An olfactory groove meningioma is a skull-base meningioma arising from the cribriform plate and frontoethmoidal dura of the anterior cranial fossa. It grows between the frontal lobes, causes progressive frontal lobe compression, and often presents with anosmia, personality changes, cognitive decline, visual impairment, and massive bifrontal edema. These tumors frequently cause hyperostosis of the cribriform plate and can extend inferiorly into the ethmoid sinuses or superiorly into the interhemispheric fissure.
Their slow growth leads to late diagnosis, often when large.

 

Q. What are the key anatomical structures relevant to olfactory groove meningiomas?

 

Anterior Cranial Fossa Anatomy

Floor formed by frontal bone, cribriform plate, and planum sphenoidale.

The cribriform plate houses olfactory fila and forms the site of dural attachment for most OGMs.

The crista galli is a midline projection to which falx attaches; hyperostosis here is common.

The ethmoid labyrinth and sinuses lie just below, important for risk of CSF leak.

 

Vascular Relationships

The anterior cerebral arteries (ACAs) run along the interhemispheric fissure.

Tumor typically displaces ACAs laterally. The A2 segments and pericallosal arteries can be splayed across the superior pole. Recurrent artery of Heubner may be at risk during devascularization.

 

Frontal Lobe Considerations

OGMs compress the basal medial frontal lobes causing behavioral/personality changes. They often induce extensive vasogenic edema, due to venous compression and pial invasion.

 

Olfactory Apparatus

Olfactory nerves run from nasal mucosa through the cribriform foramina to olfactory bulbs. Small tumors may allow unilateral preservation via pterional or unilateral subfrontal route. Large tumors typically destroy both bulbs, producing irreversible anosmia.

 

Venous Drainage

The anterior superior sagittal sinus and frontal bridging veins drain the medial frontal lobes. Retraction injury or venous sacrifice increases risk of edema or venous infarct.

 

Optic Apparatus

Large OGMs may compress optic nerves/chiasm anteriorly or inferiorly.

Can cause visual decline via mass effect or vasogenic edema.

 

Q. Is embryology relevant in the development of olfactory groove meningiomas?

 

Only indirectly. OGMs arise from meningothelial cells associated with neural crest; derived dura of the anterior cranial base and mesodermal components of the cribriform plate. Embryologically, the anterior skull base forms from a combination of prechordal mesoderm and neural crest cells, which explains the tendency of meningiomas in this region to produce hyperostosis and invade bone.

 

Q. How common are olfactory groove meningiomas?

 

OGMs account for 8–13% of all intracranial meningiomas (Al-Mefty).

More common in middle-aged to elderly women, consistent with general meningioma epidemiology.

Present later than other skull base tumors because symptoms are subtle and slowly progressive.

Can reach giant sizes (>4–6 cm) before diagnosis.

 

Q. What are the key pathological features of olfactory groove meningiomas?

 

Most OGMs are WHO Grade 1, meningothelial or transitional types.

Tend to produce hyperostosis of underlying bone due to tumor infiltration or reactive osteoblastic activity. Microscopic invasion of dura and bone is common. Pial invasion is associated with increased edema.

 

Q. What is the WHO 2021 integrated classification’s relevance to OGMs?

 

Most OGMs remain Grade 1, unless atypical features present:

High mitotic index

Brain invasion

Necrosis

Sheeting architecture

 

Molecular markers:

NF2 mutations are less common than convexity tumors.

TERT promoter mutation or CDKN2A/B deletion upgrades tumor to Grade 3.

SMO and AKT1 mutations seen in anterior skull base meningiomas.

 

Q. What is the typical origin and growth pattern of OGMs?

 

Originate from cribriform plate, frontoethmoidal region, falcine dura anteriorly. Grow symmetrically upward, expanding between the frontal lobes (“butterfly pattern”). May extend downward into the ethmoid sinuses or nasal cavity. Frequently extend posteriorly into interhemispheric fissure.

 

Q. What are the classic presenting symptoms?

 

Olfactory Impairment

Anosmia or hyposmia is the earliest symptom.

Often unnoticed by the patient.

 

Behavioral and Cognitive Changes: Frontal lobe compression causes:

Apathy

Disinhibition

Personality change

Impaired judgment

Memory decline

Often misdiagnosed as psychiatric or degenerative conditions.

 

Visual Symptoms:

Due to compression of optic nerves/chiasm.

May present with blurred vision, decreased acuity, field defects.

 

Headache: Common, due to mass effect or edema.

Seizures: Less common than in convexity tumors, but possible if extension to frontal cortex present.

 

Large Tumor Presentation:

Gait disturbance

Incontinence (frontal lobe syndrome)

Features of increased intracranial pressure

 

Q. Why do OGMs cause such marked frontal lobe edema?

 

Mechanisms include:

Venous outflow obstruction from compression of frontal bridging veins.

Pial invasion altering blood–brain barrier.

Mass effect on medial frontal lobes.

Hyperostotic bone pressing on dura and venous channels.

Extensive edema correlates with postoperative recovery challenges.

 

Q. What findings on examination may suggest an OGM?

 

Complete anosmia.

Frontal release signs (grasp, snout reflex).

Apathy, impaired executive function.

Optic disc pallor if chronic compression is present.

Rarely, proptosis from anterior extension.

 

Q. What are the classic radiologic features of an olfactory groove meningioma on CT and MRI?

 

CT typically shows a midline anterior skull-base mass arising from the cribriform plate with hyperostosis of the olfactory groove or crista galli. Bone infiltration is common and may extend into ethmoid sinuses. Calcification may be present. MRI demonstrates an extra-axial lesion with a broad dural attachment, isointense signal on T1 and T2, and homogeneous contrast enhancement. A dural tail may be present. Prominent bifrontal vasogenic edema out of proportion to tumor size is characteristic. Tumor may elevate and laterally displace the anterior cerebral arteries, and may compress the optic apparatus posteriorly.

 

Q. What MRI findings help distinguish OGMs from other anterior skull-base meningiomas?

 

OGMs typically arise from the midline cribriform plate and therefore show symmetrical bifrontal displacement, lateral splaying of the ACAs, and early involvement of olfactory bulbs. Tuberculum sellae meningiomas elevate the chiasm and displace ACAs superiorly rather than laterally. Planum sphenoidale meningiomas extend posteriorly toward the chiasm earlier than OGMs. Prominent frontal lobe edema is more pronounced in OGMs due to venous congestion and pial invasion.

 

Q. How does an OGM appear on angiography when performed?

 

Angiography shows a mass with primary feeders from the anterior and posterior ethmoidal arteries (branches of the ophthalmic artery). There may be tumor blush or early venous filling. ACAs are displaced laterally. Preoperative embolization is rarely helpful because of ophthalmic artery risk.

 

Q. What imaging signs help predict the risk of postoperative edema or venous infarction?

 

Severe preoperative bifrontal edema, compression or distortion of frontal draining veins, invasion of pial surfaces, and hyperostosis causing venous obstruction all increase postoperative edema risk. Large tumors with tight interhemispheric corridors also predispose to venous congestion after devascularization.

 

Q. What is the differential diagnosis of an anterior cranial fossa mass in this region?

 

Differential diagnoses include planum sphenoidale meningioma, tuberculum sellae meningioma, esthesioneuroblastoma (especially when there is intranasal extension with cystic superior poles), sinonasal carcinoma with intracranial extension, metastatic lesions, and large olfactory neuroepitheliomas. Arachnoid cysts and dermoids are rare differentials but may appear anteriorly.

 

Q. How do you differentiate OGM from esthesioneuroblastoma on imaging?

 

Esthesioneuroblastoma often shows a dumbbell-shaped mass through the cribriform plate with enhancement in both nasal cavity and anterior cranial fossa and may have peripheral cysts at the intracranial margin. OGMs are entirely dural-based with hyperostosis and lack the multilobulated appearance. Esthesioneuroblastoma may enhance heterogeneously and invade the nasal cavity more aggressively.

 

Q. What are the principles of management for olfactory groove meningiomas?

 

Management depends on tumor size, symptoms, and radiologic progression. Small, asymptomatic tumors may be observed. Symptomatic tumors, especially those causing personality change, visual decline, or significant edema, require surgical resection. Surgery aims for gross total removal including involved dura and hyperostotic bone. Approach selection depends on tumor size, height, lateral extension, olfactory preservation goals, and surgeon experience.

 

Q. When is observation appropriate in a patient with OGM?

 

Observation is appropriate for elderly or frail patients with small, minimally symptomatic lesions, especially if anosmia already exists and the tumor is slow-growing. Regular MRI surveillance every 6 to 12 months is required. Significant growth or new cognitive deficits prompt reconsideration for surgery.

 

Q. When is surgery clearly indicated?

 

Surgery is indicated for symptomatic tumors causing personality change, seizures, visual deficits, significant edema, or mass effect. Surgery is also indicated for tumors extending inferiorly through the cribriform plate with risk of CSF leak or infection, or for patients with progressive radiologic enlargement.

 

Q. What are the main surgical options for OGM and what factors influence the choice of approach?

 

Major approaches include bifrontal subfrontal (bicoronal), unilateral subfrontal or pterional/orbitofrontal, and extended endoscopic endonasal (EEA). 

Choice depends on tumor size, height above planum, lateral extension, vascular encasement, olfactory preservation goals, bone involvement, sinus extension, and surgeon expertise.

Bifrontal approach is preferred for large midline tumors, tumors with significant lateral extension, and tumors with hyperostosis requiring bone removal.

Pterional/orbitofrontal approach is useful for unilateral or moderately sized tumors where unilateral olfaction may be preserved.

EEA is used for midline tumors with predominant inferior extension, minimal lateral spread, and when early devascularization and avoidance of brain retraction are priorities.

 

Q. What are the advantages of the bifrontal (bicoronal) subfrontal approach?

 

This approach provides excellent midline exposure, allows early access to tumor base and devascularization, facilitates bilateral frontal lobe decompression, allows removal of hyperostotic bone, and supports complete reconstruction of the anterior skull base. It is ideal for giant tumors. Both ACAs and their branches are well visualized from above.

 

Q. What are the disadvantages of the bifrontal approach?

 

It requires significant frontal lobe retraction, increases risk of venous injury to frontal bridging veins, may worsen postoperative edema, and commonly violates the frontal sinus, increasing risk of CSF leak. It sacrifices remaining olfaction if present. The large exposure increases operative time and potential blood loss.

 

Q. What are the advantages of the unilateral subfrontal or pterional/orbitofrontal approach?

 

This approach reduces brain retraction, especially when combined with extradural anterior clinoidectomy or orbitotomy. It allows potential unilateral olfactory preservation, provides early access to ipsilateral feeding vessels, and avoids frontal sinus entry if the incision is placed carefully. It is excellent for small to medium tumors with asymmetric extension.

 

Q. What are the disadvantages of the pterional/orbitofrontal approach?

 

Exposure of the contralateral side is limited. Superior extension beyond the falx may be difficult to reach. Large midline tumors may result in blind spots. Hyperostotic bone cannot be widely removed without converting to a larger exposure. Contralateral ACA branches may not be fully visualized.

 

Q. What are the advantages of the extended endoscopic endonasal approach (EEA)?

 

EEA provides a direct midline, brain-retraction-free route with early devascularization at the skull-base dura. It avoids manipulation of frontal lobes and venous structures, reducing edema. It allows aggressive removal of hyperostotic bone and reconstruction from below. It is ideal for tumors with inferior extension through ethmoid sinuses.

 

Q. What are the disadvantages or limitations of EEA?

 

It carries a higher risk of postoperative CSF leak, requires extensive reconstruction of the skull base, and may not permit complete resection of lateral tumor components beyond the medial orbit or optic nerves. Vascular control may be more limited than with transcranial routes. Very large or superiorly projecting tumors may not be fully accessible.

 

Q. When do you choose bifrontal over pterional or EEA?

 

A bifrontal approach is chosen for giant midline tumors, tumors with significant lateral expansion, those with superior extension into interhemispheric fissure, when wide removal of hyperostotic bone is needed, or when bilateral ACA visualization is necessary. It is also chosen when the tumor rises significantly above the planum and is not accessible from below.

 

Q. When is EEA superior to open approaches?

 

EEA is superior when the tumor is midline, relatively flat against the skull base, has significant inferior extension, and does not extend far laterally beyond the medial orbital walls. It is also advantageous when avoidance of frontal lobe retraction is a priority, particularly in patients with severe preoperative edema.

 

Q. How do you manage hyperostosis in OGMs?

 

Removal of hyperostotic bone is essential to reduce recurrence risk. In bifrontal approaches, the hyperostotic crista galli and involved cribriform plate are drilled away. Reconstruction is required to prevent CSF leak. In EEA, hyperostotic bone is drilled directly from below while preserving vascularized mucosa for reconstruction.

 

Q. How do you manage the frontal sinus if violated during a bifrontal approach?

 

The sinus is exenterated, mucosa fully removed, and nasofrontal ducts obliterated. Fat graft packing or pericranial flap is used to isolate the sinus from the intracranial space. Proper sealing reduces risk of postoperative CSF leak or mucocele formation.

 

Q. How will you perform a bifrontal (bicoronal) subfrontal approach for an olfactory groove meningioma?

 

I will position the patient supine with the head elevated, slightly extended, and secured in a three-pin fixation device. I will avoid excessive extension to protect venous drainage. I will mark and infiltrate a bicoronal incision behind the hairline, elevate the scalp flap anteriorly, and preserve a generous vascularized pericranial flap for skull-base reconstruction. I will expose the frontal bone down to the orbital rims.

 

I will perform a bifrontal craniotomy extending from one temporal line to the other, staying above the frontal sinus if possible. If the frontal sinus is entered, I will exenterate the mucosa, pack the cavity with fat, and prepare it for obliteration later. I will remove the anterior skull base bone overlying the crista galli and drill hyperostotic bone to expose the tumor attachment. I will open the dura in a curvilinear fashion and protect the frontal veins.

 

I will gently elevate the frontal lobes with minimal retraction, using gravity and CSF drainage from the lumbar drain if needed. I will identify the tumor capsule and begin internal decompression using bipolar cautery and suction. Once the tumor softens, I will progressively debulk it toward the base, preserving arachnoid planes around the ACAs and their branches.

 

I will devascularize the tumor early by coagulating its dural base along the cribriform plate and frontoethmoidal dura. I will dissect the tumor from the medial frontal lobes, preserving pial surfaces. I will carefully follow the capsule toward the interhemispheric fissure and across the midline to free both sides symmetrically.

 

When I reach the inferior extension, I will separate the tumor from the nasal mucosa while maintaining watertight dural margins. I will drill all hyperostotic bone and remove the crista galli completely. I will remove any tumor extension into the ethmoid sinuses if accessible from above.

 

After confirming complete resection, I will reconstruct the anterior skull base using the pericranial flap, securing it over the defect to prevent CSF leak. I will close the dura primarily or with a graft, replace the bone flap, secure it with titanium plates, and close the scalp in layers.

 

Q. What are the key advantages of the bifrontal approach during surgery?

 

The bifrontal approach gives me wide midline exposure, allows symmetrical access to both frontal lobes, permits removal of hyperostotic bone, gives direct access to the tumor base for early devascularization, and allows full visualization of both A2 segments. It is ideal for giant tumors or those with significant bone invasion.

 

Q. What are the main risks during the bifrontal approach?

 

I must protect the frontal bridging veins, avoid aggressive frontal lobe retraction, prevent venous infarction, handle the frontal sinus meticulously, and manage large dead space after removal. I must be careful around A2 branches, especially Heubner. Postoperative edema is a significant concern due to manipulation of swollen frontal lobes.

 

Q. How will you perform a pterional/orbitofrontal approach for olfactory groove meningioma?

 

I will position the patient supine with the head rotated 30 degrees away from the side of approach and slightly extended. I will perform a standard frontotemporal (pterional) incision, elevate the scalp, and dissect the temporalis muscle inferiorly. I will fashion a pterional craniotomy and flatten the sphenoid wing with drilling. If needed, I will remove part of the orbital roof or perform a small orbitotomy to increase anterior exposure.

 

I will open the dura in a curvilinear fashion and use CSF drainage from the sylvian fissure to relax the brain. I will gently retract the frontal lobe posteriorly and medially to expose the olfactory groove region from one side. I will identify the ipsilateral olfactory tract and bulb, preserving them when possible. I will expose the tumor capsule from the anteromedial direction.

 

I will begin by devascularizing the tumor base as much as possible from the ipsilateral side. I will internally debulk the tumor to collapse the capsule and gradually mobilize it from the medial frontal lobe, falx, and ACAs. I will follow the tumor across to the contralateral side by working under the falx, limiting excessive traction.

 

As I progress, I will detach the tumor from the cribriform plate region and carefully separate it from the nasal mucosa. I will drill any accessible hyperostotic bone. I will remove the tumor completely as long as the contralateral capsule is reachable without excessive traction. I will achieve meticulous hemostasis and close the dura Watertight.

 

I will replace the bone flap, secure the orbitotomy if performed, and close the wound in layers.

 

Q. How will you perform an endoscopic endonasal approach (EEA) for an olfactory groove meningioma?

 

I will position the patient supine with the head slightly elevated and in slight extension. I will work with a binarial endoscopic four-hand technique. I will laterally outfracture the middle turbinates and perform a wide sphenoethmoidectomy to expose the skull base from lamina papyracea to lamina papyracea.

 

I will identify the cribriform plate, planum sphenoidale, and fovea ethmoidalis. I will elevate mucosa and drill the bone of the cribriform plate, removing hyperostotic bone until dura is exposed widely. I will create a large dural opening over the tumor base, allowing early devascularization of the feeding vessels from the anterior and posterior ethmoidal arteries.

 

I will debulk the tumor centrally using suction and ultrasonic aspirator, then work circumferentially to detach it from the frontal lobes while maintaining the arachnoid plane. I will follow the tumor superiorly until the capsule releases into the anterior cranial fossa. I will protect the ACAs and their branches by maintaining traction-free dissection from below.

 

I will address lateral extensions as far as anatomically safe without compromising optic nerves or medial orbits. I will remove hyperostotic bone completely and clear any tumor invading the ethmoid sinuses.

I will reconstruct the skull base using a multilayer technique with fascia, fat graft, and a vascularized nasoseptal flap to ensure a watertight seal. I will use lumbar drainage selectively.

 

Q. What are the intraoperative limitations of EEA?

 

Lateral and superior extensions may be inaccessible, vascular control is limited compared to craniotomy, reconstruction requires expertise, and CSF leak risk is higher. Tumors encasing ACAs are not ideal for this approach.

 

Q. What are the important intraoperative principles across all approaches?

 

I will debulk first, detach later. I will protect frontal veins to reduce edema. I will minimize frontal lobe retraction and use CSF drainage for relaxation. I will maintain arachnoid planes around ACAs and Heubner. I will devascularize early by addressing the dural base. I will remove the hyperostotic bone to reduce recurrence. I will ensure a watertight skull-base reconstruction.

 

Q. What is the role of adjuvant radiotherapy in olfactory groove meningiomas?

 

Adjuvant radiotherapy is recommended when subtotal resection is performed, when the tumor shows atypical or malignant features, or when molecular findings such as TERT mutation or CDKN2A/B deletion upgrade the tumor’s biological risk. Fractionated radiotherapy or stereotactic radiosurgery can control residual disease effectively, especially along the skull base or in locations where resection is unsafe. For WHO Grade 1 tumors with gross total resection, radiotherapy is not routinely required.

 

Q. When is stereotactic radiosurgery preferred for OGMs?

 

Stereotactic radiosurgery is preferred when the residual tumor is small, well circumscribed, not compressing the optic apparatus closer than tolerance limits, and situated along the skull base or in lateral extensions not amenable to EEA or reoperation. It is particularly useful for recurrent smaller lesions and in medically fragile patients.

 

Q. What factors increase the likelihood of recurrence?

 

Residual hyperostotic bone, incomplete dural removal, aggressive histologic features, pial invasion, atypical or malignant pathology, and molecular alterations such as TERT mutation or CDKN2A/B deletion increase recurrence risk. Tumors invading the sinuses or extending beyond safe surgical corridors also exhibit higher recurrence rates.

 

Q. How do you manage recurrence after initial subtotal resection?

 

Management includes radiologic surveillance for early detection of growth. If the recurrent tumor is small and accessible, reoperation may be performed with careful attention to prior scar tissue and vascular displacement. Radiosurgery or fractionated radiotherapy is often preferred to avoid additional morbidity. Molecular profiling may guide prognosis and follow-up intensity.

 

Q. What are the common postoperative complications after resection of olfactory groove meningiomas?

 

Complications include CSF leak, frontal lobe edema, venous infarction, anosmia, meningitis, seizures, hemorrhage, visual deterioration, and frontal syndrome with behavioral changes. Craniotomy-related complications include infection, wound healing issues, and sinus-related problems such as mucocele formation. EEA-specific complications include CSF leak and sinonasal morbidity.

 

Q. Why is postoperative edema frequently seen after OGM surgery?

 

The frontal lobes are often edematous preoperatively due to venous congestion and pial invasion. Surgical manipulation, retraction, or venous injury worsens edema. Postoperative venous outflow obstruction and the collapse of frontal lobes after tumor removal also contribute. Adequate venous preservation and slow decompression help mitigate edema.

 

Q. How do you prevent CSF leak during anterior skull-base surgery?

 

I will perform meticulous dural closure, remove all hyperostotic bone to achieve clean margins, and use a vascularized pericranial flap for reconstruction in bifrontal approaches. In EEA, I will use multilayer reconstruction with fascia, fat, and a vascularized nasoseptal flap, supported by tissue sealants and temporary lumbar drainage when necessary.

 

Q. How do you manage postoperative CSF leak?

 

Initial measures include lumbar drainage and head elevation. Persistent leaks require re-exploration of the repair or reinforcement with additional grafts. In EEA leaks, endoscopic revision with flap reinforcement is preferred. Antibiotic coverage and monitoring for meningitis are essential.

 

Q. What are the visual complications after OGM surgery and why do they occur?

 

Visual complications may include decreased acuity or field deficits due to optic nerve manipulation, vascular compromise, or edema postoperatively. Excessive traction on the frontal lobes or inadequate decompression of the optic apparatus may worsen vision. Rarely, postoperative hemorrhage can affect the chiasm or optic nerves.

 

Q. What neurocognitive changes may occur after surgery?

 

Temporary cognitive slowing, apathy, or impaired executive function may persist due to preoperative compression or postoperative edema. Gradual improvement occurs in most patients. Permanent deficits are associated with large tumors, prolonged compression, or venous infarction.

 

Q. What is the prognosis after resection of olfactory groove meningiomas?

 

Prognosis is excellent for WHO Grade 1 tumors when gross total resection is achieved. Long-term control rates exceed 85 to 90 percent. Cognitive recovery depends on preoperative severity and venous preservation. WHO Grade 2 or 3 tumors have higher recurrence rates and require closer surveillance and adjuvant therapy.

 

Q. What factors predict favorable surgical outcomes?

 

Smaller tumor size, minimal edema, preserved venous structures, complete dural and bone removal, and WHO Grade 1 histology predict good outcomes. Early diagnosis before significant frontal-lobe compression also improves cognitive recovery. Skilled skull-base reconstruction reduces complications.

 

Q. How do you structure follow-up after OGM surgery?

 

I will obtain an immediate postoperative MRI within 48 to 72 hours to assess resection extent. For WHO Grade 1 tumors with gross total resection, yearly MRI for 5 years is appropriate. If residual tumor is present or histology shows atypia, imaging every 6 months for the first 2 years is recommended, followed by annual scans. WHO Grade 3 tumors require imaging every 3 to 4 months initially.

 

Q. What special considerations are needed in elderly patients?

 

Elderly patients may present with significant frontal-lobe dysfunction that mimics dementia. Edema tolerance is lower, and venous injury is more dangerous. Minimally invasive approaches or observation may be appropriate for small tumors. Reconstruction strategies must account for frailty and wound healing.

 

Q. What clinical pearls help reduce morbidity in OGM surgery?

 

I will prioritize venous preservation, minimize frontal retraction, perform early devascularization, and avoid rapid decompression of tense frontal lobes. I will remove the hyperostotic bone thoroughly to prevent recurrence. I will handle the frontal sinus meticulously and construct a robust skull-base repair. I will anticipate edema and tailor postoperative care accordingly.

 

Recalls:

 

OGMs classically present with anosmia, personality change, and large bifrontal edema.
CT shows hyperostosis; MRI shows a midline extra-axial mass displacing ACAs laterally.
Bifrontal approach is ideal for giant midline tumors requiring extensive bone removal.
Pterional approach may preserve unilateral olfaction and avoid frontal sinus violation.
EEA avoids brain retraction and offers early devascularization for midline tumors.
Hyperostotic bone removal is essential to reduce recurrence.
CSF leak prevention relies on meticulous multilayer skull-base reconstruction.
Cognitive recovery depends heavily on edema control and venous protection.
WHO 2021 markers like TERT mutation determine prognosis and adjuvant needs.
Long-term MRI surveillance is key, especially after STR or atypical histology.