Traumatic Cervical Spinal Cord Research Articles

Biomechanics of nonacute cervical spinal cord trauma.

Biomechanics of nonacute cervical spinal cord trauma.

Cardiovascular instability following acute cervical spinal cord trauma.

Irregularities in vital sign (pulse, blood pressure, cardiac rhythm) recordings are commonly observed following acute spinal cord injury. These abnormalities have been generally attributed to autonomic instability. However, there have been no clinical reports that evaluate these problems in a large group of acutely injured patients. Therefore, this study was performed on 45 patients with acute cervical spinal cord injuries to evaluate the incidence, severity, and risk factors for cardiovascular instability. This investigation revealed that there is a direct correlation between the severity of the cord injury and the incidence and severity of cardiovascular problems. Endotracheal suctioning with or without documented hypoxia are major causes of severe bradycardia and cardiac arrest within the first 2 weeks after trauma. Careful monitoring of severely injured patients and attention to the warning signs of cardiovascular instability can reduce the risk of life-threatening emergencies.

Cervical spine injuries resulting from collision sports.

Acute traumatic lesions of spine as a result of ‘collision sports’ such as football, wrestling, and boxing are of particular significance since these injuries most frequently involve the cervical spine in males, and the resulting neurologic deficit if permanent, is tetraplegia. Forty-six (3.5 per cent) of 1305 patients with spinal cord injury sustained cervical spinal cord trauma during collision sports and 84 per cent of these remained tetraplegie. Their neurological patterns of deficit, radiological abnormalities, mechanism of injury and management are presented in detail. To minimise the severity of neurological deficit some preventive measures are also outlined.

Minimyelogram in cervical spinal cord trauma.

Fifty-eight patients with a clinical or radiographic diagnosis of cervical spinal cord injury underwent Pantopaque myelography on an emergency basis. Twenty-five per cent of these patients demonstrated evidence of spinal cord compression after reduction by spinal traction, as evidenced by the presence of a myelographic defect. Less than half of these patients had a defect that the authors thought required emergency surgical decompression. Two of the five patients so operated upon demonstrated an improvement in neurological function after operation that was much greater than that which would have been predicted before operation. The finding of these few patients who made a significant improvement after operation may justify the myelographic investigation of all patients with evidence of serious cervical spinal cord injury. Based on our experience, Pantopaque myelography may offer adequate, accurate, and useful information for the immediate management of spinal cord-injured patients.

Minimyelogram in cervical spinal cord trauma

Fifty-eight patients with a clinical or radiographic diagnosis of cervical spinal cord injury underwent Pantopaque myelography on an emergency basis. Twenty-five per cent of these patients demonstrated evidence of spinal cord compression after reduction by spinal traction, as evidenced by the presence of a myelographic defect. Less than half of these patients had a defect that the authors thought required emergency surgical decompression. Two of the five patients so operated upon demonstrated an improvement in neurological function after operation that was much greater than that which would have been predicted before operation. The finding of these few patients who made a significant improvement after operation may justify the myelographic investigation of all patients with evidence of serious cervical spinal cord injury. Based on our experience, Pantopaque myelography may offer adequate, accurate, and useful information for the immediate management of spinal cord-injured patients. (Neurosurgery, 7: 219-224, 1980)

Management of cervical spinal cord trauma in Southern California.

Acute cervical spinal cord injuries were reviewed in 356 patients treated by the neurosurgical community in Southern California. Neurological recovery was compared in operated and nonoperated patients with complete and incomplete cervical myelopathies. The complications of nonsurgical and surgical therapy are identified. No neurological improvement was noted in any patient with a complete lesion who underwent early surgical decompression. In those with incomplete sensorimotor paralysis, it was difficult to document any effect of surgical decompression on neurological recovery. Patients with some degree of sensory preservation had a similar incidence of motor recovery in both surgical and nonsurgical groups. With complete sensorimotor paralysis, anterior cervical fusion within the first week of injury was associated with increased pulmonary morbidity.

Changes in evoked potentials after experimental cervical spinal cord injury in the monkey

Rhesus monkeys were subjected to acute cervical spinal cord trauma after chronic implantation of both cortical and deep electrodes. The method of injury was acute flexion-compression in the mid-cervical region. After stimulation of the sciatic nerve with a stimulus just above threshold at 10-sec intervals for 1 msec, evoked potentials were recorded from the contralateral sensory cortex, ventral posterior lateral nucleus of the thalamus, internal capsule, and the brain stem reticular formation. The evoked potential was still present immediately after injury, but starting at approximately 20–90 sec after the injury it began to disappear rapidly. Thereafter, the primary evoked response could not be demonstrated until it began to reappear about 24 hr after the injury; however, no averaged evoked response was ever obtained from the brain stem reticular formation, even after 6 days. The loss of the evoked response is thought to coincide with the onset of primary hemorrhage and edema, demonstrated in the cord. A synchronous 16-cycle spindle activity, which seems to be time-locked to the stimulus and not present in any control recording, began to appear about 30 min after the injury and became more prominent in ensuing days. This 16-cycle activity, characteristic of fast sleep spindles, coupled with the loss of the evoked response in the brain stem reticular formation may account for the transient loss of consciousness that occurs in the monkeys after the cervical injury, and for the persistent alteration of the conscious level we have noted.