Giant arachnoid cyst associated with acute subdural haematoma: A case report

Abstract

Arachnoid cysts are extra-cerebral, intra-arachnoidal cerebrospinal fluid collections – the most frequent congenital developmental intracranial cystic lesions. They are often diagnosed incidentally during imaging exams acquired for different reasons, and are usually asymptomatic. Rare complications are post-traumatic rupture with consequent subdural haematomas. Spontaneous bleeding should be acknowledged as a rare but possible complication of this benign lesion. We report on the case of a patient presenting with a giant arachnoid cyst extending to the left frontal, temporal and parietal lobes associated with acute subdural haematoma without history of trauma.

Introduction

Arachnoid cysts (ACs) are the most frequent congenital developmental intracranial cystic lesions.¹ They can be recognised at any age, but they are usually diagnosed in childhood. They are extra-cerebral, intra-arachnoidal cerebrospinal fluid collections, and are detected in 1.4% of the patients undergoing brain magnetic resonance imaging (MRI).² The pathogenesis and natural course are unclear. They are often diagnosed incidentally during imaging exams acquired for different reasons, and are usually asymptomatic. Rare complications of ACs are subdural haematomas.^1–10 We report on the case of a patient presenting with a giant AC extending to the left frontal, temporal and parietal lobes associated with acute subdural haematoma without previous head trauma.

Case description

A 76-year-old man affected by Alzheimer’s disease presented with worsening paraesthesia on the right side and severe visual deficits. Recent history revealed mild headache, which became more severe and resistant to mild analgesia and bed rest. The level of consciousness was normal. No previous head trauma was revealed. The patient had not taken any drugs likely to cause bleeding. A computed tomography (CT) scan (Figure 1) showed a subacute, mixed, septated subdural haematoma, measuring approximately 25 mm, with signs of recent bleeding located in the left frontotemporal-parietal region; a 7 mm midline shift was appreciable too.

Figure 1.

Non-enhanced CT scan in the axial plane. A giant AC in the left frontotemporal-parietal region ((a)–(h)) with a subdural haematoma ((e)–(h)) in the left frontoparietal region. A shift of the midline is also appreciable ((d)–(f)). CT: computed tomography; AC: arachnoid cyst.

A giant AC was diagnosed in the frontotemporal-parietal region, extending to the convexity and reaching the ambiens cistern and the lamina quadrigemina. Focal thinning of the adjacent left temporal bone was evident. There were no signs of subarachnoid haemorrhage.

A subsequent MRI (Figure 2) was acquired to define clearly the presence of a large cystic lesion in the left frontotemporal-parietal region. It was homogeneously hypointense in T1-weighted sequences, and hyperintense on T2-weighted sequences. Additionally, the presence of the subdural collection was confirmed.

Figure 2.

Non-enhanced MRI scan. A T2-weighted scan in (a) the axial and (b) the coronal plane, (c) a T1-weighted scan in the sagittal plane, (d) FLAIR in the axial plane and ((e)–(f)) a T1-weighted scan in the axial plane. MRI confirmed a large cystic lesion in the left frontotemporal-parietal region, homogeneously hypointense in T1-weighted images and hyperintense in T2-weighted images. The acute subdural collection was confirmed with the typical high signal in FLAIR. In (f), the hypotrophy of the left parietal lobe surrounding the cyst is also evident. MRI: magnetic resonance imaging.

Surgery consisting of a frontotemporal craniotomy was performed to evacuate the subdural haematoma (Figure 3). The AC was completely removed, and the histological specimen of the cyst wall confirmed the neuroradiological diagnosis.

Figure 3.

Non-enhanced CT scan in the axial plane. Postoperative control showing substantial evacuation of the subdural haematoma, arachnoid cyst remotion and midline shift resolution. CT: computed tomography.

After the intervention the clinical symptoms completely resolved. Written informed consent for patient information and images to be published was provided by the patient.

Discussion

The first description of ACs dates back to the 19th century as part of an autopsy report.¹¹ ACs are benign intra-arachnoidal collections filled with clear, colourless fluid nearly identical to cerebrospinal fluid (CSF) within CSF cisterns and major cerebral fissures, intimately bordered by the arachnoid membrane. They represent 1% of lesions occupying the intracranial space.¹ The pathogenesis is unclear. They may derive from an alteration of the CSF flow during the early phase of subarachnoid space formation, leading to the rupture of the developing webbed arachnoid and thus the formation of a false passage. Another theory involves the splitting of the arachnoid membrane during delamination from the overlying dura.¹ They are mainly congential lesions. In some cases, ACs arise after inflammatory events, trauma, intracranial haemorrhages or infections.

ACs are more frequent in males,³ who make up two thirds of the cases. They can develop anywhere in the subarachnoid space, intimately related to the cisterns. The middle cranial fossa is the most common site, and the majority of them commonly occur on the left side.^4,12 The supratentorial location is significantly more common than the infratentorial.¹³ Infrequent sites include the perisellar region, the cerebello-pontine angle, the retrocerebellar space, the cerebral convexity and the quadrigeminal lamina cisterns.¹⁴

ACs are usually discovered during the first two decades of life as incidental findings. Their natural history is poorly understood, and most of them remain silent for many years. However, cases of spontaneous resolution or sudden progressive enlargement have been reported.¹ Normally, patients do not report any signs or symptoms, even with large lesions. However, larger ACs can have a mass effect on adjacent structures, producing papilloedema, headache, hydrocephalus or seizures.¹⁵ Symptomatic AC account for 5% of all cases.^5,6 Headache is the most frequent symptom, and can present with cysts in any location (clivus, sylvian fissure, vermis, etc.). The supratentorial location is more often associated with seizures. In the rare symptomatic cases, symptoms may arise from an increase in intracystic fluid or more rarely haemorrhage into the cyst itself and/or adjacent subdural space. Subdural hematomas as a complication of ACs usually occur after head trauma. They have been observed in the course of sporting activities, such as soccer.⁷ Vessels surrounding the AC are not supported by normal tissue. This predisposes them to rupture, even after low-energy trauma. Bleeding may result from the rupture of the outer arachnoid cyst wall containing fragile bridging vessels, allowing blood to accumulate within subdural compartments and finally producing a subdural haematoma. Subsequent re-bleeding or osmotic influx of fluid could explain the gradual increase in the subdural or intracystic fluid collection.⁸ Only a few cases of rupture of spontaneous ACs with subdural haematoma have been reported in the literature.^5,9,10

ACs appear on CT scans as circumscribed extra-axial hypodense lesions without contrast-enhancement. On the other hand, in post-traumatic cases, the margins of isointense ACs are not clearly defined. In these cases, their location and relationship to adjacent structures are best detected with T1-weighted MRI sequences. Cyst fluid has a low signal on T1-weighted images and a high signal on T2-weighted images. They do not show signal restriction on diffusion-weighted imaging. A distinctive feature is that they do not communicate with the ventricular system, which makes differential diagnosis with poroencephalic cysts that usually communicate with lateral ventricles.

Bony erosion and remodelling features suggestive of longstanding processes are usually associated with ACs. These findings are secondary to chronic fluid accumulation with transmitted pulsation. Depending on the size and location of the cyst, hypoplasia of the adjacent brain could be associated too. In this case, a fine linear septation, representing the arachnoid membrane, divided the subdural haemorrhage from the cyst itself. The subdural collection had a nearly isointense signal on T1-weighted sequences and increased signal intensity on Flair sequences – findings consistent with active bleeding.

The annual risk for haemorrhage in patients with an arachnoid cyst remains negligible (<0.1%).³ Most subjects are asymptomatic and are conservatively observed. Symptomatic patients undergo surgery. Ruptured ACs producing subdural hematomas must be promptly evacuated with surgical decompression.

Conclusions

The widespread use of CT and MRI has increased the frequency of diagnosed incidental ACs, as well as the detection of their possible complications. Because of this, it is important to recognise that subdural haemorrhage could be associated with the rupture of ACs. Finally, ACs represent a predisposing factor for subdural haematoma.

Patients are usually asymptomatic, in which case arachnoid cysts are managed conservatively and the outcome is generally good. If the arachnoid cyst instead ruptures after trauma or spontaneously leading to subdural haematoma with mass effect, surgical decompression is mandatory.

Funding

This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.