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*Corresponding author: Mohamed Aziz. Copyright © 2025 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution License 4.0. Angiomatous meningioma: Case report of a rare tumor and a brief review of the literature Amanda Canellas 3, Lady Gonzalez Perez 3, Melissa Perez 3, Thomas Saliba 2, Shabnam Yazdanpanah 2, Alireza Izadian Bidgoli 2, Javier Aleman 4, Jessica Jahoda 1, 5 and Mohamed Aziz 1, * 1 Research Writing and Publication (RWP), LLC, NY, USA. 2 American University of the Caribbean School of Medicine, Sint Maarten. 3 St. George's University School of Medicine, Grenada. 4 Universidad Iberoamericana (UNIBE), Santo Domingo, Dominican Republic. 5 Memorial Healthcare System, Pembroke Pines, FL, USA. World Journal of Biology Pharmacy and Health Sciences, 2025, 24(02), 108-117 Publication history: Received on 27 September 2025; revised on 02 November 2025; accepted on 05 November 2025 Article DOI: https://doi.org/10.30574/wjbphs.2025.24.2.0986 Abstract Angiomatous meningioma (AM), a rare World Health Organization (WHO) Grade I subtype of meningioma, which presents special diagnostic and therapeutic challenges. Our patient is a 56-year-old male with a history of cranial radiation therapy 15 years ago, who was presenting with progressive neurological symptoms, including severe headaches, generalized tonic-clonic seizures, personality change, and left homonymous hemianopia. The imaging studies revealed a large (5.2 x 4.8 x 4.1cm) heterogeneously enhancing, highly vascular mass in the right parietooccipital area with severe peritumoral edema and mass effect. The complexity of the diagnosis was due to the high vascularity and dural location, as well as the patient's history The multidisciplinary tumor board discussion recommended surgical resection. During surgery, the tumor was markedly vascular (more than 60% of mass volume) and required extreme attention to hemostasis when performing a Simpson Grade II resection. Pathology showed a WHO Grade I AM with numerous local vascular spaces, meningothelial cells, hyalinized perivascular sclerosis, and atrophic nuclear atypia. EMA, CD31, CD34, progesterone receptor, and SSTR2A were positive; EMA and Ki-67 were low, and molecular analysis revealed monosomy 22. Even after reexploration due to postoperative hemorrhage, the patient had full neurological recovery. Postoperative seizure risk continued to be controlled at four-year follow-up. This case highlights the diagnostic complexity and rarity of AMs, especially in patients with prior radiation treatment, and demonstrates how good prognoses can be achieved with extensive, specialized treatment despite initial complications. Keywords: Angiomatous meningioma; Vascular; Radiation-Induced Meningiomas; MR Spectroscopy; Simpson Grade I resection. 1. Introduction Meningioma is a tumor that arises from the meningeal membranes covering the brain and spinal cord. Although meningioma is not a tumor of the brain parenchyma, it may cause neurological impairment by exerting mass effect on surrounding brain tissue, cranial nerves, and vessels. It is the most common primary tumor of the brain. Most meningiomas have a slow growth pattern and are often asymptomatic, as they may mature over a long period. Nonetheless, the resultant mass effect can cause serious neurological morbidity depending on their size and the location of their anatomical position. [1]
World Journal of Biology Pharmacy and Health Sciences, 2025, 24(02), 108-117 109 Like other morphologically different forms of meningiomas, the AM subtype characterizes a morphologic variant in which there is a vivid proliferation of vascular channels that may take up more than half of the tumor mass and may result in severe peritumoral edema and massive surgeries because of the threat of severe bleeding. [2] Although they are usually benign, their various histological subtypes may pose a lot of diagnostic and management challenges. AM is one of these very rare variants comprising only 2-2.5% of all meningiomas. [3] [4] Earlier, AM was considered a separate entity due to its abundant vascularity forming a network embedded in meningothelial cells. This prominent feature made it difficult to differentiate from other vascular neoplasias of the central nervous system. [5] However, over time and as molecular profiling and IHC have advanced, the classification and biological behavior were clarified, and it is currently classified as a WHO grade I meningioma subtype in the most recent 2021 WHO Classification of Tumors of the Central Nervous System. [6] AM has unique radiological and pathological features, often posing a diagnostic dilemma and requiring a comprehensive diagnostic approach that includes advanced imaging, histopathological studies, immunohistochemical (IHC) analyses, and molecular studies. [7] [8] Moreover, prior cranial radiation therapy history, as in the case of our patient, is also a known risk factor for the development of meningioma, which further complicates the management of the patient and long-term monitoring. [8] Due to their rarity, AMs remain underrepresented in the literature. Most of our knowledge has been derived from retrospective series or individual case reports. This case report aims to highlight the clinical, radiological, and pathological peculiarities of AM, underscore the diagnostic complexities, and discuss treatment options for this rare meningioma, thereby expanding knowledge of this tumor. 2. Case presentation 2.1. Clinical presentation A 56-year-old man was referred to the neurology department by his primary physician because of the progressive and gradual onset of neurological symptoms. The patient started experiencing mild and intermittent headaches, which occurred in the frontal region and became severe and persistent after 18 months. In the last 6 months, he experienced three generalized tonic-clonic seizures, and that is the reason why he was referred to the neurologist. Gradual personality changes were noted by family members, including irritability, social withdrawal, and an inability to function effectively. Occasional visual symptoms were progressive, including left homonymous hemianopia and diplopia. His wife said that he had undergone previous cranial radiation therapy 15 years ago to treat a pituitary adenoma. No family history of CNS tumors or genetic syndromes were reported. Medical history included pituitary adenoma status post transsphenoidal resection and adjuvant radiation therapy, controlled hypertension, and type 2 diabetes mellitus. 2.2. Physical examination Neurologically, the patient presented with left homonymous hemianopia (confirmed by confrontational testing of the visual field) and mild right hemiparesis (4+/5 strength), as well as slight impairment in cognitive ability, as indicated by a Montreal Cognitive Assessment (MoCA) score of 24/30. There was bilateral papilledema. No other focal neurological impairments were detected. The initial lab tests included a complete blood count, an extensive metabolic panel, coagulation studies, and tumor markers (CEA, PSA), all of which were within the normal range. The level of antiepileptic drug was therapeutic after the initiation of seizure control by levetiracetam. 2.3. Imaging findings The CT head scan showed a heterogeneously enhancing, large mass in the right parieto-occipital area, measuring 5.2 x 4.8 x 4.1cm, with severe surrounding vasogenic edema and a mild mass effect, resulting in an 8 mm midline shift. The MRI Brain Scan with Ggadolinium of the lesion exhibited a signal of isointensity on the T1-weighted images and heterogeneous hyperintensity on the T2/FLAIR images. Subsequent contrast imaging revealed intense, heterogeneous enhancement, along with multiple prominent feeding vessels and draining veins. There was thickening and increased enhancement of the dura mater in a linear fashion, tapering away from a lesion (dural tail sign). Massive perilesional edema was spread into the white matter. CT angiography revealed that the vascular supply originated from branches of the middle meningeal artery and the superficial temporal artery, and the early venous drainage suggested high-flow features. The MR Spectroscopy showed a high choline (Cho) peak and a low N-acetylaspartate (NAA) peak, indicating a neoplastic process. 2.4. Differential diagnosis and multidisciplinary tumor board discussion The main clinical/radiological considerations included angiomatous meningioma (WHO Grade I), hemangiopericytoma/solitary fibrous tumor, metastatic disease, high-grade glioma with prominent vascularity,
World Journal of Biology Pharmacy and Health Sciences, 2025, 24(02), 108-117 110 arteriovenous malformation with mass formation, atypical meningioma with prominent vascularity, and primary CNS lymphoma. The dural-based location with a dural tail sign, high-intensity enhancement, and high vascularity supported the diagnosis of angiomatous meningioma as the leading differential diagnosis. The case was discussed in the neurooncology tumor board, which included representatives from neurosurgery, neuro-oncology, radiation oncology, and neuropathology. Due to the symptomatic presentation of the patient, mass effect, and tumor size, surgery was recommended as the initial treatment. The observed high vascularity on imaging raised the debate over whether to use preoperative embolization or direct surgical intervention, with a focus on meticulous hemostasis. 2.5. Surgical excision A right parieto-occipital craniotomy was done using frameless stereotactic navigation. The tumor's intraoperative appearance showed very high vascularity (it was estimated at more than 60% of the mass volume), necessitating the use of multiple bipolar coagulation tools and hemostatic agents. Ultrasonic aspiration was employed to debulk the tumor, with caution being taken not to cut off feeding vessels until tumor volume had been reduced. The tumor was lobulated, well-circumscribed, and highly vascularized on its surface. Complete tumor resection was made possible by a Simpson Grade II resection, in which the dura attachments to the tumor are coagulated rather than resected, as in a Simpson Grade I resection, to decrease the risk of uncontrolled bleeding significantly. Some of the intraoperative measures included controlled hypotension, the essential application of hemostatic agents (Surgicel, Gelfoam), careful bipolar coagulation, and temporary occlusive arterial blockage. The blood loss was severe (800mL) but tolerated. Hemostasis was done thoroughly before closing. 2.6. Pathology findings, immunohistochemistry, and molecular studies The removed tumor was composed of several fragments of soft, highly vascular, reddish-brown tissue, measuring a total aggregate of 5.8 x 4.2 x 3.7 cm. Gross examination displayed a heterogeneous tumor surface with prominent dense vascularity interspersed with more solid areas. The tumor exhibited several cystic spaces filled with blood. Microscopic examination revealed features of a meningioma with a large angiomatous component, indicating high angiogenesis and proliferation of ectatic blood vessels with thin walls, comprising approximately 65 percent of the tumor mass. The vascular structures ranged in size from capillary-like to larger, dilated channels lined by endothelial layers. The regular meningothelial cells were arranged in lobules and indistinct whorls, with oval nuclei and eosinophilic cytoplasm, between the vascular components. There were no psammoma bodies. Prominent hyalinized perivascular sclerosis was noted in many areas of the tumor. Scattered large, bizarre (but not atypical) nuclei that were not mitotically active were noted throughout the tumor. These abnormal cells are histologically referred to as ancient change or degenerative nuclear atypia and are not considered signs of malignancy. (Figure 1 A, B, C, D) There was no evidence of brain invasion, necrosis, or atypical features, and mitotic activity was very rare (less than 1-2 mitoses per 10 high-power fields). Immunohistochemistry (IHC) revealed that meningothelial cells exhibited strong, diffuse EMA (epithelial membrane antigen) staining. The extensive vascular network was characterized by positive staining for CD31 and CD34. The tumor cells also expressed progesterone receptor and SSTR2A. The tumor cells were negative for CK7, CK20, TTF-1, S-100, and Ki-67 proliferation index was low <2%. Molecular studies did not identify any pathogenic mutations. The results of the chromosomal analysis revealed monosomy 22, a characteristic of meningioma genetics. No molecular changes were identified that could be targeted therapeutically. Pathology provided a final diagnosis of angiomatous meningioma, 5 cm, WHO Grade I, completely resected. 2.7. Postoperative management Postoperative hemorrhage at the surgical site, which was identified on a routine 6-hour CT scan, complicated the recovery of the patient and was characterized by an enhanced state of drowsiness and focal neurological impairments. Re-exploration, due to an emergency, showed a small point of arterial bleeding, which was controlled using bipolar coagulation. It was followed by transient cerebral edema, which was treated with dexamethasone and mannitol. The patient's neurological condition progressively improved over 72 hours. These complications led to an 8-day stay in the hospital. On discharge, he had weak residual right-sided weakness but intact cognition and mild, stable visual field impairments. 2.8. Follow-up and outcome The WHO Grade I and full resection of the patient’s tumor were good prognostic indicators. Nonetheless, radiation therapy history can also contribute to a slight risk of recurrence and the need to continue monitoring it. A follow-up plan was worked out including, MRI brain with gadolinium at 3 months, 6 months, and annually following 2 years of seizure-free life, and neurological examination at 6 months and subsequently annually. Gradual tapering of the anti-
World Journal of Biology Pharmacy and Health Sciences, 2025, 24(02), 108-117 111 epileptic medication was to be considered after 2 years of continuous seizure-free life. There was endocrine follow-up because of the history of pituitary tumor, and patient education about seizure precautions and symptom recognition. The patient achieved full neurological recovery after 9 months, and the mass effect symptoms had resolved. Proper antiepileptic management was able to bring about long-term seizure control. There was a restoration of quality of life with the least long-term sequelae. The patient did not exhibit any signs of recurrence or complications at four-year followup. Figure 1 Microscopic examination of the excised angiomatous meningioma 1A: Low power view showing angiomatous meningioma with vascular component (orange arrow), meningeal cell component (green arrow), with the mass attachment to the dura (blue arrow) (H&E stain X20); 1B: Low power view showing prominent vascular component (>65% of the tumor mass) showing vascular structures of different sizes, from capillary-like to the larger and dilated channels lined by endothelial layers (H&E stain X20); 1C: High power view showing prominent perivascular hyalinized sclerosis (H&E stain X40); 1D: High power view showing scattered large, bizarre (but not atypical) nuclei that are not mitotically active. These abnormal cells are histologically referred to as ancient change or degenerative nuclear atypia and are not considered signs of malignancy (H&E stain X60). 3. Discussion 3.1. Background: (History, epidemiology, WHO classification) While meningiomas are now well-understood and defined within neuropathology, this was not always the case, and the field's early terminology reflects a period of scientific ambiguity. Early medical literature termed meningiomas as "fungoid tumors," "epitheliomas," and "dural sarcomas," highlighting uncertainty in their "histogenesis." [4] Over time, the terminology suited better the clinical and pathological realities, and “meningioma” became the preferred term, popularized by Harvey Cushing in the 1920s for tumors arising from the meninges. [10] The development of other techniques in microscopy and IHC provided the means to subclassify meningiomas into multiple variants of histology. [11] As in the case of other morphologically distinct variants of meningiomas, the AM subtype describes a morphologic variant where an abundance of vascular channels developed in the framework of the meningioma. [12] Due to its prominent vascularity, AM is diagnostically challenging, as it may be mistaken for other vascular neoplasms, such as hemangioblastoma and hemangiopericytoma. The meningiomas have been one of the most heterogeneous, both histologically and clinically, of all primary intracranial tumors since their formal classification. [2] [4] AMs are rare.
World Journal of Biology Pharmacy and Health Sciences, 2025, 24(02), 108-117 112 However, the unusual vascularity of these tumors has caused diagnostic difficulties and the necessity to differentiate them from other highly vascular tumors of the CNS. [7] Recent reviews note that the biological behavior of AMs typically falls into the range of other WHO Grade I entities, but since they are less common, much of what we know about them is based on small retrospective series and case studies. [6] [7] Depending on the specific series, meningiomas make up about 20-30% of primary brain tumors annually, resulting in a yearly incidence of approximately 4.5 per 100,000. [6] [11] About 80% of meningiomas diagnosed are benign based on World Health Organization Grade I classification. [2] In addition, most subtypes of meningiomas are more common and exhibit a higher incidence ratio in females. [4] However, unlike typical meningiomas, AMs appear to have a slightly higher male-to-female ratio. They are most common in middle-aged patients, though there is limited specific age-range data. [7] Due to the rarity of AMs, most current literature is limited to retrospective surgical series and case reports, and not large, population-based studies. Meningiomas are classified into three histologic grades (I, II, III) that correlate with tumor recurrence and aggressiveness. [6] The fibrous, meningothelial, transitional, and psammomatous subtypes of the WHO Grade I (benign) variants are the more common ones, and some less common variants include microcystic, angiomatous, metaplastic, secretory, and lymphoplasmacyte-rich meningiomas. [9] The angiomatous subtype is characterized by numerous vascular channels. However, these are often thin-walled and are surrounded by the other constituents of a meningioma (i.e., meningothelial or spindle cells). The vascular component is usually present and predominantly so. [12] It is important to note that the sheer vascularity of the AM cannot elevate its grade classification, unless the angiomatous meningioma expresses other atypical or malignant characteristics, such as increased mitotic activity, invasion of adjacent brain tissue, or necrosis as per the recent classification adjustments. [13] The 2021 (5th edition) WHO classification of meningiomas incorporates specific molecular alterations, such as TERT promoter mutations or homozygous deletion of CDKN2A/B. [6] [14] In the current classification, AM must also not harbor high-risk molecular alterations. Otherwise, high-risk molecular alterations may elevate a meningioma's classification. In addition, there is a general lack of AM subtype-specific molecular data, so it is still treated the same as other Grade I variants, unless more aggressive behavior is demonstrated. [6] [7] Finally, the WHO classification still includes AMs as benign (Grade I) meningiomas. However, this classification might need to be revised if atypical or molecular adverse factors are identified. 3.2. Pathogenesis and pathophysiology AMs are characterized by a distinct genetic profile in contrast to the common meningiomas that usually have monosomy of chromosome 22 and NF2 gene mutations. Studies showed that in AM, there is a high prevalence of multiple chromosomal polysomies, including chromosomes 5 and 13, as well as chromosome 20, which are more common than the common NF2 aberrations in meningiomas. [15]. This implies a rather non-NF2-dependent pathogenesis. Table 1 summarizes the comparison of chromosomal abnormalities and mutations between common meningiomas and angiomatous meningiomas. Table 1 Comparison of chromosomal abnormalities and mutations between common meningiomas and angiomatous meningiomas Feature Common Meningiomas Angiomatous Meningiomas Common Chromosomal Abnormalities Monosomy of chromosome 22 or a complete lack of copy number aberrations. Loss of chromosome 22q is most frequent. Multiple chromosomal polysomies (gains of entire chromosomes) represent a distinct genetic profile. Most Frequent Polysomies (Gains) Typically, few or none. Highly recurrent gains, especially of chromosomes 5, 13, and 20. Common Gene Mutations NF2 gene mutation/inactivation is the major driver (40%-60% of sporadic cases). Other mutations include TRAF7, KLF4, AKT1, PIK3CA, and SMO. Generally characterized by an absence of the common driver mutations found in other subtypes, including NF2 mutations. An angiogenic switch, in which a set of mutations enables unregulated neovascularization, is a process required for tumor growth beyond 2 mm [13]. This high angiogenesis is an additional cause of peritumoral brain edema, which is
World Journal of Biology Pharmacy and Health Sciences, 2025, 24(02), 108-117 113 characteristic of high vascularity and elevated levels of vascular endothelial growth factor (VEGF) [13]. Although moderate to severe nuclear atypia may be detected, it is generally thought to be of a degenerative process as opposed to an expression of aggressive behavior [15]. 3.3. Comparative analysis of our case with the existing literature 3.3.1. Clinical presentation and radiology findings Our case of AM has distinct clinical and radiological features compared with similar cases reported in the literature. The patient had several typical findings in line with previous reports, such as seizures, recurrent headaches, cognitive and visual impairment, hemiparesis, as well as mass effect. [17] [18] [19] Additionally, this case is consistent with the AM reports in patients who had prior radiation therapy. [19] However, this presentation was, characterized by strong personality changes, which were probably caused by the mass effect and the involvement of the frontal lobe by the tumor. The same mass effect also explained the elevated intracranial pressure and papilledema. Although the final pathology of this tumor was deemed a WHO Grade I AM, it is important to note that it exhibited both common and uncommon radiological features. If the tumor has surrounding edema, draining veins, and tumor necrosis, it is generally considered more atypical and more malignant. [16] The size and location of the tumor are also significant factors in determining tumor grade, as Grade I tumors are typically located on the floor of the skull, while higher grades are found in the dome of the skull. [16] This patient also had severe vasogenic edema around the tumor, causing an 8 mm midline shift, which is rare for lower-grade benign meningiomas, but common for AMs. [16] MR Spectroscopy showed a high choline peak and a low N-acetylaspartate (NAA) peak for this patient, which can be used to differentiate meningioma from other brain tumors. [20] A dural tail sign is often seen in meningiomas but is not exclusive to them; therefore, precautions should be taken when interpreting imaging studies. [20] 3.3.2. Diagnosis (Pathology, immunohistochemistry, and molecular findings) Our case demonstrates a typical diagnostic picture that is compatible with AM, which agrees with the existing literature. Pathologically, the angiomatous nature, with a predominant tumor component and a significant number of thin-walled ectatic blood vessels within meningothelial cells organized in lobules, is typical of this rare type. [7] [12] Clear hyalinized perivascular sclerosis and dispersed large, bizarre nuclei, which is considered a degenerative change, but not malignancy, is another evidence in favor of the WHO Grade. [7] EMA, CD31, and CD34 are typical meningioma and vascular markers. IHC of AMs shows strong, diffuse EMA positivity in meningioma cells, as well as CD31 and CD34 positivity in the extensive vascular network. [3] The presence of progesterone receptor and SSTR2A and the absence of CK7, CK20, TTF-1, S-100, and low index of Ki-67 (<2 percent) support the benign nature and similarity to common meningioma immunophenotype. [3] The fact that there were no other pathogenic mutations in our case, even though radiation has been used in the past, supports the initial diagnosis of a Grade I angiomatous meningioma, which has a unique genetic context in contrast to other types of meningioma. [15] 3.3.3. Management and outcomes Management strategy and surgical difficulties with hypervascularity AMs are benign World Health Organization (WHO) Grade I neoplasms [6] [21], however, their marked hypervascularity distinguishes their surgical treatment from that of less vascular meningiomas. Maximal safe resection is the foundation of management, as the extent of surgical resection remains the best predictor of long-term recurrence risk. [22] The goal of gross total resection (Simpson Grade I) is often limited by the need for meticulous hemostasis in the AMs, frequently necessitating a Simpson Grade II resection where dural attachments are coagulated rather than excised. [6] The profound hemostatic challenges of this pathology exemplified by the significant intraoperative bleeding and acute postoperative complication observed in this case, highlight the literature's discussion on specialized techniques to manage hemorrhage. [23] [24] Preoperative embolization (POE) is a widely used adjunct, supported by evidence showing that it reduces the tumorto-blood loss ratio and can prolong recurrence-free survival. [8] [23] However, the routine application of POE remains controversial due to a documented risk of procedural complications, including stroke and hemorrhage, ranging from 2.9% to 5.6%. [24] [25] For high-flow tumors like AM, the benefit of devascularization in reducing acute surgical risk may outweigh the procedural risks, a conclusion supported by the serious morbidity experienced in cases without POE.
World Journal of Biology Pharmacy and Health Sciences, 2025, 24(02), 108-117 114 Extent of resection and adjuvant therapy The Simpson Grade II resection achieved in this patient significantly elevated the long-term risk of local recurrence, even for a WHO Grade I tumor. [26] The hazard ratio for retreatment following Grade II/III resection is reported to be 4.9 times higher than that of following Grade I resection, as incomplete resection increases the probability of regrowth over the course of 10 to 20 years. [6] [27] Subtotal resection (STR) typically prompts consideration of Adjuvant Radiation Therapy (ART) for both Grade I and higher-grade meningiomas. [22] [28] However, recent long-term analyses (over 10 years) suggest that ART for WHO Grade I residuals may paradoxically increase recurrence rates and a higher risk of malignant transformation in certain cohorts. [29] The management decision to pursue aggressive observation, rather than immediate ART, is therefore justified as a conservative strategy to mitigate these potential long-term risks. Salvage therapy, such as stereotactic radiosurgery (SRS), remains an option should definite progression be observed. [6] [22] Outcomes and prognostic implications The patient's excellent four-year recurrence-free survival and functional recovery align with the generally favorable short-term outcomes expected for WHO Grade I tumors. [21] However, the long-term prognosis is complicated by the confluence of the Grade II resection and the suspected underlying etiology: The patient’s history of prior cranial radiation 15 years earlier falls within the established latency period for radiationinduced meningiomas (RIMs), which averages 17.5 to 29.7 years. [23] [30] RIMs are recognized in the literature as biologically more aggressive than sporadic meningiomas, with recurrence rates reported between 21% and 33%, even among Grade I subtypes. [8] This history acts as a potent, independent risk factor for future progression. This high-risk profile is presented by the surveillance and seizure management protocols used by the patient. It has been recommended that all meningiomas, whether low-grade or not, which are not fully excised, should have indefinite annual MRI scans. In the case of tumor-related epilepsy, it is standard practice to continue taking anti-epileptic drugs (AEDs) for over one year in patients with preoperative seizures [31], and only when the patient is free of seizures after 1 to 2 years, should one consider the gradual reduction of these medications. [29] While management successfully achieved acute neurologic control, the combination of technical surgical limitations (Grade II EOR) and profound biological risk (suspected RIM etiology) dictates a lifelong, stringent surveillance protocol to address the cumulative probability of late recurrence. 4. What have we learned from this case? This example of AM can be useful in clinical practice in several ways. To begin with, the history of previous cranial radiation therapy in the patient provides evidence of a recognized risk factor of developing meningioma, which explains the significance of long-term monitoring in patients who have a history of meningioma (even the benign types). Secondly, the non-specific and progressive neurological symptoms, such as headaches, seizures, and personality changes, underscore the insidious nature of these tumors and the high index of suspicion required in patients with unexplained neurological symptoms and signs. The large peritumoral edema and mass effect, despite the WHO Grade I of the tumor, support the idea that even the histologically benign meningiomas may lead to severe neurological impairment and necessitate aggressive treatment. Thirdly, the extensive vascularity observed on imaging and confirmed intraoperatively, resulting in significant blood loss, highlights the importance of rigorous preoperative planning and surgical technique for AM. The discussion of preoperative embolization, which is not indicated in this case, is an important consideration for high-vascularity lesions. The experience of the successful Simpson Grade II resection, which strikes a balance between sufficient tumor destruction and a low risk of bleeding, offers a practical solution to the dilemma of dealing with such problematic situations. Lastly, the postoperative complication of hemorrhage and resultant temporary cerebral edema, even with successful resection, is a reminder that although post-surgical complications may be immediate, careful observation and timely actions may prevent them. What ultimately happened to the patient as he recovered his full neurological function and managed his seizures in the long term, however, demonstrates the benefits that can be attained through prompt, correct management.
World Journal of Biology Pharmacy and Health Sciences, 2025, 24(02), 108-117 115 Abbreviation • Angiomatous meningioma (AM); • Adjuvant Radiation Therapy (ART); • Immunohistochemical (IHC); • Subtotal resection (STR) 5. Conclusion This case of angiomatous meningioma is discussed to emphasize the diagnostic and management challenges of the uncommon subtype, especially in patients with previous history of cranial radiation. The main point of this report is that even WHO Grade I tumors may have a high mass effect, a high percentage of vascularity, and acute postoperative conditions, which make them hard to plan and hard to operate on. The case supports the value of considering a wider range of diagnoses and demonstrates that positive long-term neurologic outcomes are possible with multidisciplinary care. Through this experience, we hope to contribute to the medical community by learning about angiomatous meningiomas and highlighting the need for close observation in vulnerable patients and for devising culturally specific intervention measures to help patients recover to the best of their ability. Compliance with ethical standards Acknowledgments Special thanks to Jennifer Paz, Elizabeth Sanchez, and Sara Naser for their assistance in reviewing the final manuscript. Additionally, we appreciate the assistance of Grammarly's language editor, which provided valuable writing support by identifying and correcting errors in grammar, spelling, punctuation, and style, ultimately enhancing the manuscript. Disclosure of conflict of interest All authors make the following declarations: • Payment/services information: All authors have declared that they received no financial support from any organization for the submitted work. • Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might be interested in the submitted work. Data access statement All relevant data are included in the paper. Author contributions All authors contributed equally to producing this manuscript. Statement of informed consent Consent for the publication of this case was obtained from the patient. The paper has been sufficiently anonymized to maintain the patient's confidentiality. References [1] Meyer HJ, Wienke A, Surov A. ADC values of benign and high grade meningiomas and associations with tumor cellularity and proliferation–A systematic review and meta-analysis. Journal of the Neurological Sciences. 2020 Aug 15;415:116975. [2] Raghunathan A, Giannini C. Histopathology of meningiomas. Biological and Clinical Landscape of Meningiomas. 2023 Jul 12:35-45. [3] Ogasawara C, Philbrick BD, Adamson DC. Meningioma: a review of epidemiology, pathology, diagnosis, treatment, and future directions. Biomedicines. 2021 Mar 21;9(3):319.
World Journal of Biology Pharmacy and Health Sciences, 2025, 24(02), 108-117 116 [4] Brown NJ, Pennington Z, Kuo CC, Gendreau J, Chakravarti S, Singh R, Douse DM, Van Gompel JJ. Meningioma: a biography—tumor forever tied to the origins and “soul of neurosurgery”. World neurosurgery. 2023 Oct 1;178:191-201. [5] Nowosielski M, Galldiks N, Iglseder S, Kickingereder P, Von Deimling A, Bendszus M, Wick W, Sahm F. Diagnostic challenges in meningioma. Neuro-oncology. 2017 Nov 29;19(12):1588-98. [6] Louis DN, Perry A, Wesseling P, Brat DJ, Cree IA, Figarella-Branger D, Hawkins C, Ng HK, Pfister SM, Reifenberger G, Soffietti R. The 2021 WHO classification of tumors of the central nervous system: a summary. Neuro-oncology. 2021 Aug 1;23(8):1231-51. [7] Verma PK, Nangarwal B, Verma J, Dwivedi V, Mehrotra A, Das KK, Maurya VP, Bhaisora KS, Singh J, Srivastava AK, Behari S. A clinico-pathological and neuro-radiological study of angiomatous meningioma: Aggressive look with benign behaviour. Journal of Clinical Neuroscience. 2021 Jan 1;83:43-8. [8] Jung IH, Kim JY, Park SH, Chang WS. Consecutively occurring radiation-induced meningiomas with various pathologic diagnoses: a case report. Journal of the Korean Society of Stereotactic and Functional Neurosurgery. 2021 Sep 24;17(2):103-9. [9] Liu Y, Lin W, Zheng X, Huang Y, Li Y, Deng X. Clinical and imaging features of angiomatous meningioma: a retrospective analysis of 28 cases. J Clin Neurosci. 2021;83:43–8. [10] Barthélemy EJ, Sarkiss CA, Lee J, Shrivastava RK. The historical origin of the term “meningioma” and the rise of nationalistic neurosurgery. Journal of Neurosurgery. 2016 Nov 1;125(5):1283-90. [11] Franca RA, Della Monica R, Corvino S, Chiariotti L, De Caro MD. WHO grade and pathological markers of meningiomas: clinical and prognostic role. Pathology-Research and Practice. 2023 Mar 1;243:154340. [12] Hwang J, Kong DS, Seol HJ, Nam DH, Lee JI, Choi JW. Clinical and radiological characteristics of angiomatous meningiomas. Brain tumor research and treatment. 2016 Oct 31;4(2):94. [13] Ansari SF, Shah KJ, Hassaneen W, Cohen-Gadol AA. Vascularity of meningiomas. InHandbook of clinical neurology 2020 Jan 1 (Vol. 169, pp. 153-165). Elsevier. [14] Soni N, Ora M, Bathla G, Szekeres D, Desai A, Pillai JJ, Agarwal A. Meningioma: molecular updates from the 2021 World Health Organization Classification of CNS Tumors and imaging correlates. American Journal of Neuroradiology. 2025 Feb 1;46(2):240-50. [15] Abedalthagafi MS, Merrill PH, Bi WL, Jones RT, Listewnik ML, Ramkissoon SH, Thorner AR, Dunn IF, Beroukhim R, Alexander BM, Brastianos PK. Angiomatous meningiomas have a distinct genetic profile with multiple chromosomal polysomies including polysomy of chromosome 5. Oncotarget. 2014 Sep 25;5(21):10596. [16] Hale AT, Wang L, Strother MK, Chambless LB. Differentiating meningioma grade by imaging features on magnetic resonance imaging. Journal of Clinical Neuroscience. 2018 Feb 1;48:71-5. [17] Yang L, Ren G, Tang J. Intracranial angiomatous meningioma: a clinicopathological study of 23 cases. International Journal of General Medicine. 2020 Dec 30:1653-9. [18] Gkasdaris G, Vasiljevic A, Cartalat S, Pelissou-Guyotat I, Guyotat J, Dumot C, Picart T, Berhouma M. Purely cystic meningioma: Case report and systematic review of the literature. Clinical Neurology and Neurosurgery. 2022 Dec 1;223:107498. [19] Demaisip PD, Juangco DN, Nic Junn CT, Alvarez N. A Meningioma with Extensive Peritumoral Edema Mimicking Metastatic Brain Tumor: A Case Report. Brain Tumor Research and Treatment. 2023 Apr 1;11(2):140-4. [20] Lyndon D, Lansley JA, Evanson J, Krishnan AS. Dural masses: meningiomas and their mimics. Insights into imaging. 2019 Feb 6;10(1):11. [21] Hasselblatt M, Nolte KW, Paulus W. Angiomatous meningioma: a clinicopathologic study of 38 cases. The American journal of surgical pathology. 2004 Mar 1;28(3):390-3. [22] Rogers L, Barani I, Chamberlain M, Kaley TJ, McDermott M, Raizer J, Schiff D, Weber DC, Wen PY, Vogelbaum MA. Meningiomas: knowledge base, treatment outcomes, and uncertainties. A RANO review. Journal of neurosurgery. 2015 Jan 1;122(1):4-23. [23] Chun YS, Oh CW, Han JS, et al. Preoperative embolization significantly reduces blood loss to tumor volume ratio. J Cerebrovasc Endovasc Neurosurg. 2013;15(3):148-154. doi:10.7461/jcen.2013.15.3.148.