Traumatic intracranial pseudoaneurysms of cortical middle cerebral artery and posterior cerebral artery branches presenting as subdural hematomas in elderly patients: A two-case report

Abstract

Background:

Traumatic intracranial pseudoaneurysms (TIPAs) are exceedingly rare, representing <1% of all intracranial aneurysms, and are associated with high morbidity and mortality. They often remain occult on initial imaging, particularly when masked by concomitant subdural hematomas (SDHs).

Case Description:

We report two patients with traumatic pseudoaneurysms presenting as evolving SDHs. To the best of our knowledge, this is one of the few reports describing cortical middle cerebral artery (MCA) and posterior cerebral artery (PCA) pseudoaneurysms manifesting as SDHs in elderly patients. Case 1: An 86-year-old man presented with interhemispheric and tentorial SDHs. Serial computed tomography and magnetic resonance imaging (MRI) revealed progressive thickening and a 10 mm enhancing lesion. Cerebral angiography confirmed a 4.5 × 6.5 mm PCA pseudoaneurysm, which was successfully treated with Onyx embolization. He remained neurologically intact with stable follow-up imaging. Case 2 : An 83-year-old woman sustained a fall with left convexity, falcine, and tentorial subacute SDHs. MRI demonstrated a 7 mm focal contrast enhancement within the hematoma, and cerebral angiography during prophylactic middle meningeal artery embolization revealed a 5.8 × 5.6 mm distal MCA pseudoaneurysm. TIPA was treated with microsurgical clipping. She ultimately made a full recovery with near complete resolution of the SDH.

Conclusion:

These cases illustrate that TIPAs may remain angiographically occult early and present only with an evolving SDH. Key diagnostic red flags include recurrent or tentorial SDH and focal cortical enhancement on MRI. Multidisciplinary management with timely angiographic evaluation and tailored surgical and/or endovascular therapy is essential to reduce the risk of catastrophic rebleeding.

INTRODUCTION

Subdural hematoma (SDH), defined as blood accumulation within the potential space between the dura and arachnoid, is most often traumatic in origin.[18] Other causes include acceleration–deceleration injury, intracranial hypotension, vascular malformations, and iatrogenic complications.[3] While venous bleeding from bridging veins predominates, arterial bleeding, particularly from dural or cortical vessels, can also occur. Arterial-source SDH is diagnostically challenging as it often mimics venous bleeding, and pseudoaneurysms may not be visible on initial scans, especially studies without contrast. Rarely, this arises from traumatic intracranial pseudoaneurysms (TIPAs).[10,14]

TIPAs account for fewer than 1% of all intracranial aneurysms and are histologically false aneurysms formed by arterial wall disruption contained by surrounding tissue.[20] They carry mortality rates approaching 50%.[5] Previous reports describe TIPAs from distal middle cerebral artery (MCA)[1] and posterior cerebral artery (PCA)[2,4] branches presenting as acute or delayed SDH. Murakami et al. first reported a ruptured traumatic pseudoaneurysm mimicking spontaneous SDH in 2003,[11] while later, Miyazaki et al. described a false aneurysm associated with vasospasm, leading to a SDH.[8] Management options include microsurgery (clipping, trapping, bypass, or resection)[17,19] and endovascular strategies such as coil or liquid embolic occlusion.[6,15]

Here, we present two elderly patients with cortical MCA and PCA pseudoaneurysms manifesting as SDHs, underscoring the importance of serial neuroimaging, angiographic evaluation, and tailored multidisciplinary treatment.

CASE DESCRIPTION

Case 1 - Delayed presentation of vascular pathology

Presentation

An 86-year-old man with past medical history of chronic myeloid leukemia, hypertension (HTN), hyperlipidemia (HLD), chronic kidney disease, coronary artery disease, and atrial fibrillation, on Apixaban 2.5 mg twice daily, experienced a mechanical fall on the street, also sustaining a scalp laceration. He denied loss of consciousness, seizures, vomiting, visual changes, weakness, or confusion. Glasgow Coma Scale (GCS) was 15 at the time of admission.

Imaging

Initial non-contrast computed tomography (CT) scan revealed acute SDHs along the interhemispheric fissure, left tentorium, and a small left hemispheric collection without significant mass effect [Figure 1A]. The patient was discharged after 3 days of stable SDH on serial CT scans. Follow-up CT scan 23 days after the initial trauma showed a decrease in density but an increase in thickness from 1.0 cm to 1.4 cm and mild progression of mass effect and rightward displacement of the posterior septum pellucidum. SDH volume was estimated at 42.5 mL, using TeraRecon for measurement. Magnetic resonance imaging (MRI) from this second admission demonstrated subacute-to-chronic left temporal-occipital-parietal SDH (maximal thickness 14 mm), right occipital SDH (4 mm), and a 10 mm enhancing lesion along the medial temporal cortex, adjacent to the hematoma [Figure 1B]. CT-Angiography (CT-A) showed a 1.1 cm circumscribed hyperdense structure within the anterior aspect of the SDH collection, which demonstrated enhancement on the arterial phase. A diagnostic angiogram was recommended at this point, as an aneurysm could not be excluded from CT-A.

Figure 1:

Pre-embolization and post-embolization imaging studies showing an intracranial pseudoaneurysm in Case #1. (A) Initial non-contrast computed tomaography showing SDH along the left tentorium (red arrow). (B) Magnetic resonance imaging with contrast, before embolization, showing a 10 mm enhancing lesion (red arrow) along the medial temporal cortex adjacent to the hematoma. (C) Cerebral angiography showing a 4.5 × 6.5 mm pseudoaneurysm (red arrow) arising from the posterior lateral temporal branch of the left PCA. (D) Post-procedural imaging showing successful target vessel sacrifice of the pseudoaneurysm (red arrow). PCA: Posterior cerebral artery, SDH: Subdural hematoma.

Intervention

Twenty-six days from initial presentation, cerebral angiography confirmed a 4.5 × 6.5 mm pseudoaneurysm arising from the posterior lateral temporal branch of the left PCA [Figure 1C]. Significant time was taken to evaluate the entrance of the pseudoaneurysm. It was determined that sacrifice of the lateral posterior temporal branch of the left PCA was necessary. Endovascular occlusion of the pseudoaneurysm was performed using Onyx 18, a liquid embolic system. Coil embolization was considered but felt to be technically challenging given the small vessel caliber and irregular pseudoaneurysm morphology. N-Butyl cyanoacrylate glue was an alternative liquid embolic option; however, Onyx was preferred for its slow and controlled delivery, allowing for catheter repositioning and limiting the likelihood of non-target embolization. Parent artery tolerance was assessed clinically. With the patient neurologically intact at baseline and the distal nature of the posterior lateral temporal branch, sacrifice of this vessel was deemed acceptable with low risk of significant functional deficit. Both the vessel and pseudoaneurysm were noted to be occluded.

Hospital course

Endovascular embolization with Onyx was successful, and the patient did not experience any subjective neurological deficits. He remained neurologically intact on assessment and was discharged home. Apixaban was held on admission, and reversal agent, andexant alfa, was administered, given the intracranial hemorrhage. Anticoagulation was held for 8 days and resumed for 2 days before the second admission. Anticoagulation was held again at second admission and not resumed, given the ongoing risk of pseudoaneurysm rebleeding and the patient’s clinical stability.

Follow-up

At 1-month follow-up, scans showed the evolving sequelae of Onyx embolization with continued decrease in SDH sizes. There was no new or enlarging hemorrhage present [Figure 1D]. The patient remained neurologically intact, with no new deficits or complications.

Case 2 - early detection during intervention

Presentation

An 83-year-old woman with past medical history of metastatic breast cancer, on denosumab and exemestane, diabetes mellitus, HTN, and HLD, on Aspirin 81 mg daily, presented immediately after falling down a flight of stairs, sustaining scalp lacerations. She reported dizziness before the fall but denied loss of consciousness, headache, vomiting, weakness, visual disturbance, or seizures. GCS on admission was 15.

Imaging

Initial CT scan showed left convexity, falcine, and tentorial SDHs with minimal mass effect and a 2.7 mm rightward displacement of the septum pellucidum [Figure 2A]. SDH volume was estimated at 61.9 mL, using TeraRecon for measurement. No obvious lesion was identified on an initial CT scan without contrast. Three days post-fall, MRI revealed a 7 mm focal contrast-enhancing lesion within the left convexity hematoma, raising suspicion for vascular injury [Figure 2B]. Repeat CT demonstrated hematoma thickening (11–12 mm) with an increased midline shift of 6 mm, and increased SDH volume of 66 mL [Figure 2C].

Figure 2:

Pre-embolization and post-embolization imaging studies showing an intracranial pseudoaneurysm in Case #2. (A) Initial non-contrast computed tomography (CT) showing left SDH (red arrow) with minimal mass effect. (B) Magnetic resonance imaging with contrast on day 3, before embolization, revealing 7 mm focal contrast-enhancing lesion within the left convexity hematoma (red arrow). (C) Delayed post-contrast CT demonstrating hematoma thickening with increased midline shift and redemonstrating 7 mm focal contrast-enhancing lesion (red arrow). (D) Cerebral angiography revealing pseudoaneurysm (red arrow) arising from a distal cortical branch of the left MCA. (E) Postoperative cerebral angiography showed a completely occluded pseudoaneurysm (red arrow). (F) Post-procedural CT showed a stable SDH with mild midline shift. MCA: Middle cerebral artery, SDH: Subdural hematoma.

Intervention

On day 8 of her hospitalization, cerebral angiography revealed a 5.8 × 5.6 mm pseudoaneurysm arising from a distal cortical branch of the left MCA [Figure 2D]. Incidental findings included three unrelated aneurysms: Right superior hypophyseal artery (2 mm), left ophthalmic segment (2 mm), and left A1-A2 junction (1.5 mm). Given their small size (≤2 mm), all three incidental aneurysms were deemed low rupture risk per established guidelines and were recommended for surveillance imaging rather than immediate intervention. In the context of the patient’s metastatic breast cancer, the risk–benefit profile further favored non-operative management with follow-up magnetic resonance angiography at 6–12 months.

The patient underwent embolization of the left middle meningeal artery (MMA) to prevent the development of chronic SDH, given the timing of progression and her age. One day later, she was taken to the operating room for surgical clipping of the ruptured pseudoaneurysm through left craniotomy. The decision to proceed with open microsurgical clipping rather than endovascular treatment was driven by several factors. The pseudoaneurysm arose from a distal cortical MCA branch located immediately beneath the convexity SDH, making it surgically accessible. Simultaneous hematoma evacuation during the same operative approach offered the additional benefit of mass effect relief. Endovascular coiling was considered less favorable given the irregular pseudoaneurysm morphology and the small, tortuous cortical branch. This posed technical challenges for microcatheter navigation. Onyx embolization was felt to carry a higher risk of non-target cortical embolization at this superficial location. While the patient’s age of 83 years and metastatic cancer status were acknowledged, her functional status was good (GCS 15), and she was deemed an acceptable surgical candidate after multidisciplinary discussion. Intraoperatively, two titanium vascular clips were placed proximally and distally along this cortical vessel, trapping the pseudoaneurysm and point of extravasation.

Hospital course

Microsurgical clipping of the aneurysm was technically successful, confirmed by CT-A and digital subtraction angiography [DSA ] [Figure 2E] postoperatively. On postoperative day 4, the patient developed altered mental status and global aphasia, with right-sided weakness on day 6. These symptoms were transient and resolved within 72 h. MRI at this time revealed tiny foci of restricted diffusion within the left angular region and subarachnoid hemorrhage within the sulci of the left hemisphere. The very small sub-millimeter diameter of the foci of restricted diffusion limited the likelihood of correlation with parent vessel occlusion. Angiography-related small embolic events were likely the underlying etiology. Two-day video electroencephalography monitoring showed the left hemisphere focal nearly continuous delta slowing, which may have been evidence of a focal cerebral disturbance over the area. Clinical presentation seemed to be secondary to SDH-induced cortical spreading depolarizations.[7,9] The patient was cleared from a neurosurgical perspective, but she remained hospitalized for the treatment of her metastatic disease. She remained neurologically intact for the remainder of her stay and was discharged to her home.

Follow-up

At postoperative day 6, the CT scan showed stable hematomas with mild midline shift [Figure 2F]. SDH volume was estimated at 56.4 mL, using TeraRecon for measurement. Last scan completed 103-day postoperatively showed microsurgical clipping with near complete resolution of the left greater than right SDH in the supratentorial compartment, with a reparative dural thickening along the left parietotemporal convexity. There was no residual mass effect. A summary of cases is found in Table 1.

Table 1:

Combined patient characteristics and clinical outcomes.

DISCUSSION

TIPAs of cortical branches presenting as SDHs in the elderly are under-reported, likely under-recognized, and clinically hazardous. Murakami et al. described a ruptured pseudoaneurysm initially mimicking spontaneous SDH,[11] Miyazaki et al. reported a false aneurysm with associated vasospasm,[8] and Cho et al., documented recurrent SDH due to a distal MCA pseudoaneurysm missed on initial scans.[1] Ciochon and Fuga reported presentations the most similar to Case 2, with tentorial SDHs associated with distal PCA pseudoaneurysms.[2,4] These cases illustrate that diagnostic delay is often experienced by patients with this condition. A summary of comparative literature on cortical-branch TIPAs presenting as SDHs can be found in Table 2. Taken together, these studies suggest that TIPAs should be suspected in the following three scenarios: recurrent or unexplained SDH after evacuation,[11] tentorial or interhemispheric SDH distribution,[3,4] or focal cortical contrast enhancement on MRI.

Table 2:

Comparative literature on cortical-branch TIPAs presenting as SDH.

Diagnostic challenges

These cases add on prior literature by demonstrating the delayed radiographic evolution of cortical-branch traumatic pseudoaneurysms and highlighting the importance of repeat vascular imaging when MRI or CT findings are discordant or when SDH distribution is atypical.

Cerebral angiography, or DSA, remains the gold standard for TIPAs diagnosis, where repeat DSA is warranted when initial studies are negative.[20] Although untreated pseudoaneurysms may resolve spontaneously, diagnostic cerebral angiography with occlusion of the aneurysm is appropriate because of the high mortality rate associated with rupture (40–60%) and the unpredictable nature of the lesion.[12] Diagnostic cerebral angiograms were completed in both cases and confirmed the diagnosis of the TIPAs. MRI can suggest the diagnosis by demonstrating focal cortical enhancement. This focal cortical enhancement likely reflects active extravasation or pooling of contrast material within the pseudoaneurysm sac, as well as reactive changes in the adjacent cortex and leptomeninges from the hemorrhagic and inflammatory milieu. Unlike true saccular aneurysms with intact arterial walls, pseudoaneurysms lack a complete wall structure and are contained only by surrounding fibrous tissue. This makes them susceptible to contrast accumulation on delayed imaging sequences. This pathological correlate distinguishes pseudoaneurysm-related enhancement from other causes of cortical enhancement, such as cortical vein thrombosis, encephalitis, or neoplastic leptomeningeal involvement. The focal cortical enhancement seen on MRI, at day 3 in Case 2 and day 24 in Case 1, was the first diagnostic “red flag” in both cases. The vascular injury was obscured, though, by the concurrent SDH, highlighting a challenge of using this imaging modality for diagnosis.

CT-A was also performed in Case 1, before cerebral angiography. It showed the presence of a vascular lesion, but it is important to consider in clinical decision making that this imaging modality has a lower sensitivity for pseudoaneurysms, especially small distal branch lesions and those obscured by adjacent hematoma.[13] Visualization in this case may have been facilitated by time, as the study was performed 25 days after the initial trauma, providing further evidence that repeat imaging is essential even if initial scans are negative.[16] The delayed radiographic evolution of TIPAs is a known phenomenon.[12] Case 1 also underscores the dynamic nature of TIPAs, where seemingly benign, uncomplicated SDHs at presentation subsequently progress into a more complex intracranial pathology.

Serial SDH volume measurements, obtained through TeraRecon semi-automatic segmentation, served as a quantitative adjunct to guide clinical decision-making. In Case 2, progressive volumetric expansion from 61.9 mL to 66 mL, combined with the increased midline shift and hematoma thickening, reinforced the urgency of definitive intervention and informed the timing of surgical planning. Although no predetermined volume threshold triggered intervention, the trajectory of expansion along with clinical findings supported the multidisciplinary team’s decision to proceed with surgery.

Therapeutic strategies

Management of TIPAs must be individualized, balancing surgical and endovascular approaches. Microsurgical strategies include clipping, trapping, resection, or bypass. Wang et al. reported 12 surgically treated cases, emphasizing the durability of direct aneurysm exclusion.[19] Tirado et al. described MCA-MCA bypass following resection of a ruptured distal MCA pseudoaneurysm.[17] Endovascular approaches offer less invasive alternatives, particularly useful in elderly or comorbid patients. Techniques include coil embolization,[6] liquid embolic occlusion with Onyx,[15] and parent artery sacrifice when collaterals are sufficient. It is important to note that definitive exclusion of the lesion, rather than hematoma evacuation alone, is required to prevent recurrence.[6,15]

In our series, Case 2 utilized a combined approach (MMA embolization followed by craniotomy for clipping given the distal cortical branch location), while Case 1 was successfully managed with endovascular Onyx embolization. It is worth noting that middle meningeal artery embolization in Case 2 was performed prophylactically to reduce the risk of chronic SDH progression, a role well-supported in the literature for bridging-vein-source SDHs. However, its efficacy in arterial-source SDHs, such as those caused by pseudoaneurysms, is less established. MMA embolization reduces dural arterial supply and may theoretically decrease hematoma membrane neovascularization, but the primary driver of SDH expansion in pseudoaneurysm cases is the aneurysm itself, which requires definitive exclusion. In our case, MMA embolization was performed as an adjunct given the concurrent SDH burden and concern for membrane formation. Surgical clipping remained the definitive treatment. These strategies highlight that treatment should be tailored to lesion location, vessel caliber, and patient frailty.

Limitations

This report has several limitations. As a two-case series, the observations are descriptive and intended to generate hypotheses rather than provide generalizable conclusions. The retrospective nature of the review introduces potential information bias, particularly regarding timing, selection, and interpretation of imaging studies. Follow-up was limited, restricting our ability to comment on long-term aneurysm stability, recurrence risk, and functional outcomes.

Histopathological confirmation was not available in either case, so the diagnosis relied exclusively on radiographic and angiographic features. In addition, both patients were elderly, which limits the applicability of the findings to younger trauma populations with different vascular and physiologic profiles. Our institution’s ready access to advanced neuroimaging (contrast-enhanced MRI, DSA) and neurointerventional expertise may not reflect the resources of all centers, particularly those in resource-limited settings. These limitations should be considered when interpreting the broader implications and external validity of our findings.

CONCLUSION

We report two rare cases of TIPAs arising from cortical branches of the MCA and PCA, both presenting as SDHs in elderly patients. These cases highlight several key points. First, diagnostic vigilance is essential. TIPAs may be angiographically occult initially and should be suspected in recurrent, atypical (tentorial or interhemispheric), or abnormally evolving SDHs. Focal cortical enhancement on MRI is a critical red flag. Next, serial neuroimaging and angiography are necessary, where CT-A is a useful modality, especially if DSA is not readily available. DSA should not be deferred when MRI shows focal cortical enhancement, and repeat DSA should be performed when suspicion remains despite negative initial studies. Furthermore, management strategies should be tailored to the patient. Elderly or frail patients may benefit from minimally invasive endovascular strategies, while microsurgical approaches remain definitive in selected cases. Optimal outcomes require coordination between neurosurgery, neurointerventional radiology, and critical care teams.

By integrating these lessons into practice, clinicians may improve early recognition and tailored treatment of TIPAs, ultimately reducing the risk of catastrophic rebleeding and mortality. Future studies should evaluate standardized follow-up imaging protocols and functional outcomes to better guide management of these rare but high-risk lesions.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent :

The manuscript contains only fully de-identified clinical information and images. No identifying information is included, and the patient cannot reasonably be identified from the material presented.

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript, and no images were manipulated using AI.

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