In 1969, Newton classified cerebral arteriovenous malformation (CAVM) into pure pial, mixed dural-pial and pure dural types, and analyzed 20 mixed dural-pial arteriovenous malformation (DPAVM) patients. DPAVM frequently received a portion of blood supply from dural meningeal arteries. The dural contribution may arise from meningeal branch of the internal carotid, the external carotid and the vertebral arteries [1]. Pial CAVMs were generally thought to be congenital, whereas dural CAVMs were acquired. Acquired dural CAVMs were well known to develop secondary to sinus thrombosis or trauma [1–4].

The treatment of CAVMs is based on an objective comparison of natural risks with operative treatment risks. DPAVMs are usually large in size and complicated [5]. The treatment of DPAVMs usually requires a combination of three therapeutic modalities, including endovascular therapy, microsurgery and stereotactic radiosurgery. The cure rate is extremely low, and morbidity and mortality is high [6, 7]. Moreover, ARUBA showed that medical management is superior to medical management with interventional therapy for the prevention of death or stroke in patients with unruptured CAVMs [8]. On conditions that complete obliteration or resection is less feasible and that symptoms confuse patients persistently, how to alleviate or eliminate symptoms such as epilepsy, headache and focal neurological dysfunction (FND) seems important for unruptured DPAVM patients. Both dural and pial branches have blood supply to the nidus in DPAVM, whether the occlusion of dural or pial artery branch is more efficient for symptom alleviation is not well known.

In this retrospective study, we compared the symptom alleviation rate of DPAVM patients presented with epilepsy, headache or FND, to examine whether dural or pial blood supply artery branch occlusion is more efficient for symptom alleviation.

In this retrospective study, we discovered that symptom alleviation rate is higher in patients who were embolized via dural branches or both dural and pial branches than patients who were embolized via pial branches. The potential reason may be that the stimulations, which are caused by pulsatile dural feeding artery, exerted on dura and cortex are relieved. The result of our cohort could remind us that dural blood supply artery approach may have advantage over pial blood supply artery approach in symptom alleviation of unruptured DPAVM patients presented with epilepsy, headache or FND.

The incidence of CAVM is around 1.1–1.3/100,000 [11, 12]. Participation of dural meningeal branches in the supply of CAVM is relatively uncommon. In 1958, Krayenbuhl and Yasargil [13] noted dural contribution in 1 of 90 patients with CAVM. Newton analyzed 129 CAVMs and 20 were DPAVMs [1]. The incidence rate of DPAVMs in the current study is 7.1%. The pathogenesis of mixed DPAVM is still controversial. The presence of abnormal communications between the pial and dural arteries in the embryonic stage may lead to the development of mixed DPAVM [6]. Venous hypertension secondary to sinus thrombosis is believed to be the primary mechanism responsible for the formation of DPAVM. Lawton speculated that increased cortical venous pressure might decrease cerebral perfusion and increase ischemia, and that dural CAVM formation might be the result of aberrant angiogenesis [14]. Large CAVMs are more likely to develop into DPAVMs. This may because large nidus contains more concealed abnormal communications between the pial and dural arteries, which would undoubtedly provide more chances for the formation of dural-pial CAVM when venous hypertension happens [5]. More than 50.0% of the nidus in this study are >6 cm and 93.3% are >3 cm, which is consistent with previous studies.

Clinical presentations of CAVMs are ICH, epilepsy, headache and FND. The most common presentation is ICH and seizure is the second most common symptom [15]. Tong et al. reported an analysis of 3299 CAVM patients in china, among which 57.9% presented with hemorrhage, 20.9% with epilepsy and 14.9% with chronic headache [16]. In this study, the percentage of hemorrhage presentation (30.0%) is lower and epilepsy presentation (36.7%) is higher. Deep and infratentorial location is indication of CAVM hemorrhage [17, 18]. The percentage of deep and infratentorial location DPCAM in this cohort is small, so it is logically feasible that the percentage of hemorrhage presentation is small. It seems that DPAVM patients are more inclined to present with epilepsy. This may because DPAVM group has higher percentage of cortical located nidus. Nidus that are more adjacent to cortical may stimulate pial mater and cerebral cortex, which will cause abnormal discharge. Moreover, pulsatile veins and obstruction of venous efflux caused by venous hypertension may increase the incidence of seizures [19].

This is a retrospective study. The generalizability of our results is limited by the small sample size. There are only a few cases in each category based on various occlusion arteries. We could only describe with frequencies and our conclusion still needs a large prospective study to confirm.

For DPAVM patients presented with epilepsy, headache and FND, embolization via dural blood supply branches may be more efficient for symptom alleviation. Large cohort study is needed to confirm the generalizability.