessments and functional ability evaluations. Sixty percent of patients with complete cervical spinal cord injuries improved at least one Frankel or American Spinal Injury Association (ASIA) grade at the last follow-up review. Thirty percent regained the ability to walk and 20% had return of bladder function 1 year postinjury. Thirty-three percent of the patients with complete thoracic spinal cord injuries improved at least one Frankel or ASIA grade. Approximately 10% of the patients regained the ability to walk and had return of bladder function. As of the 12-month follow-up review, 92% of patients demonstrated clinical improvement after sustaining incomplete cervical spinal cord injuries compared to their initial neurological status. Ninety-two percent regained the ability to walk and 88% regained bladder function. Eighty-eight percent of patients with incomplete thoracic spinal cord injuries demonstrated significant improvements in neurological function 1 year postinjury. Eighty-eight percent were able to walk and 63% had return of bladder function. The authors conclude that the enhanced neurological outcome that was observed in patients after spinal cord injury in this study was in addition to, and/or distinct from, any potential benefit provided by surgery. Early and aggressive medical management (volume resuscitation and blood pressure augmentation) of patients with acute spinal cord injuries optimizes the potential for neurological recovery after sustaining trauma.

scholarly journals Sulcal artery syndrome presenting as an incomplete Brown–Sequard syndrome – Report of an unusual case and review of the literature

2020 ◽  
Vol 29 (1) ◽  
pp. 59-63
Author(s):  
May Myat Win ◽  
Monica Saini ◽  
Shrikant Digambarrao Pande ◽  
Kappaganthu Venkatesh Prasanna
Keyword(s):  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Vertebral Artery Dissection ◽  
Artery Occlusion ◽  
Sudden Onset ◽  
Artery Dissection ◽  
Spinal Cord Infarction ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Brown Sequard Syndrome

Sulcal arteries perfuse the anterior two-thirds of the spinal cord, and spinal cord infarction as a result of sulcal artery occlusion is rare. Most reported cases are associated with vertebral artery dissection, and commonly involve the cervical spinal cord. A 74-year-old man presented with sudden onset weakness and numbness after a brief bout of abdominal pain. Further investigations concluded that this was sulcal artery syndrome. We report a case of sulcal artery syndrome affecting the thoracic spinal cord presenting as Brown–Sequard syndrome. Sulcal artery syndrome usually has good prognoses, unlike anterior spinal artery infarction.

scholarly journals Analysis of 82 cases of spinal cord injury treated by ozone [abstract]

2019 ◽  
Vol 3 (4) ◽  
Author(s):  
Xirzat Abdukeram ◽  
Muhtar Rixit ◽  
Dilare Mahmut
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Internal Fixation ◽  
Cervical Spinal Cord ◽  
Spinous Process ◽  
Axon Growth ◽  
Epidural Injection ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Cord Injury

PURPOSE: To investigate the feasibility and clinical efficacy of ozone in the treatment of spinal cord injury so as to restore the function and sensation of the limbs. METHODS: From May 2007 to July 2016, 82 patients with spinal cord injury were treated, including 24 females and 58 males, with an average age of 32.1 years. Among all the research, 26 cases of cervical spinal cord injury, 12 cases of paraplegia in the thoracic spinal cord, 44 cases of paraplegia in the lumbar spine, all of whom had muscle strength 0 and had incontinence. Frankel classification, grade A is 69 cases, B class is 13 cases. 12 cases of spinous process wire fixation was performed; in 61 cases, internal pedicle screw fixation, and no internal fixation was required in 9 cases. In these patients, we did epidural injection of 2-8 mL of ozone at 35 mcrg/mL with the C arm. In 4 cases we did spinal canal decompression and internal fixation and we used an epidural catheter into the epidural and subarachnoid cavity to directly inject 2-8 mL of ozone at 35 mcrg/mL; after catheter withdrawal, we did ozone injection in the scar segment with the C arm to increase acurracy of the technique. RESULTS: In 10 patients, the treatment produced no neurological improvement; the remaining 72 patients, from the 3rd postoperative day, feeling started to recover. We observed 22 patients during 26 months that could stand up and walk with crutches and 18 patients of them could control defecation and 16 patients could feel the defecation; 14 cases could do slight activities with their lower extremities; 12 patients reached mild forearm movement. CONCLUSION: The key to the repair of the injured spinal cord is provided through the axon growth; ozone can play a worthy role in the release of scar and allow nerve axons to grow and access some function recovery.

scholarly journals C2 spinal cord stimulation induces dynorphin release from rat T4 spinal cord: potential modulation of myocardial ischemia-sensitive neurons

2008 ◽  
Vol 295 (5) ◽  
pp. R1519-R1528 ◽  
Author(s):  
XiaoHui Ding ◽  
Fang Hua ◽  
Kristopher Sutherly ◽  
Jeffrey L. Ardell ◽  
Carole A. Williams
Keyword(s):  
Spinal Cord ◽  
Myocardial Ischemia ◽  
Dorsal Horn ◽  
Cervical Spinal Cord ◽  
Ibotenic Acid ◽  
Opioid Antagonist ◽  
Sprague Dawley ◽  
Thoracic Spinal Cord ◽  
Central Processing ◽  
Thoracic Spinal

During myocardial ischemia, the cranial cervical spinal cord (C1–C2) modulates the central processing of the cardiac nociceptive signal. This study was done to determine 1) whether C2 SCS-induced release of an analgesic neuropeptide in the dorsal horn of the thoracic (T4) spinal cord; 2) if one of the sources of this analgesic peptide was cervical propriospinal neurons, and 3) if chemical inactivation of C2 neurons altered local T4 substance P (SP) release during concurrent C2 SCS and cardiac ischemia. Ischemia was induced by intermittent occlusion of the left anterior descending coronary artery (CoAO) in urethane-anesthetized Sprague-Dawley rats. Release of dynorphin A (1-13), (DYN) and SP was determined using antibody-coated microprobes inserted into T4. SCS alone induced DYN release from laminae I–V in T4, and this release was maintained during CoAO. C2 injection of the excitotoxin, ibotenic acid, prior to SCS, inhibited T4 DYN release during SCS and ischemia; it also reversed the inhibition of SP release from T4 dorsal laminae during C2 SCS and CoAO. Injection of the κ-opioid antagonist, nor-binaltorphimine, into T4 also allowed an increased SP release during SCS and CoAO. CoAO increased the number of Fos-positive neurons in T4 dorsal horns but not in the intermediolateral columns (IML), while SCS (either alone or during CoAO) minimized this dorsal horn response to CoAO alone, while inducing T4 IML neuronal recruitment. These results suggest that activation of cervical propriospinal pathways induces DYN release in the thoracic spinal cord, thereby modulating nociceptive signals from the ischemic heart.

Leptomeningeal spread of intramedullary spinal cord tumors

1988 ◽  
Vol 69 (2) ◽  
pp. 295-300 ◽  
Author(s):  
William O. Bell ◽  
Roger J. Packer ◽  
Kathy R. Seigel ◽  
Lucy B. Rorke ◽  
Leslie N. Sutton ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Recent Literature ◽  
Cervical Spinal Cord ◽  
Spinal Cord Tumors ◽  
Thoracic Spinal Cord ◽  
Intramedullary Spinal Cord ◽  
Content Type ◽  
Leptomeningeal Spread ◽  
The Past ◽  
Thoracic Spinal

✓ Three patients with intramedullary spinal cord tumors and secondary leptomeningeal spread of their tumors are presented. Two patients had astrocytomas and one had a ganglioglioma. Two tumors were located in the cervical spinal cord and one within the thoracic spinal cord. Review of the past and recent literature shows leptomeningeal dissemination of spinal cord tumors to be relatively rare, but it should be suspected and investigated in any patient whose condition deteriorates following removal of a spinal cord neoplasm.

scholarly journals Intramedullary Subependymoma of the Cervical Spinal Cord: A Case Report and Review of the Literature

2019 ◽  
Vol 08 (01) ◽  
pp. 064-068
Author(s):  
Eiralí Chapa ◽  
Juana González ◽  
Mauricio Morquecho ◽  
José Martínez ◽  
Mariana Flores ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Epithelial Membrane Antigen ◽  
Cervical Spinal Cord ◽  
Resonance Imaging ◽  
Nuclear Pleomorphism ◽  
Thoracic Spinal Cord ◽  
Intramedullary Lesion ◽  
Thoracic Spinal ◽  
The Central Nervous System ◽  
Diffuse Positivity

AbstractSubependymoma is a rare tumor of the central nervous system, representing 0.2 to 0.7% of all intracranial tumors. They are usually found in the fourth ventricle or in the walls of the lateral ventricles, often remaining asymptomatic. Subependymomas occur rarely in the cervical or thoracic spinal cord. Since its first description in the spinal cord by Boykin et al in 1954, only 47 cases have been reported. A 49-year-old man presented with a 4-year-long-lasting neck pain, which radiated to the upper right extremity for 4 years. It was insidious at onset and revealed gradual progression, difficulty in performing fine hand movements, and hyperalgesia. Magnetic resonance imaging revealed irregular hyperintensity of T2 and dilatation of the spinal cord from C4 to T1 with associated edema and an intramedullary lesion with central location. During the surgical event, a transoperative biopsy was performed that revealed loose fibrillary networks and groups of nuclei showing mild pleomorphism and microcystic formations. Histologically, we observed groups of cells with mild nuclear pleomorphism embedded in a dense, thin, glial fibrillar fundus, and microcystic formations. Immunohistochemical staining revealed diffuse positivity for the glial fibrillary acidic protein, and negative for the epithelial membrane antigen. Subependymoma accounts for 8.3% of all ependymal tumors. There are few descriptions of the cytologic features of the subependymoma because this neoplasm is rare and most commonly found incidentally in autopsies.

Progressive motor impairment from a critically located lesion in highly restricted CNS-demyelinating disease

2018 ◽  
Vol 24 (11) ◽  
pp. 1445-1452 ◽  
Author(s):  
B Mark Keegan ◽  
Timothy J Kaufmann ◽  
Brian G Weinshenker ◽  
Orhun H Kantarci ◽  
William F Schmalstieg ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Demyelinating Disease ◽  
Cervical Spinal Cord ◽  
Motor Impairment ◽  
Subcortical White Matter ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Demyelinating Lesions ◽  
Magnetic Resonance Imaging Mri

Objective: To report progressive motor impairment from a critically located central nervous system (CNS) demyelinating lesion in patients with restricted magnetic resonance imaging (MRI)-lesion burden. Methods: We identified 38 patients with progressive upper motor-neuron impairment for >1 year, 2–5 MRI CNS-demyelinating lesions, with one seemingly anatomically responsible for progressive motor impairment. Patients with any alternative etiology for progressive motor impairment were excluded. A neuroradiologist blinded to clinical evaluation reviewed multiple brain and spinal-cord MRI, selecting a candidate critically located demyelinating lesion. Lesion characteristics were determined and subsequently compared with clinical course. Results: Median onset age was 47.5 years (24–64); 23 (61%) women. Median follow-up was 94 months (18–442); median Expanded Disability Status Scale Score (EDSS) at last follow-up was 4.5 (2–10). Clinical presentations were progressive: hemiparesis/monoparesis 31; quadriparesis 5; and paraparesis 2; 27 patients had progression from onset; 11 progression post-relapse. Total MRI lesions were 2 ( n = 8), 3 ( n = 12), 4 ( n = 12), and 5 ( n = 6). Critical lesions were located on corticospinal tracts, chronically atrophic in 26/38 (68%) and involved cervical spinal cord in 27, cervicomedullary/brainstem region in 6, thoracic spinal cord in 4, and subcortical white matter in 1. Conclusion: Progressive motor impairment may ascribe to a critically located CNS-demyelinating lesion in patients with highly restricted MRI burden. Motor progression from a specific demyelinating lesion has implications for understanding multiple sclerosis (MS) progression.

Influence of CNS T2-focal lesions on cervical cord atrophy and disability in multiple sclerosis

2019 ◽  
Vol 26 (11) ◽  
pp. 1402-1409 ◽  
Author(s):  
Emanuele Pravatà ◽  
Paola Valsasina ◽  
Claudio Gobbi ◽  
Chiara Zecca ◽  
Gianna C Riccitelli ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Neurological Impairment ◽  
Cervical Cord ◽  
Focal Lesions ◽  
Cross Sectional ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Upper Thoracic

Background: Mechanisms associated with cervical spinal cord (CSC) and upper thoracic spinal cord (TSC) atrophy in multiple sclerosis (MS) are poorly understood. Objective: To assess the influence of brain, CSC and TSC T2-hyperintense lesions on cord atrophy and disability in MS. Methods: Thirty-four MS patients underwent 3T brain, cervical and thoracic cord magnetic resonance imaging (MRI) and Expanded Disability Status Scale (EDSS) score assessment. CSC/TSC lesion number and volume (LV), whole-brain and cortico-spinal tract (CST) LVs were obtained. Normalized whole CSC and upper TSC cross-sectional areas (CSAn) were also derived. Age- and sex-adjusted regression models assessed associations of brain/cord lesions with CSAn and EDSS and identified variables independently associated with CSAn and EDSS with a stepwise variable selection. Results: CSC CSAn (β = −0.36, p = 0.03) and TSC CSAn (β = −0.60, p < 0.001) were associated with CSC T2 LV. EDSS (median = 3.0) was correlated with CSC T2 LV (β = 0.42, p = 0.01), brain (β = 0.34, p = 0.04) and CST LV (β = 0.35, p = 0.03). The multivariate analysis retained CSC LV as significant predictor of CSC CSAn ( R2 = 0.20, p = 0.023) and TSC CSAn ( R2 = 0.51, p < 0.001) and retained CSC and CST LVs as significant predictors of EDSS ( R2 = 0.55, p = 0.001). Conclusions: CSC LV is an independent predictor of cord atrophy. When neurological impairment is relatively mild, central nervous system (CNS) lesion burden is a better correlate of disability than atrophy.

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