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Spinal Injuries
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
For each mechanism of injury described earlier, there may be complete or incomplete (partial) cord injury. The distinction between complete and incomplete cord injury cannot, however, be made until the patient has recovered from spinal shock. Spinal shock is defined as the complete loss of all neurological function, including reflexes, anal tone and autonomic control, below the level of spinal cord injury. Spinal shock is unrelated to hypovolaemia or neurogenic shock and is effectively spinal concussion. It usually involves a period of 24–72 hours of complete loss of sensory, motor and segmental reflex activity with flaccid paralysis and areflexia below the level of the injury. Despite this profound paralysis, areas of the cord are still capable of a full recovery. Therefore, assessment of neurological status (ASIA Score) for outcome prediction reasons must be done after this period.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Spinal cord injury (SCI) describes damage to the spinal cord resulting in loss of mobility or sensation. SCI is a lifelong condition affecting over 40,000 people in the UK (NICE 2016). The spinal cord does not have to be severed for loss of function to occur; bruising and tearing can cause long-term injury. Fractured vertebrae do not necessarily cause spinal cord injury.
Pharmacokinetic-Pharmacodynamic Correlations of Corticosteroids
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
Helmut Möllmann, Stefan Baibach, Günther Hochhaus, Jürgen Barth, Hartmut Derendorf
Ultra-high doses of corticosteroids (0.5 to 10 g/d) are used to treat various diseases such as spinal cord injury, cardiac infarction, and arthritis, as well as for inhibition of graft rejection.134 These high doses result in plasma and tissue concentrations of 10−4 to 10−5 mol/1, which is far above receptor saturation (10−6 to 10−8 mol/1).58 Efficacy cannot be explained by a receptor-mediated effect. Despite the common clinical application, not much is known about the mode of action. Therapy for the acute spinal cord injury is under intense investigation and is reviewed by several authors.4,157–159 The main mechanism seems to be facilitation of the spinal cord impulse generation, due to hyperpolarization of the resting membrane potential as well as enhancing the excitability of spinal motor neurons. Additionally, improved blood flow in the injured spinal cord was reported. Interference with vasoconstrictor effects, sympathetic response, prostaglandin and thromboxan synthesis, and direct vasodilatation are all proposed mechanisms. During hypoxia induced by spinal cord injury, free radicals are generated in the membrane, which attack unsaturated lipids and inhibit neuronal key enzymes such as the sodium/potassium-ATPase.4 There is evidence that large doses of corticosteroids, especially MP, protect the membrane from free radicals.160
Effect of selegiline as a monomine oxidase B inhibitor on the expression of neurotrophin mRNA levels in a contusion rat model of spinal cord injury
Published in Neurological Research, 2023
Alireza Abdanipour, Mojgan Mirzaei, Iraj Jafari Anarkooli, Parvin Mohammadi
Hind limb scores were recorded 3, 7, 14, 21 and 28 days after injury. In a spinal cord injury model, this test was performed to assess motor function. The behavioral study was conducted in two phases: the pre-test and the main test. In the preliminary test, all rats received 21 BBB points. Statistically significant differences between groups were determined using a one-way analysis of variance. The Tukey post hoc test showed significant differences between the selegiline treated group compared to the untreated contusion, sham and laminectomy groups at day 14 and 21 as follows: day of 14 (Contusion: 2.75 ± 0.72, laminectomy: 19.20 ± 0.73, sham: 4.5 ± 1.25, treatment: 8.91 ± 1.17); day of 21 (Contusion: 3.08 ± 0.63, laminectomy: 20.6 ± 0.24, sham: 4.5 ± 1.25, treatment: 11.16 ± 0.73); day of 28 (Contusion: 3.5 ± 0.65, laminectomy: 20.6 ± 0.24, sham: 5 ± 1.29, treatment: 12.5 ± 0.5) (Figure 1).
Regenerative replacement of neural cells for treatment of spinal cord injury
Published in Expert Opinion on Biological Therapy, 2021
William Brett McIntyre, Katarzyna Pieczonka, Mohamad Khazaei, Michael G. Fehlings
Another common line of treatment following spinal cord injury involves physical rehabilitation, which has been associated with functional improvements. Fundamentally, physical activity is able to mitigate cellular pathophysiology, which makes it a promising conjunctive therapy. At the level of the neuron, exercise is associated with a decrease in neuronal apoptosis [32] and a reduction in motor neuron dendritic atrophy, thus indicating that it is beneficial for maintaining synaptic integrity [33]. Interestingly, exercise induces upregulation of the expression of proteins and trophic factors that are involved in the survival of motor neurons and sensory neurons. As such, exercise may have ranging implications for different types of neurons [33]. In the context of oligodendrocytes, physical activity may reduce demyelination and/or improve remyelination, as it is associated with an increased number of myelinated axons in a model of peripheral nerve damage [34]. Finally, exercise is associated with a decrease in phagocytic and reactive glia, which may restrict glial scar formation [32].
Exosomes derived from GIT1-overexpressing bone marrow mesenchymal stem cells promote traumatic spinal cord injury recovery in a rat model
Published in International Journal of Neuroscience, 2021
Yongjun Luo, Tao Xu, Wei Liu, Yuluo Rong, Jiaxing Wang, Jin Fan, Guoyong Yin, Weihua Cai
Spinal cord injury from trauma severely impairs motor and sensory function. Emerging data from preclinical studies in the past decades had offered potential therapy helpful for this severe and even fatal disease. To date, however, most proven therapeutic modality was able to show a limited positive effect on neurological outcome. A great deal of efforts was still necessary to invest in the study of SCI. The process of neural rehabilitation after SCI is complex, with neuron apoptosis, glial scar formation and neuroinflammation involved, hampering the neural functional recovery. In this study, we tried to prove GIT1-overexpressing BMSC-derived Exos could alleviate the neurons apoptosis, attenuate neuroinflammation and inhibit microglia formation and finally the axonal could regenerate and neural function was able to recover.