In Reply: Is the Optic Nerve Head Structure Impacted by a Diagnostic Lumbar Puncture in Humans?
We thank García-Montesinos and associates for their interest in our work1 and we appreciate their comments. The authors point out certain similarities between our recent work and their previous publication: in a prospective case series study including 12 eyes of 7 patients suffering from intracranial hypertension (ICH), they assessed morphologic changes in deep structures of optic nerve head (ONH) after reducing ICH and papillo-edema by mean of medical or surgical intervention.2 As expected, they reported a significant reduction of both retinal nerve fiber layer and prelaminar tissue thicknesses. Nevertheless, they did not find any significant change in Bruch membrane opening diameter, nor in anterior relative lamina cribrosa position: a nonsignificant posterior or anterior bowing of this structure being observed depending on the level of initial ICH.
First, García-Montesinos and associates remark that they did not find in our study any mention about cerebrospinal fluid pressure (CSFP), intraocular pressure (IOP) or translaminar pressure difference. We would point out that as mentioned in our study, for ethical reasons, we could not measure CSFP, bearing in mind that none of our patients were suffering from ICH. We reported, however, baseline IOP for each eye included in the study but did not repeat this measure after lumbar puncture (LP), assuming the fact that short-term fluctuations of IOP may not affect deep ONH position (the time duration of our study was about 360 min vs. 3.5 to 10.9 mo in Garcia-Montesinos’ one).
Secondly, the authors hypothesize from their study and our results that a LP in patients with papillo-edema could also significantly affect deep ONH structures. As both studies did not find any significant difference in lamina cribrosa position and Bruch membrane opening diameter after resolution of papillo-edema or LP and considering the point that none of our studies evaluated the effect of LP in patients suffering from papillo-edema, we could not address such a conclusion. Indeed, although Garcia-Montenisos and colleagues suspect “a linear relationship between the volume of CSF removed and the amount of CSF pressure relieved,” we would like to point out that this relationship, as well as the determination of translaminar pressure difference (defined in their study as “equal to IOP minus IC pressure”), is not as linear and simple in its determination. Indeed, Killer et al3 recently demonstrated that the subarachnoid space surrounding the ONH was divided into distinct compartments by anatomic arrangement related to trabeculae, septa and stout pillars made of cytoplasmic bridges arranged between the arachnoid and the meningeal pia layers. This optic nerve sheath compartment syndrome4 (or optic nerve chamber syndrome5) may offer the possibility that a 1-way valve mechanism explains local entrapment as well as reduced influx of CSF, buffering acute variations of spinal CSFP among deep ONH structures.
Third, Garcia-Montesinos and associates note that immediately after LP, patients were asked to stay in a supine position between optical coherence tomography scans, pointing out that CSFP as well as IOP levels differs between supine and sitting position. As optical coherence tomography and IOP measurements were only done in sitting position in our real life study, we believe that this transient supine position did not made any difference in IOP nor CSFP values once the sitting position restored, the only parameter impacting CSFP being then the natural restoration of CSF and/or the potential existence of a CSF leakage.
Finally, the aim of our study was to evaluate if diagnostic LP, one of the most commonly performed invasive tests with 280,000 procedures each year in France, was a safe procedure regarding deep ONH structures in normal patients, and we never aimed to extrapolate our results to patients with ICH.