Brady Huang, MD and Per-Lennart Westesson, MD, PhD, DDS
Clinical
Presentation:
An 36-year-old male with a sudden onset of headache during a weight lifting exercise. A CT and CT angiogram of the head were performed for clinical suspicion of subarachnoid hemorrhage.
Radiological Findings:
Figures 1 & 2: Two selected axial images from a non-contrast enhanced CT scan at the level of the midbrain and suprasellar cistern demonstrate an area of increased attenuation (white arrows) within the interpeduncular cistern, consistent with subarachnoid blood in this region. No blood is seen in the suprasellar cistern or sylvian fissures. A subsequent CT angiogram (CTA) was negative for an aneurysm.
Discussion: The incidence of subarachnoid hemorrhage (SAH) is about 6/100,000 patient years, with a case fatality rate of ~50%. Patients present with a sudden-onset, explosive headache, however only half describe an instantaneous onset, the other half describing an onset in seconds to even a few minutes. In addition, when explosive headache is the only symptom, the chance of SAH as the cause is only 10%. The cause of SAH is due to a ruptured aneurysm in 85% of cases, nonaneurysmal perimesencephalic hemorrhage (PMH) in 10%, and rare conditions in the remaining 5% [1].
PMH is most likely due to rupture of pontomesencephalic veins (PMVs). PMH was first described by van Gijn et al. in 1985, and is characterized by the accumulation of subarachnoid blood around the midbrain in the absence of an aneurysm or other bleeding source on angiography [2]. The typical distribution of bleeding is anterior to the brainstem, with extension to the basal parts of the sylvian fissures, but rarely completely filling the lateral sylvian or anterior interhemispheric fissures, as can be seen in aneurysmal SAH [3]. There is no further treatment once a posterior circulation aneurysm is excluded. Patients have an eventful clinical course, and generally a good outcome [4].
The PMVs are comprised of the pontine veins, the interpeduncular veins, and lateral mesencephalic veins. In order to investigate the frequency and anatomy of PMVs, Teksam et al. retrospectively reviewed 211 CTAs performed in 211 consecutive patients [5]. PMVs were visualized in 11 (5.2%) patients. In addition, a false positive non-enhanced CT (NECT) for SAH was found in a patient with a nonaneurysmal perimesencephalic pattern due to a large anterior PMV in the interpeduncular cistern. However, in patients with a perimesencephalic pattern of hemorrhage, the cause is of arterial origin in 5% of cases [3].
If a SAH is seen on NECT, CTA is generally the next exam of choice, having replaced catheter-directed digital subtraction angiography (DSA) given its time constraints and risks. However, there has been debate whether or not to proceed with DSA after a negative CTA in patients with a perimesencephalic pattern of hemorrhage, which has been recently explored. Velthuis et al. examined 48 patients with SAH, and observers agreed in 38 (95%) in differentiating between perimesencephalic and nonperimesencephalic patterns of hemorrhage on NECT. No patients with a perimesencephalic pattern of hemorrhage were found to have an aneurysm on CTA or DSA [6]. Ruigrok et al. performed a comprehensive decision analysis determining the method of choice for excluding a vertebrobasilar aneurysm in patients with a perimesencephalic pattern of hemorrhage, using a 4% prevalence of a vertebrobasilar aneurysm in a perimesencephalic pattern, a 97% sensitivity and specificity of CTA, and a 99.5% sensitivity and 100% specificity of DSA. Four different diagnostic strategies were explored including no further investigation, DSA alone, CTA without subsequent DSA if negative, and CTA followed by DSA. Expected utilities were calculated and were 99.09 for CTA only, 98.6 for no further investigation, 98.22 for DSA, and 96.34 for CTA and DSA. DSA was preferred strategy only if the complication rate was <0.2%. These findings suggest that CTA alone may be an adequate diagnostic strategy [7].
References:
van Gijn J, Rinkel GJ. Subarachnoid haemorrhage: diagnosis, causes and management. Brain. 2001 Feb;124(Pt 2):249-78. [Medline]
van Gijn, J, van Dongen KJ, Vermeulen M, Hijdra A. Perimesencephalic hemorrhage: a nonaneurysmal and benign form of subarachnoid hemorrhage. Neurology. 1985 Apr;35(4):493-7. [Medline]
Rinkel GJ, Wijdicks EF, Vermeulen M, Ramos LM, Tanghe HL, Hasan D, Meiners LC, van Gijn J. Nonaneurysmal perimesencephalic subarachnoid hemorrhage: CT and MR patterns that differ from aneurysmal rupture. AJNR Am J Neuroradiol. 1991 Sep-Oct;12(5):829-34. [Medline]
Rinkel GJ, Wijdicks EF, Hasan D, Kienstra G, Hageman L, Franke C, Vermeulen M, van Gijn J. Outcome in patients with subarachnoid haemorrhage and negative angiography according to pattern of haemorrhage on computed tomography. Lancet. 1991 Oct 19;338(8773):964-8. [Medline]
Teksam M, Casey S, McKinney A, Michel E, Truwit CL. Anatomy and frequency of large pontomesencephalic veins on 3D CT angiograms of the circle of Willis. AJNR Am J Neuroradiol. 2003 Sep;24(8):1598-601. [Medline]
Velthuis BK, Rinkel GJ, Ramos LMP, Witkamp TD, van Leeuwen MS. Perimesencephalic hemorrhage. Exclusion of vertebrobasilar aneurysms with CT angiography. Stroke. 1999 May;30(5):1103-9. [Medline]
Ruigrok YM, Rinkel GJ, Buskens E, Velthuis BK, van Gijn J. Perimesencephalic hemorrhage and CT angiography: A decision analysis. Stroke. 2000 Dec;31(12):2976-83. [Medline]
Osborn AG, Blaser S, Salzman K. Diagnostic Imaging: Brain. W.B. Saunders Company 2004; i:3:6-7
