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Intrathecal Pressure After Spinal Cord Injury To the Editor: Martirosyan and colleagues1 provide evidence that cerebrospinal fluid drainage, combined with induced hypertension, improves spinal cord perfusion after acute spinal cord injury in pigs. We congratulate the authors for performing this work but urge caution in the interpretation of these data. Our data, obtained from patients with severe spinal cord injury, show that different compartments form after spinal cord injury: the intrathecal compartment above the injury, the intrathecal compartment at the site of injury where the spinal cord is compressed against the dura, the intrathecal compartment below the injury, and the extrathecal compartment (Figure).2 When the spinal cord is swollen and compressed against the dura, there is no communication between the intrathecal compartment above the injury and the intrathecal compartment below. We showed that each of these compartments has a different pressure profile, with the highest pressure in the intrathecal compartment at the site of injury when the patient lies horizontally. Therefore, drainage of cerebrospinal fluid from the intrathecal compartment below the injury will not decompress the cord at the injury site. Our recent clinical trial shows that laminectomy combined with expansion duroplasty is required to decompress the swollen spinal cord.3 Lumbar cerebrospinal fluid drainage after spinal cord injury, as used in the pig study by Martirosyan et al1 and the earlier clinical trial by Kwon et al,4 would

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reduce intrathecal pressure at the injury site only if the spinal cord is not compressed against the surrounding dura. Unfortunately, in most patients with severe spinal cord injury, the spinal cord is compressed against the surrounding dura; therefore, drainage of cerebrospinal fluid from the lumbar region will not reduce intrathecal pressure at the injury site.2 Disclosure The author has no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article.

Marios C. Papadopoulos, MD Department of Neurosurgery St. George's, University of London London, United Kingdom

REFERENCES 1. Martirosyan NL, Kalani MY, Bichard WD, et al. Cerebrospinal fluid drainage and induced hypertension improve spinal cord perfusion after acute spinal cord injury in pigs. Neurosurgery. 2015;76(4):461-468. 2. Werndle MC, Saadoun S, Phang I, et al. Monitoring of spinal cord perfusion pressure in acute spinal cord injury: initial findings of the injured spinal cord pressure evaluation study. Crit Care Med. 2014;42(3):646-655. 3. Phang I, Werndle MC, Saadoun S, et al. Expansion duroplasty improves intraspinal pressure, spinal cord perfusion pressure and vascular pressure reactivity index in patients with traumatic spinal cord injury: injured spinal cord pressure evaluation study. J Neurotrauma. 2015;32(12):865-874. 4. Kwon BK, Curt A, Belanger LM, et al. Intrathecal pressure monitoring and cerebrospinal fluid drainage in acute spinal cord injury: a prospective randomized trial. J Neurosurg Spine. 2009;10(3):181-193. 10.1227/NEU.0000000000000862

In Reply: Intrathecal Pressure After Spinal Cord Injury

FIGURE. The 4 compartments that form after spinal cord injury. 1, Intrathecal compartment above the injury; 2, extrathecal compartment; 3, intrathecal compartment at the injury site (spinal cord compressed against dura); 4, Intrathecal compartment below the injury site. CSF, cerebrospinal fluid.

E500 | VOLUME 77 | NUMBER 3 | SEPTEMBER 2015

We thank Dr Papadopoulos for his important comments regarding our article on the role of cerebrospinal fluid (CSF) dynamics after spinal cord injury. We agree that the results of translational studies should be carefully interpreted before they are implemented in clinical practice. Our experiments, which investigated the effects of CSF drainage and induced hypertension on spinal cord blood flow after moderate spinal cord injury, demonstrated significant improvement of spinal cord blood flow after combined CSF drainage and hypertensive treatment. As evidenced by our ability to continuously drain CSF from the intrathecal space below the site of the injury, we surmised that, contrary to Dr Papadopoulos’ suggestion, there was not a complete blockage of CSF drainage. We purposely chose a moderate injury model, because the disruptive effects on autoregulation are less than those in a severe model.1,2 Furthermore, in our human clinical observational experience,

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