Neurochirurgie 60 (2014) 55–58
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Clinical case
Suprasellar arachnoid cyst after subdural haemorrhage in an infant. A case based update Kyste arachnoïdien suprasellaire après hématome sous-dural du nourrisson. Mise au point. À propos d’un cas M.-H. Sonnet , A. Joud , J.-C. Marchal , O. Klein ∗ Service de neurochirurgie pédiatrique, université de Lorraine, hôpital d’Enfants, CHU de Nancy, 4, rue du Morvan, 54500 Vandœuvre-lès-Nancy, France
a r t i c l e
i n f o
Article history: Received 23 October 2013 Accepted 4 January 2014 Available online 18 March 2014 Keywords: Suprasellar Arachnoid cyst Head trauma Subdural haemorrhage Paediatric neurosurgery
a b s t r a c t Introduction. – Brain arachnoid cysts (AC) are congenital or acquired malformations. Their prevalence in children ranges between 0.2 and 2.3% of the studied populations. Few reported studies exist where AC appears after a subdural haemorrhage. Methods. – We present one case of a symptomatic suprasellar AC after post-traumatic subdural haemorrhage in an infant. Results. – After endoscopic ventriculocystostomy, the child quickly improved and the cyst reduced in size. The child was monitored for 22 months and his neurocognitive development remained normal. Conclusion. – Our case led us to the hypothesis that the inflammatory process due to subdural haemorrhage may locally result in arachnoiditis, and thus to the creation of a neomembrane, and eventually to cyst formation. This is also the case with the development of post-traumatic spinal AC. © 2014 Elsevier Masson SAS. All rights reserved.
r é s u m é Mots clés : Suprasellaire Kyste arachnoïdien Traumatisme crânien Hématome sous-dural Neurochirurgie pédiatrique
Introduction. – Les kystes arachnoïdiens (KA) cérébraux sont des malformations congénitales ou acquises. Leur prévalence chez l’enfant se situe entre 0,2 et 2,3 % des populations étudiées. Il existe peu d’études mentionnant l’apparition d’un KA dans les suites d’une hémorragie sous-durale. Méthodes. – Nous rapportons le cas d’un KA suprasellaire symptomatique faisant suite à un hématome sous-dural du nourrisson. Résultats. – L’état clinique de l’enfant s’est rapidement amélioré après ventriculo kystostomie endoscopique et le kyste a diminué de taille. L’enfant est suivi depuis 22 mois et son développement neurocognitif est normal. Conclusion. – Notre cas conduit à l’hypothèse qu’un phénomène inflammatoire dû à un hématome sousdural peut aboutir localement à une arachnoïdite et ainsi à la création d’une néomembrane et donc à la formation du kyste. Cela est déjà le cas pour le développement des KA spinaux post-traumatiques. © 2014 Elsevier Masson SAS. Tous droits réservés.
1. Background Arachnoid cysts (AC) are congenital [1] or acquired malformations [2]. Recent findings regarding their prevalence in children (all type of cysts, whether symptomatic or not) range between 0.2
∗ Corresponding author. E-mail addresses: [email protected], [email protected] (O. Klein). 0028-3770/$ – see front matter © 2014 Elsevier Masson SAS. All rights reserved. http://dx.doi.org/10.1016/j.neuchi.2014.01.003
and 2.3% of the studied populations [3,4] certainly increasing due to more accurate indications of neuroradiological explorations. The association between AC and subdural haematoma is well known and numerous cases have been described where subdural effusion complicates AC [5–8]. However, very few studies exist where AC appears after a subdural haemorrhage [9,10], as in the case described in our case report. Hopefully, this case will bring new insights regarding AC pathogenesis, where there still remains controversies.
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Fig. 1. A and B. The first CT-scan showing a subdural haematoma and parietal fracture. A et B. Premier scanner montrant un hématome sous-dural et une fracture pariétale.
2. Illustrative case We report the case of a two-month-old baby who slipped from his mother’s arms and fell down the stairs. Upon arrival at the emergency unit, the child was asleep and difficult to wake-up; he lost consciousness but recovered after two thoracic compressions. The physical examination did not show any focal neurologic signs. The infant presented with frontal and parietal bruises. An emergency CT-scan revealed a bilateral frontal subdural hematoma with acute bifrontal, bitemporal, and left parietal bleeding associated with a left parietal fracture (Fig. 1A and B). Initially, there was no surgical indication. There were no signs of haemorrhage in the fundi, and the EEG showed focal right anterior slow activity, and preventive treatment using phenobarbital was given to the patient. The infant’s clinical state worsened by the fourth day of hospitalisation, and a new CT-scan showed an increase of the haematoma. As a result, an emergency external drainage of the subdural space was performed (Fig. 2). His clinical state rapidly improved, and five days later, the drain was removed. Ten days after surgery, the child was discharged and sent home with an anti-epileptic treatment. Three months later, the infant was still doing fine, and the neurological exam showed no anomalies. However, the CT-scan revealed the presence of a suprasellar cyst, possibly linked to the third ventricle. A close-up surveillance was proposed. Seven months after trauma, an MRI showed an increase in the lesion size, which blocked the two interventricular foramen, causing hydrocephalus (Fig. 3A and B). The lesion had signal intensity
Fig. 2. CT-scan after subdural drainage. Scanner après drainage de l’hématome sous-dural.
comparable to that of cerebrospinal fluid on all the weightings. Therefore, we concluded that it was most likely an AC. The child rapidly underwent an endoscopic ventriculocystostomy (Fig. 4) allowing a slow decrease of the ventricular dilatation and the cyst
Fig. 3. A and B. Axial and sagittal T2-weighted MRI (seven months after the trauma), showing a suprasellar cyst with hydrocephalus by obstruction of both the interventricular foramen by the cyst. A et B. IRM en coupe axiale et sagittale, en séquence pondérée T2 (sept mois après le traumatisme), montrant un kyste suprasellaire avec une hydrocéphalie par blocage des deux foramen interventriculaires par le kyste.
M.-H. Sonnet et al. / Neurochirurgie 60 (2014) 55–58
57
size (Fig. 5). Twenty-two months later, the child had a normal neurocognitive development, and CT-scan showed a continuing decrease of both ventricular and cyst size (Fig. 6A and B). 3. Discussion
Fig. 4. Endoscopic view of the cyst obstructing the right interventricular foramen, before fenestration. Vue endoscopique du kyste obstruant le foramen interventriculaire droit, avant fenestration.
Fig. 5. Postoperative CT-scan after endoscopic treatment showing a slow decrease of the cyst. Scanner postopératoire, après traitement endoscopique, montrant une diminution lente du volume du kyste.
Different hypothesis have been proposed regarding the development of an AC. An historical hypothesis, reported by Robinson [11], suggested that ACs were due to agenesis of the brain structure, known as the temporal lobe agenesis syndrome. It has been shown, however, that there is no loss of brain tissue, and that these cysts are primarily a congenital disorder causing a subsequent brain displacement. In 1977, Contreras et al. were the first to link head trauma to AC [10]. Three years later, Fox and Al-Mefty described a case were they proposed that the cyst was an extension of the membrane of Liliequist, probably split by factors such as haemorrhage or infection [12]. Page and Robinson discussed the creation of arachnoid pockets containing cerebrospinal fluid (CSF), due to the post-traumatic oedema leading to the splitting of the arachnoid membrane [7]. Lesoin et al. argues, moreover, that these pockets contain blood, lysing and produce a hyperosmotic protein-rich environment, supporting by the fact “that in certain cases, red blood cells pigment deposits were found on the cyst wall membrane, and also that these cysts are found in the same anatomical locations as certain intracranial haematomas” [13]. Furthermore, Yanaka et al., in 1988, mentioned the role of inflammatory process as a mechanism of fluid-filling of the cyst [14]. In contrast, Choi and Kim reported microscopic findings of traumatic cysts biopsies, which where the same as congenital cysts. For these authors, head trauma could lead to abnormal splitting of the arachnoid endomeninx in infancy, a delicate period where cisterns are formed [9]. Pierre-Kahn et al. made a similar point of view: they observed that temporal subarachnoid spaces progressively regress in early childhood, so they hypothesised “that any peri- or postnatal event, such as haemorrhage or inflammatory process, could easily lead to the formation of a cyst by impeding this process of regression” [15]. In our case, the cyst developed soon after the trauma. Our hypothesis was that inflammatory process due to subdural haemorrhage, may locally lead to arachnoiditis, and thus to the creation of a neomembrane, and then to cyst formation (one could hypothesise that it is a close mechanism to the development of septas in ventricles during severe meningitis with the difference that they are leptomeningeal formations and not arachnoid formations). Then fluid-filling of the cyst may occur by a slit-valve mechanism,
Fig. 6. A and B. CT-scan one month after endoscopic treatment: decrease of both the ventricular dilatation and the cyst. A et B. Scanner cérébral réalisé un mois après le traitement endoscopique : diminution à la fois de la dilatation ventriculaire et du volume du kyste.
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M.-H. Sonnet et al. / Neurochirurgie 60 (2014) 55–58
as observed during endoscopic procedure [16,17], emphasised by the increased CSF pressure due to a possible pulsatile pump mechanism. An analogy can be made between the development of posttraumatic spinal AC and suprasellar AC. These cysts may occur after a direct injury of the arachnoid matter, due first to a dural tear [18,19], and then to the presence of blood involving arachnoiditis, despite the fact that in most cases they are extradural cysts, whereas intracranial cysts are intradural [1]. 4. Conclusion We present an exceptional case of suprasellar AC after subdural haemorrhage in an infant. These cases are seldom described in the literature. Our case supports the theory that inflammatory process (from bleeding) may be the first step to the development of AC. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article. References [1] Hanieh A, Simpson DA, North JB. Arachnoid cysts: a critical review of 41 cases. Childs Nerv Syst 1988;4(2):92–6. [2] Oberbauer RW, Haase J, Pucher R. Arachnoid cysts in children: a European cooperative study. Childs Nerv Syst 1992;8(5):281–6. [3] Al-Holou WN, Yew AY, Boomsaad ZE, Garton HJ, Muraszko KM, Maher CO. Prevalence and natural history of arachnoid cysts in children. J Neurosurg Pediatr 2010;5(6):578–85. [4] Kim BS, Illes J, Kaplan RT, Reiss A, Atlas SW. Incidental findings on pediatric MR images of the brain. AJNR Am J Neuroradiol 2002;23(10):1674–7.
[5] Bilginer B, Onal MB, Oguz KK, Akalan N. Arachnoid cyst associated with subdural hematoma: report of three cases and review of the literature. Childs Nerv Syst 2009;25(1):119–24. [6] Mori K, Yamamoto T, Horinaka N, Maeda M. Arachnoid cyst is a risk factor for chronic subdural hematoma in juveniles: twelve cases of chronic subdural hematoma associated with arachnoid cyst. J Neurotrauma 2002;19(9):1017–27. [7] Page A, Paxton RM, Mohan D. A reappraisal of the relationship between arachnoid cysts of the middle fossa and chronic subdural haematoma. J Neurol Neurosurg Psychiatry 1987;50(8):1001–7. [8] Parsch CS, Krauss J, Hofmann E, Meixensberger J, Roosen K. Arachnoid cysts associated with subdural hematomas and hygromas: analysis of 16 cases, long-term follow-up, and review of the literature. Neurosurgery 1997;40(3): 483–90. [9] Choi JU, Kim DS. Pathogenesis of arachnoid cyst: congenital or traumatic? Pediatr Neurosurg 1998;29(5):260–6. [10] Contreras C, Copty M, Langelier R, Gagne F. Traumatic suprasellar arachnoid cyst. Surg Neurol 1977;8(3):196–8. [11] Robinson RG. The temporal lobe agenesis syndrome. Brain 1964;87:87–106. [12] Fox JL, Al-Mefty O. Suprasellar arachnoid cysts: an extension of the membrane of Liliequist. Neurosurgery 1980;7(6):615–8. [13] Lesoin F, Dhellemmes P, Rousseaux M, Jomin M. Arachnoid cysts and head injury. Acta Neurochir (Wien) 1983;69(1–2):43–51. [14] Yanaka K, Enomoto T, Nose T, Maki Y. Post-inflammatory arachnoid cyst of the quadrigeminal cistern. Observation of development of the cyst. Childs Nerv Syst 1988;4(5):302–5. [15] Pierre-Kahn A, Hanlo P, Sonigo P, Parisot D, McConnell RS. The contribution of prenatal diagnosis to the understanding of malformative intracranial cysts: state of the art. Childs Nerv Syst 2000;16(10–11):619–26. [16] Schroeder HW, Gaab MR. Endoscopic observation of a slit-valve mechanism in a suprasellar prepontine arachnoid cyst: case report. Neurosurgery 1997;40(1):198–200. [17] Santamarta D, Aguas J, Ferrer E. The natural history of arachnoid cysts: endoscopic and cine-mode MRI evidence of a slit-valve mechanism. Minim Invasive Neurosurg 1995;38(4):133–7. [18] Rawlings 3rd CE, Nashold Jr BS. Traumatic extradural spinal cysts: a case report and review of the literature. Br J Neurosurg 1989;3(3):403–8. [19] Hernandez-Leon O, Perez-Nogueira FR, Corrales N. [Postraumatic epidural arachnoid spinal cyst: case report]. Neurocirugia (Astur) 2011;22(3): 267–70.
Disponible en ligne sur
ScienceDirect www.sciencedirect.com
Clinical case
Suprasellar arachnoid cyst after subdural haemorrhage in an infant. A case based update Kyste arachnoïdien suprasellaire après hématome sous-dural du nourrisson. Mise au point. À propos d’un cas M.-H. Sonnet , A. Joud , J.-C. Marchal , O. Klein ∗ Service de neurochirurgie pédiatrique, université de Lorraine, hôpital d’Enfants, CHU de Nancy, 4, rue du Morvan, 54500 Vandœuvre-lès-Nancy, France
a r t i c l e
i n f o
Article history: Received 23 October 2013 Accepted 4 January 2014 Available online 18 March 2014 Keywords: Suprasellar Arachnoid cyst Head trauma Subdural haemorrhage Paediatric neurosurgery
a b s t r a c t Introduction. – Brain arachnoid cysts (AC) are congenital or acquired malformations. Their prevalence in children ranges between 0.2 and 2.3% of the studied populations. Few reported studies exist where AC appears after a subdural haemorrhage. Methods. – We present one case of a symptomatic suprasellar AC after post-traumatic subdural haemorrhage in an infant. Results. – After endoscopic ventriculocystostomy, the child quickly improved and the cyst reduced in size. The child was monitored for 22 months and his neurocognitive development remained normal. Conclusion. – Our case led us to the hypothesis that the inflammatory process due to subdural haemorrhage may locally result in arachnoiditis, and thus to the creation of a neomembrane, and eventually to cyst formation. This is also the case with the development of post-traumatic spinal AC. © 2014 Elsevier Masson SAS. All rights reserved.
r é s u m é Mots clés : Suprasellaire Kyste arachnoïdien Traumatisme crânien Hématome sous-dural Neurochirurgie pédiatrique
Introduction. – Les kystes arachnoïdiens (KA) cérébraux sont des malformations congénitales ou acquises. Leur prévalence chez l’enfant se situe entre 0,2 et 2,3 % des populations étudiées. Il existe peu d’études mentionnant l’apparition d’un KA dans les suites d’une hémorragie sous-durale. Méthodes. – Nous rapportons le cas d’un KA suprasellaire symptomatique faisant suite à un hématome sous-dural du nourrisson. Résultats. – L’état clinique de l’enfant s’est rapidement amélioré après ventriculo kystostomie endoscopique et le kyste a diminué de taille. L’enfant est suivi depuis 22 mois et son développement neurocognitif est normal. Conclusion. – Notre cas conduit à l’hypothèse qu’un phénomène inflammatoire dû à un hématome sousdural peut aboutir localement à une arachnoïdite et ainsi à la création d’une néomembrane et donc à la formation du kyste. Cela est déjà le cas pour le développement des KA spinaux post-traumatiques. © 2014 Elsevier Masson SAS. Tous droits réservés.
1. Background Arachnoid cysts (AC) are congenital [1] or acquired malformations [2]. Recent findings regarding their prevalence in children (all type of cysts, whether symptomatic or not) range between 0.2
∗ Corresponding author. E-mail addresses: [email protected], [email protected] (O. Klein). 0028-3770/$ – see front matter © 2014 Elsevier Masson SAS. All rights reserved. http://dx.doi.org/10.1016/j.neuchi.2014.01.003
and 2.3% of the studied populations [3,4] certainly increasing due to more accurate indications of neuroradiological explorations. The association between AC and subdural haematoma is well known and numerous cases have been described where subdural effusion complicates AC [5–8]. However, very few studies exist where AC appears after a subdural haemorrhage [9,10], as in the case described in our case report. Hopefully, this case will bring new insights regarding AC pathogenesis, where there still remains controversies.
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M.-H. Sonnet et al. / Neurochirurgie 60 (2014) 55–58
Fig. 1. A and B. The first CT-scan showing a subdural haematoma and parietal fracture. A et B. Premier scanner montrant un hématome sous-dural et une fracture pariétale.
2. Illustrative case We report the case of a two-month-old baby who slipped from his mother’s arms and fell down the stairs. Upon arrival at the emergency unit, the child was asleep and difficult to wake-up; he lost consciousness but recovered after two thoracic compressions. The physical examination did not show any focal neurologic signs. The infant presented with frontal and parietal bruises. An emergency CT-scan revealed a bilateral frontal subdural hematoma with acute bifrontal, bitemporal, and left parietal bleeding associated with a left parietal fracture (Fig. 1A and B). Initially, there was no surgical indication. There were no signs of haemorrhage in the fundi, and the EEG showed focal right anterior slow activity, and preventive treatment using phenobarbital was given to the patient. The infant’s clinical state worsened by the fourth day of hospitalisation, and a new CT-scan showed an increase of the haematoma. As a result, an emergency external drainage of the subdural space was performed (Fig. 2). His clinical state rapidly improved, and five days later, the drain was removed. Ten days after surgery, the child was discharged and sent home with an anti-epileptic treatment. Three months later, the infant was still doing fine, and the neurological exam showed no anomalies. However, the CT-scan revealed the presence of a suprasellar cyst, possibly linked to the third ventricle. A close-up surveillance was proposed. Seven months after trauma, an MRI showed an increase in the lesion size, which blocked the two interventricular foramen, causing hydrocephalus (Fig. 3A and B). The lesion had signal intensity
Fig. 2. CT-scan after subdural drainage. Scanner après drainage de l’hématome sous-dural.
comparable to that of cerebrospinal fluid on all the weightings. Therefore, we concluded that it was most likely an AC. The child rapidly underwent an endoscopic ventriculocystostomy (Fig. 4) allowing a slow decrease of the ventricular dilatation and the cyst
Fig. 3. A and B. Axial and sagittal T2-weighted MRI (seven months after the trauma), showing a suprasellar cyst with hydrocephalus by obstruction of both the interventricular foramen by the cyst. A et B. IRM en coupe axiale et sagittale, en séquence pondérée T2 (sept mois après le traumatisme), montrant un kyste suprasellaire avec une hydrocéphalie par blocage des deux foramen interventriculaires par le kyste.
M.-H. Sonnet et al. / Neurochirurgie 60 (2014) 55–58
57
size (Fig. 5). Twenty-two months later, the child had a normal neurocognitive development, and CT-scan showed a continuing decrease of both ventricular and cyst size (Fig. 6A and B). 3. Discussion
Fig. 4. Endoscopic view of the cyst obstructing the right interventricular foramen, before fenestration. Vue endoscopique du kyste obstruant le foramen interventriculaire droit, avant fenestration.
Fig. 5. Postoperative CT-scan after endoscopic treatment showing a slow decrease of the cyst. Scanner postopératoire, après traitement endoscopique, montrant une diminution lente du volume du kyste.
Different hypothesis have been proposed regarding the development of an AC. An historical hypothesis, reported by Robinson [11], suggested that ACs were due to agenesis of the brain structure, known as the temporal lobe agenesis syndrome. It has been shown, however, that there is no loss of brain tissue, and that these cysts are primarily a congenital disorder causing a subsequent brain displacement. In 1977, Contreras et al. were the first to link head trauma to AC [10]. Three years later, Fox and Al-Mefty described a case were they proposed that the cyst was an extension of the membrane of Liliequist, probably split by factors such as haemorrhage or infection [12]. Page and Robinson discussed the creation of arachnoid pockets containing cerebrospinal fluid (CSF), due to the post-traumatic oedema leading to the splitting of the arachnoid membrane [7]. Lesoin et al. argues, moreover, that these pockets contain blood, lysing and produce a hyperosmotic protein-rich environment, supporting by the fact “that in certain cases, red blood cells pigment deposits were found on the cyst wall membrane, and also that these cysts are found in the same anatomical locations as certain intracranial haematomas” [13]. Furthermore, Yanaka et al., in 1988, mentioned the role of inflammatory process as a mechanism of fluid-filling of the cyst [14]. In contrast, Choi and Kim reported microscopic findings of traumatic cysts biopsies, which where the same as congenital cysts. For these authors, head trauma could lead to abnormal splitting of the arachnoid endomeninx in infancy, a delicate period where cisterns are formed [9]. Pierre-Kahn et al. made a similar point of view: they observed that temporal subarachnoid spaces progressively regress in early childhood, so they hypothesised “that any peri- or postnatal event, such as haemorrhage or inflammatory process, could easily lead to the formation of a cyst by impeding this process of regression” [15]. In our case, the cyst developed soon after the trauma. Our hypothesis was that inflammatory process due to subdural haemorrhage, may locally lead to arachnoiditis, and thus to the creation of a neomembrane, and then to cyst formation (one could hypothesise that it is a close mechanism to the development of septas in ventricles during severe meningitis with the difference that they are leptomeningeal formations and not arachnoid formations). Then fluid-filling of the cyst may occur by a slit-valve mechanism,
Fig. 6. A and B. CT-scan one month after endoscopic treatment: decrease of both the ventricular dilatation and the cyst. A et B. Scanner cérébral réalisé un mois après le traitement endoscopique : diminution à la fois de la dilatation ventriculaire et du volume du kyste.
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M.-H. Sonnet et al. / Neurochirurgie 60 (2014) 55–58
as observed during endoscopic procedure [16,17], emphasised by the increased CSF pressure due to a possible pulsatile pump mechanism. An analogy can be made between the development of posttraumatic spinal AC and suprasellar AC. These cysts may occur after a direct injury of the arachnoid matter, due first to a dural tear [18,19], and then to the presence of blood involving arachnoiditis, despite the fact that in most cases they are extradural cysts, whereas intracranial cysts are intradural [1]. 4. Conclusion We present an exceptional case of suprasellar AC after subdural haemorrhage in an infant. These cases are seldom described in the literature. Our case supports the theory that inflammatory process (from bleeding) may be the first step to the development of AC. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article. References [1] Hanieh A, Simpson DA, North JB. Arachnoid cysts: a critical review of 41 cases. Childs Nerv Syst 1988;4(2):92–6. [2] Oberbauer RW, Haase J, Pucher R. Arachnoid cysts in children: a European cooperative study. Childs Nerv Syst 1992;8(5):281–6. [3] Al-Holou WN, Yew AY, Boomsaad ZE, Garton HJ, Muraszko KM, Maher CO. Prevalence and natural history of arachnoid cysts in children. J Neurosurg Pediatr 2010;5(6):578–85. [4] Kim BS, Illes J, Kaplan RT, Reiss A, Atlas SW. Incidental findings on pediatric MR images of the brain. AJNR Am J Neuroradiol 2002;23(10):1674–7.
[5] Bilginer B, Onal MB, Oguz KK, Akalan N. Arachnoid cyst associated with subdural hematoma: report of three cases and review of the literature. Childs Nerv Syst 2009;25(1):119–24. [6] Mori K, Yamamoto T, Horinaka N, Maeda M. Arachnoid cyst is a risk factor for chronic subdural hematoma in juveniles: twelve cases of chronic subdural hematoma associated with arachnoid cyst. J Neurotrauma 2002;19(9):1017–27. [7] Page A, Paxton RM, Mohan D. A reappraisal of the relationship between arachnoid cysts of the middle fossa and chronic subdural haematoma. J Neurol Neurosurg Psychiatry 1987;50(8):1001–7. [8] Parsch CS, Krauss J, Hofmann E, Meixensberger J, Roosen K. Arachnoid cysts associated with subdural hematomas and hygromas: analysis of 16 cases, long-term follow-up, and review of the literature. Neurosurgery 1997;40(3): 483–90. [9] Choi JU, Kim DS. Pathogenesis of arachnoid cyst: congenital or traumatic? Pediatr Neurosurg 1998;29(5):260–6. [10] Contreras C, Copty M, Langelier R, Gagne F. Traumatic suprasellar arachnoid cyst. Surg Neurol 1977;8(3):196–8. [11] Robinson RG. The temporal lobe agenesis syndrome. Brain 1964;87:87–106. [12] Fox JL, Al-Mefty O. Suprasellar arachnoid cysts: an extension of the membrane of Liliequist. Neurosurgery 1980;7(6):615–8. [13] Lesoin F, Dhellemmes P, Rousseaux M, Jomin M. Arachnoid cysts and head injury. Acta Neurochir (Wien) 1983;69(1–2):43–51. [14] Yanaka K, Enomoto T, Nose T, Maki Y. Post-inflammatory arachnoid cyst of the quadrigeminal cistern. Observation of development of the cyst. Childs Nerv Syst 1988;4(5):302–5. [15] Pierre-Kahn A, Hanlo P, Sonigo P, Parisot D, McConnell RS. The contribution of prenatal diagnosis to the understanding of malformative intracranial cysts: state of the art. Childs Nerv Syst 2000;16(10–11):619–26. [16] Schroeder HW, Gaab MR. Endoscopic observation of a slit-valve mechanism in a suprasellar prepontine arachnoid cyst: case report. Neurosurgery 1997;40(1):198–200. [17] Santamarta D, Aguas J, Ferrer E. The natural history of arachnoid cysts: endoscopic and cine-mode MRI evidence of a slit-valve mechanism. Minim Invasive Neurosurg 1995;38(4):133–7. [18] Rawlings 3rd CE, Nashold Jr BS. Traumatic extradural spinal cysts: a case report and review of the literature. Br J Neurosurg 1989;3(3):403–8. [19] Hernandez-Leon O, Perez-Nogueira FR, Corrales N. [Postraumatic epidural arachnoid spinal cyst: case report]. Neurocirugia (Astur) 2011;22(3): 267–70.
