[Experimental spinal injuries under the action of longitudinal impact loads].
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Traumatic CNS injury is one of the most important health issues in our society and is a risk to all athletes, both in competitive and recreational sports. Our understanding of the pathophysiology has improved tremendously in the last 20 years. This progress has led to the identification of several possible treatments for improving outcome following spinal cord injury and traumatic brain injury. As no panacea exists, improvements in experimental models have empowered researchers in their search for novel therapeutic strategies.
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In the last decade, by application of detailed methods of care, the previously accepted complications of urinary infection, pressure sores and motor skeletal problems of contractures and spasm, have largely been eliminated from the clinical picture of patients with spinal paralysis. Many professionals in medicine have contributed to these advances. Long-term or extended care in the area of tetraplegia and paraplegia need further stimulation, with continued application of all those methods used in acute rehabilitation in properly organized spinal units.
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Vertebral artery injury may complicate cervical spine injury and may result in severe neurological impairment. We present a case of a 54 year-old male who sustained a hyperextension injury of the neck during horse-back riding with cervical spine dislocation of C3/4. As a consequence of right-sided traumatic vertebral artery thrombosis and extension of the thrombus into the basilar artery the patient developed a brainstem and bilateral cerebellar infarction with fatal outcome. In a review of the literature the characteristics of 33 cases with vertebral artery injuries following cervical spine trauma and with associated neurological complications are described. The problems of vertebral artery injury are discussed concerning diagnosis and therapy.
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Using a conjugate of substance P and the ribosome-inactivating protein saporin, neurons expressing the neurokinin-1 receptor in lamina I of the spinal cord were targeted to determine their role in the expression of a spontaneous pain behavior following intraspinal injections of quisqualic acid in the rat. Treatment was carried out at the time of injury in order to prevent the onset of the behavior, and following onset in order to evaluate the potential clinical utility of this intervention. Treatment at the time of injury resulted in significant decreases in onset-time and severity of pain behavior, while treatment at the time of onset led to a significant reduction of the spontaneous self-directed behavior. The results suggest that the substrate for at-level pain following spinal cord injury includes a population of spinal neurons expressing the neurokinin-1 receptor in the superficial laminae of the spinal cord.
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