Intracranial aneurysm pathogenesis

Intracranial aneurysm pathogenesis

Until now, the exact etiology of intracranial aneurysms formation remains unclear.

Time-dependent and site-dependent morphological changes and the level of degradation molecules may be indicative of the vulnerability of aneurysm rupture 1).

Miyata et al. proposed the contribution of a structural change in an adventitia, i.e., vasa vasorum formation, to the rupture of IAs 2).

Intracranial aneurysm risk factors.

see Intracranial aneurysm genetics.

see Intracranial aneurysm pathophysiology.

see Intracranial aneurysm hemodynamics.

In addition to ambiental factors (smoking, excessive alcohol consumption and hypertension), epidemiological studies have demonstrated a familiar influence contributing to the pathogenesis of intracranial aneurysms, with increased frequency in first- and second-degree relatives of people with subarachnoid hemorrhage.

Data suggest that macrophage-derived Matrix metalloproteinase 2 and Matrix metalloproteinase 9, may play an important role in the progression of intracranial aneurysms. The findings will shed a new light into the pathogenesis of cerebral aneurysms and highlight the importance of inflammatory response causing the degeneration of extracellular matrix in the process of this disease 3).

Investigations strongly suggest that the pathophysiology is closely associated with chronic inflammation in vascular walls. Nuclear factor kappaB (NF-kappaB) has a key role in the formation and progression.

Children with Sickle Cell Disease (SCD) are at risk for developing multiple intracranial aneurysms, and a high index of suspicion must be maintained during the interpretation of routine magnetic resonance imaging or angiography of the brain 4).

Dental bacterial DNA can be found using a quantitative polymerase chain reaction in both ruptured and unruptured aneurysm walls, suggesting that bacterial DNA plays a role in the pathogenesis of cerebral aneurysms in general, rather than only in ruptured aneurysms 5).

Thrombospondin type-1 domain-containing protein 1 is a protein that in humans is encoded by the THSD1 gene.

The protein encoded by this gene contains a type 1 thrombospondin domain, which is found in thrombospondin, a number of proteins involved in the complement pathway, as well as extracellular matrix proteins. Alternatively spliced transcript variants encoding distinct isoforms have been observed.

As illustrated by THSD1 research, cell adhesion may play a significant role in IA 6).

A study discovered that harmful variants in THSD1 (Thrombospondin type-1 domain-containing protein 1) likely cause intracranial aneurysm and subarachnoid hemorrhage in a subset of both familial and sporadic patients with supporting evidence from two vertebrate models 7).

A report identified THSD1 mutations in familial and sporadic IA patients and shows that THSD1 loss results in cerebral bleeding in 2 animal models. This finding provides new insight into IA and subarachnoid hemorrhage pathogenesis and provides new understanding of THSD1 function, which includes endothelial cell to extracellular matrix adhesion 8).

Toll‑like receptor (TLR) 2/4 serves an important regulatory role in nerve tissue injury. However, the downstream and potential mechanisms remain to be elucidated. The present study was designed to investigate the roles of the TLR2/4‑major myeloid differentiation response gene 88 (MyD88)‑NF‑κB signaling pathway in the development of an intracranial aneurysm. The expression of TLR2, TLR4, and MyD88 in the blood of normal controls and patients with intracranial aneurysms were detected by quantitative PCR and ELISA. Human brain vascular smooth muscle cells were treated by Angiotensin II (Ang II) to evaluate the involvement of the TLR2/4‑MyD88‑NF‑κB signaling pathway in the process. The in vitro experiment was divided into four groups: The control group, an Ang Ⅱ group, an Ang Ⅱ + small interfering (si)RNA control group, and an Ang Ⅱ + TLR2‑group. Cell viability, migration, apoptosis, and expression of TLR2, TLR4, MyD88, NF‑κB, and phosphorylated (p‑)p65 expression was detected. The results demonstrated that the expression of TLR2, TLR4, MyD88, and NF‑κB at mRNA and protein levels in patients with an intracranial aneurysm was significantly higher compared with corresponding protein in normal controls (P&lt;0.05). <em>In vitro</em> experiments demonstrated that Ang Ⅱ treatment increased the cell proliferation and migration rate but reduced the apoptotic rate compared with the control (P&lt;0.05). The expression of TLR2, TLR4, MyD88, NF‑κB, and p‑p65 was significantly increased in the Ang II group (vs. control; P&lt;0.05). By contrast, TLR2‑short interfering RNA reduced the cell proliferation and migration rate and reduced the expression of TLR2, TLR4, MyD88, NF‑κB, and p‑p65 (vs. Ang Ⅱ + short interfering RNA control; P&lt;0.05). In conclusion, the data of the present study indicated that the TLR2/4‑MyD88‑NF‑κB signaling pathway is involved in the intracranial aneurysm pathogenesis 9).


1)

Yamaguchi T, Miyamoto T, Kitazato KT, Shikata E, Yamaguchi I, Korai M, Shimada K, Yagi K, Tada Y, Matsuzaki Y, Kanematsu Y, Takagi Y. Time-dependent and site-dependent morphological changes in rupture-prone arteries: ovariectomized rat intracranial aneurysm model. J Neurosurg. 2019 Sep 13:1-9. doi: 10.3171/2019.6.JNS19777. [Epub ahead of print] PubMed PMID: 31518986.
2)

Miyata H, Imai H, Koseki H, Shimizu K, Abekura Y, Oka M, Kawamata T, Matsuda T, Nozaki K, Narumiya S, Aoki T. Vasa vasorum formation is associated with rupture of intracranial aneurysms. J Neurosurg. 2019 Aug 16:1-11. doi: 10.3171/2019.5.JNS19405. [Epub ahead of print] PubMed PMID: 31419795.
3)

Aoki T, Kataoka H, Morimoto M, Nozaki K, Hashimoto N. Macrophage-derived matrix metalloproteinase-2 and -9 promote the progression of cerebral aneurysms in rats. Stroke. 2007 Jan;38(1):162-9. Epub 2006 Nov 22. PubMed PMID: 17122420.
4)

Saini S, Speller-Brown B, Wyse E, Meier ER, Carpenter J, Fasano RM, Pearl MS. Unruptured Intracranial Aneurysms in Children With Sickle Cell Disease: Analysis of 18 Aneurysms in 5 Patients. Neurosurgery. 2015 Feb 12. [Epub ahead of print] PubMed PMID: 25710108.
5)

Pyysalo MJ, Pyysalo LM, Pessi T, Karhunen PJ, Lehtimäki T, Oksala N, Öhman JE. Bacterial DNA findings in ruptured and unruptured intracranial aneurysms. Acta Odontol Scand. 2016 May;74(4):315-20. doi: 10.3109/00016357.2015.1130854. Epub 2016 Jan 18. PubMed PMID: 26777430.
6)

Xu Z, Rui YN, Hagan JP, Kim DH. Intracranial Aneurysms: Pathology, Genetics, and Molecular Mechanisms. Neuromolecular Med. 2019 May 4. doi: 10.1007/s12017-019-08537-7. [Epub ahead of print] Review. PubMed PMID: 31055715.
7)

Rui YN, Xu Z, Fang X, Menezes MR, Balzeau J, Niu A, Hagan JP, Kim DH. The Intracranial Aneurysm Gene THSD1 Connects Endosome Dynamics to Nascent Focal Adhesion Assembly. Cell Physiol Biochem. 2017;43(6):2200-2211. doi: 10.1159/000484298. Epub 2017 Oct 25. PubMed PMID: 29069646.
8)

Santiago-Sim T, Fang X, Hennessy ML, Nalbach SV, DePalma SR, Lee MS, Greenway SC, McDonough B, Hergenroeder GW, Patek KJ, Colosimo SM, Qualmann KJ, Hagan JP, Milewicz DM, MacRae CA, Dymecki SM, Seidman CE, Seidman JG, Kim DH. THSD1 (Thrombospondin Type 1 Domain Containing Protein 1) Mutation in the Pathogenesis of Intracranial Aneurysm and Subarachnoid Hemorrhage. Stroke. 2016 Dec;47(12):3005-3013. Epub 2016 Nov 15. Erratum in: Stroke. 2017 Aug;48(8):e240. PubMed PMID: 27895300; PubMed Central PMCID: PMC5134902.
9)

Zhang X, Wan Y, Feng J, Li M, Jiang Z. Involvement of TLR2/4‑MyD88‑NF‑κB signaling pathway in the pathogenesis of intracranial aneurysm. Mol Med Rep. 2021 Jan 26. doi: 10.3892/mmr.2021.11869. Epub ahead of print. PMID: 33655339.

Pituitary Surgery During Covid-19

Pituitary Surgery During Covid-19

see Precautions for endoscopic transnasal skull base surgery during the COVID-19 pandemic


During the Covid-19 pandemic, every hospital has had to change its internal organization. The nature of the transsphenoidal corridor exposes the pituitary surgery team to an increased risk of virus exposure 1).

It was reported that the aerosolization and mucosal involvement increase the risk of viral transmission during operation. Therefore, transcranial is a safer surgical approach during the COVID-19 pandemic.

Nine cases of pituitary adenomas have presented with urgent manifestations. The endoscopic endonasal approach was performed in eight patients, while a craniotomy was selected for a recurrent pituitary adenoma. Pre- and postoperative thorough clinical evaluations with chest CT scans were performed. Other strict infection control measures have been applied.

In 8 weeks duration starting from the past days of February 2020, we have operated on four females and five males of pituitary adenomas. Visual deterioration was the main presenting symptom. The driving factor for surgery was saving vision in eight patients. Fortunately, the postoperative course was uneventful for all patients. No suspected COVID-19 infection has been reported in any patient or health-care team except one patient. In our city, PCR test was routinely not available 2).


A retrospective cohort study was conducted of all patients who underwent high-priority endoscopic nasal surgery or anterior skull base surgery between 23rd March and 15th June 2020 at University Hospitals Birmingham NHS Trust.

Twenty-four patients underwent endonasal surgery during the study period, 12 were males and 12 were females. There was no coronavirus-related morbidity in any patient.

This observational study found that it is possible to safely undertake urgent endonasal surgery; the nosocomial risk of coronavirus disease 2019 can be mitigated with appropriate peri-operative precautions 3).

A 21-year old male, who required urgent surgery because of progressive visual disturbance due to giant pituitary adenoma. On brain MRI with contrast, it was revealed an extra-axial tumor extending anteriorly over planum sphenoidal with the greatest diameter was 5.34 cm. A transcranial approach was chosen to resect the tumor. Near-total removal of the tumor was achieved without damaging the vital neurovascular structure. The visual acuity was improved and no significant postoperative complication. Pathology examination revealed pituitary adenoma.

Transcranial surgery for pituitary adenoma is still an armamentarium in neurosurgical practice, especially in the COVID-19 pandemic to provide a safer surgical approach 4).


The goal of a paper of Penner et al. is to illustrate the feasibility of pituitary region surgery during the SARS-CoV-2 pandemic.

After two negative COVID tests were obtained, three patients with macro GH-secreting tumors, and two patients with micro ACTH-secreting tumors resistant to medical treatment underwent surgery during the pandemic. During the surgery, every patient was treated as if they were positive.

Neither operator nor patient has developed COVID symptoms. The two neurosurgeons performing the operations underwent two COVID swabs, which resulted in negative.

Pituitary surgery is high-risk non-urgent surgery. However, the method described has so far been effective and is safe for both patients and healthcare providers 5).


The impact of COVID-19 on pituitary surgery. ANZ J Surg. 2020 Apr 25. doi: 10.1111/ans.15959. [Epub ahead of print] PubMed PMID: 32336017 6).


A 47-year-old male COVID-19 positive patient presented to the Emergency Department with a left frontal headache that culminated with diplopia, left eye ptosis, and left visual acuity loss after 5 days. Transsphenoidal hypophysectomy was uneventfully performed, and the patient was discharged from the hospital on postoperative day four. It additionally describes in detail the University of Mississippi Medical Center airway management algorithm for patients infected with the novel coronavirus who need emergent surgical attention 7).


A 72-year-old woman who required urgent endonasal transsphenoidal surgery (eTSS) because of progressive visual field disturbance due to pituitary adenoma, in whom we conducted reverse-transcriptase-polymerase-chain-reaction (RT-PCR) for COVID-19 and chest CT before eTSS. We took care of her by following the rule for suspected infection patient and safely completed her treatment without medical staff infection. Under COVID-19 pandemic state, essentially careful management including RT-PCR test and chest CT should be taken for the high infection risk surgeries to avoid the outbreak through the hospital. And the cost of the RT-PCR test for the patients should be covered by the government budget 8).


1)

Quillin JW, Oyesiku NM. Status of Pituitary Surgery During the COVID-19 Pandemic. Neurol India. 2020 May-Jun;68(Supplement):S134-S136. doi: 10.4103/0028-3886.287685. PMID: 32611904.
2)

Arnaout MM, Bessar AA, Elnashar I, Abaza H, Makia M. Pituitary adenoma surgeries in COVID-19 era: Early local experience from Egypt. Surg Neurol Int. 2020 Oct 29;11:363. doi: 10.25259/SNI_472_2020. PMID: 33194296; PMCID: PMC7655998.
3)

Naik PP, Tsermoulas G, Paluzzi A, McClelland L, Ahmed SK. Endonasal surgery in the coronavirus era – Birmingham experience. J Laryngol Otol. 2020 Nov 4:1-4. doi: 10.1017/S0022215120002364. Epub ahead of print. PMID: 33143753; PMCID: PMC7729149.
4)

Golden N, Niryana W, Awyono S, Eka Mardhika P, Bhuwana Putra M, Stefanus Biondi M. Transcranial approach as surgical treatment for giant pituitary adenoma during COVID 19 pandemic – What can we learn?: A case report. Interdiscip Neurosurg. 2021 Feb 25:101153. doi: 10.1016/j.inat.2021.101153. Epub ahead of print. PMID: 33654658; PMCID: PMC7906516.
5)

Penner F, Grottoli S, Lanotte MMR, Garbossa D, Zenga F. Pituitary surgery during Covid-19: a first-hand experience and evaluation [published online ahead of print, 2020 Jul 10]. J Endocrinol Invest. 2020;10.1007/s40618-020-01354-x. doi:10.1007/s40618-020-01354-x
6)

Mitchell RA, King JA, Goldschlager T, Wang YY. The impact of COVID-19 on pituitary surgery. ANZ J Surg. 2020 Apr 25. doi: 10.1111/ans.15959. [Epub ahead of print] PubMed PMID: 32336017.
7)

Santos CDSE, Filho LMDCL, Santos CAT, Neill JS, Vale HF, Kurnutala LN. Pituitary tumor resection in a patient with SARS-CoV-2 (COVID-19) infection. A case report and suggested airway management guidelines. Braz J Anesthesiol. 2020 Mar-Apr;70(2):165-170. doi: 10.1016/j.bjane.2020.05.003. Epub 2020 Jun 10. PMID: 32834194; PMCID: PMC7283047.
8)

Akai T, Maruyama K, Takakura H, Yamamoto Y, Morinaga Y, Kuroda S. Safety management in urgent endonasal trans-sphenoidal surgery for pituitary adenoma during the COVID-19 pandemic in Japan – A case report. Interdiscip Neurosurg. 2020 Dec;22:100820. doi: 10.1016/j.inat.2020.100820. Epub 2020 Jul 10. PMID: 32835016; PMCID: PMC7347482.

Posttraumatic leptomeningeal cyst

Posttraumatic leptomeningeal cyst

Posttraumatic leptomeningeal cysts (PTLMC) (sometimes just traumatic leptomeningeal cysts), AKA growing skull fractures consists of a fracture line that widens with time.

The term cyst is actually a misnomer, as it is not a cyst, but an extension of the encephalomalacia 1).

Posttraumatic leptomeningeal cysts were first described in 18162).

Very rare, occurring in 0.05–0.6% of skull fracture3) 4). Usually requires both a widely separated fracture AND a dural tear.

Mean age at injury: < 1 year; over 90% occur before age 3 years 5) (formation may require the presence of a rapidly growing brain 6)), although rare adult cases have been described 7)8) 9) (a total of 5 cases in the literature as of 1998 10)).

The pathophysiology and some aspects of its management are still controversial.

It is thought they occur secondary to skull fractures causing dural tears allowing the leptomeninges and/or cerebral parenchyma to herniate into it

Pulsations from CSF erode the fracture margin, resulting in eventual expansion and non-union.

It occurs due to a wide skull defect with underlying dural defect and changes in pressure gradients within the skull cavity. Neglected cases may develop progressive neurological deficits and complications after second head trauma 11).

Enlarging scalp mass

Seizures

Focal neurological deficit

Headache

Most often presents as scalp mass (usually subgaleal), although there are reports of presentation with head pain alone 12).

Kitumba and Mascarenhas presented a rare case of an adult with excruciating headache secondary to a post-traumatic fronto-orbital leptomeningeal cyst 13)

PTLMCs rarely occur > 6 mos out from the injury. Some children may develop a skull fracture that seems to grow during the initial few weeks that is not accompanied by a subgaleal mass, and that heals spontaneously within several months; the term “pseudogrowing fracture” has been suggested for these 14).

They can rupture and cause diffuse subgaleal CSF collection 15).

Radiographic findings: progressive widening of fracture and scalloping (or saucering) of edges.

round or oval lucency with smooth margins

CT scan is the modality of choice for the evaluation of leptomeningeal cyst. It consists of a lytic calvarial lesion with scalloped edges, in which encephalomalacia invaginates. The following features may also be present

extracranial brain herniation

hydrocephalus

unilateral ventricular dilatation

porencephalic cyst.

Guler I, Buyukterzi M, Oner O, Tolu I. Post-traumatic leptomeningeal cyst in a child: computed tomography and magnetic resonance imaging findings. J Emerg Med. 2015 May;48(5):e121-2. doi: 10.1016/j.jemermed.2014.12.042. Epub 2015 Feb 3. PMID: 25662419.

Not to be confused with arachnoid cysts (AKA leptomeningeal cysts, which are not posttraumatic).

Posttraumatic intradiploic leptomeningeal cyst.

Skull tumor 16).

eosinophilic granuloma

calvarial metastases

epidermoid cyst

osteomyelitis

congenital calvarial defect

Although usually asymptomatic, the cyst may cause a mass effect with neurologic deficit.

Distal cortical artery aneurysms: often associated with an overlying s skull fracture, sometimes a growing skull fracture


Neglected GSF can rupture and cause diffuse subgaleal CSF collection 17).

If early growth of a fracture line with no subgaleal mass is noted, repeat skull films in 1–2 months before operating (to rule out pseudogrowing fracture). In young patients with separated skull fractures (the width of the initial fracture is rarely mentioned), consider obtaining follow-up skull film 6–12 mos post-trauma. However, since most PTLMCs are brought to medical attention when the palpable mass is noticed, routine follow-up X-rays may not be cost-effective.

Treatment of true PTLMC is surgical, with dural closure mandatory. Since the dural defect is usually larger than the bony defect, it may be advantageous to perform a craniotomy around the fracture site, repair the dural defect, and replace the bone 18).

The dural substitutes used are either autografts (which may not be enough) or artificial grafts (which are foreign-body implantations and which also may be too expensive in a low-resource practice).

Adeleye presented the surgical description of the use of the cyst capsule as a cost-free autologous graft in the surgical repair of the dural defects of two cases of traumatic leptomeningeal cyst 19).

Pseudogrowing fractures should be followed with X- rays and operated only if expansion persists beyond several months or if a subgaleal mass is present.

Liu et al. performed a retrospective review of 27 patients with GSF, who were grouped according to 3 different GSF stages.

Over a period of 20 years, 27 patients with GSF (16 males and 11 females) were treated in the authors’ department. The mean follow-up period was 26.5 months. Six patients were in the pre-phase of GSF (Stage 1), 10 patients in the early phase (Stage 2), and 11 in the late phase (Stage 3). All patients underwent duraplasty. All 6 patients at Stage 1 and 5 patients at Stage 2 underwent craniotomy without cranioplasty. Five patients at Stage 2 and all of the patients at Stage 3 underwent cranioplasty with autologous bone and alloplastic materials, respectively. Among all patients, 5 underwent ventriculoperitoneal shunt placement. Symptoms in all patients at Stages 1 and 2 were alleviated or disappeared, and the cranial bones developed without deformity during follow-up. Among patients with Stage 3 GSF, no obvious improvement in neurological deficits was observed. Three patients underwent additional operations because of cranial deformation or infection.

The authors identify the stages of GSF according to a new hypothesis. They conclude that accurately diagnosing and treating GSF during Stages 1 and 2 leads to a better prognosis 20)

Kulkarni et al. presented a 14-year-old child who developed sudden-onset, diffuse, soft, fluctuant, circumferential swelling of the head after a road traffic accident. He had sustained a head injury at the age of 3-months leading to an asymptomatic soft swelling over the skull which was left untreated. The present CT scan of the brain showed a bony defect with ragged edges and cerebrospinal fluid (CSF) collection in subgaleal space circumferentially. He underwent exploration, duroplasty, and cranioplasty and had a good outcome.

Neglected GSF can rupture and cause diffuse subgaleal CSF collection. It should be managed with dural repair and cranioplasty 21).

Kitumba D, Mascarenhas L. Rare case of an adult with excruciating headache secondary to post-traumatic fronto-orbital leptomeningeal cyst. Neurochirurgie. 2020 Nov;66(5):410-411. doi: 10.1016/j.neuchi.2020.06.126. Epub 2020 Aug 7. PMID: 32777233 22).


A 4-year-old boy was brought to the emergency department after suffering from head trauma caused by a fall from a rooftop where he was treated conservatively at a local hospital. Later, he developed swelling in the occipital region and was brought to the department of neurosurgery where he was operated on. After the first surgery, recurrence of swelling was seen after a postoperative period of 2 months, and a computed tomography scan reported persistent epidural hygroma with extension into the subcutaneous space. The second surgery was performed, and a 12-month follow-up did not show any recurrence of swelling in the patient 23).

A full-term infant born after a nontraumatic, forceps-assisted spontaneous delivery, who developed an increasing cystic swelling over the left frontoparietal area that crossed over coronal and sagittal sutures. The lesion was initially misinterpreted as cephalhematoma. Clinical and radiological follow-up established the correct diagnosis of leptomeningeal cyst.

The collection was initially tapped. Surgical treatment was undertaken thereafter, consisting of decompression and resection of the cyst and dural repair. Two months after follow-up, the patient remains asymptomatic and the porencephalic cavity remains isolated from the extradural space, with no evidence of new fluid collections 24).

A 53-year-old female presented with a post-traumatic leptomeningeal cyst manifesting as bulging of the scalp, dizziness, and tinnitus. She had known of the bulging of her forehead for about 20 years. She had suffered an injury to the head in childhood. Brain CT revealed a bone cyst associated with a round bone defect in the left frontal bone, bulging of the very thin outer layer, and the defective inner layer. She was treated surgically with a diagnosis of a skull tumor, but only gray cystic membranous tissue was found. The dural defect was repaired with fascia and the bone defect with bone cement. Bulging of the skull in adults can be caused by a bone cyst originating from a skull fracture 25).

12 patients diagnosed and treated between 1980 and 2002. 11 patients were under the age of 3 years and one patient was 5 years old at the moment of HI. The most common cause of injury was a fall from height. In the initial plain x-rayfilms, 11 patients showed a diastatic skull fracture and one patient only had a linear fracture. At this time, CT scan showed cortical contussion underlying the fracture in every case. The mean time between injury and presentation of GSF was 11.6 weeks. Diagnosis was made by palpation of the cranial defect and confirmed with skull x-rayfilms. The most frecuent location of GSF was in the parietal region. Associated lesions like hydrocephalus, encephalomalacia, leptomenigeal cysts, brain tissue herniation and ipsilateral ventricular dilatation, were found in the preoperative CT or MRI. All patients underwent a dural repair with pericranium or fascia lata. The cranial defect was covered with local calvarial bone fragments in every case. Only one patient needed a cranioplasty with titanium mesh. Every child with a skull fracture must be followed until the fracture heals. Patients under the age of 3 years with a diastatic fracture and a dural tear, demostrated by TC or MRI, are more prone to develop GSF. In these cases, early repair must be adviced in order to prevent progressive brain damage 26).

A growing skull fracture associated with cerebrospinal fluid rhinorrhoea following trauma sustained in adult life. The natural history of its development, diagnosis, and the results of surgery are discussed. The literature is reviewed with regard to aetiology, incidence, imaging characteristics and management of this rare post-traumatic complication 27).

A lump in the right parietal region of this 53-year-old man prompted a computed tomography (CT) scan. The patient denied any symptoms and was in good health. The examination confirmed a firm, non-tender, non-pulsatile mass in the right parietal region of the skull. The CT scan demonstrated a 4 x 3 cm area of irregular bone destruction involving both the inner and outer table of the skull. At operation a distinctly raised paper-thin outer table was noted, and underneath was a soft, tan-colored mass, which measured approximately 2 x 2 cm and was connected to the underlying brain through a 1 cm dural defect. The extradural portion of the mass was amputated, the dura repaired with a pericranium patch, the skull defect was repaired with a split-thickness bone graft, and the final pathology was congruent with a gliotic brain 28).

Meloche BR, Sansregret A, Grégoire H, Gagnon J, Massicotte P. Un cas de kyste leptoméningé post-traumatique [A case of post-traumatic leptomeningeal cyst]. Union Med Can. 1967 Oct;96(10):1214-9. French. PMID: 5601803.

PEYSER E, WEISSBERG D. Post-traumatic arachnoidal cyst. Report of an unusual case. J Neurosurg. 1961 Jul;18:551-3. doi: 10.3171/jns.1961.18.4.0551. PMID: 13735101.


2) , 7) , 10) , 28)

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6)

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13) , 22)

Kitumba D, Mascarenhas L. Rare case of an adult with excruciating headache secondary to post-traumatic fronto-orbital leptomeningeal cyst. Neurochirurgie. 2020 Nov;66(5):410-411. doi: 10.1016/j.neuchi.2020.06.126. Epub 2020 Aug 7. PMID: 32777233.
14)

Sekhar LN, Scarff TB. Pseudogrowth in Skull Fractures of Childhood. Neurosurgery. 1980; 6:285–289
15) , 17) , 21)

Kulkarni AV, Dikshit P, Devi BI, Sadashiva N, Shukla D, Bhat DI. Unusual Complication of a Neglected Growing Skull Fracture. Pediatr Neurosurg. 2021 Feb 24:1-5. doi: 10.1159/000513102. Epub ahead of print. PMID: 33626526.
16) , 25)

Kurosu A, Fujii T, Ono G. Post-traumatic leptomeningeal cyst mimicking a skull tumour in an adult. Br J Neurosurg. 2004 Feb;18(1):62-4. doi: 10.1080/02688690410001660463. PMID: 15040717.
19)

Adeleye AO. Posttraumatic leptomeningeal cyst capsule as a cost-free autograft for its repair: case illustrated technical reports. Neurosurg Rev. 2020 Aug 8. doi: 10.1007/s10143-020-01364-6. Epub ahead of print. PMID: 32772295.
20)

Liu XS, You C, Lu M, Liu JG. Growing skull fracture stages and treatment strategy. J Neurosurg Pediatr. 2012 Jun;9(6):670-5. doi: 10.3171/2012.2.PEDS11538. PMID: 22656261.
23)

Harsh V, Gond PK, Kumar A. Post-Traumatic Diploic Leptomeningeal Cyst with Bilateral Posterior Cranial Fossa Epidural Hygroma: A Management Dilemma? World Neurosurg. 2020 Aug;140:258-261. doi: 10.1016/j.wneu.2020.05.129. Epub 2020 May 21. PMID: 32445897.
24)

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27)

Gupta V, Sinha S, Singh AK, Kumar S, Singh D. Growing skull fracture of ethmoid: a report of two cases. J Craniomaxillofac Surg. 2000 Aug;28(4):224-8. doi: 10.1054/jcms.2000.0141. PMID: 11110154.
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