- Email: [email protected]
Cranial fasciitis of the petrous temporal bone
Accepted Manuscript Title: Cranial Fasciitis of the Petrous Temporal Bone Author: Thomas M. Fissenden M.Reza Taheri Samantha Easley Ashkan Monfared PII: DOI: Reference:
S0165-5876(14)00282-1 http://dx.doi.org/doi:10.1016/j.ijporl.2014.05.014 PEDOT 7133
To appear in:
International Journal of Pediatric Otorhinolaryngology
Received date: Revised date: Accepted date:
31-1-2014 16-4-2014 7-5-2014
Please cite this article as: Thomas M.Fissenden, M.Reza Taheri, Samantha Easley, Ashkan Monfared, Cranial Fasciitis of the Petrous Temporal Bone, International Journal of Pediatric Otorhinolaryngology http://dx.doi.org/10.1016/j.ijporl.2014.05.014 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Cranial Fasciitis of the Petrous Temporal Bone Thomas M. Fissenden, MD1; M. Reza Taheri, MD, PhD2; Samantha Easley, MD3;
ip t
Ashkan Monfared, MD1 From Division of Otolaryngology – Head & Neck Surgery1, Departments of Radiology2
us
Send Correspondence to:
cr
and Pathology3, George Washington University, Washington, D.C.
Thomas M. Fissenden, MD at the Department of Otolaryngology – Head & Neck
an
Surgery, 2021 K Street NW, Suite 206, Washington, D.C. 20006
M
Phone: 412-576-2094
d
Fax: 202-741- 3382
Ac ce pt e
Email: [email protected] Author Contributions:
All authors contributed equally and extensively to this paper Conflicts of Interest:
We have no conflicts to disclose Word Count: 972
Page 1 of 15
Thomas M. Fissenden, MD1; M. Reza Taheri, MD, PhD2; Samantha Easley, MD3; Ashkan Monfared, MD1 From Division of Otolaryngology – Head & Neck Surgery1, Departments of Radiology2
cr
Send Correspondence to:
ip t
and Pathology3, George Washington University, Washington, D.C.
us
Thomas M. Fissenden, MD at the Department of Otolaryngology – Head & Neck Surgery, 2021 K Street NW, Suite 206, Washington, D.C. 20006
an
Phone: 412-576-2094
M
Fax: 202-741- 3382
d
Email: [email protected]
Ac ce pt e
Author Contributions:
All authors contributed equally and extensively to this paper Conflicts of Interest:
We have no conflicts to disclose Word Count: 1006
Abstract
Page 2 of 15
Cranial fasciitis (CF) is a rare benign neoplastic lesion affecting the pericranium and deep fascia of the scalp. We report a case confined to the temporal bone, resembling a malignant destructive lesion. The mass was identified during myringotomy for recurrent
ip t
unilateral otitis media. Biopsy was consistent with CF, which was partially resected. The patient has remained disease free for 12 months. Due to its rarity, no defined treatment
cr
algorithm for CF exists. Despite aggressive features on radiology, they may respond very
Ac ce pt e
d
M
an
us
well to partial resection.
Page 3 of 15
Introduction: Cranial fasciitis is a histologically indistinguishable subtype of nodular fasciitis first described in 1980 by Lauer and Enzinger.1 Typically, lesions originate from the deep
ip t
fascia of the scalp or periosteum of the cranium and present as a solitary lesion in the
cr
parietotemporal region2. There has been at least one report of a purely intracranial lesion and very few prior cases of cranial fasciitis involving the petrous portion of the temporal
us
bone 2, 3, 4. We present a case of a lesion found to involve the meso and hypotympanum
an
extending to the petrous apex medial and inferior to the petrous carotid. Case Report:
M
A 13-month-old male underwent myringotomy at an outside facility for recurrent unilateral otitis media and was found to have a “red fleshy mass” in the right middle ear
d
space obstructing the opening of the eustachian tube. He had no additional clinical signs
Ac ce pt e
or symptoms resulting from the mass apart from otitis media. CT of the temporal bone was obtained for the initial imaging characterization. The erosions of the inferior aspect of the otic capsule suggested presence of an aggressive tumor (Figure 1). The intimate relationship of this enhancing temporal bone lesion with the petrous segment of the internal carotid artery and the jugular foramen was observed on subsequent MRI (Figure 2). Although these imaging features are not pathognomonic for a particular entity, they supported the presence of an aggressive tumor, with rhabdomyosarcoma being included in the differential. Operative exploration was carried out in two interval procedures, both via a postauricular tympanoplasty approach. These demonstrated a white-tan mass deep to the
Page 4 of 15
edematous, erythemetous mucosa involving the meso and hypotympanum and extending through the hypotympanum to the petrous apex. It was also found to be intimately associated with the carotid artery and the eustachian tube. Due to the aggressive
ip t
characteristics of mass on MRI as well as the limited data available regarding the behavior of these tumors in the temporal bone, a near-total resection of the mass was
cr
carried out in order to increase the likelihood of resolution as well as to ensure patency of
us
the eustachian tube. A micro-doppler was used to trace out the petrous carotid so that only a small residual of tumor was left on the wall of the artery. The ossicles, facial nerve
an
and chorda tympani were completely intact. Follow up imaging at six months and one year post-operatively showed no residual tumor. He was also followed with routine
d
further episodes of otitis media.
M
audiometry, which demonstrated resolution of the eustachian tube dysfunction. He had no
Ac ce pt e
On gross examination the specimen consisted of multiple, friable fragments of pink-white soft tissue. Intraoperative microscopic frozen section examination was consistent with a spindle cell lesion with benign features. Microscopic examination of paraffin-embedded sections showed a cellular
proliferation exhibiting areas of storiform growth in a variably fibrous and hypocellular, myxoid background (Figure 3). The proliferation was composed of spindle-shaped cells with a “tissue culture-like” appearance. The lesional cells have pale basophilic cytoplasm and elongated to ovoid nuclei with dense chromatin and inconspicuous nucleoli. There was no evidence of cytologic pleomorphism or atypical mitotic figures. Portions of the lesion contained hemosiderin and scattered lymphocytes. Foci of extravasated red cells were also present (Figure 4).
Page 5 of 15
By immunohistochemistry, the lesional cells were reactive for smooth muscle actin and vimentin (Figure 5), findings consistent with a myofibroblastic population. Immunohistochemical stains for S-100 and beta-catenin were negative. The morphologic
ip t
appearance and immunophenotype supported a diagnosis of nodular fasciitis, cranial type (cranial fasciitis).
cr
Discussion:
us
Cranial fasciitis is an uncommon clinical entity and its involvement of the temporal bone is usually confined to the external ear. 5 It typically presents in children as
an
a solitary, rubbery mass, most commonly located on the temperoparietal scalp, though they may occur anywhere on the cranium. They characteristically undergo a rapid period
M
of expansion, which eventually stabilizes 1,2. The present case solely involved the temporal bone presenting with eustachian tube obstruction.
d
Histologically the differential diagnosis includes malignant sarcomas
Ac ce pt e
(leiomyosarcoma, fibrosarcoma) and benign lesions such as fibromatosis, dermatofibroma and benign peripheral nerve sheath tumor 6,5. The lack of cellular pleomorphism, herringbone growth pattern and atypical mitoses should assist in separating cranial fasciitis from malignant tumors 6,5. The presence of characteristic morphologic features and the use of pertinent immunohistochemical stains can help to exclude other benign entities.
Radiologically, cranial fasciitis can demonstrate features concerning for more
aggressive processes. They typically appear as an isolated lytic skull lesion, with an accompanying soft tissue mass that enhances with contrast administration 7. These features correlate well with the fact that most lesions originate from the deep fascia of the
Page 6 of 15
scalp with an expansive growth phase. They may demonstrate neo-bone formation and calcifications within the soft tissue component7. They commonly erode the outer calvarium, and have been shown to invade the inner table as well as the dura1. There is
ip t
also at least one case report of a purely intracranial lesion3. The pathogenesis of cranial fasciitis is largely unknown, however, it is thought to
cr
be reactive or inflammatory in nature rather than truly neoplastic 8, 9.
us
Treatment options vary and should be tailored to the individual clinical scenario. In any case, a tissue diagnosis should be formally obtained via a biopsy and histological
an
evaluation. Histopathologic examination is required for definitive diagnosis as clinically cranial fasciitis may mimic an aggressive neoplastic process10. Most cases of cranial
M
fasciitis are self-limiting and are unlikely to recur if completely excised 6, 10. Although, spontaneous regression is not the norm, there has been at least one reported case making
d
an argument for observation in select situations11. Surgical excision is the favored
Ac ce pt e
treatment, however alternative treatment options have been demonstrated, specifically at least one report of full clinical resolution following intralesional corticosteroid injection12. If the lesion is large, disfiguring, intracranial or invading vital structures, surgery may be the more reasonable option. Even lesions that cannot be completely excised due to risk of damage to critical surrounding structures may demonstrate complete clinical regression2. Curettage of the underlying bone may be warranted, as a case of recurrence has been reported 13.
Page 7 of 15
Conflict of interest statement: We, the authors, have no conflicts to report.
ip t
Acknowledgements: We would like to acknowledge Ashley Hill, MD, Chief of the Department of Pathology
cr
at Children’s National Medical Center for her contributions to the pathology section of
Ac ce pt e
d
M
an
us
the paper as well as for providing images of the slides for the paper.
Page 8 of 15
References 1. Lauer DH, Enzinger FM. Cranial fasciitis of childhood. Cancer. 1980 Jan
ip t
15;45(2):401-6. 2. Clapp CG, Dodson EE, Pickett BP, Lambert PR. Cranial fasciitis presenting as an
cr
external auditory canal mass. Arch Otolaryngol Head Neck Surg. 1997 Feb;123(2):223-5.
us
3. Sayama T, Morioka T, Baba T, Ikezaki K, Fukui M. Cranial fasciitis with massive intracranial extension. Childs Nerv Syst 1995; 11: 242–245.
an
4. Pollack IF1, Hamilton RL, Fitz C, Kassam A, Snyderman CH. Congenital reactive myofibroblastic tumor of the petrous bone: case report. Neurosurgery. 2001 Feb;
M
48(2):430-5.
d
5. Thompson LDR, Fanburg-Smith JC, Wenig BM. Nodular fasciitis of the external ear
Ac ce pt e
region: A clinicopathologic study of 50 cases. Ann Diagn Pathol 2001; 5: 191-8. 6. Thompson LDR. Nodular fasciitis. Ear Nose Throat J. 2002; 830. 7. Keyserling HF, Castillo M, Smith JK. Cranial fasciitis of childhood. AJNR Am J Neuroradiol. 2003 Aug; 24(7):1465-7.
8. Sarangarajan R, Dehner, LP. Cranial and extracranial fasciitis of childhood: A clinicopathologic and immunohistochemical study. Hum Pathol 1999; 30(1): 87-92. 9. Bemrich-Stolz CJ, Kelly DR, Muensterer OJ, Pressey JG. Single institution series of nodular fasciitis in children. J Pediatr Hematol Oncol 2010; 32(5):354-357. 10. Hussein MR. Cranial fasciitis of childhood: a case report and review of literature. J Cutan Pathol 2008; 35: 212-214.
Page 9 of 15
11. Adler R, Wong CA. Cranial fasciitis simulating histiocytosis. J Pediatr. 1986 Jul; 109(1):85-8. 12. Lee JY, Kim YC, Shin JH. Cranial fasciitis treated with intralesional corticosteroids.
ip t
Int J Dermatol. 2004 Jun; 43(6):453-5. 13. Sajben FP, Eichenfield LF, O'Grady TC, Cunningham BB. Cranial fasciitis of
us
cr
childhood. Pediatr Dermatol 1999; 16: 232–234.
an
Figure 1: Cranial Fasciitis of the Petrous Temporal Bone. Coronal CT scan of the temporal bone after the administration of intravenous contrast shows erosion of the undersurface of the otic capsule (black arrowhead) by a temporal bone lesion (solid white arrow). The lesion extends to the petrous segment of the internal carotid artery (dashed arrow).
M
Figure 2: Cranial Fasciitis of the Petrous Temporal Bone. MRI shows a temporal bone lesion (arrow) that is isointense to muscle on T1 weighted imaging (A) and mixed signal
d
intensity but predominantly hyperintense to muscle on T2 weighted imaging (B). The
Ac ce pt e
axial time of flight MRA of the head and neck shows the close juxtaposition of the lesion to the proximal portion of the petrous segment of the internal carotid artery and the jugular foramen (C). The lesion does not arise from either the internal carotid artery or the jugular vein (C). The frond-like extension of this homogenously enhancing tumor along the fascial place is evident after the administration of intravenous contrast (D) Figure 3: Cranial fasciitis is composed of spindle cell proliferation, exhibiting areas of storiform growth in a variably fibrous and hypocellular, myxoid background (H&E, 10X, inset 40X). Figure 4: Foci of extravasated erythrocytes are seen between the myofibroblasts (H&E, 40X).
Page 10 of 15
Figure 5: Immunohistochemistry demonstrated cells staining for smooth muscle actin and
Ac ce pt e
d
M
an
us
cr
ip t
vimentin.
Fig. 1.
Page 11 of 15
ip t cr us an
Ac ce pt e
d
M
Fig. 2.
Page 12 of 15
ip t cr us an M d
Ac ce pt e
Fig. 3.
Page 13 of 15
ip t cr us an M d
Ac ce pt e
Fig. 4.
Page 14 of 15
ip t cr us an M d
Ac ce pt e
Fig. 5.
Page 15 of 15
S0165-5876(14)00282-1 http://dx.doi.org/doi:10.1016/j.ijporl.2014.05.014 PEDOT 7133
To appear in:
International Journal of Pediatric Otorhinolaryngology
Received date: Revised date: Accepted date:
31-1-2014 16-4-2014 7-5-2014
Please cite this article as: Thomas M.Fissenden, M.Reza Taheri, Samantha Easley, Ashkan Monfared, Cranial Fasciitis of the Petrous Temporal Bone, International Journal of Pediatric Otorhinolaryngology http://dx.doi.org/10.1016/j.ijporl.2014.05.014 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Cranial Fasciitis of the Petrous Temporal Bone Thomas M. Fissenden, MD1; M. Reza Taheri, MD, PhD2; Samantha Easley, MD3;
ip t
Ashkan Monfared, MD1 From Division of Otolaryngology – Head & Neck Surgery1, Departments of Radiology2
us
Send Correspondence to:
cr
and Pathology3, George Washington University, Washington, D.C.
Thomas M. Fissenden, MD at the Department of Otolaryngology – Head & Neck
an
Surgery, 2021 K Street NW, Suite 206, Washington, D.C. 20006
M
Phone: 412-576-2094
d
Fax: 202-741- 3382
Ac ce pt e
Email: [email protected] Author Contributions:
All authors contributed equally and extensively to this paper Conflicts of Interest:
We have no conflicts to disclose Word Count: 972
Page 1 of 15
Thomas M. Fissenden, MD1; M. Reza Taheri, MD, PhD2; Samantha Easley, MD3; Ashkan Monfared, MD1 From Division of Otolaryngology – Head & Neck Surgery1, Departments of Radiology2
cr
Send Correspondence to:
ip t
and Pathology3, George Washington University, Washington, D.C.
us
Thomas M. Fissenden, MD at the Department of Otolaryngology – Head & Neck Surgery, 2021 K Street NW, Suite 206, Washington, D.C. 20006
an
Phone: 412-576-2094
M
Fax: 202-741- 3382
d
Email: [email protected]
Ac ce pt e
Author Contributions:
All authors contributed equally and extensively to this paper Conflicts of Interest:
We have no conflicts to disclose Word Count: 1006
Abstract
Page 2 of 15
Cranial fasciitis (CF) is a rare benign neoplastic lesion affecting the pericranium and deep fascia of the scalp. We report a case confined to the temporal bone, resembling a malignant destructive lesion. The mass was identified during myringotomy for recurrent
ip t
unilateral otitis media. Biopsy was consistent with CF, which was partially resected. The patient has remained disease free for 12 months. Due to its rarity, no defined treatment
cr
algorithm for CF exists. Despite aggressive features on radiology, they may respond very
Ac ce pt e
d
M
an
us
well to partial resection.
Page 3 of 15
Introduction: Cranial fasciitis is a histologically indistinguishable subtype of nodular fasciitis first described in 1980 by Lauer and Enzinger.1 Typically, lesions originate from the deep
ip t
fascia of the scalp or periosteum of the cranium and present as a solitary lesion in the
cr
parietotemporal region2. There has been at least one report of a purely intracranial lesion and very few prior cases of cranial fasciitis involving the petrous portion of the temporal
us
bone 2, 3, 4. We present a case of a lesion found to involve the meso and hypotympanum
an
extending to the petrous apex medial and inferior to the petrous carotid. Case Report:
M
A 13-month-old male underwent myringotomy at an outside facility for recurrent unilateral otitis media and was found to have a “red fleshy mass” in the right middle ear
d
space obstructing the opening of the eustachian tube. He had no additional clinical signs
Ac ce pt e
or symptoms resulting from the mass apart from otitis media. CT of the temporal bone was obtained for the initial imaging characterization. The erosions of the inferior aspect of the otic capsule suggested presence of an aggressive tumor (Figure 1). The intimate relationship of this enhancing temporal bone lesion with the petrous segment of the internal carotid artery and the jugular foramen was observed on subsequent MRI (Figure 2). Although these imaging features are not pathognomonic for a particular entity, they supported the presence of an aggressive tumor, with rhabdomyosarcoma being included in the differential. Operative exploration was carried out in two interval procedures, both via a postauricular tympanoplasty approach. These demonstrated a white-tan mass deep to the
Page 4 of 15
edematous, erythemetous mucosa involving the meso and hypotympanum and extending through the hypotympanum to the petrous apex. It was also found to be intimately associated with the carotid artery and the eustachian tube. Due to the aggressive
ip t
characteristics of mass on MRI as well as the limited data available regarding the behavior of these tumors in the temporal bone, a near-total resection of the mass was
cr
carried out in order to increase the likelihood of resolution as well as to ensure patency of
us
the eustachian tube. A micro-doppler was used to trace out the petrous carotid so that only a small residual of tumor was left on the wall of the artery. The ossicles, facial nerve
an
and chorda tympani were completely intact. Follow up imaging at six months and one year post-operatively showed no residual tumor. He was also followed with routine
d
further episodes of otitis media.
M
audiometry, which demonstrated resolution of the eustachian tube dysfunction. He had no
Ac ce pt e
On gross examination the specimen consisted of multiple, friable fragments of pink-white soft tissue. Intraoperative microscopic frozen section examination was consistent with a spindle cell lesion with benign features. Microscopic examination of paraffin-embedded sections showed a cellular
proliferation exhibiting areas of storiform growth in a variably fibrous and hypocellular, myxoid background (Figure 3). The proliferation was composed of spindle-shaped cells with a “tissue culture-like” appearance. The lesional cells have pale basophilic cytoplasm and elongated to ovoid nuclei with dense chromatin and inconspicuous nucleoli. There was no evidence of cytologic pleomorphism or atypical mitotic figures. Portions of the lesion contained hemosiderin and scattered lymphocytes. Foci of extravasated red cells were also present (Figure 4).
Page 5 of 15
By immunohistochemistry, the lesional cells were reactive for smooth muscle actin and vimentin (Figure 5), findings consistent with a myofibroblastic population. Immunohistochemical stains for S-100 and beta-catenin were negative. The morphologic
ip t
appearance and immunophenotype supported a diagnosis of nodular fasciitis, cranial type (cranial fasciitis).
cr
Discussion:
us
Cranial fasciitis is an uncommon clinical entity and its involvement of the temporal bone is usually confined to the external ear. 5 It typically presents in children as
an
a solitary, rubbery mass, most commonly located on the temperoparietal scalp, though they may occur anywhere on the cranium. They characteristically undergo a rapid period
M
of expansion, which eventually stabilizes 1,2. The present case solely involved the temporal bone presenting with eustachian tube obstruction.
d
Histologically the differential diagnosis includes malignant sarcomas
Ac ce pt e
(leiomyosarcoma, fibrosarcoma) and benign lesions such as fibromatosis, dermatofibroma and benign peripheral nerve sheath tumor 6,5. The lack of cellular pleomorphism, herringbone growth pattern and atypical mitoses should assist in separating cranial fasciitis from malignant tumors 6,5. The presence of characteristic morphologic features and the use of pertinent immunohistochemical stains can help to exclude other benign entities.
Radiologically, cranial fasciitis can demonstrate features concerning for more
aggressive processes. They typically appear as an isolated lytic skull lesion, with an accompanying soft tissue mass that enhances with contrast administration 7. These features correlate well with the fact that most lesions originate from the deep fascia of the
Page 6 of 15
scalp with an expansive growth phase. They may demonstrate neo-bone formation and calcifications within the soft tissue component7. They commonly erode the outer calvarium, and have been shown to invade the inner table as well as the dura1. There is
ip t
also at least one case report of a purely intracranial lesion3. The pathogenesis of cranial fasciitis is largely unknown, however, it is thought to
cr
be reactive or inflammatory in nature rather than truly neoplastic 8, 9.
us
Treatment options vary and should be tailored to the individual clinical scenario. In any case, a tissue diagnosis should be formally obtained via a biopsy and histological
an
evaluation. Histopathologic examination is required for definitive diagnosis as clinically cranial fasciitis may mimic an aggressive neoplastic process10. Most cases of cranial
M
fasciitis are self-limiting and are unlikely to recur if completely excised 6, 10. Although, spontaneous regression is not the norm, there has been at least one reported case making
d
an argument for observation in select situations11. Surgical excision is the favored
Ac ce pt e
treatment, however alternative treatment options have been demonstrated, specifically at least one report of full clinical resolution following intralesional corticosteroid injection12. If the lesion is large, disfiguring, intracranial or invading vital structures, surgery may be the more reasonable option. Even lesions that cannot be completely excised due to risk of damage to critical surrounding structures may demonstrate complete clinical regression2. Curettage of the underlying bone may be warranted, as a case of recurrence has been reported 13.
Page 7 of 15
Conflict of interest statement: We, the authors, have no conflicts to report.
ip t
Acknowledgements: We would like to acknowledge Ashley Hill, MD, Chief of the Department of Pathology
cr
at Children’s National Medical Center for her contributions to the pathology section of
Ac ce pt e
d
M
an
us
the paper as well as for providing images of the slides for the paper.
Page 8 of 15
References 1. Lauer DH, Enzinger FM. Cranial fasciitis of childhood. Cancer. 1980 Jan
ip t
15;45(2):401-6. 2. Clapp CG, Dodson EE, Pickett BP, Lambert PR. Cranial fasciitis presenting as an
cr
external auditory canal mass. Arch Otolaryngol Head Neck Surg. 1997 Feb;123(2):223-5.
us
3. Sayama T, Morioka T, Baba T, Ikezaki K, Fukui M. Cranial fasciitis with massive intracranial extension. Childs Nerv Syst 1995; 11: 242–245.
an
4. Pollack IF1, Hamilton RL, Fitz C, Kassam A, Snyderman CH. Congenital reactive myofibroblastic tumor of the petrous bone: case report. Neurosurgery. 2001 Feb;
M
48(2):430-5.
d
5. Thompson LDR, Fanburg-Smith JC, Wenig BM. Nodular fasciitis of the external ear
Ac ce pt e
region: A clinicopathologic study of 50 cases. Ann Diagn Pathol 2001; 5: 191-8. 6. Thompson LDR. Nodular fasciitis. Ear Nose Throat J. 2002; 830. 7. Keyserling HF, Castillo M, Smith JK. Cranial fasciitis of childhood. AJNR Am J Neuroradiol. 2003 Aug; 24(7):1465-7.
8. Sarangarajan R, Dehner, LP. Cranial and extracranial fasciitis of childhood: A clinicopathologic and immunohistochemical study. Hum Pathol 1999; 30(1): 87-92. 9. Bemrich-Stolz CJ, Kelly DR, Muensterer OJ, Pressey JG. Single institution series of nodular fasciitis in children. J Pediatr Hematol Oncol 2010; 32(5):354-357. 10. Hussein MR. Cranial fasciitis of childhood: a case report and review of literature. J Cutan Pathol 2008; 35: 212-214.
Page 9 of 15
11. Adler R, Wong CA. Cranial fasciitis simulating histiocytosis. J Pediatr. 1986 Jul; 109(1):85-8. 12. Lee JY, Kim YC, Shin JH. Cranial fasciitis treated with intralesional corticosteroids.
ip t
Int J Dermatol. 2004 Jun; 43(6):453-5. 13. Sajben FP, Eichenfield LF, O'Grady TC, Cunningham BB. Cranial fasciitis of
us
cr
childhood. Pediatr Dermatol 1999; 16: 232–234.
an
Figure 1: Cranial Fasciitis of the Petrous Temporal Bone. Coronal CT scan of the temporal bone after the administration of intravenous contrast shows erosion of the undersurface of the otic capsule (black arrowhead) by a temporal bone lesion (solid white arrow). The lesion extends to the petrous segment of the internal carotid artery (dashed arrow).
M
Figure 2: Cranial Fasciitis of the Petrous Temporal Bone. MRI shows a temporal bone lesion (arrow) that is isointense to muscle on T1 weighted imaging (A) and mixed signal
d
intensity but predominantly hyperintense to muscle on T2 weighted imaging (B). The
Ac ce pt e
axial time of flight MRA of the head and neck shows the close juxtaposition of the lesion to the proximal portion of the petrous segment of the internal carotid artery and the jugular foramen (C). The lesion does not arise from either the internal carotid artery or the jugular vein (C). The frond-like extension of this homogenously enhancing tumor along the fascial place is evident after the administration of intravenous contrast (D) Figure 3: Cranial fasciitis is composed of spindle cell proliferation, exhibiting areas of storiform growth in a variably fibrous and hypocellular, myxoid background (H&E, 10X, inset 40X). Figure 4: Foci of extravasated erythrocytes are seen between the myofibroblasts (H&E, 40X).
Page 10 of 15
Figure 5: Immunohistochemistry demonstrated cells staining for smooth muscle actin and
Ac ce pt e
d
M
an
us
cr
ip t
vimentin.
Fig. 1.
Page 11 of 15
ip t cr us an
Ac ce pt e
d
M
Fig. 2.
Page 12 of 15
ip t cr us an M d
Ac ce pt e
Fig. 3.
Page 13 of 15
ip t cr us an M d
Ac ce pt e
Fig. 4.
Page 14 of 15
ip t cr us an M d
Ac ce pt e
Fig. 5.
Page 15 of 15