METHODS OF PHYSIOTHERAPY FOR STUDY IN A SPINAL INSULT

2018 ◽  
Vol 28 (7) ◽  
pp. 2565-2566
Author(s):  
Daniela Popova ◽  
Mariela Filipova
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Back Pain ◽  
Young People ◽  
Hemorrhagic Stroke ◽  
Muscle Spasm ◽  
Spinal Cord Tissue ◽  
Blood Diseases ◽  
Cord Injury ◽  
Ischemic Spinal Cord Injury

Spinal stroke is a disease that is rare in neurological practice. Affects young people, mostly at the age of 30 years [2]. It may be ischemic or haemorrhagic. Etiological, ischemic spinal stroke is caused by atherosclerosis of the aorta and blood vessels of the spinal cord, muscle spasm, vasculitis, pregnancy, hemangioma or hernia [3, 4]. Hemorrhagic stroke is caused by dysplasia, tumors and blood diseases involving increased bleeding [1]. Spinal infarction most commonly develops in the basal spinal artery pool, which is responsible for the blood supply of the anterior 2/3 of the spinal cord tissue. Often, the disease starts with a sudden back pain with an enigmatic nature (in the area of the thoracic segment - Th 8), a gradually occurring weakness in the limbs and hypestesia, pelvic-tangle disorders [5]. The gait is very difficult to impossible.Purpose of the study: To test neurological tests in patients with spinal ischemic spinal cord injury. Assess their accessibility and reliability.

scholarly journals METHODS OF PHYSIOTHERAPY FOR STUDY IN A SPINAL INSULT

2018 ◽  
Vol 28 (7) ◽  
pp. 2565-2566
Author(s):  
Daniela Popova ◽  
Mariela Filipova
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Back Pain ◽  
Young People ◽  
Hemorrhagic Stroke ◽  
Muscle Spasm ◽  
Spinal Cord Tissue ◽  
Blood Diseases ◽  
Cord Injury ◽  
Ischemic Spinal Cord Injury

Spinal stroke is a disease that is rare in neurological practice. Affects young people, mostly at the age of 30 years [2]. It may be ischemic or haemorrhagic. Etiological, ischemic spinal stroke is caused by atherosclerosis of the aorta and blood vessels of the spinal cord, muscle spasm, vasculitis, pregnancy, hemangioma or hernia [3, 4]. Hemorrhagic stroke is caused by dysplasia, tumors and blood diseases involving increased bleeding [1]. Spinal infarction most commonly develops in the basal spinal artery pool, which is responsible for the blood supply of the anterior 2/3 of the spinal cord tissue. Often, the disease starts with a sudden back pain with an enigmatic nature (in the area of the thoracic segment - Th 8), a gradually occurring weakness in the limbs and hypestesia, pelvic-tangle disorders [5]. The gait is very difficult to impossible.Purpose of the study: To test neurological tests in patients with spinal ischemic spinal cord injury. Assess their accessibility and reliability.

scholarly journals Poststroke Pain – but Multiple Pain Mechanisms

2010 ◽  
Vol 15 (1) ◽  
pp. 24-26 ◽  
Author(s):  
Vinjamuri Chari ◽  
Eldon Tunks
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Low Back Pain ◽  
Back Pain ◽  
Heterotopic Ossification ◽  
Hemorrhagic Stroke ◽  
Central Pain ◽  
Low Back ◽  
Pain Mechanisms ◽  
Cord Injury

A 42-year-old man presented with acute left hemiplegia due to a right frontotemporal hemorrhagic stroke and left-sided pain. While the initial presentation suggested central poststroke pain, subsequent investigations also implicated heterotopic ossification of the left hip and amplification of previous low back pain by the new central pain. While heterotopic ossification has been commonly associated with brain injury, spinal cord injury or osseous injury, it is only rarely associated with stroke. Poststroke pain may be multifactorial, and discovering the pain mechanisms has important implications for treatment.

Neuroprotective Effect of Epidural Electrical Stimulation against Ischemic Spinal Cord Injury in Rats

2005 ◽  
Vol 103 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Manabu Kakinohana ◽  
Hideki Harada ◽  
Yasunori Mishima ◽  
Tatsuhiko Kano ◽  
Kazuhiro Sugahara
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Electrical Stimulation ◽  
Neuroprotective Effect ◽  
Spinal Cord Ischemia ◽  
Aortic Occlusion ◽  
Cord Injury ◽  
Optimal Setting ◽  
Transient Aortic Occlusion ◽  
Ischemic Spinal Cord Injury

Background Electroconvulsion therapy is likely to serve as an effective preconditioning stimulus for inducing tolerance to ischemic brain injury. The current study examines whether electrical stimuli on the spinal cord is also capable of inducing tolerance to ischemic spinal cord injury by transient aortic occlusion. Methods Spinal cord ischemia was induced by occlusion of the descending thoracic aorta in combination with maintaining systemic hypotension (40 mmHg) during the procedure. Animals implanted with epidural electrodes were divided into four groups according to electrical stimulation and sham. Two groups consisted of rapid preconditioning (RE group, n = 8) and sham procedure (RC group, n = 8) 30 min before 9 min of spinal cord ischemia. In the two groups that underwent delayed preconditioning, rats were exposed to 9 min of aortic occlusion 24 h after either pretreatment with epidural electrical stimulation (DE group, n = 8) or sham (DC group, n = 8). In addition, rats were exposed to 6-11 min of spinal cord ischemia at 30 min or 24 h after epidural electrical stimulation or sham stimulation. The group P50 represents the duration of spinal cord ischemia associated with 50% probability of resultant paraplegia. Results Pretreatment with electrical stimulation in the DE group but not the RE group protected the spinal cord against ischemia, and this stimulation prolonged the P50 by approximately 15.0% in the DE group compared with the DC group. Conclusions Although the optimal setting for this electrical preconditioning should be determined in future studies, the results suggest that epidural electrical stimulation will be a useful approach to provide spinal protection against ischemia.

A systematic review of the prevalence of musculoskeletal pain, back and low back pain in people with spinal cord injury

2013 ◽  
Vol 36 (9) ◽  
pp. 705-715 ◽  
Author(s):  
Christina Michailidou ◽  
Louise Marston ◽  
Lorraine H. De Souza ◽  
Ian Sutherland
Keyword(s):  
Systematic Review ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Low Back Pain ◽  
Back Pain ◽  
Musculoskeletal Pain ◽  
Low Back ◽  
Cord Injury

Transforaminal Lumbar and Thoracic Interventions and Ischemic Spinal Cord Injury

2016 ◽  
Author(s):  
Scott E. Glaser ◽  
Rinoo Shah
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Infarction ◽  
Supporting Evidence ◽  
Steroid Injections ◽  
Epidural Steroid Injections ◽  
Root Cause ◽  
Cord Injury ◽  
Epidural Steroid ◽  
Ischemic Spinal Cord Injury

Transforaminal epidural steroid injections have been shown to be associated with catastrophic neurologic complications secondary to spinal cord infarction. The reflexive, ad hoc response of practitioners to these injuries has been to recommend risk minimization strategies to prevent embolism of the injected particulate steroids and to use nonparticulate steroids. This focus on distal embolism as the sole or primary cause of catastrophic outcomes lacks conclusive supporting evidence and does not suffice to protect the patient from paraplegia as it fails to address the root cause of the complications. A root cause analysis of the procedure provides evidence that the injection technique itself—the “safe triangle”—creates a risk of arterial damage and sequelae leading to ischemia of the spinal cord. The evidence is strong that the only way to mitigate or eliminate the risk of paraplegia is to use a different technique to perform transforaminal injections: the Kambin triangle approach. This change in technique is the only definitive solution that addresses the root cause of these catastrophic sequelae associated with transforaminal epidural steroid injections. Key Words: Artery of Adamkiewicz, ischemic spinal cord injury, Kambin triangle, safe triangle, transforaminal epidural injection

Spinal Cord Tissue Bridges Validation Study: Predictive Relationships With Sensory Scores Following Cervical Spinal Cord Injury

2021 ◽  
Author(s):  
Andrew C. Smith ◽  
Denise R. O’Dell ◽  
Wesley A. Thornton ◽  
David Dungan ◽  
Eli Robinson ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
External Validation ◽  
Inpatient Rehabilitation ◽  
Spinal Cord Tissue ◽  
Light Touch ◽  
Post Injury ◽  
Data Set ◽  
Cord Injury ◽  
Predictive Relationships

Background: Using magnetic resonance imaging (MRI), widths of ventral tissue bridges demonstrated significant predictive relationships with future pinprick sensory scores, and widths of dorsal tissue bridges demonstrated significant predictive relationships with future light touch sensory scores, following spinal cord injury (SCI). These studies involved smaller participant numbers, and external validation of their findings is warranted. Objectives: The purpose of this study was to validate these previous findings using a larger independent data set. Methods: Widths of ventral and dorsal tissue bridges were quantified using MRI in persons post cervical level SCI (average 3.7 weeks post injury), and pinprick and light touch sensory scores were acquired at discharge from inpatient rehabilitation (average 14.3 weeks post injury). Pearson product-moments were calculated and linear regression models were created from these data. Results: Wider ventral tissue bridges were significantly correlated with pinprick scores (r = 0.31, p < 0.001, N = 136) and wider dorsal tissue bridges were significantly correlated with light touch scores (r = 0.31, p < 0.001, N = 136) at discharge from inpatient rehabilitation. Conclusion: This retrospective study’s results provide external validation of previous findings, using a larger sample size. Following SCI, ventral tissue bridges hold significant predictive relationships with future pinprick sensory scores and dorsal tissue bridges hold significant predictive relationships with future light touch sensory scores.

Inhibition of x-irradiation–enhanced locomotor recovery after spinal cord injury by hyperbaric oxygen or the antioxidant nitroxide tempol

2007 ◽  
Vol 6 (4) ◽  
pp. 337-343 ◽  
Author(s):  
Virany H. Hillard ◽  
Hong Peng ◽  
Kaushik Das ◽  
Raj Murali ◽  
Chitti R. Moorthy ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Hyperbaric Oxygen ◽  
Spinal Cord Tissue ◽  
Irradiation Site ◽  
Injury Site ◽  
Locomotor Recovery ◽  
Locomotor Function ◽  
Cord Injury ◽  
X Irradiation

Object Hyperbaric oxygen (HBO), the nitroxide antioxidant tempol, and x-irradiation have been used to promote locomotor recovery in experimental models of spinal cord injury. The authors used x-irradiation of the injury site together with either HBO or tempol to determine whether combined therapy offers greater benefit to rats. Methods Contusion injury was produced with a weight-drop device in rats at the T-10 level, and recovery was determined using the 21-point Basso-Beattie-Bresnahan (BBB) locomotor scale. Locomotor function recovered progressively during the 6-week postinjury observation period and was significantly greater after x-irradiation (20 Gy) of the injury site or treatment with tempol (275 mg/kg intraperitoneally) than in untreated rats (final BBB Scores 10.6 [x-irradiation treated] and 9.1 [tempol treated] compared with 6.4 [untreated], p < 0.05). Recovery was not significantly improved by HBO (2 atm for 1 hour [BBB Score 8.2, p > 0.05]). Interestingly, the improved recovery of locomotor function after x-irradiation, in contrast with antiproliferative radiotherapy for neoplasia, was inhibited when used together with either HBO or tempol (BBB Scores 8.2 and 8.3, respectively). The ability of tempol to block enhanced locomotor recovery by x-irradiation was accompanied by prevention of alopecia at the irradiation site. The extent of locomotor recovery following treatment with tempol, HBO, and x-irradiation correlated with measurements of spared spinal cord tissue at the contusion epicenter. Conclusions These results suggest that these treatments, when used alone, can activate neuroprotective mechanisms but, in combination, may result in neurotoxicity.

Effect of anti—rat interleukin-6 antibody after spinal cord injury in the rat: inducible nitric oxide synthase expression, sodium- and potassium-activated, magnesium-dependent adenosine-5′-triphosphatase and superoxide dismutase activation, and ultrastructural changes

2001 ◽  
Vol 95 (1) ◽  
pp. 64-73 ◽  
Author(s):  
Metin Tuna ◽  
Sait Polat ◽  
Tahsin Erman ◽  
Faruk Ildan ◽  
A. Iskender Göçer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Tissue ◽  
Inos Activity ◽  
Content Type ◽  
Cord Injury ◽  
Oxide Synthase ◽  
Fine Print ◽  
Inducible Nitric Oxide

Object. The inflammatory cells that accumulate at the damaged site after spinal cord injury (SCI) may secrete interleukin-6 (IL-6), a mediator known to induce the expression of inducible nitric oxide synthase (iNOS). Any increased production of NO by iNOS activity would aggravate the primary neurological damage in SCI. If this mechanism does occur, the direct or indirect effects of IL-6 antagonists on iNOS activity should modulate this secondary injury. In this study, the authors produced spinal cord damage in rats and applied anti—rat IL-6 antibody to neutralize IL-6 bioactivity and to reduce iNOS. They determined the spinal cord tissue activities of Na+-K+/Mg++ adenosine-5′-triphosphatase (ATPase) and superoxide dismutase, evaluated iNOS immunoreactivity, and examined ultrastructural findings to assess the results of this treatment. Methods. Seventy rats were randomly allocated to four groups. Group I (10 rats) were killed to provide normal spinal cord tissue for testing. In Group II 20 rats underwent six-level laminectomy for the effects of total laminectomy alone to be determined. In Group III 20 rats underwent six-level T2–7 laminectomy and SCI was produced by extradural compression of the exposed cord. The same procedures were performed in the 20 Group IV rats, but these rats also received one (2 µg) intraperitoneal injection of anti—rat IL-6 antibody immediately after the injury and a second dose 24 hours posttrauma. Half of the rats from each of Groups II through IV were killed at 2 hours and the other half at 48 hours posttrauma. The exposed cord segments were immediately removed and processed for analysis. Conclusions. The results showed that neutralizing IL-6 bioactivity with anti—rat IL-6 antibody significantly attenuates iNOS activity and reduces secondary structural changes in damaged rat spinal cord tissue.

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