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(Stroke. 2004;35:2753.)
© 2004 American Heart Association, Inc.
Letters to the Editor |
Department of Neurosurgery, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
To the Editor:
We read with great interest the article by van der Schaaf and colleagues1 in the July 2004 issue of Stroke in which the authors sought to assess the contribution of venous drainage patterns in the etiology of perimesencephalic hemorrhage (PMH). PMH, defined by a negative 4-vessel angiographic study as bleeding in the cisterns around the midbrain, is associated with an excellent outcome.2 Using computed tomography angiography, van der Schaaf and colleagues found that patients with PMH had primitive venous drainage directly into dural sinuses instead of via the vein of Galen, as with patients having aneurysmal subarachnoid hemorrhage. They also observed that the side of the PMH related to the side of the primitive drainage. They concluded that these results support the venous origin of PMH. Although van der Schaaf and colleagues found differences in the venous drainage of these patients, they neglected to present direct evidence showing that primitive venous drainage led to hemorrhage around the midbrain. They speculated that direct venous pressure from the dural sinus might cause the rupture of the perimesencephalic veins. However, their speculation is not substantiated because other cerebral veins with direct connection to the dural sinus never rupture under normal circumstances. Moreover, if this variation of venous drainage were a cause of bleeding, it would have a high chance of rebleeding in the follow-up because venous drainage is not easily changed.
We would like to bring to the authors attention our study of PMH3 in which small bulges on the basilar artery were found in 2 patients by 3D rotational angiography. These lesions were thought to be intramural hematomas due to arterial dissection and to be responsible for the hemorrhage in each case. This finding matches the distribution of the hematomas, and the spontaneous healing of the dissection could explain the absence of rebleeding. The small bulges showed spontaneous resolution, but they were too small to be detected by computed tomography angiography, such as that employed by van der Schaaf and colleagues. Therefore, we would like to emphasize that some of the PMH were of arterial origin. Nonetheless, the study by van der Schaaf and colleagues, which focuses on venous drainage, provides an important contribution to the literature. We congratulate the authors on their careful observations.
References
Department of Radiology, University Medical Center Utrecht, Utrecht, The Netherlands
Department of Neurology, University Medical Center Utrecht, Utrecht, The Netherlands
We appreciate the interest of Dr Matsumaru and colleagues in our article on the venous drainage patterns in the etiology of perimesencephalic hemorrhage (PMH).1
Dr Matsumaru focuses our attention on their observation in 2 patients with a perimesencephalic pattern of hemorrhage, who had small bulges on the basilar artery that disappeared on follow-up imaging. These bulges were supposed to be intramural hematomas due to arterial dissection, and were not visible on standard DSA but only on the 3-D angiography.2 The authors emphasized that some of the patients with a PMH might have had an arterial origin.
We are aware that in patients with a perimesencephalic pattern of hemorrhage, the cause is of arterial (vertebrobasilar) origin in 5% of the cases.3 We also agree that an abnormal venous drainage is not the definitive cause in all patients with a PMH. However in patients with a unilateral primitive variant, the blood was always found on the side of the primitive drainage, which suggests a relation between the primitive venous variant and the bleeding. Four patients in our series had a "normal" venous drainage system in both hemispheres. We cannot substantiate the suggestion that in these 4 patients the PMH was caused by bleeding from small intramural hematomas. None of these patients underwent DSA.4 Three of these 4 patients were scanned on a single-slice CTA scanner; the resolution of this scanner does allow the detection of such small bulges. The fourth patient, however, was scanned on a multislice CT scanner. Multislice (MS) CTA provides a high resolution and small vascular details can be detected.5 In this patient we reviewed the CTA using multiplanar reconstruction in 3 directions and maximum intensity projection, but we did not find any irregularity on the vessel wall of the basilar artery.
Dr Matsumaru and coauthors also mention that other cerebral veins with direct connection to the dural sinus never rupture under normal circumstances and therefore think that our speculation that direct venous pressure from the dural sinus might cause rupture of the perimesencephalic veins is not substantiated. The authors also point out that if this variation in venous drainage were a cause of bleeding, it would have a high chance of rebleeding because the venous system is not easily changed.
We would like to emphasize that primitive variants lack fusion of the 3 primitive veins during the embryologic development of the Galenic system.6 This deficiency of anastomosis might make these vessels more prone to rupture due to sudden increase in venous pressure. Even though other veins do connect directly to the dural sinuses, the perimesencephalic fine venous network is usually protected from sudden pressure changes by the drainage from the basal vein of Rosenthal through the Galenic system into the straight sinus. It is possible that a more direct connection to a dural sinus makes this network more vulnerable to pressure changes. Some of the primitive veins cross the tentorial margin, which might lead to torsion or friction and therefore make these primitive variants even more prone to rupture. We speculate that the spontaneous healing of the venous system by fibrous tissue firms the vessel wall of the vein on its weakest point, thereby preventing it from rerupture.
Arterial dissections are a frequent cause of the hemorrhage in patients with subarachnoid hemorrhage, but without an aneurysm on angiography.7 In most patients with subarachnoid hemorrhage from intracranial dissections, the pattern of hemorrhage is not confined to the perimesencephalic cisterns, but comparable to an aneurysmal pattern of hemorrhage7 Moreover, intracranial dissections leading to a subarachnoid hemorrhage have a 30% risk of rebleeding.8 These characteristics are unlike those from PMH, and we do not think that arterial dissections are a frequent cause of PMH. The relatively benign symptoms at onset, the clinical course without rebleeding or secondary ischemia, and the localized pattern of hemorrhage favor a venous source in the majority of these patients. The observation of Dr Matsumaru et al offers an interesting vision in the etiology of PMH, which may hold true for some patients with a perimesencephalic pattern of hemorrhage. The higher resolution of the MS CT scanners and 3D angiography will provide more insight on this finding in the future.
References
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