Spinal cord injury without radiographic abnormalities in children

1982 ◽  
Vol 57 (1) ◽  
pp. 114-129 ◽  
Author(s):  
Dachling Pang ◽  
James E. Wilberger
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cervical Cord ◽  
Content Type ◽  
Age Related ◽  
Surgical Fusion ◽  
Flexion Extension ◽  
Cord Injury ◽  
Upper Cervical ◽  
Long Term Prognosis

✓ Spinal cord injury in children often occurs without evidence of fracture or dislocation. The mechanisms of neural damage in this syndrome of spinal cord injury without radiographic abnormality (SCIWORA) include flexion, hyperextension, longitudinal distraction, and ischemia. Inherent elasticity of the vertebral column in infants and young children, among other age-related anatomical peculiarities, render the pediatric spine exceedingly vulnerable to deforming forces. The neurological lesions encountered in this syndrome include a high incidence of complete and severe partial cord lesions. Children younger than 8 years old sustain more serious neurological damage and suffer a larger number of upper cervical cord lesions than children aged over 8 years. Of the children with SCIWORA, 52% have delayed onset of paralysis up to 4 days after injury, and most of these children recall transient paresthesia, numbness, or subjective paralysis. Management includes tomography and flexion-extension films to rule out incipient instability, and immobilization with a cervical collar. Delayed dynamic films are essential to exclude late instability, which, if present, should be managed with Halo fixation or surgical fusion. The long-term prognosis in cases of SCIWORA is grim. Most children with complete and severe lesions do not recover; only those with initially mild neural injuries make satisfactory neurological recovery.

Deterioration following spinal cord injury

1987 ◽  
Vol 66 (3) ◽  
pp. 400-404 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Sharen Knowlton ◽  
Steven R. Garfin ◽  
Melville R. Klauber ◽  
Howard M. Eisenberg ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cervical Cord ◽  
Skeletal Traction ◽  
Systemic Complications ◽  
Content Type ◽  
Management Procedures ◽  
Cord Injury ◽  
Specific Management ◽  
Fine Print

✓ The results are presented of a prospective study of the course of 283 spinal cord-injured patients who were consecutively admitted to five trauma centers participating in the Comprehensive Central Nervous System Injury Centers' program of the National Institutes of Health. Of the 283 patients, 14 deteriorated neurologically during acute hospital management. In 12 of the 14, the decline in neurological function could be associated with a specific management event, and in nine of these 12 the injury involved the cervical cord. Nine of the 14 patients who deteriorated had cervical injuries, three had thoracic cord injuries, and two had thoracolumbar junction injuries. Management intervention was identified as the cause of deterioration in four of 134 patients undergoing operative intervention, in three of 60 with skeletal traction application, in two of 68 with halo vest application, in two of 56 undergoing Stryker frame rotation, and in one of 57 undergoing rotobed rotation. Early surgery on the cervical spine when cord injury is present appears hazardous, since each of the three patients with a cervical cord injury who deteriorated was operated on within the first 5 days. No such deterioration was observed following surgery performed from the 6th day on. In two other patients, deterioration did not appear to be related to management but was a direct product of the underlying disease or of systemic complications. Deterioration following hospitalization for spinal cord injury is relatively uncommon — 4.9% in this large series. In most instances, decline in function could be attributed to specific management procedures. These changes must not be interpreted as representing failure to provide optimal care but rather should be seen as the inevitable product of an attempt to manage patients with spinal cord and column injuries, many of which are clearly unstable.

The neurological and skeletal outcome in patients with closed cervical spinal cord injury

1987 ◽  
Vol 66 (5) ◽  
pp. 690-694 ◽  
Author(s):  
William H. Donovan ◽  
Dennis Kopaniky ◽  
Eweline Stolzmann ◽  
R. Edward Carter
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Callus Formation ◽  
Cervical Spinal Cord ◽  
Fracture Site ◽  
Cervical Spinal Cord Injury ◽  
Spinal Stability ◽  
Content Type ◽  
Surgical Fusion ◽  
Cord Injury

✓ Sixty-one patients with closed cervical spinal cord injury were cared for within a defined protocol and followed for at least 1 year. Neurological recovery and healing of spinal structures were evaluated at intervals. Forty-three patients were managed without surgical intervention at the site of spine trauma, and the incidence of spontaneous fusion (”autofusion”) was noted. Surgical fusion was performed on 17 patients, mainly to restore spinal stability and alignment. One patient underwent laminectomy without fusion. In both the surgical fusion and the autofusion groups, there were significant numbers of patients who improved neurologically, including some designated as having a complete spinal cord lesion at the initial neurological examination. As expected, better spinal alignment was achieved in the surgical group, although alignment in the nonsurgically treated group was generally acceptable. The majority of patients developed radiographically apparent callus formation anterior to the injured vertebral bodies, regardless of the mechanism of injury or the method of treatment. After 3 months all patients who underwent surgical fusion achieved spinal stability, as did the majority of patients in the autofusion group. Only individuals with flexion-distraction injuries who did not undergo surgical fusion appeared to be at risk for progressive spinal column deformity. Neither retropulsion of bone fragments nor angulation at the fracture site appeared to correlate with a poor neurological outcome, since improvement in neurological function occurred similarly in patients with and without these deformities.

Recurrent spinal cord injury without radiographic abnormalities in children

1988 ◽  
Vol 69 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Ian F. Pollack ◽  
Dachling Pang ◽  
Robert Sclabassi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Soft Tissues ◽  
Spinal Cord Injuries ◽  
Dorsal Column ◽  
Neurological Deficits ◽  
Spinal Instability ◽  
Content Type ◽  
Flexion Extension ◽  
Cord Injury

✓ Spinal cord injury without radiographic abnormality is a well-known entity in the pediatric age group. Agerelated elasticity of the vertebral ligaments as well as immaturity of the osseous structures in the pediatric spine allow momentary subluxation in response to deforming forces. The resultant neurological injuries range from transient dorsal column dysfunction to complete cord transection. Between 1960 and 1985, 42 such injuries were treated at the Children's Hospital of Pittsburgh. Management of these radiographically occult spinal cord injuries consisted of cervical immobilization for 2 months in a hard collar and restriction of contact sports. Recurrent cord injury occurred in eight cases during the 2-month immobilization period. A clearly defined traumatic episode was identified in seven of the eight patients, although in four children the recurrent trauma to the spine was trivial. Five of the children removed their collars briefly before the second injury, and two children incurred reinjury with the hard collar in place. The remaining child was too young for hard-collar immobilization, and recurrent neurological deterioration occurred during sleep. Serial flexion-extension films failed to detect frank instability in any of the eight cases. The children most susceptible to reinjury were those who sustained mild or transient neurological deficits from an initial cord injury and who rapidly resumed normal activities. Radiographically occult spinal instability resulting from the initial injury to the vertebral and paravertebral soft tissues presumably made these children vulnerable to recurrent spinal cord injury, often from otherwise insignificant trauma. During the last 21 months, 12 additional children have been managed with a more stringent protocol combining neck immobilization in a rigid cervical brace for 3 months and restriction of both contact and noncontact sports, together with a major emphasis on patient compliance. With this new protocol, no recurrent cord injuries have been documented.

Cardiovascular and Metabolic Responses to Electrical Stimulation-Induced Leg Exercise in Spinal Cord Injury

1997 ◽  
Vol 36 (04/05) ◽  
pp. 372-375 ◽  
Author(s):  
J. R. Sutton ◽  
A. J. Thomas ◽  
G. M. Davis
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Spinal Cord Injury ◽  
Cardiac Output ◽  
Electrical Stimulation ◽  
Knee Flexion ◽  
Flexion Extension ◽  
Cord Injury ◽  
Leg Exercise ◽  
Leg Muscle

Abstract:Electrical stimulation-induced leg muscle contractions provide a useful model for examining the role of leg muscle neural afferents during low-intensity exercise in persons with spinal cord-injury and their able-bodied cohorts. Eight persons with paraplegia (SCI) and 8 non-disabled subjects (CONTROL) performed passive knee flexion/extension (PAS), electrical stimulation-induced knee flexion/extension (ES) and voluntary knee flexion/extension (VOL) on an isokinetic dynamometer. In CONTROLS, exercise heart rate was significantly increased during ES (94 ± 6 bpm) and VOL (85 ± 4 bpm) over PAS (69 ± 4 bpm), but no changes were observed in SCI individuals. Stroke volume was significantly augmented in SCI during ES (59 ± 5 ml) compared to PAS (46 ± 4 ml). The results of this study suggest that, in able-bodied humans, Group III and IV leg muscle afferents contribute to increased cardiac output during exercise primarily via augmented heart rate. In contrast, SCI achieve raised cardiac output during ES leg exercise via increased venous return in the absence of any change in heart rate.

The effects of methylprednisolone and the ganglioside GM1 on acute spinal cord injury in rats

1994 ◽  
Vol 80 (1) ◽  
pp. 97-111 ◽  
Author(s):  
Shlomo Constantini ◽  
Wise Young
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Body Weight Loss ◽  
Ganglioside Gm1 ◽  
Rat Spinal Cord ◽  
Neuroprotective Effects ◽  
Content Type ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Fine Print

✓ Recent clinical trials have reported that methylprednisolone sodium succinate (MP) or the monosialic ganglioside GM1 improves neurological recovery in human spinal cord injury. Because GM1 may have additive or synergistic effects when used with MP, the authors compared MP, GM1, and MP+GM1 treatments in a graded rat spinal cord contusion model. Spinal cord injury was caused by dropping a rod weighing 10 gm from a height of 1.25, 2.5, or 5.0 cm onto the rat spinal cord at T-10, which had been exposed via laminectomy. The lesion volumes were quantified from spinal cord Na and K shifts at 24 hours after injury and the results were verified histologically in separate experiments. A single dose of MP (30 mg/kg), given 5 minutes after injury, reduced 24-hour spinal cord lesion volumes by 56% (p = 0.0052), 28% (p = 0.0065), and 13% (p > 0.05) in the three injury-severity groups, respectively, compared to similarly injured control groups treated with vehicle only. Methylprednisolone also prevented injury-induced hyponatremia and increased body weight loss in the spine-injured rats. When used alone, GM1 (10 to 30 mg/kg) had little or no effect on any measured variable compared to vehicle controls; when given concomitantly with MP, GM1 blocked the neuroprotective effects of MP. At a dose of 3 mg/kg, GM1 partially prevented MP-induced reductions in lesion volumes, while 10 to 30 mg/kg of GM1 completely blocked these effects of MP. The effects of MP on injury-induced hyponatremia and body weight loss were also blocked by GM1. Thus, GM1 antagonized both central and peripheral effects of MP in spine-injured rats. Until this interaction is clarified, the authors recommend that MP and GM1 not be used concomitantly to treat acute human spinal cord injury. Because GM1 modulates protein kinase activity, protein kinases inhibit lipocortins, and lipocortins mediate anti-inflammatory effects of glucocorticoids, it is proposed that the neuroprotective effects of MP are partially due to anti-inflammatory effects and that GM1 antagonizes the effects of MP by inhibiting lipocortin. Possible beneficial effects of GM1 reported in central nervous system injury may be related to the effects on neural recovery rather than acute injury processes.

scholarly journals Age-related variation in mobility independence among wheelchair users with spinal cord injury: A cross-sectional study

2016 ◽  
Vol 39 (2) ◽  
pp. 180-189 ◽  
Author(s):  
Timo Hinrichs ◽  
Veronika Lay ◽  
Ursina Arnet ◽  
Inge Eriks-Hoogland ◽  
Hans Georg Koch ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Cross Sectional ◽  
Wheelchair Users ◽  
Related Variation ◽  
Age Related ◽  
Cord Injury

Cervical Cord-Canal Mismatch: A New Method for Identifying Predisposition to Spinal Cord Injury

2017 ◽  
Vol 108 ◽  
pp. 112-117 ◽  
Author(s):  
Aria Nouri ◽  
Julio Montejo ◽  
Xin Sun ◽  
Justin Virojanapa ◽  
Luis E. Kolb ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
New Method ◽  
Cervical Cord ◽  
Cord Injury

Therapeutic trial of hypercarbia and hypocarbia in acute experimental spinal cord injury

1984 ◽  
Vol 61 (5) ◽  
pp. 925-930 ◽  
Author(s):  
Ronald W. J. Ford ◽  
David N. Malm
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Mortality Rates ◽  
Therapeutic Trial ◽  
Tissue Preservation ◽  
Content Type ◽  
Experimental Spinal Cord Injury ◽  
Cord Injury ◽  
Fine Print

✓ Hypocarbia, normocarbia, or hypercarbia was maintained for an 8-hour period beginning 30 minutes after acute threshold spinal cord injuries in cats. No statistically significant differences in neurological recovery or histologically assessed tissue preservation were found among the three groups of animals 6 weeks after injury. No animal recovered the ability to walk. It is concluded that maintenance of hypercarbia or hypocarbia during the early postinjury period is no more therapeutic than maintenance of normocarbia. Mortality rates and tissue preservation data suggest, however, that postinjury hypocarbia may be less damaging than hypercarbia.

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