Tissue damage in herniated brain parenchyma into giant arachnoid granulations: demonstration with high resolution MRI

Abstract

Background

Brain herniation (BH) into arachnoid granulation has been remarkable in recent years.

Purpose

To evaluate the damage in herniated parenchyma into the giant arachnoid granulation (GAG) and to investigate the clinical–demographic importance of this damage.

Material and Methods

Patients with BH into GAG were retrospectively included in the study. Each of the patients had at least one high-resolution 3D magnetic resonance imaging (MRI) sequence. The arachnoid granulation dimensions, locations, and origin of herniated parenchyma were evaluated by two experienced radiologists. The demographic and symptomatic features of the patients were recorded from the hospital database.

Results

A total of 27 patients (21 females, 6 males; age range 6–71 years; mean age 41.3 years) were found to contain BH into GAG. It was most commonly seen in the transverse sinus (67%); the origin was most common in the cerebellar parenchyma (56%). Abnormal signal and morphology were detected in herniated parenchyma in 11 (47%) patients, atrophy in six, and atrophy and gliosis in five. The most common complaints were headache (47%), while other frequent symptoms were vertigo (15%) and blurred vision (11%). There was a statistically significant positive correlation between frequency of damage in herniated brain parenchyma and the maximal size of GAG (P<0.05).

Conclusion

In patients with BH into GAG, parenchymal damage may be associated with various symptoms, such as headache and vertigo, although they have not been statistically proven. It is important to carefully evaluate hernia tissue, as the risk of tissue damage may increase in larger GAGs.

Keywords

Giant arachnoid granulation brain herniation high-resolution magnetic resonance imaging

Introduction

Arachnoid granulations, which are hypertrophied arachnoid villi, are the pocket formation of cerebrospinal fluid (CSF) into the dural sinuses. They are usually detected randomly in the transverse and superior sagittal sinus, where they are most common (1,2). When their size exceeds 1 cm, they are referred to as giant arachnoid granulations (GAG) (3 –5).

Brain herniation (BH) into arachnoid granulation is a rare condition (0.32%) that has attracted attention recently (6,7), and its physiopathology has not yet been fully revealed. Some authors argue that pre-existing arachnoid granulation creates weakness in the dural structure and herniation occurs with fluctuations in intracranial pressure (8). In the experimental study performed on rats and new-world monkeys, it has been shown that BH into arachnoid granulation is reversed with reduced intracranial pressure (9). However, the occurrence of BH in cases without symptoms of pressure increase revealed the controversy that this situation may also develop spontaneously (10 –12).

Although it is generally asymptomatic clinically, it can cause symptoms such as headaches and tinnitus. Symptoms have been shown mostly in protrusions towards the temporal bone mastoid fragment and are thought to be secondary to erosion and leakage of cerebrospinal fluid (CSF) (7,8,13,14).

While conventional magnetic resonance imaging (MRI) sequences can easily detect arachnoid granulation, they may be unable to determine its content. In recent years, especially with the advances in high-resolution MRI techniques, the anatomical structure can be determined with much more accuracy. Thus, it was seen that BH was more frequent than previously thought. By using volumetric three-dimensional (3D) high-resolution MR images, besides the brain parenchyma, the presence of damage can be easily observed (15 –17).

In a recent retrospective study, Battal et al. (7) evaluated the presence of incidental brain herniations into the dural venous sinuses or calvarium with high-resolution T1-weighted (T1W) or T2-weighted (T2W) MR sequences. Nevertheless, the authors did not specifically examine parenchymal damage in arachnoid granulation and evaluated both small and giant arachnoid granulation. In our daily practice, we have rarely observed parenchymal damage in GAG patients with BH in patients using volumetric 3D high-resolution cerebral MRI sequences. Thus, the aim of the present study was to demonstrate herniated tissue damage in GAG patients with BH and to investigate their relationship with symptoms and demographic features. To the best of our knowledge, this is first study that specifically demonstrates herniated tissue damage in GAG with volumetric 3D high-resolution MRI sequences and its clinical results.

Material and Methods

Patients

We included consecutive patients who underwent brain MRI in our hospital between January 2015 and February 2017 in this retrospective study. Approval was received for the present study from our institutional review board. It was a retrospective review of medical records and written informed consent was not required.

During the aforementioned period, we obtained a list of patients with arachnoid granulation in the radiology reports from our institution’s database. Images of the patients were examined by two radiologists, with 13 and 5 years of experience, respectively. All patients had 3D high-resolution MR images as well as conventional MR sequences. Patients with a lesion > 1 cm and meeting the standard arachnoid granulation diagnostic criteria were identified. Subsequently, patients with brain parenchymal herniation into GAG in question were included in the study. At the same time, information was obtained from our hospital database about the patients’ symptoms. Among the exclusion criteria were those who had surgery before and had artifacts affecting evaluation. No patient had pathological correlation.

MRI technique

Studies were performed on a 3-T MR scanner (Magnetom Skyra; Siemens Healthcare, Erlangen, Germany) using standard head coils. All MR studies started with the localizer and continued with conventional sequences consisting of axial spin-echo (SE) T1, coronal and sagittal turbo spin-echo (TSE) T2, axial fluid-attenuated inversion recovery (FLAIR), pre-contrast 3D T1 magnetization prepared rapid gradient echo (MPRAGE), and post-gadolinium (0.1 mmol/kg) 3D T1 acquisitions. All of patients had 3D-sampling perfection with the application of optimized contrasts using different flip angle evolution (SPACE) sequences. Routine MRI sequence parameters are listed in Table 1. In addition, constructive interference in steady-state (CISS), phase-sensitive T1 inversion recovery imaging, contrast-enhanced MR venography (CE-MRV), and susceptibility weighted imaging (SWI) were available in some cases. A workstation was used to create multi-plane images from high resolution 3D T1W and T2W datasets.

Table 1.

3-T MR scanner imaging sequence parameters.

Sequence	TR/TE (ms)	Inversion time (ms)	Flip angle (°)	Slice thickness (mm)	FOV (mm)
SE T1	450/8	–	–	4	256 × 182
TSE T2	3100/90	–	–	4	256 × 182
FLAIR	10 000/120	2000	–	4	256 × 182
3D T1 MPRAGE	15/8	300	15	1.25	256 × 256
3D T2 SPACE	3200/400	–	Variable	1	256 × 256

FLAIR, fluid attenuation inversion recovery; FOV, field of view; SE, spin-echo; TE, echo time; TR, rotation time; TSE, turbo spin-echo.

Imaging analysis

High-resolution monitors and a communication system (Syngo Via console, software v. 2.0; Siemens Medical Solutions, Erlangen, Germany) were used to examine all cerebral MR images. Analysis of all patients with BH to GAG was done by two experienced radiologists with consensus. In each case, the mean diameter and location of the arachnoid granulation were recorded first. Then, the origin and location of the brain herniation were noted. Signal characteristics of herniated parenchyma were examined and the presence of atrophy (sulcal or folia dilatation) or atrophy and gliosis (hyperintensity on T2W images) was evaluated for each case carefully.

Statistical analysis

For descriptive statistics, percentage (%) and median data values were used for discrete data and continuous data, respectively. SPSS version 20 software (SPSS for Windows; SPSS, Chicago, IL, USA) was used for performing the statistical analysis. The Chi-square test in categorical data groups and the independent samples t-test were used for the comparison of continuous variables with normal distributions, and the Mann–Whitney U and Kruskal Wallis tests were used for the data that did not conform to normal distributions in the Kolmogorov–Smirnov test. P values < 0.05 were considered statistically significant.

Results

As a result of the MR studies that were retrospectively analyzed, 27 patients with BH into GAG were included in the study (21 female, 6 males; age range = 6–71 years; mean age = 41.3 years). The demographic data of the patients are presented in Table 2.

Table 2.

Demographic data of the patients with GAG.

Patient no.	Age (years)	Sex	Location of GAG	Origin of BH	Longest size of GAG (mm)	Damage of BH	Symptoms	Accompany AG
1	38	F	Transverse sinus	Cerebellum	11	Atrophy	Vertigo	Single
2	33	F	Transverse sinus	Temporal Lobe	10	No	No	No
3	16	F	Transverse sinus	Temporal Lobe	16	No	No	No
4	55	F	Occipital intraosseous	Occipital Lobe	42	Atrophy + gliosis	Vertigo	No
5	55	M	Transverse sinus	Temporal Lobe	12	No	Headache	No
6	37	F	Transverse sinus	Temporal Lobe	12	Atrophy	Other symptoms	Single
7	38	M	Straight sinus	Cerebellum	10	No	No	Single
8	14	F	Transverse sinus	Occipital Lobe	15	Atrophy	Blurred vision	No
9	35	M	Transverse sinus	Temporal Lobe	17	No	Headache	Multiple
10	6	M	Transverse sinus	Temporal Lobe	15	Atrophy + gliosis	Headache	No
11	53	F	Transverse sinus	Cerebellum	14	No	Blurred vision	Multiple
12	27	F	Transverse sinus	Cerebellum	18	Atrophy + gliosis	Headache	Multiple
13	60	M	Transverse sinus	Cerebellum	28	No	Vertigo	Multiple
14	65	F	Occipital intraosseous	Cerebellum	18	Atrophy	Headache	Single
15	46	M	Sigmoid sinus	Cerebellum	10	No	Headache	Multiple
16	29	F	Transverse sinus	Cerebellum	10	No	No	No
17	42	F	Occipital intraosseous	Cerebellum	18	Atrophy + gliosis	Vertigo	Multiple
18	32	F	Transverse sinus	Occipital Lobe	11	No	Headache	Single
19	47	F	Occipital intraosseous	Cerebellum	16	No	Other symptoms	No
20	47	F	Sigmoid sinus	Temporal Lobe	18	No	Other symptoms	No
21	37	F	Transverse sinus	Temporal Lobe	10	No	Blurred vision	No
22	39	F	Transverse sinus	Cerebellum	18	Atrophy	Headache	Multiple
23	47	F	Transverse sinus	Cerebellum	18	Atrophy + gliosis	Headache	Single
24	45	F	Transverse sinus	Temporal Lobe	12	No	No	No
25	71	F	Sigmoid sinus	Cerebellum	11	No	Other symptoms	Multiple
26	57	F	Occipital intraosseous	Cerebellum	17	Atrophy	Headache	Multiple
27	44	F	Transverse sinus	Cerebellum	17	No	Headache	No

AG, arachnoid granulation; BH, brain herniation; GAG, giant arachnoid granulation.

All patients had conventional MR sequences as well as T1 MPRAGE and high-resolution T2 SPACE images. No patient had more than one BH into GAG detected. Of the 27 patients, seven had additional cranial pathologies such as meningioma (n = 1), small vessel disease (n = 4), and non-specific white matter plaque (n = 2). GAGs were located differently among the patients: 18 (67%) were located in the transverse sinus; 5 (19%) occipital intraosseous; 3 (11%) sigmoid; and 1 (3%) straight sinus. The dimensions of GAG in the longest axis were in the range of 10–42 mm (mean = 15 mm). The accompanying arachnoid granulation was detected in a total of 15 (56%) patients: two in six patients; and multiple in nine patients. No significant relation was found between arachnoid granulation dimensions nor between herniation origin and gender (P > 0.05).

The origin of brain herniation was determined as the cerebellum in 15 (56%) patients, temporal lobe in 9 (33%), and occipital lobe in 3 (11%). Eight (53%) cerebellar herniations were protruded to the transverse sinus, 4 (27%) of them were into occipital bone, 2 (13%) were in the sigmoid sinus, and 1 (7%) was in the straight sinus (Fig. 1). While only 1 (11%) temporal herniations was in the sigmoid sinus (Fig. 2), the others were observed in the transverse sinus. Of the occipital lobe herniations 2 (67%) were localized in the transverse sinus and one was in the occipital intraosseous location.

Fig. 1.

A 38-year-old asymptomatic male patient: axial oblique (a) and sagittal oblique (b) high-resolution 3D T2 SPACE MRI sequence show herniation (frames) of the right superior cerebellar folia into the straight sinus. There is no damage of the herniated parenchyma. Post-contrast dynamic MR venography (c) reveals protrusion (frame) of the GAG into the straight sinus. GAG, giant arachnoid granulation; MRI, magnetic resonance imaging.

Fig. 2.

A 34-year-old male patient with suspected convulsion: coronal (a), sagittal (b), and axial (c) phase-sensitive T1 inversion recovery MR images show herniation (frames) of the normal temporal gyrus into the GAG the in left sigmoid sinus. GAG, giant arachnoid granulation; MRI, magnetic resonance.

Damage in herniated parenchyma was seen in 11 (41%) patients. Ten (91%) of the subgroups were female (average age = 21 years). In six of them, there was only atrophy, and in five patients, atrophy and gliosis (Figs. 3 and 4) were identified. The origins of damaged BH were the cerebellum in 7 (64%) patients, the occipital lobe in 2 (18%) patients, and the temporal lobe in 2 (18%) patients. In the statistical analysis, a significant relationship was found between GAG size and damage of herniated parenchyma (P = 0.03). As the GAG size increased, the frequency of damage increased. The rate of parenchymal damage was more common in women with BH compared to men. However, there was no statistically significant relationship between parenchymal damage and gender (P = 0.12). According to the information obtained, the males were more symptomatic (83%) and the most common accompanying symptom was headache in 11 (41%) patients. In addition, four of the patients had dizziness, three had blurred vision, and four had other complaints. While 11 (50%) of the symptomatic patients had atrophy or gliosis, five patients who were asymptomatic had no BH damage. No significant difference was found between BH damage and symptoms (P = 0.34). Only three of the patients with additional cranial pathologies were symptomatic, and they experienced a headache.

Fig. 3.

A 55-year-old female patient with headache: axial (a), coronal (b), and sagittal (c) plane high-resolution 3D T2 SPACE and axial FLAIR (d) MR images show intraosseous parenchymal herniation (frames) of the right occipital gyrus into occipital GAG. There is parenchymal atrophy with gliosis (blue arrowheads). GAG, giant arachnoid granulation.

Fig. 4.

A 47-year-old female patient with headache: coronal plane high resolution 3D T2 SPACE (a), coronal plane high resolution 3D T1 MPRAGE (b), and axial plane FLAIR sequence (c) show herniation (frames) of the atrophic and gliotic left cerebellar folia into the GAG the in left transverse sinus. Post-contrast dynamic MR venography 3D MIP image (d) reveals a filling defect (frame) of the GAG in the left transverse sinus. GAG, giant arachnoid granulation; MIP, maximum intensity projection; MR, magnetic resonance.

Discussion

BH into arachnoid granulation is a rare condition, although it may become noticeable with the use of high-resolution MR techniques. Evaluation of the imaging findings of herniated parenchyma into arachnoid granulation is very low in the literature (15,16,18). To the best of our knowledge, there have been no other studies that have specifically evaluated the relationship between damage of herniated parenchyma into GAG and its clinic effect. The authors of this article concentrate purely on the high-resolution 3D MR image features of herniated parenchyma into GAG.

The most common location of GAG with parenchymal herniation was the transverse sinus (67%), and the cerebellar parenchyma was the most common herniated tissue (56%). These findings are supported in other studies (7,17). In a MRI study of 38 patients, multiple arachnoid granulations with BH were found in 58% of cases (18). In another imaging study, multiple arachnoid granulation accompanying arachnoid granulation with BH were detected in 4/21 patients (15). In our cases, 15 (56%) of the patients were accompanied by another arachnoid granulation. However, there was no parenchymal herniation in these areas. Although additional arachnoid granulation was found in 52% of female patients and 67% of male patients, no relationship was established with gender.

Although it has generally been understood that arachnoid granulation did not occur in early childhood and occurred with age, there is evidence of child cases in the literature (18 –20). In the present study, three patients were aged < 18 years. In two of these patients, herniated parenchymal damage was detected. One had only atrophy, the other had atrophy and gliosis, and both were symptomatic. No correlation was found between the patient’s age and parenchymal damage.

Damage in herniated parenchyma can occur as a result of different pathophysiological processes separately or together. One of them is tethering of the parenchyma by bridges between the piamater-arachnoid membranes in the herniated sac. At the same time, damage can occur as a result of the restriction in the vessels passing through the classical herniated neck, that is, strangulation. In addition, inflammatory processes can increase the occurrence of damage by causing fibrosis (15). One of the important findings of the present study is that it determines the relationship between GAG size and risk of BH damage. As the size of the GAG increases, the risk of parenchymal herniation damage increases. This can be explained by the greater tethering effect in larger arachnoid granulations. However, the neck size of the arachnoid granulation and the herniated parenchyma size are also important factors beyond the arachnoid granulation size for the tethering effect. Because of the retrospective nature of the present study, we could not specifically evaluate the herniated parenchyma size and the neck size of the arachnoid granulation. A prospective study with a larger number of patients and utilizing well-defined selection criteria and histopathologic correlation is necessary to fully evaluate the reliability of this theory.

Malekzadehlashkariani et al. (18) performed an imaging study with 68 patients with BH and identified atrophy and/or gliosis in 31 (46%) cases. All of the damaged parenchymal herniation’s originated from cerebellar parenchyma and no supratentorial origin has been reported. They did not find a significant relationship between symptoms and parenchymal damage. However, they emphasized that in the case of seizures, there may be supratentorial gliosis at the microscopic level. In another study performed by Liebo et al. (15), 21 brain parenchymal hernias were detected in 16 patients; of them, 7 (33%) had abnormal signals in the herniated parenchyma. Although two of the cases were supratentorial, the damage was only shown in the cerebellar parenchyma. In the literature, damage of the supratentorial parenchymal hernia has been demonstrated in two case studies. One of them was shown incidentally in the parietal lobe, and no association with the patient’s symptom was detected (21). In another study, spastic progressive paresis of his left lower limb due to damage in the frontal lobe herniation was shown (22). In the present study, damage of the herniated parenchyma into GAG was seen in 41% of cases. All these patients were symptomatic, with blurred vision and vertigo in occipital patients and headache and other symptoms in temporal ones. Because the blurred vision and vertigo are not specific to occipital lobe lesions, we searched the hospital database to determine whether the ophthalmologic examination results were consistent with primary occipital visual cortex damage, but no ophthalmologic examination results could be found for the patient. The most commonly associated symptom in previous studies is headache, although this is not statistically significant. In the present study, headache was most frequently accompanied symptom, and it was noteworthy that there was an existing symptom in all patients with herniated parenchymal injury. In other symptomatic cases, the reason for the absence of damage may be due to its microscopic level. The symptomatology and the clinical significance of this entity have been reported controversially and the argument still continues in the literature. The presented symptoms, especially headache, may be associated with other accompanied pathologies or incidental. To clarify this, further studies with high-resolution imaging and pathological correlation are required in the larger case group.

Arachnoid granulation is accepted as an incidental detected finding in approximately two-thirds of the individual performed conventional MR sequences (23,24). MRI plays an important role in differential diagnosis, especially with thrombus and mass as well as guiding the surgeon before the operation.

The widespread use of high-resolution MR techniques in the future may also indicate that parenchymal herniation and parenchymal damage within arachnoid granulations are much more prevalent than previously thought (7,17). In this case, different views may arise in terms of the appropriate treatment approach, especially in symptomatic cases. Patients who are asymptomatic despite showing parenchymal damage in MRI may not be followed until they exhibit symptoms. However, in symptomatic cases associated with parenchymal injury, follow-up and surgical decompression may be required.

The present study has some limitations. First, there was no pathological confirmation of any patient. Therefore, neither confirmation could be performed in cases where damage was detected in MRI nor was it possible to determine whether there was a microscopic pathology in the undamaged patients and its possible relationship with symptoms. Second, all retrospective studies have inherent limitations. Clinical features of patients and MRI indications were obtained from hospital records. Third, patients did not have follow-up MR images. Therefore, it was not possible to see if the damage occurred in symptomatic patients or if the damage developed with the change in GAG size. Finally, the FLAIR sequence is the most useful sequence for detection of the parenchymal damage and gliosis. Because our routine brain MR protocol does not have a volumetric thin section (1 mm) FLAIR sequence, we used a thick (4–5 mm) sequence parameter in this retrospective study. Therefore, we may have missed some gliotic signal changes. Moreover, although we have a volumetric thin section T2 SPACE sequence for all the patients, T2W sequences may be misleading for the determination of the gliotic signal.

In conclusion, in cases where GAG contains brain parenchyma, tissue damage such as atrophy and gliosis can be seen. This damage can be determined at almost any age and may be associated with various symptoms, though unproven. The most common accompanying symptom is headache, but it may vary depending on the location where the damage occurred. The fact that the risk of damage increases as the arachnoid granulation size increases is especially important in terms of symptoms and possible treatment-follow-up that may arise in these patients. The use of high-resolution MRI techniques in the differential diagnosis and follow-up of these patients is much more valuable and reliable.

Footnotes

Declaration of conflicting interests

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

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iDs

Hayri Ogul

Mecit Kantarci

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