Sphenopalatine Foramen

Pathways of Spread

Of course, the pathways of spread of juvenile angiofibroma will influence the choice of the surgical approach (Fig. 8.29).

Owing to its nature, juvenile angiofibroma tends to grow along the paths of least resistance, causing displacement of adjacent soft tissues, rather than invasion. Adherence can be present, particularly when the lesion contacts the dura, but dural or brain infiltration is rare (Danesi et al. 2000; Scholtz et al. 2001).

Its peculiar dual pattern of bone involvement (remodeling and destruction) is likely to result from two different mechanisms of interaction between juvenile angiofibroma and bony structures. Displacement of the periosteal invested cortical surfaces causes remodeling and thinning, with only late breakthrough and destruction, whereas the direct growth of juvenile angiofibroma along perforating arteries into the cancellous root of the sphenoid lets the lesion extend into the medullary content of the sphenoid (floor of sphenoid sinus, greater wing). This could explain why the vidian canal (invested by a periosteal layer), though the closest to the growing lesion, shows more frequently enlargement of its anterior third, rather

Fig. 8.29. Pathways of spread of juvenile angiofibroma. A, extent through the sphenopalatine foramen into the nasal fossa (1) and - via the choana - into the nasopharynx (2); through the erosion of the sphenoid sinus floor into the sphenoid sinus (3). B, extent from the pterygopalatine fossa along the foramen rotundum (actually a groove or a complete bone canal) (4), into the cancellous bone of the greater wing of the sphenoid (5), and into the masticator space (6)

than destruction. Moreover, further posterior extension into the canal is infrequent, and usually observed in advanced lesions.

Due to the knowledge of the elementary interactions of juvenile angiofibroma with surrounding structures and its constant site of origin, the patterns of spread are highly predictable (Lloyd et al. 2000b; Schick and Kahle 2000).

From its site of origin in the pterygopalatine fossa, the juvenile angiofibroma extends medially into the nasal cavity and nasopharynx - the areas of least resistance - via enlargement and erosion of the sphenopalatine foramen. Growth of tumor anteriorly indents the postero-superior maxillary sinus wall, resulting in anterior bowing of the sinusal wall, the so-called antral sign, described by Holman and Miller on lateral plain X-ray (Lloyd and Phelps 1986) (Fig. 8.30) . The lateral extent, via an enlarged pterygo-maxil-lary fissure, gives rise to infratemporal fossa spread. Extension into this space is demonstrated by detecting the "finger-like projections" of the enhancing juvenile angiofibroma characterized by sharp and lobulated margins (Fig. 8.31). In this area, the least resistant structure consists of the fat tissue between the pterygoid muscles, usually splayed.

From the pterygo-maxillary fissure, the lesion can also access the apex of the orbit through the inferior orbital fissure, and further extends into the middle cranial fossa via the superior orbital fissure (Fig. 8.32).

Posterior spread from pterygopalatine fossa is almost certainly the most dangerous for the patient because it enables the juvenile angiofibroma to penetrate the cancellous bone of the root of pterygoid process. From this site, juvenile angiofibroma extends both medially, into the floor of the sphenoid sinus, and laterally, into the greater wing (Lloyd et al. 1999). As the center of growth of the intrasinusal component of juvenile angiofibroma is located at the intersection between the floor and the lateral wall, there is evidence to suggest that the intrasinusal extension comes from the root of the pterygoid, rather than being due to upward extension from the choana. Lateral spread allows the juvenile angiofibroma to replace the diploe of the greater wing, usually with late erosion of the inner table.

The key to detecting the diploic invasion consists of differentiating its medullary content from the lesion on the basis of CT density and MR signal. On CT, this is achieved by the strong enhancement of juvenile angiofibroma within the diploe. On MR, the optimal discrimination is obtained by combining a plain T1 with a post-contrast T1 with or without fat

Sphenopalatine Foramen

Fig. 8.29. Pathways of spread of juvenile angiofibroma. A, extent through the sphenopalatine foramen into the nasal fossa (1) and - via the choana - into the nasopharynx (2); through the erosion of the sphenoid sinus floor into the sphenoid sinus (3). B, extent from the pterygopalatine fossa along the foramen rotundum (actually a groove or a complete bone canal) (4), into the cancellous bone of the greater wing of the sphenoid (5), and into the masticator space (6)

Pterygopalatine Space Boundaries

Fig. 8.30a,b. Juvenile angiofibroma. SE T1 after contrast administration, sagittal plane. a The lesion infiltrates the medullary bone of clivus, the intracranial cortical boundary being detectable only in its inferior part (white opposing arrows). Reactive thickening of the adjacent dura of prepontine cistern (white arrowhead). Submucosal growth along the undersurface of the sphenoid bone is appreciated (black arrows). b The lesion indents the posterior wall of the maxillary sinus, reaches the inferior orbital fissure (black arrows) and spreads along the foramen rotundum (white arrows)

Fig. 8.30a,b. Juvenile angiofibroma. SE T1 after contrast administration, sagittal plane. a The lesion infiltrates the medullary bone of clivus, the intracranial cortical boundary being detectable only in its inferior part (white opposing arrows). Reactive thickening of the adjacent dura of prepontine cistern (white arrowhead). Submucosal growth along the undersurface of the sphenoid bone is appreciated (black arrows). b The lesion indents the posterior wall of the maxillary sinus, reaches the inferior orbital fissure (black arrows) and spreads along the foramen rotundum (white arrows)

Superior Orbital Fissure Axial Few

Fig. 8.31a,b. Juvenile angiofibroma. CT (a) and SE T1 (b) after contrast administration, both in the axial plane. a Finger-like projections of the juvenile angiofibroma grow into the infratemporal fossa. The posterior wall of the maxillary sinus is remodeled and interrupted (black arrows). A small part of the lesion extends posteriorly to the pterygoid plates (into the pterygoid fossa) along the medial pterygoid muscle (white arrows). b The enhancing juvenile angiofibroma occupies the left masticator space (black arrows). Laterally it borders the temporalis muscle, posteriorly it reaches the foramen ovale. An enlarged middle meningeal artery is detected (white arrowheads). Remodeling of posterolateral maxillary sinus wall is seen (white arrows)

Fig. 8.31a,b. Juvenile angiofibroma. CT (a) and SE T1 (b) after contrast administration, both in the axial plane. a Finger-like projections of the juvenile angiofibroma grow into the infratemporal fossa. The posterior wall of the maxillary sinus is remodeled and interrupted (black arrows). A small part of the lesion extends posteriorly to the pterygoid plates (into the pterygoid fossa) along the medial pterygoid muscle (white arrows). b The enhancing juvenile angiofibroma occupies the left masticator space (black arrows). Laterally it borders the temporalis muscle, posteriorly it reaches the foramen ovale. An enlarged middle meningeal artery is detected (white arrowheads). Remodeling of posterolateral maxillary sinus wall is seen (white arrows)

Figure 8.32. Juvenile angiofibroma. Enhanced SE T1 in the coronal plane. The juvenile angiofibroma invades the sphenoid sinus through the floor. A second component reaches the cavernous sinus (white arrows) through the foramen (groove) rotundum, running above the maxillary nerve (arrowhead)

saturation (Fig. 8.33). The latter makes it possible to easily distinguish the hyperintense enhanced juvenile angiofibroma from the suppressed signal of the normal bone marrow. An alternative option to reduce marrow signal on T1 sequences consists of decreasing the TR and selecting thinner sections: while the signal of bone marrow greatly diminishes, juvenile angiofibroma maintains its hyperintensity. Replacement of the cancellous structure of the clivus can be observed in advanced lesions that completely fill the sphenoid sinuses and displace both the lateral walls and the roof.

Juvenile angiofibroma shows two different types of intracranial invasion: extent along a canal, and spread through bone destruction. It is interesting to note that even medium size lesions may gain access into the middle cranial fossa by growing along the foramen rotundum, and running lateral to the cavernous sinus to reach the anterior aspect of the Meckel's cave. Generally, the second pattern occurs when huge lesions break through the inner table of the greater wing or the lateral sphenoid sinus walls. Regardless of the pattern of intracranial access, infiltration of the dura is very rare. In fact, it has been recently reported that even when cross sectional imaging suggests cavernous sinus invasion or internal carotid artery involvement, a dissection plane can

Embolization Angiofibroma

Fig. 8.33. Juvenile angiofibroma. Enhanced SE T1 in the coronal plane. The juvenile angiofibroma completely replaces the cancellous bone of both the left pterygoid root and the greater sphenoid wing. The inferior orbital fissure is reached through a defect of the lateral wall of sphenoid sinus (thin black arrows). Intracranial growth is appreciated along the floor of middle cranial fossa (white arrows). The extracranial component of the lesion invades the infratemporal fossa. The lateral pterygoid muscle is inferiorly displaced (thick black arrows)

Fig. 8.33. Juvenile angiofibroma. Enhanced SE T1 in the coronal plane. The juvenile angiofibroma completely replaces the cancellous bone of both the left pterygoid root and the greater sphenoid wing. The inferior orbital fissure is reached through a defect of the lateral wall of sphenoid sinus (thin black arrows). Intracranial growth is appreciated along the floor of middle cranial fossa (white arrows). The extracranial component of the lesion invades the infratemporal fossa. The lateral pterygoid muscle is inferiorly displaced (thick black arrows)

be found in most cases, making complete removal feasible (Danesi et al. 2000).

8.7.5.2 Angiography

Surgical resection is currently the most widely accepted treatment for juvenile angiofibroma. Due to its high vascularization, surgical removal can sometimes be difficult because of significant intraoperative hemorrhage, resulting in incomplete resection and higher rate of persistence. Pre-operative embolization was introduced in 1972 to obtain lesion devasculariza-tion and facilitate complete excision of the tumor (Roberson et al. 1972). Nowadays, the availability of intra-arterial digital subtraction angiography, micro-catheters, and embolic agents - such as PVA particles - makes superselective embolization of feeders easier and safer (Valavanis and Christoforidis 2000). Though some authors questioned the usefulness of this procedure, as in their experience no significant difference in surgical bleeding was observed, there is increasing evidence that embolization is a safe and effective method to reduce intra-operative blood loss (Siniluoto et al. 1993; Moulin et al. 1995; Li et al. 1998). Nevertheless, the shrinkage of lesion achieved by embolization has been indicated as a contributory cause to incomplete excision of juvenile angiofibroma by McCombe et al. (1990).

At present, the role of angiography is to provide a detailed map of feeders, demonstrating the recruitment of internal carotid artery, vertebral or contralateral external carotid artery branches, and to obtain preoperative devascularization.

According to Lasjaunias et al. (1980), the angio-graphic findings of juvenile angiofibroma consist of moderate enlargement of feeding arteries, intense "parenchymal" blush, absence of large arteriovenous shunts, or early venous return (Fig. 8.34).

The pattern of arterial feeders recruited is predictable in most cases. It is strictly related to the pathways of spread, but not to the actual size of the lesion, though most large lesions are multi-compartmental. In our experience of 15 patients treated by exclusive endonasal excision, there was no correlation between the volume of juvenile angiofibroma and the number of feeding vessels (Nicolai et al. 2003). However, recruitment of internal carotid artery, vertebral branches was significantly more frequent among lesions with several external carotid artery feeders. Notably, though internal carotid artery feeders

Angiofibromas Picture

Fig. 8.34a,b. Juvenile angiofibroma. Enhanced SE T1 in the coronal plane (a); intra-arterial DSA (b). a On MR, the lesion shows a prevalent endoluminal growth within the nasopharynx. Upwards extension in the pterygoid root and within the sphenoid sinus is also appreciated. b DSA demonstrates vascular feeders arising from the distal part of the sphe-nopalatine artery; a more prominent blush is observed at the level of the nasal part of the lesion b a

Fibroma Juvenile Dsa

Fig. 8.35a,b. Juvenile an-giofibroma. Enhanced SE T1 in the sagittal plane (a); intra-arterial DSA (b). a The lesion fills the sphenoid sinus. Infiltration of the clivus is demonstrated by the encroachment of both its cortical layers and replacement of the medullary content. b DSA demonstrates the several subtle feeders from the internal carotid artery, not embolized b

Fig. 8.35a,b. Juvenile an-giofibroma. Enhanced SE T1 in the sagittal plane (a); intra-arterial DSA (b). a The lesion fills the sphenoid sinus. Infiltration of the clivus is demonstrated by the encroachment of both its cortical layers and replacement of the medullary content. b DSA demonstrates the several subtle feeders from the internal carotid artery, not embolized b a were demonstrated in approximately 47% of cases (Fig. 8.35), intracranial extent was present only in 13%.

During the last decade the availability of small particles and microcatheters has made it possible to reach even peripheral small branches of the external carotid artery, preserving adjacent normal vessels from being devascularized by the more proximal occlusion obtained by Gelfoam or Spongel embolization (Fig. 8.36). In fact, the goal of embolization is to achieve vessel occlusion at the capillary level. Consequently, polyvinyl-alcohol particles with a minimal size of 150 pm have been suggested, as significant arteriovenous shunts have been demonstrated for particles of 50 pm or less by nuclear medicine techniques (Schroth et al. 1996).

The rate of minor and major complications for embolization of external carotid artery branches is negligible, approximately 4% (Ungkanont et al. 1996).

It is evident that the major challenge to angiog-raphy regards the management of juvenile angio-fibroma vascularization by internal carotid artery feeders. Advanced lesions with intracranial extent have been successfully excised after pre-operative embolization of external carotid artery branches with acceptable blood loss, despite involvement of the internal carotid artery branches in the blood supply. Devascularization by direct tumor puncture and embolization, advocated by Casasco et al. (1999), entails an unacceptable risk of major neurologic complications. Balloon occlusion and sacrifice of the internal carotid artery is required in rare cases (Casasco et al. 1999).

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  • AMALDA
    What causes an enhancing lesion of the foramen rotundum?
    7 years ago

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