Cerebral aneurysms are relatively common, occurring in up to 2% of adults without risk factors for subarachnoid hemorrhage (SAH) [1]. Cerebral aneurysm diagnosis raises substantial concerns because of the potential risk of rupture and subsequent hemorrhage. Ruptured aneurysms can lead to both intracranial and SAHs, with SAH being particularly dangerous owing to severe complications, including vasospasm. Vasospasm is a reversible narrowing of the cerebral arteries that typically begins within the first few days after SAH and can progress to cerebral ischemia. Despite the availability of effective therapeutic options, including pharmacological agents (such as nimodipine) and interventional procedures, vasospasm remains a leading cause of morbidity and mortality [2]. Thus, prompt and continuous monitoring is essential in patients with SAH for detecting vasospasms early.

Digital subtraction angiography (DSA) is currently the gold standard for diagnosing vasospasms. However, it is an invasive procedure with inherent risks. For decades, transcranial Doppler (TCD) and transcranial color-coded Doppler (TCCD) have been recognized as valuable, noninvasive diagnostic tools for detecting and monitoring vasospasm [3]. Key parameters include: (1) mean flow velocity (MFV), calculated as (EDV×2+PSV)/3, where EDV is the end-diastolic velocity and PSV is the peak systolic velocity, and (2) the Lindegaard index (LI), which is the ratio between the MFV in the middle cerebral artery (MCA) and in the ipsilateral extracranial internal carotid artery (ICA) (MFV^MCA/MFV^ICA). An MFV exceeding 120 cm/sec in the MCA suggests vasospasm [4], whereas an LI >3 supports the diagnosis of vasospasm and helps exclude hyperemia as a cause of the elevated velocity [5]. Although Doppler techniques offer advantages such as bedside assessment and high tolerability, they are operator-dependent, which may result in reduced reproducibility and increased variability. The primary endovascular treatment options for ruptured cerebral aneurysms include coil embolization [6] and other devices such as flow-diverter stents or Woven EndoBridge. In these scenarios, TCCD monitoring can detect vasospasm following SAH and assess the endovascular treatment efficacy by evaluating the residual blood flow within the aneurysm. Here, we report the case of a patient with a ruptured right MCA aneurysm who was treated with acute coil embolization. The patient was monitored using TCCD to detect vasospasm and evaluate the outcome of embolization.

A 57-year-old man with no significant medical history, current medications, or history of smoking was admitted to the hospital because of confusion and psychomotor agitation. Two days prior, he had developed a severe diffuse headache. On admission, neurological examination revealed a coma (Glasgow Coma Scale score of 8, with an eye response of 1, a verbal response of 2, and a motor response of 5) and hypotonia of the left hemibody. A cerebral computed tomography (CT) scan (Fig. 1) showed a right frontal intracranial hemorrhage along with SAH (Fisher grade 4). CT angiography (CTA) identified a cerebral aneurysm in the right MCA at the M1–M2 branch bifurcation. The patient was subsequently analgosedated and intubated by an intensivist and admitted to the angiography operating room.

DSA confirmed the presence of a saccular, dysmorphic aneurysm with a narrow neck and a small bleb at its base. Mild vasospasm of the right MCA was also observed. Following multidisciplinary discussion, endovascular treatment with coil embolization was performed. Two coils were placed within the aneurysm to achieve subtotal embolization, as confirmed by post-procedural angiographic examination (Fig. 2). Post-procedure, the patient was transferred to the intensive care unit (ICU). Serial cerebral CT scans showed gradual hemorrhage reabsorption and the absence of hydrocephalus or a midline shift. TCCD monitoring was initiated the day after embolization to assess vasospasm and evaluate embolization outcomes.

In this case, TCCD was employed to not only monitor vasospasm, but also evaluate embolization using advanced imaging techniques such as Micro-V technology [7] and Bright-Flow three-dimensional (3D) technology. TCCD examinations were performed twice daily after endovascular treatment for 15 days. Although daily TCCD assessments were conducted, only the results from days with significant changes are reported here. The initial TCCD assessment on the first posttreatment day revealed normal MFV and color findings in the right MCA. However, TCCD examination on the second posttreatment day showed focal aliasing in color mode at high pulse repetition frequency values proximal to the coils in the distal M1 segment of the right MCA. At this site, the MFV was 133 cm/sec, indicating a mild focal vasospasm (Fig. 3A). Bright-Flow 3D imaging also revealed residual blood flow within the aneurysm, confirming incomplete embolization, as indicated by post-procedural DSA. On the fourth posttreatment day, extended aliasing suggested vasospasm progression in a distoproximal direction. Local velocities increased further, with MFV reaching 171 cm/sec, indicating moderate vasospasm (Fig. 3B). At the TCCD follow-up on the seventh posttreatment day, the morphological progression of aliasing had nearly reached the MCA origin. The MFV decreased slightly to 161 cm/sec, likely because of the extended length of the narrowed segment. Subsequent daily TCCD examinations continued to show residual vasospasm without further significant progression until the twelfth posttreatment day, when TCCD evaluation revealed resolution of both aliasing and spectral acceleration. This progression and its subsequent regression were well documented by TCCD, as shown in the Supplementary Video 1, where color-mode imaging highlighted the distoproximal extension of aliasing in the MCA, followed by complete resolution on the twelfth posttreatment day. However, all TCCD assessments consistently demonstrated residual blood flow within the aneurysm, indicating incomplete embolization (Fig. 4). Clinically, the patient exhibited no signs of delayed cerebral ischemia. He experienced a rapid recovery of consciousness following the withdrawal of analgosedation, along with a gradual improvement in his neurological deficits, specifically mild left brachial paresis, which had been present since hemorrhage onset. Serial CT revealed no evidence of ischemic lesions. The patient was transferred to the neurosurgery unit on day 18 in a stable neurological condition (alert and without significant sensorimotor deficits) and subsequently discharged to a rehabilitation clinic on day 24 with a modified Rankin scale score of 1.

TCD and TCCD use for posttreatment monitoring of endovascularly treated aneurysms represents a relatively novel approach. Few studies have explored the application of Doppler techniques in this context [8,9]. Collectively, these studies suggest that Doppler techniques are reliable tools for monitoring aneurysms after endovascular treatment. Based on our experience, TCCD offers distinct advantages over traditional TCD. This is primarily due to the morphological insights provided by TCCD, which allow direct visualization of both the color-coded blood flow and endovascular coils, typically appearing as hyperechogenic structures (Fig. 5A). Consequently, morphological data complemented the hemodynamic parameters in assessing vasospasm and determining the completeness of aneurysm embolization or full-flow diversion (Fig. 5B).

The TCCD offers several advantages. One significant benefit is its noninvasive nature, which avoids the DSA-associated risks. Additionally, it facilitates bedside assessments, making it particularly valuable in the ICU setting, where patient mobility is limited. TCCD also enables the direct visualization of endovascular devices, particularly coils, which is challenging with CT or magnetic resonance imaging owing to metal artifacts. Furthermore, advanced techniques, such as Micro-V and Bright-Flow 3D, enhance residual blood flow detection within the aneurysm, signaling incomplete embolization (Fig. 6). In our case, such a residual flow was evident, emphasizing the utility of TCCD in influencing subsequent therapeutic decisions. However, TCCD is highly operator-dependent and thus subject to variability. Although DSA remains the gold standard for diagnosing vasospasm and assessing aneurysm reperfusion, TCCD serves as an invaluable adjunct, particularly for monitoring vasospasm and identifying residual flow within the aneurysm.

This methodological limitation warrants further consideration. To ensure comparability with the velocity cutoffs reported in the literature, which are predominantly derived from TCD studies, we did not apply angle correction during velocity measurements with the TCCD. However, in the case of the MCA, the lack of angle correction did not introduce significant discrepancies in velocity readings compared to angle-corrected values. As previously mentioned, MFV is the most critical hemodynamic parameter for detecting vasospasms. Nonetheless, an elevated MFV can result from conditions other than vasospasm, such as hyperemia. Hyperemia may arise from autoregulation, hypertension, or hypervolemia.

The LI has been proposed to distinguish between vasospasms and hyperemia. This ratio, calculated by dividing the MFV in the MCA by that in the ipsilateral ICA, helps differentiate between the two conditions. LI >3 suggests vasospasm, indicating a significantly higher velocity in the MCA than in the ICA. Conversely, LI <3 indicates similar velocities in both arteries, suggesting hyperemia rather than vasospasm. In our case, the LI was not measured because of the clear visualization of the proximal MCA segment with normal MFV, which excluded hyperemia as a possible explanation for the increased velocity. Moreover, using advanced 3D modes such as Bright-Flow 3D enhances the ability to directly visualize vessel narrowing using TCCD. The ability to observe the affected artery in color mode allows for differentiation between velocity reductions due to vasospasm regression and those resulting from extended arterial narrowing in severe vasospasm (>90% stenosis). This capability is particularly useful in the later stages of TCCD monitoring.

TCCD is a valuable tool for detecting and monitoring vasospasms in cases of SAH caused by ruptured aneurysms treated with endovascular procedures. Additionally, it has potential as a technique for assessing the outcomes of endovascular treatment, particularly in identifying cases of subtotal embolization.