TO THE EDITOR: We read with great interest the article by Lenga et al.1 (Lenga P, Hohaus C, Hong B, et al: Giant intracranial aneurysms of the posterior circulation and their relation to the brainstem: analysis of risk factors for neurological deficits. J Neurosurg 131:403–409, August 2019). In their study, the authors examined the risk factors for cranial nerve deficits, motor deficits, and disability in patients with giant intracranial aneurysms of the posterior circulation (GPCirAs). They found that higher degrees (incidence and magnitude) of neurological deficits and disability were significantly associated with aneurysm volume but not with brainstem displacement.
Although it appears logical that the extent of brainstem displacement will be correlated with the volume (diameter) of the aneurysm sac, the results in this study differ from this logic. We think that the method of measuring the brainstem displacement is inappropriate. In the article by Lenga et al., the basis of measuring brainstem displacement is analogous to that for measuring basilar invagination (BI).1 Brainstem displacement (ΔMT) is measured as the distance between the highest tip of the GPCirA and the McRae line, as is done in cases of BI. Applying this method of measurement to aneurysms is not justified. Aneurysms arising from posterior circulation will displace the brainstem away from the clivus, predominantly posteriorly, and the ideal method for measuring brainstem displacement may be the perpendicular distance from the Wackenheim clivus canal line.2 Vertebral artery (VA)–posterior inferior cerebellar artery aneurysms arising posterolaterally may displace the brainstem anteriorly or medially, and in these particular cases, axial T2-weighted MRI may be more accurate for assessing brainstem displacement in the respective directions.
An essential point to note here is that since the vertebrobasilar arterial system is ventral to the brainstem, it is expected to displace the brainstem away from the clivus (and not away from the foramen magnum, as assumed in the present article). Being a caudal structure, the odontoid tip is expected to displace the brainstem predominantly superiorly, with additional posterior displacement when associated with atlantoaxial dislocation. Thus, this methodology for measuring BI is inappropriate for measuring brainstem displacement, and it might have affected the results. Also, with the authors’ method a distal aneurysm will cause greater brainstem displacement; for example, an aneurysm of the basilar artery (BA)–superior cerebellar artery junction will produce greater brainstem displacement than a VA-BA junction aneurysm of same volume because the distance is measured with reference to the McRae line.
We think that, because of this inappropriate method of measurement, the authors could not find a correlation between GPCirA volume and the extent of brainstem displacement. And because of this fallacy, the authors reported that “the actual craniodorsal [italics added] displacement of the brainstem by the GPCirA and GPCirA volume seem to be 2 separate risk factors.” A modified and more logical method to measure brainstem displacement away from the clivus may find a correlation between aneurysm volume and brainstem displacement and also between brainstem displacement and neurological deficits/disability.
Disclosures
The authors report no conflicts of interest.
References
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Lenga P, Hohaus C, Hong B, Kursumovic A, Maldaner N, Burkhardt JK, : Giant intracranial aneurysms of the posterior circulation and their relation to the brainstem: analysis of risk factors for neurological deficits. J Neurosurg 131:403–409, 2019
