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Magnetic resonance imaging (MRI) findings of giant arachnoid granulation. Axial T1-weighted imaging (T1WI) (a) and coronal T2-weighted imaging (T2WI) (b) of the brain revealed a protruding nodular lesion causing compression within the anterior superior sagittal sinus in the midline, showing high signal intensity on T2WI and low intensity on T1WI, similar to that of the cerebrospinal fluid (CSF) signal. Coronal T2WI (b) and enhanced sagittal T1WI (c) showed narrowing with compression of the dural sinus and right-sided displacement of the cortical vein adjacent to the lesion. Enhanced axial T1WI (d) revealed that the cortical vein drained to the frontal pole AG lesion and into the superior sagittal sinus.

Magnetic resonance imaging (MRI) findings of giant arachnoid granulation. Axial T1-weighted imaging (T1WI) (a) and coronal T2-weighted imaging (T2WI) (b) of the brain revealed a protruding nodular lesion causing compression within the anterior superior sagittal sinus in the midline, showing high signal intensity on T2WI and low intensity on T1WI, similar to that of the cerebrospinal fluid (CSF) signal. Coronal T2WI (b) and enhanced sagittal T1WI (c) showed narrowing with compression of the dural sinus and right-sided displacement of the cortical vein adjacent to the lesion. Enhanced axial T1WI (d) revealed that the cortical vein drained to the frontal pole AG lesion and into the superior sagittal sinus.

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Case presentation: A 6-year-old girl complained of diplopia and headache over a 2-week period after sustaining a minor head injury. Her neurological examinations were normal, but visual examination identified bilateral papilledema. Magnetic resonance imaging of the brain revealed a protruding nodular lesion causing compression within the anterior...

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... [1][2][3][4][5] Arachnoid granulations and herniation of cerebral tissue into the venous sinuses have also been reported as rare and benign phenomena, with most patients being asymptomatic. [6][7][8][9][10][11][12][13] We describe the case of a pediatric patient with symptomatic intracranial hypertension from the herniation of ectopic cerebellar tissue into the dural venous sinuses. This resulted in stenosis of the torcula and bilateral transverse sinuses. ...
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BACKGROUND Venous sinus stenosis has been implicated in intracranial hypertension and can lead to papilledema and blindness. The authors report the unique case of a cerebellar transtentorial lesion resulting in venous sinus stenosis in the torcula and bilateral transverse sinuses that underwent resection. OBSERVATIONS A 5-year-old male presented with subacute vision loss and bilateral papilledema. Imaging demonstrated a lesion causing mass effect on the torcula/transverse sinuses and findings of increased intracranial pressure (ICP). A lumbar puncture confirmed elevated pressure, and the patient underwent bilateral optic nerve sheath fenestration. Cerebral angiography and venous manometry showed elevated venous sinus pressures suggestive of venous hypertension. The patient underwent a craniotomy and supracerebellar/infratentorial approach. A stalk emanating from the cerebellum through the tentorium was identified and divided. Postoperative magnetic resonance imaging showed decreased lesion size and improved sinus patency. Papilledema resolved and other findings of elevated ICP improved. Pathology was consistent with atrophic cerebellar cortex. Serial imaging over 6 months demonstrated progressive decrease in the lesion with concurrent improvements in sinus patency. LESSONS Although uncommon, symptoms of intracranial hypertension in patients with venous sinus lesions should prompt additional workup ranging from dedicated venous imaging to assessments of ICP and venous manometry.
... Of the 147 persons with documented gender, GAGs involved 80 (54%) females and 67 (46%) males and were similarly distributed across sex (1.2:1 female-to-male ratio) ( Table 2). The afflicted persons included infants [15], children [10,[16][17][18][19][20], adolescents [17,[21][22][23][24], and adults across a wide age spectrum [10,15,45] (range, 0.33 to 91 years; mean, 43 ± 20 years). Interestingly, one pediatric case was reported by parents since birth [16]. ...
... Diagnosis of GAG on imaging workup (Table S1) was accomplished by visualization of round-to-ovoid, irregular or oblong, unilocular or multilocular cystic-appearing structures with or without internal septations, and with internal CSF-like density or signal intensity and communication with the subarachnoid space on MRI with and/or without contrast [8,13,15,17,19,20,[22][23][24][25][26]28,30,31,[36][37][38][39] (Figure 4A), MR angiogram/venogram [10,23,25,[34][35][36][39][40][41][42], CT with and/or without contrast, or CT angiogram [8,21,25,27,28,31,34,35] ( Figure 4B). GAGs were also identified as well-delineated focal calvarial defects on plain X-ray [13,15] or as focal filling defects within the DVS on conventional angiography and/or on cross-sectional studies [11]. ...
... Several individuals experienced misdiagnosis or delayed diagnosis of GAG [7,22,43,45]. Since symptoms were sometimes initially interpreted as subacute or chronic DVS thrombosis, hypercoagulability workup and medical treatment were initiated to manage symptoms of presumed coagulopathy, infection, or related processes [12,14,19,22,23,25,26,33,35,36,39,41,43]. Patients were treated with acetazolamide [19,32,41,43], NSAID, anticephalgic medication, or other analgesia [12,23,33,34,43], other anticoagulants [22,35,36], antiepileptics [39], furosemide [41], mannitol [41], prednisolone [25], decongestants [14], and/or antibiotics [14,44] (each in 1 to 4 of 169 patients, or <3%). ...
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