Pretreatment with Calpain Inhibitor CEP-4143 Inhibits Calpain I Activation and Cytoskeletal Degradation, Improves Neurological Function, and Enhances Axonal Survival After Traumatic Spinal Cord Injury

2002 ◽  
Vol 74 (4) ◽  
pp. 1646-1655 ◽  
Author(s):  
P. A. Schumacher ◽  
R. G. Siman ◽  
M. G. Fehlings
1988 ◽  
Vol 69 (3) ◽  
pp. 399-402 ◽  
Author(s):  
Joseph M. Piepmeier ◽  
N. Ross Jenkins

✓ Sixty-nine patients with traumatic spinal cord injuries were evaluated for changes in their functional neurological status at discharge from the hospital, and at 1 year, 3 years, and 5+ years following injury. The neurological examinations were used to classify patients' spinal cord injury according to the Frankel scale. This analysis revealed that the majority of improvement in neurological function occurred within the 1st year following injury; however, changes in the patients' status continued for many years. Follow-up examinations at an average of 3 years postinjury revealed that 23.3% of the patients continued to improve, whereas 7.1% had deteriorated compared to their status at 1 year. An examination at an average of 5+ years demonstrated further improvement in 12.5%, with 5.0% showing deterioration compared to the examinations at 3 years. These results demonstrate that, in patients with spinal trauma, significant changes in neurological function continue for many years.


2021 ◽  
Vol 15 ◽  
Author(s):  
Hong-jun Zou ◽  
Shi-Wu Guo ◽  
Lin Zhu ◽  
Xu Xu ◽  
Jin-bo Liu

Traumatic spinal cord injury (TSCI) leads to pathological changes such as inflammation, edema, and neuronal apoptosis. Methylprednisolone (MP) is a glucocorticoid that has a variety of beneficial effects, including decreasing inflammation and ischemic reaction, as well as inhibiting lipid peroxidation. However, the efficacy and mechanism of MP in TSCI therapy is yet to be deciphered. In the present study, MP significantly attenuated the apoptotic effects of H2O2 in neuronal cells. Western blot analysis demonstrated that the levels of apoptotic related proteins, Bax and cleaved caspase-3, were reduced while levels of anti-apoptotic Bcl-2 were increased. In vivo TUNEL assays further demonstrated that MP effectively protected neuronal cells from apoptosis after TSCI, and was consistent with in vitro studies. Furthermore, we demonstrated that MP could decrease expression levels of IBA1, Il-1α, TNFα, and C3 and suppress A1 neurotoxic reactive astrocyte activation in TSCI mouse models. Neurological function was evaluated using the Basso Mouse Scale (BMS) and Footprint Test. Results demonstrated that the neurological function of MP-treated injured mice was significantly increased. In conclusion, our study demonstrated that MP could attenuate astrocyte cell death, decrease microglia activation, suppress A1 astrocytes activation, and promote functional recovery after acute TSCI in mouse models.


Neurocirugía ◽  
2009 ◽  
Vol 20 (3) ◽  
pp. 245-254 ◽  
Author(s):  
A. Çolak ◽  
A. Karaoğlan ◽  
M. Kaya ◽  
A. Sağmanligil ◽  
O. Akdemir ◽  
...  

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Graham Ka Hon Shea ◽  
Paul Aarne Koljonen ◽  
Ying Shing Chan ◽  
Kenneth Man Chee Cheung

AbstractDegenerative cervical myelopathy (DCM) presents insidiously during middle-age with deterioration in neurological function. It accounts for the most common cause of non-traumatic spinal cord injury in developed countries and disease prevalence is expected to rise with the aging population. Whilst surgery can prevent further deterioration, biological therapies may be required to restore neurological function in advanced disease. Cell replacement therapy has been inordinately focused on treatment of traumatic spinal cord injury yet holds immense promise in DCM. We build upon this thesis by reviewing the pathophysiology of DCM as revealed by cadaveric and molecular studies. Loss of oligodendrocytes and neurons occurs via apoptosis. The tissue microenvironment in DCM prior to end-stage disease is distinct from that following acute trauma, and in many ways more favourable to receiving exogenous cells. We highlight clinical considerations for cell replacement in DCM such as selection of cell type, timing and method of delivery, as well as biological treatment adjuncts. Critically, disease models often fail to mimic features of human pathology. We discuss directions for translational research towards clinical application.


2018 ◽  
Vol 1 (2) ◽  
pp. 34
Author(s):  
Mochamad Targib Alatas

Early surgical treatment for traumatic spinal cord injury (SCI) patients has been proven to yield better improvement on neurological state, and widely practiced among surgeons in this field. However, it is not always affordable in every clinical setting. It is undeniable that surgery for chronic SCI has more challenges as the malunion of vertebral bones might have initiated, thus requires more complex operating techniques. In this case series, we report 7 patients with traumatic SCI whose surgical intervention is delayed due to several reasons. Initial motoric scores vary from 0 to 3, all have their interval periods supervised between outpatient clinic visits. On follow up they demonstrate significant neurological development defined by at least 2 grades motoric score improvement. Physical rehabilitation also began before surgery was conducted. These results should encourage surgeons to keep striving for the patient’s best interest, even when the injury has taken place weeks or even months before surgery is feasible because clinical improvement for these patients is not impossible. 


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