To the Editor:—
The paper by Angle et al. 1is a well-designed and carefully conducted study that clearly delineates the effect of epidural needle design and insertion technique on fluid leak through dural tissue after puncture in vitro . The goal of the study was to help define methods that might decrease the incidence of “spinal headache” when the meninges are accidentally punctured during attempted epidural anesthesia/analgesia. Clearly, this is a laudable goal.
The assumptions that underlie this study design are that persistent cerebrospinal fluid leak through a hole in the meninges is responsible for spinal headache and that the hole in the dura mater is responsible for the persistent cerebrospinal fluid leak. The first assumption is probably correct; however, to my knowledge there are no data to support the idea that the hole in the dura mater, as opposed to the arachnoid mater, is responsible for the persistent cerebrospinal fluid leak. After all, cerebrospinal fluid resides in the subarachnoid space, not the subdural space, and it is entirely possible that it is the nature of the hole in the arachnoid mater that determines whether patients develop spinal headache.
This is certainly not to suggest that the clinical studies demonstrating that parallel insertion of a beveled spinal needle reduces the risk of spinal headache are in error. Clearly, parallel insertion does result in a lower risk of spinal headache. However, the conventional wisdom that ascribes the reduced risk to the nature of the hole in the dura mater has no valid experimental basis. Specifically, because the current study by Angle et al. and similar studies by others failed to address the potential role of the arachnoid mater in persistent cerebrospinal fluid leak, their conclusions as to mechanism are of little or no value, and extrapolation of their findings to the clinical arena are not warranted.
It is hard to conceive of an in vitro study design that would produce a valid model of cerebrospinal fluid leak through the spinal meninges. A more appropriate model would be one in which the spinal meninges of an animal were punctured in vivo and the animals sacrificed at various time points thereafter to determine the nature of the hole in the dura and the arachnoid membranes. In this way, the healing process could be examined and the “rate-limiting” menix identified. In the absence of experimental data that clearly identify the dura mater as the menix responsible for persistent cerebrospinal fluid leak, studies like that of Angle et al. should not be considered to provide any insight into the mechanism responsible for spinal headache or the methods that can be used to prevent it.
University of Washington, Seattle, Washington. chrisb@u.washington.edu
