Parenchymal Hypointense Foci Associated with Developmental Venous Anomalies: Evaluation by Phase-Sensitive MR Imaging at 3T

Discussion

Our results demonstrated that the prevalence of hypointense foci, indicating microhemorrhage or CM, was higher (62.3%) than previously reported. According to previous studies, CM occurs in up to 18% of patients with DVA,^7,9 whereas DVA is present in 8–33% of patients with CM.^5,8⇓–10 The discrepancy in the prevalence of hemorrhage and CM between this study and previous studies may be related to several factors. First, susceptibility-weighted MR imaging was used in the present study but not in prior studies. Susceptibility-weighted MR imaging is a high-resolution 3D gradient-echo MR imaging technique with phase postprocessing that accentuates the paramagnetic properties of blood products, such as deoxyhemoglobin, intracellular methemoglobin, and hemosiderin. As a result, it is quite sensitive to the presence of even small amounts of hemorrhage. Previous studies have reported susceptibility-weighted MR imaging is more sensitive in detecting CM than T2*, which in turn is much better than T1 or T2.^15,16 Susceptibility-weighted MR imaging has also been specifically recommended when imaging DVAs because of their association with CM.¹⁷ Second, 3T MR was used in the present study but not in prior studies, and the susceptibility effect in higher field strength increases the conspicuity of paramagnetic substances. Additionally, we could detect hypointense foci more frequently in the peripheral regions of medullary veins in comparison to a previous study that used T2-weighted imaging and T1-weighted spoiled gradient-recalled acquisition in steady state imaging with gadobutrol enhancement at 3T.¹³ This may result from the increased detectability of minute hemorrhage and CM in the peripheral region of medullary veins in response to the increased conspicuity of paramagnetic substances with PSI at 3T.

The incidence of WMH in the drainage territory of DVA in this study was >50%, whereas reported WMH rates on MR imaging were 12.5% and 28.3%.^7,11 Although we have no good explanation for this discrepancy, variations in the imaging parameters and the scanners themselves could produce different results. For example, we used a 3T MR system, whereas both previous studies were mainly investigated by 1.5T MR systems. Moreover, the discrepancy may be due to the differences in the populations and readers among these reports.

This study also demonstrated a significant relationship between hypointense foci and WMH, which may reflect leukoaraiosis that histopathologically includes edema, demyelination, and gliosis resulting from chronic venous hypertension caused by anomalous venous drainage. That supposition is based on several reports of stenosis of the draining vein, which leads to chronic venous congestion,^7,18,19 and on a report of reduced cerebral blood flow in the drainage territory of the DVA, which suggests the presence of altered hemodynamics.^20⇓–22 Alternatively, some case reports have described de novo formation of CM in the drainage territory of DVA.^23⇓–25 Although the exact events leading to de novo formation of CM in patients with DVA is unclear, some investigators have speculated that development of venous hypertension and resultant microhemorrhages from the fragile vessel wall of the DVA may induce reactive angiogenesis.^26,27 Relative ischemia can result in production of angiogenic factors and stimulation of growth of new vessels.²⁸ However, the neovasculature lacks vasoregulatory capacity, and its fragility makes it susceptible to bleeding. This leads to repeated hemorrhage and formation of abnormal vessels, which eventually results in CM formation.^13,29 Hong et al¹³ reported that the angioarchitectural factors of DVA cause disturbances in blood flow and may lead to CM within the territory of DVA by increasing venous pressure. Taken together, these data suggest that venous congestion caused by angioarchitectural or other factors leads to WMH and subsequent CM formation. Hence, these 2 phenomena are likely to occur simultaneously.

In the present study, there was no significant association between the presence of hypointense foci and the presence of clinical symptoms. However, CM is generally considered to be an active lesion characterized by dynamic behaviors, including enlargement, regression, and de novo formation. Furthermore, several studies have reported that clinical presentation of patients with both DVA and CM is nearly always related to CM, reflecting its potential for epileptogenesis and symptomatic hemorrhage.^5,9,29,30 Although no association was found between hypointensities and presence of clinical symptoms or indications, patients with hypointensities had higher rates of being symptomatic than those without (71% versus 52%) in the present study. This result shows a tendency that supports previous assumptions of CM being a dynamic lesion with the potential to cause bleeding and other symptoms. If analyzed with a larger population, there may be a significant association. Therefore, careful follow-up examination with the use of susceptibility-weighted MR imaging should be performed to assess whether there is a change in size of the hypointense foci, and further follow-up survey is needed to predict symptomatic ICH.

This study has several limitations. First, the study population was relatively small, and further studies in a large population are required to validate the present results. Second, hypointense foci may have represented dystrophic calcification or thrombosis rather than microhemorrhage and CM. However, only 1 among 14 patients with hypointense foci on PSI showed calcification on CT. Therefore, it is unlikely that calcification around the DVA plays a major role in the hypointensity on PSI, though minute calcification can coexist with hemorrhage.