British Journal of Radiology (2006) 79, 79-82
© 2006 British Institute of Radiology
doi: 10.1259/bjr/94682952
Non-haemorrhagic subdural collection complicating rupture of a middle cranial fossa arachnoid cyst
C Offiah, BSc, FRCS, FRCR,
W St Clair Forbes, MA, DMRD, FRCR and
J Thorne, FRCS
Departments of Neuroradiology, Hope Hospital, Salford Royal Hospitals NHS Trust, Stott Lane, Salford, Manchester M6 8HD and Royal Manchester Children's Hospital, Central Manchester and Manchester Children's University Hospitals NHS Trust, Manchester, UK
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Abstract
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Arachnoid cysts are a common incidental finding on routine brain imaging and, for the most part, their presence is uneventful. Occasionally they may be associated with haemorrhage into the subdural compartment. Rarer still is simple rupture of the contents of the arachnoid cyst into the extra-axial space. MRI can help distinguish between these two rare occurrences an important distinction to make as this may assist in directing the treating clinician toward the most appropriate management plan.
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Introduction
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Arachnoid cysts are a well-recognized benign intracranial lesion occuring most commonly in the middle cranial fossa. Although most are small and asymptomatic, they may be associated with a complicated course most typically causing mass effect or hydrocephalus. Spontaneous and post-traumatic intracystic and subdural haemorrhage has also been reported. We describe a case of the very rare complication of symptomatic rupture of a middle cranial fossa cyst into the subdural compartment without haemorrhage. Despite extensive literature review, there has been no previous description of this.
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Case report
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An 8-year-old boy presented with a history of intermittent headaches, vomiting and double vision over a period of several weeks, the onset of which was related to a fall playing football when he struck his head on concrete. No loss of consciousness occurred at the time of the injury. On examination, his Glasgow coma scale (GCS) was 15 and there was no focal neurology, cranial nerve deficit or papilloedema. CT performed on admission demonstrated a low-attenuation right-sided subdural collection isodense to cerebrospinal fluid (CSF) causing moderate mass effect, compression of the ipsilateral ventricle and effacement of the cortical sulci. No focal intraparenchymal abnormality was present. A left middle cranial fossa arachnoid cyst was also noted (Figure 1
). The patient underwent burr-hole drainage of the right subdural collection and at surgery fluid consistent with CSF was seen to escape under pressure.

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Figure 1. (a) Unenhanced CT brain demonstrating a right subdural effusion causing mass effect and (b) a left middle cranial fossa arachnoid cyst. The right Sylvian fissure demonstrates notable prominence of low (cerebrospinal fluid) density consistent with an underlying right-sided middle cranial fossa arachnoid cyst.
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He was discharged a few days later following improvement but re-admitted shortly after that with recurrence of his symptoms and a notable right-sided scalp swelling. A repeat CT scan (not shown) demonstrated re-accumulation with a slight increase in size of the right subdural collection, which remained low-attenuation. The left arachnoid cyst remained unchanged and evidence of a small right Sylvian fissure arachnoid cyst persisted. Right-sided extracranial soft-tissue swelling was also demonstrated. Ultimately, a subdural-peritoneal shunt was placed on the right and his subsequent recovery was unremarkable. Prior to his discharge, a CT scan was performed which showed only a thin residual right-sided subdural collection with some associated subdural air, but no residual mass effect. The left-sided arachnoid cyst was noted as previously. The small right-sided arachnoid cyst has become more readily appreciated with resolution of the ipsilateral subdural fluid (Figure 2
).

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Figure 2. Unenhanced CT brain following shunt drainage of the right subdural collection. Only a small residual effusion remains (with some air). The left middle cranial fossa cyst appears unchanged. The presence of the right middle cranial fossa cyst is more readily appreciated.
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Since his discharge, a MR scan of the brain has been performed (7 months since the index admission). The subdural collection has completely resolved. The right-sided middle cranial fossa arachnoid cyst has increased significantly in size since the preceding CT examination obtained during the admission some 6 months previously. The left-sided arachnoid cyst has remained unchanged in size (Figure 3
).

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Figure 3. Axial T2 weighted MR brain performed 6 months later, confirming the re-accumulation of the right middle cranial fossa arachnoid cyst as indicated by the interval increase in size as well as the presence of the unaltered left middle cranial fossa arachnoid cyst. No subdural collection was present this time.
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The patient remains clinically well and the subdural-peritoneal shunt in situ.
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Discussion
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Arachnoid cysts derive from the meninx primitive, embryologically, which is the primitive membrane ensheathing the developing central nervous system (CNS). As subarachnoid CSF accumulates, this meninx cavitates and resorbs under normal circumstances leaving only the subarachnoid space and the arachnoid membrane. During this process, the arachnoid membrane may split with secretion of fluid by the arachnoid cells into the resulting cleft ultimately yielding a cyst the so called arachnoid cyst which is truly intra-arachnoid anatomically [13].
Both intracystic haemorrhage and rupture of middle cranial fossa arachnoid cysts into the subdural space resulting in acute or chronic subdural haematoma either spontaneous or post-traumatic have been well documented in the medical literature [114]. Bleeding occurs due to tearing of an unsupported bridging vein or veins that are stretched by the cyst and susceptible to rupture by a rise in intracystic pressure [5, 7, 15]. What has not been highlighted in the radiological literature is the occurrence of arachnoid cyst rupture into the subdural compartment resulting in progressive symptoms of raised intracranial pressure, despite the lack of haemorrhage. Appreciation of this complication does appear to have implications in relation to the management of these patients and is a valuable differential to highlight to the referring clinician. This is because there potentially remains a communication between the arachnoid cyst and the subdural compartment following rupture so that, despite burr hole drainage of the collection, there remains predisposition to re-accumulation of cyst fluid in the subdural compartment and therefore the increased probability of drain insertion being required as an immediate definitive treatment. An important imaging manoeuvre to assist in this differentiation would be early MRI as the signal characteristics of the subdural collection would aid distinction between acute or subacute haemorrhage, as opposed to rupture of arachnoid cyst contents into the subdural compartment. In the case of the latter, the signal characteristics of the subdural fluid would present as isointense to cyst contents (and to CSF).
It would appear that very minor trauma, if any, is required for arachnoid cyst rupture to occur [6]. In our case study the head injury that preceded the onset of symptoms was not associated with any loss of consciousness at the time suggesting that the insult was indeed a minor one. Rupture has been reported to occur in cases following the Valsalva manoeuvre during various activities such as swimming [4, 5]. There have been sporadic reports in the medical literature regarding spontaneous disappearance of middle cranial fossa arachnoid cysts following rupture or haemorrhage into the subdural space with eventual resorption [4, 5]. Various mechanisms have been proposed for such resolution [46]. However, in our case report the cyst was seen to increase in size consistent with re-accumulation after the subdural collection had been treated and had begun to resolve. Presumably, diversion of the subdural accumulation with shunt placement reduced the intracranial pressure enough for the arachnoid cyst to re-accumulate. The re-accumulation of the right-sided arachnoid cyst in this case may also have been aided by the widely conjectured "flap-valve" effect that may result after a tear in the inner cyst wall following rupture that allows passage of CSF from subarachnoid space into the cyst, but closure of the tear in the outer membrane that allowed cyst contents to egress from the cyst into the subdural compartment [4, 5, 9].
Forty-eight percent of arachnoid cysts occur in the middle cranial fossa. Only 20% occur in the posterior fossa [1015]. It is reported that only middle cranial fossa cysts rupture [15] and this is supported by a review by Rogers et al that demonstrated six cases of subdural haematomas, which were all associated with middle cranial fossa arachnoid cysts [9]. In our experience arachnoid cysts are frequently bilateral; the presence of a middle cranial fossa arachnoid cyst and a contralateral subdural fluid collection should therefore raise the possibility of rupture of a contralateral arachnoid cyst as a consideration, particularly if early MRI fails to confirm the presence of haemorrhagic subdural fluid contents.
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Conclusion
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We have demonstrated the rare complication of rupture of a middle cranial fossa arachnoid cyst into the subdural space without haemorrhage following minimal trauma. Although it is well recognized that arachnoid cysts may be associated with acute and eventually chronic subdural blood following rupture due to tearing of the vessels that bridge the cyst wall, non-haemorrhagic rupture into the subdural compartment is an important radiological differential diagnosis to consider in order to direct the clinical/surgical management of such patients optimally as the imaging appearances of these two entities on CT examination can be identical. In such cases, early MRI would be a valuable adjunct.
Received for publication August 3, 2004.
Revision received January 9, 2005.
Accepted for publication May 6, 2005.
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