Tencer A F, Huber P, Mirza S K
Orthopedic Sciences Laboratory, University of Washington, Seattle, Washington, USA.
Annu Proc Assoc Adv Automot Med. 2003;47:383-98.
Several hypotheses have been proposed to explain the mechanism of injury in whiplash including, pressure on nerve root ganglia, stretching of facet capsules, or damage to facet articular cartilage. These injury mechanisms have not been directly compared in the same study. A comparison could provide insight into the most likely mechanism of whiplash injury. Twenty eight volunteers underwent rear impacts with head and chest acceleration data collected. The same apparatus was used to test 11 cervico-thoracic human cadaveric spines with an instrumented headform attached. Head acceleration, individual vertebral kinematics from high speed video, local nerve root pressure, and facet joint contact pressures were collected during impacts. Each specimen was tested first at an impact acceleration similar to that of volunteers, who reported minimal or no symptoms after the test, then at double the acceleration. Head X (forward) and Z (upward) accelerations of cadaveric specimens were very similar in time sequence and magnitude to those of unprepared volunteers. Pressure around the lower cervical nerve roots ranged from 2.7kPa to 10kPa, and occurred generally after chest but before peak head acceleration. Facets at C4-5 and C5-6 had the highest probability (64% and 71% respectively) of pinching. Neither pressure rise nor pinching changed significantly with increased acceleration. Vertebral intersegmental extension rotations (4 ( o ) -9.5 ( o ) ) and posterior translations (3.7-8.9 mm) peaked near maximum head excursion into the head restraint, at the time of peak head acceleration. Vertebral shear translations showed the largest (and only significant) increases with increased impact acceleration. This data implies that facet shearing was most sensitive to the increased acceleration in this experiment and may be a primary mechanism of cervical spine injury in rear impacts.
为了解释挥鞭样损伤的机制,人们提出了几种假说,包括神经根神经节受压、小关节囊拉伸或小关节软骨损伤。这些损伤机制尚未在同一研究中进行直接比较。进行比较可能有助于深入了解最可能的挥鞭样损伤机制。28名志愿者接受了后向撞击,并收集了头部和胸部的加速度数据。使用相同的装置对11个附有仪器化头模的颈胸段人体尸体脊柱进行测试。在撞击过程中收集头部加速度、高速视频中的单个椎体运动学、局部神经根压力和小关节接触压力。每个标本首先在与志愿者相似的撞击加速度下进行测试,这些志愿者在测试后报告症状轻微或无症状,然后在加速度加倍的情况下进行测试。尸体标本的头部X(向前)和Z(向上)加速度在时间序列和大小上与未准备的志愿者非常相似。下颈椎神经根周围的压力范围为2.7kPa至10kPa,通常在胸部之后但在头部加速度峰值之前出现。C4-5和C5-6节段的小关节发生挤压的概率最高(分别为64%和71%)。随着加速度的增加,压力升高和挤压均无明显变化。椎体节段间伸展旋转(4(°)-9.5(°))和向后平移(3.7-8.9mm)在头部最大程度向后靠在头枕上时、头部加速度峰值时达到峰值。随着撞击加速度的增加,椎体剪切平移显示出最大(也是唯一显著)的增加。这些数据表明,在本实验中,小关节剪切对加速度增加最为敏感,可能是后向撞击中颈椎损伤的主要机制。