Idiopathic extracranial internal carotid artery vasospasm: case report and systematic review.

BACKGROUND: Idiopathic extracranial internal carotid artery vasospasm (IEICAV) is characterized by spontaneous, recurrent, and reversible vasoconstriction of the cervical internal carotid artery (ICA). The etiology remains elusive, and no effective treatment has been established. The present study presents a case of recurrent IEICAV with migraine-like symptoms and conduct a systematic review on IEICAV. METHODS: A retrospective analysis was conducted on a case involving medical history, radiological data, treatment, and outcomes. A systematic review of published IEICAV cases was conducted through database searching in PubMed, Embase, and Web of Science from inception until May 2024. RESULTS: A 22-year-old female with recurrent headaches, blurred vision, and aphasia was diagnosed with bilateral IEICAV through angiography. Magnetic resonance imaging demonstrated a novel cerebral infarction during a prolonged episode. Treatment with topiramate successfully controlled recurrence in a 5-month follow-up. The systematic review included 36 IEICAV cases reported by literature. Bilateral involvement of extracranial ICAs was observed in 25 (69.4%) cases. Cerebral infarction was identified in 31 (88.9%) cases. Despite various treatment attempts including vasodilators, antiplatelet, anticoagulants, glucocorticoids, and other medical or surgical intervention, the recurrent rate increased in 5 (13.9%) cases, decreased in 10 (27.8%) cases, and remained unchanged in 4 (11.1%) cases. CONCLUSIONS: The elusive mechanism of IEICAV brings great difficulty into managing recurrence. Preventing IEICAV-related infarction related to secondary factors like hypoperfusion may be crucial for maintaining life quality. Further research is essential for advancing treatment strategies and a case-by-case approach is needed in identifying and eliminating possible triggers for vasospastic episodes.

Successful administration of clazosentan in subarachnoid hemorrhage patient with severe heart failure.

Background: Clazosentan, an endothelin receptor antagonist, has been shown to prevent cerebral vasospasms following subarachnoid hemorrhage (SAH) effectively. However, clazosentan-induced pulmonary edema is a frequently reported adverse effect and a primary reason for discontinuing treatment. The presence of preexisting heart conditions predisposes patients to severe pulmonary edema; thus, the administration of clazosentan is generally contraindicated. Case Description: We report the successful administration of clazosentan in a 58-year-old female patient with SAH and severe heart failure (Takotsubo cardiomyopathy). The patient initially presented with a ruptured left internal carotid posterior communicating artery aneurysm, leading to SAH. She successfully underwent neck clipping, and postoperative treatment to prevent cerebral vasospasm, including clazosentan, was initiated. Following the emergency surgical intervention, she exhibited pulmonary edema and diffused left ventricular hypokinesis with an ejection fraction of 10-20%. Although drug-induced pulmonary edema emerged after the administration of clazosentan, tailored fluid management based on daily cardiac function and ventilator management in response to pulmonary edema enabled the completion of a 2-week clazosentan therapy regimen. This approach guaranteed the patient's stability throughout the treatment period. Neither cerebral vasospasm nor cardiopulmonary complications were observed. Conclusion: This case highlights the importance of a multidisciplinary approach in managing complex patients with severe cardiac comorbidities undergoing clazosentan therapy.

Acute coronary syndrome due to coronary vasospasm: a case report.

Coronary vasospasm can lead to decreased cardiac perfusion and result in acute coronary syndrome. Here is a case of a 49-year-old man presented to the emergency department with epigastric pain and nausea with normal initial electrocardiogram. However, 6 h later, the patient experienced severe chest pain prompting a repeat electrocardiogram demonstrating inferior ST-segment elevation with troponin I levels peaked at 1.2 ng/ml (normal range: 0.00-0.02 ng/ml). Coronary angiography revealed angiographic stenosis in the left circumflex territory of a left dominant system which resolved with intracoronary nitroglycerin administration indicating ischemia with nonobstructive coronary arteries secondary to coronary vasospasm. He was discharged on isosorbide mononitrate and amlodipine therapy and had no recurrence of symptoms during follow-up.

[Box: see text].

Perfusion imaging for delayed cerebral ischemia detection in patients following ruptured aneurysmal subarachnoid hemorrhage: Interrater reliability assessment.

BACKGROUND: Delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH) is associated with adverse neurological outcomes. Early and accurate diagnosis of DCI is crucial to prevent cerebral infarction. This study aimed to assess the diagnostic accuracy and interrater agreement of the visual assessment of neuroimaging perfusion maps to detect DCI in patients suspected of vasospasm after aSAH. METHODS: In this case-control study, cases were adult aSAH patients with DCI who underwent magnetic resonance perfusion or computed tomography perfusion (CTP) imaging in the 24 h prior to digital subtraction angiography for vasospasm diagnosis. Controls were patients with dizziness and no aSAH on CTP imaging. Three independent raters, blinded to patients' clinical information, other neuroimaging studies, and angiographic results, visually assessed anonymized perfusion color maps to classify patients as either having DCI or not. Tmax delay was classified by symmetry into no delay, unilateral, or bilateral. RESULTS: Perfusion imaging of 54 patients with aSAH and 119 control patients without aSAH was assessed. Sensitivities for DCI diagnosis ranged from 0.65 to 0.78, and specificities ranged from 0.70 to 0.87, with interrater agreement ranging from 0.60 (moderate) to 0.68 (substantial). CONCLUSION: Visual assessment of perfusion color maps demonstrated moderate to substantial accuracy in diagnosing DCI in aSAH patients.

Optical coherence tomography catheter-induced vasospasm of the left anterior descending artery: A case report.

Optical coherence tomography (OCT) helps identify coronary artery disease of different etiologies. Vasospasm from OCT catheter is a rarely reported complication that is more commonly seen in the right coronary artery. We report a case of OCT-catheter induced vasospasm of the left anterior descending artery that resolved with administration of nitroglycerine. Interventionalists need to weary of the occurrence of catheter-related coronary artery spasm to avoid stenting when not necessary.

Diagnosis and treatment of coronary spasm in China: a case report.

Background: Coronary vasospasm (CVS) is a common cardiovascular condition, yet its implications should not be underestimated. Regrettably, the current diagnostic and treatment standards for CVS in China are not standardized, severely affecting the quality of life for patients with this condition. Case presentation: A 68-year-old male presented to the hospital one month prior due to recurrent chest pain. Coronary angiography (CAG) revealed a mid-segment muscle bridge with plaque formation in the left anterior descending artery, followed by pharmacological balloon angioplasty. The primary diagnosis post-operation was acute non-ST elevation myocardial infarction (NSTEMI) and coronary artery myocardial bridging. This time, the patient experienced nocturnal chest pain with a dynamic increase in troponin levels. Emergency CAG showed the left anterior descending and right coronary arteries were fine, with segmental narrowing reaching 95%-99%. Intravascular ultrasound (IVUS) indicated negative remodeling of the mid-segment lumen associated with myocardial bridging, with the smallest lumen area being 2.19 mm2. After intracoronary administration of nitroglycerin, the original most narrowed lumen area increased to 8.81 mm2. Consequently, a definitive diagnosis of CVS with coronary artery myocardial bridging was made, and the medication treatment plan was promptly adjusted. The patient's symptoms disappeared, and he was discharged. Follow-up after more than three months showed no recurrence of symptoms. Conclusion: In cases where provocative agents are contraindicated, CAG combined with IVUS can optimize the differential diagnosis of CVS. There is an urgent need in China to improve epidemiological data on CVS and establish standardized diagnostic and treatment protocols.

Iatrogenic arterial vasospasm during mechanical thrombectomy requiring treatment with intra-arterial nimodipine might be associated with worse outcomes.

BACKGROUND AND PURPOSE: Vasospasm is a common iatrogenic event during mechanical thrombectomy (MT). In such circumstances, intra-arterial nimodipine administration is occasionally considered. However, its use in the treatment of iatrogenic vasospasm during MT has been poorly studied. We investigated the impact of iatrogenic vasospasm treated with intra-arterial nimodipine on outcomes after MT for large vessel occlusion stroke. METHODS: We conducted a retrospective analysis of the multicenter observational registry Endovascular Treatment in Ischemic Stroke (ETIS). Consecutive patients treated with MT between January 2015 and December 2022 were included. Patients treated with medical treatment alone, without MT, were excluded. We also excluded patients who received another in situ vasodilator molecule during the procedure. Outcomes were compared according to the occurrence of cervical and/or intracranial arterial vasospasm requiring intraoperative use of in situ nimodipine based on operator's decision, using a propensity score approach. The primary outcome was a modified Rankin Scale (mRS) score of 0-2 at 90 days. Secondary outcomes included excellent outcome (mRS score 0-1), final recanalization, mortality, intracranial hemorrhage and procedural complications. Secondary analyses were performed according to the vasospasm location (intracranial or cervical). RESULTS: Among 13,678 patients in the registry during the study period, 434 received intra-arterial nimodipine for the treatment of MT-related vasospasm. In the main analysis, comparable odds of favorable outcome were observed, whereas excellent outcome was significantly less frequent in the group with vasospasm requiring nimodipine (adjusted odds ratio [aOR] 0.78, 95% confidence interval [CI] 0.63-0.97). Perfect recanalization, defined as a final modified Thrombolysis In Cerebral Infarction score of 3 (aOR 0.63, 95% CI 0.42-0.93), was also rarer in the vasospasm group. Intracranial vasospasm treated with nimodipine was significantly associated with worse clinical outcome (aOR 0.64, 95% CI 0.45-0.92), in contrast to the cervical location (aOR 1.37, 95% CI 0.54-3.08). CONCLUSION: Arterial vasospasm occurring during the MT procedure and requiring intra-arterial nimodipine administration was associated with worse outcomes, especially in case of intracranial vasospasm. Although this study cannot formally differentiate whether the negative consequences were due to the vasospasm itself, or nimodipine administration or both, there might be an important signal toward a substantial clinical impact of iatrogenic vasospasm during MT.

Progress of Brain Hypothermia Treatment for Severe Subarachnoid Hemorrhage-177 Cases Experienced and a Narrative Review.

The benefits of hypothermia for the treatment of subarachnoid hemorrhage (SAH) remain controversial. In 1999, we initiated brain hypothermia treatment (BHT) in the hyperacute phase to mitigate the evolution of early brain injury in patients with World Federation of Neurological Surgeons (WFNS) grade V SAH. In June 2014, we introduced endovascular cooling to maintain normothermia for seven days following the initial BHT period. Immediately after the decision to treat the sources of bleeding, cooling was initiated, with a target temperature of 33-34°C. Bleeding sources were extirpated primarily by clipping with decompressive craniectomy. Patients were rewarmed at a rate of ≤1°C/day after ≥48 hours of surface cooling. After being rewarmed to 36°C, temperatures were controlled with antipyretic (chronologically divided into groups A-C with 47, 46, and 46 patients, respectively) or endovascular (group D, 38 patients) cooling. Overall, 177 patients (median age, 62 [52-68] years; 94 [53.1%] women; onset-to-arrival time, 36 minutes [28-50]) were included. The median Glasgow Coma Scale (GCS) score upon admission was 4 (3-6). Median core body temperature was 36 (35.3-36.6)°C on arrival, 34.6 (34.0-35.3)°C on entering the operating room, 33.8 (33.4-34.3)°C upon starting the microsurgical or interventional radiology procedure, and 33.7 (33.3-34.2)°C upon admission to the intensive care unit. There were no significant differences in age, sex, GCS score, pupillary findings, location of bleeding sources, or treatment methods. There were 69 (39.0%) overall favorable outcomes (modified Rankin Scale score of 0-3) at 6 months and 11 (23.4%), 18 (39.1%), 17 (37.0%), and 23 (60.5%) in groups A-D, respectively (p = 0.0065). The outcomes of patients with WFNS grade V SAH improved over time. Herein, we report our experience using BHT for severe SAH through a narrative review.

Comment on, "Gene expression in a canine basilar artery vasospasm model: a genome-wide network-based analysis".

The study by Sasahara et al. (2008) offers a comprehensive exploration of the molecular mechanisms underlying cerebral vasospasm following subarachnoid hemorrhage, utilizing genome-wide microarray technology and network-based analysis in a canine model. Their work identifies significant gene expression changes, particularly in IL-6, IL-8, and CCL2, which are implicated in cell signaling, host-pathogen interactions, and immune responses. Despite the study's methodological rigor, it is limited by a single time-point analysis and the use of non-injected controls, which may not fully account for procedural effects. Future studies should include a time-course analysis and more appropriate controls, as well as isolate specific cell types to enhance the relevance of the findings. Further research could explore therapeutic interventions targeting the identified pathways, particularly those involved in calcium signaling and inflammation, to develop more effective treatments for cerebral vasospasm.

Symptomatic cerebral vasospasm after posterior fossa surgery in pediatric patients: single-center study and systematic literature review.

PURPOSE: The most common cause of cerebral vasospasm is subarachnoid hemorrhage, less frequently it occurs after trauma, infection, and tumor resection. Vasospasm in children is rare and has not been systematically investigated in posterior fossa surgery. METHODS: The authors undertook a single-center retrospective study of all the pediatric patients who underwent surgery on the posterior fossa and presented with postoperative symptomatic vasospasm in the period from January 2018 to February 2024. Subsequently, a systematic literature review in accordance with the PRISMA guidelines was performed in the PubMed and Scopus databases to identify the published papers on symptomatic vasospasm after posterior fossa surgery in children. RESULTS: Of the 178 patients who underwent surgery on the posterior fossa, only one patient was diagnosed with symptomatic diffuse vasospasm on postoperative day 21. The systematic literature review provided further 9 children. The underlying pathology comprised 8 intra-axial lesions with 4 medulloblastomas, 1 schwannoma in the medulla oblongata, 1 pilocytic astrocytoma, 1 primitive neuroectodermal tumor, and 1 arteriovenous malformation. The extra-axial lesions were 1 hypoglossal schwannoma and 1 oculomotor nerve schwannoma. CONCLUSION: Iatrogenic symptomatic vasospasm after posterior fossa surgery in children is a rare complication with an outcome ranging from complete recovery to the death of the patient. It is important for all staff involved in the care of patients undergoing surgery on the posterior fossa to be aware of this rare postoperative complication. The small number of patients affected does not allow a substantiated conclusion to be drawn about predictive risk factors.

Symptomatic Vasospasm Refractory to Clazosentan after Subarachnoid Hemorrhage of Ruptured Vertebral Artery Dissecting Aneurysm: Clinical Implications from Two Contrasting Cases.

Clazosentan prevents vasospasms after aneurysmal subarachnoid hemorrhage (SAH). However, clinical data on patients with SAH with ruptured vertebral artery dissecting aneurysms (VADAs) are limited. We report the case of a 49-year-old male patient with mild-grade (WFNS grade 1) thick and diffuse (modified Fisher grade 3) SAH who underwent endovascular trapping of a ruptured VADA, resulting in a poor functional outcome with a modified Rankin Scale score of 4 due to severe symptomatic vasospasm refractory to clazosentan, requiring repeated rescue endovascular therapies and chronic communicating hydrocephalus. A retrospective analysis of the clot density in the basal and Sylvian cisterns, assessed by the Hounsfield unit (HU) values of serial CT scans, in this patient showed persistent higher values, distinct from another VADA case that showed a decline in HU values with a good clinical course. These results imply the limited effectiveness of clazosentan in cases of thick and diffuse SAH after a ruptured VADA, even in good-clinical-grade patients treated with less invasive modalities. The HU values may become a simple quantitative marker for predicting symptomatic vasospasms and chronic hydrocephalus.

Subarachnoid hemorrhage-associated brain injury and neurobehavioral deficits are reversed with synthetic adropin treatment through sustained Ser1179 phosphorylation of endothelial nitric oxide synthase.

Background: Subarachnoid hemorrhage (SAH) is a life-threatening vascular condition without satisfactory treatment options. The secreted peptide adropin is highly expressed in the human brain and has neuroprotective effects in brain injury models, including actions involving the cerebrovasculature. Here, we report an endothelial nitric oxide synthase (eNOS)-dependent effect of synthetic adropin treatment that reverses the deleterious effects of SAH. Methods: We tested the molecular, cellular, and physiological responses of cultured brain microvascular endothelial cells and two mouse models of SAH to treatment using synthetic adropin peptide or vehicle. Results: SAH decreases adropin expression in cultured brain microvascular endothelial cells and in murine brain tissue. In two validated mouse SAH models, synthetic adropin reduced cerebral edema, preserved tight junction protein expression, and abolished microthrombosis at 1 day post-SAH. Adropin treatment also prevented delayed cerebral vasospasm, decreased neuronal apoptosis, and reduced sensorimotor deficits at seven days post-SAH. Delaying initial treatment of adropin until 24 h post-SAH preserved the beneficial effect of adropin in preventing vasospasm and sensorimotor deficits. Mechanistically, adropin treatment increased eNOS phosphorylation (Ser1179) at 1 & 7 days post-SAH. Treating eNOS-/- mice with adropin failed to prevent vasospasm or behavioral deficits, indicating a requirement of eNOS signaling. Conclusions: Adropin is an effective treatment for SAH, reducing cerebrovascular injury in both the acute (1 day) and delayed (7 days) phases. These findings establish the potential of adropin or adropin mimetics to improve outcomes following subarachnoid hemorrhage.

MiRNA expression profiling reveals a potential role of microRNA-148b-3p in cerebral vasospasm in subarachnoid hemorrhage.

Cerebral vasospasm (CVS) is an important contributor to delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage (aSAH), leading to high morbidity and long-term disability. While several microRNAs (miRNAs) have been implicated in vasospasm, the underlying mechanisms for CVS remain poorly understood. Our study aims to identify miRNAs that may contribute to the development of CVS. Whole-blood samples were obtained during or outside of vasospasm from aSAH patients whose maximal vasospasm was moderate or severe. MiRNAs were isolated from serial whole-blood samples, and miRNA sequencing was performed. Differentially expressed miRNAs were identified and the expression levels in patients' samples were verified using real-time qPCR. The biological functions of identified miRNA were evaluated in human brain endothelial cells (HBECs). MiRNA profiling revealed significant upregulation of miR-148b-3p in patients during CVS. We demonstrated that miR-148b-3p directly targeted and decreased the expression of ROCK1, affecting cell proliferation, migration, and invasion of HBECs through the ROCK-LIMK-Cofilin pathway. We propose that the upregulation of miRNA-148b-3p plays a role in the development of CVS by regulating actin cytoskeletal dynamics in HBECs, which is crucial for vascular function. Our study highlights miR-148b-3p as a potential diagnostic marker as well as therapeutic target for CVS following aSAH.

Microsurgery and vasospasms: Spasms' predictive factors during harvesting.

BACKGROUND: Vasospasm (VS) in microsurgery is a source of surgical complications, repeat operations, stress for the patient and the surgical team, as well as increased length of stay. Various risk factors have been identified but knowledge regarding the implicated mechanism remains limited. HYPOTHESIS: Our objective was to determine if the harvesting conditions for microsurgical toe transfers could increase the risk of VS. Our secondary objective was to determine the correlation between VS occurrence before flap division, and the occurrence of vascular complications after completion of vascular anastomoses. PATIENTS AND METHODS: Primary endpoints were the existence of locoregional anaesthesia of the lower limb, the Gilbert classification, the nature of the graft taken from the foot, the characteristics of the patients and smoking status. Our secondary endpoints were the presence of secondary VS or microsurgical failure. This series consists of 14 toe transfers over a 30-month period. Primary VS was defined as occurring prior to flap division, while secondary VS occurred after transfer. RESULTS: In this series, we identified 4 cases of primary VS. The average age of the operated population was 30.6 ± 11.2 years (16-58). The patients who presented with primary VS had a mean age of 35.3 ± 16.2 years (21-58), with no statistical difference with the other group (p = 0.54). There was a statistically significant difference between the absence of locoregional anaesthesia and the occurrence of primary VS in toe transfer (p = 0.0008). Microsurgical failure occurred in 1 case. This failure was linked to the presence of a primary VS. Gilbert's classification and type of graft were not predictive of VS (p = 0.15 and p = 0.08, respectively). The occurrence of secondary VS was statistically linked to the occurrence of primary VS (p = 0.009). DISCUSSION: The occurrence of VS remains unpredictable and the effectiveness of available treatments is debated in the literature. Faced with the failure of curative treatments, this study aimed to determine predictive factors for VS. The existence of secondary VS, when prolonged and non-responsive to conventional measures, can lead to anastomotic revision. Performing locoregional anaesthesia on the lower limb makes it possible to effectively combat the occurrence of VS. The absence of primary VS was correlated with an absence of secondary VS and an absence of microsurgical failure. In addition to controlling vasospasm, regional anaesthesia provides effective analgesia at the harvesting site. LEVEL OF EVIDENCE: IV.

"Spasms in Silence": A case of coronary vasospasm-induced ventricular fibrillation.

A 56-year-old man presented following an aborted cardiac arrest. His initial ECGs showed episodes of transient repolarization abnormalities. Coronary vasospasm can be a precipitant for ventricular arrhythmia in these patients, underpinning the importance of continuous ECG for accurate diagnosis and management.

The potential of disulfiram as a drug to improve the prognosis after the onset of subarachnoid hemorrhage.

Subarachnoid hemorrhage due to rupture of intracranial aneurysms has a poor outcome, making this disease being the social problem. Inflammation evoked by the increase in intracranial pressure and the clot in the subarachnoid space after the onset of SAH exacerbates neuronal death and vasospasm, resulting in the poor outcome and severe aftereffects. Here, FROUNT mediates CCR2 and CCR5 signaling as an intracellular molecule binding to these chemoattractant receptors which facilitate the migration of inflammatory cells, such as macrophages, in situ to trigger inflammation there. Animal model of subarachnoid hemorrhage was established in rats through intrathecal injection of autologous blood. The effect of the FROUNT inhibitor, disulfiram, on survival rate, neuronal death in hippocampus or vasospasm was then examined. The intrathecal administration of disulfiram significantly suppressed the infiltration of CD68-positive macrophages and myeloperoxidase-positive neutrophils toward the clot in the cistern in situ. In this condition, disulfiram ameliorated the death of animals after the onset of subarachnoid hemorrhage in rats. In addition, disulfiram suppressed both the two major events after subarachnoid hemorrhage, the neuronal death in hippocampus and vasospasm. The pharmacological inhibition of CCR2 and CCR5 signaling by disulfiram could thus be the therapeutic strategy to improve the outcome of subarachnoid hemorrhage.

Volatile Sedation in Neurointensive Care Patients After Aneurysmal Subarachnoid Hemorrhage: Effects on Delayed Cerebral Ischemia, Cerebral Vasospasm, and Functional Outcome.

BACKGROUND: Volatile anesthetics have shown neuroprotective effects in preclinical studies, but clinical data on their use after aneurysmal subarachnoid hemorrhage (aSAH) are limited. This study aimed to analyze whether the use of volatile anesthetics for neurocritical care sedation affects the incidence of delayed cerebral ischemia (DCI), cerebral vasospasm (CVS), DCI-related infarction, or functional outcome. METHODS: Data were retrospectively collected for ventilated aSAH patients (2016-2022), who received sedation for at least 180 hours. For comparative analysis, patients were assigned to a control and a study group according to the sedation used (intravenous vs. volatile sedation). Logistic regression analysis was performed to identify independent predictors of DCI, CVS, DCI-related infarction, and functional outcome. RESULTS: Ninety-nine patients with a median age of 58 years (interquartile range: 52-65 years) were included. Forty-seven patients (47%) received intravenous sedation, while 52 patients (53%) received (additional) volatile sedation with isoflurane (n = 30, 58%) or sevoflurane (n = 22, 42%) for a median duration of 169 hours (range: 5-298 hours). There were no significant differences between the 2 groups regarding the occurrence of DCI, angiographic CVS, DCI-related infarction, or functional outcome. In a multivariable logistic regression analysis, the use of volatile anesthetics had no impact on the incidence of DCI-related infarction or the patients' functional outcome. CONCLUSIONS: Volatile sedation in aSAH patients is not associated with the incidence of DCI, CVS, DCI-related infarction, or functional outcome. Although we could not demonstrate neuroprotective effects of volatile anesthetics, our results suggest that volatile sedation after aSAH has no negative effect on the patient's outcome.

Postoperative Symptomatic Cerebral Vasospasm: Requiring Attention Following an Uneventful Resection of an Epidermoid Cyst - A Case Report and Literature Review.

Cerebral vasospasm associated with epidermoid cyst can be caused by tumor content spillage, such as spontaneous rupture and postsurgical resection. Symptomatic cerebral vasospasm following the resection of an intracranial epidermoid cyst is a rare but serious complication that lacks a consensus on treatment. Case presentation: A 10-year-old girl underwent an uneventful complete resection of a left cerebellopontine angle epidermoid cyst. On the second postoperative day (POD 2), she exhibited reduced speech, confusion, and hyperventilation followed by hypocapnia. On POD 4, she developed right hemiparesis and dysphasia. Cerebral magnetic resonance imaging showed restricted diffusion areas in her left temporal and parietal lobes and the dorsal thalamus. Magnetic resonance angiograms confirmed narrowing of the proximal middle cerebral arteries, consistent with vasospasm. Conservative management, consisting of intravenous hydration and corticosteroid administration, proved effective in resolving her symptoms and radiologic vasospasm. On POD 8, the extensive restricted diffusion areas notably decreased in size. Her right hemiparesis was completely resolved, and her dysphasia gradually improved over time. At the 1-year follow-up, she exhibited moderate transcortical sensory dysphasia. To our knowledge, this study is the first to report on a pediatric case of symptomatic cerebral vasospasm following an epidermoid cyst resection. The combination of tumor content spillage and hyperventilation may contribute to the occurrence of cerebral vasospasm and subsequent ischemia. This complication should be acknowledged after a complete and uneventful resection.