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Traumatic Spinal Cord Injury (traumatic + spinal_cord_injury)

Distribution by Scientific Domains
Medical Sciences80%

Selected Abstracts

Traumatic spinal cord injury and concomitant brain injury: a cohort study

ACTA NEUROLOGICA SCANDINAVICA, Issue 2010
E. M. Hagen
Hagen EM, Eide GE, Rekand T, Gilhus NE, Gronning M. Traumatic spinal cord injury and concomitant brain injury: a cohort study. Acta Neurol Scand: 2010: 122 (Suppl. 190): 51,57. © 2010 John Wiley & Sons A/S. Objective,,, To assess the temporal trends in the incidence and demographic characteristics of traumatic spinal cord injury (TSCI) with clinical concomitant traumatic brain injury (TBI), in an unselected, geographically defined cohort, 1952,2001. Material and methods,,, The patients were identified from hospital records. TBI was classified as none, mild, moderate, and severe. Results,,, Of 336 patients, 157 (46.7%) patients had a clinical concomitant TBI. Clinical TBI was classified as mild in 30.1%, moderate in 11.0% and severe in 5.7%. The average annual incidence increased from 3.3 per million in the first decade to 10.7 per million in the last. Alcohol was the strongest risk factor of clinical TBI (OR = 3.69) followed by completeness of TSCI (OR = 2.18). Conclusions,,, The incidence of TSCI with concomitant TBI has increased during the last 50 years. Alcohol and completeness of injury are strong risk factors. Increased awareness of dual diagnoses is necessary. [source]

Disruption of the hyaluronan-based extracellular matrix in spinal cord promotes astrocyte proliferation

GLIA, Issue 1 2005
Jaime Struve
Abstract Astrocyte proliferation is tightly controlled during development and in the adult nervous system. In the present study, we find that a high-molecular-weight (MW) form of the glycosaminoglycan hyaluronan (HA) is found in rat spinal cord tissue and becomes degraded soon after traumatic spinal cord injury. Newly synthesized HA accumulates in injured spinal cord as gliosis proceeds, such that high-MW HA becomes overabundant in the extracellular matrix surrounding glial scars after 1 month. Injection of hyaluronidase, which degrades HA, into normal spinal cord tissue results in increased numbers of glial fibrillary acidic protein (GFAP)-positive cells that also express the nuclear proliferation marker Ki-67, suggesting that HA degradation promotes astrocyte proliferation. In agreement with this observation, adding high- but not low-MW HA to proliferating astrocytes in vitro inhibits cell growth, while treating confluent, quiescent astrocyte cultures with hyaluronidase induces astrocyte proliferation. Collectively, these data indicate that high-MW HA maintains astrocytes in a state of quiescence, and that degradation of HA following CNS injury relieves growth inhibition, resulting in increased astrocyte proliferation. © 2005 Wiley-Liss, Inc. [source]

Model of traumatic spinal cord injury in Macaca fascicularis: similarity of experimental lesions created by epidural catheter to human spinal cord injury

JOURNAL OF MEDICAL PRIMATOLOGY, Issue 6 2006
Shanker Nesathurai
First page of article [source]

Traumatic spinal cord injury and concomitant brain injury: a cohort study

ACTA NEUROLOGICA SCANDINAVICA, Issue 2010
E. M. Hagen
Hagen EM, Eide GE, Rekand T, Gilhus NE, Gronning M. Traumatic spinal cord injury and concomitant brain injury: a cohort study. Acta Neurol Scand: 2010: 122 (Suppl. 190): 51,57. © 2010 John Wiley & Sons A/S. Objective,,, To assess the temporal trends in the incidence and demographic characteristics of traumatic spinal cord injury (TSCI) with clinical concomitant traumatic brain injury (TBI), in an unselected, geographically defined cohort, 1952,2001. Material and methods,,, The patients were identified from hospital records. TBI was classified as none, mild, moderate, and severe. Results,,, Of 336 patients, 157 (46.7%) patients had a clinical concomitant TBI. Clinical TBI was classified as mild in 30.1%, moderate in 11.0% and severe in 5.7%. The average annual incidence increased from 3.3 per million in the first decade to 10.7 per million in the last. Alcohol was the strongest risk factor of clinical TBI (OR = 3.69) followed by completeness of TSCI (OR = 2.18). Conclusions,,, The incidence of TSCI with concomitant TBI has increased during the last 50 years. Alcohol and completeness of injury are strong risk factors. Increased awareness of dual diagnoses is necessary. [source]