Diverse arachnoid cyst morphology indicates different pathophysiological origins
© Rabiei et al.; licensee BioMed Central Ltd. 2014
Received: 19 October 2013
Accepted: 3 February 2014
Published: 3 March 2014
There are few, limited, and to some extent contradictory, reports on the cellular and subcellular morphology of arachnoid cysts. In the literature cyst membranes are described as similar to, or as vastly different from, normal arachnoid membranes.
This paper reports electron microscopic analyses of symptomatic cysts from 24 patients (12 males and 12 females; age 10–79), that underwent fenestration surgery. Fourteen cysts were located in the middle cranial fossa (temporal), one in the interpeduncular cistern, five in the posterior fossa, and four were overlying the frontal cortex.
Microscopic findings confirmed the diverse nature of this clinical condition. Twelve cyst walls resembled normal arachnoid, four had a conspicuous core of dense fibrous tissue with a simple epithelial lining, and the remaining aberrant cysts exhibited non-arachnoid luminal epithelia with plentiful microvilli and/or cilia, and also nervous tissue components in the wall. The possible identity and origin of various cyst types are discussed. We hypothesize that cysts are formed mostly at an early stage of embryonic development, as a teratological event.
Cysts with various epithelial linings and extracellular components most likely have different barrier properties and fluid turnover characteristics. Further studies are needed to elucidate relations between cyst morphology, fluid composition, pathogenesis, and clinical behaviour including growth rate and relapse tendency.
Arachnoid cysts (AC) are fluid filled cyst-like structures that are anatomically connected with the arachnoid mater and can be found throughout the cranial-spinal axis with a preponderance in the middle cranial fossa . Several mechanisms have been proposed to explain their formation such as splitting or duplication of the arachnoid membrane [2–4], trauma [5, 6], and in a few cases genetic factors [7–11]. Some of these cysts expand over time which has variously been explained by fluid entering through one-way valves [12–15], due to fluid secretions by cells lining the cyst lumen [16, 17], or by osmosis .
The ultrastructure of the arachnoid cyst membrane has been sparsely studied previously. Rengachary and Watanabe described the ultrastructure of three arachnoid cysts and found the cyst wall to be very similar to normal arachnoid mater . A cyst membrane similar to normal arachnoid tissue was also reported by Go et al. [16, 19]. However, there have also been reports of cyst membranes containing other types of tissue, e.g. choroid plexus and respiratory-like epithelium [20–23]. We decided to study the morphology of symptomatic arachnoid cysts with the main focus on electron microscopy in 24 consecutive cases operated in our department.
The study was performed as a prospective explorative study. It was approved by the Regional Ethical Committee (380–09) and all patients gave their written consent to participate in the study. In the pediatric cases written consent was given by the patients’ parents.
Demographic and clinical data in relation to cyst morphology
Connective tissue cysts
No. of cases (with head trauma)
Age; range and median (years)
2 Posterior fossa
3 Posterior fossa
1 Interpeduncular cistern
Patients were operated under general anaesthesia with a craniotomy and microsurgical fenestration of the cyst wall. The procedure commenced with puncture and cyst fluid collection followed by excision of part of the cyst wall. This membrane was subjected to microscopical analyses. All patients were re-examined 3 months after surgery with the same test battery and MRI. Reference (control) material was obtained from normal-looking arachnoid mater from the cisterna magna of 5 consecutive patients with Chiari type I malformation undergoing first surgery (3 females, 2 males, age 19–61 years). The surgical samples were divided into two parts. One small piece, for routine histopathological diagnosis, was fixed in 4% formaldehyde; no material was reserved for immunohistological analyses. The major part was immersed for 24 to 72 h in a mixture of 2% formaldehyde + 2.5% glutaraldehyde + 0.02% sodium azide in 0.05 M Na cacodylate buffer, pH 7.2. This sample was prepared for transmission and scanning electron microscopy (TEM and SEM). Pieces intended for TEM were postfixed in 1% osmium tetroxide + 1% potassium hexacyanoferrate in 0.1 M cacodylate followed by en bloc staining with uranyl acetate and dehydration in ethanol. Specimens were infiltrated with epoxy resin and cured by heat according to routine methods. Sections were cut with a Leica UC6 ultramicrotome (Leica Microsystems, Vienna, Austria) fitted with diamond knives. Semithin sections 1 μm thick were examined by light microscopy after treatment with Richardson’s stain (0.5% Azur II and 0.5% Methylene blue). Ultrathin sections were contrasted with uranyl acetate and lead citrate before examination in a digitized LEO 912AB Omega electron microscope (Carl Zeiss SMT, Oberkochen, Germany). Digital image files were acquired with a MegaView III or Veleta CCD camera (Olympus-SiS, Münster, Germany). For samples prepared for SEM the aldehyde fixation was followed by repeated osmification according to the OTOTO protocol . Specimens were then dehydrated in ethanol, ending in hexamethyldisilazane, which was allowed to evaporate. They were mounted on aluminum stubs and sputter coated with palladium before examination in a Zeiss 982 Gemini field emission scanning electron microscope (Carl Zeiss).
Patient history revealed no instances of complications during birth or early childhood. Only four patients reported head trauma. All head traumas were minor and there was no correlation between head trauma and cyst location or type (Table 1). All patients improved after cyst fenestration as determined at follow-up. Three patients had temporary postoperative complications; one had meningitis, one status epilepticus and one a transient postoperative aphasia
Samples from 20 patients underwent routine pathological-anatomical diagnosis (four were omitted for technical reasons). The structure of these samples was considered to agree with arachnoid cyst morphology.
Detailed morphology – general cyst wall composition
Cysts composed of arachnoid-like tissue (12 cases).
Summary of the morphological characteristics of cysts in the respective groups
Connective tissue cysts
Connective tissue layer
Thick; major part of cyst wall
Dominant on both sides
Sometimes present on dural side
One to several layers
Stratified or single layer
Tight and adherence junctions, desmosomes
Elaborate; tight, adherence, and gap junctions, desmosomes
Glial cell processes
Present in one cyst
A multilayered subdural meningothelium formed very complex cellular extensions in whorls and wide extracellular spaces (Figure 3a). In spite of these elaborate cell interactions the en face SEM examination as a rule revealed a smooth and structure-less continuous surface (not shown). The core of the cyst wall consisted of a trabecular connective tissue with widely spaced cells and scattered microvessels. The cyst lumen (Figure 3c; SEM image) was mostly lined by a single layer of flattened epithelial cells with organized junctions and a moderate number of short microvilli. Regions of multilayered arachnoid epithelium also occurred.
These cyst walls were generally thicker than in the other groups and had a dominating core of dense connective tissue with scattered cellular elements. The epithelium on both aspects of the cyst was single-layered (Figure 3b) except for a few strands of meningothelial appearance on the subdural side. The luminal aspect could indicate some desquamation of cells and showed few microvilli (Figure 3d).
iii) Cysts with aberrant structure (8 cases).
Detailed morphology – barrier-mediating structural features of cysts
Arachnoid membrane from Chiari patients
This is, to the best of our knowledge, the first prospective study on the detailed morphology of the walls of intracranial cysts, diagnosed as arachnoid cysts (ACs) from clinical criteria. The study material is also the largest hitherto reported with 24 patients. The most striking overall results are that (i) only half of the samples had a cyst wall arrangement in good agreement with arachnoid tissue; (ii) four cysts made up a morphologically distinct group with a dominant core of cell-poor dense connective tissue lined by a thin squamous epithelium; and (iii) the architecture and cellular composition of the remaining group was variable with an obvious admixture of various elements of an expected intracerebral origin or location, e.g. ciliated epithelia, glial and neuronal components.
None of these findings is unique, a number of case reports exist based on few patients that demonstrate the variability of the arachnoid cyst entity [21–23, 25]. Thus, the present study extends and confirms the notion that clinical ACs are a heterogeneous group of pathological conditions. The origin and cause(s) of cyst formation as well as the pathogenic mechanisms behind their expansion into clinically evident cysts have attracted interest over decades . It is noteworthy, that our thorough penetration of patient histories gave no indication as to causative mechanisms behind cyst development. This observation, which is in harmony with previous reports, supports per se that these cysts are spontaneous and formed at an early stage, probably as a teratological event [27–29]. It is conceivable that cysts lined and composed of cells characteristic of normal arachnoid originate as errors in the normal splitting of the perineural mesenchymal layers that are destined to form the meninges during early nervous system development. Although there are reports on genetic mechanisms behind AC in combination with more severe encephalic disturbances [30–37] it is not likely that isolated cysts in otherwise healthy patients could be linked to specific genetic errors.
The fibrous cysts in the present report in one respect share morphology with normal dura through the dominance of densely organised cell-poor connective tissue. It might thus be assumed that they reflect erroneous positioning of mesenchymal islands destined for development into dura mater. Experimental evidence based on transgenic techniques indicates that the barrier-forming arachnoid and adjacent dural layers differentiate from a common cell lineage expressing prostaglandin D2 synthase (PGD2S) of neural crest origin at forebrain level and mesodermal origin from midbrain level and posteriorly . In addition, inactivation of the neurofibromatosis type 2 gene during a critical embryonic and early postnatal time window gave rise to meningioma development in PGD2S -positive cell layers with a meningothelial or fibroblastic histological character. These neoplasm types were in continuity with the respective arachnoid and dural layers . It seems justified to speculate that the cited observations on meningioma pathogenesis could have bearing on the developmental mechanisms for cyst formation.
An alternative interpretation of the fibrous cysts is that instead they reflect an equivalent of mature scar or capsule tissue, for example after an early and limited hemorrhage. A recent study presented a “2 hit” process for development of arachnoid cysts with both a congenital histological defect in the development of the arachnoid membrane and a later event of head trauma or hemorrhage [39, 40]. This type of mechanism was not evident for the patients in our study, none of whom reported a complication during birth or early childhood and only a few of them reported head trauma.
Cyst-lining epithelial cells equipped with cilia or numerous microvilli indicate a possible origin from ependymal and choroid lineages, respectively. Similarly, the presence of nervous tissue in the group of aberrant extracerebral cysts, anatomically connected with the arachnoid, reasonably represents true malpositioning of neural tube progenitor cells. We lack knowledge of relevant reference literature in the neuro-developmental field that would give clues on possible pathogenetic mechanisms behind such failures in the control of normal development. In a few case reports, authors discuss the possibility that CNS cysts lined by strongly-ciliated epithelia, due to the similarity to respiratory epithelium, are even derived from endodermal progenitors [41, 42]. From morphological criteria, the ciliated epithelia encountered in the present material are best compared with the ventricular ependymal lining. Particularly, the simultaneous presence of cilia and numerous long and slender microvillus-like projections are characteristic of ependymal cells . Retrospectively, we realize that the enigma of cell lineage could have been further elucidated by immunohistological analyses, e.g. seeking expression of cytokeratins, gfap, and CD99, to distinguish ependyma from respiratory-like lining. This was not possible in this study due to lack of suitable material.
Regionally the ciliated epithelia also presented a probable secretory morphology that differed from normal ependyma. Whether or not such a differentiation would result in effects on cyst fluid composition or turnover is beyond the scope of the present study. Nevertheless, this finding points at the possibility that cyst wall epithelium can actively modify cyst fluid. This hypothesis is also supported in a recent study by Berle et al. . We plan to extend the study and try to find correlates between morphology, fluid chemistry, and clinical properties, including postoperative events, of the various cyst types.
The examined tissue samples invariably had a tight and continuous epithelial lining with seemingly ordered junctions between cells. This would implicate that the luminal epithelium, the primary exchange barrier, limits free exchange of cyst fluid by restricting the possibility for paracellular flow. The degree of resistance should, on the other hand, vary considerably between the attenuated blood capillary endothelium-like junctions of the lowest single layered epithelium, and the elaborate intercellular pathways with multiple specific junctional elements of more complex epithelia. In addition, the variations of stromal thickness and composition including vascularization, and of the arrangement of cells at the dural aspect of cysts, must influence the net fluid exchange properties of cyst walls. Recent studies have focused interest on active mechanisms for cyst fluid accumulation. For example, Berle et al.  reported that cyst fluid had a composition distinct from cerebrospinal fluid which would require active transport mechanisms. However, considering the drastically different cellular architecture of cyst walls reported here it seems unjustified to expect that cyst fluid is a unitary entity. As an example, assuming that the various epithelia described preserve functional activities characteristic of their normal location, a cyst lined with choroid-like epithelium should conceivably have the potential for fluid formation resembling CSF production  whereas the simplest epithelia should lack such activity. Obviously, these considerations urge for further elucidation of possible correlates between cyst fluid contents and cyst wall morphology.
All patients in this study were operated with microsurgical decompression through craniotomy. It is well known that intracranial cysts can re-occlude years after surgery requiring secondary surgery [47, 48]. To our knowledge risk factors for reoccurrence have so far not been identified. The cyst morphology could be of importance for long-term surgical outcome. Accordingly, the present work may provide a valuable basis for analysis of cases that might present as future relapses.
This study on 24 patients established that arachnoid cysts have variable organization of epithelial linings and extracellular components suggesting different barrier properties and fluid turnover characteristics. Further studies are needed to elucidate relations between cyst morphology, cyst pathogenesis, and clinical behavior, including growth rate and relapse tendency. Cyst morphology might be a relevant factor since some cysts become symptomatic [49–51] while others are asymptomatic for years [52–54].
The skilled preparation work of Mrs Yvonne Josefsson and Ms Kanita Cukur of the Electron Microscopy Unit is gratefully acknowledged. Professor Claes Nordborg is acknowledged for his review of the cyst samples in the pathology department. This work was supported by grants from the Lundberg Research Foundation and the ISNF (Insamlingsstiftelsen för Neurologisk Forskning).
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