Rai Survendra Kumar Rajdeo, Rai Pooja Survendra Kumar
Department of Neurosurgery, Seth Gordhandas Sunderdas Medical College and King Edward Memorial Hospital, Sion, Mumbai, Maharashtra, India.
Department of Biochemistry, Lokmanya Tilak Municipal Medical College and Lokmanya Tilak Municipal General Hospital, Sion, Mumbai, Maharashtra, India.
Asian J Neurosurg. 2015 Oct-Dec;10(4):245-51. doi: 10.4103/1793-5482.162680.
The etiopathogenesis of syringomyelia is still an enigma. The authors present a novel theory based on fluid dynamics at the craniovertebral (CV) junction to explain the genesis of syringomyelia (SM). The changes in volume of spinal canal, spinal cord, central canal and spinal subarachnoid space (SSS) in relation to the posterior fossa have been analysed, specifically during postural movements of flexion and extension. The effect of fluctuations in volume of spinal canal and its contents associated with cerebrospinal fluid (CSF) flow dynamics at the CV junction have been postulated to cause the origin and propagation of the syringomyelia. The relevant literature on the subject has been reviewed and the author's theory has been discussed.
Volume of spinal canal in flexion is always greater than that in extension. Flexion of spine causes narrowing of the ventral subarachnoid space (SAS) and widening of dorsal SAS while extension causes reverse changes leading to fluid movement in dorsal spinal SAS in flexion and ventral spinal SAS in extension. Cervical and lumbar spinal region with maximum bulk hence maximum area and volume undergo maximum deformation during postural changes. SSS CSF is the difference between the volume of spinal canal and spinal cord, varies in flexion and extension which is compensated by changes in posterior fossa (CSF) volume in normal circumstances. Blocked SAS at foramen magnum donot permit spinal SAS CSF exchange which during postural changes is compensated by cavitatory/cystic (syrinx) change at locations in cervical and lumbar spine with propensity for maximum deformation. Augmentation of posterior fossa volume by decompression helps by normalization of this CSF exchange dynamics but immobilizing the spinal movement theoretically will cease any dynamic volume changes thereby minimizing the destructive influence of the fluid exchange on the cord. Thus, this theory strengthens the rational of treating patients by either methodology.
脊髓空洞症的发病机制仍是一个谜。作者提出了一种基于颅颈(CV)交界处流体动力学的新理论,以解释脊髓空洞症(SM)的成因。分析了椎管、脊髓、中央管和脊髓蛛网膜下腔(SSS)相对于后颅窝的体积变化,特别是在屈伸姿势运动期间。推测CV交界处与脑脊液(CSF)流动动力学相关的椎管及其内容物体积波动的影响会导致脊髓空洞症的起源和扩散。回顾了该主题的相关文献并讨论了作者的理论。
屈曲时椎管体积总是大于伸展时。脊柱屈曲导致腹侧蛛网膜下腔(SAS)变窄,背侧SAS变宽,而伸展则导致相反变化,导致屈曲时背侧脊髓SAS和伸展时腹侧脊髓SAS中的液体流动。因此,体积最大、面积和体积最大的颈段和腰段脊髓在姿势改变时变形最大。SSS脑脊液是椎管和脊髓体积之间的差值,在屈伸时会发生变化,在正常情况下由后颅窝(脑脊液)体积的变化来补偿。枕骨大孔处受阻的SAS不允许脊髓SAS脑脊液交换,在姿势改变期间,这种交换由颈段和腰段脊柱中倾向于最大变形部位的空洞化/囊性(空洞)变化来补偿。通过减压增加后颅窝体积有助于使这种脑脊液交换动力学正常化,但理论上固定脊柱运动将停止任何动态体积变化,从而将液体交换对脊髓的破坏影响降至最低。因此,该理论强化了采用任何一种方法治疗患者的合理性。