A ruptured aneurysmal subarachnoid hemorrhage and vasospasm initially manifesting as acute ischemic stroke: a case report

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J Neurocrit Care. 2024;17(2):75-78

Publication date (electronic) : 2024 November 11

doi : https://doi.org/10.18700/jnc.240026

Joongwon Park, MD, Wonseok Jeon, MD, Junho Choi, MD, Chulho Kim, MD, PhD

Department of Neurology, Hallym University College of Medicine, Chuncheon, Korea

Corresponding authors: Chulho Kim, MD, PhD Department of Neurology, Hallym University College of Medicine, 1 Hallimdaehak-gil, Chuncheon 24252, Korea Tel: +82-33-240-5255, Fax: +82-33-255-1338 E-mail: gumdol52@naver.com

Received 2024 August 11; Revised 2024 September 13; Accepted 2024 September 26.

Abstract

INTRODUCTION

The diagnostic approach in patients presenting with dysarthria and unilateral motor weakness without definite hemorrhagic features on initial imaging often leans towards identifying ischemic stroke rather than hemorrhage. This case report highlights a patient whose initial brain computed tomography (CT) scan, showed no clear signs of hemorrhage, despite the presentation of relevant symptoms, making the diagnosis challenging. However, the patient’s age (51 years) and history of thunderclap headache prompted further evaluation, facilitating the final diagnosis of vasospasm-induced ischemic stroke caused by a ruptured cerebral aneurysm.

This case illustrates the importance of considering all forms of ischemia with similar presentations, and emphasizes the need for a comprehensive medical history and thorough imaging, including angiography. In particular, the treatment did not involve antithrombotic therapy, instead focusing on addressing vasospasm, highlighting the necessity of accurate diagnosis to guide appropriate treatment.

CASE REPORT

A 51-year-old male presented to the emergency department with weakness in his left upper and lower limbs and dysarthria, which developed on the day of admission. He had no known underlying medical conditions, no specific family history, and no relevant medical interventions, but had a 20-pack-year smoking history. The patient reported intermittent left upper and lower limb weakness and dysarthria, which developed 2 days prior to admission. Upon neurological examination, dysarthria was noted, while muscle strength in the left upper and lower limbs was reduced to grade 4 on the Medical Research Council scale. Although the patient was involved in a car accident on the day of admission, he was unable to recall the details of the accident.

Brain CT performed in the emergency department showed no clear signs of hemorrhage (Fig. 1A and B), leading to the initial consideration of ischemic stroke rather than hemorrhage. However, given the patient's age (51 years) and the history of thunderclap headache the day before admission, hemorrhagic stroke could not be ruled out, prompting further investigation with multiphase brain CT angiography, magnetic resonance imaging, and digital subtraction angiography. These imaging studies revealed infarctions in the bilateral middle cerebral artery (MCA) territories (Fig. 1C), as well as an aneurysm in the left anterior cerebral artery (Fig. 2A and B). A brain CT imaging taken 1 day after hospital admission revealed a hypodense area corresponding to an infarct in the left Sylvian cortex (Fig. 1D). Additionally, vasospasms were observed bilaterally in the MCAs and posterior cerebral arteries (Fig. 2). The patient was administered intravenous nimodipine the day after hospital admission, while aneurysmal clipping was performed on the third day of the visit. No additional intra-arterial administration of nimodipine or angioplasty was performed. On the fourth day postoperatively, intravenous nimodipine was replaced with peroral nimodipine. After aneurysmal clipping, the patient underwent daily monitoring for vasospasm using transcranial Doppler (TCD) daily. Vasospasm persisted on TCD on postoperative day 7, but cerebral angiography performed on day 11 (Fig. 1E) confirmed that the vasospasm had improved significantly; therefore, TCD monitoring was discontinued. The patient's neurological status significantly improved, allowing him to resume normal daily activities.

Fig. 1.

Images taken during additional diagnostic work-up. Brain computed tomography (CT) angiography showing an aneurysm in the left anterior cerebral artery (long white arrows; A, B). Further, bilateral middle cerebral artery (B, C) and posterior cerebral artery narrowing (white arrows) were observed in CT angiography (A). Brain CT image taken 1 day after hospital admission showing a hypodense area corresponding to an infarct in the left Sylvian cortex (arrow, D). Cerebral angiography on day 11 confirmed significant improvement of the vasospasm (E).

Fig. 2.

Initial diagnostic evaluation in the emergency department. Non-enhanced brain computed tomography image (A) showing an ambiguous sign of hemorrhage (white arrows), with no clear hemorrhage in the basal and interhemispheric cistern (B). Diffusion-weighted imaging showing multiple diffusion restrictive lesion in bilateral middle cerebral artery territories (white arrows) (C).

DISCUSSION

In contrast to other reports, the present patient presented with an initial CT scan that did not clearly reveal cerebral hemorrhage, and his initial manifestations suggested ischemia rather than hemorrhage. However, owing to the possibility of a hemorrhagic infarction, further imaging was performed, which revealed evidence of a ruptured anterior cerebral artery aneurysm and vasospasm across the main intracerebral arteries. Consequently, antithrombotic treatment was not administered, and treatments targeting vasospasm and aneurysmal repair were initiated.

Cerebral vasospasm, defined as a prolonged but reversible narrowing of the cerebral arteries, typically begins days after subarachnoid hemorrhage (SAH) [1,2]. Vasospasm can occur in 50%–90% of patients following cerebral aneurysm rupture [3]. Vasospasm typically begins 3–4 days after headache (aneurysmal rupture), peaks in severity between 7–10 days, and can last as long as 21 days. In this patient, it is possible that cerebral ischemia associated with vasospasm occurred within 24 hours of the onset of the thunderclap headache. Some reports have noted vasospasm occurring as early as 1–2 days after aneurysmal rupture; thus, we believe it likely that this case also had a short interval between aneurysmal rupture and delayed cerebral ischemia (DCI) due to vasospasm [4,5]. If the information for the headache and the onset of symptom are lacking, distinguish between vasospasm-induced cerebral infarction and a classic ischemic stroke can be challenging [6]. It is thus crucial to identify hemorrhage in the initial imaging studies; however, as in the present case, minimal hemorrhage can obscure the findings, leading to delayed or incorrect diagnosis. Misdiagnosis of the etiology of cerebral ischemia can lead to recurrence and worsening of hemorrhage, potentially resulting in fatal outcomes. Therefore, thorough history-taking of neurological symptoms and additional imaging studies are essential.

We propose stroke in this patient was a vasospasm-induced hemodynamic infarction. Hemodynamic infarction often occurs bilaterally into the cortical watershed zone, whereas embolic infarction is commonly observed as a small and discrete infarct unilaterally in the cortical area [7]. The delayed contrast transit into the corresponding right MCA territory and sluggish contrast filling on transfemoral catheter angiography imaging indicate that the symptoms in the present case were caused by hemodynamic infarct [8].

Differentiating between DCI due to vasospasm following aneurysmal rupture and reversible cerebral vasoconstriction syndrome (RCVS) is important. DCI events are commonly reported to be accompanied by aneurysmal rupture and worsening of neurologic deficits rather than headache, whereas RCVS events are more commonly reported to be accompanied by spasms and thunderclap headache [9]. Angiographically, vasospasm in DCI is predominantly distributed in proximal arteries with large segmental narrowing; however, in RCVS, multifocal and segmental narrowing can be seen distally, including in the proximal cerebral arteries [10]. As such, it is appropriate to categorize this case as DCI due to vasospasm of aneurysmal SAH, rather than RCVS.

In conclusion, even when the initial imaging does not prominently display hemorrhage, the possibility of SAH due to cerebral aneurysm rupture and associated vasospasm should be considered in patients presenting with symptoms of cerebral infarction. The importance of an accurate diagnosis in preventing the exacerbation of hemorrhage and misuse of antithrombotic treatments cannot be overstated. This case underscores the necessity of a thorough history-taking, including inquiries regarding symptoms such as thunderclap headaches, as well as additional imaging for vascular assessment, to ensure accurate diagnosis and appropriate management.

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