A Case of Convexity Meningioma Presenting With Acute Subdural Hematoma: A Case Report With a Pooled Analysis of 63 Reported Cases

Abstract

Meningioma-associated acute subdural hematoma (ASDH) is an exceedingly rare clinical entity, and its hemorrhagic mechanisms remain poorly understood. A 65-year-old man presented with progressive headache without a history of trauma. Neurological examination revealed no focal deficits. Computed tomography demonstrated a left convexity acute subdural hematoma, while magnetic resonance imaging revealed a small adjacent extra-axial lesion with mild contrast enhancement. Digital subtraction angiography showed only minimal tumor staining and no evidence of vascular malformation. The patient underwent gross total resection of the tumor and evacuation of the hematoma. Histopathological examination confirmed a meningothelial meningioma with focal disruption of intratumoral venous structures, intratumoral hemorrhage, necrosis, and focal areas of increased proliferative activity. The postoperative course was uneventful, and the patient recovered without neurological deficits. Previously reported cases are discussed to provide clinical context and highlight the diverse presentations and management strategies of this rare condition. Although rare, meningioma should be considered a potential source of non-traumatic ASDH. Because reliable preoperative predictors of hemorrhage have not been established, management should be individualized according to tumor-hematoma continuity, neurological status, surgical feasibility, and patient preferences.

Introduction

Acute subdural hematoma (ASDH) is a common traumatic intracranial hemorrhage, most frequently caused by rupture of bridging veins. Elderly patients with cerebral atrophy are particularly vulnerable to rotational forces resulting from minor falls or head trauma. ASDH can lead to life-threatening mass effect and often requires urgent surgical evacuation, sometimes combined with decompressive craniectomy. However, ASDH may also occur in the absence of trauma. Non-traumatic ASDH has been associated with ruptured intracranial aneurysms, coagulopathy related to antithrombotic therapy, and intracranial tumors [1-3]. Intratumoral hemorrhage is relatively common in malignant hypervascular tumors such as glioblastoma, metastatic brain tumors, and pituitary adenomas presenting with pituitary apoplexy. In contrast, meningioma-associated ASDH is exceedingly rare, with only a limited number of cases reported in the literature [4,5]. Several mechanisms have been proposed to explain hemorrhage in meningiomas, including rupture of fragile intratumoral vessels, disruption of adjacent bridging veins, and secondary venous congestion. However, the factors predisposing individual meningiomas to hemorrhage remain poorly understood [6,7]. Because of the rarity of this condition, we combined a detailed case report with a review of previously published cases to provide additional clinical context. We therefore report this rare case together with a pooled analysis of previously reported cases to summarize the currently available evidence and generate hypotheses regarding clinical presentation, hemorrhagic mechanisms, and prognostic factors.

Case presentation

A 65-year-old man presented with a four-day history of left occipital headache without any neurological deficits. The intensity of the headache was stable and described as a persistent pressure-like sensation. T2-weighted magnetic resonance imaging, computed tomography (CT), contrast-enhanced MRI, and CT angiography revealed a left-sided ASDH, a vertebral artery aneurysm, and a left convexity extra-axial mass located in the lower parietal region (Figure 1A-1D). The hematoma appeared contiguous with the tumor.

Figure 1. Radiological findings.

(A) Axial T2-weighted MRI demonstrates a small extra-axial mass at the left convexity (arrowhead).

(B) Non-contrast CT reveals an acute subdural hematoma over the left convexity (arrowhead), without evidence of skull fracture.

(C) Coronal contrast-enhanced MRI shows a dural-based lesion with mild enhancement (arrowhead), suggestive of meningioma, appearing contiguous with the subdural hematoma.

(D) Three-dimensional CT angiography demonstrates a coexisting vertebral artery aneurysm (arrowhead), without radiological continuity with the hematoma, suggesting that the aneurysm is unlikely to be the bleeding source.

The patient had a history of well-controlled hypertension treated with antihypertensive medications. He denied any history of recent trauma or falls within the preceding six months. Non-contrast CT demonstrated no skull fracture or subcutaneous hematoma (Figure 1B). CTA demonstrated a saccular vertebral artery aneurysm measuring 5 mm. No radiological continuity between the vertebral artery aneurysm and the subdural hematoma was observed on MRI or CT, suggesting that the aneurysm was unlikely to be the source of bleeding.

Based on the imaging findings and previous reports, the extra-axial tumor, presumed to be a meningioma, was considered the most likely source of the ASDH. Contrast-enhanced MRI demonstrated only mild tumor enhancement (Figure 1C). In addition, digital subtraction angiography in the anteroposterior and lateral views demonstrated only faint tumor staining, suggesting relatively low vascularity (Figure 2A-2B).

Figure 2. External carotid artery angiography.

(A) Lateral projection demonstrating minimal tumor blush in the convexity region (arrow).

(B) Posteroanterior projection showing faint and poorly defined tumor staining (arrow), indicating relatively low vascularity.

Although the tumor was relatively small (maximum diameter, approximately 15 × 13 mm) and did not exert a significant mass effect on the cerebral cortex, surgical resection was selected because imaging suggested continuity between the tumor and the hematoma, the coexistence of a vertebral artery aneurysm created diagnostic uncertainty, and a definitive histopathological diagnosis was considered important. After discussion of both conservative and surgical options, the patient elected surgical treatment. A left frontoparietal craniotomy was performed two days after diagnosis. Upon dural opening, an ASDH was encountered and carefully evacuated. No active bleeding was identified from cortical vessels.

The tumor was subsequently exposed and appeared firm and well demarcated from the surrounding brain. Careful inspection did not reveal a definitive bleeding source outside the tumor. Two potential bleeding sources were considered: the tumor itself and adjacent structures, including the dura or cortical surface, particularly given the presence of sulcal subarachnoid hemorrhage on preoperative imaging. However, no definitive extratumoral bleeding source was identified intraoperatively. Gross total resection was achieved without complications. The patient was discharged on postoperative day 8 and remained neurologically intact, corresponding to a favorable outcome.

Histopathologically, the tumor was diagnosed as meningothelial meningioma (Figure 3A). Focal necrosis and intra-peritumoral hemorrhage were observed (Figure 3B). Immunohistochemical staining demonstrated focal disruption of intratumoral venous structures (Figure 3C), and the proliferative activity was assessed by Ki-67 immunostaining (Figure 3D). Although focal hot-spot areas demonstrated a Ki-67 labeling index of up to 40%, no brain invasion, increased mitotic activity, or other CNS WHO 2021 grade 2 criteria were identified on pathological examination. Therefore, the tumor was classified as a meningothelial meningioma, CNS WHO grade 1. These findings suggested that both intratumoral and peritumoral hemorrhage may have contributed to the formation of the subdural hematoma.

Figure 3. Histopathological findings.

(A) Hematoxylin and eosin (H&E) staining shows a densely cellular tumor composed of polygonal meningothelial cells arranged in whorls and fascicular patterns, consistent with meningothelial meningioma.

(B) Areas of intratumoral hemorrhage (arrowhead) and necrosis (arrow) are observed.

(C) Immunohistochemical staining for CD34 demonstrates disrupted vascular architecture with focal vascular wall rupture (arrow).

(D) Ki-67 immunostaining demonstrates a focal hot spot (arrow) with a proliferative index of up to 40%. Despite this focal finding, no brain invasion, increased mitotic activity, or other CNS WHO 2021 grade 2 criteria were identified.

Scale bars = 1 mm.

Discussion

We report a rare but clinically meaningful case of a benign intracranial tumor-meningioma presenting with ASDH. In our institution, this represents the only case of meningioma-associated ASDH over the past 10 years, underscoring its extreme rarity. This case provides three important clinical insights. First, clinicians should consider meningioma as a potential source of non-traumatic ASDH. Second, even relatively small and radiologically hypovascular meningiomas, such as in our case, may induce symptomatic intracranial hemorrhage, suggesting that current surgical indications based primarily on tumor size or apparent vascularity may not fully capture rare hemorrhagic presentations. Third, an isolated headache in the absence of trauma does not exclude tumor-related ASDH.

Overview of previously reported cases

To provide clinical context for this rare presentation, we performed a literature review of previously reported cases of meningioma-associated ASDH. PubMed was searched on January 12, 2026, using the search term "meningioma associated with acute subdural hematoma." Only English-language articles were included. Reference lists of eligible articles were manually screened to identify additional reports. Only cases with histologically confirmed meningioma and sufficient clinical information regarding presentation, treatment, and outcome were included in the pooled analysis. The study selection process is summarized in Figure 4. Because the available evidence consisted exclusively of published case reports and small case series, the present pooled analysis should be regarded as an exploratory synthesis intended to summarize currently available evidence and generate hypotheses rather than establish definitive prognostic factors. The heterogeneous nature of the included reports should be considered when interpreting the findings. Furthermore, publication bias and selective reporting are unavoidable because unusual or clinically severe presentations are more likely to be published than uneventful cases.

Figure 4. Flow diagram of the literature review and case selection process.

Records were identified through a PubMed search using the search term "meningioma associated with acute subdural hematoma" and by manual screening of reference lists. After exclusion of articles without individual patient data, insufficient clinical information, or unrelated content, eligible reports with histologically confirmed meningioma-associated acute subdural hematoma were included in the pooled analysis.

Compared with previously reported cases, our case has several notable features, particularly the relatively small tumor size and scarce radiological vascularity. Among the 63 cases, the median age was 62 years (IQR, 50-68), with a female predominance (39/63, 61.9%). Headache was the most frequent presenting symptom (17/63, 27.0%), followed by severe disturbance of consciousness (14/63, 22.2%). Tumor size varied widely, ranging from 8 mm to 7 cm. Overall prognosis was favorable in 46 of 56 patients with available outcome data (82.1%), whereas 10 of 56 patients (17.9%) experienced severe disability or death. Although outcomes appeared better than those observed in trauma-related ASDH [8,9], they were less favorable compared with the overall prognosis of meningiomas [8].

The reported hemorrhage rate in malignant intracranial tumors ranges from 5.1% to 14.6% [10,11]. Rapid tumor proliferation, formation of structurally abnormal, fragile vessels, and secondary tumor necrosis have been proposed as mechanisms of hemorrhage in malignant gliomas and metastatic tumors [11,12]. In contrast, hemorrhage associated with meningioma is relatively uncommon. Several hypothetical mechanisms have been proposed to explain bleeding in meningioma-associated ASDH: (1) disruption of fragile intratumoral vessels resulting in subdural extension of hemorrhage [7,13]; (2) rupture of adjacent bridging veins or fragile neovascular structures surrounding the tumor, including feeding vessels [6,13]; (3) secondary hemodynamic alterations due to tumor invasion or compression, leading to venous congestion and subsequent hemorrhagic infarction [14,15]; and (4) systemic influences such as hypertension or antithrombotic medications [16,17]. Overall, the available evidence suggests that the mechanism of hemorrhage is likely multifactorial. In our case, the patient had no history of trauma and was not receiving antithrombotic therapy.

Histopathological examination demonstrated focal laceration of intratumoral vessels. In addition, areas of tumor necrosis were identified. Although the overall proliferative activity was not remarkable, focal hot-spot regions demonstrated a Ki-67 labeling index of up to 40%, suggesting localized proliferative activity. Such focal biological aggressiveness may contribute to vascular fragility through progressive necrosis and structural vessel compromise.

However, alternative bleeding mechanisms cannot be completely excluded. Sulcal subarachnoid hemorrhage was present on preoperative imaging, and rupture of adjacent cortical vessels, bridging veins, or other extratumoral vascular structures may also have contributed to hematoma formation. Although no definitive extratumoral bleeding source was identified intraoperatively, the precise origin of hemorrhage remains uncertain.

While the precise mechanism of hemorrhage remains incompletely understood, the identification of preoperative risk factors for hemorrhage may have greater clinical relevance than determining a single underlying mechanism. Such risk factors could potentially be incorporated into individualized management strategies. However, because the proposed mechanisms are derived primarily from isolated case reports and pathological observations, the relative contribution of each mechanism remains uncertain. Future studies incorporating standardized pathological evaluation and molecular characterization may further clarify the biological basis of hemorrhage in meningiomas.

Our case was classified as the meningothelial subtype, which represents the most common histological variant of meningioma. Among the previously reported cases of meningioma-associated ASDH, the meningothelial subtype has likewise been the most frequently observed. Prior literature examining the distribution of histological subtypes demonstrated no significant difference in the proportion of meningothelial meningiomas between hemorrhagic and non-hemorrhagic cases. In contrast, angiomatous meningioma has been reported more frequently among ASDH-associated cases compared with non-hemorrhagic cohorts, suggesting that high vascularity may increase the risk of hemorrhage [4]. However, from a clinical standpoint, the histological subtype cannot be reliably determined preoperatively and therefore cannot serve as a practical determinant for surgical decision-making in asymptomatic meningiomas.

Notably, in our case, angiography and contrast-enhanced MRI did not demonstrate marked hypervascularity, such as strong gadolinium enhancement or prominent tumor staining. This observation suggests that even meningiomas without apparent radiological hypervascular features may give rise to ASDH. Interestingly, despite the limited radiological evidence of tumor vascularity, the histopathological examination demonstrated intratumoral hemorrhage, focal vascular disruption, and necrosis.

Several explanations may account for this apparent radiology-pathology discrepancy. Angiography primarily visualizes larger feeding vessels and may not detect fragile microvascular abnormalities within the tumor. In addition, vascular injury may have occurred intermittently before imaging acquisition and therefore may not have been evident at the time of angiography. Venous congestion or rupture of fragile intratumoral microvessels may also contribute to hemorrhage without producing marked angiographic hypervascularity. Another important consideration concerns surgical strategy, namely whether staged surgery or one-step tumor removal with hematoma evacuation is better. In previously reported cases, clinical deterioration due to hematoma expansion was documented in only five patients. Nevertheless, when technically feasible, simultaneous evacuation of the hematoma and tumor resection may reduce the risk of rebleeding or hematoma progression, as suggested in prior reports [7]. However, approximately one-third of meningiomas associated with ASDH have been located at the skull base (Table 1).

Lesions in cranial base regions such as the posterior fossa or sphenoid ridge often require advanced microsurgical techniques and, in some cases, intraoperative neurophysiological monitoring to preserve critical neurological structures [18]. Therefore, a one-stage procedure may represent a technically demanding operation compared with isolated hematoma evacuation.

Although both the hematoma and tumor were relatively small and could potentially have been managed conservatively, several factors supported surgical intervention in the present case. First, imaging consistently demonstrated anatomical continuity between the extra-axial tumor and the ASDH, raising suspicion that the lesion represented the bleeding source. Second, the coexistence of a vertebral artery aneurysm created diagnostic uncertainty that could not be completely resolved without histological confirmation. The aneurysm measured 5 mm and showed no radiological continuity with the hematoma on CT angiography or MRI. Therefore, it was considered unlikely to represent the source of hemorrhage. Following treatment of the meningioma-associated ASDH, conservative management with periodic radiological surveillance was selected for the aneurysm. Third, previous reports have described neurological deterioration associated with tumor-related ASDH, further supporting definitive surgical management when the tumor is considered the bleeding source [6,7]. Finally, after discussion of conservative and surgical options, the patient elected definitive surgical treatment. 

Importantly, the management strategy adopted in the present case should not be interpreted as supporting routine surgical resection of all small asymptomatic convexity meningiomas. Treatment decisions should continue to be individualized according to current guideline recommendations, imaging findings, clinical presentation, and patient preference. Accordingly, hemorrhagic risk alone should not be considered an indication for prophylactic surgery in otherwise asymptomatic patients.

An additional consideration is the current surgical indication for small, asymptomatic meningiomas, particularly those located at the convexity. According to the European Association of Neuro-Oncology (EANO) guidelines, gross total resection is recommended for symptomatic or progressively enlarging meningiomas, whereas a watch-and-wait strategy is considered appropriate for small, asymptomatic tumors [19]. Thus, routine surgical resection of all small, radiographically stable meningiomas would likely constitute overtreatment. However, clinicians should inform patients that, although rare, tumor-related intracranial hemorrhage remains a potential complication. Optimization of modifiable systemic risk factors should also be considered. Although systemic hypertension and antithrombotic therapy have not been definitively established as independent risk factors for hemorrhage in meningioma, several studies have demonstrated an increased risk of intracranial hemorrhage in patients with malignant brain tumors receiving anticoagulation [20,21]. If the mechanisms of bleeding in meningioma share similarities with those in malignant tumors, antithrombotic therapy could plausibly contribute to hemorrhagic risk in selected patients. 

We analyzed available reported cases identified through our literature review. Patients were categorized into a favorable outcome group (good recovery or mild disability) and an unfavorable outcome group (severe disability or death). Statistical analyses were performed using R software (R Foundation for Statistical Computing, Vienna, Austria). Given the heterogeneity of the included reports, differences in outcome definitions, and incomplete reporting of several clinical variables, all statistical analyses were considered exploratory. Accordingly, the objective of the pooled analysis was to identify potential prognostic signals rather than establish causal or definitive predictors.

Given the substantial heterogeneity across reports, the statistical findings should be interpreted as descriptive and exploratory rather than confirmatory. Continuous variables were compared using the t-test, and categorical variables were analyzed using Fisher’s exact test. In univariate analyses, advanced age and severe disturbance of consciousness were significantly associated with poor outcome, whereas gender, tumor size, tumor location, and histological subtype were not. Because only 10 unfavorable outcome events were identified, the number of covariates included in the multivariate logistic regression model was restricted to two in order to minimize the risk of model overfitting.

Variables that were statistically significant in univariate analyses (age ≥70 years and severe disturbance of consciousness) were therefore included in the final multivariate model. Multivariate analysis demonstrated that age ≥70 years (OR 8.36, 95% CI 1.86-37.3, p=0.02) and severe disturbance of consciousness (OR 7.13, 95% CI 1.62-31.2, p=0.006) were significantly associated with an unfavorable outcome. Posterior fossa location showed a suggestive association but did not reach statistical significance (OR 19.3, 95% CI 1.77-211, p=0.08). The particularly wide confidence interval reflects the small number of posterior fossa cases and should not be interpreted as evidence of a large effect size.

Limitations

This study has several limitations. First, it is based on a single case together with a pooled analysis of previously published case reports and small case series, limiting generalizability and introducing potential publication and selection biases. Second, the literature search was performed using a single electronic database without a pre-registered review protocol. Third, clinical variables and outcome definitions were not uniformly reported across studies, resulting in missing data and potential misclassification. Finally, because only 10 unfavorable outcome events were available, the multivariable analysis was exploratory and may have been statistically unstable despite restricting the number of covariates. The wide confidence intervals further reflect the limited sample size. Therefore, the identified associations should be regarded as hypothesis-generating rather than definitive. Larger, systematically collected multicenter datasets are required to validate these findings and better define hemorrhagic risk factors in meningioma.

Conclusions

In summary, reliable clinical or radiological markers for predicting meningioma-associated ASDH have not yet been established. Although histopathological findings in the present case suggest possible mechanisms of hemorrhage, the precise bleeding source remains uncertain and is likely multifactorial. Despite its rarity, meningioma should be recognized as a potential cause of non-traumatic ASDH. Clinical decision-making should remain individualized.