Abstract: Objective To investigate the surgical access and surgical technique of saddle-nodal meningioma and the treatment results. Methods Retrospective analysis of 25 cases of saddle-nodal meningiomas treated by microsurgery. The tumors ranged in size from 2.5 to 6 cm, and all patients presented with visual loss. All patients underwent craniotomy, unilateral inferior frontal approach in 14 cases, pterygoid point approach in 8 cases, and bilateral frontal transversal fissure approach in 3 cases. The results were 9 cases of Simpson grade I resection, 16 cases of grade II resection, and no surgical death. Postoperative visual acuity improved in 16 cases, no change in 5 cases, and visual acuity decreased in 4 cases. Conclusion With proper surgical access and micro-neurosurgical techniques, most saddle node meningiomas can be completely resected and the patient’s visual acuity can be improved. Keywords meningioma, saddle node, microsurgery In 1899, Steward reported the first case of saddle node meningioma found incidentally during autopsy. In 1916, Cushing performed the first successful total resection of a meningioma of the saddle node. In 1938, Cushing and Eisenhardt reported 24 cases of surgically treated saddle-nodule meningiomas. Saddle-nodal meningiomas are common intracranial tumors, accounting for approximately 5% to 10% of all intracranial meningiomas [1,3,5]. The authors retrospectively analyzed 25 cases of saddle node meningioma admitted to our hospital in the past 2 years and summarized them as follows. Materials and methods 1. General data: 8 male and 17 female cases in this group, aged 36-71 years, average 54.5 years. The disease duration ranged from one month to 84 months. Visual disturbance was the most common first symptom, and all cases showed visual disturbance. 17 patients showed unilateral visual loss, 8 showed bilateral visual loss; 16 cases had uni-temporal visual field defects, 5 cases had typical bilateral temporal visual field defects, 4 cases had normal visual field, and 8 cases had severe visual loss (visual acuity lower than 1 foot and several fingers in front of the eyes). Headache was found in 12 cases. Endocrine function tests were normal in all cases. CT showed occupying lesions in the saddle area, 16 cases with equal density, 9 cases with slightly high density, 5 cases with calcification, 9 cases with osteophytes in the saddle nodes and pterygoid plateau, 17 cases with normal pterygoid saddle, 8 cases with enlargement, and MRI showed equal T1 or slightly long T2 signal with uniform enhancement. Twelve cases were associated with peritumoral cerebral edema, and 21 cases were seen with dural tail sign. The tumor diameter (d) was less than 3 cm in 8 cases, 3 cm < d ≤ 5 cm in 12 cases, and d > 5 cm in 5 cases. 3. Surgical methods: Different surgical approaches were used according to the operator’s surgical experience and tumor size and growth pattern. There were 14 cases of unilateral inferior frontal approach, 8 cases of pterygoid approach and 3 cases of bilateral frontal approach through longitudinal fissure. The cerebrospinal fluid was first released to fully reduce the cranial pressure, and then the tumor base was cut by electrocoagulation to block the blood supply. At this stage, it is important to identify and protect the anterior cerebral artery and anterior communicating artery bilaterally; at the later stage, the tumor below the optic nerve and optic cross and the tumor invading the optic nerve canal are removed. The key at this stage is to identify and protect the pituitary stalk and the penetrating vessels emanating from the medial wall of the internal carotid. The arachnoid membrane covers the surface of important structures such as optic nerve, optic cross and internal carotid artery, so the operation should be performed at the interface between the tumor and the arachnoid layer, which can avoid direct damage to these structures and protect the small penetrating vessels in the arachnoid membrane, which can facilitate the recovery of visual function after surgery. Finally, the basal dura mater was removed and the invaded skull was ground down. All tumors were completely resected, including 9 cases that reached Simpson grade I resection and 16 cases that reached grade II resection, and there was no surgical death. Pathological diagnosis: endothelial cell meningioma in 12 cases, fibroblast type in 8 cases, and mixed type in 5 cases. Postoperative visual acuity improved in 16 cases, no change in 5 cases, and visual acuity was reduced in 4 cases. Postoperatively, 4 cases had different degrees of uveitis, which was controlled by posterior pituitary gland or mydriasis. The postoperative follow-up period was from 2 months to 18 months for 19 patients through outpatient review and telephone contact. 12 cases resumed normal work and life, 5 cases took care of themselves, and 2 cases needed family care. Due to the short follow-up period, no case of tumor recurrence was found. Discussion 1. Clinical manifestations and differential diagnosis The main manifestation of saddle node meningioma is visual dysfunction, and some patients may have headache. Unilateral vision loss accounts for about 68%, bilateral vision loss accounts for 32%, and severe vision loss accounts for about 32%. Visual field defects are often asymmetric and do not always present as bilateral temporal visual field defects [2]. Because saddle-nodule meningiomas and pituitary adenomas have similar clinical and imaging presentations, they are often misdiagnosed with each other. Saddle-nodule meningiomas are isosignal in the T1-weighted phase and high-signal in the T2-weighted phase of magnetic resonance. Meningiomas show markedly uniform enhancement after contrast injection, whereas pituitary adenomas tend to be heterogeneous and mildly enhancing. The small pterygoid saddle, osteophytes, dural caudal sign and identifiable pituitary glands that are disproportionate to the lesion facilitate the accurate diagnosis of meningioma. Pituitary adenomas tend to present with bilateral temporal visual field defects, and a significant number of saddle node meningiomas present with a single temporal visual field defect. Hypopituitarism and hypothalamic dysfunction may also be reported in the literature, but are rare. Hypothalamic glioma has similar visual field changes as saddle-nodal meningioma, but it has obvious symptoms of hypothalamic dysfunction [3]. 2.Microsurgical anatomy The saddle node meningioma originates from the saddle node, optic cross sulcus, pterygoid bone and saddle septum. The saddle node is a tiny bony protrusion on the body of the pterygoid bone, separating the anterior top of the pterygoid saddle from the anterior optic cross sulcus. The saddle septum attaches anteriorly to the anterior bed process and the superior margin of the saddle node, and posteriorly to the posterior bed process and the superior margin of the saddle dorsum, and is on average 8 mm (5-13 mm) long and 11 mm (6-15 mm) wide. This could explain why saddle node meningiomas smaller than 1.5 cm do not produce symptoms unless they originate from the optic foramen. The barrier structures that limit tumor growth in the area of the saddle nodes and septum are: laterally, the internal carotid artery, the posterior communicating artery, and the arachnoid membrane of the carotid pool; anteriorly, the optic nerve and its surrounding arachnoid membrane; posteriorly, the pituitary stalk, funiculus, and Liliequist’s membrane; and superiorly, the optic cross and its arachnoid structures, the end plate, the A1 segment of the anterior cerebral artery, and the anterior communicating artery. Therefore, the only growth pathway of the tumor is to spread above the pterygoid plateau, optic nerve and optic cross [2,3]. As the tumor grows, the arachnoid at the base of the optic cross pool is lifted upward and covers the surface of the tumor. As the tumor continues to grow, it invades adjacent structures, such as the internal carotid artery, the end plate and the interpeduncular pool, and the arachnoid membrane and cerebrospinal fluid form a barrier between the tumor and the neural tissue. Since the optic nerve is fixed to the optic foramen, as the tumor grows, the optic nerve can become angulated and further compressed, and both sides of the optic nerve can be wrapped to different degrees. The internal carotid artery may be displaced laterally, but not as significantly as the optic nerve. The tumor may slowly burrow between the optic nerve and the internal carotid artery and may sometimes encapsulate the internal carotid artery, but the surface of the internal carotid artery is still covered with the arachnoid layer. The anterior artery located dorsal to the optic cross may be stretched by the tumor, and tumors larger than 3.5 cm in diameter may encapsulate the anterior artery. Posteriorly, the tumor may enter the interpeduncular pool and displace the pituitary stalk posteriorly. The tumor does not adhere to the dura mater of the slope and dorsal saddle due to the arachnoid membrane. The tumor can grow forward to the pterygoid plateau. The effect of saddle node meningioma on the visual pathway is different from that of anterior cranial fossa base tumor, the former elevates the optic nerve and the optic cross, the latter has a downward compressive effect [2,4]. There are three main surgical approaches for saddle-nodal meningioma: (1) bilateral inferior frontal approach; (2) unilateral inferior frontal approach; and (3) pterygoid approach. 3.1 Bilateral inferior frontal approach: The advantage is that it can provide a wide and direct view, fully expose the bilateral optic nerve, internal carotid artery and anterior artery, and facilitate the reconstruction of the anterior cranial fossa base. The disadvantages are high trauma, easy damage to the olfactory nerve and frontal cortex, the need to open the frontal sinus, the risk of cerebrospinal fluid leakage and meningitis, and the longest distance to reach the greater saddle area [1,2,3]. 3.2 Unilateral inferior frontal approach: the unilateral inferior frontal approach has no significant advantages, but has more disadvantages. The surgical path is longer than that of the pterygoid point via the lateral fissure; the protruding orbital roof often blocks the surgical field of view, and the frontal lobe brain tissue needs to be excessively stretched for exposure, which is easy to contaminate the brain tissue; the exposure of the ipsilateral optic nerve and the lower part of the internal carotid artery is limited; the olfactory nerve is easily damaged; the frontal sinus needs to be opened, and there is a risk of cerebrospinal fluid leakage and meningitis; the huge tumor often causes the lateral fissure to shift outward, which makes early release of cerebrospinal fluid for decompression difficult and often requires transitional stretching of frontal lobe brain tissue and cause brain tissue damage [2,3,5]. 3.3 Pterygopoint approach: the pterygopoint approach has obvious advantages, including the following aspects: ① the shortest path to the saddle area, which facilitates surgical operation; ② it can fully expose the bilateral optic nerve gap and provide a lateral view through the carotid pool; ③ it facilitates olfactory nerve protection; ④ it does not need to open the frontal sinus, which avoids the risk of cerebrospinal fluid leakage and meningitis; ⑤ early release of cerebrospinal fluid from the lateral fissure pool can fully retract the brain tissue, which facilitates brain tissue protection; ⑥Early confirmation of important structures such as optic nerve and internal carotid artery facilitates intraoperative spatial localization [1,2,3,5]. During the operation, the base of the tumor is cut off by electrocoagulation at the pterygoid plateau and saddle nodes, and this operation is performed in the midline. The tumor above the anterior part of the optic nerve is removed first, and the tumor below the posterior part of the optic nerve is left for later removal. The ipsilateral optic nerve is first confirmed, and the tumor is explored along the medial edge of the ipsilateral optic nerve and the anterior edge of the optic cross toward the contralateral side and removed in pieces until the medial edge of the contralateral optic nerve and the contralateral internal carotid artery are confirmed, avoiding damage to the arachnoid around the optic nerve as much as possible during this procedure [2,4,6]. After the optic nerve and optic cross are revealed, the next step is to begin to separate and resect the tumor above and behind the optic cross. The A1 segment of the ipsilateral anterior cerebral artery is identified first, and the posterior border of the tumor is separated along the A1 segment of the anterior artery and the posterior edge of the optic cross, and the tumor is resected in pieces to expose the anterior communicating artery and the contralateral anterior artery, which may be wrapped around the anterior artery when the tumor is large. Finally, the tumor below the optic nerve and optic cross is removed. As more tumors are removed, there is sufficient surgical space at this stage. The main focus of this stage is to identify and protect the pituitary stalk and the penetrating branches to the optic nerve, optic cross and pituitary gland emanating from the medial wall of the internal carotid artery. During the pterygopoint approach, there is limited exposure of the tumor below the ipsilateral optic nerve and internal carotid artery, which can be resolved by rotating the surgical bed. Small lesions entering the optic canal can be directly separated and resected, while large lesions need to be removed by grinding the anterior bed process and opening the optic canal to remove the lesion [6,7,8]. 5. Prognosis Improvement of visual acuity after surgery for saddle node meningioma accounts for 50-60%, about 17-28% have no change, and 10-25% have deterioration of visual acuity. Tumors larger than 3 cm are less likely to improve visual acuity after surgery. If the tumor diameter is less than 3 cm, the preoperative vision loss is less than 50%, and the symptoms do not last more than 2 years, the patient’s postoperative vision recovery is more likely to be better. The prognosis for visual acuity is poor in tumors invading the optic foramen. The literature reports that the morbidity and mortality rate of saddle node meningioma is 0-7%. With the development of microneurosurgical techniques the morbidity and mortality rate has been significantly reduced and many now report zero morbidity and mortality after surgery mainly due to the poor physical condition of the patient [1,3,9].