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Spinal Cord Disease
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
The surface of the spinal cord is richly interwoven with circumflex anastomoses arising from the anterior and posterior spinal arteries. A relative hypovascularity exists in the mid-thoracic region from about T4 to T8, which is the most vulnerable part of the spinal cord to ischemia. Venous drainage occurs via the median posterior and the anterior spinal veins. The lack of venous valves may permit retrograde spreading of abdominal infectious and malignant processes to the spinal cord.
Spine
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
Radicular and spinal veins drain into the internal vertebral venous plexus (of Batson) that later drain into the azygos system and the superior vena cava through the vertebral, intercostal and lumbar veins. The plexus communicates with the basilar sinus in the brain and with the pelvic veins and inferior vena cava. In patients with increased intra-abdominal pressure, blood is diverted from the inferior vena cava to the plexus, leading to engorgement of epidural veins. For example, in pregnant women, this increases the risk of accidental venous puncture during the conduct of epidural anaesthesia and decreases the effective epidural space volume, thereby requiring a smaller volume of local anaesthetic.
The Spinal Cord and the Spinal Canal
Published in Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand, Pediatric Regional Anesthesia, 2019
Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand
Spinal veins are arranged in a manner very similar to spinal and radicular arteries (Figure 1.52). Small peripheral branches from the posterior horns and posterior funiculi unite. Within the pia mater, they form three posterior (two posterolateral and one posteromedian) spinal veins that communicate with each other by coronal veins, thus contributing to the constitution of the epidural venous plexus (or internal vertebral venous plexus) between the dura mater and the ligamenta flava. These veins are drained by several posterior radicular veins and connect with the external vertebral venous plexus (Figure 1.53).
Association between subarachnoid hemorrhage-induced hydrocephalus and hydromyelia: pathophysiological changes developed in an experimental model
Published in Neurological Research, 2023
A ‘craniospinal pressure dissociation’ theory was postulated by Williams [6]. This theory posited that significant pressure changes during daily activities may increase the intrathoracic pressure, as reflected in the spinal CSF through the epidural spinal veins [6]. The CSF flow from the cranial to the SAS reflects expansile brain motion during the cardiac cycle, especially in the arterial pulse. A syrinx cavity is frequently accompanied by a myelomalacia area. The progression of a syrinx cavity transmits the pressure to the medulla spinalis surface. The syrinx does not require communication between the central channel and the ventricular system. The dorsal root entry zone and the perivascular spaces can influence the communication between the central channel and extracellular spaces of the medulla spinalis. This mechanism can play a primary role in compensating for the changes occurring in the perimedullary CSF flow. However, pathologies and iatrogenic conditions, such as spinal meningitis, SAH, peridural anesthesia, intramedullary spinal surgery, infarction, trauma, and spinal injuries, frequently cause arachnoid scarring that impaired this mechanism [24,25]. Both parenchymal (extracanalicular) syringes and paracentral dissections of central channel syringes are lined with glial or fibroglial tissues that are frequently ruptured into the SAS. The fibroglial tissue is characterized by Wallerian degeneration, neuronophagia, and central chromatolysis. The clinical presentation in patients varies depending on the affected tracts and nuclei with this cavity [2,24,25].
Resolution of isolated syringomyelia after removing thoracic disc herniation
Published in British Journal of Neurosurgery, 2020
Youssef El Ouadih, Guillaume Coll, Yakouba Haro, Remi Chaix
Despite the fact that many pathophysiology mechanisms have been suggested to explain syrinx formation, the exact one has not yet been clarified.13,14 One of these theories suggests that the origin of the positive pressure gradient between the spinal medulla and the subarachnoid spaces which surround it is due to the Venturi effect.15 The Venturi effect is the application of Bernoulli's law which governs the flow of a non-viscous, incompressible fluid (a laminar flow in a tube). The viscosity of the CSF is similar to water. Bernoulli’s theorem is based on the principle of conservation of the kinetic energy of a fluid. Thus, if the flow rate of the fluid is constant and the diameter decreases, the speed necessarily increases; because of the conservation of energy, the kinetic energy increase results in a decrease of elastic energy: (depression). This depression produces a suction effect creating a centrifugal positive transmedullary pressure gradient at the origin of the syrinx. The syrinx should not be considered as a simple dilation of the intramedullary canal that would fill the LCS. Disturbance of the intramedullary capillary exchanges (which must be considered as resorption zones of the LCS) secondary to the venous return alteration of the transmedullary pressure gradient that tends to collapse the spinal veins would lead to an accumulation of plasma ultrafiltrate. This accumulation of plasma ultrafiltrate combined with the suction effect is believed to be at the origin of the syringomyelic cavity.
Acute neuro-Behçet’s disease with longitudinal extensive transverse myelitis in a patient receiving long-term anti-TNF-α therapy
Published in Modern Rheumatology Case Reports, 2019
Jun Ishizaki, Takuya Matsumoto, Koichiro Suemori, Katsuto Takenaka, Hitoshi Hasegawa
Anti-TNF-α therapy is effective in NBD with or without myelitis [9–15]. In addition, anti-TNF-α therapy prevents acute NBD in small-scale studies [8,12]. However, in our patient, acute NBD with LETM occurred during the administration of IFX despite the inhibition of TNF-α activity without the development of anti-IFX neutralising antibodies. This indicates that the onset of acute NBD with LETM may be elicited through other mechanisms, except a mechanism mediated by TNF-α, and that anti-TNF-α therapy does not necessarily prevent the onset of NBD. From autopsy and biopsy studies, venous vasculitis has an important role in the pathophysiology of LETM in NBD [39,40]. The intrinsic venous system that interconnects with many vertical and transmedullary anastomotic channels exists in the spinal cord. Small veins connect to the anterior or posterior spinal veins that run longitudinally along the spinal cord surface. Therefore, small-vessel obstructions caused by vasculitis at multiple sites along the spinal veins may induce stagnation and oedema mainly in the central gray matter longitudinally. The onset of LETM in our case may be caused by this mechanism.